General Flashcards
fiid use
What is the equation for oxygen delivery (DO2)?
What is the equation for arterial oxygen content (CaO2)?
The equation for oxygen delivery (DO2) is…
DO2 (mL/min) = Q × CaO2
Where Q is the cardiac output and CaO2 is the arterial oxygen content.
The equation for arterial oxygen content (CaO2) is…
CaO2 (mL O2/dL) = (1.34 × Hb × SaO2) + (0.0031 × PaO2)
Where Hb is the hemoglobin concentration, SaO2 is the arterial oxygen saturation, and PaO2 is the arterial oxygen tension.
Oxygen dissolved in arterial blood (0.003 x PaO2) raises the total value by only a small amount. If PaO2 is increased, there is little change in CaO2 and it is therefore considered of little significance by most when determining oxygen content. Optimizing Hgb amount is one way to ensure maximal oxygen content.
Each gram of normal Hb can bind ~1.34 mL of oxygen.
According to Henry’s law, the amount of dissolved oxygen is related to the partial pressure of oxygen and the solubility coefficient. The solubility coefficient of oxygen is 0.003 mL O2/dL/mm Hg, so the amount of oxygen dissolved in the plasma is 0.003 mL O2/dL/mm Hg × PaO2.
What is the Fick Principle?
The Fick principle
The Fick equation [CO = VO2 / (CaO2 – CvO2)] can be used to calculate cardiac output on the basis of total oxygen consumption divided by the differences between arterial and mixed oxygen content. This makes it a more accurate measure of cardiac output than simply measuring heart rate or blood pressure.
CO = VO2 / (CaO2 – CvO2)
CaO2= (1.34 x hgb x SaO2) + (0.003 x PaO2)
VO2 (total uptake of oxygen consumption into the blood; measured by the difference between inhaled and expired oxygen)
CaO2 (arterial oxygen content, measured off a systemic artery)
CvO2 (venous oxygen content, measured off the pulmonary artery)
Calculating oxygen saturation from an ABG and a mixed venous gas provides the gradient between arterial and venous oxygen content.
EXAMPLE:
CO = (200 mL/min) / (140 mL O2/L blood – 100 mL O2/L blood)
CO = 200/40 = ~5 L/min
Equation for SVR
SVR = (MAP - RAP) / CO x 80
Typically, CVP is substituted for RAP.
The conversion factor “80” is used to change units from “mm Hg/L/min” to “dynes x sec/cm^5.”
MAP = (SBP + 2DBP)/3 or MAP= DP + 1/3 (PP)
Equation for MAP
MAP = (SBP + 2DBP)/3
or
MAP= DP + 1/3 (PP)
MAP = (CO x SVR) +CVP
Equation for PVR
PVR= 80 (MPAP-PAOP) /CO
MPAP (Mean pulmonary arterial pressure)
PAOP (pulmonary artery occlusion pressure)
The conversion factor “80” is used to change units from “mm Hg/L/min” to “dynes x sec/cm^5.”
NOTE:
LA pressure or LVEDP can be used instead of PAOP.
Pulmonary Artery Occlusion Pressure (PAOP) can be used as a proxy for _.
Pulmonary Artery Occlusion Pressure (PAOP) can be used as a proxy for LVEDP.
Describe LaPlace’s law as it pertains to myocardial wall tension.
T = Pr/2h
T = wall tension
P= Pressure
r = radius
h= thickness
For PPV or SVV to be valid for the prediction of fluid responsiveness, various conditions must be met:
For PPV or SVV to be valid for the prediction of fluid responsiveness, various conditions must be met:
* Mechanical ventilation with positive pressure ventilation at 8-10 mL/kg tidal volume (NOT spontaneously breathing patients)
* PEEP of ≥ 5 cm H20
* Regular cardiac rhythm
* Closed thoracic cavity with normal intrathoracic pressures
* Normal intra-abdominal pressure
Fluid responsiveness can be viewed as an increase in stroke volume or cardiac output after a fluid bolus. Accurate predictors of fluid responsiveness in patients who are being treated with mechanical ventilation include systolic and pulse pressure variation and stroke volume variation. The greater the variation of the systolic pressure and pulse pressure with positive pressure breaths while mechanically ventilated, the more likely the patient will respond to volume administration with an increase in cardiac output or stroke volume. Minimal to absent pulse pressure variation with respiration indicates that the patient may not have a hemodynamic response to volume resuscitation.
Negative Pressure Pulmonary Edema
Causes:
Risk factors:
Pathophysiology:
Signs/symptoms:
Treatments:
Negative Pressure Pulmonary Edema
Causes: upper airway obstruction [eg. laryngospasm (#1), bitting of ETT]
Risk factors: airway obstruction, young, fit, men, otolaryngology surgery
Pathophysiology: exaggerated negative intrathoracic pressure increases RV return and pulmonary hydrostatic pressure causing pulmonary edema, also increases LV afterload worsening pulmonary edema, mechanical stress from breathing against a closed glottis induces breaks in the alveolar epithelial and pulmonary microvascular membranes resulting in increased pulmonary capillary permeability
Signs/symptoms: Absence of breath fog, suprasternal and supraclavicular retractions, paradoxical chest and abdomen movements (abdominal breathing), loss of ETCO2/volumes, hypoxia, pink/frothy sputum, bilateral fluffy pulmonary infiltrates on CXR
Treatments: relieve obstruction, PPV (via ETT or CPAP), FiO2 100%, +/- diuretics
NOTE:
Triggering stimuli within the larynx tend to be more potent when preexisting inflammation of the upper airway is present such as patients with severe GERD or recent URI.
What are causes of overdampening seen on an arterial line trace?
Overdampening is caused by factors that increased resistance within the tubing or increase compliance of the tubing.
* Blood clot
* Air bubble
* Addition of stop cocks
* Thin tubing
Overdampening is seen on a trace as a loss of dicrotic notch and flattened waveform. Systolic blood pressure will be underestimated. Diastolic pressure will be overestimated. MAP will remain accurate.
Fix by flushing line if clot, pulling back to remove air, and removing stopcocks or an extra length of tubing.
CBF increases linearly with PaCO2 between ____ to ___ mm Hg
CBF increases linearly with PaCO2 between 20 to 80 mm Hg.
Beyond 80 mm Hg, CBF tends to plateau.
NOTE:
CO2 readily cross the blood-brain barrier while H+ ions do not. Respiratory acid-base derrangement (ie respiratory acidosis) have a greater affect on CBF than metabolic acid-base derrangements (ie metabolic acidosis).
CBF increases 1-2cc/100mg/min for each 1mmHg increase of PaCO2.
CBF changes in response to CO2 are not sustained. After 6-8hrs the CSF will compensate by excreting bicarbonate.
In healthy adults, CBF is autoregulated with respect to MAP between a MAP range of ____ to _____ mm Hg.
In order to maintain adequate cerebral oxygenation, CBF undergoes extensive regulation in the human body.
In healthy adults, CBF is autoregulated with respect to MAP between a MAP range of 50 to 150 mm Hg.
NOTE:
The cerebral autoregulation curve is right-shifted in chronic hypertension. Long term antihypertensive therapy can reverse the right shift towards a normal cerebral autoregulation curve.
Define controlled hypotension.
Controlled hypotension is defined as a reduction of the systolic blood pressure to 80-90 mm Hg, a reduction of mean arterial pressure (MAP) to 50-65 mm Hg or a 30% reduction of baseline MAP.
Increases in brain activity lead to local increases in cerebral metabolic rate (CMR), which leads to proportional changes in cerebral blood flow (CBF). This relationship is referred to as ________________________.
Increases in brain activity lead to local increases in cerebral metabolic rate (CMR), which leads to proportional changes in cerebral blood flow (CBF). This relationship is referred to as flow-metabolism coupling
Hypoxia has minimal effect on CBF above tensions of _______, but below that level CBF rises dramatically.
Hypoxia has minimal effect on CBF above tensions of 50 mm Hg, but below that level CBF rises dramatically.
NOTE:
Compared to PaCO2, PaO2 has much less of an effect on CBF.
What methods are used for neurologic monitoring during carotid endarterectomies?
Neurologic monitoring in a patient undergoing carotid endarterectomy (CEA) is primarily utilized to promptly identify changes in cerebral blood flow (CBF) to prevent brain hypoperfusion while a carotid artery is clamped. This monitoring is utilized to guide both surgical interventions (e.g. carotid shunt placement) and the maintenance of anesthesia (e.g. increasing cerebral perfusion pressure).
Monitoring modalities that are most often used to detect these changes in CBF include electroencephalogram (EEG), somatosensory-evoked potentials (SSEP), transcranial Doppler (TCD), and cerebral oximetry.
EEG is often thought of as the “Gold Standard” for the detection of electrical brain activity perturbations attributed to decreases CBF during CEA. This arises from studies in the 1970s that validated EEG against the true gold standard of CBF measurement, 133Xe radiotracer washout method. While these studies demonstrated that EEG was adequate to detect regional changes in CBF, because of the extremely low incidence of intraoperative stroke, no prospective study has validated EEG to reduce the incidence of stroke during CEA. Controversy abounds regarding the use of EEG during CEA especially when it is the practice of a surgeon to place a carotid shunt in all patients prophylactically. It is further complicated by the fact that the majority of the studies validating EEG in this role utilized a full 16-channel EEG, while in practice a 4 channel (2 per hemisphere) EEG is utilized for simplicity of monitoring. While sensitivity and specificity of detecting intraoperative cerebral injury both approached 100% in a 16 channel EEG, these were slightly less when a 4 channel EEG was utilized. Regardless, this monitor reflects a functional assessment of brain electrical activity and is utilized routinely to detect regional decreases in CBF and guide therapy during CEA.
SSEPs generally remain intact until CBF decreases to under 15 mL/100 g/minute. This is an additional monitor that has been shown to have a similar clinical efficacy to EEG when selective shunting (shunting patients undergoing CEA when intraoperative evidence of cerebral hypoperfusion arises) is utilized. Also, as the SSEP signal is averaged over minutes instead of instantaneously as in EEG, SSEPs may have a lower failure rate than EEG, but clinically these two monitoring modalities are very similar. Where controversy regarding the clinical efficacy of EEG exists in preventing the development of intraoperative cerebral injury, even fewer outcome data exist to guide the use of this monitoring modality in CEA.
TCD monitoring utilized ultrasonography to most often image the MCA by obtaining a view window through the thin temporal bone. Utilizing the Doppler effect, the flow velocity of red blood cells in the MCA can be approximated. Because this is an ultrasound monitor, atherosclerotic emboli burden can be quantified by counting the number of high-intensity transient signals (HITSs) that the highly echogenic emboli generate as they pass through the plane of the ultrasound Doppler. The use of this monitoring modality makes two major assumptions regarding CBF. First is that the velocity of blood flow correlates with CBF, and second is that increasing the embolic burden increases the likelihood of cerebral injury. The first assumption here regarding Doppler flow velocity and CBF is controversial, with many data both supporting and criticizing this claim, but the second has been borne out in multiple studies. If utilized, TCD flow velocity reductions of greater than 50% are generally thought to be an indicator for shunting, TCD monitoring is also the only monitor that allows for the detection of cerebral hyperemia, or increased blood flow, following removal of an obstructive carotid lesion. Sustained doubling of flow may be an indicator for the anesthesia provider to decrease CPP if clinically prudent. The intraoperative use of this monitor is limited by the difficulty in maintaining an appropriate view window, though new head-mount systems are mitigating this limitation and this technology is becoming more utilized throughout the perioperative period.
Cerebral oximetry, or near-infrared spectroscopy (NIRS), is a monitor that is simple to both apply and interpret. It operates under the principle that as less oxygen is delivered to the brain due to decreased CBF, more oxygen is proportionately extracted from cerebral arterial blood, and therefore oxygen saturation in cerebral venous blood will decrease. Practically, this monitor is applied as a pad across the forehead and detects oxygen saturation in cerebral venous blood across the prefrontal cortex. While, in theory, this monitor seems useful in detecting decreased oxygen delivery to the brain and may prevent intraoperative cerebral injury, the data regarding its use in this capacity is mixed.
Contradictory evidence regarding intraoperative findings of cerebral oximetry, EEG/SSEP, and TCD all exist, and no single monitor has yet been validated as the gold standard for the prevention of cerebral injury during CEA.
At what PaCO2 does hypocapnia become dangerous?
At a PaCO2 level below 25 mmHg, the vasoconstriction response to PaCO2 is blunted.
At PaCO2 levels of 20 mmHg, cerebral ischemia occurs due to a leftward shift in the oxyhemoglobin dissociation curve, with a subsequent decrease in CBF. Anaerobic metabolism and decreased oxygen consumption occur at PaCO2 levels below 20 mmHg.
Temperature changes CBF by ___% to ___% for every 1 degree Celsius.
Temperature changes CBF by 6% for every 1 degree Celsius, due to corresponding changes in CMRO2 (metabolism).
CBF decreases in hypothermia and increases in hyperthermia.
This has led to extensive use of hypothermia for multiple types of surgeries including cardiac, thoracic aneurysm repair, and cerebral aneurysm repair.
NOTE:
Cerebral blood flow is also directly affected by a number of other factors that DO NOT AFFECT metabolism including arterial partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) and mean arterial blood pressure (MAP).
Which volatile anesthetics cause cerebral vasodilation?
-
ALWAYS KEEP MAC <1.0 IN NEURO CASES WHERE ICP IS A CONCERN!!!
Which volatile anesthetic tends to decrease CO compared to others?
Sevoflurane
All volatile anesthetics cause reduction in myocardial contractility.
However, Isoflurane and Desflurane compensate with an increase in heart rate due to preserved carotid baroreceptor reflex and thus little/no change in overall CO.
Sevoflurane blunts carotid baroreceptor reflex.
NO, on the other hand, tends to increase sympathetic output increasing HR and CO.
Nitrous Oxide
MOA
NMDA antagonist (noncompetitive) - primary anesthetic effect
GABA-A agonist - anxiolysis
Opioid receptor agonist (indirect, induces release of endogenous opioids) - analgesic
Nitric oxide’s primary anesthetic effect is through its inhibition of NMDA receptors.
What effect does Nitrous Oxide have on SVR and PVR?
PVR- increases (esp in pts with pulmonary HTN and mitral stenosis)
SVR- increases
Nitrous oxide is commonly combined with potent volatile anesthetics to maintaine general anesthesia. Nitrous oxide increases sympathetic activity and vascular resistance when given in a 40% concentration. When N2O is combined with volatile anesthetics, systemic vascular resistance and BP are greater than when equipotent concentrations of the volatile anesthetics are evaluated without N2O. These effects might not be due soley sympathetic activation from N2O per se, but may be partially attributed to a decreases in concentration of the coadministered potent volatile anesthetic required to achieve a MAC equivalent when using N2O.
Explain how nitrous oxide can cause diffusion hypoxia?
The relatively higher concentrations of nitrous oxide (up to 70%) required to maintain general anensthesia compared to other potent inhaled anesthetics and its low solubility result in the rapid alveolar elimination of large amounts of nitrous oxide following cessation of the anesthetic. The flooding of nitrous oxide results in the displacement of oxygen and CO2 in the alveoli, leading to a temporary hypoxia.
Diffusion hypoxia can last for 5-10 minutes. Treat with supplemental oxygen.
What characteristic of nitrous oxide contributes to its rapid removal from the body compared to volatile anesthetics?
Nitrous oxide has decreased fat solubility relative to volatile anesthetics. Thus, leading to lower accumulation of nitrous oxide in fat tissue and faster removal from the body after discontinuation.
In fact, Nitrous oxide’s solubility is relatively similar in the fat, muscle, and vessel-rich groups.
In contrast, the volatile anesthetics have much higher fat solubility than the muscle and vessel rich groups.
What effect does hypoxia have on SVR and PVR?
SVR- vasodilation
PVR- vasoconstriction (HPV)
Hypoxia produces vasodilation in systemic circulation due to local nitric oxide production. In the acute phase nitric oxide induced vasodilation tends to dominate over chemoreceptor induced sympathetic discharge and circulating catecholamines.
Hypoxia produces vasoconstriction in pulmonary circulation due to increased intracellular calcium within endothelial cells in setting of low oxygen (mechanism of HPV).
Dexmedetomidine
MOA
a2 agonist
At the brainstem, Dexmedetomidine acts within the pons at the locus cereleus (responsible for arousal, primary source of adrenergic neurotransmitters in the brain) inhibiting the presynaptic release of norepinephrine to produce sedation (sedation resembles natural sleep pattterns, w/ delta waves on EEG)
At the spinal cord, Dexmedetomidine acts on interneurons in the doral horn causing hyperpolarization and decreasing substance P and glutamate transmission to produce analgesia.
NOTE:
Dexmedetomidine is more selective for a2 than clonidine.
(a2:a1 receptor ratio 1600:1 vs a2:a1 receptor ratio 220:1)
Dexmedetomide commonly causes bradycardia and hypertension after an initial bolus dose (brady from the baroreceptor reflex). If followed by an infusion, bradycardia and hypotension can be seen. The reported overall frequency of side effects are hypotension > hypertension > bradycardia.
What effect does Dexmedetomidine have on CMRO2 and CBF?
CMRO2- decreases
CBF- decreases
Dexmedetomidine demonstrates a dose-dependent reduction in CBF which is correlated to a decrease in CBV.
This action is primarily mediated by its ability to reduce CMRO2 through its alpha-2 receptor agonism.
By decreasing CMRO2, cerebral autoregulation will concomitantly decrease CBF and therefore CBV despite the vasodilating effect on Dexmedetomidine.
Dose reduction of Dexmedetomidine is recommended in patients with:
Dose reduction of Dexmedetomidine is recommended in patients with severe hepatic dysfunction.
Dexmedetomidine is metabolized and cleared by the liver. Dose reduction is not required with renal insufficiency.
NOTE:
Dexmedetomidine has no CYP450 drug interactions.
Does Dexmedetomidine affect the ventilatory response to hypercarbia?
NO, Dexmedetomidine does not affect the ventilatory response to hypercarbia. Ventilatory response to hypercarbia is present even at doses associated with unresponsiveness.
Dexmedetomidine does, however, decrease minute ventilation.
NOTE:
Elimination half life is 2-3 hrs.
Context sensitive half life is 4 min after a 10 minute infusion and 250 min after an 8 hr infusion.
What is the mechanism by which ketamine increases HR and BP?
1) Direct sympathetic stimulation
2) Inhibits catecholamine reuptake
3) Vagal nerve inhibitor
NOTE:
In catecholamine depleted states (critical illness, shock), ketamine can cause a paradoxical decrease in HR and/or BP.
Ketamine Side Effects:
CNS
Cardiovascular
Respiratory
See attached picture
NOTE:
Ketamine should be avoided in patients with increased ICP, increased IOP, severe or uncontrolled CAD, severe liver disease (metabolized in liver), severe renal dysfunction (exreted by kidneys), pregnancy, and underlying psychiatric disease associated with psychosis.
Ketamine produces dissociative anesthesia that can be described as a trance-like cataleptic unconcious state (eyes open, spontaneous respiration, unconcious, nonresponsive to painful stimuli).
The dissociative state seems to result from a functional dissociation: inhibition of thalamocortical pathways and stimulation of the limbic regions of the brain.
Psychomimemtic effects of ketamine (vivid dreams, hallucinations) can be minimized with concomitant use of benzodiazepines.
The risk of laryngospasm due to secretions is higher with IM administration than with IV adminstration.
Ketamine
Subanesthetic dose for chronic pain patients?
0.3mg/kg bolus prior to incision
0.25mg/kg bolus every hour or 0.25mg/kg/hr infusion
Ketamine has been shown to be an effect adjunct in the management of post-operative pain. Antagonism of the NMDA receptor by ketamine is thought to decrease 1) central sensitization 2) opioid tolerance and 3) pain intensity. Thus reducing postoperative opioid requirements as well as nausea and vomiting.
NOTE:
Ketamine should be avoided in patients with increased ICP, increased IOP, severe or uncontrolled CAD, severe liver disease (metabolized in liver), severe renal dysfunction (exreted by kidneys), pregnancy, and underlying psychiatric disease associated with psychosis.
Ketamine produces dissociative anesthesia that can be described as a trance-like cataleptic unconcious state (eyes open, spontaneous respiration, unconcious, nonresponsive to painful stimuli).
The dissociative state seems to result from a functional dissociation: inhibition of thalamocortical pathways and stimulation of the limbic regions of the brain.
Psychomimemtic effects of ketamine (vivid dreams, hallucinations) can be minimized with concomitant use of benzodiazepines.
The risk of laryngospasm due to secretions is higher with IM administration than with IV adminstration.
Ketamine has a context-sensitive half life similar to ____________.
Ketamine has a context-sensitive half life similar to Propofol.
Define context-sensitive half time (CSHT).
Context sensitive half time describes the time required for the plasma concentration of a drug to decrease by 50% after stopping an infusion of the drug.
It reflects primarily two opposing processes: drug plasma clearance and drug redistribution.
Drugs with a slow plasma clearance and a high rate of tissue to plasma redistribution will have a high CSHT.
Drugs with rapid plasma clearance and a low rate of tissue to plasma redistribution will have a low CSHT.
Keep in mind that CSHT’s are different from elimination half-lives since the latter are the result of metabolism and excretion from the whole body, not just the plasma.
EXAMPLES:
Fentanyl (green), like propofol, is highly lipophilic and has a large volume of distribution. However, fentanyl has a longer CSHT than propofol due to its rapid redistribution. The rapid redistribution back to plasma prevents the plasma concentration from quickly falling after the infusion is stopped, even though fentanyl is rapidly cleared.
Alfentanil (purple0 has a small volume of distribution due to its lower lipid solubility and high degree of protein binding (90%). SInce much less of the drug redistributes into the peripheral tissues, redistribution back to the plasma does not significantly affect plasma concentration. This explains why the CSHT of alfentanil does not increase after about two hours of infusion. Note, however, for short infusions of alfentanil the CSHT is higher than fentanyl. This occurs since the plasma clearance of alfentanil is significantly lower than fentanyl .
Remifentanil (red) has a flat and low CSHT curve. Remifentanil is hydrolyzed by plasma esterases. It has a very high plasma clearance.
The blood supply to the brain comes from two sources:
The blood supply to the brain comes from two sources:
70% from the internal carotid arteries.
30% from the basilar artery (formed by the two vertebral arteries).
The internal carotid arteries and basilar artery form the circle of Willis, which supply the brain via the anterior, middle, and posterior cerebral arteries.
Cerebellar dysfunction and symptoms:
see picture
Diseases affecting the basal ganglia:
see picture
Blood:Brain Barrier
NOTE:
Water moves across the BBB specifically by chanel-mediated transport by aquaporin-4.
Brain Venous Drainage
The venous drainage of the brain consists of deep and superficial veins that drain into dural venous sinuses, which are valveless vessels between the dura mater and the skull periosteum. All dural venous sinuses eventually drain into the sigmoid sinuses, which empty into the internal jugular vein.
The artery of Adamkiewicz (also referred to as the great anterior radiculomedullary artery or arteria radicularis magna) can be found spanning across several vertebral levels most commonly between ____ and ____ supplying the watershed zone of the lumbar and sacral spinal cord.
The artery of Adamkiewicz (also referred to as the great anterior radiculomedullary artery or arteria radicularis magna) can be found spanning across several vertebral levels most commonly between T9 and L2 (left side) supplying the watershed zone of the lumbar and sacral spinal cord.
The spinal cord receives its blood supply from three major vascular structures - one anterior spinal artery and two posterior spinal arteries. The anterior spinal artery provides vascular supply to the anterior portion of the spinal cord. In particular, the anterior two-thirds of the spinal cord is dependent vascularly from the anterior spinal artery. The two posterior spinal arteries provide vascular supply to the posterior spinal cord. However, only the posterior one-third of the spinal cord is dependent vascularly from the posterior spinal arteries.
The artery of Adamkiewicz provides blood supply to the thoracolumbar anterior spinal cord and may be ligated during a thoracoabdominal aortic aneurysm (TAAA) repair or damaged during surgical manipulation of the axial skeleton. The use of MEPs provides the perioperative team with a modality to detect relative decreases in spinal cord perfusion pressure (SCPP). Such decreases in SCPP may be treated intraoperatively in order to reduce the risk of postoperative paraplegia.
What factors decreased evoked potentials?
What factors have minimal/no effect on evoked potentials?
What factors increase evoked potentials?
DECREASE
Inhalational agents including nitrous oxide
(All of the volatile anesthetics produce dose-dependent effects)
Anemia (hgb <10, reducing O2 carrying capacity)
MINIMAL/NO EFFECT
Propofol
Dexmedetomidine
Opiates
INCREASE
Ketamine
Etomidate
OTHER:
Somatosensory evoked potentials (SSEP) are used intraoperatively to assess lateral and posterior spinal cord perfusion. Detection of the SSEP signal takes place in the patient’s brain. Motor evoked potentials (MEP) are used to evaluate anterior spinal cord perfusion. Detection of MEP signaling occurs distally in the peripheral musculature.
Brain Waves
G-BAT-D
What EEG findings would be observed at an optimal depth of general anesthesia with Propofol TIVA?
Alpha and slow-delta oscillations
The _____________ tract carries signals of pain and temperature from the periphery to the somatosensory cortex.
The lateral spinothalamic tract carries signals of pain and temperature from the periphery to the somatosensory cortex.
Which specific nerve fibers transmit pain impulses?
Type A, delta fibers
The ________ tract carries signals of fine touch, pressure, vibration, proprioception from the periphery to the somatosensory cortex.
The dorsal column tract carries signals of fine touch, pressure, vibration, proprioception from the periphery to the somatosensory cortex.
The ________ tract carries signals of proprioception from the periphery to the cerebellum.
The spinocerebellar tract carries signals of proprioception from the periphery to the cerebellum.
An isoelectric EEG indicates cerebral silence and the maximal decrease in ____________.
An isoelectric EEG indicates cerebral silence and the maximal decrease in CMRO2
Burst suppression, however, is the desired EEG pattern when using an infusion of pentobarbital (also applies to infusions of propofol or etomidate). It allows a maximal reduction in CMRO2 while indicating that regular EEG activity will return predictably following cessation of the infusion..
Describe the Monro-Kellie Doctrine.
The importance of ICP was recognized more than 200 years ago and is referred to as the Monro-Kellie Doctrine (or hypothesis), which states that
1) The brain is enclosed in a nonexpandable case of bone
2) The brain parenchyma is nearly incompressible
3) The volume of blood in the cranial cavity is therefore nearly constant
4) A continuous outflow of venous blood from the cranial cavity is required to make room for incoming arterial blood.
The intracranial vault is composed of 3 compartments:
1) Brain parenchyma
2) Blood volume (arterial & venous)
3) Cerebral spinal fluid (CSF)
Intracranial hypertension and elevated ICP occur when the volume of one of the compartments increases, and further compensation by a decrease in another compartment is no longer possible.
Normal ICP in healthy adult is between __–___ mm Hg.
TBW is made up of ____ extracellular fluid and ____ intracellular fluid.
Extracellular fluid volume is further subdivided into ____ interstitial fluid and ____ plasma fluid.
How is % TBW different in different sexes/age groups?
TBW is made up of 1/3 extracellular fluid and 2/3 intracellular fluid.
Extracellular fluid volume is further subdivided into 3/4 interstitial fluid and 1/4 plasma fluid.
TBW 60% in men
TBW 50% in women
Neonates have the highest TBW (most extracellular, hence why they need high doses per kilo because of the greater volume of distribution)
Elderly have the lowest TBW (decrease in TBW with age)
NOTE:
When different fluids are given, they distribute differently in the different compartments. Dextrose 5% distributes across the extracellular and intracellular compartments. Normal saline and balanced crystalloids remain in the extracellular compartment and distribute in the interstitial and intravascular compartment. Colloids, in theory, remain entirely in the intravascular compartment when the glycocalyx is intact but become less efficacious when the glycocalyx is disrupted.
The luminal side of the capillary endothelium is lined by the glycocalyx, a network of proteoglycans and glycoproteins. The glycocalyx plays a pivotal role in fluid physiology. The capillary lumen and the interstitial space are separated by the glycocalyx, which creates a protected region called the subglycocalyx space without protein, which augments intravascular hydrostatic pressure. The glycocalyx retains plasma constituents and prevents their extravasation to the interstitial space. However, the glycocalyx can be disrupted by inflammatory states (for example, during sepsis and surgery) and excessive fluid administration.
Define Volume of Distribution (VD)
The volume of distribution (Vd) is a pharmacokinetic parameter representing an individual drug’s propensity to either remain in the plasma or redistribute to other tissue compartments.
By definition, Vd is a proportionality constant that relates the total amount of drug in the body to the plasma concentration of the drug at a given time.
The following equation can represent VD:
Volume of Distribution (L) = Amount of drug in the body (mg) / Plasma concentration of drug (mg/L)
Based on the above equation:
A drug with a high VD has a propensity to leave the plasma and enter the extravascular compartments of the body, meaning that a higher dose of a drug is required to achieve a given plasma concentration. (High VD -> More distribution to other tissue)
Conversely, a drug with a low VD has a propensity to remain in the plasma meaning a lower dose of a drug is required to achieve a given plasma concentration (Low VD -> Less distribution to other tissue).
Drugs with a high degree of plasma protein binding, lower degree of tissue protein binding, and hypdrophilic nature have a small VD.
Differentiate zero-order and first-order kinetics.
ZERO ORDER:
For some drugs, elimination may depend on the action of a specific enzyme or transporters. These enzymes or transporters can reach their maximum capacity and become saturated.
When saturation is reached at a given plamsa concentration, the amount of drug removed is a constant amount per unit time regardless of the plasma concentration.
In zero-order kinetics, drug elimination occurs in a linear declining manner.
Examples- Phenytoin, Ethanol, Aspirin (PEA)
A simple analogy would be an athlete signing an autograph on a picture. Regardless of the total amount of photographs that must be signed, the athlete can only sign one autograph every 15 seconds. The rate-limiting factor of this analogy and zero-order kinetics is time.
FIRST ORDER:
Approximately 95% of drugs used in clinical practice are eliminated by first-order kinetics. Drugs are eliminated primarily the liver or kidneys.
In first-order kinetics, drug elimination occurs in an exponentially declining manner with the rate of elimination being proportional to the plasma concentration.
The amount of drug removed is a constant fraction per unit time rather than a constant amount.
To utilize the same analogy, now the entire team can sign the photographs. The more photographs there are to sign, the more athletes can sign. The rate-limiting factor of this analogy and in first-order kinetics is the initial concentration.
SUMMARY::
Zero = constant amount, linear
First = constant fraction, exponential
How to calculate left-sided Coronary Perfusion Pressure (CPP):
Left-sided Coronary perfusion pressure (CPP) is represented as the difference between the aortic diastolic pressure (AoDP) and the left ventricular end-diastolic pressure (LVEDP).
CPP = AoDP - LVEDP
Left coronary perfusion predominately occurs in diastole.
Right coronary perfusion, however, occurs throughout the cardiac cycle (systole & diastole).
Right-sided CPP during systole = AoSP-RVEDP
Right-sided CPP during diastole = AoDP-RVEDP
Diastolic predominance in right coronary flow can occur with chronic pulmonary artery hypertension due to RV hypertrophy.
Which volatile anesthetics increases coronary blood flow?
Isoflurane, Desflurane, and Sevoflurane
Isoflurane is the most potent.
NOTE:
Volatile anesthetics administered before or immediately after some time of ischemic event can reduce the size of any myocardial infarct that may have occurred. This is thought to be due to reduced loading of calcium into myocardial cells.
Why do neonates have decreased oxygen reserve compared to adults?
Tidal volumes in the neonate are similar to the adult on a volume per kg basis.
They have increased respiratory rates which thereby increases the neonate’s minute ventilation as compared to the adult. The neonate has a higher minute ventilation due to their higher oxygen consumption.
The neonate’s closing volume is higher and can approach their normal tidal volume which can result in premature closure of small airways.
With a similar functional residual capacity compared to the adult but a higher minute ventilation, the neonate’s ratio of minute ventilation to FRC is two to three times higher.
This leads to a decreased oxygen reserve but a faster inhalation induction in the neonate.
Why do pregnant women have decreased oxygen reserve compared to average adults?
Many respiratory changes occur in the obstetric patient due to both anatomic and hormonal alterations.
As the pregnancy progresses, the diaphragm moves more cephalad which causes a decrease in the functional residual capacity.
In order to compensate for this change, the thoracic rib cage increases in anteroposterior and transverse diameter which aids to cause only a slight decrease in the total lung capacity overall.
The functional residual capacity decreases by about 20-30% as does the expiratory reserve volume and residual volume. In addition, there is an increase in the inspiratory reserve volume.
Airway resistance remains unchanged as progesterone relaxes the bronchiolar smooth muscle which combats the increased airway resistance due to upper airway edema.
These changes contribute to a rapid desaturation during apnea and necessitate prompt airway intervention to avoid complications.
When should thrombocytopenia be treated in the perioperative period?
There are not clearly defined cut-off values that mandate platelet transfusion.
It is largely accepted that severe thrombocytopenia with platelet levels of less than 10,000/µL should receive transfusion for increased risk of spontaneous bleeding.
For minor surgeries, the platelet levels should be greater than 30,000/µL.
For major surgery, levels greater than 50,000/µL are appropriate.
For neurosurgical operations the level should be greater than 100,000/µL.
Nasotracheal Intubation (NTI):
Indications
Absolute contraindications
Relative contraindications
Nasotracheal Intubation (NTI)
Indications:
- Impending airway compromise
(Nasotracheal intubation is typically performed on the awake patient in this case to avoid loss of airway protection reflexes during the process of intubation. NTI causes less gagging and is better tolerated in awake patients than oral intubation)
- Intraoral/oropharyngeal surgery
- Rigid laryngoscopy
- Maxillofacial or orthognathic surgery
- Complex intraoral procedures involving mandibular reconstruction
- Dental surgery
Absolute contraindications:
- Previous history of old or recent skull base fractures (basilar fracture)
- Anterior skull base fractures (may result in passage of the tube intracranially)
- Midface instability
- Coagulopathy (that can predispose patient to epistaxsis)
Relative contraindications:
- Recurrent epistaxis
- Large nasal polyps
- Known/suspected nasal foreign body
- Recent nasal surgery
Oral antiplatelets include:
Aspirin - irreversible COX-1 and COX-2 inhibitor
Clopidogrel (Plavix)- P2Y12 receptor inhibitor
Ticagrelor (Brilinta)- P2Y12 receptor inhibitor
Prasugrel (Effient)- P2Y12 receptor inhibitor
Dipyridamole- PDE3 inhibitor
Antiplatelet drugs are commonly prescribed in patients with compromised arterial blood flow to prevent platelet aggregation in syndromes such as coronary artery disease, peripheral artery disease, or ischemic strokes. Because anticoagulants tend to prevent clot formation in the venous system, antiplatelet drugs will tend to be used in patients with occlusive arterial disease. The antiplatelet drugs that are used in clinical practice tend to work through one of three mechanisms, though there are other novel anti-platelet medications outside of these.
These mechanisms include cyclooxygenase (COX) inhibition, P2Y12 receptor inhibition, and glycoprotein IIB/IIIA inhibition. Of these, the glycoprotein IIB/IIIA inhibitors can only be given via an intravenous route. Inhibition of any of these pathways will lead to a decrease in ultimate thromboxane production and decreased platelet aggregation.
Aspirin irreversibly inhibits COX-1 and COX-2 in the arachandonic pathway preventing the production of what three compounds from arachadonic acid?
Aspirin irreversibly inhibits COX-1 and COX-2 in the arachandonic pathway preventing the production of:
* Thromboxane- platelet aggregation, vasoconstrictor
* Prostacyclin- platelet activation, vasodilator
* Prostaglandin- vascular tone
NOTE:
With low dose ASA therapy, prostacylcin production is selectively spared decreasing clot formation and vasoconstriction seen with thromboxane production while still allowing vasodilation from prostacyclin.
Clopidogrel (Plavix) and Ticagrelor (Brilinta)
MOA
Clopidogrel (Plavix) irreversibly inhibits P2Y12 receptor on platelets, thus preventing ADP-mediated platelet activation and aggregation.
Ticagrelor (Brilinta) reversibly inhibits P2Y12 receptor on platelets, thus preventing ADP-mediated platelet activation and aggregation.
NOTE:
Though Brilinta prevents blood from clotting more effectively, it also tends to have an increased risk of side effects compared to Plavix, such as a higher chance of bleeding.
Recommendation for stopping oral antiplatelets before surgery?
Aspirin = 7-10 days
Plavix and Brilinta = 5 days
Prasugrel- 7 days
NOTE:
Aspirin can be safely continued in patients undergoing minor surgery.
Patients on Aspirin for primary or secondary prevention should discuss whether the risks outweights the benefits with surgeon.
Patients on Aspirin for a prior hx of PCI should continue unless the risk of bleeding outweights the benefits of preventing MI.
Aspirin should be continued until the day of surgery for patients with a hx of CAD scheduled for an elective CABG but P2Y12 inhibitors should be stopped 5 days before elective CABG.
Aspirin should be continued until the day of surgery for patients scheduled for elective carotid endarterectomy.
Warfarin should be held how many days before surgery?
5 days
(check INR)
Apixaban (Eliquis) and Rivaroxaban (Xarelto) should be held how many days before surgery?
5 days
Dabigatran should be held how many days before surgery?
5 days
Recommendation for perioperative steroid supplementation?
Perioperative steroid supplementation with hydrocortisone should be administered to patients taking >20mg/day of prednisone (or equivalent) for at least 3 weeks in the previous year and may be considered in patients taking 10-20mg/day.
Chronic corticosteroid use can lead to suppression of HPA axis and places patients at risk for developing secondary adrenal insufficiency in the setting of abrupt cessation of their glucocorticoids or in the setting of high physiologic stress (eg. surgery). This occurs since the adrenal gland is unable to secrete cortisol in response to stress and a patient’s chronic steroid dose is adequate only for daily activity and minor stress.
The most dangeous manifestation is hemodynamic instability that is not responsive to fluids or pressors.
There is no proven optimal regimen for perioperative steroid replacement. Based on the data, patients who take 5-10mg/day of prednisone (or equivalent) do not usually have clinically significant HPA axis suppression and therefore do not need perioperative corticosteroid supplementation. Patients who take > 20mg day of prednisone (for longer than 3 weeks within the last year) are at risk for AI and should be supplemented based on the amount of anticipated surgical stress. Patients on steroid doses between these two levels may benefits from supplementation.
Patients using > 2g/day of topical steroids or > 800 mcg/day of inhaled steroids on a long-term basis should probably also receive supplementation.
NOTE:
Primary adrenal insufficiency: low glucocorticoid + low mineralocorticoid
Secondary adrenal insufficiency: low glucocorticoid (no electrolyte abnormalities)
What oral antiplatelet is a prodrug that requires hepatic oxidation to become active?
Clopidogrel (Plavix)
Prasugrel (Effient)
Clopidogrel (Plavix) is a prodrug that requires activation by hepatic cytochromes, most specifically CYP 2C19 in order to exert its clinical effect. This active metabolite will then bind to the platelet adenosine diphosphate (ADP) receptor and prevent platelet aggregation.
This characteristic of Clopidogrel caused the US Food and Drug Administration to release a black box warning regarding its use. Because around 2 to 14% of the population has a mutant phenotype of CYP 2C19, these patients are at an increased risk of thrombotic death due to the failure of clopidogrel therapy due to decreased conversion of clopidogrel into its active metabolite.
Ticagrelor (Brilinta) is NOT a prodrug.
NOTE:
Clopidogrel (Plavix) is associated with Thrombotic Thrombocytopenic Purpura (TTP).
Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of Warfarin (Coumadin)?
Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of Warfarin (Coumadin)?
CYP2C9
NOTE:
Polymorphisms are variants in DNA sequence that occurs in at least 1% of the population and can lead to altered patient response to medications.
Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of BB’s, CCBs, antiarrthymics, Tramadol, Codeine, Oxycodone, Hydrocodone, Hydromorphone?
Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of BB’s, CCBs, antiarrthymics, Tramadol, Codeine, Oxycodone, Hydrocodone, Hydromorphone?
CYP2D6
NOTE:
Polymorphisms are variants in DNA sequence that occurs in at least 1% of the population and can lead to altered patient response to medications.
Which oral opioids are prodrugs?
Codeine
Tramadol
Oxycodone
Hydrocodone
Hydromorphone
NOTE:
All metabolized by CYP 2D6
Hydromorphone (Dilaudid) is metabolized by the liver into hydromorphone-3-glucuronide which can accumulate in patients with renal dysfunction and result in…
Hydromorphone (Dilaudid) is metabolized by the liver into hydromorphone-3-glucuronide which can accumulate in patients with renal dysfunction and result in cognitive dysfunction and myoclonus.
Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of fentanyl, alfentanil, sufentanil, midazolam, diazepam, amide local anesthetics, methadone, dexamethasone?
Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of fentanyl, alfentanil, sufentanil, midazolam, diazepam, amide local anesthetics, methadone, dexamethasone?
CYP3A4
NOTE:
Polymorphisms are variants in DNA sequence that occurs in at least 1% of the population and can lead to altered patient respone to medications.
Midazolam inhibits CYP3A4 which can prolong the effects of Fentanyl.
What pertinent medications are metabolized by CYP3A4?
Fentanyl
Alfentanil
Sufentanil
Midazolam
Diazepam
Amide local anesthetics
Dxamethasone
Methadone
Polymorphisms of what receptor is associated with red hair and may affect sensitivity to general anaesthetics and pain response?
Polymorphisms of what receptor is associated with red hair and may affect sensitivity to general anaesthetics and pain response?
MC1R
Red hair results from distinct mutations of the melanocortin-1 receptor (MC1R).
There is some evidence suggesting that redheads
are less sensitive to general anaesthetics and this
has been linked to variants MC1R gene.
Medications that induce and inhibit of CYP450
See picture
Factors that can affect the block height during spinal anesthesia include:
Factors that can affect the block height during spinal anesthesia include:
-Baricity (most important factor for the spread of local anesthetic and the level of block)
- Medication (dose and baricity)
- Patient (cerebrospinal fluid volume, older age, and pregnancy),
- Procedure (patient position, epidural injection before or after spinal injection) factors.
Mechanism by which epidurals reduce risk of postoperative ileus?
Epidurals used for postoperative analgesia reduce the risk of postoperative ileus. The proposed mechanism is increased gastrointestinal peristalsis (sympatholitic) and reduced overall opiod consumption.
What is more effective for pain relief, local based or opioid base epidurals?
**Local based epidural
**
Epidural administration of any anesthetic agent including local anesthetics and opioids has been shown to produce superior analgesia to the same medications administered systemically, regardless of the type of surgery being performed. The proposed mechanism for this significantly improved pain control involves the direct effect of administration on nociceptive inputs into the central nervous system.
The use of a local anesthetic based epidural regimen has been shown to provide the best postoperative pain control. Opioid-based epidural analgesics provide superior pain control to systemic opioid-based analgesic regimens, though they are inferior to a local anesthetic based epidural regimen. The hydrophilicity of opioids plays a role in this superior pain control, with epidural administration of hydrophilic opioids generally equating an equianalgesic dosing of systemic hydrophilic opioids. Therefore, some suggest only using lipophilic opioids such as fentanyl in the epidural space for immediate postoperative pain control.
The use of opioids in combination with local anesthetics in epidural analgesia may be beneficial, however, definitive data on this point are lacking.
Furthermore, patient-controlled epidural analgesia (PCEA) has been shown to be inferior to continuous epidural infusions (CEI) of analgesic medications. Proposed mechanisms for this finding include the delayed action of local anesthetics in the epidural space, as well as benefits of a continual bathing of the pertinent nerve roots in CEI when compared to the intermittent coverage provided by PCEA. CEI may have increased incidences of medication-related side effects secondary to the increased amounts of medication administered in CEI compared to PCEA, and the benefits of CEI should be weighed against these possible complications. In clinical practice, many choose an epidural regimen that combines both CEI and PCEA.
Mechanism by which epidurals reduce risk of postoperative ileus?
Epidurals containing a local anesthetic (with or without opioid) for postoperative analgesia reduces risk of postoperative ileus.
The proposed mechanism is increased gastrointestinal peristalsis and reduced overall opioid use.
The increased gastrointestinal motility is thought to come from regional blockade of sympathetic nervous system (sympathectomy) and the epidural leaving the parasympathetic nervous system innervation of the gastroinestinal tract unopposed.
NOTE:
Single dose neuraxial opioids do not offer sympathectomy and are not superior to epidurals in regards to risk of post-op ileus.
Perfusion territories of LAD, LCX, RCA
LAD - anterior wall (including anteroseptal and anteroapical) and left atrium
LCX - lateral wall (including anterolateral and inferolateral)
RCA - most of the right atrium, lateral right ventricle, and basal and mid inferior left ventricular wall
Do most people have right dominant or left dominant circulation in the heart?
There is some variability in the extent of additional coverage by the RCA.
In most “right dominant” individuals (85%), there is additional coverage through a posterior descending artery (PDA) branch from the RCA that provides perfusion to the apical inferior wall and superior-posterior interventricular septum.
Approximately 5% of individuals have what is referred to as left dominant circulation, in which the PDA is a branch of the LCX.
Approximately 10% of individuals are co-dominant, in which the PDA receives blood supply from both the RCA and the LCX.
In 60% of individuals, the sinoatrial (SA) node is also supplied by the RCA. The LAD provides perfusion to the SA node in the other 40% of individuals.
The “upper airway” consists of the _________ and the _________.
The “lower airway” consists of the trachea, bronchi, bronchioles, and alveoli.
The “upper airway” consists of the Pharynx (naso-, oro-, hypo-) and the Larynx.
The pharynx is divided into the naso-, oro-, and hypopharynx.
The nasopharynx begins at the nasal cavity and ends at the soft palate
The oropharynx begins at the soft palate and continues to the hyoid bone.
The hypopharynx begins at the epiglottis and ends at the cricoid cartilage. The hypopharynx connects the oropharynx to the esophagus and larynx.
The larynx contains the epiglottis and vocal cords and extends from the superior border of the epiglottis to the cricoid cartilage.
Transexamic acid (TXA) is a ____________ and will help decrease hemorrhage.
Transexamic acid (TXA) is a anti-fibrinolytic and will help decrease hemorrhage.
The primary management technique of resuscitation in trauma patients is transfusion of blood products in a 1:1:1 ratio and this is often started with ________ and _________, followed by _________when available.
The primary management technique of resuscitation is transfusion of blood products in a 1:1:1 ratio and this is often started with packed red blood cells and fresh frozen plasma, followed by platelet therapy when available.
1PRBC: 1FFP: 1plts
In cases where transfusion cannot be delayed, what type of uncrossmatched can be given?
Type O, Rh negative
As type O blood lacks the A and B antigens it will not be hemolyzed by the presence of anti-A and anti-B antibodies in the recipient’s blood. This is why type O blood is considered the universal RBC donor and why it is preferentially administered in situations where emergency transfusion is necessary.
That said, some donors of type O blood produce high titers of anti-A and anti-B antibodies which could potentially cause hemolysis of recipient RBCs if they express the A or B antigen. It is for this reason that type O Rh-negative packed RBCs are preferred to whole blood as packed RBCs contain a lower volume of donor plasma and therefore decreased amount of potential anti-A and anti-B antibodies.
If a sufficient volume of uncrossmatched type O Rh-negative whole blood is administered it is considered unsafe for a patient with either an A, B, or AB blood type to receive type-specific RBC transfusions until it is confirmed that the serum titers of anti-A and anti-B antibodies have decreased to a safe level.
Which blood products should not be transfused through a fluid warmer?
ALL blood products are SAFE to transfuse through a fluid warmer including PRBCs, platelets, FFP, and cryopercipitate.
NOTE:
It was previously thought that warming platelets would result in damage to platelets but no evidence supporting this.
Using a fluid warmer is advised when giving >2 units of blood products or 3L of fluid to prevent reduction of core temperature and hypothermia.
Warfarin
MOA
Vitamin-K antagonist
Warfarin is a vitamin-K antagonist that inhibits the enzyme vitamin K epoxide reductase, decreasing the synthesis of active forms of Vitamin K.
As a result there is a decrease in the gamma carboxylation of the glutamate residues on factor II, VII, IX, X, Protein C, Protein S.
Warfarin is used in the management of atrial fibrillation, mechanical assist devices, and artificial heart valves.
Warfarin reversal
PCC or FFP
IV Vitamin K
Four patients on Warfarin with major bleeding or requiring immediate surgery which reversal agent is preferred?
PCC
FFP requires time for type and screen, time for thawing, large volumes (10-30cc/kg), is less reliable than PCC.
IV Vitamin K should still be given with PCC to generate new clotting factors.
IV Vitamin K takes 6-8 hours to correct INR.
Components of Prothrombin Complex Concentrate (PCC)?
Prothrombin Complex Concentrate (PCC):
Vitamin K–dependent clotting factors (II, VII, IX, X, Protein C, Protein S)
NOTE:
Brand Name: Kcentra
PCC reverses the effect of warfarin (a coumarin anti-coagulant) and is used in cases of significant bleeding in patients with a coagulopathy (INR > 8.0, prolonged prothrombin time, raised d-dimer). Examples include gastrointestinal haemorrhage or intracranial haemorrhage.
Thromboelastogram (TEG)
Thromboelastogram (TEG)
The Parkland formula is a well-established protocol to determine the initial fluid administration required for burn patients.
Parkland formula: 4 mL/kg x weight (kg) x %TBSA over 24 hours.
Half the volume is given over the first 8 hours.
After 24 hours, colloids are preferred to continue resuscitating.
“Wallace Rules of 9” to calculate %TBSA (see picture)
Emergence delirium is a transitory state of agitation that occurs during the recovery from anesthesia characterized by hyperactive behavior, disturbances of awareness, and hypersensitivity that does not respond to consoling measures lasting up to 30 minutes..
Medications to prevent emergence delirium include at/near the end of surgery include a single dose of IV….
Medications to prevent emergence delirium include…
Propofol
Fentanyl
Ketamine
Dexmedetomidine
Midazolam
What are signs that a patient is going through phase II of emergence?
Tearing
Salivation
Grimacing
Gagging/coughing/swallowing
Increased HR
Increased BP
NOTE:
Signs correspond to return of cranial nerve function (VII, IX, and X) in the pons and upper medulla.
Reaching for ETT can occur in phase II of emergence and does not provide evidence that the patient is ready for extubation.
What are signs that a patient is going through stage III of emergence?
Response to oral commands
Spontaneous eye opening
NOTE:
Spontaneous eye opening is the last sign seen. Occurs well after an appropriate return of motor function and responsiveness to commands. Generally, patients tend to keep their eyes closed even after conciousness has returned. They may respond reliably to verbal commands but do not yet open their eyes spontaneously despite a substantial return of motor functions.
Reaching for ETT can occur in phase II of emergence and does not provide evidence that the patient is ready for extubation.
Emergence delirium is terminated either spontaneously or after the administration of….
Emergence delirium is terminated either spontaneously or after the administration of midazolam, propofol, clonidine, dexmedetomidine, fentanyl, or ketamine.
Risk factors for emergence delirium include…
The two main risk factors for developing emergence delirium are patient age (2-6 years) and type of anesthetic.
Emergence delirium occurs most commonly with less-soluble volatile anesthetics (sevoflurane and desflurane).
Emergence delirium vs. post-operative delirium (POD) ?
Emergence delirium occurs during or immediately after emergence from general anesthesia
POD is usually notable from postoperative day 1 and up to 1 week after surgery.
Predisposing factors for Post-Operative Delirium (POD) are:
Predisposing factors for Post-Operative Delirium (POD) are:
* Age > 65 years
* Male sex
* Preexisting cognitive impairment or depression
* Pre-existing functional impairment
* Sensory impairment (e.g. visual and hearing deficiencies)
* Medication (opioids, benzodiazepines, anticholinergics)
* High-risk surgical procedures (cardiac, thoracic, orthopedic operations esp hips)
What is postoperative cognitive dysfunction (POCD)?
POCD is characterized by new cognitive deficits including impaired memory, inability to combine tasks, and impaired psychomotor dexterity that can be seen immediately postoperative and can last for up to six months. POCD typically resolves in days to months, but it may persist in 1% of patients.
Risk factors for developing postoperative cognitive dysfunction (POCD)- **increasing age, low educational level, history of CVA without deficits. **
Procedural risk factors include major surgeries (especially cardiac and major orthopedic surgeries) and long surgeries, and intraoperative complications (such as extensive blood loss) are independent risk factors for POCD.
In contrast to delirium, fluctuating state of conciousness and hallucinations are not seen with POCD, and POCD typically resolves within days to months but may persist in 1% of patients. Chronic POCD is important to identify because it is associated with an increased incidence of 1-year mortality.
Does Propofol TIVA prevent emergence delirium?
YES. The use of propofol total intravenous anesthesia is associated with a significant reduction in risk.
Does Ketamine prevent emergence delirium?
Ketamine reduces the incidence of emergence delirium in patients who have undergone general anesthesia with volatile anesthetics.
It can be given as a bolus of 1 mg/kg IV followed by an infusion of 1 mg/kg/hr or as a single dose of 0.25 mg/kg IV at the end of surgery.
Maintaining end-tidal volatile concentrations of ______ MAC or above can significantly reduce the risk of awareness.
Maintaining end-tidal volatile concentrations of **0.7 **MAC or above can significantly reduce the risk of awareness.
MAC-awake =
MAC-awake = ~0.4-0.5
MAC-awake is the MAC value at which voluntary reflexes (no longer opens eyes to command, shouting, shaking) and perceptive awareness are lost.
NOTE:
Interestingly, the MAC-awake is generally higher at induction (0.4-0.5 MAC in order for loss of conciousness) than at emergence (as low as 0.15 MAC to regain conciousness). Mechanism is unclear.
ASA recommends maintaining at least 0.7 MAC during general anesthesia to significantly reduce the risk of awareness.
MAC-movement=
MAC-movement= 1.0
MAC-EI=
MAC-EI= ~1.3
MAC necessary to prevent laryngeal response to endotracheal intubation.
MAC-BAR=
MAC-BAR= 1.7-2.0
MAC-BAR is the MAC at which the adrenergic response to noxious stimuli is blunted.
BAR (blunt adrenergic response)
Risk factors for intraoperative awareness
PROVIDER
Use of paralytics (#1)
TIVA
PATIENT
Obesity
Difficult intubation
Chronic alcohol, benzo, opioid use
SURGERY
C-sections (highest rate)
Cardiac surgery w/ bypass
Emergency/trauma surgery
NOTE:
Incidence of intraoperative awareness in 1:14,000-19,000.
Paralytics- physiological response of purposeful movement to surgical stimulus is absent
TIVA- unable to monitor depth of anesthesia compared to anesthetic end-titdal CO2 (use BIS monitor)
Difficult intubation/obesity- wearing off of induction dose, higher doses of anesthetic required for obese patients
Chronic alcohol use induces CYP450 2E1 which metabolizes inhalation agents, opioids, and benzos.
Cardiac surgery w/ bypass- use of lower dose of anesthesia due to poor cardiac reserve.
C-section- due to difficult intubation, short duration between induction and surgical incision, use of lower doses of anesthetic agents due to concerns for fetal or maternal wellbeing (incidence 1:256-1,600)
Emergency/trauma- use of lower anesthetic doses due to hemodynamic instability.
Does the addition of opioids affect BIS values?
NO
Opioids do not affect BIS values (eg. Propofol gtt with Remi gtt)
SIADH causes hypo or hypernatremia?
Hyponatremia
Diabetes Insipidus (DI) causes hypo or hypernatremia?
Hypernatremia
Diabetes insipidus (DI) leads to low urine osmolality (<300 mOsm/kg) and high plasma osmolality (>305 mOsm/kg) due to the loss of antidiuretic hormone (ADH), resulting in an inability to concentrate urine and massive diuresis. Hypernatremia (>145 mEq/L) occurs from excessive water loss.
Diabetes Insipidus (DI):
Types
Causes
Treatment
Diabetes insipidus is often caused by damage to the pituitary or hypothalamus, as in severe head injury or near brain death (central DI) or in reduced renal sensitivity to ADH (nephrogenic DI), which can occur from certain renal diseases (eg, chronic renal failure, pyelonephritis, polycystic kidney disease), electrolyte disturbances (eg, chronic hypokalemia or hypercalcemia), or certain drugs (eg, amophotericin B, demeclocycline, lithium). While patients with DI are generally euvolemic, they make become hypovolemic if they do not consume enough water.
The treatment for central DI is ADH replacement with vasopressin or desmopressin.
The treatment for nephrogenic DI is salt restriction, thiazide diuretics, and correcting any electrolyte disturbances along with discontinuation of drugs that may be contributing to the pathologic state.
SIADH
Causes
Treatment
Causes:
CNS distrubance (stroke, infection,hemorrhage, trauma)
Malignancy (small cell lung cancer, head/neck)
Hormone deficiency (hypopituitarism and hypothyroidism)
Drugs (carbamazepine, oxcarbazepine, chlorpropamide, cyclophosphamide, SSRIs)
Infection (PNAs, HIV)
Hereditary SIADH
Treatment:
Salt tablets
Water restriction
Furosemide (to increase plasma osmalility)
Hypertonic saline
Vasopressin antagonists (conivaptan, tolvaptan)
The rate of correction is an important factor. It should not exceed more than 8 mEq/L per 24 hours or 0.5 to 1 mEq/L per hour. More rapid correction can result in osmotic demyelination of the CNS, leading to severe lethal complications such as osmotic demyelination syndrome (“locked-in” syndrome), causing quadriplegia.
Serum osmolality=
Serum osmolality= 2[Na] + BUN/2.8 + glucose/18
Sodium is the largest contributor to plasma osmolality and is the most abundant positive ion of the extracellular fluid compartment.
Osmolality is defined as the number of osmotically active particles per kilogram and can be estimated by the equation 2 x [Na+] + [Glucose]/18 + [BUN]/2.8. Normal plasma osmolality ranges from 275-290 mOsm/kg. The serum Na+ is multiplied by 2 to account for the sodium salts such as sodium chloride and sodium bicarbonate. The 18 and 2.8 are used to convert the units for glucose and BUN in mg/dL to mOsm/kg. Thus, in normal healthy patients, the determinants of plasma osmolality are Na+, glucose, and urea with Na+ being the primary determinant.
NOTE:
Uosm: Posm ratio of > 1.5 indicates pre-renal pathology (dehydration, hypovolemia).
Chronic alcohol use commonly results in what electrolyte abnormalities?
Hyponatremia
Hypokalemia
Hypomagnesemia
Respiratory alkalosis
Hyperuricemia
Fenoldapam
MOA
D1-agonist
Fenoldopam is a dopamine agonist that acts on the dopamine-1 receptor, causing vasodilation, especially of the splanchnic, mesenteric, and renal arterioles, which can increase renal blood flow. This promotes diuresis and natriuresis.
Fenoldopam does appear to have some potential as an antihypertensive (second-line) because it does not have the same tachyphylaxis or rebound hypertensive properties as other nitrovasodilators.
It has a rapid onset (10min) and short duration (10min)
For severe hypertension, initiate treatment at 0.2 mcg/kg/minute then increases by 0.3 to 0.5 mcg/kg/minute at 20 to 30 minute intervals until target blood pressure is reached or until reaching a max of 0.8 mcg/kg/minute.
Risk factors for post-CABG AKI?
AKI occurs in up to 30% of patients following cardiac surgery. Mortality increases by 60-80% in post-cardiopulmonary bypass patients who go on to require renal replacement therapy.
Preoperative creatinine greater than 1.2mg/dL, combined valve and bypass procedures, emergency surgery, and preoperative intraaortic balloon pump are risk factors most strongly correlated with post-CABG AKI.
Other well-known minor risk factors include: female gender, CHF, depressed LVEF, COPD, insulin-requiring DM.
SIDE NOTE:
Dopaminergic agents (Dopamine, Fendoldapam) agonize D1 and D2 receptors and induce vasodilation in the renal, mesenteric, peripheral, and coronary arteries. Specifically, within the kidney, the D1 receptor seems to be concentrated in the medulla, while the D2 receptor tends to be more prevalent in the renal cortex. By stimulating either of these receptors but especially the D1 receptor, blood flow will theoretically increase in the renal medulla and help to prevent the ischemic injury that is implicated in perioperative AKI. Despite this theoretical benefit, no decrease in the incidence of acute kidney injury has been seen with the perioperative administration of these drugs.
Fenoldopam = D1 agonist
Dopamine= D1 and D2 agonist (also beta and alpha agonist)
What effect do prostaglandins have centrally and peripherally in regards to pain?
NSAIDs are COX-II inhibitors and lead to a decrease in the production of prostaglandins.
Prostaglandin E2 is the key mediator of both central and peripheral pain sensitization.
Centrally, prostaglandins enhance pain transmission at the level of the dorsal horn by increasing the release of substance P and glutamate from first-order pain neurons, increasing the sensitivity of second-order pain neurons, and inhibiting the release of neurotransmitters from the descending pain-modulating pathways.
Peripherally, prostaglandins do not directly mediate pain; rather, they contribute to hyperalgesia by sensitizing nociceptors to other mediators of pain sensation such as histamine and bradykinin.
Gabapentin
MOA?
How long does it take for nerve regeneration following cryoanalgesia for post-thoractomy pain?
1-3 months
In healthy patients, succinylcholine will cause an increase of plasma potassium levels by approximately _____ mEq/L.
In healthy patients, succinylcholine will cause an increase of plasma potassium levels by approximately 0.5 mEq/L.
Why does Succinylcholine commonly cause bradycardia in children?
Bradycardia occurs most often in children because children have a high vagal tone. Children have a high vagal tone because they have more acetylcholine receptors in the SA node. Succinylcholine is metabolized by pseudocholinesterase to succinylmonocholine which has cholinergic activity. Bradycardia can be prevented by predaministration of atropine.
Bradycardia can also occur in adults when a second dose is given.
Is Cerebral Palsy a contraindication for Succinylcholine?
NO.
Succinylcholine has been used in children with CP for more than 50 yr without a single report of a hyperkalaemic response.
Keep in mind however that cerebral palsy patients have an increased incidence of gastroesophageal reflux and aspiration.
Lambert-Eaton Syndrome is a disorder involving auto-antibodies prejunctional calcium.
How do these patients respond to DMR and NDMR?
Lambert-Eaton Syndrome
DMR: Increased sensitivity
NDMR: Increased sensitivity
Neostigmine is ineffective for reversal of NDMR
Myasthenia gravis is an auto-immune disorder involving auto-antibodies binding to the extracellular acetylcholine receptors.
How do these patients respond to DMR and NDMR?
Myasthenia Gravis
DMR: Resistant
NDMR: Increased sensitivity
Weakness in Myasthenia Gravis ________ with activity whereas weakness in Lambert Eaton ________ with activity.
Weakness in Myasthenia Gravis WORSENS with activity whereas weakness in Lambert Eaton IMPROVES with activity.
Several risk factors have been identified that predict the requirement for postoperative ventilation in patients with MG who are undergoing anesthesia including:
Several risk factors have been identified that predict the requirement for postoperative ventilation in patients with MG who are undergoing anesthesia including:
* Evidence of bulbar symptoms preoperatively
* History of myasthenic crises
* Disease duration of six years or more
* Pyridostigmine dose of >750 mg daily
* History of COPD
* Vital capacity of less than 2.9 L (in some sources, ~2 L)
* Serum acetylcholine receptor antibody level >100 nM/mL
* Intraoperative blood loss of >1 L
Myasthenia gravis is an autoimmune disorder in which a patient develops antibodies against nicotinic acetylcholine receptors at the neuromuscular junction, resulting in activity-exacerbated weakness. Most patients have anti–acetylcholine receptor antibodies, although some patients have antibodies against muscle-specific tyrosine kinase or lipoprotein-related protein 4.
The primary symptom of MG is weakness of skeletal muscles that is exacerbated by repetitive use. Although any muscle group can be affected, muscles controlled by cranial nerves tend to be most affected, predisposing patients to bulbar symptoms that can cause aspiration. A myasthenic crisis can be caused by poor disease control, stress, hyperthermia, or infection and is characterized by respiratory failure with muscle weakness, often requiring intubation and mechanical ventilation.
Diagnosis of MG is primarily based on clinical history, serodiagnostic testing, and electrodiagnostic testing. Treatment most commonly consists of cholinesterase inhibitors (eg, pyridostigmine), steroids, intravenous immunoglobulin, and/or immunosuppression. Plasmapheresis is sometimes used in patients who are in crisis or who have refractory symptomatology.
There is an association of thymoma with MG, and many patients undergo thymectomy.
__________ is a measure of the synthetic function of the liver.
Prothrombin time (PT) is a measure of the synthetic function of the liver as the liver synthesizes the coagulation factors that affect the PT.
The liver produces all vitamin K dependent factors including factors II, VII, IX, and X along with protein C and protein S. PT is used to assess procoagulant capabilities of these Vit K dependent factors. These clotting factors are not synthetized in teh case of severe hepatic dysfunction leading to prolonged PT. Among these factors, factor VII has the shortest half life (4 hours) and can therefore serve as an early and reliable measure of possible liver dysfunction. PT measures the activity of factors I, II, V, VII, and X which are components of the extrinsic clotting pathway.
PT is the most sensitive standard laboratory test for acute changes in or the current status of the synthetic function of the liver.
Other measures of hepatic synthetic function include fibrinogen (half-life of four days) and albumin (half-life of 20 days).
NOTE:
Albumin accounts for 15% of proteins synthesized by the liver.
Liver disease reduces what coagulation factors?
II, V, VII, IX, X, XI
NOTE:
VIII and vWF are increased in liver disease as they are produced by endothelial cells (extrahepatic)
“348 outside the livers gate”
Coagulation management in liver disease?
Which coagulation factors are NOT produced by the liver?
III, IV, VIII
“348 outside the liver’s gate”
The recommended duration of DAPT in a patient with a drug-eluting stent is at least _____ months before holding for an elective surgery.
The recommended duration of DAPT in a patient with a drug-eluting stent is at least 6 months before holding for an elective surgery.
The guidelines now state that noncardiac elective surgery should be delayed optimally for at least 6 months, but, at 3 months, interruption of DAPT for surgery may be considered for time-sensitive surgeries (eg oncological).
After an MI, patients should wait ____ days after balloon angioplasty, ____ days after BMS, ____ days if no coronary intervention, and ____ days after DES for elective noncardiac surgery.
After an MI, patients should wait 14 days after balloon angioplasty, 30 days after BMS, 60 days if no coronary intervention, and 180 days after DES for elective noncardiac surgery.
The liver recieves ______% of cardiac output.
The liver is supplied by the hepatic artery and portal vein. The hepatic artery delivers _____% of the blood volume and the portal vein delivers ____%.
The liver recieves 25% of cardiac output.
The hepatic artery delivers 25% of the blood volume and the portal vein delivers the other 75%.
Despite the disproportionate blood flow, both vessels each supply 50% of the liver’s oxygen due to the hepatic artery carrying more oxygenated blood.
The portal blood flow is regulated by the hepatic arterial buffer response system which can increase blood flow via the hepatic artery by as much as 100%. This system is driven by the local concentration of adenosine, a metabolic byproduct of the liver. When portal venous blood flow is reduced, adenosine accumulates resulting in vasodilation of the hepatic artery and increasing blood flow via the hepatic artery.
Which diuretics can cause hypo-chloremic metabolic alkalosis?
Loop diuretics
Thiazide diuretics
What are the five classes of diuretics?
- Osmotic (Mannitol, a sugar alcohol)
- CA inhibitors (ACTZ, Brinzolamide)
- Loop (Furosemide, Torsemide, Bumetanide, Ethacrynic Acid)
- Thiazides (HCTZ, chlorthalidone)
- K sparing (Spironolactone [Aldactone], Eplerenone, Amiloride, Triamterene)
Pneumonic: SEAT BELT
Spironolactone, Eplerenone, Amiloride, Triamterene
Bumetanide, Ethacrynic Acid, Lasix (Furosemide), Torsemide
Mannitol
Effects?
Increased plasma volume
Increased CO
Increased BP
Decreased ICP
Increased PCWP (caution w/ HF patients as can cause pulmonary edema)
Increased RBF and UOP (increases osmotic pressure in PCT and loop of henle, decreasing passive reabsoprtion of water)
Hyponatremia (diultional)-> Hypernatremia (hemoconcentrated)
Hypokalemia vs. hyperkalemia
Metabolic acidosis (dilution of bicarb)
NOTE:
Rapid bolus of mannitol can acutally cause a transient increase in ICP. Appropriate bolus dose is 0.25-1g/kg over at least 10-15min.
Acetazolamide is a diuretic that inihbits CA in the PCT which can cause what acid-base disorder?
Hypokalemic metabolic acidosis
NOTE:
CA in the PCT works to increase Na, Cl, and HCO3 reabsorption. Inhibition of CA by acetazolamide causes Na, Cl, and HCO3 excretion.
Loop and thiazide diuretics can cause what acid-base disorder?
Hypokalemic hypochloremic metabolic alkalosis
Acetazolamide and K sparing diuretics can cause what acid-base disorder?
Hyperchloremic metabolic acidosis
Loop diuretics inhibit which transporter?
Thiazide diuretics inhibit which transporter?
Loop inhibits NaKCl(2)
Thiazide inhibits NaCl
K+ Sparing Diuretics
MOA
Spironolactone & Eplerenone are competitive antagonists of mineralocorticoid receptor sites.
Amiloride and Triamterene directly block sodium channels.
Overall, K+ sparing diuretics prevent K+ secretion by antagonizing the effects of aldosterone in the collecting tubules.
Equation for sodium deficit
Sodium deficit= 140-plasma Na x TBW
TBW (Total Body Water)= weight (kg) x 0.6
Symptomatic patients with serum Na+ < 120 mEq/L should have their serum osmolality corrected by 3% hypertonic saline (HS). Serum electrolytes should be assessed regularly and HS should be discontinued once symptoms resolve and/or Na+ rises above 120 mEq/L. Central pontine myelinolysis (CPM), a demyelinating CNS lesion, may result from rapid increase in serum osmolality during HS therapy. Typically, 50% of the Na+ deficit is corrected during the first 24 hours, and the rate of hypertonic saline administration should never be higher than 100 mL/hr.
EX:
Serium sodium= 110mEq/L
Sodium deficit = (140 mEq/L – 110 mEq/L) x (100 kg x 0.6) = 1800 mEq
Describe the effects of PPV on the following:
VR/preload
RV afterload
RV SV
Pulmonary vascular resistance
LV afterload
LV SV
CO
Describe the effects of PPV on the following:
VR/preload- decreases
RV afterload- increases
RV SV- decreases
Pulmonary vascular resistance- increases
LV stroke volume- decreases
CO- decreases
Although PPV can decrease the work of breathing, it can have significant hemodynamic effects.
Positive pressure ventilation results in an increase in intrathoracic pressure that compresses the inferior vena cava and right atrium, decreasing venous return to the heart. In addition, the increased intrathoracic pressure increases the afterload on the right ventricle. The increase in alveolar pressures compresses the pulmonary valsculature leading to an increase in pulmonary vascular resistance, increasing the right ventricular afterload. Combining the decreased preload and increased afterload leads to a decreased right ventricular stroke volume.
Effects seen on the left side of the heart include a decreased preload (due to decreased right-sided stroke volume). A decreased afterload also occurs due to a reduction in the left ventricular end-systolic transmural pressure and an increased gradient between the intrathoracic aorta and extrathoracic systemic circuit; however, this is minor compared to the reduced preload. The decreased preload results in a decrease in left ventricular stroke volume and in overall cardiac output.
How can Transfusion-related acute lung injury (TRALI) be differentiated by a Transfusion-associated circulatory overload (TACO)?
CVP is normal in TRALI.
CVP is elevated in TACO.
Normal CVP = 8-12mmHg
TRALI occurs most often after the administration of fresh frozen plasma (FFP) and platelets and carries a mortality of up to 5%. Anti-HLA antibodies have been implicated, though an immune response is not always evident. A “two-hit” theory has thus been proposed that includes an initial priming insult followed by transfusion as the “second hit.” TRALI typically develops rapidly after transfusion, usually within six hours. It presents as chills, fever, respiratory distress or increased inspiratory pressures in the mechanically ventilated patient, and noncardiogenic pulmonary edema. Bilateral patchy infiltrates are commonly seen with TRALI as inflammatory mediators lead to fluid extrusion in the lungs. No signs of heart failure.
Transfusion-associated circulatory overload (TACO) results from the rapid administration of more blood products than the patient’s cardiovascular status can support. Hypertension and elevated central venous pressure (CVP) are more common in the initial phases of TACO due to volume overload. Progression to cardiovascular collapse can result in hypotension in TACO as well, though signs of heart failure are typically seen.
TRALIs occur most often after administration of what product(s)?
FFP
Platelets
Commonly used guidelines for the application of HBO therapy in CO poisoning include:
Commonly used guidelines for the application of HBO therapy in CO poisoning include:
1. HbCO level >25%
- Neurologic impairment (including dizziness and loss of consciousness)
- Evidence of acute cardiac abnormalities (ischemia, arrhythmias, ventricular failure)
Carbon monoxide is an odorless, nonirritating gas that binds to hemoglobin with an affinity 200 times greater than that of oxygen.
When a patient is exposed to smoke from a fire or combustion of any kind, carbon monoxide toxicity should be assumed until proven otherwise. Clinical effects of HbCO include headache, nausea, vomiting, dizziness, myocardial ischemia, loss or altered consciousness, and fetal distress during pregnancy. Carboxyhemoglobin and HbO2 absorb light at the same wavelength; thus, a standard pulse oximeter will not detect carbon monoxide levels.
Increasing PaO2 will hasten the removal of CO from the blood. The half-life of HbCO is 200 to 300 minutes when patient is breathing room air, and it is about 40 to 80 minutes when 100% O2 at 1 atm is administered. With HBO therapy, the half-life of HbCO becomes 15 to 30 min at 2.5 atm.
Hyperbaric oxygen therapy increases oxygen delivery to the tissues by increasing the amount of oxygen dissolved in the plasma PaO2. It has been hypothesized that the increased PaO2 “pushes” the CO molecules off hemoglobin. Hyperbaric oxygen therapy will reduce the half-life of HbCO even further.
NOTE:
Dissolved oxygen within the blood is independent of circulating carbon monoxide. The PaO2 should therefore be increased during CO poisoning in order to increase arterial oxygen content. This may be achieved through 100% face mask oxygen, endotracheal intubation with 100% FiO2, or hyperbaric oxygen (HBO) treatment. This latter form of treatment subjects the patient to 2-3 atmospheres of oxygen. This allows PaO2 to reach approximately 1500-2500 mm Hg.
Why is it that new generation carbon dioxide absorbents (calcium hydroxide, calcium chloride) are much less likely to react with volatile anesthetics and produce carbon monoxide?
New generation carbon dioxide absorbents (calcium hydroxide, calcium chloride) do not contain strong bases (such as sodium hydroxide or potassium hydroxide).
Old generation carbon dioxide absorbents include soda lime and barium hydroxide.
Volatile anesthetic degradation can produce carbon monoxide (Desflurane > Isoflurane > Sevoflurane).
Dessicated (dried out) absorbents generate significantly more carbon monoxide and may lead to carbon monoxide poisoning.
Which volatile anesthetics blunt hypoxic pulmonary vasocontriction (HPV)?
ALL volatile anesthetics blunt hypoxic pulmonary vasocontriction, but at HIGH DOSES.
Though earlier animal studies indicated that volatile anesthetics (especially halothane) potently inhibited HPV, this effect was most profound at high doses—such as those required to produce 1.5-2.0 MAC. Such inhibition may be related to the direct vasodilatory properties of volatile agents. Newer volatile anesthetics like isoflurane, sevoflurane, and desflurane do not appear to inhibit HPV as profoundly, and their clinical effects on HPV are virtually negligible at doses around 1.0 MAC.
Why do patients with COPD sometimes become hypercapnic with supplemental O2 administration?
1) Blunting of HPV
Patients with advanced COPD who otherwise exhibit substantially elevated shunt fractions due to the presence of under-ventilated and hypoxic alveoli, are therefore highly dependent on HPV to maintain adequate gas exchange.
Unfortunately this tenuous balance is easily disrupted. When supplemental O2 is applied, PAO2 increases in under-ventilated alveoli, decreasing the degree of HPV and increasing blood flow to those alveolar units. However, these under-ventilated alveoli continue to maintain a high CO2 tension (PACO2) which disfavors the release of CO2 from the pulmonary capillary blood. The result is a significant increase in systemic CO2 retention with the rapid development of hypercapnia.
2) Haldane Effect (minor contributor)
Increase in arterial O2 tension will result in more CO2 offloading from hemoglobin.
What electrolyte derrangements are seen in Refeeding Syndrome?
Hypokalemia
Hypophosphatemia
Hypomagnesemia
“Leave Me a Plate Please”=
Low Mag, Phosp, Potassium
Total parenteral nutrition is an intravenous infusion of nutrients used to support patients who cannot receive enteral feeding. It typically contains dextrose, amino acids, and lipids to support the patient’s metabolism as well as the electrolytes sodium, chloride, potassium, magnesium, phosphate, and, sometimes, calcium. Total parenteral nutrition also contains the vitamins and trace minerals required to support metabolism; however, TPN is associated with several notable derangements in electrolyte levels if it is not properly managed.
Hypophosphatemia (phosphate level below 2.5mg/dL) is common in patients receiving TPN. The glucose loading in TPN causes an intracellular shift of phosphate, causing a precipitous drop in phosphate with the initiation of TPN. Phosphate levels below 1 mg/dL may cause seizures, heart failure, tachypnea, hemolytic anemia, and death. A slowly advanced TPN regimen and frequent phosphate monitoring and repletion can mitigate this complication.
Hypomagnesemia and hypokalemia are also frequently seen in patients receiving TPN. When a patient develops hypomagnesemia, hypokalemia, and hypophosphatemia after initiating TPN, this is termed refeeding syndrome. Calcium is the electrolyte that is often elevated in patients receiving TPN, which is why calcium is sometimes omitted from TPN solutions. Before TPN is initiated, assessing and correcting for any electrolyte abnormalities is essential.
Some common causes of hypophosphatemia are…
Some common causes of hypophosphatemia are
- Catecholamine therapy (intracellular redistribution of phosphate)
- Refeeding syndrome (insulin-induced cellular phosphate uptake)
- Alcoholism or malnutrition (inadequate intake or absorption)
- Acute alkalemia (hyperventilation causing respiratory alkalosis and intracellular redistribution of phosphate)
- Renal impairment (diuretic therapy, renal tubular defects)
- Gastrointestinal losses (malabsorption syndrome or use of phosphate-binding antacids)
Hypophosphatemia = phosphate <2.5 mg/dL
Phosphate is an electrolyte that plays an important role in cellular energy, and hypophosphatemia can lead to respiratory, neurologic, and hematologic manifestations. This occurs especially when levels drop below 1 mg/dL, which can result in significant organ dysfunction.
Loop diuretics can cause hypo/hyper-calcemia?
Hypocalcemia
Thus, loop diuretics (eg. Lasix) is often used to treat hypercalcemia.
Thiazide diuretics can cause hypo/hyper-calcemia?
Hypercalemica
Thiazide-induced blockade of Na+ entry enchances the Na+/Ca2+ antiporter activity and increases overall reabsorption of Ca2+
NOTE:
Thiazides are useful in the prevention of calcium-containing kidney stones caused by hypercalciuria.
What effect do diurectics have on the Frank-Starling curve?
Diuretics, such as Lasix, will decrease preload or LVEDV and therefore cause a left-shift along the curve. It will NOT shift the curve up.
The Frank-Starling curve is shifted down and to the right with increased afterload or decreased inotropy (eg systolic heart failure). Decreased afterload and increased inotropy will shift the curve up and to the left. Increased LVEDV for a given state of inotropy and afterload will shift the curve up and to the left. Decreases in LVEDV (eg diuretics) will cause a left shift along the curve.
First line treatment of hypercalcemia?
First line treatment: Rehydration (isotonic saline)
Patients with hypercalcemia are often significantly dehydrated. Rehydration lowers calcium levels slightly via a dilutional effect. Additionally, rehydration prevents sodium and calcium reabsorption from the thick ascending limb of the loop of Henle.
Second line treatment: Loop diuretics, calcitonin, bisphosphonates
NOTE:
Metabolic acidosis causes hypercalcemia (increased ionization of calcium and thus less protein binding).
Metabolic alkalosis causes hypocalcemia (decreased ionization of calcium and thus more protein binding).
Symptoms of hypermagnesemia?
Treatment of hypermagnesemia?
Normal serum magnesium levels are between 1.5 and 2.5 mg/dL.
Hypermagnesemia is > 2.5 mg/dL and can result from kidney impairment, overuse of magnesium-based laxatives or enemas, over-infusion of magnesium in preeclampsia treatment, and disorders such as milk-alkali syndrome.
Hypermagnesemia results in neurotoxicity by decreasing transmission of the impulse across the neuromuscular junction, resulting initially in diminished deep tendon reflexes. As the magnesium levels rise (table), the reflexes disappear.
Cardiotoxicity results from magnesium acting as a calcium and potassium channel blocker, disrupting cardiac function and leading to complete heart block and cardiac arrest (> 12 mg/dL). Due to its calcium channel blocker effects, magnesium can lead to hypotension, bradycardia, and changes seen on electrocardiogram (ECG), including prolonged PR interval and widened QRS.
Stopping the source of magnesium is the first step in the treatment of hypermagnesemia. If the patient is symptomatic, calcium gluconate can be administered. The elimination of magnesium can be further increased by adding a loop diuretic and increasing diuresis with normal saline. If the patient has renal failure, dialysis is indicated.
Describe the Haldane Effect.
The Haldane effect is a physicochemical phenomenon which describes the increased capacity of blood to carry CO2 under conditions of decreased haemoglobin oxygen saturation (ie hypoxia).
More CO2 binds to haemoglobin at lower oxygen saturation. This effect facilitates the removal of CO2 from the tissues
Describe the Bohr Effect.
The Bohr effect describes hemoglobin’s lower affinity for oxygen secondary to increases in the partial pressure of carbon dioxide and/or decreased blood pH (ie. hypercapnia, acidosis).
This lower affinity, in turn, enhances the unloading of oxygen into tissues to meet the oxygen demand of the tissue.
Describe the ACLS management of bradycardia
First line treatment is Atropine
Atropine is indicated for symptomatic bradycardia regardless of the conduction cause.
However, it may be ineffective for second-degree Type II and third-degree blocks.
Which NMBAs undergo Hoffman Elimination?
Cisatracurium
Atracurium
NOTE:
Cisatracurium is a nondepolarizing neuromuscular blocking agent that is of intermediate duration (20-50 min) ,with an onset of 4 to 6 minutes. It was created to reduce the histamine release associated with atracurium. Because of its potency, 5 times less cisatracurium is used compared to atracurium, resulting in a minimal histamine release. Cisatracurium is not reliant on liver or kidney function because it spontaneously degrades in the plasma via Hofmann elimination and ester hydrolysis into inactive metabolites. As a result, it is used clinically in patients with severe renal dysfunction. The Hofmann elimination is pH- and temperature-dependent, with an increase in pH increasing degradation and hypothermia slowing down the degradation.
Hoffman Elimination is increased under what two conditions?
Increased pH
Increased temperature
Which NMBAs undergo metabolism by pseudocholinesterase?
Succinylcholine
Mivacurium
NOTE:
Patients with pseudocholinesterase deficiency will have prolonged neuromuscular blockade.
Also note ester local anesthetics are metabolized by pseudocholinesterases as well.
Somethings “SMeLs” fishy
What medications are metabolized by RBC and plasma esterases?
Clevidipine
Esmolol
Remifentanil
NOTE:
Hence fast onset/offset of each.
Which NMBAs are reversed by Sugammadex?
Rocuronium
Vecuronium
“Sugammadex RV”
Duration of action:
Atropine
Glycopyrrolate
Duration of action:
Atropine 15-30min
Glycopyrrolate 2-4hrs
Induction dose and onset time for non-depolarizing NMBAs?
Is Rocuronium safe to use in renal failure?
YES
Rocuronium is metabolized by the liver and eliminated primarily by the hepatobiliary system (70%) and to a lesser degree renally eliminated. Because of this the elimination of rocuronium is slightly extended in renal failure but has not been shown to be significant clinically.
Which NMBAs can cause prolonged muscular blockade in patients with renal failure?
PANCURONIUM
Pancuronium is the most dependent on renal metabolism, and its pharmacokinetics would be most significantly impacted in the setting of renal disease (neuromuscular blockade is prolonged).
The metabolite of pancuronium, 3-desacetylpancuronium, is half as potent as its parent compound and can accumulate in renal failure due to its significant (85%) renal elimination, leading to prolongation of the neuromuscular blockade.
VECURONIUM
Vecuronium is primary eliminated through the biliary system. However, there is a small amount of vecuronium that is eliminated by the kidneys. Additionally, vecuronium has an active metabolite, 3-desacetylvecuronium, which has about 80% the potency of vecuronium and is primarily eliminated through the kidneys.
The duration of action of vecuronium is also increased with age, which means that the same dose of vecuronium will have longer lasting effects. One study showed the duration increases from 44 minutes to 73 minutes; dosing could therefore be decreased by 36% per this study.
“Very Prolonged in renal failure”
Define ED95 as it relates to paralytics.
ED95 is the median dose required to achieve 95% reduction in maximal twitch response from baseline in 50% of the population.
Describe TURP syndrome.
During TURP, the wide plexus of venous sinuses is often opened and the absorption of the irrigation fluid causes a group of symptoms and findings that is called TURP syndrome.
Absorption of the irrigation fluid (2000 ml or more) may lead to TURP syndrome which causes headaches, anxiety, confusion, dyspnoea, arrhythmia, hypotension and seizures and can be fatal if not treated.
The symptoms of TURP are generally caused by an excessive fluid load in circulation. Different symptoms may occur depending on the solute used in the irrigation fluid.
Excessive absorption of the irrigation solutions used during TURP, which are highly hypotonic can cause dilutional hyponatremia and hypo-osmolality resulting in severe neurological symptoms.
Describe the Hepatic Arterial Buffer Response (HABR).
The hepatic arterial buffer response (HABR) is the system within the liver responsible for maintaining constant hepatic blood flow and is *unaffected by intravenous or volatile anesthetics. *
The system functions in a manner such that when portal venous blood flow decreases, the hepatic artery vasodilates to maintain perfusion. The main determinant controlling this hepatic blood flow is adenosine. It is produced in the space of Mall which surrounds the hepatic vasculature and diffuses into the portal vein. When the portal venous blood flow decreases, the adenosine accumulates resulting in vasodilation of the hepatic artery increasing blood flow to the liver by the hepatic artery.
_____________ is the only anesthetic that increases blood flow to the liver.
Propofol is the only anesthetic that increases blood flow to the liver.
The effects of anesthetics on hepatic blood flow stem from their ability to alter perfusion to the liver. Total hepatic blood flow is the sum of portal venous blood flow plus the hepatic artery blood flow. When there is a reduction in portal venous blood flow, the hepatic artery increases blood flow via the hepatic arterial buffer response.
Volatile anesthetics reduce portal venous blood flow by decreasing mean arterial pressure and cardiac output. Despite this, isoflurane, desflurane, and sevoflurane mostly preserve total hepatic blood flow at 1 minimum alveolar concentration (MAC) by leaving the hepatic arterial buffer response intact. At concentrations higher that 1 MAC, isoflurane will reduce total hepatic blood flow in a dose-dependent manner. Intravenous and neuraxial anesthetics also alter blood flow. Propofol increases hepatic blood flow, while barbiturates, benzodiazepines, dexmedetomidine, and etomidate have little effect on hepatic blood flow but may decrease somewhat. Ketamine does not alter hepatic blood flow.
Use of propofol, an intravenous anesthetic, results in an increase in blood flow to the liver, and it is the only anesthetic to increase blood flow.
NOTE:
Glucagon, D1 agonism, B2 agonsim, Adenosine (A2 agonism) all increase HBF.
Propofol
Metabolism?
Hepatic metabolism
Propofol has a very high hepatic extraction ratio (near 1)
Does Propofol or Etomidate have a higher incidence of superficial thrombophlebitis?
ETOMIDATE
Thrombophelbitis is a condition where a vein becomes inflamed related to a thrombus that has formed in the vein (thrombo-phleblitis).
Risks include small vein, slow injection, and high doses.
Etomidate is poorly water-soluble and therefore formulated as a solution in PEG. This preparation of PEG is analogous to an extremely hyperosomolar solution compared to normal serum osmolality. Hyperosmolality is thought to be the major contributing factor in pain on injection and venous irritation. There are reports of phlebitis and thrombophlebitis after injection with PEG preparations of Etomidate up to 7 days after surgery.
Glucagon is a catabolic peptide secreted by the pancreatic α-cells located in the islets of Langerhans in response to __________, __________, and __________.
Glucagon is a catabolic peptide secreted by the pancreatic α-cells located in the islets of Langerhans in response to hypoglycemia, B2 stimulation (eg. epinephrine, NE), and cortisol.
Glucagon
MOA
Glucagon activates G-protein coupled recepotors activating adenyl-cyclase to increase cAMP levels.
Results:
- Increased gylcogenolysis
- Increased gluconeogenesis
- Inhibition of glycogenesis
- Increased lipolysis
- GI muscle relaxation
- Decreases biliary and LES tone
- Increases hepatic and splanchnic blood volume
- Positive chronotrope (increases HR)
- Positive inotrope (increases contractility)
NOTE:
Glucagon enhances activation of adenyl cyclase in the myocardium but its effects are not blocked by beta blockers.
Glucagon may be useful in treatment of beta blocker overdose by increasing cAMP in the myocardium while bypassing the second messenger system.
Glucagon is contraindicated in pheochromocytoma due to the risk of hyperglycemia and severe hypertension.
By what mechanism does nitric oxide produce vasodilation in pulmonary vasculature?
Activation of guanylate cyclase and increase in cGMP.
Another medication that is commonly used to increase intracellular cGMP is nitroglycerin. This medication is rapidly converted to NO in the body and this vasodilatory effect is leveraged to provide systemic vasodilation, either when a patient is having anginal symptoms or in more controlled circumstances in the operating room or ICU.
The medication sildenafil, originally created to treat pulmonary hypertension, has the same clinical effect as iNO. Sildenafil is a phosphodiesterase V inhibitor (which breaks down cGMP) and causes its clinical effect through the relaxation of smooth muscle in the pulmonary vasculature identically to iNO.
If arterial air embolism is suspected while on cardiopulmonary bypass what measures should be taken?
If arterial air embolism is suspected while on cardiopulmonary bypass it is reasonable to…
Initiate steep Trendelenburg positioning
Deep hypothermia (decrease CRMO2)
Retrograde cerebral perfusion
Mantain arterial oxygenation
Permissive hypercapnia (cerebral vasodilation)
Maintain/elevate CPP
FFP contents?
Factors II, VII, V, VIII, IX, X, XI
NOTE:
Used to treat dilutional coagulopathy during massive transfusion, coagulopathy related to hepatic deficiency, TTP, specific factor deficiencies, Warfarin reversal, anti-thrombin III deficiency.
Which factors are the least stable in FFP requiring FFP to be frozen?
Factor V
Factor VIII
NOTE:
Factor V and VIII are the least stable in blood products and can degrade above 4 degrees celcius.
This is mainly why FFP is frozen for storage.
FFP can be transfused up to 5 days after thawing, at which significant reductions occur in factor V and factor VIII.
PCC contents?
Factors II, VII, IX, X, Protein C, Protein S
Cryopercipitate contents?
Factors VIII, XIII, fibrinogen, vWF
_ units of cryopercipitate will typically raise a 70kg patient’s fibrinogen by 70mg/dL.
10 units of cryopercipitate will typically raise a 70kg patient’s fibrinogen by 70mg/dL.
NOTE:
Cryopercipitate contains approximately 200mg/unit of fibrinogen.
Cryopercipitate is often given during massive transfusion after several units of other blood products have been given.
Checking fibrinogen levels during massive transfusion can assist with management of cryopercipitate.
Cryopercipitate is also used to treat vWF disease and hemophilia A.
What is the role of factor VIII in massive transfusion?
Use of factor VIII during massive transfusion is theoretical and not proven.
Factor VIII levels have to decrease to below 30% to alter hemostasis.
Because PRBCs contain very little coagulation factors, it is theoretical that levels could decrease during massive transfusions.
However, both fresh frozen plasma and cryoprecipitate contain factor VIII; these products are typically transfused during a massive transfusion protocol thus administration of factor VIII concentrate is not necessary.
Equation for volume of FFP needed to correct INR:
Amount FFP Needed (mL) = (Target Level - Present Level) * kg
For example, let’s say we have a 70kg patient who is bleeding with an INR of 7.5 and our goal INR is 1.4. We would need (40% - 5%) * 70 kg, which is 2450 mL of FFP to make this correction. A single unit of FFP typically is 200-250 mL.
Hemophilia A is an X-linked recessive disorder caused by deficiency of factor _______
Hemophilia B is an X-linked recessive disorder caused by deficiency of factor _______
Hemophilia A is an X-linked recessive disorder caused by deficiency of factor VIII (treatment: desmopressin, factor VIII concentrate)
Hemophilia B is an X-linked recessive disorder caused by deficiency of factor IX (treatment: recombinant factor IX)
Definition and calculation of Ideal Body Weight (IBW)
Ideal body weight (IBW) is the optimal weight associated with maximum life expectancy for a given height.
Ideal body weight (male) = height (cm) – 100
Ideal body weight (female) = height (cm) – 105
Calculation of Lean Body Weight (LBW)
Lean body weight (male) = 1.1 (weight [kg]) – 128 (weight / height) ^ 2
Lean body weight (female) = 1.07 (weight [kg]) – 148 (weight / height) ^ 2
Propofol should be dosed based on _____________ body weight.
Propofol should be dosed based on lean body weight.
Rocuronium should be dosed base on _______ body weight.
Rocuronium should be dosed base on ideal body weight.
Specific medications in anesthesia and how dosage should be calculated:
Total body weight:
Lean body weight:
Ideal body weight:
Specific medications in anesthesia and how dosage should be calculated:
Total body weight: succinylcholine, maintenance infusion dose of propofol
Lean body weight: induction dose of propofol, fentanyl
Ideal body weight: rocuronium, vecuronium
Note that obese patients have increased butrylcholinesterase activity and increased ECF hence sucinnylcholine should be based on total body weight.
How does the pharmacokinetics of non-depolarizing NMBAs differ in the elderly compared to young patients? (ie onset, duration, redosing)
The following changes occur in the elderly (≥65 years) affecting the function, duration, and elimination of NMBAs:
* Increased total body fat
* Decreased total body water
* Decreased lean body mass
* Decreased renal and hepatic blood flow
* Decreased hepatic function
* Decreased glomerular filtration rate
* Decreased cardiac output
As a result of a decrease in cardiac output, the circulatory time is increased, leading to a slower onset for NMBAs. Prolongation of the duration of action is also seen due to decreased metabolism and clearance for NMBAs that rely on hepatic and renal excretion and metabolism as well as distribution due to changes in blood flow and body mass. In addition, there is a decrease in the dosing requirements for maintenance of the neuromuscular blockade, which is evident clinically by an increased duration between dosing intervals required to maintain the same depth of neuromuscular blockade compared to that in younger patients.
What are the six clinical characteristics used to calculate a patients Revised Cardiac Risk Index (RCRI)?
IHD
CHF
CVA
DM requiring insulin
Cr >2
High risk procedure
Using a risk stratification scoring system such as the Revised Cardiac Risk Index (RCRI) is helpful in determining patients at risk of postoperative mortality from MI on the basis of their risk factors. The risk of an adverse cardiac event increases with the number of risk factors present. The RCRI establishes a 30-day mortality risk for patients, depending on the risk inherent to the surgery itself (according to the RCRI scoring system, “high risk” surgeries include intraperitoneal, intrathoracic, or suprainguinal vascular surgery), history of ischemic heart disease, history of congestive heart failure, history of stroke, poor kidney function, or insulin-dependent diabetes.
On the basis of the original data used to create the RCRI, the risk of a major cardiac event is 0.4% with zero points, 1% with one point, 2.4% with two points, and 5.4% with three or more points.
Other factors to consider prior to surgery involve preoperative functional capacity evaluation, cardiac markers, and using pharmacologic or treadmill stress testing to establish a functional cardiac baseline. The American College of Cardiologists and the American Heart Association recommendations require that all patients must be able to achieve an activity level equal to 4 or more metabolic equivalents (MET) prior to undergoing surgery as studies have shown that patients who cannot achieve 4 METs are at increased risk of adverse perioperative cardiac events.
Define emergent, urgent, time-sensitive, and elective procedures.
An emergency exists when life or limb is threatened if the patient is not in the operating room within six hours.
An urgent procedure is required when life or limb is threatened if the patient is not in the operating room within 24 hours.
A time sensitive procedure can be delayed 1-6 weeks for evaluation if it will change management.
An elective procedure can be delayed up until one year.
How is a phase II block is characterized?
A phase II block can be seen in which patients?
Aphase II block is characterized by fade of TOF, tetanic fade, and post-tetanic potentiation.
A phase II block is seen with the following:
1) Non-depolarizing NMBAs
2) Prolonged exposure to succinylcholine (repeated doses > 4mg/kg, infusions)
3) Single dose of succinylcholine in a patient with pseudocholinesterase deficiency
NOTE:
A single, normal dose of succinylcholine should only produce a phase I block often preceeded by muscle fasiculation. A phase I block is characterized by a diminished but equal height in the TOF.
Why is it that non-depolarizing NMBAs cause a phase II block but a single dose of succinylcholine produces a phase I block (and not a phase II block)?
Non-depolarizing NMBAs also block presynaptic acetylcholine receptors.
Succinylcholine does not block presynaptic acetylcholine receptors.
A single dose of Succinylcholine will produce a phase _ block.
A single dose of Succinylcholine will produce a phase 1 block.
Repeated dose of Succinylcholine or infusion of Succinylcholine will produce a phase _ block.
Repeated dose of Succinylcholine or infusion of Succinylcholine will produce a phase II block.
Succinylcholine administered to a patient with pseudocholinesterase deficiency will produce a phase _ block.
Succinylcholine administered to a patient with pseudocholinesterase deficiency will produce a phase II block.
What is post-tetanic potentiation?
Phenomenom where tetanic stimulation increases the effect of a single twitch applied immediately after.
Occurs due to increased Ca2+ in presynaptic neurons and thus increase in acetylcholine at the motor endplate.
It is most useful when deep levels (TOFC = 0) are present.
TOF count and corresponding % nACR blockade:
0:
1:
2:
3:
4:
TOF count and corresponding % nACR blockade:
0: 100%
1: 90%
2: 80%
3: 70-80%
4: < 70%
The recommended target for intraoperative blood glucose levels is <________ mg/dL.
The recommended target for intraoperative blood glucose levels is <180 mg/dL.
When should Metformin be held for surgery?
The classic teaching is that Metformin must be stopped the day before surgery for fear of lactic acidosis forming in the perioperative period.
Miller Clinical Anesthesia states that “Metformin does not have to be routinely discontinued the day before surgery.” The problem with routine discontinuation of Metformin is the possibility of worsening glycemic contnrol, something we know is problematicand causes poor outcomes. The risk of lactic acidosis is very low and exists in patients who then go on to develop renal and hepatic failure while taking Metformin.
In specific patients with renal or hepatic failure who are being exposed to IV contrast or having procedures with significant blood loss or hemodynamic instability, it may be reasonable to hold Metformin.
Should ACE inhibitors be continued on the day of surgery?
The issue of perioperative continuation of angiotensin converting enzyme inhibitors and angiotensin receptor blockers is not entirely settled.
The 2014 ACC/AHA guidelines state is it “reasonable” to continue them perioperatively, but anesthesia textbooks urge caution as they **may cause refractory hypotension. **
In a more recent large prospective observational study, continuation of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers was associated with a higher risk of death and postoperative vascular events.
Should diuretics be continued on the day of surgery?
Whether or not to stop a diuretic is controversial and depends on the patient’s history and the surgery planned.
Most experts would recommend holding the diuretic especially for a surgery that has the potential for volume shifts (eg open abdominal) and significant blood loss.
The concern with continuation includes volume management, potential hemodynamic derrangements, and electrolytes abnormalities. Potassium derrangements can lead to arrhythmias, altered response to muscle relaxants, and potentiation of ileus.
Studies have NOT shown an increased risk of intraoperative hypotension when the patient is on chronic therapy.
What effect do carbohydrate-rich drinks given 2h before surgery have on insulin sensitivity?
Carbohydrate-rich drinks given 2h before surgery INCREASES insulin sensitivity.
A systematic review of 17 studies (1445 patients) showed carbohydrate loading reduced postoperative insulin resistance.
In patients undergoing major abdominal surgery, carbohydrate loading has also been associated with a reduced hospital length of stay.
Should patients on long-term beta-blockers take their beta-blocker on the day of surgery?
YES.
According to the American College of Cardiologists/American Heart Association 2014 guidelines, patients taking long-term or chronic beta-blockers should continue these medications through the perioperative period including the day of surgery.
Results of several well-powered studies have provided evidence that individuals who stop taking their long-term beta-blockers within 48 hours of surgery have an elevated mortality risk of cardiac ischemia after noncardiac surgery.
OTHER:
Beta-blocker therapy is an important treatment consideration for high-risk patients undergoing non-cardiac surgery. Identifying patients at high risk for ischemia, either from their risk factors or their planned surgery, and considering beta-blocker therapy preoperative is potentially beneficial to alter their risk of major adverse cardiac events. Patients with known inducible ischemia may receive even more benefit from preoperative beta-blocker therapy and thus it should be highly considered in that patient population. It is known that beta-blocker therapy should not be started within 1 day of surgery as that significantly increases the risk of stroke and death. Thus the recommendation from most experts/guidelines is to initiate therapy at least 2 days, but preferably 7-45 days prior to surgery. Additionally, anyone who is currently on a beta-blocker should have that medication continued in the perioperative period.
Holding of which two anti-hypertensives the morning of surgery can lead to rebound hypertension?
Beta Blockers
Clonidine
NOTE:
Holding Clonidine can also lead to severe delirium.
The herbal supplement Ginseng can raise what perioperative concerns?
Hypoglycemia
Shown to decrease postprandial blood glucose in patients with and without diabetes. In the setting of perioperative fasting prior to surgery this can result in hypoglycemia. Animal studies demonstrate direct stimulation of insulin release.
Bleeding
Potentially irreversible platelet inhibition- inhibition of platelet aggregation that may be permanent and may increase bleeding. May also interefere with Warfarin anticoagulation.
NOTE:
Patients should hold Ginseng 7-14 days prior to surgery.
Herbal supplements starting with the letter “G” inhibit platelet aggregation and can increase risk of bleeding (Garlic, Ginger, Ginseng, Ginko)
The herbal supplement St. John’s wort can raise what perioperative concerns?
Delayed emergence
Altered drug metabolism
(CYP450 inducer can affect benzos, lidocaine, alfentanil, warfarin, digoxin)
Risk of serotonin syndrome
(SNRI-inhibitor risk of serotonin syndrome with other meds)
The herbal supplement Garlic can raise what perioperative concerns?
Bleeding
It inhibits platelet aggregation and increases fibrinolysis. Can increase risk of bleeding especially when patients are on other antiplatlet agents.
NOTE:
Garlic should be held 7 days prior to surgery.
Herbal supplements starting with the letter “G” inhibit platelet aggregation and can increase risk of bleeding (Garlic, Ginger, Ginseng, Ginko)
The cardioselective (β1) blockers include:
The cardioselective (β1) blockers may be remembered by using the mnemonic “BEAM” (Bisoprolol, Esmolol, Atenolol, and Metoprolol).
Which NMBAs have enhanced effects in patients with renal dysfunction due to decreased clearance?
Vecuronium, Pancuronium
“Very Prolonged” in renal failure
Pancuronium is the most dependent on renal clearance and prolongation has been reported in patients with significant renal impairment.
How does Sugammadex affect oral contraceptive efficacy?
Sugammadex is a reversal agent for the steroidal neuromuscular blocking medications rocuronium and vecuronium.
Sugammadex is amodified y-cyclodextrin with an 8-member ring with a central core that encapsulates the steroid nucleus of rocuronium and vecuronium (intermediate-acting neuromuscular blocking agents).
Sugammadex is relatively selective for steroidal neuromuscular blocking drugs but does additionally bind to the steroidal portions of toremifene, flucloxacillin, progesterone, and fusidic acid.
Oral contraception has been known to be affected by sugammadex, with the administration of sugammadex being equivalent to missing 1 daily oral dose; thus, it is recommended to use alternative means of birth control for 1 week after sugammadex administration.
Incidence of intraoperative anaphylaxis to Sugammadex?
Estimated to be anywhere between 1:5000 to 1:20,000.
Sugammadex is a synthetic, modified γ-cyclodextrin. Therefore, a patient with hypersensitivity to cyclodextrins is at significantly increased risk for an anaphylactic reaction to sugammadex, and its use is contraindicated.
Coronary Perfusion Pressure (CPP) =
The CCP is determined by the difference between aortic diastolic pressure (AoDP) and left ventricular end-diastolic pressure (LVEDP) by the equation CPP = AoDP − LVEDP.
Describe the sensory and motor innervation of the larynx.
Larynx is innervated by two nerves branching from VAGUS NERVE (CN X)
SUPERIOR LARYNGEAL NERVE:
Sensory: internal branch supplies sensation to mucosa from epiglottis to vocal cords
Motor: external branch supplies CRICOTHYROID MUSCLE (lengthens vocal cords).
RECURRENT LARYNGEAL NERVE:
Sensory: mucosa below vocal cords
Motor: ALL OTHER INTRINSIC MUSCLES of larynx except cricothyroid muscle
The left recurrent laryngeal nerve branches off the left vagus nerve, loops under the aorta, and travels superiorly between the esophagus and trachea. The right recurrent laryngeal nerve branches off the right vagus, loops under the right subclavian artery, and travels superiorly between the esophagus and trachea on the right.
Describe the symptoms of…
RLN injury (unilateral, bilateral)
SLN injury (unilateral, bilateral)
If there is a unilateral recurrent laryngeal nerve injury, there will be ipsilateral paralysis of all intrinsic laryngeal muscles except for the cricothyroid muscle. Thus, on inspiration, the paralyzed vocal cord will not abduct properly. The patient may be asymptomatic or present with hoarseness. With phonation, the paralyzed vocal cord will have assumed a paramedian position due to the unopposed action of the cricothyroid muscle. With time, the unparalyzed vocal cord will move toward the paralyzed vocal cord, and phonation will improve.
In bilateral recurrent laryngeal nerve injury, the vocal cords will not abduct properly and may present as fixed airway obstruction.
In unilateral superior laryngeal nerve injury, there will be decreased pitched and weakened voice.
Bilateral superior laryngeal nerve injury is rare and will present with coughing; choking episodes; and a weak, husky voice.
What two nerves should be anesthetized for awake nasal FOB intubation?
Two other nerves that should be anesthetized for an awake nasal FOB intubation include:
Glossopharyngeal Nerve (CN IX)
(Sensory innervation to posterior 1/3 of tongue, pharynx, and areas above epiglottis0
Trigeminal Nerve (CN V)-
Ophthalmic Branch (V1): sensory innervation to anterior portion of nasopharynx
Maxillary Branch (V2): Sensory innervation to posterior portion of nasopharynx
Gag reflex
Afferent Limb:
Efferent Limb:
Glossopharyngeal Nerve (IX)
(Afferent limb)
Vagus Nerve (X)
(Efferent limb)
The gag reflex (or pharyngeal reflex) is triggered by afferent signaling via the glossopharyngeal nerve (CN IX) and produces pharyngeal muscle contraction mediated primarily by the bilateral vagus nerves (CN X). This reflex prevents entry of debris into the hypopharynx and thus protects against aspiration and asphyxiation. However, the gag reflex may also complicate airway management and provoke emesis in an awake or lightly anesthetized patient.
Oculocardiac reflex
Afferent Limb:
Efferent Limb:
Oculocardiac reflex
Afferent Limb: Trigeminal nerve, ophthalmic division (V1)
Efferent Limb: Vagus (X)
Triggered by
1) Direct pressure on the eye
2) Traction on EOM
3) Retrobulbar block
What is the Bainbridge reflex?
The Bainbridge reflex is mediated by type-B stretch sensitive mechanoreceptors in the right atrium and cavoatrial junction.
When cardiac preload is increases, stretch receptors send signals via the vagus nerve (CN X) to the medulla.
Medulla sends efferent response to inhibit parasympathetic activity which increases heart rate.
What situations can result in advancement of the ETT into the mainstem?
Head/neck flexion
Trendelenburg
Pneumoperiotneum/insufflation
NOTE:
Trendelenburg and pneumoperitoneum/insufflation doesnt actually move the tip of the ETT but pushes the lung up and trachea cephaled relative to the tip of the ETT.
Conversely, head/neck extension and reverse RT will cause cephalad movement of the ETT.
With respect to head/neck flexion and extension just remember that the “hose follows the nose”
Major contraindications for LMA use include but are not limited to:
Major contraindications for LMA use include, but are not limited to:
* Patients with a high risk for aspiration of gastric contents (full stomach, hiatal hernia, gastroesophageal reflux disease, intestinal obstruction, and delayed gastric emptying)
* Lung disease (low compliance, high airway resistance)
* Airway obstructions (glottic, subglottic)
* Lmited mouth opening (generally less than 1.5 cm)
OTHER:
Most (2 in 3) patients that have aspirated are asymptomatic by two hours and require no additional intervention. Of those who develop respiratory symptoms (1 in 3), non-invasive or invasive ventilation may be temporarily required, and there is a mortality of approximately 10%. Patients who are ventilated > 48 hours have a nearly 50% mortality rate.
Factors that decrease and increase lower esophageal sphincter tone?
See picture
NOTE:
Although routinely used to decrease risk of aspiration, recent evidence suggests cricoid pressure may actually increase for reflux in anesthetized patients. Cricoid pressure decreases LES tone without influencing gastric pressure. This leads to a decreased barrier pressure (difference between LES pressure and gastric pressure) and therefore potentially increases the risk of aspiration. The clinical signficance of this however has not been determined. Opponents of cricoid pressure affirm that succinylcholine increases LES tone making the need for cricoid pressure during RSI questionable.
Succinylcholine increases LES tone and intragrastric pressure, but LES > intragastric pressure. Unless the patient has an incompetent LES, there is no increased risk of aspiration.
Lower esophageal sphincter (LES) pressure is approximately _ mmHg.
Lower esophageal sphincter (LES) pressure is approximately 25 mmHg.
Gastric effects of medications used for aspiration prophylaxis:
Overinflation of small-fitting LMAs is asssociated with what specific injuries?
Although it is uncommon, laryngeal mask airway (LMA) use has been associated with lingual, hypoglossal, and recurrent laryngeal nerve injuries.
These complications have been associated with overinflation of a small-fitting cuff, prolonged operative time (>2-4 hours), lidocaine lubrication, difficult insertion, use of nitrous oxide, and cervical joint disease. Pressure neuropraxia from the LMA tube and/or cuff is the most common cause of these nerve injuries.
The increased oropharyngeal soft tissue pressure leads to injury of the lingual nerve, hypoglossal nerve (CN XII), and recurrent laryngeal nerve, which may cause tongue numbness, oropharyngeal swelling, and transient vocal cord palsy leading to difficulty with phonation. The use of nitrous oxide(NO2) can cause an increase of up to 30 mmHg in LMA cuff pressure on the soft tissue because NO2 can displace air within the cuff. Adjusting LMA placement and/or changing to a larger size LMA is appropriate when more than the recommended air insufflation is required to maintain a mask seal (typically, 60 cm H2O or 44 mmHg).
Correct positioning may be best verified by generating an airway pressure of 20 cm H2O and the ability to ventilate manually using the reservoir bag.
Which antacid may be given to patients at increased risk of pulmonary aspiration?
Sodium Citrate
NOTE:
According to the ASA guidelines, medications should not be routinely administered preoperatively solely to reduce pulmonary aspiration risk in patients who have no apparent increased risk of pulmonary aspiration. The ASA guidelines state that medications can be given to high-risk patients. High-risk patients typically include those with multiple aspiration risk factors, such as diabetic gastroparesis, hiatal hernia, inappropriate fasting status, morbid obesity (body mass index >40 kg/m2, now known as class III obesity), nasogastric tube in place, pregnancy, and symptomatic gastroesophageal reflux disease. The overall goal of using these medications is to decrease gastric volume and increase pH.
SAMBA Guidelines for Risk Factors for PONV
Female sex
Age <50 years
Nonsmoker
History of PONV or motion sickness
Use of post-operative opioids
Specific surgeries (laparoscopic esp chole, gynecologic)
Use of volatile anesthetics or NO
Long duration of anesthesia
Medications for PONV target the chemoreceptor trigger zone (CTZ) in the area postrema of the brainstem. The CTZ contains dopamine (D2), histamine (H1), muscarinic acetylcholine (M1), neurokinin (NK1), opioid, and serotonin (5HT3) receptors. Multimodal use of dopamine antagonists (e.g. IV droperidol 0.625 mg, haldol), histamine antagonists (diphenhydramine, promethazine), neurokinin antagonists (aprepitant), muscarinic antagonists (scopolamine), serotonin antagonists (IV ondansetron 4 mg, palonosetron), and steroids (dexamethasone 4mg) may be used for PONV.
Famotidine (Pepcid)
MOA
Famotidine (Pepcid)
MOA: H2-antagonist; Increases gastric pH and deceases gastric volume
Onset (IV): 30min
Metoclopramide (Reglan)
MOA
Metoclopramide (Reglan)
MOA: Dopamine (D2) antagonist; Decreases gastric volume, no effect on gastric pH, relaxation of pyloric sphincter and
duodenal bulb, increases lower esophageal
sphincter tone
Onset (IV): 3 min
Metoclopramide is a weak antiemetic, and, at a dose of 10 mg IV, it is not thought to be effective when used in combination with other antiemetics for prophylaxis. Metoclopramide is a more effective antiemetic at 25 to 50 mg, but, at these higher doses, the risk of adverse effects such as tachycardia, hypotension, and extrapyramidal symptoms is also higher. The current SAMBA guidelines suggest using metoclopramide only when other dopamine antagonists (such as droperidol) are not available.
Dexamethasone
MOA
1) NR3C1 agonist (anti-inflammatory effect)
Glucocorticoids such as dexamethasone agonize nuclear receptor subfamily 3, group C, member 1 (NR3C1), also known as the glucocorticoid receptor (GCR). Agonism of NR3C1 aka GCR treats inflammation. GCR regulates metabolism and immunity in most cells. In macrophages, upregulation of GCR leads to increased expression of anti-inflammatory proteins and inhibition of the expression of pro-inflammatory proteins.
2) Phospholipase A2 inhibitor (analgesic effect)
Corticosteroids also inhibit prostaglandin synthesis at phospholipase A2 at the beginning of the arachidonic acid pathway; thus, they have similar analgesic effects to NSAIDs, which block COX at the next step in the pathway.
Aprepitant (Emend)
MOA
NK1 antangonist
Aprepitant antagonizes the NK1 receptors in the CTZ. It blocks the actions of dopamine, NK1, and NK2.
Early trials have shown equal efficacy between aprepitant and ondansetron for their effects on nausea; however, aprepitant has been shown to be more efficacious against vomiting. IV Aprepitant has good efficacy for the prevention of vomiting for up to 48 hours postoperatively.
Aprepitant has not been shown to cause any changes in ECG, whereas several other antinausea medications such as droperidol, haloperidol, and ondansetron can cause QT prolongation.
Many of the antinausea, antiemetic medications target receptors in the chemoreceptor trigger zone (CTZ) (also known as the area postrema) along with the nearby nucleus tractus solitarius (both located in the medulla oblongata of the brainstem) are felt to contain dense quantities of emetogenic chemoreceptors.
Receptors identified in this area so far include dopamine, NK1, acetylcholine, serotonin, histamine (D-NASH).
What anti-emetic is effective in patients with PONV in PACU despite receiving prophylaxis?
Droperidol (Inapsine)
MOA: Dopamine (D2) antagonist
Dose: 0.625-1.25mg
Which medications should be avoided or used with caution in patients with glaucoma?
Dexamethasone
Scopalamine patch (anti-cholinergic)
Benadryl (anti-histamine, anti-cholinergic)
Glaucoma is a group of eye disorders in which the optic nerve is damaged and leads to visual loss. Most commonly this is caused by elevated intraocular pressure (IOP) which then impairs capillary blood flow to the optic nerve.
Open-angle glaucoma: IOP elevated due to impaired aqueous humor drainage in the setting of an antomically open anterior chanmber angle (angle between iris and cornea).
Closed-angle glaucoma: acute, sudden onset of eye pain and blurred vision. Result of closure of the angle between iris and cornea. Considered an emergency requiring immediate IOP reduction (via medication or surgery).
Several classes of perioperative medications should be used cautiously or avoided in patients with glaucoma. Medications that cause mydriasis (eg. anticholinergics, antihistamines) can impair aqueous humor drainage and acutely increase intraocular pressure (IOP). Their use is contraindicated in patients with or at risk for closed angle glaucoma and should be used cautiously in patients with open angle glaucoma.
Corticosteroids can increase IOP and even cause steroid-induced glaucoma and they should be used cautiously in patients with glaucoma.
Zofran does not cause or worsen glaucoma and is safe to use.
Atropine and glycopyrrolate (although anti-cholinergics, antimuscarinics) are generally considered safe to use in either population.
What are the five components of the modified Aldrete scoring system that is used to determine when a patient can be discharged from PACU?
Conciousness
Activity
Circulation
Respiration
Oxygenation
NOTE:
Patients can be discharged with a score of >9
Administration of _________ quickly and reliably treats extrapyramidal symptoms caused by antidopaminergic PONV medication administration.
Administration of an anticholinergic medication such as benztropine or diphenhydramine quickly and reliably treats extrapyramidal symptoms caused by antidopaminergic medication administration.
Second-line therapies include benzodiazepines, beta blockers, and atropine.
Thinks B’s for EPS - Benztropine, Benadryl, Benzos, BBs.
Although often effective for the treatment of postoperative nausea and vomiting (PONV), antidopaminergic drugs (e.g. droperidol, metoclopramide, prochlorperazine) can cause extrapyramidal symptoms (EPS) by altering the cholinergic-dopaminergic balance in the central nervous system, notably in the basal ganglia. They work by restoring the CNS cholinergic-dopaminergic balance.
Extrapyramidal side effects include acute dystonias (abnormal movement or posturing due to involuntary/sustained muscle contractions), akathisia (restlessness and the need to be in constant motion), and tardive dyskinesia (involuntary repetitive or purposeless movements)
A transdermal scopolamine patch must be applied ______ hours prior to the patient’s entering the operating room
A transdermal scopolamine patch must be applied ≥2 hours prior to the patient’s entering the operating room
Scopolamine
MOA
M1 anatgonist
H1 antagonist
NOTE:
Scopolamine is able to cross the blood-brain barrier
Scopolamine
Adverse effects
Sedation
Agitation
Dizziness
Blurred vision (20%)
Mydriasis (pupil dilation)
Cycloplegia (paralysis of accomadation)
Dry mouth (xerostomia)
NOTE:
Elderly patients are particularly more sensitive to scopolamine because 1) increased blood:brain permeability and 2) decrease ACH neurotransmission.
Due to its mydriatic and cycloplegic effects, scopolamine is contraindicated in patients with glaucoma.
Scopolamine should be avoided in patients with preclampsia as it can cause seizures (eclampsia).
The glottic closure reflex is mediated by…
Vagus Nerve- SLN
(Afferent limb)
Vagus Nerve (X)- RLN
(Efferent limb)
A critical physiologic function of the glottis is to prevent the entry of solids or liquids into the trachea and, thus, guard against pulmonary aspiration. The glottic closure reflex is an important contributor to this function in awake patients, allowing the vocal cords to rapidly and involuntarily adduct in response to stimulation of the supraglottic airway, at which point the entry of debris into the tracheobronchial tree may be imminent. However, this key mechanism is often undesirable when the airway is instrumented perioperatively because glottic closure may produce acute airway obstruction and render ventilation impossible. Inappropriate activation of the glottic closure reflex produces laryngospasm, which may evolve into an airway emergency.
The internal branch of the superior laryngeal nerve (a branch of the vagus nerve), which supplies sensory innervation to the portion of the hypopharynx above the glottis and the superior aspects of the vocal cords, is the main afferent mediator of the glottic closure reflex arc. This nerve registers stimulation at the hypopharynx as a result of direct instrumentation, pooled secretions, or other irritants. Activation of the reflex arc then leads to the abrupt closure of the glottis—that is, laryngospasm—via the motor functions of the bilateral recurrent laryngeal nerves at the vocal cord adductors (especially the lateral cricoarytenoid and transverse arytenoid muscles). Severe complications of laryngospasm may include hypoxia, hypercapnia, negative-pressure pulmonary edema, and death due to asphyxiation.
Additional Information:
The efferent branch of the laryngospasm reflex is mediated by the recurrent laryngeal nerve. The recurrent laryngeal nerve innervates all the intrinsic muscles of the larynx, with the exception of the cricothyroid muscle which is innervated by the external branch of the superior laryngeal nerve. The lateral cricoarytenoid and transverse arytenoid muscles are major adductors of the vocal cords. Additionally, the cricothyroid muscle tenses the vocal cords. These muscles are responsible for laryngospasm.
The larynx is a hollow structure composed of muscles and cartilage that extends from the epiglottis to the inferior aspect of the cricoid cartilage. The nerves that supply innervation to sensory and motor aspects of the larynx are the superior laryngeal and recurrent laryngeal nerves. The superior laryngeal nerve is divided into the external and internal branches. The internal branch supplies all sensation to the mucosa above the vocal folds. The external branch supplies the motor innervation to the cricothyroid muscle. The recurrent laryngeal nerve supplies sensory innervation below the vocal cords as well as all motor innervation to the laryngeal muscles except the cricothyroid muscle.
Treatment of laryngospasm
1) Deep suction (remove offending agent)
2) Positive pressure w/ 100% FiO2
3) Larson maneuver
4) Deepen anesthetic (Propofol), Succinylcholine (0.1-0.5mg/kg IV)
5) Reintubation w/ full dose induction agent and NMB
Laryngospasm refers to the sudden and forceful spasm of the true vocal cords that results in complete occlusion of the tracheal opening. This condition arises as an exaggerated laryngeal closure reflex that is triggered by either a mechanical or chemical stimuli of the pharynx or larynx. These stimuli tend to be more potent in the setting of pre-existing local inflammation as is present in patients with severe gastroesophageal reflux disease or in patients with a recent upper respiratory tract infection. Of the upper airway reflexes, the laryngeal closure reflex is the most resistant to the deepening of anesthesia, while the coughing reflex is the most sensitive.
Laryngospasm may be clinically diagnosed based upon the clinical judgment of the anesthesiologist. In general, apparent and increasing abdominal and chest wall efforts to breathe without evidence of air movement, such lack of ETCO2, lack of mask fogging, or worsening desaturation. These inspiratory efforts may manifest as suprasternal retractions, paradoxical chest and abdominal movements, and supraclavicular retractions. These signs will typically arise during the patient’s clinical course as they are proceeding through stage 2 of anesthesia during either induction or emergence.
**Treatment of laryngospasm varies according to the source or guidelines but generally follows the following algorithm. First, the irritant stimulus is removed if apparently present. This may include suctioning of the airway to remove excess secretions. Second, airway manipulation is attempted using a chin-lift and jaw-thrust maneuver in combination with continuous positive airway pressure (CPAP) administered with 100% oxygen through a tight-fitting mask. Up to 86% of patients who develop laryngospasm and are treated with CPAP and positive pressure ventilation will develop clinically significant abdominal distension which may require decompression via an orogastric or nasogastric tube in order to prevent regurgitation and subsequent aspiration of gastric contents.
**
Pressure in the “laryngospasm notch” just anterior to the pinna of the ear and under the angle of the mandible may be attempted at this time in order to stimulate and awaken the patient in an effort to proceed through stage 2 of anesthesia faster. This is referred to as the Larson maneuver. Should air movement not be apparent with this maneuver, either deepening of the anesthetic back into phase 3 of anesthesia or the administration of a muscle relaxant may be considered. The choice between these courses of action will depend on the availability of intravenous access. If IV access is available, propofol administration may be sufficient to reverse the laryngeal muscle spasm, though the patient will often become apneic following this course of action. In a case such as this question where IV access is not obtained, intramuscular succinylcholine may be administered to relax the laryngeal musculature. Intramuscular atropine should be considered if succinylcholine is administered given the risk of profound bradycardia and cardiac arrest following its administration.
It must be noted that hypoxemia will eventually cause the laryngeal musculature to relax and permit positive pressure ventilation. Waiting until this occurs, however, is not recommended, as this degree of hypoxia will raise the risk of severe bradycardia and cardiac arrest. The longer that the patient experiences laryngospasm, the greater their risk is for post-obstruction pulmonary edema, though this risk is relatively low in younger patients and increases to adult levels as they approach puberty. The cause for this protection against post-obstructive pulmonary edema is simply that younger patients are unable to generate sufficiently negative intrathoracic pressures to cause injury during upper airway obstruction.
NOTE:
If IV access unavailable Succinylcholine can be given IM (4mg/kg)
Laryngospasm
Afferent Limb:
Efferent Limb
Laryngospasm
Afferent Limb: Superior laryngeal nerve (internal branch)
Efferent Limb: Recurrent laryngeal nerve
The Posterior Cricoarytenoid Muscle is supplied by RLN and is the only muscle that causes _______ of the vocal cords.
The Posterior Cricoarytenoid Muscle is supplied by RLN and is the only muscle that causes ABDUCTION of the vocal cords.
Therefore, RLN damage leads to unopposed tensing and adduction of the cords.
The carotid bodies have chemoreceptors sensitive to changes in PaO2.
PaO2 values of around _ mmHg generate nerve impulses that are transmitted to the central respiratory centers in the medulla via the sinus nerve of Hering, an afferent branch of CN ____, which increases ventilatory drive (increased RR, TV, & MV).
The carotid bodies have chemoreceptors sensitive to changes in PaO2.
PaO2 values of around 60mmHg generate nerve impulses that are transmitted to the central respiratory centers in the medulla via the sinus nerve of Hering, an afferent branch of CN IX, which increases ventilatory drive (increased RR, TV, & MV).
Central chemoreceptors in the medulla are affected by increased PaCO2 and decreased CSF pH. The peripheral chemoreceptors, such as the carotid and aortic bodies, are affected by a decrease in PaO2 (< 60 mmHg), an increase in PaCO2, and a decrease in arterial pH.
The main peripheral chemoreceptor is the carotid body located at the bifurcation of the common carotid artery. It detects changes in the PaO2, PaCO2, and pH, with PaO2 being the most significant driver. When PaO2 is < 60 mmHg, signals are sent via the glossopharyngeal nerve to the medulla to increase respiration by tidal volume and respiratory rate, increasing minute ventilation. The response to a decreased arterial pH and increased PaCO2 is minor. Damage to the carotid body, such as in carotid endarterectomy, can lead to altered responses to hypoxemia, especially when there is denervation of the carotid bodies.
When only one side is affected, it may result in a decreased ventilatory response to mild hypoxemia. When both sides are affected, such as in bilateral carotid endarterectomy, there is a complete loss of ventilatory response to acute hypoxia, leading to a higher than normal resting PaCO2. When both carotid bodies are affected, the central chemoreceptors are the drivers for changes in ventilation. Opioid administration may cause the impaired ventilatory response to be exacerbated.
Injury to what cranial nerve during a radical neck dissection would attenuate a patient’s hypoxic respiratory drive?
CN IX (glossopharyngeal)
Unilateral- moderate attenuationn
Bilateral- obliteration
Below PaO2 of 100mmHg, increased neuronal activity along IX.
Below PaO2 of 60mmHg, increased neuronal activity along IX and these signals results increased ventilatory drive.
A 10 cm change in the height of the level of the transducer will change the reading by ____ mmHg in the opposite direction.
A 10 cm change in the height of the level of the transducer will change the reading by 7.5 mmHg in the opposite direction.
Why might a patient become hypotensive in PACU following a carotid endarterectomy?
Carotid sinus hypersensitivity
Hypersensitivity or reactivation of the carotid sinus can result after CEA, leading to decreased in systemic BP.
NOTE:
Increased systemic BP results in activation of carotid and aortic arch baroreceptors,* increasing signaling* via cranial nerves IX and X to the medulla, resulting in reflex vasodilation. The converse is true, with decreased signaling along the cranial nerves.
Which hormones contribute to intraop hyperglycemia?
Cortisol
Growth hormone
Glucagon
Catecholamines
NOTE:
Hyperglycemia in patients with diabetes who undergo surgery is associated with increased rates of surgical site infection, MI, stroke, and death.
How can cerebral salt wasting be differentiated from SIADH?
Cerebral salt wasting is another cause of hyponatremia in patients with CNS disturbances. The mechanism is not well understood, but generally leads to inappropriate renal salt wasting, which leads to hyponatremia and low plasma osmolarity along with high urine sodium and urine osmolarity. These are the same electrolyte disturbances seen in SIADH, so the main distinguishing factor is that patients with cerebral salt wasting are hypovolemic.
SIADH: Euvolemic, hypervolemic
CSW: Hypovolemic
Side effects of thiazide diuretics include…
Side effects of thiazide diuretics include
- Hyponatremia
- Hypokalemia
- Hypochloremia
- Metabolic alkalosis
- Hypercalcemia
- Hyperuricemia
- Hyperlipidemia
Loss of EMG response from a Nerve Integrity Monitoring (NIM) tube can be do to…
1) RLN damage (unilateral= stridor, hoarseness, bilateral= aphonia, airway obstruction)
2) Malpositioning of NIM tube (use glidescope)
3) Paralytic (thus, use succinylcholine and remi gtt)
4) Secretion accumulation (suction, glyco)
The ventilatory drive is dependent on both peripheral and central chemoreceptors.
Central chemoreceptors originate in the central medullary centers and are responsive to _______changes in the cerebrospinal fluid (CSF).
Peripheral chemoreceptors are located in the aortic body and carotid bodies are primarily responsive to changes in _______.
The ventilatory drive is dependent on both peripheral and central chemoreceptors.
Central chemoreceptors originate in the central medullary centers and are responsive to ACID-BASE changes in the cerebrospinal fluid (CSF).
Peripheral chemoreceptors are located in the aortic body and carotid bodies are primarily responsive to changes in PaO2 (the carotid bodies are most responsible for changes in ventilation and the aortic bodies are most responsible for hemodynamic changes).
Obstructive lung disease will result in a FEV1/FVC ratio being < _____% of predicted.
Obstruction is seen as a result of the FEV1/FVC ratio being <70% of predicted.
Both FEV1 and FVC are reduced as is the ratio of FEV1 to FVC.
Restrictive type lung conditions demonstrate decreases in the FEV1 and FVC. However, the FEV1/FVC proportions remain normal.
For the following andrenergic receptors, describe the involved receptor subunit, second messenger, and effects:
a1
a2
B1-3
(see photo)
G protein-coupled receptors are composed of three elements: receptor with seven transmembrane helices, G-protein (Gs, stimulates adenylyl cyclase; Gi, inhibits adenylyl cyclase; and Gq, stimulates phospholipase C), and a second messenger (eg, cAMP).
Review the following G-protein coupled receptors
G protein-coupled receptors are composed of three elements: receptor with seven transmembrane helices, G-protein (Gs, stimulates adenylyl cyclase; Gi, inhibits adenylyl cyclase; and Gq, stimulates phospholipase C), and a second messenger (eg, cAMP).
Describe how PPV can cause oliguria.
Oliguria is defined as urine output less than 0.5 mL/kg/hr.
Positive pressure ventilation increases intrathoracic pressure which can decrease urine output through four main effects:
1) Impaired renal perfusion and renal venous drainage
2) Decreased preload and increased right ventricular afterload
3) Stimulation of the sympathetic nervous system
4) Release of inflammatory cytokines
Increased intrathoracic pressure increases IVC pressure. This directly decreases renal perfusion (by impairing venous drainage) which decreases urine production. Increased intrathoracic pressure also increases right ventricle afterload and reduces venous return, thereby decreasing preload. These two effects can decrease cardiac output which further decreases renal perfusion and urine production. Additionally, they can reduce left atrial volume which decreases atrial natriuretic peptide (ANP) release. Since ANP promotes sodium and water excretion, a decrease can contribute to oliguria. Finally, decreased preload signals the posterior pituitary to release antidiuretic hormone (ADH) which increases renal water reabsorption and decreases urine output.
Through the changes above, PPV decreases cardiac output and systemic blood pressure. This causes carotid and aortic baroreceptor-mediated increases in sympathetic nervous system (SNS) activity. This leads to stimulation of the renin-angiotensin-aldosterone system (RAAS), renal vasoconstriction, antidiuresis, and antinatriuresis, all of which can contribute to oliguria.
Finally, positive pressure ventilation, particularly with high tidal volume and low PEEP, can stimulate the release of pro-inflammatory cytokines and other inflammatory mediators. These are thought to be responsible for acute lung injury seen with positive pressure ventilation. However, the inflammatory mediators can also cause acute inflammation in the kidneys leading to acute kidney injury from renal epithelial cell dysfunction and apoptosis. This is less likely to be seen intraoperatively but may be a contributor to postoperative oliguria. Lung-protective ventilation strategies significantly decrease this risk.
The most sensitive and specific test for the detection of an acute hemolytic transfusion reaction is ________________.
The most sensitive and specific test for the detection of an acute hemolytic transfusion reaction is the direct antiglobulin test (DAT) which is also known as a direct Coombs test.
In this test, red blood cells (RBCs) are drawn from the patient that is suspected of having immune-mediated hemolytic anemia (e.g. acute hemolytic transfusion reaction). If these donor RBCs are coated in antibodies that are bound to antigens on the RBC surface, then when they are exposed to anti-human antibodies (Coombs reagent), the anti-human antibodies will bind to all of the antibodies on the RBCs and cause agglutination.
What triggers the release of renin?
Renin is created and stored by the cells in the afferent arterioles of the kidney. Renin secretion can be caused by 3 different mechanisms:
1) Hyponatremia (chemoreceptors in macula densa)
2) Hypotension (baroreceptors within JGA)
3) B1 activity
Decreases in blood pressure, such as that displayed by the patient above, would cause a release of renin into the serum by at least one of these mechanisms. Renin then acts by cleaving the peptide angiotensinogen to create angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE).
Angiotensin II (Ang II) has several effects, which combine to increase systemic perfusion in patients. The most immediate response to Ang II is an increase in blood pressure caused by an increase in systemic vascular resistance. Ang II activates the angiotensin1 (AT1) receptors on vascular smooth muscle cells, causing constriction of the arterioles. Ang II also augments the sympathetic nervous system by inhibiting norepinephrine reuptake into nerve terminals. It also stimulates the release of catecholamines from the adrenal medulla. In addition, Ang II causes a centrally mediated increased thirst and enhances the release of vasopressin. These effects are almost immediate, but are not long-lasting.
Ang II also has longer lasting effects in the body. In addition to its effects on blood pressure, it stimulates remodeling of the cardiovascular system, causing hypertrophy of cardiac cells and increased collagen deposition. It also has profound effects on the kidney, causing a decrease in the urinary excretion of both sodium and water.
Lastly, Ang II stimulates the adrenal cortex to synthesize and release aldosterone. Aldosterone also acts on the kidneys to decrease the urinary excretion of sodium and water. This ultimately leads to an increase in blood volume and therefore blood pressure.
Contraindications to BiPAP
Contraindications to BiPAP:
Cardiac or respiratory arrest
Severe agitation
Voluminous secretions/vomiting/GI bleeding
Inability to protect airway (GCS < 8)
Facial trauma
Hemodynamic instability
A common complication (25-45%) of sitting craniotomies is ____________
A common complication (25-45%) of sitting craniotomies is Venous Air Embolism (VAEs).
It occurs because non-collapsible venous channels such as venous sinuses can be violated during surgery and air is entrapped in them due to the negative pressure gradient between the surgical site and the heart. VAEs generally travel to the heart and, if small, can be absorbed in the pulmonary vasculature. However, if large, they can cause pulmonary occlusion, increased pulmonary pressures, and even right heart failure with decreased cardiac output.
The most sensitive method of detecting VAEs is via TEE with precordial doppler being second. In some instances or at some institutions, it is commonplace to have a right atrial catheter in place for these surgeries in order to aspirate air if a VAE is detected.
Treatment of Venous Air Embolism (VAE)?
1) Flood field with normal saline (or pack with wet gauze)
2) Administer 100% FiO2 & discontinue NO if using
3) Head down, left lateral positioning (if feasible)
4) Vasopressors & inotropes
5) Aspiration via RA catheter (if present)
6) TEE (highest sensitivity for diagnosing VAE)
-
OTHER: Hyperbaric oxygen has some demonstrated efficacy if there is cardiac, pulmonary, or neurological defects, however, it is not typically available in a rapid time frame.
Most sensitive method for detecting VAE?
TEE
Methods for detecting VAE from most to least sensitive are as follows: transesophageal echo (TEE), precordial Doppler, end-tidal carbon dioxide, pulmonary artery pressures, central venous pressure, and electrocardiogram.
What opthalmic complication is commonly seen in prone surgeries?
Postoperative visual loss is most commonly associated with surgeries in the prone position.
A small percentage of these cases (~10%) are a consequence of central retinal artery occlusion, which is directly correlated to poor positioning and increased pressure on the eyes. Periorbital and scleral edema can be found on exam of these patients.
However, most cases (~90%) of postoperative visual loss are secondary to ischemic optic neuropathy, which to date is still considered an idiopathic process. It is not thought to be the result of optic globe compression or faulty positioning. It is however associated with prone position, Mayfield pin use, anesthetic duration >6 hours, blood loss greater than 1000 mL, preexisting retinal disease, diabetes, hypertension, atherosclerosis, and anemia
Causes of HAGMA
A CAT MUDPILE
Diarrhea causes what acid/base derrangment?
Metabolic acidosis
Excessive diarrhea leads to GI losses of bicarb.
“Bicarbarrhea”
The major hemoglobin in adults is hemoglobin _______.
The major hemoglobin in adults is hemoglobin A (HbA), which consists of four globin polypeptide chains; two α chains and two β chains.
The major hemoglobin in utero and the first 6 months of life is ____________.
The major hemoglobin in utero and the first 6 months of lfie is fetal hemoglobin (HbF), which is composed of two α globin chains and two γ globin chains.
Hence, Infants with beta-thalassemia minor or major, however, are asymptomatic at birth.
Beta-thalassemia minor- patients are heterozygotes, inheriting only one defective Beta globulin allele.
Beta-thalassemia major-patients are homozygotes, inheriting two defective beta alleles. Severe symptoms after 6 months- anemia 2/2 hemolysis w/ hepatosplenomegaly.
Initial treatment for patients with suspected sepsis or septic shock includes initiation of fluid administration (_____mL/kg recommended) within the first hour and completion within three hours of initial presentation.
Initial treatment for patients with suspected sepsis or septic shock includes initiation of fluid administration (30 mL/kg recommended) within the first hour and completion within three hours of initial presentation.
Fluid boluses are preferred to treat hypotension before initiating vasopressors and should be continued until blood pressure and tissue perfusion is adequate or if patients are nonresponsive to fluid resuscitation.
Multiple randomized trials and meta-analyses has provided no evidence of significant difference in mortality between albumin and crystalloid solutions in managing sepsis or septic shock (SAFE trial).
What effect does norepinephrine (levophed) have on cardiac output?
Administration of norepinephrine (α1 > α2 > β1) leads to intense vasoconstriction, causing slight reflex bradycardia. Despite the bradycardia, cardiac output is maintained via a decrease in venous capacitance, resulting in an increase in preload and stroke volume. The β1 increase in myocardial contractility further increases the stroke volume, and, despite a decrease in heart rate, cardiac output is maintained or slightly increased.
Patients who have had a heart transplant in the past will having resting heart rates between - bpm.
Patients who have had a heart transplant in the past will having resting heart rates between 90-110 bpm.
Due to loss of cardiac autonomic plexus. Parasympathetic nervous system no longer innervates the heart.
What are the three components of the quick sequential organ failure assessment (qSOFA)?
The qSOFA criteria are scored from 0-3 with one point for each of the following: altered mental status (GCS < 15), respiratory rate ≥ 22, and systolic blood pressure ≤ 100 mm Hg.
The quick sequential organ failure assessment (qSOFA) is a screening tool developed from the SOFA (see below) that can be used to identify adult ICU patients with a suspected infection that are likely to have a prolonged ICU stay or poor outcome. Additionally, the qSOFA score can be used in adult out-of-hospital, emergency room, and general ward patients with suspected infection to identify those that are more likely to have poor outcomes typical of sepsis. In either case, a score of ≥ 2 indicates a worse prognosis. A significant benefit of the qSOFA compared to the full SOFA is its ability to be a quick, repeatable bedside assessment tool that does not require calculated or laboratory values.
It is important to recognize that although SOFA and qSOFA are discussed in detail within the 2016 third international consensus definitions for sepsis and septic shock (“Sepsis-3”), neither tool is used to diagnose sepsis or functions as a stand-alone definition for sepsis. Rather, the assessments should be used to identify patients with a potentially worse prognosis and perhaps prompt an escalation of care. Additionally, a positive qSOFA score can be used to prompt consideration of possible infection in patients not otherwise recognized as having an infection. Failure to meet ≥ 2 qSOFA/SOFA criteria should not cause a delay in care otherwise deemed necessary.
The SOFA includes assessments of respiration (PaO2/FiO2), coagulation (platelet count), liver function (bilirubin), cardiovascular function (MAP and pressor dose), mental status (GCS), and renal function (creatinine and urine output) with each category scored from 0-4. The full details of the system can be found in the Sepsis-3 reference and are beyond the scope of this question.
Contrainidications to enteral feeding in ICU patients?
The primary indication for initiating nutritional support is preventing or treating malnutrition among patients unable or unwilling to sustain sufficient oral intake.
Enteral nutrition should be initiated within 48 hours of a critically ill patient’s admission without contraindications to enteral feeding.
Enteral nutritional support should not be initiated in patients with** intractable vomiting and diarrhea, bowel obstruction, gastrointestinal ischemia or bleeding, hemodynamic instability, severe and protracted ileus, or high-output fistulas. **
Patients who are initiated on early enteral nutritional support have a lower incidence of infection and mortality.
A rapid shallow breathing index (RSBI) of _______ is a sufficiently low respiratory rate to tidal volume ratio and is consistent with readiness for extubation.
A rapid shallow breathing index (RSBI) of < 105 is a sufficiently low respiratory rate to tidal volume ratio and is consistent with readiness for extubation.
Criteria for extubation include
* Resolution of the process that initially necessitated mechanical ventilation
* Hemodynamic stability
* Adequate oxygenation on minimal fractured of inspired oxygen (< 40%-50%)
* The ability to protect the airway and clear secretions
* Favorable respiratory mechanics. Favorable respiratory mechanics values include a negative inspiratory force (NIF) of more than −20 cm H2O, an RSBI of < 105, and a vital capacity of > 10 mL/kg
*
The RSBI, also known as the Yang Tobin index, reflects the breathing pattern that predicts postextubation respiratory distress: RSBI = respiratory rate / tidal volume (L).
A result > 105 indicates a rapid shallow breathing pattern, while a result < 105 is consistent with readiness for extubation.
Physiological consequences of abdominal compartment syndrome
Abdominal compartment syndrome is defined as new organ dysfunction with significant intra-abdominal hypertension (increase in intra-abdominal pressures >20 mmHg with or without intra-abdominal perfusion pressure <50 mmHg). This syndrome can be caused by multiple clinical conditions, including liver transplants, major abdominal/trauma surgery, burn injuries (requiring large amounts of fluids), severe bowel obstruction, massive fluid resuscitation, pancreatitis, peritonitis, ascites, and intraperitoneal hemorrhage.
The intra-abdominal pressure can be measured with an indwelling Foley catheter and by using the same pressure tubing apparatus used for arterial line blood pressure monitoring. The Foley catheter is then clamped distal to the instillation port, and 50 mL of normal saline is instilled within the bladder, measuring intravesicular pressure. Immediate management for this syndrome after it has been recognized includes immediate paracentesis and opening the abdomen for urgent decompression. Intra-abdominal pressure may be chronically elevated (up to 12 mmHg) in obese adults. However, this has not been shown to be associated with end-organ dysfunction.
Manometry tubing in CVC kits can be attached to the catheter to confirm placement by connecting the catheter to the tubing and raising the tubing vertically to measure the pressure. The blood in the column of blood should be <_ cm and will vary with respiration (expiration: goes up, inspiration goes down).
Manometry tubing in CVC kits can be attached to the catheter to confirm placement by connecting the catheter to the tubing and raising the tubing vertically to measure the pressure. The blood in the column of blood should be < ____ cm and will vary with respiration (expiration: goes up, inspiration goes down).
NOTE:
Tip of catheter should be at inferior aspect of SVC for internal jugular CVCs.
Benfits of low frequency vs. high frequnecy probes
Linear- high frequency
Curvilinear- low frequency
Phased array- low frequency
High frequency probes (linear) provide improved resolution of superficial structures. Low frequency probes (curvilinear) provides deeper penetration (good for deep structures or on obese patients). Phased array probe (low frequency) is used for cardiac examination.
Acoustic Impedance (Z1) =
Acoustic Impedance (Z1) is the product of the density of a medium and the propagation speed of sound through that medium.
Ultrasound reflection that occur at the interface of different mediums are due to the changes in acoustic impedance.
Since propagation speed changes only slightly between biological mediums, acoustic impedance is primarily dependent upon density.
Z1 = p1 x c1
Winter’s Formula
PCO2 (Expected) = (1.5 * [HCO3]) + 8 +/- 2
Winters’ formula gives an expected value for the patient’s PCO2; the patient’s actual (measured) PCO2 is then compared to this.
If the two values correspond, respiratory compensation is considered to be adequate.
If the measured PCO2 is higher than the calculated value, there is also a primary respiratory acidosis.
If the measured PCO2 is lower than the calculated value, there is also a primary respiratory alkalosis.
Causes of NAGMA
HARDASS
Hyperchloremia/Hyperailmentation
Addision’s Disease
Renal tubular acidosis
Diarrhea (loss of bicarb in stool)
Acetazolamide
Spironolactone
Saline infusion
Primary hyperparathyroidism can cause what acid/base disturbance?
Hyperchloremic metabolic acidosis
In primary hyperparathyroidism, parathyroid hormone (PTH) levels are elevated. Parathyroid hormone has been shown to be an important inhibitor of renal bicarbonate reabsorption. Increased renal bicarbonate loss leads to a metabolic acidosis. Furthermore, PTH has been shown to inhibit the sodium chloride cotransporter in the distal convoluted tubule of the nephron leading to hyperchloremia. Although not particularly common, patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.
A normal alveolar-arterial (A-a) oxygen gradient is in the range of ____ to ___ mm Hg.
A normal alveolar-arterial (A-a) oxygen gradient is in the range of 5 to 10 mm Hg.
An increased A-a gradient indicates a barrier to oxygen transfer.
Elevations in the A-a gradient would be seen as a result of a ventilation-perfusion mismatch in the lungs. Examples would include pneumonia, acute respiratory distress syndrome, obstructive lung disease, atelectasis, and pulmonary embolism.
In conditions of high altitude or alveolar hypoventilation (eg, opioid-induced respiratory depression, obesity-hypoventilation syndrome, peripheral neuropathy, myasthenia gravis), the A-a gradient will remain within normal limits.
What is respiratory splinting?
Respiratory splinting is defined as reduced inspiratory effort due to sharp pain during inspiration. As a result, patients hypoventilate with decreased chest wall movement and decreased functional residual capacity, leading to atelectasis and hypoxemia, the potential requirement for intubation and mechanical respiratory support, and an increased risk of pneumonia.
Patients with splinting may have rapid shallow breathing, a weak cough, and decreased mucociliary clearance.
Thoracic epidurals have been shown to be effective in reducing the morbidity of splinting.
In an otherwise healthy individual without parenchymal lung disease, the peripheral chemoreceptors will begin to stimulate the respiratory centers in the brainstem when the arterial oxygen tension drops below _______ mmHg.
In an otherwise healthy individual without parenchymal lung disease, the peripheral chemoreceptors will begin to stimulate the respiratory centers in the brainstem when the arterial oxygen tension drops below 50 mmHg.
As can be seen in the Figure below, by the position of the star on the below curve this arterial oxygen partial pressure occurs right before a precipitous drop in arterial hemoglobin oxygen saturation. Because of this relationship between arterial oxygen tension and hemoglobin saturation, a PaO2 of around 50 mmHg is roughly the lowest physiologically sustainable arterial oxygen tension before oxygen delivery to the tissues begins to become extremely inefficient. Thus, the body will generate a robust hypoxic ventilatory drive should arterial oxygen tension drop below this point in order to ensure adequate oxygen delivery to the tissues. In situations where hypoxic drive is blunted, such as during anesthesia, it is even more important to ensure SpO2 remains > 85% as oxygen delivery is not fully effective below this level.
Recovery of which muscle/nerve ensures adequate recovery of the diaphragm?
The adductor pollicis muscle is supplied by the ulnar nerve and responsible for adduction of the thumb. This muscle can be stimulated by placing two electrodes over the course of the **ulnar nerve **at the wrist or placement of electrodes over the dorsal and palmar sides of the hand between the first and second digits. This muscle is relatively sensitive to neuromuscular blockade.
Recovery at this location lags behind the diaphragm ensuring adequate respiratory function if adequate response is obtained.
Blockade of which muscle/nerve ensures adequate intubating conditions?
The corrugator supercilii muscle is responsible for movement of the eyebrow and is innervated by the facial nerve. This muscle most resembles blockade effects upon the laryngeal adductors and can be useful to determine favorable intubating conditions.
Severe Aortic Stenosis (AS) is defined as:
Aortic Valve Jet Velocity (m/s):
Mean Gradient (mmHg):
Aortic Valve Area (cm^2):
Severe Aortic Stenosis (AS) is defined as:
Aortic Valve Jet Velocity: > 4 m/s
Mean Gradient (mmHg): > 40mmHg
Aortic Valve Area (cm^2): < 1.0
Stress Response to Surgery
Hemodynamic goals in a patient with hypertrophic obstructive cardiomyopathy (HOCM) include:
Hemodynamic goals in a patient with hypertrophic obstructive cardiomyopathy (HOCM) include:
- Adequate full preload
- Increased afterload (phenylephrine preferred, avoid vasodilators)
- Depressed myocardial contractility (avoid inotropes)
- Normal to low heart rate (BBs)
- Sinus rhythm
Which vasopressor is most susceptible to tachyphylaxis?
Ephedrine
What is the cause of acute hemolytic transfusion reactions?
Transfusion of an ABO-incompatible unit of packed red blood cells (PRBCs) results in an Acute Hemolytic Transfusion Reaction (AHTR), in which recipient IgM-mediated antibodies attack donor cell ABO blood group antigens.
Laboratory testing will result in a positive direct Coombs test.
What three hormones modulated potassium?
Aldosterone
Insulin
Cortisol
Define Strong Ion Difference (SID)
SID < 0 causes what acid/base disturbance?
SID > 0 causes what acid/base disturbance?
Strong Ion Difference (SID) is difference between the sum of the strong cations minus the sum of strong anions.
SID = (strong cations) − (strong anions) = (Na + K + Ca2 + Mg2) − (Cl + lactate)
SID is normally ~40 mEq/L due to unmeasured anions (such as lactic acid and keto acids).
When the SID is > 0, the unmeasured ions result in alkalosis.
When the SID is < 0, the results is acidosis.
The following strong ion changes result in the following SID changes:
↓ [Na+] → ↓ SID and acidosis
↑ [Na+] → ↑ SID and alkalosis
↑ [Cl−] → ↓ SID and acidosis
↑ organic acids → ↓ SID and acidosis
Medications that can cause hyperkalemia:
NOTE:
Beta 2 agonism causes activation of Na/K ATPase shifting K intracellulary and can cause hypokalemia (Terbutaline also works in this way). So Beta 2 antagonist will have the opposite effect causing hyperkalemia.
Mannitol is hypertonic will draw water intravascularly and K will follow.
ACE-i and ARBs prevent aldosterone release from the adrenal cortex.
The most common complication of an autologous blood transfusion is _____________.
The most common complication of an autologous blood transfusion is infection caused by improperly stored blood.
Autologous transfusion DOES NOT place the recipient at risk of immune-mediated reactions.
Autologous transfusions reduce the incidence of complications associated with allogenic donor blood, such as hemolytic and non-hemolytic (febrile, urticarial, and post-transfusion purpura) reactions resulting from donor proteins triggering an immune-mediated reaction in the recipient. Autologous blood does not contain non-self antigens and does not trigger these reactions. Transfusion-related immunomodulation (TRIM) results from the downregulation of several immune functions following allogenic, but not autologous, transfusion.
Hypocalcemia cause QT ________
Hypercalcemia cause QT ________
Hypocalcemia cause QT prolongation
Hypercalcemia cause QT shortening
NOTE:
QTc prolongation (>440ms in men, > 460ms in women)
QT interval varies with HR. QT is shorter at fast heart rates, QT is longer at slow heart rates.
QT interval can be corrected for heart rate:
QTc = QT/cardiac cycle (seconds)
Autonomic dysreflexia (AD) occurs most often in patients with spinal lesions above what spinal level?
Autonomic dysreflexia (AD) (also known as autonomic hyperreflexia) occurs most often in patients with spinal lesions above the midthoracic (T5-7) level. These levels correspond with the splanchnic outflow distribution within the sympathetic nervous system. Autonomic dysreflexia has been known to occur in patients with a lesion as low as T10, although lesions at or above T6 involve the highest risk.
Autonomic dysreflexia occurs when a noxious cutaneous or visceral stimulus below the SCI causes a signal to be transmitted to the dorsal root of the spinal cord. An increase in sympathetic outflow and vasoconstriction occurs below the level of the lesion.
Examples of triggering events include bladder or bowel distension, cystoscopy and other urinary tract procedures, surgical stimulation of the pelvic region, uterine contraction and manipulation during childbirth, and lower extremity burns and surgery.
When there is no spinal cord injury, inhibitory impulses from the brain modulate the sympathetic outflow. When there is a lesion at the midthoracic level (T5-7) or above, this inhibition is blocked so the sympathetic outflow goes unchecked. Spinal cord reflexes from the above stimuli trigger sympathetic activity (preganglionic sympathetic nerves) along the splanchnic outflow tract, but because of the SCI, inhibitory impulses from higher CNS centers (e.g., cerebral cortex, cerebellum, and brain stem) cannot reach below the level of the SCI. Accordingly, intense generalized vasoconstriction occurs below the level of the SCI while reflex cutaneous vasodilation occurs above the level of SCI (usually in proportion to the magnitude of the inciting stimulation).
Signs and symptoms of AH reflect the imbalance outlined above. The intense sympathetic response below the level of injury can cause acute hypertension (at least 20-40 mm Hg above baseline), reflex bradycardia, cardiac arrhythmias (e.g., premature ventricular contractions or atrial-ventricular conduction abnormalities), and myocardial infarction. Hypertension can further lead to headaches, blurred vision, retinal hemorrhage, intracranial hemorrhage, stroke, seizure, and/or cerebral edema. Additionally, the intense vasoconstriction leads to cool, dry, pale skin below the level of the SCI. The reflex cutaneous vasodilation above the level of the SCI leads to nasal congestion, sweating, and warm, flushed skin on the upper extremities, shoulders, neck, and face.
Prevention of AH during surgery is best done with spinal or epidural anesthesia with a local anesthetic and/or deep general anesthesia. Narcotic-only regional anesthesia and sedation techniques do not reliably prevent AH.
Treatment includes cessation of the triggering event and administration of direct vasodilators, such as sodium nitroprusside, nitroglycerin, or nicardipine. Beta-blockers should be used cautiously as they can worsen reflexive bradycardia and, if given in the setting of unopposed α-stimulation, may lead to severe vasoconstriction, hypertensive crisis, and congestive heart failure.
In the sympathetic nervous system, all post-ganglionic neurons release norepinephrine with the exception of what two organs?
Sweat glands
Post-ganglionic neurons secrete acetylcholine
Adrenal glands (medulla)
Single preganglionic neuron secretes norepinephrine, epinephrine, and small amounts of dopamine.
NOTE:
Sympathetic neurons preganglionic neurons originate between T1-L2. Ganglia are closer to the spinal cord.
Parasympathetic neurons originate from cranial nerves III, VII, IX, X, and S2-S4. Ganglia are closer to the organ (think “para” like next to organ)
Unfractionated heparin is monitored by measuring…
PTT, ACT, or anti-Xa levels
Activated clotting time (ACT) is used to monitor the effect of high-dose UFH therapy in situations where aPTT is not clinically useful or takes too long (e.g. cardiopulmonary bypass).
The anticoagulant response to enoxaparin (Lovenox) can be monitored by measuring….
The anticoagulant response to enoxaparin (Lovenox) can be monitored by measuring factor Xa activity.
Enoxaparin binds and enhances the effects of AT3. However, the enoxaparin-induced conformational change of AT3 makes enoxaparin preferentially inhibit factor Xa.
Monitoring may be recommended in patients with extreme BMIs (high or low), renal impairment, or in pregnant patients.
Antifibrinolytics
(TXA, aminocaproic acid)
MOA
Prevent binding of plasmin to fibrin.
Plaminogen –tPA–>Plasmin
Plasmin binds to fibrin and causes clot breakdown (fibrinolysis)
Antifibrinolytics (TXA, aminocaproic acid) prevent bleeding by preventing clot breakdown.
Describe the mechanism of bronchoconstriction.
The caliber of the small airways of the lung is the primary determinant of dynamic airway resistance.
Cholinergic stimulation via the Vagus Nerve (X) of M3 receptors on the bronchiolar smooth muscle results in an influx of ionized calcium, smooth muscle contraction, and bronchoconstriction.
In contrast, the beta-2 adrenergic receptor plays a very important role in bronchiolar smooth muscle relaxation. By stimulating this receptor, there is an efflux of ionized calcium from the cell and into the sarcoplasmic reticulum causing rapid muscle relaxation.
Interestingly, when bronchospasm is mediated by a pure reflexive vagal stimulus, the bronchoconstriction tends to be in the larger airways and more central. When this same activity is stimulated by an antigen mediated histamine response the bronchoconstriction tends to be in the more distal bronchioles in the periphery of the lung.
Intraoperative bronchospasm
Signs:
Treatment:
Signs:
* Oxygen desaturation
* ETCO2 (Upsloping, decreasing, or absent)
* High PIP with minimal to no change in plateau pressures
* Decreasing tidal volumes
* Wheezing on chest auscultation
Treatment:
* FiO2 100%
* Deep anesthesia (IV propofol or ketamine bolus)
* Hand ventilate (to assess pulmonary compliance and to assess any other possible reasons for high circuit pressure)
* Albuterol
* IV epinephrine (severe) (5-10mcg/kg)
* IV steroids (severe) (125mg methylpred, takes 6 hours to have effect)
* IV magnesium sulfate (severe) (refractory bronchospasm) (2g infusion over 20min)
* Anticholinergics- atropine, glycopyrrolate (severe)
According to Poiseuville’s Law, flow (Q) =
NOTE:
Only applies to laminar flow
Reynold’s number (Re) =
If Re is < 2000, flow is most likely laminar
If Re is >4000, flow is most likely turbulent
Thus, increasing gas density, mean velocity, and length or decreasing gas viscocity will increase turbulent flow.
Low fresh gas flows in the anesthesia circuit will exhibit more laminar flow and less turbulent flow. This can help is situations in the OR such as increased airway resistance.
Capnogram with incompetent inspiratory valve
Capnogram with incompetent expiratory valve
A full cylinder of oxygen contains L and has a psig of _ .
A full cylinder of oxygen contains 660L and has a psig of 2200.
A full cylinder of nitrous oxide contains L and has a psig of _ .
A full cylinder of nitrous oxide contains 1590 L and has a psig of 745.
NOTE:
NO is a liquefied gas at ambient temperature, is stored in E cyclinders in the liquefied form under high pressures. Therefore, the pressure of NO above its liquefied form remains constant at 745psig regardless of how much liquid remains. Once all the liquefied gas has evaporated the pressure will start to fall as the gaseous NO form is used which is when ~250L (16%) of NO remains in the tank.
This is due to NO having a critical temperature of above room temperature (20 celcius) allowing it to exist as a liquid and a gas under pressurized conditions at room temperature. As gas is removed from the NO cyclinder, the liquid portion will evaporate maintaining a consistent pressure of 745mmHg until all the liquid NO is evaporated into gas form. The point when all the liquid NO is evaporated is when 16-25% of the total NO is remaining. After this point, the pressure guage will decrease proportionally to zero as the gas form is used.
Rank the volatile anesthetic gases by vapor pressure from high to low.
NO > Desflurane > Isoflurane > Sevoflurane
“N**, smoke DIS gas”
A high vapor pressure indicates the substance is more likely to evaporate at a given temperature than a susbstance with a lower vapor pressure.
Given PSI of an oxygen tank and a set flow rate how can you calculate how much time you have until the oxygen is depleted?
Time left = (Current PSI/3)/ flow rate
End-titdal CO2, volatile agents, and NO are measured by the anesthesia machine using:
End-titdal CO2, volatile agents, and NO are measured by the anesthesia machine using infrared absorption spectrophotometry (IRAS).
Inspired and expired O2 is measured by the anesthetic machine using what oxygen analyzers?
There are three main types of oxygen analyzers seen in clinical practice:
Paramagnetic
Galvanic/Clark cell
Polarographic
Management of pipeline failure or gas cross-over:
1) Disconnect the pipeline connection at the wall
2) Open the oxygen cyclinder fully
3) Ventilate by hand with the anesthesia breathing circuit
Describe a normal CVP trace
Abnormal CVP Trace:
Tall V wave
Loss of x descent
Tricuspid Regurgitation
Abnormal CVP Trace:
Tall A wave
Tall V wave
Minimal Y descent
Tricuspid Stenosis
Abnormal CVP Trace:
Tall A wave
Tall V wave
Steep X descent
Steep Y descent
Constrictive Pericarditis
Abnormal CVP Trace:
Loss of A wave
Atrial Fibrillation
Abnormal CVP Trace:
Dominant X descent
Minimal Y descent
Cardiac Tamponade
Abnormal CVP Trace:
Cannon A wave
Complete AV block
Management of stable vs. unstable ventricular tachycardia?
Stable- antiarrhythmic (Adenosine, Amiodarone)
Unstable- synchronized cardioversion
NOTE:
AV blocking agents (BB, CCB) should be avoided until WPW can be ruled out because giving AV blocking agent will encourage conduction through accessory pathway.
Amiodarone
MOA
Class III antiarrhythmic
- K+ channel blocker (prolongs duration of action potential and increases the refractory period of atrial, nodal and ventricular tissues.
- Also blocks Na+, Ca2+, b-adrenergic receptors (decreasing conduction via SA and AV node)
NOTE:
Amiodarone is the only antiarrhytmic with little to no negative inotropic effects, making it a good option for patients with reduced ejection fraction.
Amiodarone is commonly used to treat ventricular tachycardia, persistent ventricular fibrillation after defibrillation, refractory atrial fibrillation.
What is the most common side effect of Amiodarone?
Bradycardia
Bradycardia as a result of calcium channel blocking properties of Amiodarone.
Bradycardia is more common than QTc prolongation (>440ms in men, > 460ms in women).
MOA:
* K+ channel blocker (prolongs duration of action potential and increases the refractory period of atrial, nodal and ventricular tissues.
* Also blocks Na+, Ca2+, b-adrenergic receptors (decreasing conduction via SA and AV node)
Labetalol
MOA
a1- antagonist (arteriolar vasodilation)
b1- antagonist (reduction in HR & contractility)
b2- antagonist AND partial agonist (overall, arteriolar vasodialtion)
NOTE:
SV and CO are typically unchanged because the arteriolar vasodilation properties of labetalol offset the decrease in HR and decrease in contractility.
Ratio of alpha:beta blockade is 1:7 when administered via IV.
One key feature of labetalol is its blockade of reflex tachycardia, seen with other vasodilators.
Duration of action: 6 hours (but can have an effect on BP for 16-18hrs).
Metabolized by liver.
Hydralazine has a duration of action of _________.
Hydralazine has a duration of action of 2-6 hours.
Fast acting anti-hypertensives including esmolol, nitroglycerin, nitroprusside have an onset of action of < 1min and have a duration of action of approximately ______________.
Fast acting anti-hypertensives including esmolol, nitroglycerin, nitroprusside have an onset of action of < 1min and have a duration of action of approximately 5-10 minutes.
What airway abnormalities are seen in patients with Acromegaly?
Associated airway abnormalities seen in acromegaly include hypertrophy of the posterior pharyngeal structures such as the epiglottis and the aryepiglottic folds.
Acromegaly leads to the expansion of cartilaginous structures in the neck, which can cause recurrent laryngeal nerve paralysis and abnormal movement of the vocal cords.
Associated chondrocalcinosis of the larynx also leads to vocal cord thickening and stricture formation.
Because of these anatomical challenges to intubation, the patient should be considered for awake fiberoptic intubation, and a smaller endotracheal tube should be considered because of possible narrowing of the cricothyroid ring and glottic opening.
How to calculate Fractional Excetion of Sodium (FeNA)?
FENa = (uNa × pCr) / (pNa × uCr) × 100%
The FENa is used to compare the value of sodium in the urine to sodium in the plasma. If there is relatively little sodium in the urine, this provides evidence that the kidneys are trying to maintain intravascular volume by reabsorbing sodium in the nephron. Higher sodium in the urine is reflected by a FENa of 3%, which generally reflects an intrarenal cause of oliguria. A FENa between 1% and 3% is indeterminate.
Patients who are taking diuretics will have a relatively high amount of sodium in the urine regardless of oliguria etiology because diuretic medications frequently inhibit sodium reabsorption in the nephron. For patients who are taking these diuretics (commonly hydrochlorothiazide and furosemide), the FEUrea can be used instead. Fractional excretion of urea is calculated in the same way as FENa but with the substitution of urea for sodium. The equation for FEUrea is
FEUrea = (uUrea x pCr) / (pUrea x uCr) × 100%
Which opioid as a longer duration of action, Morphine or Dilaudid?
Morphine
Morphine has a duration of action of approximately 4 hrs.
Dilaudid has a duration of action of approximately 2 hrs.
NOTE:
1-2-4 rule (Fentanyl 1hr, Dilaudid 2 hrs, Morphine 4hrs)
Which opioid has the fastest onset?
Alfentanil
This is due to Alfentanil’s low pKA (high unionized fraction at physiologic pH) and moderate lipid solubility.
Recall that:
1) Opioid onset of action is related to unionized fraction (pKA) and lipid solubility (lower pKA = faster onset).
2) Opioid duration of action is related to lipid solubility (low lipid solubility = longer duation).
3) Opioid analgesic potency is related to the drug’s affinity and efficacy at the mu opioid receptor.
Drugs and their active metabolites:
Lab findings of DIC:
Disseminated intravascular coagulation is often described as a thrombo-hemorrhagic disorder. Patients can present with thrombosis or bleeding at different times or simultaneously.
Disseminated intravascular coagulopathy (DIC) is a disorder characterized by systemic activation of coagulation that results in an imbalance of hemostasis. It is associated with a comorbid condition such as infection, inflammation, or malignancy which causes widespread activation of the coagulation cascade. Clinically, DIC involves diffuse thrombosis that may lead to multi-organ system failure or consumptive coagulopathy and bleeding.
Which subunit is unique to extrajunctional ACH receptors?
Mature postjunctional nAChRs have five subunits: (α2βδε)
2 α (alpha)
1 β (beta)
1 δ (delta)
1 ε (epsillon)
Immature extrajunctional nAChRs (aka fetal nAChRs) also have five subunits, but have a γ subunit (α2βδγ) in place of an ε subunit. (“epsillon at the endplate, gamma goes out”)
2 α (alpha)
1 β (beta)
1 δ (delta)
1 γ (gamma)
Postjunctional nicotinic acetylcholine receptors are ligand-gated ion channels located at the motor endplate responsible for muscle end plate depolarization. When two acetylcholine molecules bind the α subunits, the channel opens, allowing an influx of sodium and efflux of potassium to create a motor end plate potential sufficient for depolarization of the cell, which leads to muscular contraction (excitation-contraction coupling).
Immature extrajunctional receptors have long open times and low-amplitude channel currents, in contrast to mature junctional receptors that have shorter open times and high-amplitude channel currents. **The immature receptors have opening times up to 10x longer compared with mature receptors, allowing for efflux of significant amounts of potassium resulting in hyperkalemia.
**
The immature extrajunctional form is present in states of decreased muscle activity such as the fetal state prior to muscle innervation as well as immobilization, burns, upper motor neuron injury, lower motor neuron injury, or sepsis.
Immature receptors are sensitive to succinylcholine while having relative resistance to nondepolarizing NMBAs.
Conditions and Comorbidities That Increase Risk of Complications During MAC:
According to the American Society of Anesthesiologists (ASA) Closed Claims Project Database, the most common characteristics for monitored anesthesia care claims associated with oversedation leading to adverse outcomes include ASA physical status of III or IV (45% of cases), age > 70 (42%), and the use of propofol combined with other sedatives (50%).
Nearly 50% of the closed medical malpractice claims could have been prevented with better monitoring. According to the American Society of Anesthesiologists Closed Claims Project Database for monitored anesthesia care claims associated with oversedation, 12% of claims involved pulse oximetry, 20% of claims involved capnography, and 1% of claims involved both pulse oximetry and capnography, providing evidence that increased monitoring may lead to better outcomes.
The most common type of medication error is _.
The most common type of medication error is improper labeling.
NOTE:
Most medications errors occurs and adverse drug events occur within 20 minutes of induction.
Absolute contraindications for MAC?
NONE
There are no absolute contraindications for MAC.
Relative contraindications include inability to lie still enough for the procedure, inability to cooperate, and inability to cooperate with the care team.
Goal temperature of Target Temperature Management (TTM) for comatosed patients following cardiac arrest?
32-36 C
x 24hrs
How does hyothermia affect pH, PaCO2, PaO2?
What neuro, cardiovascular, respiratory, and hepatic changes occur with aging?
Nervous System
- Decreased gray/white matter
- Decreased neurotransmitters (acetylcholine, dopamine)
- Decreased epidural space
- Decreased CSF volume
- Increased permeability of dura mater
Cardiovascular System
- Decreased ventricular compliance
- Decreased beta-receptor responsiveness
- Increased sympathetic nervous system activity
- Increased stiffness of large arteries
Respiratory System
- Decreased vital capacity
- Increased residual volume
- Increased closing capacity
- Increased anatomic dead space
- Increased lung compliance
- Increased pulmonary vascular resistance
Hepatic System
- Decreased hepatic blood flow
Risk factors for post-operative AKI
Lab findings for prerenal vs. intrarenal azotemia:
Lab findings for prerenal vs. ATN
Cormack-Lehane scoring system
In 1984, a scoring system was developed by Cormack and Lehane describing the different laryngoscopic views ranging from I to IV.
Grade I view is given when the epiglottis and vocal cords are in complete view (entire glottic aperture).
Grade II includes the visualization of only the posterior aspects of the glottic aperture.
Grade III is when the epiglottis is only visible.
Grade IV view is the visualization of only the soft palate as the epiglottis or the larynx cannot be visualized.
Hyperthyroidism:
Diagnostic Algorithm
Thyroid Related Lab Abnormalities
Primary hyperthyroidism is characterized by elevated T3, T4 (free and total), elevated thyroid hormone binding ratio, and a low/ normal TSH.
Most common nerve injured in thryoid and parathyroid surgery?
The superior laryngeal nerve is the most commonly injured nerve during thyroid and parathyroid surgery.
The superior laryngeal nerve provides innervation to the cricothyroid muscle. This muscle is the only tensor of the vocal cords and is associated with a voice that tires more easily.
The symptoms are often subtle when the superior laryngeal nerve is injured, so the diagnosis may be missed. The voice may become slightly weak, hoarse, or change in pitch. The most prevalent symptom is that the patient’s voice often tires easily. The superior laryngeal nerve is more likely to be injured when the superior thyroid or parathyroid is operated on.
What factors affect local anesthetic onset?
Concentration (higher is faster)
Lipid solubility (higher is faster)
pKA (lower is faster)
Enviromental pH (higher is faster)
NOTE:
Local anesthetics are weak bases that bind to the intracellular portion of voltage gated sodium channels and prevent nerve conduction.
Although the active form of local anesthetics is the ionized form [charged cation (BH+)] the speed of onset of efffect is determined by the portion of local anesthetic in the unionized form [basic, uncharged (B)].
Essentially, anything that increases the cocentration or proportion of local anesthetic in its unionized form will speed the onset of analgesia.
pKA of a drug refers to the pH at which the drugs exists in equal parts of ionized and unionized forms. Local anesthetics with a lower pKa will have a greater unionized fraction (and faster onset) at physiological pH (7.4).
The more lipid soluble the more quickly the molecule can pass through the lipid membrane and reach its site of action.
A peripheral nerve comprises three main connective tissue sheaths:
A peripheral nerve comprises three main connective tissue sheaths:
- Endoneurium
- Perineurium
- Epineurium.
The endoneurium wraps individual axons, the perineurium covers nerve fascicles, and the epineurium surrounds the entire peripheral nerve. Most regional anesthesia blocks are performed by placing and injecting local anesthetic outside the epineurium.
TrueLearn Insight: There are generally two types of intraneural injections:
Extrafasicular blocks: Needle placement within the epineurium but outside of the perineurium avoids puncture of the fascicle. It has been referred to as an extrafascicular block or an epineural intraneural injection. On ultrasound, it may be seen as nerve swelling and separation of the fascicles. Extrafascicular injections within the epineurium may or may not cause nerve damage. Intentional injection within the epineurium is controversial and is currently being studied.
Infrafasicular blocks: Puncture of the epineurium and the perineurium places the needle within the fascicle and is called an intrafascicular block or subepineural intraneural injection. It is well accepted that intrafascicular injection can lead to permanent nerve damage and should be avoided.
Review RAAS
The RAAS is involved in the maintenance of blood pressure and water-electrolyte homeostasis.
The first enzyme involved in the system is the proteolytic enzyme renin, which is released by the juxtaglomerular apparatus of the renal cortex in response to:
1. Decreased renal perfusion pressure (glomerulus)
2. Hyponatremia (NaCl sensed my macula densa in DCT)
3. B1 stimulation
Renin then cleaves angiotensinogen, synthesized in the liver, into angiotensin I (ATI) which is then converted in the lungs by angiotensin-converting enzyme (ACE) to angiotensin II (ATII).
Angiotensin II causes:
1) Renal efferent arteriolar vasoconstriction
2) Release of aldosterone by the adrenal cortex
3) ADH release from the posterior pituitary
4) Sodium reabsorption by the proximal tubule.
Aldosterone, in turn, further stimulates sodium and water reabsorption in the distal tubules and collecting ducts leading to intravascular volume expansion.
___________is the most commonly used ventilation mode in most intensive care units.
Assist-control ventilation (AC) is the most commonly used ventilation mode in most intensive care units. Tidal volume and a minimum respiratory rate are set. It is time or pressure initiated, volume limited, and time or volume cycled. If a patient is not spontaneously breathing, AC is essentially identical to VCV. If a patient does take spontaneous breaths, the ventilator synchronizes with each spontaneous inspiration and delivers a positive pressure breath of the set tidal volume. Spontaneous breathing independent of the ventilator is not allowed.
Use of AC decreases work of breathing in spontaneously ventilating patients and allows the patient to essentially set his/her own minute ventilation above the programmed minimum. Use of AC in patients with high respiratory rates may lead to breath stacking (initiation of a breath before exhalation is fully complete) resulting in increasing auto-PEEP and baro- or volutrauma.
The attached figure illustrates AC with two synchronized breaths and one ventilator-driven breath.
In PCV (Pressure Controlled Ventilation), the airway pressure for the breath is set, and the breath size or volume is variable. This means that the volume of each breath changes depending on ___________________.
In PCV, the airway pressure for the breath is set, and the breath size or volume is variable. This means that the volume of each breath changes depending on chest wall compliance, lung compliance, and airway resistance.
NOTE:
VCV delivers a breath at a set frequency under a constant flow rate until the set volume of air is delivered. In VCV, airway pressure is a dependent variable of the breath. The volume of the breath being delivered *will not change based on intrinsic factors of the lungs. *
Pre-, intra-, post-operative risk factors for AKI:
Right lung lobe segments
“A PALM Seed Makes Another Little Palm’
The right main bronchus should give rise to a very close right take-off, which is the right upper lobe that will have three take-offs, which are the anterior, posterior, and superior lung segments of the right upper lobe. The left main bronchus has two take-offs, which are the upper and lower lobes of the left lung.
The distance between the left upper lobe bronchus and the carina is roughly double the length as the distance between the right upper lobe and carina. Therefore, it is less likely that a provider will accidentally obstruct the left upper lobe with the bronchial cuff of a left-sided tube than a provider will inadvertently obstruct the right upper lobe with the bronchial cuff of a right-sided tube.
Left lung lobe segments
ASIA ALPS
*Apico-posterior
Superior lingua
Inferior lingula
Anterior
*Antero-medial
Lateral
Posterior
Superior
Bronchial blockers are recommended over DLT in what situations?
Bronchial blockers are indicated for the following exceptions:
* Anticipated difficult airway, especially if awake fiberoptic bronchoscopy is anticipated
* Requirement for nasal intubation (a DLT cannot be advanced through the nares)
* Presence of tracheostomy (a DLT cannot be placed through the stoma)
* Distortion of tracheobronchial anatomy (eg, by vascularity, tumor)
* Requirement for selective lobar blockade
* Bronchial blockers be preferred for patients who require prolonged intubation because their use avoids the requirement for an endotracheal tube exchange
Direct IIa (thrombin) inhibitors
Direct IIa (thrombin) inhibitors
“DAB”
Dabigatran (Pradaxa) - oral
Argatroban (Acova) - IV
Bivalirudin (Angiomax)- IV
Lovenox (LMWH)
MOA
Indirect inhibtion of factor Xa
Binds to antithrombin III (ATIII) enhancing degradation of factor Xa.
NOTE:
Lovenox does not require monitoring, but can be monitored by anti-Xa levels (in patients with obesity or renal insufficiency).
Lovenox needs to be renally dosed (relies on renal clearance for up to 40% of its elimination).
Heparin (UFH)
MOA
Indirect inhibtion of factor Xa and IIa (thrombin)
Binds to antithrombin III (ATIII) enhancing degradation of factor Xa and IIa.
NOTE:
UFH is monitored with PTT, ACT, or anti-Xa levels.
UFH does not need to be renally dosed.
Used for emergent anticoagulation in ACS, PE, cardiopulmonary bypass, vascular surgery.
Reverse w/ Protamine.
Common complication is thrombocytopenia.
__________ are oral medications that specifically inhibit factors IIa or Xa.
Direct oral anticoagulants (DOACs) are oral medications that specifically inhibit factors Xa or IIa.
They are also known as new oral anticoagulants (NOACs) and include:
FEAR DABs
Edoxaban, Rivaroxaban, Apixaban are Xa inhibitors
Dabigatran is a IIa inhibitor (direct thrombin inhibitor)
Ester local anesthetics are metabolized by:
Amide local anesthetics are metabolized by:
Ester local anesthetics are metabolized by plasmacholinesterase.
Amide local anesthetics are metabolized by hepatic metabolism.
NOTE:
If it contains only 1 letter “i” then it is an ester.
If it contains 2 of the letter “i” then it is an amide.
ESTER local anesthetics undergo metabolism by pseudocholinESTERase.
Ester local anesthetics are more commonly implicated in hypersensitivity reactions compared to amide local anesthetics. This is because ester local anesthetics are metabolized to para-aminobenzoic acid (PABA) which is found in many other substances and is a known allergen. Despite this, Ig-E mediated type I hypersensitivity reactions (anaphylaxis) is extremely rare.
Which colloids can cause coagulopathy?
Synthetic colloids:
Hydroxyethyl starch (>20mL/kg/day)
Dextran
Compared to crystalloid solutions, hyperoncotic starches (eg. hydroxyethyl starch) are associated with increased risk of:
Coagulopathy
Renal injury
Anaphylactic/anaphylactoid reactions
Mortality
Factors that increase and decrease MAC:
What does a type & crossmatch test for?
Mixes the recipients serum with donor RBCs to examine for any incompatibilities that were not screened out, as well as setting aside the desired number of blood products for potential transfusion.
Factors that cause a left and right shift in the oxygen hemoglobin dissociation curve:
NOTE:
2,3-diphosphoglycerate (2,3-DPG) is an intermediate step in the glycolytic pathway and this product of cellular metabolism is a factor in the shifting of the oxyhemoglobin dissociation curve.
Given that it is indicative of cellular metabolism occurring, increases in its production shifts the curve to the right, favoring oxygen unloading at the level of the tissues.
Conditions where 2,3-DPG is decreased, such as in the storage of red blood cells or in the formation of glucose and glycogen, cause the curve to shift to the left.
Despite preservatives, such as citrate-phosphate-dextrose solution with adenine (CPDA), being used for red blood cell preservation, metabolic changes continue to occur.
Hypophosphatemia also causes a left shift. Hypophosphatemia commonly occurs secondary to sepsis, malnutrition, refeeding syndrome, acute liver injury, and DKA. Inorganic phosphate is a susbtrate for 2,3 DPG production and if hypophosphatemia is not corrected, the decrease in 2,3 DPG results in an increased affinity of oxygen for hemoglobin.
“CADET face right!” is a mnemonic that can help you remember some causes of rightward shift of the oxyhemoglobin dissociation: Carbon dioxide, Acidosis, 2,3-Diphosphoglyceric acid, Exercise, and Temperature. Cadets like to unload (fire) their guns, and a rightward shift increases oxygen unloading.
Define P50 as it pertains to the oxyhemoglobin dissociation curve.
The term P50 is designated as the partial pressure of oxygen (in mm Hg) when oxygen saturation (SaO2) is 50%. P50 can be used to relate the oxygen affinity for hemoglobin.
When the oxyhemoglobin dissociation curve shifts to the left or to the right, P50 will decrease or increase respectively.
In newborns, oxygen affinity is very high and P50 is very low (approximately 18 mm Hg). This is due to hemoglobin F, which is produced in-utero, and is useful for oxygen transfer from the maternal blood to the fetus. The presence of hemoglobin F and low 2,3-diphosphoglycerate (2,3-DPG) levels in newborns result in a very low P50. In fact, P50 is lowest in newborns.
After birth, levels of hemoglobin F begin to decline resulting in a decrease in the total hemoglobin concentration. This results in a physiological anemia of infancy. During this same period of time, 2,3-DPG levels begin to increase causing the oxyhemoglobin dissociation curve to shift to the right (P50 increases). The P50 will surpass that of an adult (27 mm Hg) and will reach a maximum of 30 mm Hg by about 12 months of age. Children will continue to have a higher P50 for the first decade of life.
In a normal adult, P50 is 27 mm Hg.
The oxygen saturation read by a standard two-wave pulse oximeter depends on the differential absorption of _ and _ light in tissue.
The oxygen saturation read by a standard two-wave pulse oximeter depends on the differential absorption of red light and infrared light in tissue.
Red light (660nm)
Infrared light (940nm)
A ratio of the absorbance of red to infrared light is calculated and that calculated number is translated to the oxygen saturation reading.
At red wavelengths, DEOXYhemoglobin aborbs MORE light than oxyhemoglobin.
At infrared wavelengths, OXYghemoglobin aborbs MORE light than deoxyhemoglobin.
NOTE:
Dyes (indocyanine green or ICG, indigo carmine, methylene blue), nail polish, ambient light, motion artifacts, vasoconstriction, hypothermia, methemoglobinemia (stuck at 85%), and carboxyhemoglobinemia (falsely elevated) will lead to inaccurate pulse ox readings.
Nail polish (esp blue, breen, and black) cause falsely low oxygen saturations by interfering with the differential absorption of 660-940nm light.
What are the three factors associated with relapse in physicians who are treated for substance abuse?
What are the three factors associated with relapse in physicians who are treated for substance abuse?
Use of opioids as the drug of abuse
Personal history of psychiatric illness
Family history of substance abuse disorder
NOTE:
Opioid is the most commonly abused substance amongst anesthesiologists.
Prevalence of chemical dependency among physicians is similar to that of the general population (10-13%)
The rate of relapse among physicians including anesthesiologists is actually lower than the general populaiton.
Review signs/symptoms of SUD among physicians (see picture)
The chromaffin cells of the adrenal medulla produce:
Dopamine
Norepinephrine
Epinephrine
Tyrosine -> DOPA -> Dopamine -> Norepinephrine -> Epinephrine
Cardiac Cycle
Methods for detecting VAE from most to least sensitive are as follows:
1) Transesophageal echo (TEE) - most sensitive
2) Precordial doppler
3) ETCO2
4) PA pressures
5) CVP
6) EKG
RCRI Scoring
NYHA Functional Classification of Heart Failure
The New York Heart Association classification of heart failure is based on symptoms.
The classification is as follows:
Class I: no limitation to normal activity
Class II: minor limitations, slight symptoms with normal activity
Class III: significant limitation to activity, comfortable only at rest
Class IV: symptoms at rest, severe limitations
What blood and/or blood-related products are considered acceptable by Jehovah’s Witness?
In 1945, the Jehovah’s Witness Governing Body banned the use of blood and/or blood-related products for transfusion on the basis of their interpretation of several biblical references. As a result, practicing Jehovah’s Witnesses are limited in the products they can receive. The table describes what is generally acceptable for Jehovah’s Witness patients.
Anesthetic considerations in patients with Parkinson’s Disease:
(see picture)
Parkinson disease is a neurodegenerative disorder caused by decreased dopaminergic neurons in the substantia nigra of the midbrain, one of a group of brain structures known as the basal ganglia, which is part of a crucial circuit for coordinating purposeful movement.
The disease manifests with progressive motor and nonmotor impairments. Motor symptoms include tremors, muscle rigidity, and bradykinesia. Nonmotor symptoms include cognitive decline in advanced stages of the disease.
Degeneration of the substantia nigra occurs in patients with Parkinson disease. This condition results in the disruption of the nigrostriatal pathway and thus decreases the striatal dopamine levels. Unlike dopamine, levodopa can cross the blood-brain barrier (BBB). Levodopa converts to dopamine in both the CNS and periphery. To increase the bioavailability of levodopa and decrease its side effects, it is often administered in combination with peripheral decarboxylase inhibitors (such as carbidopa and benserazide). Dopamine decarboxylase inhibitors prevent the conversion of levodopa to dopamine in the periphery, allowing for more levodopa to cross the BBB.
Acetylcholinesterase inhibitors are used to treat tremors (Donepizel, Galantamine, Rivastigmine).
Deep brain stimulation in Parkinson disease most commonly targets the subthalamic nucleus and the internal globus pallidus.
Triggers of aldosterone release?
1) Hyponatremia
2) Hyperkalemia
3) Angiotensin II
4) ACTH
Where is Vasopressin synthesized?
Hypothalamus
(Supraoptic & paraventricular nuclei)
Vasopressin is synthesized in the hypothalamus and *stored/released *in the posterior pituitary.
NOTE:
Anterior pituitary- synthesizes FLAT PeG. The mnemonic “FLAT PeG” can be used to recall all of the hormones released by the anterior pituitary. These are follicle stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), prolactin, endorphins, and growth hormone (GH).
Posterior pituitary- releases vasopressin and oxytocin (but both are synthesized in the hypothalamus supraoptic and paraventricular nuclei)
Digoxin
MOA
(+) INOTROPE
Digitalis is a cardiac glycoside that **inhibits the Na+/K+-ATPase **protein found within the membrane of cardiac myocytes, and this inhibition leads to an increase in intracellular sodium that subsequently increases intracellular calcium via compensatory exchange of intracellular sodium for extracellular calcium. This elevated intracellular calcium is thought to improve contractility in cardiac myocytes.
(-) CHRONOTROPE, (-) DROMOTROPE
Digitalis also stimulates the vagal nerve to slow conduction through the AV node and prolongs the refractory period in the AV node.
Digitalis is an adjunctive therapy reserved for individuals with heart failure with reduced ejection fraction (HFrEF) but can be used to manage rapid ventricular rhythms in patients with heart failure or atrial fibrillation when other therapies have failed. In patients with HFrEF, digitalis causes an improved force and velocity of contraction, increased cardiac output, and improved systolic emptying while causing reduced end-diastolic heart pressure that reduces pulmonary and systemic diastolic pressures.
de
Digoxin toxicity
Triggers?
Hypokalemia
Hypercalcemia
Hypomagnesemia
Acidosis/alkalosis
Low albumin
Hypothyroidism
Renal insufficiency
NOTE:
EKG findings include bradycardia, increased PR interval, AV block, downsloping (“scooping”) ST segments, QT shortening, PVCs, T-wave inversions or flattening.
Thiazide diuretics cause hypokalemia, hypercalcemia, and hypomagnesemia all of which can trigger digoxin toxicity.
_____________is the most commonly used induction agent for ECT and is considered the gold standard.
Methohexital s the most commonly used induction agent for ECT and is considered the gold standard.
Effects On Duration of ECT-Induced Seizure Activity:
Electroconvulsive therapy (ECT) has been used to manage psychiatric disorders since the 1930s. It can be used to treat mania, affective disorders, depression, and many other psychiatric disorders. It is typically performed three times per week for a total of 6-12 treatments. Weekly or monthly follow-up treatments are used to prevent relapses. An electrical current is applied to the brain, which precipitates a generalized motor seizure. Along with the seizure there is a large surge in the sympathetic nervous system that may result in profound hypertension and tachycardia. Electroconvulsive therapy requires minimum seizure duration of 25-30 seconds to ensure adequate antidepressant efficacy.
The anesthetic agent of choice for use during ECT depends on patient factors and length of seizure duration needed for treatment. The key is to use agents that have a neutral or attenuating effects on seizure duration.
Methohexital is the “gold standard” however it decreases seizure duration in a dose-dependent manner. Use of methohexital results in longer seizure times (versus propofol), shorter awakening times (versus thiopental), and fewer side effects (versus etomidate). With methohexital there is no change in seizure activity overall, but when compared with saline methohexital decreases the seizure duration. Methohexital will provide some blunting in hypertension and tachycardia that is observed during ECT, which gives it an advantage over other agents.
Note, medications that would decrease seizure duration (eg. Propofol, Benzos) should be avoided as an anxiolytic or induction agent during electroconvulsive therapy.
What affect does a valsalva maneuver initially have on the following parameters:
CVP
VR
HR
BP
Valsalva involves forced expiration against a clossed glottis.
CVP- increases
VR- decreases
HR- decreases
BP- decreases
Describe the phases of the cardiomyocyte action potential.
Describe the phases of the pacemaker cell action potential (SA node, AV node).
Phase 4 - slow depolarization, spontaneous inward flow of Na via funny sodium channels
Phase 0- fast depolarization, threshold met, T- type calcium channels cause calcium influx
Phase 3- repolarization, potassium efflux
NOTE:
Parasympathetic stimulation -> AcH release -> M2 muscarinic receptors (SA and AV node) –> increased pacemaker cell permeability to K+ –> hyperpolarization -> negative chronotropy, negative dromotropy, negative atria inotropy
The _________________ view is considered the optimal TEE view when a provider is monitoring for ischemia because the myocardium perfused by the three coronary arteries (left anterior descending, circumflex, and right coronary arteries) can be visualized in a single image.
The transgastric midpapillary short-axis (SAX) view is considered the optimal TEE view when a provider is monitoring for ischemia because the myocardium perfused by the three coronary arteries (left anterior descending, circumflex, and right coronary arteries) can be visualized in a single image.
TEE is the most sensitive method for detecting ischemia characterized by left ventricular systolic dysfunction.** Intraoperatively, myocardial ischemia can be detected by TEE quicker than changes on an electrocardiogram (ECG) are detected.** The transgastric midpapillary SAX views are often used when providers are monitoring for ischemia because the myocardium perfused by the three coronary arteries can be visualized in a single image. Ideally, regional wall-motion abnormalities seen in the transgastric midpapillary SAX view are confirmed in other views, including the midesophageal four-chamber, two-chamber, or long-axis planes.
Ischemia in the LAD distribution would most classically be accompanied by ST-segment or T-wave changes in what leads?
V1-V4 (Precordial Leads)
NOTE:
The LAD supplies 1/2 of the left atrium (anterior aspect), 1/2 left ventricle (anterior aspect), anterior 2/3 of the interventricular septum, the anterolateral papillary muscle, and the cardiac apex.
There are two papillary muslces in the left ventricle. The anterolateral papillary muscle is perfused by both the LAD and LCx. The posteromedial papillary muscle is perfused by the PDA however.
Ischemia in the RCA distribution would more commonly be accompanied by ST-segment or T-wave changes in what leads?
Leads II, III, or aVF
NOTE:
The RCA provides flow to both the SA and the AV node via the SA nodal and AV nodal branches. The RCA also supplies the lateral right ventricle and the cardiac apex.
Ischemia in the PDA distribution would be seen in what leads?
The PDA most commonly arises from the RCA (85% Right Dominant), and RCA ischemic changes (leads II, III, aVF) may be seen.
Isolated posterior infarctions are difficult to identify with a standard 12-lead ECG but can sometimes be identified with reciprocal changes, such as ST depression, in leads V1-V3.
NOTE:
The PDA, most commonly arising from the RCA, supplies the posterior 1/3 of the interventricular septum, the posterior inferior aspect of the heart, and the posteromedial papillary muscle.
Ischemia in the LCx distribution would most classically be accompanied by ST-segment or T-wave changes in what leads?
I, AVL, V5-V6
DAPT following DES may be held for time sensitive (non-urgent) noncardiac surgery after what time?
DAPT following DES may be held for time sensitive (non-urgent) noncardiac surgery after three months.
NOTE:
Studies have shown that the risk of in-stent thrombosis was highest 4-6 weeks after DES placement but remained elevated for up to one year.
DES have an anti-restenotic drug (chemotherapeutic agent) which reduces local neointimal hyperplasia but consequently slows endotheliazation (which is why DAPT is needed for 6 months for DES but only 1 month for BMS).
BMS are rarely used as DES have been shown to be far more superior.
The SA node and AV node are most commonly supplied by
The SA node and AV node are supplied RCA branches (SA nodal artery, AV nodal artery).
In a minority of patients, the SA and AV node may be supplied by the left circumflex.
Supply of the SA node does not dependend on coronary dominance of the patient.
In patients with right dominant heart (85%), the RCA gives right to the AV nodal artery.
The most common cause of AV nodal dysfunction and resulting complete heart block is myocardial infarction, most frequently blockage of the RCA. Revascularization results in prompt resolution of block. Ventricular pacing (transcutaneous, transvenous, or permanent pacemaker) may be needed. Atropine is typically ineffective for high degree AV blocks (Mobitz type II, third degree AV block).
Nitroglycerin and morphine should be avoided with inferior MI as they can lead to a decrease in preload and hypotension.
IABP inflates during ________ and deflates during ________.
IABP inflates during diastole and deflates during systole.
The IABP augments coronary perfusion by inflating during early diastole which improves aortic diastolic pressure. Coronary perfusion pressure (CPP) increases since CPP is the difference between aortic diastolic pressure (AoDP) and left ventricular end diastolic pressure (LVEDP): CPP = AoDP - LVEDP.
An IABP also aids in unloading the left ventricle by reducing afterload with deflation at end diastole.
The combined effect increases myocardial O2 supply and reduces myocardial O2 demand
One of the hallmark features of the arterial waveform tracing in a patient with an intra-aortic balloon pump (IABP) is the __________tracing after the dicrotic notch.
One of the hallmark features of the arterial waveform tracing in a patient with an intra-aortic balloon pump (IABP) is the augmented diastolic pressure tracing after the dicrotic notch.
What changes in the arterial waveform are seen in distal compared to proximal arteries?
Higher systolic peak
Lower diastolic nadir
Lower MAP
Delayed and less prominent dicrotic notch
Long QT syndrome can be congenital or acquired.
Causes of acquired long QT syndrome?
Acquired LQTS usually results from drug therapy, and several patient-specific and medication-related factors can enhance the risk.
Causes of acquired LQTS include antiarrhythmic drugs (quinidine, sotalol, dofetilide, ibutilide), psychotropic medications (haloperidol, methadone), erythromycin, cisapride, electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), eating disorders, coronary artery disease, and bradyarrhythmias.
NOTE:
QTc prolongation (>440ms in men, > 460ms in women)
QT interval varies with HR. QT is shorter at fast heart rates, QT is longer at slow heart rates.
QT interval can be corrected for heart rate:
QTc = QT/cardiac cycle (seconds)
What respiratory changes occur in elderly patients?
In the elderly population, normal age-related pulmonary physiological changes result from respiratory control, lung structure, and pulmonary blood flow alterations. Ventilatory responses to hypoxia, hypercapnia, and mechanical stress are impaired due to reduced central nervous system activity. Pharmacodynamic changes in the elderly include increased sensitivity to the respiratory depressant effects of benzodiazepines, opioids, and volatile anesthetics.
Age-related changes in lung structure include a loss of elastic recoil secondary to the reorganization of collagen and elastin in the lung parenchyma, leading to increased lung compliance. This increased lung compliance can result in limited maximal expiratory flow. Decreased lung elasticity is associated with enlargement of alveolar ducts and bronchioles, leading to early collapse of small airways, increasing the risk for air trapping and hyperinflation. Closing capacity (CC), defined as the volume at which small airways begin to collapse during exhalation, increases with age.
Lung volume changes in the elderly include increased anatomical dead space, CC, functional residual capacity (FRC) and decreased diffusion capacity, alveolar surface area, vital capacity, forced expiratory volume in the first second, and forced vital capacity. Residual volume increases by approximately 5% to 10% per decade. Despite these changes in lung volumes, total lung capacity is relatively unchanged in the elderly. The physiological changes between the FRC and CC cause an increased ventilation-perfusion mismatch and represent the most important mechanism for the increase in the alveolar-arterial gradient for oxygen seen in aging. The age-related decrease in height and calcification of the vertebral column and rib cage leads to a barrel chest appearance with associated diaphragm flattening. The flattened diaphragm is less efficient, and the age-related muscle mass decrease further impairs its function.
Hypoxic pulmonary vasoconstriction is blunted in the elderly (> 65 years) population, and this can cause difficulty with one-lung ventilation.
What respiratory changes occur in obese patients?
Obesity has long been recognized as significantly affecting respiratory function, including a higher respiratory rate to meet the heightened demand for ventilation in the setting of increased CO2 production and respiratory muscle inefficiency.
xcess body weight can decrease both chest wall and lung compliance. This results in a decreased functional residual capacity (FRC), vital capacity, and total lung capacity. FRC is the volume of air that remains in the lungs after a normal expiration. FRC is the sum of residual volume and expiratory reserve volume (ERV). Reduced FRC is primarily at the expense of decreased ERV while residual volume and closing capacity are unchanged. This results in lung volumes that fall below closing capacity during normal tidal volume ventilation leading to small airway collapse, ventilation-perfusion mismatch, right-to-left shunt, and arterial hypoxemia. In the supine position under general anesthesia, this effect is multiplied.
Forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) may be decreased in obesity (restrictive pattern) but are usually within normal limits. FVC/FEV1 ratio is unchanged in obesity.
The trachea can be anesthetized (translaryngeal/transtracheal block) by injecting local anesthetic transtracheally through the ____________.
The trachea can be anesthetized (translaryngeal/transtracheal block) by injecting local anesthetic transtracheally through the cricothyroid membrane.
Cough may occur with the injection, and this will help spread the local anesthetic.
Sensory, motor, and parasympathetic innervation of the trachea is via the recurrent laryngeal nerve.
Different types of pneumocytes?
The alveolus is the primary site for gas exchange in the lungs. The alveolus is primarily composed of type I alveolar cells, which cover 80% of the alveolar surface. Type I alveolar cells are squamous cells that are flat in nature, with flattened nuclei and thin cytoplasmic extensions that provide the surface area required for gas exchange. These cells are extremely susceptible to damage, highly differentiated, and metabolically limited. When they are damaged, type I alveolar cells are not replaced by other type I alveolar cells but rather by type II alveolar cells. These type II alveolar cells are interspersed among type I alveolar cells, predominantly at the alveolar-septal junctions. Unlike type I alveolar cells, type II alveolar cells are metabolically active and secrete the lung surfactant. Type II alveolar cells also play a role in pulmonary defense through the secretion of inflammatory mediators. Type III alveolar cells function as part of the immune system of the lung. They are able to migrate and ingest foreign material in the lungs.
Flow-Volume Loop:
Fixed obstruction
A fixed obstruction refers to an airway obstruction that is static and does not change with inspiration or expiration. Examples include tracheal stenosis or a large goiter. A fixed obstruction reduces flow in both the inspiratory and expiratory phases. In both phases, the flow will reach a plateau represented by a flattening of the flow-volume loop, i.e., the maximum flows during both phases will be reduced compared to a normal flow-volume loop. Note that a fixed obstruction, whether it is intrathoracic or extrathoracic, will produce a similar pattern on the flow-volume loop.
NOTE:
Flow-volume loops plot lung volume on the x-axis and flow on the y-axis. A positive value on the y-axis indicates expiration, while a negative value indicates inspiration. A continuous flow loop is formed traveling in a clockwise direction. Flow is positive as it goes towards the device during expiration, then negative as it travels away from the device (towards the patient) during inspiration.
Flow-Volume Loop:
Extrathoracic obstruction
Flow-volume loop illustrates a variable extrathoracic obstruction. Expiratory flow is relatively preserved while flow during inspiration is reduced with a plateau during this phase on the flow-volume loop.
Flow-Volume Loop:
Intrathoracic obstruction
Flow-volume loop illustrates a variable intrathoracic obstruction. Inspiratory flow is relatively preserved while flow during expiration is reduced with a plateau during this phase on the flow-volume loop.
Controlled Ventilation Modes
Continuous mandatory ventilation is the very first vent mode. It simply provides the set number of breaths and the set volume/pressure for a set time on the basis of the inspiratory/expiratory ratio. If a patient attempts to inhale between the scheduled breaths, they will not be able to draw any air, just as if they are breathing against a clamped tube. Intermittent mandatory ventilation is the next vent mode. It is an improvement compared with CMV in that, if the patient attempts to inhale between the scheduled breaths, the patient will be able to draw air. However, the breath is unsupported, and the fact that this spontaneous breath occurred does not affect the occurrence of the scheduled breaths. Both CMV and IMV are now antiquated and are no longer routinely used with modern ventilators.
Synchronized intermittent mandatory ventilation is an improvement compared with IMV in two ways. First, spontaneous breaths are supported in SIMV, either as controlled breaths or as pressure-supported breaths. Second, SIMV accounts for spontaneous breaths when mandatory breaths are scheduled. For example, if an RR of 10 is set and a patient has initiated a spontaneous breath within a six-second window after the last breath, then the spontaneous breath will be fully supported as a controlled breath (on the basis of the set volume/pressure setting) and will replace the originally scheduled breath. If a spontaneous breath has not occurred within the window, then the scheduled breath will occur at the end of the six seconds. If a second breath is attempted within the six-second window, then that breath will only be given pressure support but will not be a fully controlled breath. If the patient attempts to breathe 20 times per minute when an RR of 10 is set, then half of the breaths will consist of controlled breaths, and the other half of the breaths will be pressure-supported breaths.
Assist control is the newest vent mode. It can be easily identified because all breaths initiated by the patient will be fully supported as controlled breaths (with the set volume/pressure). It has been argued that AC is more comfortable than SIMV for the patient because, in AC mode, each of the breaths is identical and without variation. However, if the patient triggers 20 breaths per minute when 10 breaths are intended, 20 fully supported controlled breaths will be given, which may result in unintended hyperventilation. Because AC is the most commonly used vent mode, some vents abbreviate the combination of AC VC, AC PC, and AC PRVC as simply VC, PC, and PRVC, respectively; however, it is important to realize that these are actually AC vent modes.
Flow-Volume Loop:
Obstructive pattern
Flow-volume loop illustrates an obstructive pattern, such as in chronic obstructive pulmonary disease or bronchitis. This refers to lower airway obstruction and flow during expiration is lower than normal.
Difficult Airway Algorithm
ASA Physical Status Classification of Adult Patients
NOTE:
ASA physical status classification was originally created to compare anesthetic data. Nowaways is used to assess and communicate the medical comorbidities of patients. It is NOT predictive of perioperative risk.
The Guedel Classification: Stages of General Anesthesia
Stage 1: Analgesia
* Stage 1 of anesthetic depth, often referred to as the induction stage, begins with the first administration of any anesthetic drug and ends with the loss of consciousness.
* During stage 1, the patient remains in a state of analgesia and disorientation with or without amnesia.
* Patients in stage 1 will demonstrate slow and regular respirations and should be able to maintain a conversation.
Stage 2: Excitement/Delirium
* Stage 2 of anesthetic depth is characterized by the loss of consciousness and continues to the onset of autonomic breathing. Disinhibition, uncontrolled movement, and airway hypersensitivity are characteristics of stage 2.
* Patients in stage 2 are at the highest risk of laryngospasm, and airway stimulation should be avoided.
* Hypertension, tachycardia, irregular respiration, and nonpurposeful response to painful stimulus, may all indicate that a patient is in stage 2 of an anesthetic.
* Eye examination during stage 2 is characterized by loss of the eyelash reflex, divergent gaze, and reflex pupillary dilatation.
* Patients receiving a total intravenous anesthetic may exhibit fewer, if any, of the characteristic signs of stage 2 of anesthetic depth.
Stage 3: Surgical Anesthesia
* The resumption of regular, spontaneous respiration marks the entrance into stage 3 of anesthetic depth, which continues until respiratory paralysis.
* Stage 3 is the depth of anesthesia that is most desirable for surgical incision.
* During stage 3, airway reflexes become suppressed, allowing for safe airway manipulation, including insertion and removal of an endotracheal tube.
* Stage 3 can be divided into 4 separate planes of anesthesia.
* Plane I is marked by spontaneous breathing and central, constricted pupils with loss of the eyelid and conjunctival reflexes.
* Plane II is characterized by intermittent cessation of respiration along with the loss of ocular movement and laryngeal reflexes.
* Plane III is marked by the loss of function of the intercostal and abdominal musculature and the loss of the pupillary light reflex. Plane III is considered “true surgical anesthesia” and is ideal for most surgeries.
* Plane IV is demonstrated by irregular respiration and, eventually, full diaphragm paralysis, resulting in apnea. The carinal reflex is also lost in plane IV of stage 3.
Stage 4: Overdose
* Stage 4 of anesthetic depth is marked by apnea. Anesthetic overdose is the characteristic feature of stage 4.
* During stage 4, the patient’s pupils become fixed and dilated, and all reflexes and skeletal muscle tone are lost. Hypotension and bradycardia can occur, indicating brainstem and cardiovascular suppression.
* A patient in stage 4 should have anesthetic depth reduced as soon as possible or risk cardiovascular injury, neurologic injury, and death.
In 2011, a large meta-analysis (involving 55 studies and over 177,000 subjects) was published to evaluate the use of the modified Mallampati score as a prognostic test. When used as a stand-alone test, a high risk (class III or IV) modified Mallampati score demonstrated a sensitivity of _____% in predicting difficult intubation or laryngoscopy and a specificity of _____%.
In 2011, a large meta-analysis (involving 55 studies and over 177,000 subjects) was published to evaluate the use of the modified Mallampati score as a prognostic test. When used as a stand-alone test, a high risk (class III or IV) modified Mallampati score demonstrated a sensitivity of 35% in predicting difficult intubation or laryngoscopy. Like many screening tests, its specificity was much higher, determined to be 91% in this large study.
Describe the three levels of sedation.
Minimal Sedation
* Normal response to verbal stimulation
* Airway reflexes, spontaneous ventilation, and cardiovascular function are all unaffected
Moderate Sedation
* Purposeful response to verbal or tactile stimulation
* Spontaneous ventilation is adequate and no airway intervention is required
* Cardiovascular function is usually maintained
Deep Sedation
* Purposeful response to repeated or painful stimulation (reflex withdrawal from a painful stimulus is NOT considered purposeful response)
* Spontaneous ventilation may be inadequate and airway intervention may be required
* Cardiovascular function is usually maintained
General Anesthesia
* Unable to arouse even with painful stimulus
* Spontaneous ventilation is frequently inadequate and airway intervention is often required
* Cardiovascular function may be impaired
NOTE:
According to the ASA, one compares levels of sedation the major differences between moderate and deep sedation is the “airway” and “spontaneous ventilation” categories. For example, a patient may exhibit purposeful responses to repeated tactile stimulation (eg tapping, shacking) but if they repeatedly obstruct or become apneic they are techincally under deep sedation not moderate sedation.
_______________ is recommended during direct laryngoscopy and intubation in patients with known or suspected cervical spine instability.
Manual in-line stabilization (MILS) is recommended during direct laryngoscopy and intubation in patients with known or suspected cervical spine instability.
When one initially evaluates a patient with a suspected spine fracture, the presence of any of the following indicates a high risk of injury:
* High-speed (> 35 miles per hour) motor vehicle collision
* Death at the scene of a motor vehicle collision
* Fall from a height > 10 feet
* Significant closed head injury of intracranial hemorrhage seen on computed tomography
* Neurologic symptoms or signs referred to the cervical spine
* Pelvic or multiple extremity fractures
Patients with liver dysfunction who receive multiple blood transfusions can develop what electrolyte abnormality?
Hypocalcemia
Patients with liver dysfunction who receive multiple blood transfusions can develop hypocalcemia due to the calcium chelation by citrate (which is metabolized by the liver). Hypocalcemia may manifest as prolonged QT interval.
Hypermagnesemia causes QT ______________.
Hypermagnesemia causes QT prolongation.
Glucose Transporters (GLUTs)
Five GLUTs facilitate the movement of glucose across the cellular membrane. Glucose transporters 1, 2, 3, and 5 are insulin-independent transporters, while GLUT4 is the only insulin-dependent transporter. Glucose transporter 4 is responsible for most glucose uptake into adipocytes and striated muscle (skeletal and cardiac), and GLUT 2 is responsible for the uptake of glucose into the pancreas.
RBC Additives
Most blood product preservative solutions contain a mixture of citrate, phosphate, dextrose, and adenine.
Citrate is used to chelate calcium in the solution preventing coagulation from occurring.
Phosphate acts as a buffer to maintain the pH of the storage solution.
Dextrose is used to maintain a source of energy as RBCs as they are only able to undergo anaerobic glycolysis
Adenine maintains a pool of ATP for cell membrane integrity.
At two weeks of storage, metabolic changes occur, such as depletion of 2,3-diphosphoglycerate, which shifts the oxygen dissociation curve to the left, increasing oxygen affinity. By day 42, the pH decreases to 6.5, potassium concentration increases to 50 mmol/L due to RBC hemolysis and leakage, and 15-20% of RBCs are no longer viable.
Potential injuries in lithotomy position
Femoral nerve (impingement by inguinal ligament)
Obturator nerve (impingement by inguinal ligament)
Lateral femoral cutaneous nerve (impingement by inguinal ligament)
Sciatic nerve (stretch injury)
Saphenous nerve (compression against the medial condyle of the tibia with improper padding or positioning)
Common peroneal nerve (compression at the fibular head)
These injuries are associated with prolonged positioning (>2hrs)
NOTE:
Tibial Nerve = Plantarflexion + Inversion
Peroneal Nerve = Dorsiflexion + Eversion
“TIP PED”
The most common injuries during anesthesia in the lateral position are ________________.
The most common injuries during anesthesia in the lateral position are **brachial plexus injuries (brachial plexus neuropraxias). **
Cause: Axilla and neck compression (occurs when one shoulder or arm remains dependent under the ribcage or excessive lateral flexion at neck)
S/S: Loss of sensation in the affected extremity, with inability to flex the elbow, supinate the arm, or abduct and rotate the shoulder.
Prevention:
In an effort to mitigate compression of the dependent side, thoracic padding (called an “axillary roll”, an unfortunate misnomer) is used to ensure that the weight of the upper body lies on the thorax and not the dependent arm. The roll is placed under the dependent rib cage, 10 cm distal to the axillary folds, at the seventh to ninth rib. Should this padding migrate cranially into the axilla, it may actually exacerbate pressure on the brachial plexus and promote a compression injury on the dependent side. The cervical spine should also be kept in a neutral position using extra bedsheets/blankets under the head pillow, taking care to avoid flexion on the spine in either lateral direction. This can exacerbate brachial plexus injury and is best characterized by viewing the patient from the side prior to the placement of surgical drapes.
OTHER:
Traction injuries on the nondependent brachial plexus occur most frequently when the patient sags into a semi-supine posture following initial positioning. As the non-dependent arm is usually fixed to an arm board support this motion places tension on the shoulder joint and can cause traction injury.
Another common injury in the nondependent upper extremity is a suprascapular nerve injury that results from anterior flexion of the arm across the chest. This places tension on the suprascapular nerve and can result in deep and poorly characterized pain about the nondependent shoulder.
According to the Anesthesia Closed Claims Project database, the _______ nerve is the most commonly injured peripheral nerve perioperatively.
According to the Anesthesia Closed Claims Project database, the ulnar nerve is the most commonly injured peripheral nerve perioperatively.
Ulnar can occur from malpositioning or compression such as flexion of the elbow > 110° for extended periods of time during surgery (eg positioning arm over chest). Patients with ulnar nerve injuries can present with numbness, tingling, or pain at the dorsal and palmar surface of the medial one-and-a-half fingers. Motor dysfunction can include weakness of wrist flexion, flexion of the fifth digit, abduction of the fifth and fourth digit, and adduction of the thumb.
OTHER NERVE INJURIES:
A radial nerve injury can present with sensory deficits of the dorsal forearm, dorsal aspect of the first through the lateral aspect of the fourth digit. Motor dysfunction can affect extension of the forearm at the elbow. It can also present with wrist drop and decreased grip strength, depending on the location of the injury.
A musculocutaneous nerve injury would present with sensory deficits in the lateral forearm and from the elbow to the base of the thumb. Motor deficits can affect elbow flexion and forearm supination.
A median nerve injury would present with numbness of the palmar aspect of the first four digits, medial forearm, medial arm. Weakness with wrist flexion, first four digit finger flexion, opposition of the thumb, and pronation.
An axillary nerve injury would present with a sensory deficit over the lower part of the deltoid and lateral arm. Motor deficits can affect shoulder abduction above 15° and external rotation of the arm.
A _ nerve injury can occur due to overextension of the elbow.
A median nerve injury can occur due to overextension of the elbow.
Symptoms:
Numbness of the palmar aspect of the first four digits, medial forearm, medial arm.
Weakness with wrist flexion, first four digit finger flexion, opposition of the thumb, and pronation
Glasgow-Coma Scale (GCS)
Hemorrhagic Shock
Class I-IV
ASA Practice Guidelines Preoperative Fasting:
“Minimum fasting periods”
Clear liquids:
Carbohydrate drink:
Light meals:
Regular meals:
ASA Practice Guidelines Preoperative Fasting
“Minimum fasting periods”
Clear liquids: 2hrs
Carbohydrate drink: 2hrs
Light meals: 6hrs
Regular meals: 8hrs
NOTE:
Clear liquids are eliminated in the stomach in an exponential fasion. Liquids are thought to empty secondary to the pressure gradient between the stomach and duodenum.
Solid foods are eliminated in the stomach in a linear fashion. Solids are emptied from the stomach only when they have been digested to essentially liquid. Elimination of non-clear liquids depends on multiple considerations- amount of milk ingested, caloric content, ratio of fat, and amino acids. Higher fat content will take longer to eliminate.
ASA Practice Guidelines Preoperative Fasting:
“Minimum fasting periods”
Volatile anesthetics with a (higher/lower) blood:gas partition coefficients have a faster rate of alveolar (thus a slower onset of action).
Volatile anesthetics with a lower blood:gas partition coefficients have a faster rate of alveolar uptake (thus a slower onset/offset)
Blood: gas partition coefficient is inversely proportional to the speed of alveolar uptake. The higher the blood:gas partition coefficient, the slower the alveolar uptake (and longer the time of onset/offset). A larger coefficient means that the gas has a higher solubility in the blood but a slower onset of action because more anesthetic must be dissolved before it equilibriates with the tissue of the CNS.
Blood solubility, which is often described in terms of the blood:gas partition coefficient, is one of the principal determinants concerning the uptake and speed of onset of the inhaled volatile agents. The partition coefficient describes how the anesthetic is split between the two phases (blood and gas). Alveolar concentration of an anesthetic (FA) divided by the inspired concentration (FI) yields a ratio that can be used to assess the relationship of the delivered anesthetic by ventilation and the degree of anesthetic uptake/removal.
Therefore, inhaled agents with a high FA/FI ratio are associated with a low solubility, while higher blood solubility values are associated with a lower FA/FI ratio.
NOTE:
Potency is different. Potency is primarily determined by a volatile anesthetics lipid solubility (oil:gas partition coefficient)
Alveolar uptake depends on what three factors?
Minute ventilation
Alveolar blood flow (ie CO)
Blood:gas partition coefficient
Difference in alveolar vs. venous partial pressures
NOTE:
Increase rate of rise of FA/Fi include:
* High minute ventilkation
* Low cardiac output
* Relatively low blood:gas partitiion coefficients (less soluble)
* Low Parterial-Pvenous (meaning less blood uptake)
Why does the FA/Fi curve rise faster for Nitrous Oxide than Desflurane, despite the fact that Desflurane having a lower blood:gas partition coefficient (less-soluble) than Nitrous Oxide?
Why does the FA/Fi curve rise faster for Nitrous Oxide than Desflurane, despite the fact that Desflurane having a lower blood:gas partition coefficient (less-soluble) than Nitrous Oxide?
Concentration Effect
NOTE:
The cocentration effect describes the concentration of NO itself in the alveoli after its uptake into the circulation. NO is drawn into the trachea as NO is moved from the lung into the circulation further increasing the amount of NO. This effect explains why the rate of FA/Fi rise for NO is faster than desflurane, despite having a higher blood:gas partition coefficient.
The second gas effect describes how the rapid diffusion and uptake of NO concentrates the potent anesthetic (Sevoflurane) that is left behind in the alveoli.
Rank the following volatile gases from highest to lowest vapor pressure:
Sevoflurane
Isoflurane
Desflurane
NO
Rank the following volatile gases from highest to lowest vapor pressure:
NO- 38,770 mmHg
Desflurane- 669 mmHg
Isoflurane- 238 mmHg
Sevoflurane- 157 mmHg
These vapor pressures are at 20 degrees celcius and 1 atm.
At 20 degrees celcius and 1 atm all inhalation anesthetics exist in the liquid form except NO (which has a boiling point of -88 degree celicius). Although most of the inhalational anesthetics may be liquid in form, they equilibrate between the liquid and gas phases in a closed container.
Vapor pressure is proportional to temperature. As the temperature rises, the kinetic energy of the liquid increases which raises the number of molecules in the gaseous state and increases the vapor pressure. After the temperature is raised sufficiently such that the vapor pressure exceeds the atmospheric pressure in an open container, it will have reached its boiling point.
Which virus has the highest risk of seroconversion after needlestick from a patient with an active infection?
HIV
Hepatitis B
Hepatitis C
Hepatitis B
Which patient populations benefit from prophylactic treatment with antibiotics before surgical or dental procedures to try to prevent IE?
What antibiotic should be administered and when?
The list of patients who should receive prophylaxis is below:
- Patients with a prosthetic cardiac valve
- Patients who have previously had IE
- Patients with unrepaired cyanotic congenital heart disease (including palliative shunts/conduits)
- Patients with congenital heart defects which were repaired with prosthetic material within 6 months of the procedure
- Patients with repaired congenital heart disease with residual defects at the site, or adjacent to the site, of a prosthetic patch or device
- Cardiac transplantation recipients who develop cardiac valvulopathy (substantial leaflet pathology and regurgitation)
Of note, prophylaxis only applies to certain surgical procedures:
- Dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa
- Invasive respiratory tract procedures that involve incision or biopsy of the respiratory mucosa (e.g. tonsillectomy, adenoidectomy)
- Infected skin, skin structure, or musculoskeletal tissue
Antibiotics are no longer recommended for endocarditis prophylaxis for patients undergoing genitourinary or gastrointestinal tract procedures.
The preferred prophylactic regimen is Amoxicillin 2 g given as a one time oral dose 30-60 min before the procedure.
Signs/symptoms of corneal abrasion?
Foreign body sensation
Pain with blinking
Pain with eye movement
Tearing
NOTE:
Always tape eyes BEFORE masking as the mask can push high flow oxygen to eyes drying them out and mask can directly cause corneal abrasion.
Under general anesthesia, corneal reflexes are obviously impaired and they also have decreased tear production.
Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of Sedation/Analgesia
Contact dermatitis is an example of a type _______ hypersensitivity reaction.
Contact dermatitis is an example of a type IV hypersensitivity reaction.
Autoimmune hemolytic anemia is an example of a type _______ hypersensitivity reaction.
Autoimmune hemolytic anemia is an example of a type II hypersensitivity reaction.
Anaphylaxis, food, drug, and seasonal allergies are all examples of a type _______ hypersensitivity reaction.
Anaphylaxis, food, drug, and seasonal allergies are all examples of a type I hypersensitivity reaction.
In patients with a Penicillin allergy, the cross-reactivity with Cephalosporins is approximately ____ %.
In patients with a Penicillin allergy, the cross-reactivity with Cephalosporins is approximately < 1 %.
NOTE:
Anaphylactic reaction to cephalosporins is uncommon with estimates being 0.0001% to 0.1%.
An alternative may be sought if there is history of severe allergic reaction or anaphylaxis to Penicillin.
Alternative antibiotic for a patient with a true allergy to penicillin or cephalosporins?
Clindamycin or Vancomycin
NOTE:
In patients with a Penicillin allergy, the cross-reactivity with Cephalosporins is approximately < 1 %.
Anaphylactic reaction to cephalosporins is uncommon with estimates being 0.0001% to 0.1%.
By maintaining the fraction of inspired oxygen (FiO2) < _____%, the risk of operating room items becoming flammable is decreased significantly.
By maintaining the fraction of inspired oxygen (FiO2) < 30%, the risk of operating room items becoming flammable is decreased significantly.
For an operating room fire to occur, the fire triad must be present—ignition source, oxidizer, and fuel. The ignition sources are numerous and include lasers, electrosurgical units, and fiber optic cables. The oxidizers in operating room fires are either oxygen or nitrous oxide. Oxygen is a component of room air and can be more present with supplemental oxygen administered during anesthesia. Nitrous oxide is equally as efficacious as an oxidizer as oxygen and may be administered during an anesthetic. Fuel sources include gauze dressings, endotracheal tubes, mattress pads, body/facial hair, and drapes. The key to prevention is minimizing the components in the triad.
Tourniquets can be used safely for ______ hour(s).
Tourniquets can be used safely for 2 hour(s).
When inflation times are too long or tourniquet pressures are too high, damage can occur to the tissues beneath (blood vessels, nerves, muscles, and skin).
Tourniquet pain does not respond well to opioids or deepening of the anesthetic. Tourniquet deflation is the only definitive treatment of tourniquet pain.
To increase the duration of the tourniquet use, a perfusion break can occur. When the cuff is deflated, several physiological events occur such as transient metabolic acidosis, increased carbon dioxide levels, and a drop in systemic blood pressure. Care should be taken when the cuff is deflated in patients who are at risk of complications.
The cuff should be inflated to 50 mmHg above the systolic blood pressure when a tourniquet used in the arm and to 100 mmHg above the systolic blood pressure when a tourniquet is used in the leg.
Which tissues are the most radiosensitive?
Testes, ovaries, bone marrow, lymphoid tissues, and small intestines
Differentiate deterministic vs stochastic effects with respect to radiation.
When a person is exposed to ionizing radiation, damage to cells and deoxyribonucleic acid can occur, and the radiation effects can be divided into deterministic or stochastic effects (Table 1).
Deterministic effects are short-term effects that occur only after a threshold dose is reached, and, if the dose is below the threshold, no effect should occur. For deterministic effects, a larger dose results in worse severity.
Stochastic effects do not have a threshold and occur by statistical chance; a larger dose results in a greater chance of experiencing that effect. For stochastic effects, severity does not depend on the dose. The stochastic health effects can occur from either a short or a long exposure period.
Difficult Airway Algorithm
Specific (relative) indications for TIVA
Factors that cause left/right shift in oxygen-hemoglobin dissociation curve?
How does the liver metabolize lactate from lactated ringers?
The lactate in lactated ringers solution is converted to pyruvate by lactate dehydrogenase (LDH) in the liver. Pyruvate then enters the citric acid cycle to produce H2O, CO2, and bicarbonate.
Lactate in lactated ringers DOES NOT increase lactic acid levels and DOES NOT cause acidosis because it is the base conjugate of lactic acid.
Plasmalyte, in particular, contains acetate and gluconate. How does the body metabolize both?
Acetate is metabolized by the liver, muscle, and heart to bicarbonate.
Gluconate is converted to glucose by the liver which can then be used for glycolysis and citric acid cycle.
Methadone (Dolophine, Methadose) and Buprenorphine (Suboxone) have FDA approval for the treatment of Opioid Use Disorder (OUD).
MOA?
Methadone (Dolophine, Methadose)- full μ-opioid agonist, NMDA anatagonist, also acts like an SSRI in that it inhibits the serotonin transporter (SERT) .
Buprenorphine (Suboxone)- partial μ-opioid agonist, κ-antagonist
Describe the pattern seen on a Flow-Volume Loop in patients with asthma and COPD.
Intrathoracic Obstruction
Spirometry produces flow-volume loops. Different types of lung disease create stereotypical patterns on these flow-volume loops. An intrathoracic obstructive pattern is often described as having an expiratory pattern that resembles a “boot shape.” This is commonly seen in patients with chronic obstructive pulmonary disease and asthma. It is thought to be secondary to the narrowing of the upper airways and loss of elastic recoil in the lower airways.
What conditions must be met in order for dynamic values such as PPV, SVV, SPV to be accurate in the context of goal-directed fluid therapy?
A patient that is being mechanically ventilated (not spontaneous)
Tidal volumes must be 8-10 mL/kg
PEEP > 5
Sinus rhythm
Closed intrathoraic cavity with normal intrathoracic pressures
Closed abdomen with normal intraabdominal pressures
NOTE:
Arterial waveform analysis, in which variation in pulse pressure, systolic pressure, or stroke volume > 10% is considered fluid responsive, is one of the most popular mechanisms used in a GDT protocol.
What factors attenuate and potentiate hypoxic pulmonary vasoconstriction?
NOTE:
Nitroprusside and nitroglycerin produce nitric oxide and cause systemic as well as pulmonary vasodilation. Pulmonary vasodilation will blunt HPV at hypoxic alveoli.
Calcium channels blockers (eg. nicardipine) inhibits HPV by preventing calcium influx into cells.
A mediastinal mass or distal trachea tumor can cause what changes to a flow-volume loop?
Variable intrathoracic airway obstruction
Plateaued expiratory curve
A fixed upper airway obstruction (eg. tracheal stenosis, foreign body) causes what changes on a flow-volume loop?
Fixed upper airway obstruction
Plateaued inspiratory AND expiratory curve
What states causes a leftward shift without change in slope in the carbon dioxide response curve?
Metabolic acidosis
Hypoxia
A left shift amplies the patients respiratory drive and leads to hyperventilation to improve alveolar ventilation.
What states causes a rightward shift and decreased slope in the carbon dioxide response curve?
Deep anethesia
Volatile anesthetics
Propofol
Benzodiazepines
Opioids
NOTE:
The slope of the carbon dioxide response curve represents carbon dioxide sensitivity which is primarily a function of chemoreceptor thresholds. At increasing partial pressures of arterial CO2 an awake and unmedicated patient will generally respond with approximately linear increases in alveolar ventilation in order to compensate and return to normocapnia.
This response may be profoundly blunted when sedative-hypnotics, opioids, or other anesthetic medications are administered because these drugs tend to impair chemoreceptor activation and signaling. The end result is that significantly higher arterial CO2 tensions will be required to provoke an equivalent ventilatory response and patients will therefore tend to hypoventilate despitre progressive hypercapnia.
What specific types of hemoglobins (pathologic, physiologic) cause a leftward shift on the oxygen-hemoglobin dissociation curve?
LEFT
Fetal hemoglobin
Carboxyhemoglobin
Methemoglobin
Sickle hemoglobin
RIGHT
Sulfhemoglobin
How exactly do concentration-calibrated variable bypass vaporizers allow specific concentrations of volatile gases to be delivered to the patient?
By adjusting the splitting ratio (see picture).
What are the two types of dead space?
Dead space is the portion of the lung volume that is not involved in perfusion and therefore not involved in gase exchange.
Physiological dead space = anatomical dead space (oronasopharynx, trachea, bronchi, bronchioles) + alveolar dead space (alveoli that is not perfused)
In healthy individuals 30% of minute ventilation is spent on dead space ventilation. Physiological dead space is approximately 2mL/kg in the adult patient. When minute ventilation decreases below 2.1L/min ventilation is no longer effective for CO2 removal (see picture).
This means that in a healthy individual of an average 500mL TV a total of 150mL goes to the conduction airways (anatomic deadspace) and alveoli that are not perfused (alveolar dead space) and only 350mL actually participates in alveolar ventilation.
In a patient with rapid shallow breathing, when titdal volumes approach 150mL most of that volume goes to dead space ventilation and despite the apparent presence of minute ventilation the alveolar ventilation is close to zero. To put it in another way, not all minute ventilation is created equal.
How does a right-to-left intrapulmonary shunt affect speed of inhalational induction?
A right-to-left intrapulmonary shunt will slow inhalation induction.
The rate of rise for the alveolar concentration to inspired concentration (FA/Fi) will decrease. This is due to the dilution of the anesthetic agent when the venous blood that has bypassed the lungs mixes with arterial blood.
How does a right-to-left intracardiac shunt affect speed of inhalational and IV induction?
A right-to-left intracardiac shunt affect decreases speed of inhalational induction (mixing of anesthetic poor and rich blood).
A right-to-left intracardiac shunt affect increases speed of IV induction (bypasses pulmonary circulation).
How does a left-to-right intracardiac shunt affect speed of inhalational and IV induction?
Minimal/no effect for both inhalational and IV induction.
What are the most and least accurate numbers provided by a BP cuff?
MAP (most accurate)
Systolic (underestimated) - least accurate
Diastolic (overestimated)
NOTE:
BP cuff measures MAP, but systolic and diastolic are calculated.
Bladder of the cuff should cover 40% of the upper arm’s circumference and 80% of the length of the upper arm.
