Basic Exam Flashcards
What is the half life of Flumazenil?
Why is this important?
Half Life:
Midazolam: 1.7 - 2.6 hours (102 minutes - 156 minutes)
Flumazenil: 0.7 - 1.3 hours (42 min - 78 minutes)
Significantly shorter half life than benzodiazepine agonists.
This can lead to the recrudescence of sedation from benzodiazepines following the elimination of flumazenil.
Therefore, when administering flumazenil, careful attention needs to be paid to its duration of action relative to that of the benzodiazepines taken by the patient, and additional doses of flumazenil should be available.
What is the mechanism of action of Flumazenil?
*Caveat to Mechanism of Action*
Note that although flumazenil is generally considered a benzodiazepine antagonist, it exhibits a partial agonist effect.
In one study, propofol was potentiated by giving high doses of flumazenil, suggesting flumazenil has a mixed or partial agonist effect.
What is the half life of the common benzodiazepines?
Alprazolam, Diazepam, Lorazepam, Midazolam, and Temazepam
Half Life of Other Benzodiazepines (MALTD)
Midazolam is 1.7-2.6 hours (2 hours)
Alprazolam is 6-27 hours (A = Afternoon)
Temazepam is 10 hours (Tem = Ten)
Lorazepam is 11-22 hours (L = eLeven)
Diazepam is 20-50 hours (D = ~ 1 day)
For Nitrous Oxide, a full tank will read:
What volume?
What pressure?
When will the pressure start to drop?
A full tank of N2O contains 1590 L at a pressure of ~745 psig.
Pressure within a tank of N2O will remain at ~745 psig until all liquefied gas is used up which is when the tank is ~16% full (253 L).
What acid base disturbances are common with different diuretics?
Acetazaloamide?
Thiazide?
Loops?
Potassium Sparing?
Thiazide and loop diuretics can cause an Hypokalemic Hypochloremic metabolic alkalosis.
Acetazolamide and potassium sparing can cause a hyperchloremic metabolic acidosis.
How does hyperventilation affect electrolytes?
Calcium?
Potassium?
Phosphate?
Sodium?
pH?
HCO3?
Chloride?
Lactate?
Respiratory alkalosis (ETCO2 of 30-35), such as from hyperventilation, can cause electrolyte abnormalities such as hypocalcemia, hypokalemia, and hypophosphatemia.
Loss of CO2 by 10 mmHg
Rise in pH (0.1)
Decreased HCO3 (2.0 mEq/L)
Decreased Potassium (0.4 mEq/L) - After will slowly return to normal
Decrease in Sodium
Increased Chloride (Balanced decrease in Bicarb)
Increased lactate (Balanced decrease in Bicarb)
What is the relationship between hyper/hypoventilation and calcium levels?
(Explain the physiology)
Hypocalcemia can occur with respiratory alkalosis.
In response to alkalosis, hydrogen ions bound to negatively charged plasma proteins, such as albumin, are released.
Calcium, being positively charged, can then bind to albumin and other proteins decreasing the serum calcium concentration (particularly the free/ionized, active fraction). This is the mechanism behind paresthesias that occur with hyperventilation.
What are the main determinants of myocardial oxygen demand?
1. Wall tension
2. Heart rate
3. Contractility
What is the formula for wall tension?
Wall tension (T) = (P * r) / (2 h)
P is the pressure within the ventricle
r is the radius of the ventricle
h is the thickness of the ventricular wall (Increase seen in hypertrophy)
What is the downside to developing left ventricular hypertrophy?
The ventricle hypertrophies to compensate for the increased wall tension due to pressure or volume overload, such as with aortic stenosis. However, this change comes at a cost. The hypertrophied ventricle is not as compliant due to increased diastolic pressures in the ventricle. This leads to a decrease in preload*, and the hypertrophied ventricle is now more *dependent on atrial contraction to maintain LVEDV
ex: (Atrial fibrillation with diastolic heart failure is a horrible combination)
What are the two determinants of acoustic impedence of ultrasound?
Acoustic Impedance (two factors determine)
1. Density of the medium(This is the main one)
2. Propagation speed of sound through the medium
Acoustic impedance is the product of the density of a medium and the propagation speed of sound through that medium. Ultrasound reflections that occur at the interface of different mediums are due to the changes in acoustic impedance. Since propagation speed changes slightly between biological mediums, acoustic impedance is primarily dependent upon density.
How does gentamicin affect neuromuscular blockade?
What is the mechanism behind this?
Prolongs neuromuscular blockade
Gentamicin inhibits prejunctional acetylcholine release and depresses postjunctional receptor sensitivity to acetylcholine, thus prolonging paralysis in a patient who received it along with a muscle relaxant.
It is believed that aminoglycoside antibiotics antagonize calcium ions by means of its involvement in the process of acetylcholine release by nerve impulses.
What are all the antibiotics that can prolong neuromuscular blockade?
Aminoglycosides
- Lincomycin, Clindamycin, Streptomycin, kanamycin, tobramycin, neomycin, and gentamicin
Polymyxins
Tetracyclines
Muscarinic receptor agonists can act through two mechanisms, directly on the muscarinic receptor or indirectly by inhibiting the breakdown of ACh causing more ACh to be available to bind to the muscarinic receptor.
1. What are the direct acting agents are choline esters?
2. And what are the alkaloids?
3. What are the anticholinergics?
The direct acting agents are choline esters (ACh, methacholine, carbachol, bethanechol)
direct acting agents have few clinical applications due to their very short half and longer activity can be achieved by methylating the choline moiety.
Alkaloids (pilocarpine, muscarine, arecoline or acetylcholinsterase inhibitors).
The indirect acting agents are acetylcholinesterase inhibitors (physostigmine, neostigmine, pyridostigmine, edrophonium, and echothiophate). These medications are often used to improve neuromuscular function in disease states where weakness occurs such as myasthenia gravis or to help reverse the action of nondepolarizing neuromuscular blocking agents.
Anticholinergic drugs are used commonly in anesthesia practice. These medications inhibit the action of ACh by reversibly binding at the muscarinic receptor. Antimuscarinic drugs used in anesthesia practice are atropine, scopolamine, and glycopyrrolate. Both atropine and scopolamine cross the blood-brain barrier, which can result in inhibition of vagal outflow from the central nervous system. At low doses, vagal outflow can potentially be augmented.
You have your line isolation monitor alarming. What is the next step?
When the line isolation monitor alarms, the first step should be to unplug the most recent electronic device that was plugged in.
What portion of the spinal cord is perfused by the anterior spinal artery?
How many are their?
What vessel is this from?
A single (not paired) anterior spinal artery supplies the anterior two-thirds of the spinal cord.
The spinal cord blood supply is anatomically divided into an anterior and a posterior blood supply. The anterior two-thirds of the spinal cord, primarily responsible for motor function, is perfused by the anterior spinal artery (ASA), which originates from the vertebral arteries and receives contributions from various radicular vessels that arise from intercostal arteries.
Is the posterior spinal artery paired?
What is the perfusion to the posterior spinal artery?
What does it arise from?
Two posterior spinal arteries (PSA) stem from the vertebral or posterior inferior cerebellar arteries (PICA). They comprise the blood supply to the posterior one-third of the spinal cord, primarily responsible for sensation, while concurrently receiving intercostal radicular vessel contributions.
What is the origination spinal levels of Artery of Adamkiewicz?
(List the regions from most to least common)
The artery of Adamkiewicz a radicular vessel contributing to anterior spinal cord blood supply
Most commonly originates within the T9 - T12 region
Followed by the L1 - L5 region
least commonly, within the T5 - T8 region
Compare adults vs. infants in terms of:
Spinal cord* vs. *Dural Sac Ending
In adults
Spinal cord ends at about L1-L2 (Conus Medullaris)
Dural sac ends at about S1-S2.
In an infant, these landmarks are shifted slightly caudad (Inferior)
Spinal cord ending at L3-L4
Dural sac terminating at S3-S4
When performing a spinal blockade in an adult, the iliac crest is commonly used as a landmark as it generally corresponds to the level of the L4 interspace is known as What Anatomical Landmark?
Tuffier’s line
What are the 3 drugs that can decrease post-operative delirium with Ketamine administration?
Benzodiazepines, propofol, and barbiturates can decrease ketamine-induced emergence delirium.
An important consideration when using ketamine relates to the high incidence of psychomimetic reactions early in the recovery period. The most common reactions include hallucinations, nightmares, altered cognition, and altered short-term memory. Repeated doses of ketamine may decrease the severity and incidence of emergence delirium, but one of the most effective strategies for prevention of emergence delirium is the use of midazolam approximately five minutes prior to an induction with ketamine.
How does magnesium and Calcium levels affect neuromuscular blockade?
Hypocalcemia potentiates neuromuscular blockade because calcium is important for the release of vesicles containing acetylcholine from nerves at the neuromuscular junction.
When calcium levels are low, less acetylcholine is released.
With less acetylcholine being released there is less competition at the acetylcholine receptor and neuromuscular blockers have a greater effect.
Hypermagnesemia acts similarly by blocking calcium from entering alpha motor neurons and preventing the release of some of the acetylcholine containing vesicles.
How do anti-convulsants affect neuromuscular blockade?
- *Shorten Non-Depolarizing Blockade:**
- Anticonvulsants (e.g. phenytoin, carbamazepine)
What effect does Ketamine have on neuromuscular blockade?
Prolongs
What is the order or potentiating volatile anesthetics for prolonging neuromuscular blockade?
Why is this physiologically seen?
Potentiation from greatest to least for volatile anesthetics is:
desflurane* > *sevoflurane* > *isoflurane.
Desflurane is a volatile anesthetic with a low blood gas partition coefficient of 0.42.
- The low blood gas coefficient means that very little desflurane is dissolved in tissues, but that desflurane is able to rapidly equilibrate with tissues resulting in quick onset and termination of effects.
- This rapid equilibration into tissues including muscle is the reason why desflurane potentiates neuromuscular blockade more than other volatile anesthetics.
- The location of potentiation is likely at the neuromuscular junction and occurs in a dose dependent fashion.
Mechanical ventilation can be categorized by what three variables? Explain them
Ventilators need “TLC”
Mechanical ventilation can be categorized by three variables
1. Trigger - What initiates the breath and depends on ventilatory drive
2. Limit - Governor of PPV and depends on ventilatory requirements related to how much flow* and *volume are required to satisfy metabolic demands
- Cycle - What terminates the inspiratory phase and depends on the duration and ratio of inspiratory time to total breath cycle duration.
How does Morphine improve Coronary Perfusion?
Morphine improves coronary perfusion through a reduction in preload and a reduction in end-diastolic pressures (EDP) in the ventricles.
The EDV is proportional to the EDP generated within the ventricle.
The RV is perfused during both systole and diastole whereas the LV is perfused during diastole only.
Right-sided coronary perfusion pressure during systole is = (aortic systolic pressure - RVEDP).
Left-sided coronary perfusion pressure is the difference between (aortic diastolic pressure and left ventricular end-diastolic pressure (LVEDP)).
Coronary perfusion pressure is improved by REDUCING both RVEDP and LVEDP.
What is the first symptom during central nervous system toxicity of local aneshetics?
Central nervous system toxicity is first noted by circumoral and tongue numbness.
Visual and auditory disturbances (tinnitus) then follow.
The clinical scenario then progresses to dizziness/lightheadedness, muscular twitching, unconsciousness, and seizure activity. These clinical signs may then be followed by cerebral edema, increased intracranial pressure, coma, respiratory arrest, and ultimately cardiovascular depression and death. Patients who are premedicated with anticonvulsants, such as benzodiazepines or barbiturates, may have masked CNS symptoms and develop cardiovascular depression before other signs are apparent.
Areas of regional anesthesia from highest to lowest vascularity include (List the order of greatest to least)
intravenous
tracheal
intercostal
caudal/paracervical
epidural
brachial plexus
sciatic/femoral
spinal
subcutaneous
Intercostal > Caudal > Epidural > Brachial Plexus > Lower Limbs > Sub-Q “IT - ICE BaLLS” is the mnemonic
Rank the Areas of regional anesthesia from highest to lowest vascularity.
Areas of regional anesthesia from highest to lowest vascularity include:
intravenous > tracheal > intercostal > caudal/paracervical > epidural > brachial plexus > sciatic/femoral > spinal > subcutaneous.
What is the possible consequence of using lidocaine through spinal?
Lidocaine has been linked to cauda equina syndrome, causing urinary and fecal incontinence as well as gait disturbances.
This association has been documented in the setting of high concentration (5%) intrathecal lidocaine administered via narrow lumen (e.g. 27 gauge) catheters. The slow administration of 5% lidocaine through these catheters allows for pooling of the drug in the region of the cauda equina. This form of local neural toxicity may be due to demyelination.
If you have a desiccated CO2 absorbent, what is the byproduct of desflurane?
Of sevoflurane?
Carbon monoxide and heat are produced from the degradation of anesthetic agents in the presence of desiccated carbon dioxide absorbent. Among today’s volatile anesthetics, degradation of desflurane produces the most carbon monoxide.
Sevoflurane = Compound A
When would you see a Saphenous Nerve injury?
Where is the symptoms anatomically?
Injury to a saphenous nerve can cause numbness, pain, and/or paresthesias along the medial lower leg.
Perioperative saphenous nerve injury is relatively uncommon but, due to its close proximity to the great saphenous vein, is a known complication of saphenous vein harvest (e.g., vein graft harvest for coronary artery bypass grafting) or saphenous vein stripping.
Rarely, saphenous nerve block can also cause temporary or permanent nerve injury.
Damage to the saphenous nerve may result in temporary or permanent cutaneous sensory loss, pain, or paresthesias.
Anatomy:
Major sensory branch of the femoral nerve that is primarily responsible for cutaneous sensation of the medial lower leg
What does the Sciatic Nerve split into at the area of the knee?
Tibial nerve
Common Peroneal nerve
What does the superficial peroneal nerve innervate (Include MOTOR and SENSORY)?
Mixed sensory and motor nerve that innervates the peroneus longus and peroneus brevis muscles (which allow foot eversion)
Provides sensation to the lateral lower leg and most of the dorsum of the foot.
When are common peroneal nerve injuries seen?
Common peroneal nerve injury is the most common isolated mononeuropathy of the lower extremities.
Perioperative injuries can occur due to knee hyperflexion (e.g., during lithotomy position in stirrups or boots).
Excessive hip flexion leading to a sciatic nerve stretch injury can also damage nerve fibers prior to their division into the common peroneal nerve.
What is the movement responsible for deep peroneal nerve?
What is the sensory innervation of deep peroneal nerve?
What type of injury, and symptom is common from deep peroneal nerve injury?
Mixed sensory and motor nerve that innervates many major lower leg muscles which are primarily responsible for foot dorsiflexion.
Provides cutaneous sensation to a small patch of skin between the first and second toes.
Isolated injury to this nerve is most commonly caused by trauma to the lateral knee and typically leads to foot drop.
Tibial Nerve
Branch of what nerve?
What movement does this control?
The tibial nerve is a motor and sensory branch of the sciatic nerve.
It innervates the lower leg posterior compartment muscles primarily responsible for foot plantar flexion.
The tibial nerve also provides cutaneous sensation to the posterolateral lower leg and lateral foot.
Tibial nerve injury is most commonly caused by trauma to the lower leg or ankle.
Expected changes in pH, HCO3, and PaCO2 in:
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Chronic Respiratory Alkalosis
Acute respiratory acidosis should demonstrate a pH decrease of 0.05 and an HCO3- increase of 1.0 mEq/L per acute 10 mm Hg increase in PaCO2.
Chronic respiratory acidosis, pH nearly normalizes, and HCO3- concentrations increase 4-5 mEq/L per 10 mm Hg sustained increase in PaCO2.
Respiratory alkalosis becomes chronic, pH nearly normalizes and HCO3- decreases 5-6 mEq/L per 10 mm Hg sustained decrease in PaCO2.
What is the most common variant of pseudocholinesterase deficiency?
Approximately 20 genetic variants of the BCHE gene exist with the A- and K-variants being the most common.
What medicine is an anticholinesterase used to treat refractory glaucoma by causing miosis?
Since it inhibits BCHE, systemic absorption can cause up to a 95% decrease in BCHE function, thereby potentiating the effects of succinylcholine.
Echothiophate
What are the 4 phases of diastole?
There are four phases during diastole:
Isovolumetric relaxation: this phase begins with the closure of the aortic valve and continues till the opening of the mitral valve. During this time, the left ventricle is relaxing, however there is no change in the ventricular volume (isovolumetric).
Early rapid filling: this phase begins with the opening of the mitral valve. The left ventricle begins to fill with blood from the left atrium. The flow of blood is driven by the transmitral pressure gradient. This phase contributes the largest volume of blood to the left ventricle during diastole.
Diastasis (slow filling): as the left ventricle fills, the pressure difference between the left ventricle and atrium decrease. This slows down the filling considerably, and contributes approximately 5% of the preload. This phase occurs mid-diastole.
Late rapid filling (atrial contraction): the left atrium contracts, ejecting additional blood into the left ventricle. This phase can contribute 15-20% of the preload. Atrial contraction is the last phase of diastole. The mitral valve closes after the atrial contraction.
Why does the FA/FI curve rise faster for nitrous oxide compared to desflurane?
The absorption of nitrous oxide is augmented by the concentration effect, making the rate of absorption faster than desflurande despite their similar blood gas partition coefficients.
What are the 3 forms in which CO2 is transported?
Carbon dioxide is transported in the blood as:
1. Dissolved CO2
Carbon dioxide is 10 times more soluble in blood than oxygen: 0.031 mmol/L/mm Hg versus 0.003 mmol/L/mm Hg, respectively.
2. Bicarbonate *Majority*
This occurs because red blood cells and vascular endothelium contain carbonic anhydrase, an enzyme used to convert carbon dioxide to bicarbonate. The enzyme also catalyzes the reverse reaction. In either case, a transient intermediate, carbonic acid, is created.
Bicarbonate production: H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3-
3. Carbamino compounds.
Carbamino compounds also transport carbon dioxide in the blood. Carbamino compounds are produced from a reaction with proteins. The small amount of CO2 transported in this manner mostly interacts with hemoglobin proteins and to a lesser extent plasma proteins.
Carbamino compound production: R-NH2 + CO2 → R-NH-CO2- + H+
Which blood product is most likely to cause transfusion related sepsis?
Transfusion-associated sepsis is the third leading cause of transfusion-related deaths in the United States and is most commonly caused by bacterial infection from contaminated platelets.
Unlike other blood products, platelets are stored at room temperature which leads to increased bacterial growth.
What urine to plasma osmolar ratio indicates pre-renal oliguria?
A urine-to-plasma osmolar ratio (UOSM : POSM) >1.5 indicates prerenal oliguria (generally secondary to hypovolemia).
The UOSM : POSM is used to assess the tubular response of the kidneys to dehydration or hypovolemia. In this setting of prerenal oliguria, this formula evaluates the kidneys’ ability to retain Na+ and water and produce highly concentrated urine by increasing urine osmolality above 450 mOsm/kg.
By comparison, normal plasma osmolality is 280-300 mOsm/kg.
The UOSM : POSM indicates the kidneys’ ability to concentrate urine. Tubular damage and acute renal failure, therefore, may be represented by a decreased ratio.
The UOSM : POSM can also decrease with the administration of diuretics. As an aside, isosthenuria is a UOSM : POSM equal to 1.
MOA of:
Hydrochlorothiazide?
Furosemide?
Spirinolactone?
HCTZ = It works by blocking the Na/Cl co-transporter in the DCT
This causes inhibition of sodium reabsorption in the distal convoluted tubules, thereby increasing the excretion of both sodium and water.
Furosemide = Na/K/Cl in Loop of Henle Blocked
Spirinolactone = Blocks aldosterone receptor in DCT
Which of the following findings on physical examination is generally considered the BEST predictor for difficult tracheal intubation in morbidly obese patients?
Three factors obtained by history or physical exam that correlate with difficult intubations in obese patients include
1. Increased neck circumference **Best single indicator**
2. Mallampati class III or IV airway
3. Presence of obstructive sleep apnea.
In general, increased age, male sex, TMJ pathology, and abnormal upper teeth also correlate with difficult intubations.
What are the common chemo toxocities for?
Cisplatain, Carboplatin?
Acoustic nerve damage
Nephrotoxicity
Chemotoxicity for:
Vincristine
Vincristine: peripheral neuropathy
Chemotoxicity for:
Bleomycin, Busulfan
Pulmonary fibrosis
Chemo toxicity for Doxorubicin?
Cardiotoxicity
Chemo toxicity for Trastuzumab?
Cardiotoxicity
Chemo toxicity for Cyclophosphamide?
Hemorrhagic Cystitis
Chemo toxicity for 5-FU, 6-MP, methotrexate?
myelosuppression
What are the contraindications to succinylcholine therapy?
BRIGMS(S) “Brigham’s”
Burns
Relaxants - Chronic
Immobility (Prolonged)
Guillain-Barre Syndrome
MS
Stroke & Spinal Cord injury
Spinal cord injury
What are the 5 triggers for vomiting?
The vomiting center is stimulated by:
1) the chemotactic trigger zone (CTZ) located in the medulla
2) gastrointestinal tract
3) pharynx
4) visual centers
5) mediastinum
What is the onset time of Scopalamine patch?
What are the side effects of it?
Anticholinergics (e.g., scopolamine patch):
Needs to be applied prior to going back to the operating room due to its 2 to 4 hour onset time.
Can cause visual changes, dry mouth, and dizziness.
Droperidol:
Class?
Mechanism?
Dose?
Dopamine-2 receptor antagonist (e.g., droperidol, metoclopramide): droperidol is effective as an anti-emetic.
Recommended dosing is 0.625 to 1.25 mg at the end of surgery
What are the independent criteria for:
MELD Score?
vs.
Child’s Pugh?
Mnemonics to help differentiate MELD from Child-Pugh:
MELD: “I Crush Several Beers Daily” for INR, creatinine, sodium, bilirubin, dialysis
Childs-Pugh: “Pour Another Beer At Eleven” for PT, Ascites, Bilirubin, Albumin, Encephalopathy
What is a normal Strong Ion Difference?
What is the equation?
Normal human plasma has a SID of 40-44 mEq/L.
SID = ( [Na+] + [K+] + [Ca2+] + [Mg2+] ) - ( [Cl-] + [A-] )
Plasma pH Theories are determined by what 3 independent factors?
The concept of SID proposes that plasma pH is determined by three independent factors:
1. PCO2
2. SID
Strong ion difference represents the difference between the charge of plasma strong cations (sodium, potassium, calcium, magnesium) and anions (chloride and other strong anions (A-) such as lactate, sulfate, ketoacids, and nonesterified fatty acids).
3. Atot.
The latter (Atot) represents the total plasma concentration of nonvolatile buffers (e.g., albumin, globulins, and inorganic phosphate).
Large volume saline:
What happens to:
1. Bicarbonate?
2. pH?
3. SID?
4. Anion Gap?
5. Chloride level?
Large volumes and rapid administration of normal saline can produce a non-anion gap hyperchloremic metabolic acidosis. Associated laboratory values include decreased plasma HCO3-, increased plasma Cl-, decreased SID, and a normal anion gap.
Why is subendocardial ischemia seen more commonly than epicardial transmural injury?
Subendocardial ischemia is more commonly seen than transmural injury because the small capillaries and arterioles at the subendocardial level are subject to occlusive high intraventricular pressure.
The epicardial coronary arteries in comparison are distant from the high intraventricular pressures and thus generally unaffected unless acute occlusion from a thrombus, spasm, or embolism occurs.
For ST Elevation, what are your mV criteria and lead criteria for men and women, respectively?
≥ 0.1 mV in all leads other than leads V2–V3 where the following cut-points apply:
≥ 0.2 mV in men > 40 years
≥0.25 mV in men < 40 years
≥ 0.15 mV in women
What is your criteria for ST depression? and T wave inversions regarding mV and also R/S ratio?
New horizontal or down-sloping ST depression ≥ 0.05 mV in two contiguous leads and/or
T inversion ≥ 0.1 mV in two contiguous leads with prominent R wave or R/S ratio > 1
What are the sensitivities of EKG lead monitoring during surgery?
Recent studies have shown that the most sensitive lead for detection of myocardial ischemia in patients who actually had an MI is lead V4 (sensitivity of 83%) but when two precordial leads are monitored simultaneously the sensitivity increases to 97%.
A separate study suggested that adding lead II with two precordial leads increases the sensitivity for detection of myocardial ischemia to 98%.
What is the correlation between burn patient’s and neuromuscular blockers?
Which are contraindicated?
Which are not-affected (minimally)?
Patients with massive burns demonstrate resistance to NDNMBs, resulting in increased dosing requirements, due to upregulation of ACh receptors and increased plasma protein binding.
Contraindicated = Succinylcholine
Mivacurium’s dosing requirements are only slightly increased relative to other NDNMBs as it is metabolized by pseudocholinesterase, the levels of which are decreased in burn patients.
What is the pathophysiological reason that burn patient’s have increased requirements to non-depolarizing neuromuscular blockers?
Since NDNMB’s drug effect is produced by competitively inhibiting ACh receptors, the presence of more receptors means a higher dose of free drug is required to produce neuromuscular blockade manifesting as twitch depression.
Burn patients also have increased protein binding, meaning less free drugs are available to bind ACh receptors, further increasing dose requirements.
How do you adjust the doses of neostigmine and glycopyrolate for ESRD or CKD patients?
The durations of action of commonly-used anticholinesterases and anticholinergic drugs for reversal of nondepolarizing neuromuscular blockade are prolonged in the setting of CKD and ESRD.
However, no dosage alterations are required and the normal maximum recommended doses still apply.
What is the unfortunate effects of increasing your anti-cholinesterase dose for neuromuscular blockade reversal?
Increasing the dose of anticholinesterase relative to anticholinergic drug:
- Increases the risk for gastrointestinal upset
- Nausea/vomiting
- Cardiac muscarinic effects including significant bradycardia or other arrhythmias.
What is the unintended effect of increasing your anti-cholinergic relative to your anti-cholinesterase?
Increasing the dose of anticholinergic relative to anticholinesterase:
- Increases the risk for tachycardia and other arrhythmias
- Blurred vision
- Dry mouth
Confusion or hallucination may be seen with anticholinergics that cross the blood-brain barrier (e.g. atropine).
At what dose of methadone is there a significant increased risk of QT prolongation?
The risk for prolonged QT intervals is greatest in patients taking greater than 120 mg daily, however, lower doses and acute use can still prolong the QT interval.
Because methadone is metabolized by cytochrome p450, drugs inhibiting this enzyme may lead to increased methadone toxicity and further QT prolongation.
What is the mechanism for which Etomidate causes adrenal suppresion?
It causes dose-dependent inhibition of adrenal mitochondrial 11β-hydroxylase.
The enzyme 11β-hydroxylase is responsible for the conversion of 11-deoxycortisol to cortisol.
Thus, administration of etomidate causes suppression of adrenal cortisol synthesis.
What is the relationship between Pulmonary Vascular Resistance and Lung Volumes?
What is the reasoning behind this?
Pulmonary vascular resistance is affected by lung volumes.
It is lowest at FRC while increasing or decreasing lung volumes beyond FRC results in an increase in PVR.
Highest at Residual Volume and Total Lung Capacity
Pulmonary vascular resistance increases as lung volumes increase due to compression of the smaller pulmonary vessels, notably the small arterioles. As lung volumes increase, alveoli expand and the transmural (distending) pressure in and radii of the small blood vessels decrease. Therefore, PVR increases. Recall that resistance (R) is inversely proportional to vessel radius (r) to the fourth power (R ∝ 1/r4).
Pulmonary vascular resistance increases as lung volumes decrease due to what two mechanisms?
First, as the size of the alveoli decrease and especially when they collapse, the geometry of the pulmonary vessels surrounding these alveoli changes such that the vessels can essentially become kinked, resulting in a significant increase in resistance to flow.
Second, as lung volumes decrease below normal, the volume of blood in the larger pulmonary vessels decreases. This suggests a likely decrease in vessel radius and therefore increased resistance to flow.
What are the two most important factors for release of Vasopression* aka *ADH* aka *Arginine Vasopressin?
- Hyperosmolality (milliosmoles per kilogram. A normal result is typically 275 to 295 milliosmoles per kilogram)
- Reduced Effective Circulatory Volume
What is the mechanism of action of Vasopressin?
Water Balance:
Stimulates water reabsorption by increasing intracellular levels of cyclic adenosine monophosphate (cAMP) and activating protein kinase A
Vasoactive
Vasoconstriction by activating G protein and phospholipase C, which releases calcium from the sarcoplasmic reticulum. There are two classes of AVP receptors:
V1 receptors present in vascular smooth muscle
V2 receptors present in the distal and collecting tubules of the kidney
Transtracheal injection of local anesthetic will block which nerve?
Transtracheal injection of local anesthetic will block the recurrent laryngeal nerve
How long can FFP be stored after being thawed?
Why is this?
FFP is frozen for storage. It can be transfused up to 5 days after thawing
Factors VIII and V are the least stable factors in blood products and can degrade above 4 degreres Celcius.
Significant reductions in factor VIII (41 ±8%) and factor V (66 ±9%) levels.
What are the two opposing processes that determine a drug’s context sensitive half time?
- Plasma clearance
- Redistribution
What is diastasis and when does it occur?
Diastasis occurs when there is complete left ventricular relaxation and filling of the ventricle eventually slows down.
It occurs* during the *filling portion following isovolumetric relaxation.
The spead of local anesthetic in the intrathecal space is primarily determined by what 2 factors?
- Baricity of the local anesthetic solution
(Baricity refers to the density of a substance compared to the density of human cerebrospinal fluid)
Solutions that have a baricity approaching 1.000 are referred to as isobaric*, as the density of the cerebrospinal fluid is approximately 1.0003+/- 0.0003. Solutions with a baricity less than 0.999 are termed hypobaric, and are usually created by mixing the local anesthetic with distilled water. *Hyperbaric solutions are created by mixing dextrose 5-8% with the desired local anesthetic.
Hyperbaric solutions will flow in the direction of gravity and settle in the most dependent areas of the intrathecal space. Conversely, hypobaric mixtures will rise in relation to gravitational pull.
2. Patient position.
You have a patient with suspected opioid induced biliary colic, what are your drug options?
1. Atropine (Blocks parasympathetic activation)
2. Papaverine - opium alkaloid antispasmodic drug, used primarily in the treatment of visceral spasm and vasospasm (especially those involving the intestines, heart, or brain
3. Naloxone - (blocking opioid receptor activation)
How does the ETT depth become affected with neck flexion vs. neck extension?
Neck flexion - Risk of endobronchial intubation
Neck extension - Risk of ETT herniating out of the larynx.
What are the changes in ESRD disease in regard to:
Calcium levels?
Potassium levels?
Magnesium levels?
Lipid Panel?
Phosphate Levels?
- *- Hypocalcemia
- Hyperkalemia
- Hypermagnesemia
- Hyperlipidemia
- Hyperphosphatemia**
With Citrate Toxicity, what is the expected change in Calcium levels?
in Magnesium levels?
Citrate Chelates both magnesium and calcium so you have:
Hypomagnesemia and Hypocalcemia
Majority of Citrate is found in what blood products?
FFP and Platelets
(NOT PRBC)
What is the makeup of D5W in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 253
Sodium (mEq/L) None
Chloride (mEq/L) None
Potassium (mEq/L) None
Glucose (g/L) 50 grams / Liter
Lactate (mEq/L) None
What is the makeup of D5 1/4 NS in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 355
Sodium (mEq/L) 38.5
Chloride (mEq/L) 38.5
Potassium (mEq/L) None
Glucose (g/L) 50
Lactate (mEq/L) None
What is the makeup of NS in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 308
Sodium (mEq/L) 154
Chloride (mEq/L) 154
Potassium (mEq/L) None
Glucose (g/L) None
Lactate (mEq/L) None
What is the makeup of D5 1/2 NS in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 432
Sodium (mEq/L) 77
Chloride (mEq/L) 77
Potassium (mEq/L) - None
Glucose (g/L) 50
Lactate (mEq/L) - None
What is the makeup of 3% Hypertonic Saline in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 1026
Sodium (mEq/L) 513
Chloride (mEq/L) 513
Potassium (mEq/L) None
Glucose (g/L) None
Lactate (mEq/L) None
What is the makeup of LR in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 273
Sodium (mEq/L) 130
Chloride (mEq/L) 109
Potassium (mEq/L) 4
Glucose (g/L) 0
Lactate (mEq/L) 28
What is the makeup of D5LR in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 525
Sodium (mEq/L) 130
Chloride (mEq/L) 109
Potassium (mEq/L) 4
Glucose (g/L) 50
Lactate (mEq/L) 28
What is the makeup of Plasmalyte in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 294
Sodium (mEq/L) 140
Chloride (mEq/L) 98
Potassium (mEq/L) 5
Glucose (g/L) None
Lactate (mEq/L) None
What is the makeup of D5NS in terms of:
Osmolarity (mOsm/L)
Sodium (mEq/L)
Chloride (mEq/L)
Potassium (mEq/L)
Glucose (g/L)
Lactate (mEq/L)
Osmolarity (mOsm/L) 586
Sodium (mEq/L) 154
Chloride (mEq/L) 154
Potassium (mEq/L) None
Glucose (g/L) 50
Lactate (mEq/L) None
How would you summarize Boyle’s Law?
P1V1 = P2V2
“Water Boyle’s at a constant temperature”
How would you summarize Charles Law?
V1/T1 = V2/T2
“Prince Charles is under constant pressure to be king”
How would you summarize Gay-Lussac’s Law?
P1 / T1 = P2 / T2
A Culdissac “LUSSAC” has a constant volume and mass of gas
How would you summarize Henry’s Law?
C = kP
Henry’s law indicates that at a constant temperature, the concentration of a gas dissolved in a solution is directly proportional to the partial pressure of that gas: C = kP (where k is a solubility constant) or C ∝ P. As the volume percentage of a volatile anesthetic is increased, the alveolar partial pressure increases.
Example: An increased alveolar partial pressure, therefore, leads to an increased concentration of the volatile anesthetic in the blood which increases the speed of induction and depth of anesthesia.
How would you summarize Dalton’s Law?
P total =- P1 + P2 + P3
Dalton’s law (also called Dalton’s law of partial pressures) states that in a mixture of non-reacting gases, the total pressure exerted is equal to the sum of the partial pressures of the individual gases.
Why is the Desflurane vaporizer heated?
Though it vaporises very readily, it is a liquid at room temperature.
Desflurane vaporizers are typically heated to 39 °C which creates a constant desflurane vapor pressure of 2 atm within the vaporizer, independent of barometric pressure.
What is the maximum dose of neostigmine?
When is the onset/peak effect of neostigmine?
The maximum dose of neostigmine is 70-80 mcg/kg at which point a “ceiling effect” takes place.
This dose results in complete blockade of the acetylcholinesterase enzymes and occurs in approximately 10 minutes.
What is the potential downside to giving additional anticholinesterase (neostigmine) after max dose has already been given?
In some instances additional anticholinesterase medication may cause paradoxical weakening.
The anticholinesterase effect increases the amount of acetylcholine release. In an overdose, depolarization of the endplate caused by the excess acetylcholine can lead to a depolarization block, similar to that seen with succinylcholine.
What are the contraindications to ACE-Inhibitors?
- Renal Artery Stenosis
- Pregnancy
- History of angioedema (whether related to ACE-I or not).
When would you observe a sudden ETCO2 drop to absolute zero?
Circuit Disconnect
Esophageal Intubation
Kinked ETT
When would you observe a drop to ETCO2 to just above zero?
Circuit Leak
Partial Airway Obstruction
What would result in a rapid decrease in ETCO2 but not zero?
Pulmonary embolism
Circulatory Collapse
Would hypothermia cause an increase or decrease in ETCO2?
Decrease
What are some etiologies of gradual increases in ETCO2?
1. Decreased Minute Ventilation
2. Faulty Unidirectional Valve
3. Soda Lime Exhaustion
4. Insufficient Fresh Gas Flow
5. Laparoscopes are inserted into the subcutaneous space causing ETCO2 in the skin (Subcutaneous emphysema)
6. Malignant Hyperthermia
7. Thyroid Storm
How is extravasation of vasopressors best treated?
Keep IV catheter in place initially.
Aspirate about 5 mL of blood to remove as much of the drug as possible.
1. Limb elevation
2. Warm compresses (for vasopressors, cold compress for other drugs)
3. Irrigating with saline (Gault technique)
The Gault technique can be used to wash out the extravasated drug. It starts with injecting hyaluronidase (about 1500 units) into the subcutaneous tissue of the affected area. Four incisions are made at the site and saline (approx. 500 ml) is flushed through one of the incisions. This will irrigate the subcutaneous tissue and flow out the other three incisions.
Hyaluronidase is an enzyme that breaks down hyaluronic acid found in the tissue. This allows the subcutaneous tissue to become more permeable. It is typically used for vesicants, particularly in children (e.g., infant with extravasated parenteral nutrition)
4. Injection of phentolamine
Phentolamine causes the smooth muscles of blood vessels to relax and produces vasodilation. Recommended dose is 5-10 mg within 12 hours of the extravasation. Phentolamine is typically diluted to 0.5 mg/mL then injected in multiple locations, in 1 mL increments, around the border of the extravasation site.
5. Stellate ganglion block (for upper limbs).
In situations with extravasated vasopressors, a stellate ganglion block will create a sympathectomy causing vasodilation in the upper limb.
What is the timeframe in which vasopressor extravasation must be treated?
What is the definitive treatment?
Mild extravasation can lead to local necrosis and more severe extravasations may require open surgical debridement/fasciotomies. (Definitive treatment)
Extravasated vasoconstrictors usually have a 4-6 hour window before the onset of tissue necrosis.
Chemotherapeutic drugs have about 72 hours before necrosis begins.
How do you treat accidental intra-arterial injection of drugs?
Accidental intra-arterial injection of drugs can cause vasospasm and thrombosis.
Management includes injecting:
1. lidocaine
2. calcium channel blocker intra-arterially
3. A stellate ganglion block can also be useful.
Aspirin
Mechanism of Action?
Acetylsalicylic acid (ASA) blocks It is non-selective for COX-1 and COX-2 enzymes
Inhibition of COX-1 results in:
- the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan)
- This prevents the production of pain-causing prostaglandins
- Stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation
Anti-platelet or Anti-coagulant?
Mechanism of Action
Abciximab (ReoPro)
Antiplatelet
Blocks GP IIb/IIIa receptors
Anti-platelet or Anti-coagulant?
Mechanism of Action
Cilostazol (Pletal)
Antiplatelet
Lowers calcium by elevating cAMP
Anti-platelet or Anti-coagulant?
Mechanism of Action
Clopidogrel (Plavix)
Anti-platelet
Inhibit ADP Receptor activation
Anti-platelet or Anti-coagulant?
Mechanism of Action
Dipyridamole
Anti-platelet
Lowers calcium by activating cAMP
Anti-platelet or Anti-coagulant?
Mechanism of Action
Eptifibatide (Integrilin)
Anti-platelet
Blocks GP2b3a receptors
Anti-platelet or Anti-coagulant?
Mechanism of Action
Prasugrel (Effient)
Antiplatelet
Inhibit ADP Receptor Activation
Anti-platelet or Anti-coagulant?
Mechanism of Action
Ticagrelor (Brilinta)
Anti-platelet
Inhibit ADP Receptor Activation
Anti-platelet or Anti-coagulant?
Mechanism of Action
Triofiban (Aggrastat)
Anti-platelet
GP2b3a receptor inhibitor
Anti-platelet or Anti-coagulant?
Mechanism of Action
Apixaban (Eliquis)
Anticoagulant
Direct Factor Xa Inhibition
Anti-platelet or Anti-coagulant?
Mechanism of Action
Dabigatran (Pradaxa)
Anti-coagulant
Direct Factor Xa Inhibition
Anti-platelet or Anti-coagulant?
Mechanism of Action
Fondaparinux (Arixtra)
Anticoagulant
Antithrombin mediated inhibition of factor Xa
Anti-platelet or Anti-coagulant?
Mechanism of Action
Low Molecular Weight Heparin
Anti-coagulant
Antithrombin mediated inhibition of serine proteinases
LMWH binds to anti-thrombin, a serine protease inhibitor, and creates a conformational change. This change accelerates its inhibition of activated factor X in conversion of prothrombin to thrombin. Thus,thrombin cannot convert fibrinogen to fibrin strands and clot formation.
Once this change occurs LMWH is freed and can bind to another anti-thrombin molecules. LMWH also directly inhibits thrombin as it is a heterogenous mixture of molecules, some containing enough polysaccharide sequence, but this effect is much less than that of unfractionated heparin.
Anti-platelet or Anti-coagulant?
Mechanism of Action
Rivaroxaban (Xarelto)
Anticoagulant
Direct factor Xa inhibition
Anti-platelet or Anti-coagulant?
Mechanism of Action
Unfractionated Heparin
Anticoaglant
Antithrombin mediated inhibition of serine proteinases
Anti-platelet or Anti-coagulant?
Mechanism of Action
Warfarin (Coumadin)
Anti-coagulant
Inhibit vitamin K dependent coagulation factors (II, VII, IX, X)
What ionic changes occur with NMDA receptor?
The NMDA receptor is an inotropic glutamate receptor that functions as a nonspecific ion channel when activated. Activation only occurs when glutamate is bound to the receptor AND the cell is depolarized. The receptor’s effects are primarily mediated via increased intracellular calcium.
How would magnesium effect Ketamine administration?
Administration of magnesium along with ketamine can potentiate the effects of ketamine.
What are the factors that will improve defibrillation?
1. Electrode Gel
2. Applying Force (if paddles)
- 11 lbs of pressure reduces resistance
3. Biphasic Defibrillation
- Uses less energy
4. Larger Electrodes (8-12 cm)
- Paddle size is inversely proportional to transthoracic resistance
- Smaller pads can cause myocardial necrosis
Compartment Syndrome?
6 signs/symptoms?
Diagnosis?
Treatment?
6 P’s
Pain out of proportion to the injury
Paresthesias
Pain on passive movement
Palpation of a tense hard compartment
Paralysis
Pulselessness (Late sign)
Diagnosis: Compartment Pressures >30 mmHg needs a fasciotomy within 6 hours
What is the equation for Arterial Oxygen Concent (CaO2)?
(Hgb * {4/3} * SaO2) + (0.003 * PaO2)
Modified Cormack-Lehane System
2b view shows what?
Only the posterior arytenoids and the epiglottis are visible
How does pulmonary mechanics change with low thoracic or lumbar epidurals?
Peak Expiratory Pressure will decrease the most
In healthy patients, lumbar or low thoracic epidural anesthesia produces small (≤ 10%) changes in most pulmonary function parameters. However, PEP and cough strength are significantly reduced (10-40% and up to 50%, respectively) from baseline.
These two parameters are more dependent on abdominal musculature which has a higher degree of motor blockade than thoracic musculature from a lumbar or low thoracic epidural.
Note a disproportionately greater decrease in peak expiratory pressure with only a small decrease in FEV1 is in line with FEV1 being relatively effort-independent (lower peak expiratory pressure in a weaker patient is conceptually equivalent to lower effort).
How does tidal volume change with thoracic and lumbar epidurals?
Tidal volume is typically unchanged, even with a high thoracic epidural.
Definte and quantitatively define Different Levels of MAC
MAC-Awake?
MAC?
MAC-BAR?
MAC-Awake
The MAC-awake is the MAC value at which voluntary reflexes (e.g., a patient will no longer open his or her eyes to command, shouting, or shaking) and perceptive awareness are lost. It varies between 15-50% of standard MAC
MAC
minimum alveolar concentration of an inhaled anesthetic at one atmosphere that prevents movement in response to a surgical stimulus (specifically, an abdominal incision) in 50% of patients.
MAC-BAR
MAC value at which the adrenergic response (e.g., hemodynamic, sudomotor) to noxious stimuli is blunted. This has been found to be approximately 50% higher than standard MAC. Some studies estimate this value as 1.7-2.0 MAC.
MAC-awake in generally higher on induction or emergence?
Why is this?
Interestingly, the MAC-awake is generally higher at induction (40-50% standard MAC in order for loss of consciousness) than at emergence (as low as 15% standard MAC to regain consciousness)
Although the mechanism is not fully understood, it is likely due to the differences in alveolar wash-in and wash-out of anesthetic gases.
The theory of neural inertia is another proposed mechanism.
Neural inertia is defined as the tendency of the central nervous system to resist transitions between arousal states
Loss of awareness and recall typically occurs at what MAC?
Which volatile anesthetic has the most recall blocking activity and which has the least?
The loss of awareness and recall typically occurs at 0.4-0.5 standard MAC
Isoflurane likely has the most recall-blocking activity and nitrous oxide the least
Current ASA guidelines recommend maintaining at least what MAC during general anesthesia to significantly reduce the risk of awareness?
A MAC at this level effectively reduces awareness to what ratio of patients for recall of verbal stimulus.
Current ASA guidelines recommend maintaining at least 0.7 MAC during general anesthesia to significantly reduce the risk of awareness.
A MAC value of 0.627 effectively reduces awareness to 1 in 100,000 for recall of verbal stimulus.
If you have a patient with suspected TBI with GCS of 3, what is the goal of cerebral perfusion pressure (CPP)?
Even a single episode of hypotension decreases cerebral perfusion enough to affect outcomes. The CPP value to target lies within the range of 50-70 mm Hg according to current BTF (Brain Trauma Foundation) guidelines.
Avoid CPP < 50 mmHg
As far as the upper limit, aggressive attempts to maintain CPP > 70 mmHg with fluids and pressors should be avoided because of the risk of acute respiratory distress syndrome (ARDS). However, if a patient with intact autoregulation is maintaining a CPP > 70 mmHg spontaneously, that is acceptable.
How do you classify mild, moderate, and severe TBI?
TBIs are categorized by level of severity: mild, moderate, and severe.
A mild TBI is associated with a Glasgow Coma Scale (GCS) score of 13-15 and minimal to no loss of consciousness.
A moderate TBI is associated with a GCS of 9-12 and a loss of consciousness of 30 minutes or more.
A severe TBI is associated with a GCS of 3-8.
When should you start treating increased ICP in TBI?
Treatment should be initiated with ICP thresholds above 20 mmHg.
How do you adjust methadone dosing with ESRD?
Methadone also needs little adjustment in patients with renal disease.
Why should you be cautious with ESRD patients when considering giving hydromorphone?
Buildup of renally-excreted hydromorphone-3-glucuronide can lead to neuroexcitatory effects including agitation, restlessness, and myoclonus (neuroexcitatory & pro-convulsant properties)
What are two aspects of Ketorolac side effects that you should consider before administering?
Prevents the synthesis of prostaglandins.
Inhibition of PG synthesis can affect renal glomerular blood flow by causing vasoconstriction of the afferent arterioles of the glomeruli
(KIDNEY ISSUES)
Reversibly inhibits the cyclooxygenase (COX) enzyme which prevents the formation of thromboxane from arachidonic acid.
Thromboxane promotes platelet aggregation and its absence can lead to increased bleeding.
(BLEEDING AND THROMBOSIS ISSUES)
Besides Lead II, What is the best lead to monitor atrial dysrhythmias?
Lead V1 is the second-best lead for monitoring atrial arrhythmia and when using a full twelve lead ECG considering these two leads together is most effective.
The normal p-wave morphology in V1 is biphasic with an initial upward deflection as depolarization travels from the SA node anteriorly through the right atrium. There is then a terminal deflection as the current passes posteriorly through the left atrium.
What are the ways you can prevent contrast induced nephropathy in patients?
#1 = Fluid Hydration
Antioxidants such as N-acetylcysteine and ascorbic acid may also play a role in renal protection but are not as effective as fluid hydration alone.
What is the equation of SVR?
What are the normal values?
SVR = [80 * (MAP – RAP)] ÷ CO
MAP = mean arterial pressure (mm Hg)
RAP = right atrial pressure (mm Hg), central venous pressure is commonly substituted for RAP
CO = cardiac output (L/min)
80 = conversion factor which changes mm Hg/L/min (Woods unit) to dynes * sec/cm^5
What is the equation for PVR?
What are the normal values?
PVR = [80 * (MPAP – PAOP)] ÷ CO
- *MPAP** = mean pulmonary arterial pressure (mm Hg)
- *PAOP** = pulmonary artery occlusion pressure or pulmonary capillary wedge pressure (mm Hg)
- *CO** = cardiac output (L/min)
- *80** = conversion factor which changes mm Hg/L/min (Woods unit) to dynes * sec/cm^5
Normal Value = 20–130
How do you convert SVR or PVR into woods units?
Conversion of dynes * sec/cm^5 to Woods units may be achieved by dividing SVR by 80.
For example, 1520 / 80 = 19 Woods units
What are some of the complications of brachial arterial lines?
1. Thrombosis (Vascular > Infection)
2. Bleeding
3. Pseudoaneurysms
4. Arterial-Venous Fistula
5. Infection (Lower Risk)
6. Median Nerve Injury
There have been concerns that brachial artery catheterization can lead to limb ischemia due to lack of collateral vessels; however, this has not been shown to be true.
The rare instances of ischemia from brachial artery use were resolved with the catheter removal.
The radial artery is even more unlikely to have ischemia because of multiple collateral vessels.
What is the ED95 of neuromuscular blockers mean?
ED95 is the effective dose of a neuromuscular blocking drug required to achieve 95% block of a single twitch in 50% of individuals who receive this drug and dose.
What is the ED95 and Intubating dose of:
Cisatracurium?
Pancuronium?
Vecuronium?
Rocuronium?
NDNMB ED95 (mg/kg)
Dose For Intubation (mg/kg)
Cisatracurium
- 04 (0.032 - 0.05)
- 15-0.2 (3.75 - 5 x ED95)
Pancuronium
- 07
- 08-0.12 (1.2 - 1.8 x ED95)
Rocuronium
- 3
- 6-1.0 (2 - 3.3 x ED95)
Vecuronium
- 05
- 1-0.2 (2.3 - 4.7 x ED95)
What is the P50 value?
What is the normal value for an adult?
Draw the dissociation curve with axis labeled
The term P50 is designated as the partial pressure of oxygen (in mm Hg) when oxygen saturation (SaO2) is 50%.
In a normal adult, P50 is 27 mm Hg.
How does a newborn shift on the hemoglobin dissociation curve?
What is the P50 value?
Why is that?
Left Shift
In newborns, oxygen affinity is very high and P50 is very low (approximately 18 mm Hg).
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
- Low 2,3-diphosphoglycerate (2,3-DPG) levels in newborns result in a very low P50 (Note, this would cause a left shift as well)
How does the hemoglobin dissociation curve change through infancy?
What is the P50 value?
Why is this?
Right Shift
After birth, levels of hemoglobin F begin to decline (Right shift) 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.
What are the major factors that contribute to Right and Left Shift is the Hemoglobin dissociation curve?
P50 increases due to: acidosis, hypercarbia, hyperthermia, increased 2,3-DPG. Shift “RIGHT”:
Rise In 2,3-DPG, H+, and Temp.
P50 decreases due to: alkalosis, hypocarbia, hypothermia, decreased 2,3-DPG.
When does P50 value reach normal adult level?
Age 10
What is the Haldane Effect effect illustrate?
Draw the respective curve.
Illustrates that the oxygenation of hemoglobin lowers the affinity of hemoglobin for carbon dioxide
The Haldane effect describes the relationship between the carbon dioxide dissociation curve in blood and oxyhemoglobin (HbO2).
The CO2 dissociation curve, specifically, shifts to the right when the concentration of HbO2 increases in the blood.
This curve is linear since the CO2 content and the partial pressure of CO2 (PCO2) are directly correlated in a given sample of blood. The curve may be interpreted such that an increase in HbO2 results in an increased dissociation of CO2 from Hb (i.e., an increase in PCO2 but an overall unchanged value for CO2 content).
Conversely, if the concentration of HbO2 is reduced, then the affinity for carbon dioxide increases and less CO2 is available for gas exchange.
What is the Bohr Effect?
Draw the respective curve
The Bohr effect describes the binding effect of H+ to Hb chains and the oxygen release and dissociation that occurs thereafter.
Acidosis, for example, will shift the oxygen-hemoglobin dissociation curve toward the right, resulting in less attraction between Hb and O2.
Ultimately, this will permit more CO2 to be transported from the tissue to the lungs during gas exchange. The curve will shift to the left for a low PCO2 and high pH.
Supratherapeutic INR
Mild (INR < 5) & No Bleeding OR No need for emergent surgery
Treatment?
Treatment: Withholding warfarin for several days is recommended.
The half-life of warfarin therapy is 2 to 4 days thus the effects may not be seen for several days.
Supratherapeutic INR
Moderate INR (between 5 and 9 No Bleeding OR No need for emergent surgery
Treatment?
Treatment: Vitamin K can be administered orally or parenterally
- Typical adult dose is 1-2mg)
- There is no difference in efficacy between oral and intravenous vitamin K
- Higher risk of anaphylaxis with parenteral formulations; thus oral is preferred if the patient can tolerate and absorb the medication
Supratherapeutic INR
Severe INR (> 9) or there is life threatening bleeding
Treatment?
Treatment: Higher doses of vitamin K may be attempted (between 5-10mg).
Higher doses of vitamin K may render the patient temporarily resistant to further warfarin therapy for days to weeks.
Supratherapeutic INR
Emergent Surgery or If significant bleeding is present
Treatment?
1. Prothrombin complex concentrates
2. IV Vitamin K
What are the two formulations of PCC?
4-factor concentrates are preferred as they contain all vitamin K dependent coagulation factors (II, VII, IX, and X) (1972)
3-factor concentrates contain factors II, IX, and X and should be supplemented with recombinant factor VIIa to completely reverse anticoagulation.
What are the contraindications to PCC therapy?
Contraindications:
1. DIC
2. HIT - PCCs are human plasma derived products that contain low doses of heparin to prevent clotting factor activation.
What are the major concerns with FPP administration?
There are certainly risks associated with FFP transfusion; most notable are:
Transfusion related acute lung injury (TRALI)
Febrile reactions
Allergic reactions
Transfusion associated circulatory overload (TACO).
What does ASA deem the 4 distinct depths of anesthesia?
Minimal Sedation
Moderate Sedation
Deep Sedation
General Anesthesia
What are the criteria for the 4 depths of anesthesia
(Draw the table)
- Responsiveness
- Airway reflexes
- Ventilation
- Cardiovascular Function
- *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
How does the Frank Starling Curve change for Heart Failure Treatments?
Label the Axes
Include:
- Ionotropes
- Vasodilators
- Diuretics
- Ionotropes and Vasodilators
- Ionotropes, Vasodilators and Diuretics
A = Diuretics
B = Ionotropes + Vasodilators + Diuretics
C = Vasodilators
D = Ionotropes and Vasodilators
E = Ionotropes only
What is the elimination of neostigmine?
50% renal excretion
Eliminiation Half life of neostigmine:
Without renal failure/ESRD?
With renal failure/ESRD?
Without = 77 minutes
With = 181 minutes
Duration of Action of Rocuronium and Vecuronium?
46 - 73 minutes
Rocuronium
Metabolism?
Elimination?
Metabolism = 70% Hepatic
Elimination = 10% Renal Elimination
Vecuronium
Metabolism?
Elimination?
Metabolism - 50-60% Hepatic
Elimination - 25% Renal
What triggers the sub-ambient pressure alarm on the ventilator?
What are some examples:
Triggered when the pressure in the breathing circuit falls below atmospheric pressure by a predetermined amount (typically below -10 cm H2O).
Examples
- Inhalation against an increased resistance in the circuit
- Inhalation against a collapsed reservoir bag
- A malfunctioning active closed scavenging system (excessive vacuum or valve dysfunction)
- A blocked inspiratory limb during exhalation
- Accidental Placement of Nasogastric Tube or Endoscope within the trachea and use of suction = Loss of Tidal Volume and Negative pressure
What is myoclonus?
What is thought to derive from?
What is seen on EEG?
Myoclonus describes sudden jerking movements, such as those sometimes observed during induction of anesthesia
It likely results from inhibition of descending cortical inhibitory pathways.
Myoclonus can resemble seizures but EEG evidence of seizures is lacking during these episodes.
Methohexital has what side effects?
1. Myoclonus
2. Pain on Injection
3. Hiccups
What is the mechanism of action of Fenoldopam?
Dopamine-1 agonist = Increases renal blood flow despite decreased systemic arterial blood pressure
Natriuretic - Sodium excretion
Diuretic - Free water excretion
Direct renal vasodilator and can produce hypotension
What are some indications for Fenoldopam?
- A dopamine D1 receptor agonist that is used as an antihypertensive agent
- It lowers blood pressure through arteriolar vasodilation.
- Used as renal protector when renal vasoconstriction is anticipated
- Hypertensive Crisis in those with decreased renal function
How does phenytoin affect neuromuscular blockade?
Acute phenytoin administration potentiates the neuromuscular blockade of aminosteroid NDNBDs.
Chronic phenytoin administration increases a patient’s resistance to the effects of NDNBDs and reduces their duration of action by as much as 50%
For benzylisoquinoloine NMB = Variable
Why (Mechanism) are Non-depolarizing neuromuscular drugs affected by Phenytoin?
1) Increased metabolism via cytochrome P450 enzymes induction (this may explain why there is a clear effect with the aminosteroid NDNBDs, which rely on hepatic metabolism, but not with the benzylisoquinolines which undergo hepatic-independent Hofmann elimination and ester hydrolysis)
2) Increased postjunctional acetylcholine receptor density (the weak neuromuscular blocking properties of phenytoin, see below, results in postjunctional acetylcholine receptor upregulation)
3) Decreased sensitivity at the receptor sites
4) Increased end-plate anticholinesterase activity
Duing a surgery with general anesthesia, what aspect of the surgery requires the highest concentration of MAC to prevent movement:
DL, ETT placement, Surgical incision, or Tetanus to nerve stimulation?
ETT placement (MOST)
Surgical INcision
DL
Tetanus by nerve stimulation (LEAST)
Butorphanol
Mechanism?
Partial Opioid Agonist and Mixed Agonist-Antagonist
What is a normal CVP?
0 - 8 mmHg
What is a normal Mean Pulmonary Artery Pressure?
10 - 18 mmHg
What is a normal PCWP (Pulmonary Capillary Wedge Pressure)?
25 mmhg
What is a normal Cardiac Index?
2.5 - 4.2
How would PEEP improve hemodynamics in a patient with acute on chronic systolic heart failure?
Changes in:
Intrathoracic Pressure
RV Afterload
Preload
CVP
PAP
CI
PCWP
- *Raises** Intrathoracic Pressure
- *Increase** in RV Afterload
Decrease in Preload
Increase in CVP
Increase in PAP
Improved CI
Improved PCWP
What are the criteria of the Aldrete Scoring System used to dischage patients from Phase I of the PACU?
Consciousness
Activity (Moving extremities on command)
Respiration
Oxygen Saturation with O2 requirements
Circulation (BP compared to preop)
What type of shunt is created during one lung ventilation?
Right to Left Shunt
What is the most common and reliable sign of Cyanide Toxicity?
Why is this?
Elevated Anion Gap Metabolic Acidosis
Cyanide primarily causes toxicity by impairing cellular aerobic respiration. The cyanide ion (CN-) binds to the ferric ion (Fe3+) in mitochondrial cytochrome-c oxidase, inhibiting the final stage of the electron transport chain. Depletion of cellular ATP and the lactic acid produced by anaerobic metabolism can lead to profound acidosis.
Cyanide Toxicity
- Signs and Symptoms?
- PaO2 levels?
- SvO2 levels?
Signs/Symptoms:
Altered mental status, weakness, headaches, loss of consciousness, seizures, respiratory failure, and cardiac arrest, The patients blood sample may appear “cherry red” due to normal circulating levels of oxygen with impaired utilization.
PaO2 increases (Oxygen present but cannot be utilized)
SvO2 increased (oxygen present but not being utilized)
Mapleson Circuit Fresh Gas Flow (FGF) Requirements:
- FGF Mapleson A requirements for spontaneous ventilation?
- FGF Mapleson D, E, or F requirements for spontaneous ventilation?
- FGF Mapleson D, E, or F requirements for controlled ventilation?
A = Minute Ventilation
B = 2-3 times minute ventilation
C = 1-2 times minute ventilation
When a patient is on chronic dantrolene therapy, what needs to be continously monitored?
LFT’s
- Liver Dysfunction and potentially liver failure is possible
How does distance to radiation exposure protect you?
Ex: If you double the distance from the C-arm in the room, how does that decrease your radiation exposure?
Radiation intensity (exposure) with respect to distance decreases according to the inverse square law: I ∝ 1 / r^2.
Accordingly, doubling the distance from a radiation source decreases exposure by a factor of 4.
How does Bicarb administration affect BP and Calcium Levels?
Hypotension
Hypocalcemia (Transiently binds calcium and should be cautious in hypocalcemic patients)
To what degree (quantitatively) does 50 mEq of Bicarbonarte affect PaCO2?
Hypercarbia - The reaction of 50 mEq bicarbonate produces approximately 1,250 mL of CO2 which must be exhaled and is seen as a transient increase in EtCO2.
How does bicarbonate affect pulmonary vasculature?
Redistribution of Blood to the Pulmonary Vasculature
What nerves are required to perform an awake fiberoptic intubation?
Simply, CN 9 and CN 10
Specifically:
1. Internal Branch of Superior Laryngeal Nerve of CN 10
- CN 9 - Glossopharyngeal Nerve
- Recurrent Laryngeal Nerve of CN 10
Why do spinals result in hypotension?
- Arteriodilation - Due to sympathectomy
Reduction in afterload
2. Venodilation - Due to sympathectomy
Venodilation causes a reduction in preload and tends to have a more dramatic effect than arterial dilation because 75% of the total blood volume is in the venous system.
- Bradycardia - 10-15% from the spinal
- Blockade of the cardiac accelerator fibers can prevent an increased heart rate in response to hypotension, which would lead to further hypotension and bradycardia.
What is the concept of the Bezold-Jarisch Reflex?
Parasympathetic-mediated reflex occurs when stretch receptors located mainly in LV respond to an acute decrease in LV preload
The result is bradycardia and reduced contractility (and resultant hypotension).
This reflex is thought to occur to allow the ventricle additional time to fill and increase preload.
For a spinal, what dermatomes are typically affected above the spinal?
2-6 Dermatomes sensory block above level of the sensory block
What is Fractional Area Change?
Quantitative echocardiographic technique used to determine left ventricular ejection fraction.
Aortic Stenosis
What are the 3 metrics looked at to determine aortic stenosis gradients?
- Jet Velocity - (3-4 m/s)
- Mean Gradient - (25 - 40 m/s)
- Valve Area (1.0 - 1.5)
What degree angle would affect Velocity measurement as assessed by Doppler ultrasound is governed by the Doppler equation?
>20 degrees
Volatile Anesthetic effects on CBF and CMRO2 at:
>1 MAC
<1 MAC
≥1 MAC increase CBF and decrease CMRO2, causing an uncoupling of the flow-metabolism relationship.
<1 MAC = CBF balances and remains the same
How do Barbituates affect:
Cerebral Flow Metabolism & Cerebral Autoregulation?
CBF and CMRO2 % change in induction?
CBF and CMRO2 % change of isolectric EEG?
The cerebral flow-metabolism relationship and cerebral autoregulation remain intact with the use of thiopental.
Thiopental decreases both CBF and CMRO2 by 30% with induction doses
and by 50% upon achievement of an isoelectric EEG.
When would burst suppression on EEG be the goal target of reducing CMRO2?
What does burst suppression indicate?
Burst suppression on EEG is the goal target of reducing CMRO2 during an open cerebral aneurysm clipping.
Burst suppression sufficiently indicates depressed CMRO2 while providing predictability of recovery and awakening once the IV anesthetic is turned off.
What are the classic signs of Sodium Nitroprusside Toxicity?
- Elevated Mixed Venous Oxygen (PvO2)
Since cells cannot use oxygen and aerobic respiration, PVO2 becomes elevated.
- SNP (Sodium Nitroprusside) Tachyphylaxis
- Metabolic Acidosis (Lactate Buildup)
Amyl NItrate is an antidote to what poisoning?
How does this work?
Amyl nitrate works as an antidote for cyanide poisoning by converting Hb to MetHb which avidly binds cyanide, converting it to the nontoxic cyanomethemoglobin.
What are the 3 treatments for cyanide poisoning?
- Hydroxycobalamine
- Amyl NItrate
- Sodium Thiosulfate
What is the onset and duration of action of:
Cimetidine
Ranitidine
Famotidine
Cimetidine 1-1.5 hours, 3-4 hours
Ranitidine 1 hour, 9-10 hours
Famotidine 1 hour, 10-12 hours
What is the mechanism of action of Histamine H2 receptor antagonists?
Histamine H2 receptor antagonists (e.g. cimetidine, ranitidine, famotidine, nizatidine) block histamine from inducing acidic gastric fluid secretion by parietal cells.
This effectively raises gastric pH.
Raising the gastric pH prior to induction of anesthesia can reduce the severity and risk of perioperative aspiration pneumonitis.
Why do Barium Hydroxide absorbents produce more CO than soda lime?
Barium hydroxide absorbent preparations produce more carbon monoxide than soda lime due to the decreased water content of barium hydroxide absorbents.
Between different CO2 absorbers, what is the greatest at CO2 absorption?
Soda Lime
Calcium Hydroxide
Barium Hydroxide
Soda Lime
What is the composition of Soda Lime?
80% calcium hydroxide
15% water
4% sodium hydroxide
Therefore, higher-moisture absorbents (e.g., soda lime) have more water content available to react with CO2 leading to an increased CO2 absorptive capacity.
What are the factors that will increase CO production?
Desiccated CO2 absorbents
Increased Temperature
Low Fresh Gas Flows
What volatile anesthetic produces the most heat?
What voltaile anesthetic produces the most Carbon Monoxide?
CO2 absorbents + Sevoflurane = Most Heat
CO2 absorbents + Desflurane = Most CO
What absorber is the most likely to produce compound A with sevoflurane?
Soda Lime
Calcium Hydroxide
Barium Hydroxide
Barium Hydroxide
*These have been removed from US markets
Why do Calcium Hydroxide absorbents offer less CO2 absorption?
Lack Strong Bases (NaOH and KOH)
The maximum CO2 absorbed by calcium hydroxide is 10.2 liters per 100 grams absorbent whereas soda lime can absorb 26 liters of CO2 per 100 grams absorbent.
Which Absorber has the lowest incidence of compound A and Fire Production?
Soda Lime
Calcium Hydroxide
Barium Hydroxide
Calcium hydroxide absorbents, due to lower reactivity, have the lowest incidence of compound A and fire production
If you suspect a colleague of having a substance abuse problem, what is the correct answer for the exam in terms of what to do?
If you suspect a colleague of having a substance abuse problem, you should consult your state physicians health program before intervention or confrontation.
What are the indications for FFP?
- Correction of excessive microvascular bleeding (PT >1.5 times normal, PTT >2 times normal, or INR >2)
- Correction of coagulation factor deficiencies if the patient has been transfused with more than one blood volume (approximately 70 ml/kg)
- Correction of coagulation factor deficiencies for which there are no specific replacements
- Heparin resistance (antithrombin III deficiency) in a patient requiring heparin
- Coagulopathy related to hepatic insufficiency
- TTP
- Reversal of Warfarin (PCC another option)
What is the reason that FFP is used to treat Thrombotic thrombocytopenic purpura (TTP)?
Thrombotic thrombocytopenic purpura (TTP) is a platelet destruction disorder.
The inherited type involves a deficiency of vWF-cleaving protease activity (ADAMTS13 deficiency).
Fresh frozen plasma is administered in order to replete the ADAMTS13 enzyme.
Plasmapheresis may be used to treat the acquired type of TTP as it removes the acquired antibodies that damage the ADAMTS13 enzyme.
Esmolol
Selectivity?
Half Life?
Metabolism?
Esmolol is a β1-selective short acting (t1/2 = 9 min) agent that is
Rapidly metabolized by:
- Red blood cell (RBC) esterase
- Minimally hydrolyzed by pseudocholinesterase.
How do Beta Blockers affect the heart?
Beta-blockers reduce:
1. blood pressure
2. myocardial oxygen consumption
primarily by
1. decreasing heart rate
2. contractility.
They also have anti-arrhythmic properties by decreasing AV conduction and automaticity, and by increasing the atrial refractory period.
Propranolol selectivity?
Propranolol is non-selective and inhibits β1 and β2 receptors
Labetolol Selectivity?
β1, β2, and α-1 receptor blocker.
What is the ratio of selectivity of IV vs. PO Labetolol?
What is the unique about the way that labetolol can function as an anti-hypertensive?
The ratio of relative α:β potency of IV labetalol is approximately 1:7 whereas PO labetalol is 1:3.
The nature of this drug can be seen intraoperatively when labetalol administration results in decreased blood pressure without baroreceptor-triggered reflex tachycardia (as can be seen with pure vasodilating agents)
Besides labetolol, what is the only other beta blocker that has alpha antagonism properties?
Carvedilol
How are beta blockers (outside of esmolol) metabolized?
Hepatic Clearance
Exception: Atenolol (Which is renally cleared)
What is the pathophysiology of Propofol Infusion Syndrome?
The pathophysiology of PRIS relates to propofol’s ability to impair cellular free fatty acid utilization and mitochondrial activity leading to inadequate aerobic metabolism and increased reliance on anaerobic metabolism.
What arer some of the downstream effects of Propofol Infusion Syndrome?
Cardiac and skeletal muscle are particularly susceptible leading to muscle damage or necrosis that can cause cardiac failure and rhabdomyolysis.
lactic acidosis
hyperkalemia
renal failure
Hypertriglyceridemia
Hepatomegaly
Pancreatitis secondary to HLD
What color is urine with propofol infusion syndrome?
Green
Phenol excretion can cause this
How does respiratory alkalosis affect Calcium, Potassium and Phosphate levels?
All drop
What is the incidence of infection of central line?
15%
What happens if you rotate the head to the right >30 degrees to place a LEFT IJV Central Line?
It has been shown that with head rotation greater than 30 degrees that the left carotid artery and jugular vein overlap more than on the right.
If doing a carotid massage, what side should you do it on?
1. Carotid embolization on the left poses a greater risk as the left cerebral hemisphere is dominant in the majority of the population. This is also one of the reasons why right-sided carotid massage is preferred over left-sided massage.
- Another reason is that some investigations have found a greater cardioinhibitory effect on the right side.
What is the pathophysiology of performing a carotid massage?
Exert Pressure on Carotid Sinus and baroreceptors at the Transverse process of C6
The AFFERENT nerve impulses of carotid sinus baroreceptors are transmitted by the Hering’s nerves to the glossopharyngeal nerve (CN IX) (see image below).
Arterial wall stretch at the carotid sinus, within the internal carotid artery, activates the afferent impulse.
This activation leads to stimulation of the nucleus tractus solitarius (NTS) in the caudal medulla.
The NTS sends excitatory signals to other regions of the medulla which in turn inhibit stimulation of the preganglionic intermediolateral nucleus of the spinal cord which mediates the body’s sympathetic innervation.
The NTS may also stimulate vagal nuclei to activate the parasympathetic nervous system via the vagus nerve. These two effects then lead to bradycardia and hypotension.
What is the a wave on CVP tracing responsible for?
a wave: atrial contraction
What is the C wave on CVP tracing?
c wave: TV bulging into RA during RV isovolumetric contraction
What is the x descent on CVP tracing?
x descent: TV descends into RV with ventricular ejection and atrial relaxation
What is the v wave on CVP tracing?
v wave: venous return to and systolic filling of the RA
What is the y descent on cvp waveform?
y descent: atrial emptying into RV through open TV
How does atrial fibrillation reveal itself in CVP waveform?
absent a wave
How does Tricuspid Regurgitation reveal itself on CVP waveform?
Tall c waves
Tall v waves
Loss of x descent
How does Tricuspid Stenosis reveal itself on CVP wavefrom?
Tall a
Tall v waves
Minimal y descent
How does RV Ischemia present on CVP tracing?
Tall a & v waves
Steep x & y descent
M or W configuration
How does Pericardial Constriction present on CVP tracing?
Tall a & v waves
Steep x & y descent
M or W configuration
How does Cardiac Tamponade present on CVP tracing?
Dominant x descent
Minimal y descent
Draw a CVP overlapping with EKG.
What is the treatment for Methemoglobinemia resulting from G6PD?
Ascorbic Acid
Ascorbic acid also known as vitamin C, functions as an electron receptor and aids in the reduction of Fe3+ to Fe2+.
Ascorbic acid functions to reduce hemoglobin slower than methylene blue does. However, ascorbic acid does not have the hemolytic effect that methylene blue does in a G6PD deficient patient.
In a patient with G6PD deficiency the hexose phosphate pathway is dysfunctional and free radicals develop, which causes red blood cell lysis.
What is the treatment of Methemoglobinemia?
Methylene blue is often the drug of choice when treating methemoglobinemia.
Methylene blue provides an electron receptor for the reduction of methemoglobin using NADPH produced from the hexose phosphate pathway.
In a patient with G6PD deficiency the hexose phosphate pathway is dysfunctional and free radicals develop, which causes red blood cell lysis. Therefore, methylene blue should be avoided in patients with G6PD deficiency. Additionally, methylene blue is a potent reversible monoamine oxidase inhibitor (MAOI) and may interact with serotonergic psychiatric medications leading to life-threatening serotonin syndrome.
Other than G6PD deficiency, when should you avoid giving methylene blue?
Additionally, methylene blue is a potent reversible monoamine oxidase inhibitor (MAOI) and may interact with serotonergic psychiatric medications leading to life-threatening serotonin syndrome.
If an IV cannot be obtained in a patient suffering from cyanide toxicity, what is the treatment of choice?
Amyl nitrite is used to treat cyanide toxicity.
Amyl nitrate oxidizes Fe2+ to Fe3+.
Cyanide binds to methemoglobin more actively than it binds to normal hemoglobin.
Thus, by inducing a low-level of methemoglobinemia the methemoglobin in turn can sequester cyanide as cyanmethemoglobin.
Methemoglobinemia:
What occurs to Iron?
What type of anemia is caused?
Left or Right shift on Oxygen Dissociation curve?
Absorbance?
SpO2?
What should be used to monitor?
Methemoglobinemia occurs when hemoglobin becomes oxidized from Fe2+ to Fe3+.
Methemoglobin is unable to bind oxygen and causes a functional anemia, in addition to left shifting the oxygen dissociation curve.
Methemoglobin has an absorbance of 630 nm, which correlates to an oxygen saturation of 84-86% on pulse oximetry.
Co-oximetry should be used to aid in the diagnosis and treatment of methemoglobinemia. If unavailable, blood can be sent for a methemoglobin level.
Why is it that Carbon Monoxide Poisoning has a SpO2 of ~100% at high readings?
The COHb is interpreted by the pulse oximeter as a mixture of approximately 90% HbO2 and 10% HHb.
Thus, at high levels of COHb, the pulse oximeter will overestimate true SaO2, as may occur in patients with recent CO exposure.
How is SpO2 affected with Methemoglobinemia?
MetHb is formed when the heme iron is oxidized from the ferrous (Fe2+) to the ferric (Fe3+) state.
metHb is very dark and tends to absorb equal amounts of red and infrared light, resulting in a red:infrared ratio of 1.
When extrapolated on the calibration curve, a ratio of 1 corresponds with a saturation of 85%.
Thus, as metHb increases, SpO2 approaches 85% regardless of the true level of HbO2.
In order for Methemoglobinemia to be diagnosed, how much is the % increase?
What 4 drugs do anesthesiologist give that can cause this?
Drugs capable of causing methemoglobinemia (defined as greater than 1% metHb) include nitrates, nitrites, chlorates, nitrobenzenes, antimalarial agents, amyl nitrate, nitroglycerin, sodium nitroprusside, and local anesthetic agents.
What 3 dyes in the OR can produce SpO2 decreases?
How long do these decreases last?
Injections of methylene blue produce a large and consistent spurious decrease in SpO2, with readings remaining below baseline for 1 to 2 minutes.
Injection of indocyanine green decreases SpO2 to approxi- mately 80% to 90%, which lasts for a minute or less.
Injection of indigo carmine decreases the SpO2 the least, with the decrease lasting approximately 30 seconds.
What is the pathophysiology of Botulism?
(Include organism, mechanism of the bacteria in molecular detail)
Botulism is caused by the anaerobic bacillus, Clostridium botulinum.
Flaccid neuroparalysis occurs due to the prevention of acetylcholine (ACh) release from vesicles at the NMJ.
Acetylcholine is carried to the nerve terminal by vesicles which then fuse with the nerve terminal membrane via soluble N-ethylmaleimide-sensitive fusion associated protein receptor (SNARE) proteins. The collection of SNARE proteins facilitate exocytosis and then “repackaging” or reuptake of ACh.
The various toxins of C. botulinum are zinc endopeptidases that cleave the SNARE proteins and stop the fusion and release of ACh into the nerve terminal, as well as prevent reuptake back into the terminal.
What is the mechanism of action of Tetanus?
Include the organism and also the mechanism of action in molecular detail
The tetanus toxin from Clostridium tetani travels via neuronal retrograde transport up the motor neuron and enters the presynaptic terminal of inhibitory interneurons within the spinal cord. Normal modulation of fine motor movement from descending motor pathways triggers the interneurons to exert their inhibitory effects via γ-aminobutyric acid (GABA) release.
- The toxin prevents the release of GABA from the interneurons. Therefore, the inhibitory mechanism is inhibited and spastic neuroparalysis occurs.
What are the 4 sites for IO Placement?
1. Sternum
2. Proximal Humerus
3. Proximal Tibia
4. Distal Tibia
For the 4 sites of IO placement, what is the drainage of each IO site?
- Sternum = Azygos and Internal Mammary Vein
- Proximal Humerus = Axillary Vein
- Proximal Tibia = Popliteal Vein
- Distal Tibia = Greater Saphenous Vein
What are the advantages of humeral and sternal IO?
Humeral = Flow rates are higher than tibial (200 vs. 100 mL/min)
Sternal = Fast uptake of drugs (80-110 seconds) which is not that much longer than central access (60-80 seconds)
Explain in terms of ionization, pKa why Alfentanil has such a high onset of action?
pKa = 6.5
Highly un-ionized form (90%)
Lower Lipid Solubility
Compare Alfentanil to Fentanyl in terms of:
Onset:
Duration:
Potency:
Remembering “4” will get you in the appropriate range for differences between alfentanil and fentanyl.
Alfentanil has about 4 times faster onset.
Alfentanil lasts about 1/4 the duration.
Alfentanil is about 1/4 the potency (4x the dose of fentanyl).
Desflurane effects on:
BP?
Afterload?
HR?
Myocardial Function?
CO?
LV Diastolic Function?
Desflurane primarily decreases arterial pressure by decreasing afterload.
Desflurane increases heart rate, particularly when the concentration is quickly increased
Also causes dose-dependent depression of myocardial function.
Cardiac output is maintained and there is no significant effect on left ventricular diastolic function.
What are some of the extrapyramidal side effects to watch for?
- Acute dystonias (abnormal movement or posturing due to involuntary/sustained muscle contractions)
- Akathisia (restlessness and need to be in constant motion)
- Tardive dyskinesia (involuntary repetitive or purposeless movements).
What is the dose of metoclopramide that is needed to prevent PONV?
What is the respective risk of Extrapyramidal effects with these doses?
Metoclopramide has weak antiemetic effect at 10 mg (< 20 mg) and recommended dosing for PONV is 25-50 mg IV.
EPS occur in 0.3% with 10 mg and 0.6% with both 25 mg and 50 mg dosing. Marginal increase in risk of EPS to cover PONV
What are the top 2 therapies for Extrapyramidal symptoms in the PACU?
*Include doses*
-
Anticholinergics
- Benedryl 12.5 - 50 mg IV
- Benztropine
Initial dose: IM, IV, Oral: 1 to 2 mg once.
Subsequent doses: Oral: 1 to 2 mg 1 to 2 times daily.
3-8 all per True Learn but couldn’t find doses
- Trihyexyphenidyl
- Atropine
- Anti-histamines
- Benzodiazepines
- Beta-Blockers
- Dopamine Receptor Agonist
What are all the actions of Diphenhydramine?
Antihistamine (H1)
Anticholinergic activity
Inhibits serotonin reuptake
Potentiates opioid-induced analgesia
May have Local anesthetic-like properties (intracellular sodium channel blocker).
What is the concern for for venous air embolism with Nitrous Oxide?
Although nitrous oxide administration can worsen a venous air embolism, the risk is not increased significantly in intestinal surgery.
When the risk of venous air embolism is high, such as with sitting position neurosurgery, nitrous oxide should be avoided as it can increase the size of an air embolism should it occur.
What are all the contraindications to nitrous oxide?
Answers All in Bold
1. Tension pneumothorax
Expansion of a pneumothorax is the most rapidly occurring of those listed, with volume doubling occurring in only 10 minutes
Expansion of venous air emboli
Worsening of pneumocephalus
Intestinal Obstruction
100cc of gas normally
Expansion could lead to: Not closing, ischemia from lumen obstruction,
Gas-filled spaces = bowel.
One of the concerns with Bowel Distention sx cannot proceed
Blindness
How does chronic opioid use affect the hypothalamic gonadal axis?
Chronic opioid therapy has a profound effect on the adrenal and gonadal axes leading to:
increased prolactin levels (Galactorrhea)
Decreased testosterone, estrogen, cortisol, LH, and FSH.
Pre-renal
BUN:creatinine ratio
FENa
Urine Sodium (UNa)
Urine Osmolality (UOsm)
What are these values?
Pre-renal
BUN:creatinine ratio >20
FENa <1%
Urine Sodium (UNa) <10 mEq/Liter
Urine Osmolality (UOsm) >500 mOsm/kg
What are these values?
Intrinsic
BUN:creatinine ratio
FENa
Urine Sodium (UNa)
Urine Osmolality (UOsm)
What are these values?
Intrinsic
BUN:creatinine ratio <15
FENa >2%
Urine Sodium (UNa) >20 mEq/Liter
Urine Osmolality (UOsm) <350 mOsm/kg
Post-Renal
BUN:creatinine ratio
FENa
Urine Sodium (UNa)
Urine Osmolality (UOsm)
What are these values?
Post-Renal
BUN:creatinine ratio >15
FENa >4%
Urine Sodium (UNa) >40 mEq/Liter
Urine Osmolality (UOsm) <350 mOsm/kg
What is the formula for FENa
FENa = Excreted Na/Filtered Na x 100
(UNa x PCr) / (UCr x PNa x 100)
UNa – urine sodium
PNa – plasma sodium
UCr – urine creatinine
PCr – plasma creatinine
What is the exact molecular mechanism of propofol?
Propofol increases the time that the GABA-A receptors remain open after activation.
GABAA receptors, when active, allow Cl- to enter neurons and hyperpolarize the cell.
Hyperpolarization thus causes increased neuronal inhibition and unconsciousness
Why is it that dexmedotomidine can cause hypertension after bolusing?
In some instances a bolus of dexmedetomidine can cause hypertension because of activation of the sympathetic nervous system.
Alpha2 receptors are prejunctional receptors activated by What?
Alpha2 receptors are prejunctional receptors activated by norepinephrine (negative feedback loop).
The glycine receptor
- What ion channel is linked to this?
- Name an agonist?
- Name an antagonist?
Chloride
- Agonist = Alcohol
- Antagonist = Caffeine
Other than Ketamine, what are some drugs (4) that anesthesiologist can give that promote NMDA channel action?
1. PCP
2. Nitrous Oxide
3. Methadone
4. Tramadol
What is the time frame between doses that places a patient most at risk for bradycardia when administering two separate doses of succinylcholine?
What is the rationale behind this?
However, a second dose of succinylcholine, if given within approximately five minutes of the first dose, increases the risk of bradycardia.
It is thought that the hydrolytic byproducts of succinylcholine metabolism (succinylmonocholine and choline) sensitize the myocardium to the parasympathetic effects of a second dose of succinylcholine, thus leading to bradycardia.
When you simplify ICP, and how we manage this from an intraoperative perspective, what are your options?
1. Drain CSF
2. Decrease parenchymal volume
Diuretics
Steroids
3. Decrease Cerebral Blood Flow
Adjust your PaCO2 with ventilation adjustment
How does CBF pertain to PaCO2?
What is our threshold?
CBF is directly related to PaCO2, and decreasing a patients PaCO2 via hyperventilation is one of the most widely used methods of decreasing CBF and therefore ICP.
CBF changes 1 to 2 mL/100 g/min with each millimeter of mercury change in PaCO2.
Below a PaCO2 of 25 mm Hg, CBF change is attenuated because severe vasoconstriction can cause local ischemia.
Therefore care must be taken when utilizing hyperventilation as a strategy to decrease ICP as ischemia can be an unwanted consequence.
Why is the hyperventilatory therapy for decreasing CBF temporary?
When does this treatment plan not have any more lasting effect?
Ions do not readily cross the blood brain barrier, but CO2 does.
For this reason, acute changes in PaCO2 affect CBF, but changes in blood HCO3- levels have no effect.
However, after 24-48 hours, the CSF HCO3- levels have adjusted to the change, and the CBF returns to normal.
What are the pre-cautions with Methohexital in terms of seizures?
W/ seizure history or epilepsy can trigger a new-onset seizure.
W/O seizure history or epilepsy, methohexital has not been known to trigger a seizures
What are the high dose vs. low dose differences in Phenylephrine effects on?
Arterial vs. Venous constriction
Preload
Cardiac Output
Sphlanchnic Perfusion
Low Dose
Venous constriction results in improved preload from venous return and may improve cardiac output.
This is not seen in patients who have systolic heart failure, as the increased afterload can worsen cardiac output.
Notice VENOCONSTRICTION > arterial constriction
At high dose
Arterial & venous constriction → leads to decreased splanchnic perfusion
In higher doses, CO is commonly reduced due to increases in myocardial work and afterload.
The reduced splanchnic perfusion is more a result of arterial constriction than a reduction in cardiac output.
Why is LMHW more desired than Heparin (High molecula weight)?
(LMWH) more selectively inhibits activated factor X when compared to unfractionated heparin (UFH)
A longer polysaccharide chain (higher molecular weight) is required for the increased binding sites leading to thrombin inhibition.
The shorter polysaccharide chains (lower molecular weight) of LMWH is more restricted in binding solely to ATIII, therefore more selectively inhibits Xa.
Benefit =
1. Selective Xa inhibition can be desirable as factor Xa has limited function outside the coagulation system, unlike thrombin which also plays a role in the immune system and inflammatory pathways.
2. Less HIT
Why would Helium be used in the ICU?
Helium has an extremely low density and thus has an increased tendency for laminar flow.
Helium reduces airway resistance in large and medium airways (reduced resistance in turbulent flow). It can be used to decrease the work of breathing in pathologic conditions.
What is the incidence* and *treatment for Post-Dural Backache (From spinal or epidural)?
Incidence of post spinal backache = 11-13% of patients
Treatment:
Self-Limiting (Resolves in 7 days)
Mild analgesics such as acetaminophen, topical NSAIDs and patient reassurance.
Where are peripheral baroreceptors located?
Peripheral baroreceptors are located in both the:
Common carotid arteries
Aortic arch
How does the baroreceptor mediation occur in High BP vs. Low BP?
(Think about baroreceptors in the common carotid arteries and aortic arch)
When blood pressure is elevated, an increase in the baroreceptor firing in these areas causes an increase in the vagal tone (known as the baroreceptor reflex). (Stretch reflex)
In converse, decreases in blood pressure cause an inhibition of baroreceptor discharge resulting in decreased vagal tone.
When is Infective Endocarditis Prophylaxis Warranted?
1. Include What procedures qualify.
- Include what high risk cardiac conditions apply.
Infective endocarditis prophylaxis is recommended for cardiac conditions listed below PLUS:
-
1) Dental (mucosal, gingival) procedures or
2) Respiratory tract (tonsillectomy, adenoidectomy, bronchoscopy with incision/biopsy) procedures or
3) Infected skin/musculoskeletal tissue procedures* - *High risk cardiac conditions:**
1) Prosthetic cardiac valve or prosthetic material used in valve repair
2) Previous endocarditis
3) CHD only in the following categories: - Unrepaired cyanotic congenital heart disease
- Completely repaired congenital heart disease with prosthetic material or device within six months
- Repaired congenital heart disease with residual defects
4) Cardiac transplantation recipients with cardiac valvular disease
Rank the order of speed of conduction velocity between the different nerve fibers?
Type A - alpha (Fastest), beta, gamma, delta
Type B
Type C - Dorsal Root and Sympathetic (Slowest)
What is the Function of Each of these nerves?
Type A - Alpha
Type A - Beta
Type A - Gamma
Type A - Delta
Alpha = Propiroception , Motor
Beta = Touch, Pressure
Gamma = Muscle Spindles
Delta = Pain, Temp, Touch
What is the Function of Type B nerve Fibers?
Preganglionic Autonomic
What is the function of Type C - Dorsal Root?
Type C - Sympathetic Fibers?
Dorsal Root = Dull pain, Temp, Touch
Sympathetic = Postganglionic
According to the 2016 ACC/AHA guidelines, patients undergoing PCI for stable ischemic heart disease should receive dual antiplatelet therapy for:
What time period after BMS?
What time period after DES?
At least one month after BMS
At least six months after DES.
Contraindications to Metoclopramide?
- SBO (Promotility agent so not ideal)
- Parkinson’s - Increased risk of rigidity and exacerbation of extrapyramidal symptoms
- Pheochromocytoma
What P450 enzyme is affected by St. John’s Wort?
St. John’s wort is an herbal medication that is taken by patients to treat depression. St. John’s wort induces P450 3A4. This induction causes many anesthetic-related drugs to be metabolized including alfentanil and midazolam.
For local anesthetics, what is the more common for anaphylaxis and why?
Amino ester (One “i” in name) anesthetics are degraded into the metabolite para-aminobenzoic acid (PABA).
PABA is the reason for reactions to most local anesthetics.
Anaphylaxis to amino amide (2 “i” in the name) anesthetics occurs at an even lower frequency than in amino ester anesthetics.
Methylparaben, a common preservative, is often found in local anesthetics.
Methylparaben is structurally similar to PABA, and therefore cross reactivity is possible.
In the past, PABA was widely used in sunscreens as a UV filter.
Water-insoluble PABA derivatives such as padimate O are currently used in some products.
When are symptoms of a latex allergy manifested?
Who is at increased risk?
Occurs 30-60 minutes after exposure for allergies but can be immediate if anaphylaxis
More prone = Health care workers, atopic patients, and patients with spina bifida.
What is the one unique complication of a left IJV compared to the right IJV placement?
Increased Chylothorax compared to the right
In the majority of patients the thoracic duct drains into the venous system at or near the junction of the left internal jugular (IJ) vein and the left subclavian vein (SCV)
The most common configuration of the thoracic duct which is found in about 50% of the population involves the thoracic duct originating from the cisterna chyli at around the level of L1, ascending through the abdomen and thorax, and draining into the venous system at the juncture between the left IJ vein and the left SCV.
Variations exist where the thoracic duct drains in the left IJ, left SCV, left brachiocephalic, or left external jugular vein.
Due to the duct’s location, it can potentially be injured during placement of either a central line in the left IJ or in the left SCV.
What volatile anesthetic has been shown to be safest in renal failure patient’s?
The safety of desflurane exposure in patients with renal failure has been shown in various studies.
The potentially nephrotoxic inorganic fluoride concentrations found in humans after exposure to desflurane are significantly less than that after sevoflurane exposure
Unsure about this compared to isoflurane?
Why is Succinylcholine have a black box warning is pediatrics?
Succinylcholine has a Black Boxed warning specifically for this reason.
Caution should also be used in patients with muscular dystrophies (especially in children who can have potentially undiagnosed disorders), stroke patients, patients with neuromuscular disorders, or intensive care patients with prolonged immobilization.
In some patients, such as muscular dystrophy, hyperkalemia can occur secondary to rhabdomyolysis.
What is the timing window in which succinylcholine would not be contrainicated in a burn patient?
<24 hours
It is still appropriate to use succinylcholine to safely secure the airway in these patients if their injury is < 24 hours old, as there has not been enough time to experience nicotinic extrajunctional acetylcholine receptor upregulation.
What is the timeline when succinylcholine becomes harmful with neuromuscular disease?
When is the earliest effect?
When is the latest effect?
Patients with neuromuscular disease such as a stroke have risk of serious hyperkalemia after succinylcholine.
This usually peaks 7-10 days after insult, but increased K+ release may occur as soon as 2-4 days after denervation injury, or after several days of immobility.
Duration of risk has not been adequately characterized but is suspected to be for 3-6 months.
Why is Beta Blocker therapy a Class 1 Level B Recommendation to continue Beta Blockers on patient’s already on them?
A patient who is already on beta blockers should have beta blocker therapy continued in the perioperative period. Continuation of beta blocker therapy is considered Class 1 Level B evidence.
The reason for the continuation of beta-blocker therapy is that beta blocker withdrawal will allow a rebound causing increased heart rate and increased myocardial oxygen demand in the setting of surgical stress.
This increases the likelihood of a MACE
What are the risk factors defined by ACC/AHA when determining whether to start Beta Blocker therapy?
Cardiac risk factors include:
1. Hypertension
2. Cerebral vascular disease
3. Peripheral vascular disease
4. Chronic kidney disease
5. Coronary artery disease
6. Congestive heart failure,
7. Diabetes.
What are the ETT sizes that fit a sit 3-6 Unique LMA?
#3 = 6 mm
#4 = 6 mm
#5 = 7 mm
#6 = 7 mm
What are the ETT sizes that can rescue an iGEL?
#3 = 6mm
#4 = 7mm
#5 = 8mm
What are all the benefits of an epidural for GI surgeries?
Tonic inhibitory sympathetic control (T6-L2) predominates, but parasympathetic activation increases contractility.
Therefore, sympathectomy induced by epidural or spinal analgesia results in increased gut motility, especially those involving epidural catheter placement at T12 or higher.
The gastrointestinal hyperperistalsis has the advantage of providing excellent surgical conditions because of a contracted gut.
Epidural analgesia reduces the duration of postoperative ileus
The use of systemic opioids prolongs the duration of an ileus, and epidural analgesia decreases or eliminates the need for systemic opioids by minimizing postoperative pain.
Less pain also translates into decreased amount of catecholamines released which also promotes better gut contraction.
Postoperative epidural analgesia may also have a protective effect on the gastric mucosa because intramucosal pH is higher during postoperative epidural analgesia than during systemic analgesia.
Local anesthetics, given either neuraxial or systemically, have also been shown to improve intestinal perfusion as well as reduce gastrointestinal tract irritation through their anti-inflammatory properties.
Label all the components of a flow volume loop.
What would Flow-Volume Loop look like for a variable extrathoracic obstruction?
What would Flow-Volume Loop look like for a variable intrathoracic obstruction?
What would Flow-Volume Loop look like for a fixed upper airway obstruction?
What is the best block for tourniquet pain?
- Which nerve?
- Which dermatome origination?
The intercostobrachial nerve provides sensory innervation to the medial brachium and does not originate from the brachial plexus.
It originates from the T2 dermatome.
Blockade of this nerve is required when an upper arm tourniquet is required and would not be successful with any brachial plexus block technique.
What is the sensory and motor innervation of the musculocutanoeus nerve?
How do you block it?
Terminal branch of the lateral cord
Motor: Provides innervation to the biceps muscle (elbow flexion).
Sensory: It gives off the lateral antebrachial cutaneous nerve which provides sensory innervation to the lateral forearm (the site of stimulus) and thus would require supplemental block to achieve adequate anesthesia for the operation.
Block by injecting can be supplemented by injecting local anesthetic into the coracobrachialis muscle.
How is Buprenorphine able to have low physical dependence and prolonged clinical effects?
Buprenorphine has a high affinity for the μ-receptor with a half-life for dissociation from the receptor between 2-3 hours (compare to fentanyl’s 7 minutes).
This leads to a low-level of physical dependence and prolonged clinical effects, up to 6 hours, despite a metabolic and elimination half-life of 3 hours.
What is Buprenorphine potency compared to Morphine?
Buprenorphine has an analgesic potency at low doses that is 25-40 times that of morphine.
What is the cause of a febrile transfusion reaction?
Cytokines and Antibodies to Leukocyte Antigens
What is the cause of graft vs. host disease?
Donor Lymphocytes against a recipient
What is the cause of Delayed Hemolytic Transfusion reaction?
recipient antibody and complement attack on donor cells
result of recipient antibody and complement attack on donor cells
typically secondary to antibodies associated with the Rh, Kidd, or Kell systems
What is the cause of Acute Hemolytic Transfusion reactions?
recipient antibody and complement attack on donor cells
result of recipient antibody and complement attack on donor cells
typically secondary to antibodies associated with the ABO Incompatibility
When should a patient receive leukoreduction with blood products? (What patient population)
Transfusion-related CMV is a problem primarily for:
Immunocompromised patients
Neonates
Allograft recipients
Asplenic from resection or sickle cell disease.
What is the rate of seroconversion with:
HCV
HBV
HIV
HTLV
CMV
1/438 for CMV
1/366,509 for HBV
1/1,657,722 for HCV
1/1,860,883 for HIV
1/3,394,086 for HTLV.
What are the respiratory effects of laparoscopy?
- Decreased lung compliance
- Increased V/Q mismatch
- Increased inspiratory pressures
- Increased PaCO2 and decreased blood pH
What are the cardiovascular effects of laparoscopy?
Cardiac?
Vascular?
- Increased SVR, increased PVR, increased MAP
- Increased cardiac filling (e.g. increased thoracic pressure + head-down position)
- Arrhythmias (tachy or brady)
- Decreased venous return (e.g. vena cava compression + head-up position)
- Decreased ejection fraction
- Decreased renal blood flow
- Decreased splanchnic perfusion
What are the benefits of inhalational induction in an adult?
Benefits:
Stage II (excitation) is generally avoided with high concentrations of sevoflurane used for induction in the adult population.
Sevoflurane also has been administered by mask as an approach to the difficult adult airway because it preserves spontaneous ventilation and does not cause salivation.
The traditional “awake look” in the suspected difficult airway (where intravenous drugs are titrated to a level that allows direct laryngoscopy in the awake patient) has been modified to consist of spontaneous ventilation of high concentrations of sevoflurane until laryngoscopic evaluation is tolerated.
What is the mechanism of action of nicardipine?
Antagonist of calcium influx through the slow channels of cell membranes
Arterial Dilator which decreases afterload and decreases SVR
Coronary Dilator (Angina/Spasms) with minimal effect on preload
Sympathetic activation (25% get tachycardia - NOT Baroreceptor mediated)
Increases cardiac contractility
Nicardipine, nitroglycerin, and sodium nitroprusside all have what in common?
Nicardipine, nitroglycerin, and sodium nitroprusside inhibit hypoxic pulmonary vasoconstriction.
What are some common drugs that have zero order kinetics?
Drugs that typically follow zero-order kinetics are THE PAW: theophylline, heparin, ethanol, phenytoin, aspirin, warfarin.
What is the FENa formula?
FENa = [(PCr x UNa ) / (PNa x UCr)] x 100
How does Uremia lead to impaired platelet function? (Pathophysiology)
Uremia can lead to impaired hemostasis through a variety of mechanisms including, but not limited to:
1. Interference with von Willebrand factor (vWF) formation and release leading to impaired platelet activation at the site of vascular injury. ‘
Normally, platelets are activated and subsequently aggregate by binding to sub endothelial vWF.
Function of glycoprotein IIb-IIIa (GPIIb-IIIa) is abnormal in uremia.
This protein found on the surface of platelets is a receptor for fibrinogen, fibronectin, and vWF, and assists in platelet activation and aggregation.
Prostacyclin and nitric oxide synthesis are each increased in uremia.
These two compounds have platelet inhibitory effects.
Decreased tissue factor (factor III) activity.
This enzyme complexes with factor VIIa to activate factor X to factor Xa which converts prothrombin to thrombin.
What is the common side effect of large volume chloroprocaine through the epidural post-op?
Explain why.
Back pain following a large volume injection of 2-chloroprocaine is not an indication for imaging of the spine.
Back pain following injection of large volumes of 2-chloroprocaine can cause muscle spasms.
2-chloroprocaine may contain the preservative disodium ethylenediaminetetraacetic acid (EDTA).
EDTA is a known chelator of calcium.
Larger volumes of 2-chloroprocaine chelate the calcium of nearby muscle, which causes local muscle spasms.
These spasms are transient and self-relieving.
There is no need for treatment or imaging unless other signs and symptoms are present.
However, there are preservative free formulations of 2-chloroprocaine readily available so this side effect is less commonly seen.
What are the systems based side effects of Amiodarone?
CV: bradycardia, hypotension, Prolonged QTc
Pulmonary: pulmonary toxicity (with a pulmonary fibrosis appearance)
GI: Elevated LFT
Endocrine: hypothyroidism (20% of patients), life-threatening hyperthyroid storm
Dermatological: Blue/Gray Skin and Hypersensitivities
For the pulmonary fibrosis effects of amiodarone, what is thought to cause this?
What is correlated with the severity (Dosing regards)?
Antibody mediated destruction of parenchyma or cytotoxic process
Though the risk of developing side effects rises with the dosage of amiodarone, there is no set dosage limit at which it will occur.
amiodarone-induced pulmonary toxicity correlates more with the total cumulative dose than with the daily dose or plasma concentration.
Metabolism of Amiodarone
Hepatically
What is the difference in metabolism of the amide vs. ester local anesthetics?
Ester type local anesthetic, and like other esters is broken down by plasma cholinesterases.
The amide local anesthetics undergo hepatic metabolism.
What is the reason why local systemic anesthetic toxicity is not seen more with 2-Chloroprocaine?
2-chloroprocaine is so rapidly metabolized and has such low systemic toxicity that it can be delivered in much higher concentrations, up to 3%.
What is primary determinant of potency in local anesthetics?
Lipid Solubility primary determinant of potency in local anesthetics.
What is the primary determinant of duration of local anesthetics?
Protein Binding primary determinant of duration of local anesthetics.
Bier Block:
What is an important potentially devastating consequence?
When should you let down the tourniquet?
What dose and medication should you use?
Pain control is of short duration and stops almost immediately upon deflation of the tourniquet. One important complication of IVRA is systemic toxicity of local anesthetics.
For this reason, it is recommended that the tourniquet not be let down less than 20-30 minutes of local anesthetic injection
The tourniquet should be gradually released to avoid a massive washout of local anesthetic, and long-acting anesthetics such as bupivacaine should be avoided.
Dose = Amount: 40-50 mL of 0.5% Lidocaine (200-300 mg) Example dose would be 12-15 mL of 2% lidocaine (240 - 300 mg) or higher volume of dilute lidocaine
What is the length of time that a Bier Block can last?
Intravenous regional anesthesia (IVRA), also called Bier block, is an alternative to a peripheral nerve block for short (ie, 30 to 45 minutes) procedures on the hand and forearm such as carpal tunnel release, Dupuytren’s contracture release, or reduction of wrist fracture
For non-invasive cuffs, how is the MAP determined?
The point of maximal amplitude of oscillations corresponds to the mean arterial pressure (MAP).
How does the SBP, DBP and MAPs change with non-invasive oscillatory cuff monitoring?
Which is more or less reliable
MAPS = Most reliable
The values of systolic and diastolic pressures are determined using formulas that detect the rate of change in the oscillations.
Thus, systolic and diastolic pressures are less reliable than the mean arterial pressure.
Diastolic blood pressure measurement is more likely to be affected by movement since this would cause changes of similar pressure magnitude, which makes the diastolic pressure the least reliable.
How does succinylchoine affect intraocular pressures?
Intraocular pressure following succinylcholine administration can increase 5-15 mm Hg despite pretreatment with a NDNB.
When you give Succinylcholine, what can be seen with HR?
Cardiac side effects are more often seen with repeat dosing in children (Bradycardia and Asystole) and can be attenuated with the use of glycopyrrolate or atropine.
Succinylcholine more commonly causes tachycardia, mediated by catecholamine release.