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Clinical Pearls Flashcards

1
Q

Postoperative Visual Loss

A
  • POVL is rare
  • prone spine surgery has highest risk
  • 2 most common types: central retinal artery occlusion (CRAO) and ischemic optic neuropathy (ION)
  • direct pressure on globe leads to CRAO
  • inadequate oxygen delivery to optic nerve leads to ION
  • optic nerve perfusion: MAP-IOP or CVP
  • prone position: increased IOP and CVP
  • MAP may decrease during prone procedures due to hypotension or decreased CO from abdominal pressure
  • risk factors: hypotension, elevated venous pressure, anemia, blood loss, long procedure (>6h), and direct globe compression
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2
Q

Pulmonary Resection Risk Assessment

A
  1. respiratory mechanics: predicted postoperative (ppo) FEV1% (42 total lung segments)
    * ppoFEV1<40% associated w/respiratory complications and need for mechanical ventilation
  2. lung parenchymal function
    * ppoDLCO <40% associated with increased risk of both cardiac and respiratory complications
  3. cardiopulmonary interaction (exercise testing)
    * VO2 max correlates well with risk of M&M (if poor tolerance, likely ICU post-op with mechanical ventilation and staged weaning)
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3
Q

Neuromonitoring

A
  • key: maintain stable anesthetic
  • IV anesthetics: decrease amplitude and increase latency of SSEPs and MEPs
  • etomidate and ketamine increase amplitutes of SSEPs/MEPs
  • volatiles/nitrous: decrease amplitude and increase latency of SSEPs and abolish MEPs
  • muscle relaxants: little effect on SSEPs but prevent recording of MEPs
  • **optimal anesthetic: TIVA (prop/remi) without muscle relaxants (okay with just SSEPs)
  • **0.5 MAC volatile may be okay for SSEPs
  • EMGs: stimulation of a motor nerve with subsequent measured muscle response (avoid all NMBDs)
  • VEPs: extremely sensitive to IV and inhalation anesthetics (used to monitor optic nerve)
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4
Q

References

A
  • Miller’s Anesthesiology
  • Morgan & Mikhail’s Clinical Anesthesiology
  • Stoelting’s Anesthesia and Co-Existing Disease
  • Jaffe’s Anesthesiologist’s Manual of Surgical Procedures
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5
Q

ACC/AHA Guidelines on Management of Cardiac Patients for Noncardiac Surgery (2014 Update)

A
  1. Known or Risk Factors for CAD?
    Emergency? Proceed
  2. Non-emergency
    ACS? Treat
  3. No ACS
    Estimate Perioperative Risk of MACE w/RCRI or NSQIP
  4. Low risk (<1%)
    Proceed
  5. Elevated risk (>1%)
    Functional capacity >4 METS? Proceed w/o testing
  6. Functional capacity <4 METS or unknown?
    *Will testing impact decision making OR preoperative care?
    Yes–>pharmacologic stress testing then coronary revascularization if abnormal
    No–>proceed to surgery
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6
Q

Revised Cardiac Risk Index (RCRI)

A
  1. IHD
  2. CHF
  3. CVA or TIA
  4. DM w/insulin
  5. CKD (Cr 2 mg/dL)
  6. Surgery type: intrathoracic, intraperitoneal, or suprainguinal vascular

*Risk of cardiac death, nonfatal MI, and nonfatal cardiac arrest
0=0.4%
1=0.9%
2=6.6%

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7
Q

Autonomic Neuropathy

A

S&S: loss of normal HR variability, orthostatic hypotension, resting tachycardia, early satiety, peripheral neuropathy, lack of sweating, dysrhythmias
*diabetics high risk

Anesthetic Concerns

  • gastroparesis and aspiration risk
  • hypotension (impaired peripheral vasoconstriction and baroreceptor function)
  • silent ischemia
  • intraoperative hypothermia (impaired peripheral vasoconstriction)
  • impaired ventilatory response to hypoxia and hypercapnia
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8
Q

EKG Findings

A
  • RVH: RAD, tall R wave in V1
  • LAE/RAE: large P wave
  • LVH: S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm
  • LBBB: QRS > 120 msec, notched R wave in lateral leads (“M” wave), often LAD
  • RBBB: QRS > 120 msec, RSR’ in precordial leads (V1-V3), often normal axis (LV depolarization is normal)
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9
Q

Anaphylaxis v Anaphylactoid

A

Anaphylaxis

  • type 1 immediate hypersensitivity reaction involving IgE antibody-antigen interaction
  • usually requires previous exposure

Anaphylactoid
-direct, nonimmune-mediated release of vasoactive mediators from mast cells and basophils

*Clinically indistinguishable

Primary Therapy:

  • epinephrine drug of choice
  • fluids

Secondary Therapy:

  • H1 blocker (50 mg diphenhydramine IV)
  • steroid (100 mg IV hydrocortisone, fastest corticosteroid)

*Draw serum tryptase to establish conclusive dx of anaphylaxis/anaphylactoid reaction

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10
Q

Fat Embolism Syndrome

A

*fat emboli damage pulmonary capillaries causing respiratory failure

  • Major criteria: respiratory failure, CNS, petechial rash
  • Minor criteria: tachycardia, fever, jaundice, AKI, anemia, thrombocytopenia, retinal fat globules
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11
Q

Electrolyte Abnormalities and EKG Changes

A
  • hyperkalemia: peaked T waves, increased PR interval, wide QRS
  • hypokalemia: flat/inverted T waves, prominent U waves

-hypocalcemia: prolonged QT, wide QRS

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12
Q

Hypothermia

A

Causes

  • decreased heat production (decreased metabolic rate)
  • increased heat losses (peripheral vasodilation, cold room, fluids)
  • impaired heat regulation (GA, hypothalamus dz)

Consequences

  • CNS: prolonged awakening
  • CV: arrhythmias
  • Heme: impaired coagulation
  • Metabolic: prolonged drug effects, particularly NMBs
  • Mild hypothermia (33-37 C): coagulopathy 2/2 defects in platelet aggregation and adhesion (normal factor function)
  • Extreme hypothermia (<33 C): both plt and factor function impaired)
  • So: TEG more helpful in mild hypothermia (plt function not measured by PTT) and either test helpful at extreme hypothermia (coag function measure by both tests)
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13
Q

Alveolar Gas Equation

A

PAO2 = FiO2× (Pb − PH2O) − (PACO2/R)

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14
Q

Normal shunt

A
  • 3% of CO normal

* bronchial and thebesian veins (cardiac veins, drain myocardium into left heart)

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15
Q

Difficult Mask

A
  • Obesity
  • OSA
  • Beard
  • Edentulous
  • Age >55 yrs
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16
Q

Difficult Intubation

A
  • MP 3 or 4
  • Small mouth opening <2 cm
  • TM distance <6 cm
  • Thick neck

*MP score has best sensitivity (although still not great at 75%) and high specificity (high 90%)

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17
Q

Extubation Criteria

A

OR

  1. Adequate oxygenation (Sp02 >92%, PaO2 >60 mmHg)
  2. Adequate ventilation (EtCO2 < 50 mm Hg)
  3. HD stable
  4. Full reversal of muscle relaxation (TOF >0.9)
  5. Neuro intact

ICU

  1. Adequate mentation
  2. HD stable
  3. Adequate oxygenation and ventilation on minimal vent settings (ie. PS 5 mmHg, FiO2 <40%, PEEP 5)
  4. Vent Criteria (during SBT)
    - RSBI <105 (f/Vt)
    - NIF < 20 cm H20 (effort independent, strong - predictor, poor + predictor)
    - VT >5 ml/kg
    - VC >10 ml/kg
    - RR < 30

*RSBI most consistent and powerful predictor

**PSV was more effective than a T-piece (30 min) for successful spontaneous breathing trials (SBTs) among patients with simple weaning.

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18
Q

PT v PTT

A

Prothrombin Time (PT)

  • extrinsic coag pathway
  • measures warfarin, liver damage, and vit K status
  • Factors: I, II, V, VII, X
  • I (fibrinogen) and II (prothrombin)

Partial Thromboplastin Time (PTT)

  • intrinsic and common coag pathways
  • monitors heparin
  • Factors: I, II, V, VIII, IX, X, XI and XII
  • NOT measured: factors VII and XIII
  • **Both heparin and warfarin affect both PT and PTT
  • **Heparin-ATIII part of extrinsic and common pathway
  • **Warfarin-Vit K factors part of both pathways
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19
Q

Vitamin K Dependent Clotting Factors

A

II, VII, IX and X

*and proteins C and S (anti-coag factors)

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20
Q

Factor VIII

A

Only clotting factor NOT produced in the liver

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21
Q

Calcium Disorders

A

Hypercalcemia

  • bones, stones, groans (N/V), psychic overtones (lethargy, coma)
  • HTN and arrhythmias possible
  • DDX: hyperPTH, vit d toxicity, malignancy, meds (thiazides)
  • Tx: IVFs, lasix, dialysis for life-threatening hypercalcemia

Hypocalcemia

  • tetany and muscle cramping (Chvostek), respiratory weakness, CHF, arrhythmias
  • hypoPTH, vit d deficiency, citrate chelation
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22
Q

Hypoglycemia

A

S&S

  • SNS activation (diaphoresis, tachycardia, anxiety)
  • Neuro: weakness, fatigue, AMS, coma

Ddx
-exogenous insulin, insulin tumors, critical illness/sepsis, adrenal insufficiency, liver disease

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23
Q

Pheochromocytoma

A

Pre-op:

  • Phenoxybenzamine: noncompetitive, nonselective, alpha blocker
  • tachycardia from alpha 2 blockade
  • Selective, competitive, alpha 1 blockers
  • prazosin, doxazosin
  • less tachycardia and shorter elimination times may be advantageous in avoiding postoperative hypotension

Pre-op treatment until blood pressure improves (typically 10-14 days)

  • orthostatic hypotension and nasal congestion common side effects
  • hold 24 hours prior to surgery to prevent postoperative hypotension

*Beta blockade (typically B1 selective like metoprolol/esmolol) only needed for patients with predominantly epinephrine secreting tumors or patients who develop tachycardia from alpha antagonism tx

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24
Q

ARDS v TRALI

A

ARDS and TRALI
-clinically indistinguishable noncardiogenic pulmonary edema (increased pulmonary endothelial permeability/leakage)
-frothy pulmonary secretions, fever, tachycardia, dyspnea hypoxia, hypotension
Dx: acute onset hypoxemia (PaO2/FiO2 <300, SpO2 <90%), bilateral chest infiltrates on CXR, absence of cardiac failure or fluid overload (PAOP <18)
Tx: supportive (diuretics and steroids not beneficial)

*mortality rate significantly lower with TRALI (6%, compared to 40% for ARDS) and requires h/o transfusion w/in 6 hours

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25
Q

TACO v TRALI

A

TRALI

  • donor antibodies leads to activation of neutrophils on the pulmonary vascular endothelium–>release of activating factors leads to endothelial damage, capillary leakage, and acute lung injury (usually with plasma-rich blood products)
  • tx: supportive (O2 and low TVs), stop blood products and notify blood bank

TACO

  • cardiogenic (hydrostatic) pulmonary edema from volume overload during transfusion
  • tx: diuretic, inotrope and/or afterload reducer if needed

Differentiation:

  1. Signs and Symptoms
    - TRALI: low BP, fever, leukopenia
    - TACO: HTN, JVD, peripheral edema, S3 heart sound
  2. Fluid Status
    - TRALI: normovolemia or hypovolemia
    - TACO: hypervolemia
  3. Cardiac Function
    - TRALI: normal
    - TACO: impaired
  4. BNP (peptide secreted by ventricles in overload)
    - TRALI: nl
    - TACO: elevated
  5. Edema fluid to serum protein ratio
    - TRALI: high in plasma proteins
    - TACO: low in plasma protein
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26
Q

Beta Blocker Initiation

A
  • never start day of surgery

- if 3 or more risk factors (RCRI), then it may be reasonable to start, but must start 2-7 days pre op (2014 ACC/AHA)

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27
Q

Respiratory Sinus Arrhythmia

A

*Heart Rate Changes With Respiration

Bainbridge Reflex: increased heart rate during inspiration (from increased cardiac filling)

Baroreceptor Reflex: increase in BP (increased SV/CO during inspiration) leads to a decrease in HR

*Balance of these two reflexes leads to HR changes

***Bezold-Jarisch: bradycardia and hypotension in response to underfilled LV (Vagus nerve)

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28
Q

Bezold–Jarisch reflex

A

Bradycardia and hypotension in response to under-filled LV (via Vagus nerve)
*opposes baroreceptor reflex

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29
Q

cm H20 to mmHg

A

10 cm H20 = 7.5 mmHg

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30
Q

Corneal Abrasion

A
  • red and watery
  • foreign body sensation
  • photophobia
  • worse with blinking
  • tx: antibiotic ointment
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31
Q

Benzodiazepine

A
  • midazolam: short acting
  • lorazepam: intermediate acting
  • diazepam: long acting

*lorazepam may be best for EtOH withdrawal in liver disease due to its intermediate half-life

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32
Q

SIMV v AC

A

AC

  • each breath (initiated by the patient) is assisted or controlled by preset volume or pressure
  • backup rate for preset volume/pressure breath if none is initiated by patient
  • every breath is the same
  • pros: if patient weak, continue to receive full volume/pressure breaths
  • cons: risk of hyperventilation/hyperinflation (resp alkalosis)

SIMV

  • guarantees certain number of breaths (preset backup rate of certain volume/pressure)
  • mandatory breaths synchronized to coincide with spontaneous respirations
  • patient triggered breaths may be smaller
  • if the patient is taking good volumes during their spontaneous breaths, this may indicate that weaning might be possible
  • pressure support can be added to patient breaths if too small
  • pros: reduced risk of hyperventilation/hyperinflation
  • cons: increased work of breathing, reduction in CO (in patients w/reduced LV function)
  • Personal preference prevails, except in the following scenarios
    1. Patients who breathe rapidly on ACV should switch to SIMV
    2. Patients who have respiratory muscle weakness and/or left-ventricular dysfunction should be switched to ACV
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33
Q

Neurogenic Pulmonary Edema

A
  • can occur after any CNS injury
  • mechanism poorly understood
  • both cardiogenic and noncardiogenic components
  • massive sympathetic surge–>widespread vasoconstriction–>increased pulmonary blood flow
  • subsequent pulmonary leak
  • treatment largely supportive: treat CNS injury, lung protective ventilation, consider diuretics to reduce pulmonary hydrostatic pressure
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34
Q

SIADH v CSWS

A

SIADH

  • euvolemic
  • urine sodium < 100 mEq/L
  • tx: fluid restriction and diuretics

CSWS

  • hypovolemia
  • urine sodium >100 mEq/L
  • tx: fluid and sodium replacement
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35
Q

Absent Left Sided Breath Sounds

A

Right mainstem ETT v Pneumothorax
*EtCO2 decreased in pneumothorax, usually normal in endobronchial intubation

Other features of pneumothorax: decreased CO, hypotension, hyper-ressonance to percussion, contralateral tracheal shift, distended neck veins

Pneumothorax tx

  • needle decompression 2nd intercostal space, midclavicular line
  • chest tube 5th intercostal space just anterior to midaxillary line
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36
Q

Epidurals for post-op pain control

A
  • improved pain scores
  • greater mobility
  • decreased post-op pulmonary complications (less opioid induced respiratory depression, less splinting leading to hypoventilation and pneumonia)
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37
Q

SAB and TURP

A
  • T10 goal sensory level
  • provides comfort and covers bladder but also allows for early detection of bladder perforation (abdominal pain and diaphragmatic irritation/shoulder pain)
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38
Q

Pseudocholinesterase Deficiency

A

Dibucaine # (normally inhibits normal pseudocholinesterase)

  • 80%: normal (80% inhibition of enzyme by dibucaine)
  • 50%: heterozygote
  • 20%: homozygote
  • Sux lasts 4-8 hours
  • Phase 2 blockade: fade on TOF (like nondepolarizers)
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39
Q

Myocardial Oxygen Supply/Demand

A

Decreased supply: anemia, hypoxia, tachycardia, decreased CPP (hypotension, vasospasm, plaque, AS, AR, elevated LVEDP)

*Demand = HR, contractility, and wall tension (and basal O2 demand)

Increased demand: tachycardia, increased wall tension, contractility, and afterload

*myocardium is dependent on increasing coronary blood flow during times of demand, because oxygen extraction can only be minimally increased

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40
Q

Digoxin Toxicity

A
  • EKG changes, arrhythmias, fatigue, N/V, confusion, visual disturbances
  • exacerbated by hypokalemia, hypomagnesemia, and hypercalcemia

*can cause ST depression even in therapeutic range

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41
Q

Mixed SvO2

A

Normal 75% (range 60-80%)

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42
Q

Morbid Obese Risks

A
  • airway mgmt
  • pulmonary abnormalities (atelectasis, hypoxia, decreased FRC, increased CC, rapid desaturation w/apnea)
  • obesity hypoventilation syndrome (Pickwickian syndrome)
  • OSA
  • metabolic syndrome
  • DMII
  • HTN
  • CAD
  • CVA
  • DVT/PE
  • Fatty liver disease
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43
Q

Tumescent Liposuction Lidocaine Max

A

55 mg/kg

*lidocaine 4 mg/kg or 7 mg/kg w/epi

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44
Q

Celiac Plexus Block

A

Procedure:

  • prone patient, just anterior to L1 vertebral body
  • test block first w/local, then neurolytic block (alcohol or phenol)

Complications:

  • paralysis (neurolytic injection into spinal/epidural space or damage to arterial supply ie. artery of Adamkiewicz)
  • postural hypotension, intravascular injection, hemorrhage, sexual dysfunction, diarrhea
  • postural hypotension most common
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45
Q

Induction for a kid with acute epiglottitis and family history of MH?

A

IM ketamine–>IV–>airway

10 mg/kg

*maintain spontaneous respiration

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46
Q

Transplanted Heart

A
  • dependent on circulating catecholamines and preload
  • response to circulating catecholamines is normal and possibly enhanced due to denervation sensitivity (increased receptor density)
  • absence of vagal influences causes a relatively high resting HR (90-120)
  • responsive to direct acting agents: isoproterenol, epinephrine, dobutamine, dopamine
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47
Q

PEEP and Pulmonary Edema

A
  • PEEP improves oxygenation and pulmonary function by redistributing alveolar fluid to area that are less involved in gas exchange
  • recruits collapsed alveoli that are contributing to pulmonary shunting
48
Q

LAST Symptom Progression

A
  1. Nonspecific neurologic symptoms: metallic taste, circumoral paresthesias, blurred vision, tinnitus, lightheadedness/dizziness
  2. CNS excitation: agitation, shivering, muscle twitching, tremors, tonic-clonic seizures
  3. CNS depression: resolution of seizure activity, respiration depression/arrest, LOC, coma
  4. CV depression: hypotension, bradycardia, ventricular dysrhythmias, CV collapse
  • Lipid Emulsion tx: 1.5 ml/kg of 20% lipid over 1 minute, then infusion
  • LAST asystole: 1 mcg/kg epi (higher doses associated w/worse outcomes in bupi LAST)
49
Q

DO2

A

CO x (1.34 x Hgb x Sa02) + (0.003 x Pa02)

50
Q

Disadvantages to Bicarb

A
  • hypercapnia
  • tissue hypoxia due to left shift of oxy-hgb dissociation curve
  • volume overload
  • hypokalemia
  • alkali stimulation of organic acidosis (lactate)
51
Q

Serotonin Syndrome

A

Neuroexcitatory Triad

  1. Altered mental status
  2. Autonomic (fever, tachycardia, tachypnea, diarrhea)
  3. Neuromuscular (clonus, hyper-reflexia)

Causes
-SSRIs, MOAIs, antidepressants (trazodone), antiemetics (ondansetron, metoclopramide), drugs of abuse (MDMA, cocaine, amphetamine)

DDx:

  1. MH (increase in EtCO2, volatile/sux, rigidity, hyporeflexia)
  2. NLMS (dopamine antagonists, bradykinesia, “lead pipe” rigidity)
  3. Anticholinergic syndrome (nl reflexes, mydriasis, delirium, dry oral mucosa, hot skin, urinary retention)
52
Q

Thromboelastography

A

R- time to initial clot formation (reaction)

  • intrinsic pathway factor function
  • **FFP

K/alpha angle- speed of clot formation

  • thrombin and fibrin formation
  • **cryoprecipitate

MA- strength of clot

  • platelet number and function
  • **platelets

RAM it home with FFP (FFP, fibrinogen, and platelets)

53
Q

NRP

A

*Warm, dry, clear secretions, and stimulation

(30 seconds)
*If apnea or gasping or HR <100 –> PPV, SpO2 monitor, consider ECG monitor

(30 seconds)
*HR still below 100 –> ETT or LMA if needed

  • HR below 60 –> ETT, chest compressions, coordinate w/PPV, 100% O2, ECG monitor, consider UVC
  • HR still below 60 –> IV epinephrine (0.01 mg/kg IV, 0.1 mg/kg ETT)
  • consider hypovolemia and PTX if HR <60 persistently
  • compression-to-ventilation ratio (3:1 with 90 compressions and 30 breaths per minute)
  • meconium-stained amniotic fluid and presents with poor muscle tone and inadequate breathing efforts, the infant should be placed under a radiant warmer and PPV should be initiated if needed. Routine intubation for tracheal suction is no longer suggested
  • 100% oxygen whenever chest compressions are provided
  • PPV should be initiated if the infant is not breathing or the heart rate is less than 100/min after the initial steps are completed
  • Resuscitation of preterm newborns of less than 35 weeks of gestation should be initiated with low oxygen (21% to 30%), and the oxygen concentration should be titrated to achieve a preductal oxygen saturation approximating the interquartile range measured in healthy term infants after vaginal birth at sea level
  • suctioning immediately following birth (including suctioning with a bulb syringe) should be reserved for babies who have obvious obstruction to spontaneous breathing or who require positive-pressure ventilation (PPV)
  • Oxyhemoglobin saturation may normally remain in the 70% to 80% range for several minutes following birth, thus resulting in the appearance of cyanosis during that time
  • It is recommended that oximetry be used when resuscitation can be anticipated, when PPV is administered, when central cyanosis persists beyond the first 5 to 10 minutes of life, or when supplementary oxygen is administered.
  • spontaneously breathing preterm infants with respiratory distress may be supported with CPAP initially rather than routine intubation for administering PPV
  • reasonable to discontinue resuscitation in infants with an Apgar of 0 at 10 minutes of resuscitation w/undetectable HR
  • Naloxone no longer a part of the initial resuscitation efforts of infants born to opioid mothers (increased seizures and IVH)

*Hyperoxygenation–>IVH, ROP, and BPD

*Target Preductal Sp02 After Birth
1 min = 65%
2 min = 70%
3 min = 75%
4 min = 80%
5 min = 85%
10 min = 85-95%

*Preductal (RUE) most closely correlates w/CNS O2

54
Q

Transfusion Reaction

A

Acute hemolytic reaction

  • dx: decrease hgb, increase LDH, decrease haptoglobin, + Coombs test
  • tx: stop transfusion, maintain HDs, maintain UOP (fluids, diuretics), monitor for hyperkalemia, send blood back for re-cross match

Febrile non hemolytic reaction

  • most common
  • infl. from donor WBCs attacked by host antibodies
  • stop and determine if hemolytic
  • tx: acetaminophen (treat fever)
  • leukoreduction can reduce incidence

Urticarial

  • can continue transfusion
  • tx: diphenhydramine
  • washing pRBCs can reduce allergic reactions

Anaphylaxis

  • IgE mediated
  • Epi, antihistamines, steroids, fluids

TRALI
-donor antibodies react w/host WBCs–>inflammation and cytokines–>pulmonary capillary leakage

55
Q

Wide-Complex Tachycardia

A

If regular–>amiodarone 150 mg

If irregular–>probably a fib w/aberrancy
*BUT could be pre-excitated a fib (eg, WPW) in which case AV nodal agents (adenosine, diltiazem, verapamil, digoxin) are contraindicated as they can increase rate of transmission through accessory pathway and cause increased rates or VF

If any doubt–>amiodarone

56
Q

Local Anesthetic Reactions

A
  • true allergy to local anesthetics is rare
  • ester LAs have a higher incidence of allergic reactions
  • PABA (para-aminobenzoic acid) is a metabolite of esters that leads to hypersensitivity reactions (similar to methylparaben)
  • amides not metabolized to PABA
  • many manufacturers have reformulated and removed methylparaben as a preservative
  • MPF- methylparaben preservative free formulations are available
  • sodium metabisulfite is included in LAs containing epi to prevent oxidation
  • sulfite sensitivity is rare, and primarily affects a small subgroup of asthmatics
57
Q

Aortic Stenosis/Regurgitation Severity

A

AS: valve area

mild: 1.5-2.0 cm
moderate: 1.0-1.5 cm
severe: <1.0 cm
critical: <0.7 cm

AS: mean gradient
moderate: 25-40 mmHg

58
Q

Normal PAP, CI, etc

A

CO = 6 l/min
CI = 2.5-4.0 l/min/m2
CVP = <5 mmHg
*CVP > 12 indicate left heart failure

PAP: 25/15 mmHg
Mean PAP = 15 mmHg
PAWP = 10 mmHg
LVEDP = PAWP = 6-12 mmHg
*PCWP >18 mmHg in the context of normal oncotic pressure suggests left heart failure
SVR = 2000-2400 dyes*sec/cm5
PVR = <250 dynes*sec/cm5
PvO2 = 40 mmHg
SvO2 = 70% (65-75%)
59
Q

Pacemaker Settings

A

Paced-Sensed-Response

VOO: asynchronous ventricle-only pacing w/no regard to underlying rhythm

VVI

  • ventricle-only pacing
  • ventricle is sensed
  • if no event, ventricle paced
  • if ventricular activity sensed, pacemaker is inhibited
60
Q

Maximum Allowable Blood Loss

A

EBV x (Hi-Hf)/Hi

  • EBV = estimated blood volume
  • Hi = initial hematocrit
  • Hf = final lowest acceptable hematocrit
61
Q

Infective Endocarditis Prophylaxis

A

Dental Patients

  • previous IE
  • prosthetic heart material
  • unrepaired or partially repaired CHD
  • heart transplants w/valvulopathies
  • only for procedure that involve manipulation of gingival tissue or perforation of oral mucosa

NOT Indicated:
-GI/GU procedures

62
Q

Anticoagulants and Neuraxial Blocks

A

LMWH (enoxaparin)

  • Prophylaxis: 12 hours off, may resume 12 hours after block, no epidurals
  • Treatment: 24 hours off, may resume 24 hours after, no epidurals
  • restart 2 hours after catheter pull

Heparin

  • SQ prophylactic (both BID and TID): wait 4 hours to place, may resume immediately, wait 4 hours to pull epidural
  • IV: no recommendation to place(wait 4 hours?), may resume 1 hour after, wait 2-4 hours to pull
63
Q

Determinants of Myocardial Oxygen Consumption

A
  1. HR
  2. Contractility
  3. Wall tension

wall tension =(pressureradius)/2*wall thickness

64
Q

Potential Deleterious Effects of Excess Steroids

A 
Infection
Poor wound healing
Hyperglycemia
Fluid retention
Hypokalemia/hypernatremia
Fluid retention/hypertension
Immunosupression

*many side effects unproven or clinically insignificant

65
Q

Afterload Reduction in ST Changes

A

Nitroglycerin- if venodilation and preload reduction acceptable (causes afterload reduction and potentially relieves coronary vasospasm)
*Eg. LV dysfunction

Clevidipine- if venodilation and preload reduction unacceptable (reduces afterload some as well)
*Eg. AS

*CCB cause less venodilation than SNP and nitroglycerin)

66
Q

SNP and NG Mechanism of Actions

A

SNP

  • breaks down in circulation to release nitric oxide (NO)
  • it does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide
  • NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP
  • cGMP activates protein kinase G which activates phosphatases which inactivate myosin light chains
  • similar to PDE5 inhibitors (sildenafil)- increase cGMP levels by inhibiting breakdown by PDE5

NG

  • prodrug which is reduced to nitric oxide (NO)
  • activates GC–> increased levels of cGMP
67
Q

Uterine Atony

A
  • oxytocin
  • uterine massage
  • rectal misoprostol (PG), carboprost/hemabate (PG), and methergine (ergot alkaloid)
  • intrauterine balloon for tamponade (80% success rate)
  • uterine vessel clamping
  • hysterectomy
68
Q

INR and Factor Levels

A
  • INR 1.5 associated with 40% activity of Factor VII
  • vit k dependent: II, VII, IX, X
  • Normal hemostasis with 40% clotting factors
  • On discontinuation, Factor VII recovers quicker, leading to a quick reduction in INR (eg. to 1.5)
  • BUT, Factors II and X recover much slower, so INR could be normal but there’s not normal coagulation (<40% Factors II and X)
69
Q

PCCs

A

*II, VII, IX and X
(and Proteins C & S)

*Three factor PCCdoesn’t have VII

Indication

  • warfarin reversal
  • vit. K dependent clotting factor deficiency (liver disease)
  • hemophilia B (if pure factor IX is not available)
70
Q

BiPap and Pulmonary Edema

A

Contrary to popular belief, NIMV does NOT push edema fluid out of the lungs. Patients with acute CHF have an imbalance in the CO (cardiac output) of the right and left sides of the heart. With the inciting event (detailed above) the left ventricle becomes compromised but the right ventricle usually does not. So the right ventricle continues to pump forward a normal volume of blood but the left ventricle becomes unable to keep pace. Fluid backs up into the lungs resulting in capillary leak and pulmonary edema. With NIMV, the resultant positive intra-thoracic pressure decreases venous return (blood flowing back to the heart). This reduces right-sided CO to a level that the left heart can equal or even exceed. Fluid ceases to back up and will even begin to be reabsorbed as left ventricular CO improves. Pulmonary edema ceases to worsen and may even diminish, often rapidly.
*BiPap better than CPAP

71
Q

BMJ Review March 2005

NIV and Cardiogenic Pulmonary Edema

A

Cardiogenic pulmonary oedema (CPO) is a common medical emergency, and NIV has been shown to improve both physiological and clinical outcomes. From the data presented herein, it is clear that there is sufficiently high level evidence to favour the use of continuous positive airway pressure (CPAP), and that the use of CPAP in patients with CPO decreases intubation rate and improves survival (number needed to treat seven and eight respectively). However, there is insufficient evidence to recommend the use of bilevel positive airway pressure (BiPAP), probably the exception being patients with hypercapnic CPO. More trials are required to conclusively define the role of BiPAP in CPO.

72
Q

Crit Care Journal 2006 Meta-analysis

BiPap v CPAP in Cardiogenic Pulmonary Edema

A

BiPAP does not offer any significant clinical benefits over CPAP in patients with acute cardiogenic pulmonary oedema. Until a large randomized controlled trial shows significant clinical benefit and cost-effectiveness of BiPAP versus CPAP in patients with acute cardiogenic pulmonary oedema, the choice of modality will depend mainly on the equipment available.

73
Q

PDA Closure

A
  • with initiation of ventilation, arterial oxygen levels are increased and PVR decreases and flow reverses (L-R)
  • increased oxygen tension and rapid reduction in circulating PGs closes the ductus w/in 2-4 days after birth
  • hypoxia, especially in neonates, can lead to PDA as lower oxygen tension blunts stimulus for closure

*RFs: prematurity, hypoxia, RDS, acidosis

74
Q

Neonatal RDS

A
  • insufficient surfactant production (<35 weeks)
  • widespread atelectasis–>intrapulmonary shunting–>hypoxia and metabolic acidosis
  • CXR: ground glass (bilateral infiltrates) and reduce lung volumes (atelectasis)

*long term consequence: bronchopulmonary dysplasia

75
Q

Neonate monitoring for PDA closure (BP and pulse ox)

A

BP
-right arm: preductal BP preferred (left subclavian may be clamped in the event of massive bleeding from torn PDA)

Pulse ox

  • right arm (preductal) and either leg (post ductal)
  • can provide important information about shunting
  • R-to-L shunting reduces preductal oxygenation
  • aorta ligation–>loss of post ductal waveform
  • PA ligation–>decrease of pre and post ductal oxygenation (along w/decreased EtCO2)
76
Q

Retinopathy of Prematurity

A

RFs: prematurity (esp <32 weeks), LBW, cyanotic heart disease, RDS, hypoxia/hyperoxia

Goals: maintain oxygen saturation between 88-94% or PaO2 50-80 mmHg

*Relative hypoxia causes hypoxic pulmonary vasoconstriction–>increased PVR–>reduced shunt in L-to-R shunt (eg. PDA)

77
Q

Transfusion in Neonates

A

Threshold Hematocrit
<25%: healthy, full-term neonate
<40%: sick, premature neonate with reduced cardiac reserve

*Fetal hgb: left shift of oxy-hgb curve, increased oxygen consumption,

78
Q

Hypertension and Elective Surgery

A

> 180/110: delay elective surgery

79
Q

SVC Syndrome

A

S&S
-cough, SOB, JVD, headache, facial/neck/UE edema, chest pain, dysphagia, lightheadedness, orthopnea, hoarseness, nasal stuffiness, papilledema, visual changes, facial cyanosis, opacification of UE collateral veins on CT

Anesthetic Concerns

  1. airway mgmt 2/2 airway edema
  2. unreliable drug delivery through IVs in upper extremities
  3. compromised cerebral perfusion (increased cerebral venous pressure–>increased ICP–>impaired cerebral perfusion
  4. post respiratory complications: laryngospasm, bronchospasm, airway obstruction (2/2 airway edema and/or mass compression)

*difficulty airway equipment, minimize airway manipulation as much as possible to reduce edema, IV in lower extremity, maintain head up position to improve venous drainage and avoid increased airway edema and ICP, cautious fluid mgmt (too much leads to venous congestion, too little leads to decreased preload), avoid coughing/bucking during emergence (venous congestion and acute airway obstruction)

80
Q

Laryngeal Innervation

A

RLN

  • all intrinsic muscles of larynx, except cricothyroid muscle (SLN)
  • unilateral injury: abductor paralysis, w/affected cord in a paramedic position–>hoarseness
  • bilateral injury: partial v complete airway obstruction, respiratory distress w/stridor (reintubation or trach)

SLN (external branch)

  • cricothyroid muscle: tenses and adducts cords
  • injury: changes in voice quality, but not dangerous
81
Q

Postop Monitoring for OSA

A

7 hours after a postop apnea event (ASA Practice Guidelines 2006/2014)

82
Q

Central Diabetes Insipidus

A

Dx

  • copious amounts of urine despite rising serum sodium
  • increased serum osmolality
  • increased serum sodium
  • low urine specific gravity
  • increase in urine osmolality w/exogenous ADH

Tx

  • fluid replacement with 1/2 NS
  • desmopressin (DDAVP)
  • DDAVP: long-acting synthetic analogue of arginine vasopressin (made by the body)
83
Q

Thoracic Aortic Aneurysm Classification

A

DeBakey

  • Type 1: ascending aorta to descending aorta
  • Type 2: ascending aorta only (not beyond innominate artery)
  • Type 3: descending aorta (originates beyond left subclavian) and extend distal to diaphragm (IIIA) or to aorto-iliac bifurcation (IIIB)
  • Types 1 and 2 are surgical emergencies
  • Type 3 often treated medically

Stanford

  • Type A: ascending aorta (w/ or w/o arch or descending aorta) [includes DeBakey Types 1 and 2]
  • Type B: only descending aorta [includes DeBakey Types IIIA and IIIB)

*Type A most common (DeBakey 1 and 2)

84
Q

FEV1 Consistent w/Increased Risk of Postop Mechanical Ventilation

A

FEV1 < 2 L

*other parameters <50% predicted

85
Q

Spinal Drain

A

Passive drainage of CSF to a pressure of 10 mmHg

Spinal Perfusion Pressure = MAP - CSF (or CVP)
*autoregulation between 50-125 mmHg)

**aortic cross clamp–>cerebral hyperemia–>shifting of CSF in spinal compartment

86
Q

Signs of End Organ Dysfunction

A
  • lactate
  • low mixed venous O2 (<65%, nl 65-75%)
  • capillary refill >2 sec
  • ST changes
  • SSEPs/MEPs (spinal cord perfusion)
  • elevation in BUN/Cr
87
Q

PAC Signs of MI

A

Prominent a waves
-atrium contracts into a stiff LV

Increased PAOP and PA Diastolic Pressure
-ischemia induced increases in LVEDP

88
Q

Spinal Cord Blood Supply

A

Posterior 1/3 of spinal cord

  • two posterior spinal arteries
  • sensory

Anterior 2/3 of spinal cord

  • single anterior spinal artery
  • motor
  • artery of Adamkiewicz serves major supply to the anterior, lower 2/3 of spinal cord (usually left side, around T10)
  • when aortic cross-clamp applied distal to this radicular artery, risk of spinal cord ischemia is extremely low
89
Q

Hypotension on Aortic Cross-Clamp Release

A

Primary cause: central hypovolemia and resulting decrease in preload

Secondary cause:

  • distal tissue ischemia and vasoactive mediator release–>drop in SVR
  • distal tissue ischemia and acid metabolites–>decreased myocardial contractility, increased PVR, and increased capillary permeability
90
Q

Pseudocholinesterase and Other Esterases

A

Pseudocholinesterase

  • sux and mivacurium
  • also some ester local anesthetics

Non-specific plasma esterase
-remifentanil and ester local anesthetics

RBC esterase
-esmolol

91
Q

Lithium Side Effects

A
  • arrhythmias (wide QRS, AV block)
  • skeletal muscle weakness and sensitivity to NMBDs (prolonged duration of action)
  • polyuria
  • siezures
92
Q

qSOFA

A

Quick Sepsis-related Organ Failure Assessment
*Bedside prompt that may identify patients with suspected infection who are at greater risk for a poor outcome outside the ICU

  1. SBP <100 mmHg
  2. RR >22
  3. AMS (GCS <15)
93
Q

Signs of Elevated ICP/Impending Herniation

A

Dilated pupils
Vomiting
Abnormal posturing
Altered LOC

94
Q

MH v NMS

A

Both

  • tachycardia, hyperthermia, mental status changes
  • hypercapnia, metabolic acidosis
  • muscle rigidity (not present in thyroid storm/pheo)

Distinguishing

  1. NMS exhibits a slower progression
  2. Non-depolarizers lead to flaccid paralysis in NMS
  • Dantrolene used in both (adjunct in NMS)
  • Bromocriptine, dopamine agonist, used in NMS
95
Q

Regional Anesthesia in Kidney Transplant

A

-has been done successfully

Disadvantages

  • sympathectomy and blood pressure management
  • potential for uremic coagulopathy (platelet dysfunction)
96
Q

PPV and PEEP in Heart Failure/Pulmonary Edema

A
  • reduced LV preload, thereby unloading the congested heart
  • reduced LV afterload due to decreased transmural (trans thoracic) pulmonary pressures
  • reversal of hypoxia-related pulmonary vasoconstriction-decreased work of breathing and overall metabolic demand
  • improved oxygenation that may optimize oxygen supply to the stressed myocardium
  • Caution
  • excessive reduction in preload can worsen cardiac function
  • overinflation of alveoli can result in barotrauma
97
Q

NSAID/ASA and Bleeding

A
  • inhibit platelet COX (cyclooxygenase)–>thereby blocking formation of thromboxane
  • inhibits thromboxane-dependent platelet aggregation and prolonging bleeding time
98
Q

Bleeding Time

A
  • measures platelet function
  • historically used in uremia
  • prolonged by platelet disorders, vWF disease, and DIC

*not supposed to be affected by coagulopathy from factors problems (warfarin, heparin) but not very reliable

99
Q

Epidural Opioids MOA

A

Bolus

  • diffuses across the dura into the CSF
  • binds w/opioid receptors in the dorsal horn of the spinal cord
  • modifies the transmission of pain impulses to the brain via and enhances the descending inhibitory pathway

Infusion
-likely a supraspinal mechanism (venous absorption)

100
Q

NSAID MOA

A
  • reduces PG synthesis via COX inhibition
  • PGs are potent mediators of inflammation and pain
  • Cox-1: “constitutive”, always present, normal protective functions (kidney, stomach, platelet function[thromboxane A2])
  • Cox-2: “inducible”, made in response to tissue injury, expressed mainly at sites of inflammation
101
Q

Type & Screen versus Type & Cross

A

Type & Screen
-mixes recipient plasma with a panel of commercial RBCs to detect antibodies

Type & Cross

  • mixes recipient plasma with donor RBCs to detect incompatibility with a specific unit to be administered
  • slightly lower chance for hemolytic reaction
102
Q

Carbon Monoxide Poisoining

A

S&aS

  • “flu-like” (or food poisoning): headache, N/V, dizziness, weakness, confusion, chest pain
  • high levels: LOC, arrhythmias, seizures, death
  • “cherry red skin”

Causes
-cigarettes, fires, heaters, vehicle exhaust, propane

Pathophysiology

  • carboxyhemoglobin has 250 times high affinity for oxygen than hemoglobin
  • left shift in oxyhemoglobin dissociation curve–> tissue hypoxia

Diagnosis
-co-oximetry
*<5% normal, smokers ~ 10%
*symptoms 10-30%, death >30%
*Falsely high pulse ox: carboxyhemoglobin exhibits same absorption of light at 660 nm (red) as oxyhemoglobin! (other is 940 nm [infrared])
*PaO2 unaffected
*SaO2 would be affected, except standard blood gas analyzers derive the SaO2 from the PaO2 (so may be normal even with severe CO poisoining)
Treatment
-100% oxygen via non-rebreather (reduces CO half-life from 6 hours to 90 minutes)
-hyperbaric oxygen
*consider co-existing cyanide toxicity if smoke inhalation

103
Q

Cyanide Toxicity

A

Pathophysiology
-uncoupling of oxidative phosphorylation–>interruption of aerobic metabolism–> shift to anaerobic metabolism–> decreased O2 consumption, elevated lactate and severe metabolic acidosis

S&aS

  • generalized weakness, malaise, collapse, neurologic symptoms, GI symptoms, and cardiopulmonary symptoms (SVT common)
  • “cherry-red skin”, smell of bitter almonds on breath

Dx

  • falsely reassuring Sp02 (no oxygen being consumed by cells)
  • labs: high lactate, normal O2, metabolic acidosis, abnormally high VBG O2
  • rule out carboxyhemoglobin on cooximetry
  • CN levels may be drawn but results are sluggish

Tx

  • primarily aimed at uncoupling cyanide from cytochrome oxidase, allowing cells to return to aerobic metabolism via oxidative phosphorylation
  • 100% O2, ETT if indicated
  • Hydroxycobolamin: combines with CN to form cyanocobalamin (vitamin B12), which is renally excreted; also few side effects and well-tolerated by critically ill
  • nitrites also used but slower onset and more side effects
104
Q

APGAR Scoring System

A

Appearance, Pulse, Grimace, Activity, Respiration

7-10 = normal
4-6 = low
0-3 = critical

*typically performed at 1 and 5 minutes after birth

105
Q

Amniotic Fluid Embolism

A

S&S

  • First (early) phase: pulmonary HTN (2/2 pulmonary vasospasm), hypotension (2/2 right heart failure), hypoxia (V/Q mismatch), seizure, and cardiac arrest
  • Second (late) phase: LV failure, pulmonary edema, and coagulopathy
  • many don’t survive first phase
106
Q

Headaches

A

Primary

  • migraine
  • tension
  • cluster

Secondary

  • tumor
  • SAH
  • meningitis
  • TMJ
107
Q

PaO2 & SaO2

A

PaO2 60 mmHg = SaO2 90%

Normal PaO2 90-100 mmHg

*PaO2 = 100 - Age (years over 40)

108
Q

Central Line Indications

A
  1. Monitor CVP
  2. Facilitate fluid resuscitation
  3. Administer vasoactive medications
  4. Provide access for a PAC
109
Q

Bone Cement Implantation Syndrome

A

S&S
-hypotension hypoxia, dysrhythmias, pulmonary HTN, decreased CO, and cardiac arrest

Pathophysiology Mechanisms

  1. hardening/expansion of cement increases intra-medullary pressures–>embolization of bone marrow debris
    - circulating
  2. circulating methyl methacrylate–>reduced SVR
  3. release of cytokines during reaming of femoral canal
110
Q

Jet Ventilation

A

Complications

  • pneumothorax, pneumomediastinum, subcutaneous emphysema, and inadequate gas exchange (ie hypoxia/hypercapnia
  • supraglottic: gastric distention, regurgitation, and gastric rupture
  • subglottic: inadequate exhalation, hyperinflation, air-trapping, increasing airway pressures and barotrauma
  • especially dangerous in advanced COPD (prolonged expiratory phase and risk of barotrauma w/bullae)
111
Q

Abdominal Compartment Syndrome

A

S&S
-oliguria, hypotension, increased airway pressures, decreased CO, distended abdomen, CNS (increased ICP and decreased CPP)

Dx
-Foley catheter intravesical pressure >25 mmHg

112
Q

Nitric Oxide (NO)

A
  • specific pulmonary vasodilator
  • inactivated with exposure to Hgb, so does not affect SVR
  • effectiveness may be enhanced by exogenous surfactant (d/t pulmonary recruitment)
113
Q

CVP Tracing

A

“a wave” = atrial pressure. Vanishes in atrial fibrillation

“c wave” = closure of the tricuspid valve

“x descent” = ventricular systole

“v wave” = atrial filling / tricuspid closing

“y wave” = tricuspid opening

114
Q

Pre and Post Ductal Pulse Oximeters

A

Identifies an increase in right-to-left shunting through PDA

*Or coarctation

115
Q

Epi v Norepi

A

Epi: alpha 1, alpha 2, beta 1, beta 2

Norep: alpha 1, alpha 2, minimal beta 1
*No beta 2

116
Q

NMDA Antagonists

A 
Ketamine
Methadone
Tramadol
Dextromethorphan
Nitrous Oxide
117
Q

Effect of Intracardiac Shunts on Anesthetic Induction

A

Right to Left (IV): rapid induction (easy to remember – blood bypasses lungs, straight to brain)

Right to Left (volatile): slower induction

Left to Right (IV): little effect on induction

Left to Right (volatile): little effect on induction

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