Sample Questions Here are 25 sample questions that are similar to the ones that you'll find within M5. 1. Cards 38. A patient with descending thoracic aortic dissection undergoes aortic cross-clamping during the repair. Which of the following is the most likely complication:A.Cerebral haemorrhageB.Lower extremity paralysisC.Foot dropD.Horner syndromeE.Monooccular blindnessYour Notes: Expand/Contract ExplanationThe correct answer is: B: Lower extremity paralysisLower extremity paralysis complicates up to 10% of thoracic aneurysm repairs and remains permanent in about half the cases. The typical presentation is anterior spinal artery syndrome where arteries feeding the anterior spinal artery off the aorta are interrupted or hypoperfused, especially the artery of Adamkiewicz. The artery of Adamkiewicz often is the primary source of blood flow for the lumbar and low thoracic anterior spinal cord. The anterior spinal cord includes tracks for motor, light touch, pain, and temperature; therefore, interruption of blood supply results in loss of these functions in the lower extremities. Proprioception, deep touch, and vibratory sense are often spared (supplied by paired posterior spinal cord arteries). Pressure monitoring distal to the cross clamp and neurological monitors (SSEPs) are used to identify when spinal cord ischaemia may be occurring. The primary treatment is deep hypothermia (decreasing cellular oxygen consumption), but intercostal reimplantation and shunts can be used to increase blood flow to the anterior spinal artery (increasing oxygen delivery). Since perfusion of the spinal cord is dependent on a pressure gradient between anterior spinal artery pressure and CSF pressure, a spinal drain can also be placed to decrease CSF pressures. Other common complications of aortic surgery (other than the usual suspects of bleeding, infection, etc) include myocardial ischaemia, renal failure, ARDS, and gut ischaemia. Cerebral haemorrhage 12 / 13% answers Lower extremity paralysis 67 / 70% answers Foot drop 7 / 7% answers Horner syndrome 8 / 8% answers Monooccular blindness 2 / 2% answers 2. PAIN 7. Peripheral sensitization differs from central sensitization in that:A.Peripheral sensitization involves substance P (sP) and calcitonin gene-related peptide (CGRP), whereas central sensitization does notB.Central sensitization involves receptor field expansion whereas peripheral sensitization does notC.Peripheral sensitization does not contribute to central sensitizationD.Antagonism of the NMDA receptor interferes with peripheral more than central sensitizationYour Notes: Expand/Contract ExplanationThe correct answer is: B: Central sensitization involves receptor field expansion whereas peripheral sensitization does notPeripheral sensitization can occur through chemical mediators (bradykinin, prostaglandin, substance P, etc, etc), heat, frequency of stimuli, as well as other factors. This leads to a decreased threshold for nociceptor stimulation (see PAIN 5 & 6), decreased response latency (allowing more frequent discharge), and after-discharge phenomenon (spontaneous firing after the stimulus is gone). Central sensitization is due to wind-up (see PAIN 4) and sensitization of second order neurons and WDRs through neurochemical mediators (CGRP, sP, etc) (answer A), NMDA mechanisms (see below), expansion of the receptive field (see below), among other mechanisms. Various processes, including neurochemical mediators can decrease the threshold for second order neuron firing to occur (think of the opposite effect as opioids, for simplicity). Wind-up (where a small response from first order neurons leads to a larger response from second order neurons) is a complex subject that appears to have a relationship with NMDA agonism. When the NMDA receptor is stimulated, intracellular calcium levels rise, leading to the production of some of the neurochemical mediators that sensitize the second order neurons and also increase the production of aspartate and glutamate (which stimulate the NMDA receptor) (answer D). You can think of this as a positive feedback loop that can quickly spiral out of control. Receptor field expansion occurs when dorsal horn neurons (especially WDR neurons) become responsive to stimuli to which they were previously unresponsive (nonnoxious stimuli now results in noxious signaling to the brain). This occurs in the spinal cord, not in the periphery (answer B). Answer C is incorrect because increased sensitization, and therefore signaling from the periphery can lead to wind up of WDRs and therefore, central sensitization. Peripheral sensitization involves substance P (sP) and calcitonin gene-related peptide (CGRP), whereas central sensitization does not 25 / 33% answers Central sensitization involves receptor field expansion whereas peripheral sensitization does not 28 / 37% answers Peripheral sensitization does not contribute to central sensitization 12 / 16% answers Antagonism of the NMDA receptor interferes with peripheral more than central sensitization 10 / 13% answers 3. CTV 7. During one lung ventilation (OLV) in the lateral decubitus position, the patient’s pulse oximeter slowly decreases from 100% to 88% despite being on 100% oxygen, 2% sevoflurane, 30 mg rocuronium, and 200 mcg fentanyl over the past 30 minutes. Blood pressure and heart rate are both stable and at the patient’s baseline. The surgeon is in a critical part of the dissection near the pulmonary artery (PA). The next best maneuver to increase the patient’s oxygen saturation in this circumstance would be:A.Blood transfusionB.Additional rocuroniumC.5 cm H20 of PEEP to dependent lungD.5 cm H20 of CPAP to surgical lungE.Immediate double lung ventilationYour Notes: Expand/Contract ExplanationThe correct answer is: D: 5 cm H20 of CPAP to surgical lungThe problem here is shunt, and despite hypoxic pulmonary vasoconstriction (HPV) the non-dependent surgical lung is receiving enough blood flow to account for the decreased saturations. By administering CPAP (with 100% oxygen), a portion of the previously shunted flow will now be able to participate in oxygen exchange, therefore decreasing shunt. PEEP to the dependent lung is also usually effective, although not as consistently as CPAP. The reason for this is, theoretically, the increased positive pressures at end-expiration (compared to 0 with no PEEP) could divert flow away from the ventilated dependent lung and towards the nonventilated surgical lung. The advantage of PEEP in increasing oxygenation by way of opening previously atalectatic alveoli in the dependent lung typically outweighs this, but not always. Double lung ventilation is the best way to increase oxygen sats in most circumstances, but can make dissection difficult for the surgeon. In this case, the surgeon is at a critical portion of the dissection and should not be used as it may result in damage to the PA. Blood transfusion may increase oxygen carrying capacity, but will not affect the patient’s oxygen saturation. Blood transfusion 4 / 5% answers Additional rocuronium 3 / 4% answers 5 cm H20 of PEEP to dependent lung 37 / 49% answers 5 cm H20 of CPAP to surgical lung 25 / 33% answers Immediate double lung ventilation 6 / 8% answers 4. HTF 19. A 25 year old woman underwent splenectomy after suffering blunt trauma from a motor vehicle accident. Intraoperaively she received 4 units of packed red blood cells (pBRCs) and 6 units of FFP. Near the end of the case her PaO2 had decreased from 250 on 80% fiO2 to 70, and was transported to the ICU intubated. 30 minutes later she had a PaO2 of 55 on a PEEP of 15, FiO2 100%. Chest X-ray (CXR) revealed bilateral ground glass opacities. Which of the following is consistent with her diagnosis:A.Onset of pulmonary oedema within 5 minutes of transfusionB.A transient, short lived leukopaeniaC.Average resolution of lung injury after 2 weeksD.Mortality rate is extremely lowYour Notes: Expand/Contract ExplanationThe correct answer is: B: A transient, short lived leukopaeniaTransfusion related acute lung injury (TRALI) is a significant transfusion related cause of morbidity and mortality. Its onset is typically within 2 hours, usually resolves within 48 hours, and causes a syndrome indistinguishable from ARDS/ ALI. The mechanism of TRALI and ARDS is very similar, that being capillary leak syndrome causing significant non-cardiogenic pulmonary oedema. The most popular theory for the mechanism of TRALI is transfused (donor) antibodies to HLA and other recipient antigens, although other theories exist. Also important in the theory of TRALI it requires two hits (two-hit theory of ARDS). The first hit causes sequestration of neutrophils to the lung (in this case the trauma). The second hit is the immune response as described above with activation of neutrophils and the entire immune response at the site of the lungs, explaining the well documented phenomenon of a transient leukopaenia. Onset of pulmonary oedema within 5 minutes of transfusion 26 / 40% answers A transient, short lived leukopaenia 20 / 31% answers Average resolution of lung injury after 2 weeks 18 / 28% answers Mortality rate is extremely low 1 / 2% answers 5. CTV 35. During carotid endarterectomy without a shunt, stump pressure is measured at 50 mm Hg throughout the procedure, but the patient is found to have a stroke by brain MRI in the watershed area on the ipsilateral side as the surgery. Which of the following statements BEST describes why this happenedA.In the setting of high resistance, pressure does not guarantee sufficient flowB.A large embolus probably occurredC.EEG should have been used instead of stump pressureD.A stump pressure of 75 mm Hg should always be used to guarantee against ischaemiaYour Notes: Expand/Contract ExplanationThe correct answer is: A: In the setting of high resistance, pressure does not guarantee sufficient flowOhms law V =I X R in this setting can be translated to MAP = Cerebral blood flow X cerebral vascular resistance. Stump pressure assumes that collateral FLOW must be present to cause the PRESSURE. However, with high resistance minimal flow can also cause high pressure. Watershed areas refer to areas where perfusion under normal circumstances have the least amount of overlap and these are likely areas of ischaemia in the setting of low perfusion states. A large embolism would have a focalized area of ischaemia. EEG is arguably the gold standard of cereberal monitoring under general anesthesia, but is no more efficacious than other means of monitoring, including awake patients. A higher stump pressure has the same theoretical problems than the original stump pressure has. In the setting of high resistance, pressure does not guarantee sufficient flow 40 / 62% answers A large embolus probably occurred 8 / 12% answers EEG should have been used instead of stump pressure 7 / 11% answers A stump pressure of 75 mm Hg should always be used to guarantee against ischaemia 10 / 15% answers 6. ICU 4: A patient’s mixed venous saturation (Satmv) is unchanged despite an increase in the oxygen consumption (VO2), which of the following statements is most likely true:A.The extraction ratio (ER) has increasedB.The ER has decreasedC.The cardiac output (CO) has increasedD.The Sata has decreasedE.The CO has decreasedYour Notes: Expand/Contract ExplanationThe correct answer is: C: The cardiac output (CO) has increasedDon’t over-think it, its an easy straight forward question. In this case the body is consuming more oxygen, but is not extracting more oxygen (which would lower Satmv), but has an unchanged Satmv. Therefore, the delivery of oxygen has HAD to increase, which is to say there was an increase in either CO, Hb, or Sata. It all comes back to the Fick equation, which is driven home hard in the ICU section. The extraction ratio (ER) has increased 9 / 14% answers The ER has decreased 4 / 6% answers The cardiac output (CO) has increased 48 / 74% answers The Sata has decreased 2 / 3% answers The CO has decreased 2 / 3% answers 7. VA 2. Which of the following would decrease volatile anesthetic uptake:A.An increased blood/gas partition coefficientB.Decreased cardiac outputC.Decreased partial pressure of the anesthetic in venous bloodD.Increased partial pressure of the anesthetic in the alveolusE.Decreased pulmonary shuntingYour Notes: Expand/Contract ExplanationThe correct answer is: B: Decreased cardiac outputMake sure you understand that this question is about uptake, not speed of induction (discussed below). We’ll go over how they are related soon. Anesthetic uptake describes the process of the volatile gas reaching the alveolus and being taken up by the (mixed) venous blood entering the pulmonary circulation. From there, the anesthetic agent redistributes throughout the body. The avidity to which the anesthetic is taken up from the alveolus to the venous blood depends on two major factors: First, the solubility of the agent. The more soluble the agent is in blood, the more anesthetic that will be taken from the alveoli. The partition coefficient describes this in terms of how much agent will be in the blood versus the alveolus (blood / gas partition coefficient). The higher the coefficient, the higher the concentration in the blood as compared to the alveolus (it’s a simple ratio) (answer A). The second major factor determining the avidity to which the anesthetic is taken up from the alveolus to the venous blood is the difference in partial pressures between the alveolus and the venous blood. The lower the partial pressure of the agent in the blood and the higher the partial pressure in the alveolus results in the greatest pressure difference between the alveoli and pulmonary venous blood (answers C & D). Recall that gas moves from high to low pressure and that as the pressure increases (without changing resistance), so will flow (that is flow of the anesthetic from alveoli to blood). The final determinant of uptake is pulmonary blood flow. The more blood the alveoli are exposed to, the more uptake that will occur (duh!). By decreasing cardiac output, pulmonary flow decreases, and thus uptake of the anesthetic agent in the alveoli (answer D). Increasing a pulmonary shunt would do the same thing, as the alveoli are not exposed to the venous blood. Therefore, decreasing a shunt, and exposing the alveoli to more pulmonary circulation will lead to more uptake (answer E). An increased blood/gas partition coefficient 29 / 50% answers Decreased cardiac output 19 / 33% answers Decreased partial pressure of the anesthetic in venous blood 6 / 10% answers Increased partial pressure of the anesthetic in the alveolus 3 / 5% answers Decreased pulmonary shunting 1 / 2% answers 8. MON 7. Which of the following would most likely have prevented an arterial artery thrombosis following invasive arterial blood pressure monitoring:A.Using propylene catheters instead of TeflonB.Using a shorter catheterC.Performing an Allen’s test prior to catheterizationD.Using a larger gauged catheterE.Leaving the catheter in for a longer period of timeYour Notes: Expand/Contract ExplanationThe correct answer is: D: Using a larger gauged catheterThis question is good practice for two reasons. First, it’s a high yield subject. Second, it’s very confusing and designed to trick you. A larger gauged catheter is actually smaller than a smaller gauged catheter (18g vs 20g). Allen’s tests have not been shown to predict thrombosis following arterial lines (answer C). The length of catheterization and size of the catheter have the most effect (answers D & E). Other factors that increase the likelihood of ischaemia following arterial line placement are propylene composition (answer A), high dose vasopressors, artery size, puncture attempts (possibly), and female gender. Longer catheters (answer B) may be (counter-intuitively) somewhat protective. Using propylene catheters instead of Teflon 12 / 21% answers Using a shorter catheter 19 / 34% answers Performing an Allen’s test prior to catheterization 11 / 20% answers Using a larger gauged catheter 13 / 23% answers Leaving the catheter in for a longer period of time 1 / 2% answers 9. MUS 3. A scientist wants to study the effects of depolarizing muscle relaxants on a myasthenia gravis rat model. Which of the following would best serve his purpose:A.Breed for variant with mutant acetylcholine (Ach) receptors that has lower affinity for Ach moleculesB.Pretreatment with a competitive inhibitor at the alpha subunit of the Ach receptor prior to treatment with depolarizing muscle relaxantC.Pretreatment with an irreversible inhibitor at the alpha subunit of the Ach receptor prior to treatment with depolarizing muscle relaxant D.Breed for variant with increased perijunctional voltage gated sodium channelsE.Pretreatment with a drug that reduces the presynaptic accumulation of Ach in the neuron at the neuromuscular junctionYour Notes: Expand/Contract ExplanationThe correct answer is: C: Pretreatment with an irreversible inhibitor at the alpha subunit of the Ach receptor prior to treatment with depolarizing muscle relaxant Of the available choices, only C could be used to mimic myasthenia gravis. This is also an example of a question in which the reader (you) could be lead astray by making too many assumptions. Myasthenia gravis is a condition in which there are a decreased number of normal (answer A) Ach receptors on the muscle endplate. Because of this, exposure to normal doses of depolarizing muscle relaxants may not activate enough Ach receptors to result in perijunctional depolarization and thus Phase I block (see question 2). In this situation an increased dose of the depolarizing muscle relaxant is needed (to bind to just about every receptor possible) to result in depolarization. Pretreatment with a competitive inhibitor of the Ach receptor is the same as pretreatment with nondepolarizing muscle relaxants; which also, in a way mimics myasthenia gravis, in so far as that fewer receptors are available at any given time for Ach binding. Competitive binding can be overcome by increased doses of Ach. Irreversible inhibition of the Ach receptor (answer C) will more closely mimic myasthenia gravis, as at a certain dose will inhibit many, but not all, Ach receptors. Because the inhibition is noncompetitive, increased doses of depolarizing muscle relaxants cannot overcome the inhibition. In this case, like myasthenia gravis, the ability of the muscle membrane to depolarize will be based on how many Ach receptors are activated, and if there are not enough Ach receptors available (for binding), depolarization (and thus phase I block) will be impossible. Answer E, reducing the amount of presynaptic Ach, is mimicking Eaton-Lambert. Answer D, is not related to the problems of myasthenia gravis or Eaton-Lambert. Note that the ABA is madly in love with myasthenia gravis and Eaton-Lambert and its relationship with muscle relaxants (as it requires a very complete knowledge of both disease process and understanding of how neuromuscular blockers work). See Neurology Questions 24, 25, 26, 27,and 28 for more on this important concept. Breed for variant with mutant acetylcholine (Ach) receptors that has lower affinity for Ach molecules 9 / 18% answers Pretreatment with a competitive inhibitor at the alpha subunit of the Ach receptor prior to treatment with depolarizing muscle relaxant 19 / 37% answers Pretreatment with an irreversible inhibitor at the alpha subunit of the Ach receptor prior to treatment with depolarizing muscle relaxant 16 / 31% answers Breed for variant with increased perijunctional voltage gated sodium channels 2 / 4% answers Pretreatment with a drug that reduces the presynaptic accumulation of Ach in the neuron at the neuromuscular junction 5 / 10% answers 10. Neo34. You are responsible for reviewing medical records of a patient scheduled to undergo surgery at your surgery center. She is a 4 week old infant born at 36 weeks for inguinal hernia. All medical records indicate that despite a premature birth, the patient has been healthy and developing normally. Your response to this request is to:A.Allow the case to proceedB.Allow the case to proceed as long as IV caffeine is givenC.Allow the case to proceed so long as the patient is within the 25percentile of weight for ageD.Delay the surgery for 2-3 monthsE.Delay the surgery for one yearYour Notes: Expand/Contract ExplanationThe correct answer is: D: Delay the surgery for 2-3 monthsPost-anesthetic apnea in the newborn is an oral boards classic and is definitely a written boards potential as well. Post-anesthetic apnea can both be central and/or obstructive and has numerous risk factors, the greatest being pre-existing apnea. Other major risk factors are post-conceptual age at time of surgery (see below), post-conceptual age at birth, anaemia, hypothermia, infection, and various neurologic disorders. For otherwise healthy infants, most authors suggest delaying elective surgery (particularly where the patient is discharged home) until the infant is 44-60 weeks (most favor above 50). For patients with apneic spells, or pulmonary disease (such as bronchopulmonary dysplasia), surgery should be delayed until the patient is at least 6 months old. Risk of apnea can be decreased with IV caffeine or aminophylline, but the child should still be at least 44 weeks post-conceptual age (answer B). Low birth weight is a risk factor, not weight at time of surgery (answer C). Note that the patient is 40 weeks post-conceptual age in the question (36 weeks at birth + 4 weeks today). Allow the case to proceed 14 / 25% answers Allow the case to proceed as long as IV caffeine is given 2 / 4% answers Allow the case to proceed so long as the patient is within the 25percentile of weight for age 8 / 15% answers Delay the surgery for 2-3 months 23 / 42% answers Delay the surgery for one year 8 / 15% answers 11. AA30. Which of the following are NOT effects of opioids:A.Urinary retentionB.Increased gastric secretionC.Decreased lower esophageal sphincter toneD.Stimulation of the chemotactic trigger zoneYour Notes: Expand/Contract ExplanationThe correct answer is: B: Increased gastric secretionOpioids have many undesired systemic effects and you should expect that you will get a question on these. The effects vary on drug and dose, and most sources do a poor job of making large sweeping generalizations that’s easy to remember. So, lets make some generalizations, even though there are exceptions, so we have a starting point. Gastrointestinal and genitourinary symptoms are often overlooked by anesthesiology residents, partly because they are not emphasized in clinical practice (we think CNS, respiratory, and cardiac) and the complications of these drugs often present after the patient has left the PACU. Urinary retention is seen early and often following neuraxial (especially spinal) opioids but do occur with systemic opioids as well (mediated by mu and delta receptors). The urinary retention is typically responsive to very low dose naloxone. Opioids decrease GI motility, gastric secretions, and pancreatic secretions. These effects are partially reversed with methylnaltrexone (an opioid antagonist that cannot pass the blood brain barrier), which I mention here because it might show up on the boards but not worthy of an entire question devoted to it. Opioids also decrease lower esophageal tone and increase GERD symptoms. In the biliary track, opioids increase the tone of the sphincter of Oddi, which in severe cases can lead to symptoms of abdominal distress, angina-like chest pain, and increased amylase & lipase. Opioids also likely directly stimulate the chemotactic trigger zone and increase nausea and vomiting. Other board worthy effects of opioids as discussed elsewhere and within this section are respiratory depression through decreasing CO2 responsiveness, increased OSA symptoms, decreased cough reflex, muscle rigidity, decreased sympathetic outflow, and some opioids stimulate a large amount of histamine release (morphine, meperidine). Urinary retention 5 / 10% answers Increased gastric secretion 37 / 71% answers Decreased lower esophageal sphincter tone 6 / 12% answers Stimulation of the chemotactic trigger zone 4 / 8% answers 12. NPA 23. Which of the following can lead to worsening contractures in a patient with myotonic dystrophy (MyoD):A.AtropineB.NeostigmineC.RocuroniumD.HyperthermiaE.DantroleneYour Notes: Expand/Contract ExplanationThe correct answer is: B: NeostigmineThere are four big perioperative concerns with patients with MyoD for anesthesiologists 1) contractures; 2) sensitivity to anesthetics; 3) aspiration risk; and 4) theoretical increased risk of malignant hyperthermia (which is probably FALSE!). Regarding contractures, three big things to avoid: 1) succinylcholine (see neurology question 21 – sustained contractures); 2) reversal of muscle relaxation with anticholinerestases (sustained contractures); and 3) hypothermia leading to shivering and then contractures. Contractures can be so severe, ventilation and intubation is impossible. Atropine 2 / 4% answers Neostigmine 33 / 60% answers Rocuronium 6 / 11% answers Hyperthermia 12 / 22% answers Dantrolene 2 / 4% answers 13. IA 4. Following a 2 mg/kg dose of propofol, a patient has profound hypotension. Which of the following LEAST likely contributed to this:A.Decreased systemic vascular resistance (SVR)B.Decreased left ventricular end-diastolic volume (LVEDV)C.Decreased stroke volumeD.Interruption of sympathetic outflowE.Impaired baroreceptor reflexYour Notes: Expand/Contract ExplanationThe correct answer is: D: Interruption of sympathetic outflowPropofol can be thought of primarily as an afterload reducer (answer A), but also affects preload (answer B) and contractility (answer C). Propofol affects the baroreceptor response to hypotension as well. Recall that the baroreceptors decrease their rate of firing in response to hypotension, therefore decreasing sympathetic inhibition, see Cardiac Physiology Question 14. Although this would technically be interruption of sympathetic outflow, this is still the only answer that is not clearly correct, so you are forced to choose it. This is the type of questions that residents find unclear and ambiguous on the boards (sadly). Decreased systemic vascular resistance (SVR) 9 / 17% answers Decreased left ventricular end-diastolic volume (LVEDV) 6 / 11% answers Decreased stroke volume 4 / 7% answers Interruption of sympathetic outflow 17 / 31% answers Impaired baroreceptor reflex 18 / 33% answers 14. NEU 2. A 25 year old man following traumatic brain injury (TBI) has a measured intracranial pressure (ICP) of 28 cc H20 through an external ventricular drain (EVD), and mean arterial pressure (MAP) of 60. The EVD has been draining 12 cc of cerebral spinal fluid (CSF) an hour and is set to drain above a pressure of 20 cm H20. Which of the following is the next most important step in this patient’s management:A.Decrease the level of the drain to 15 cm H20B.Apply intermittent suction to the EVDC.Flush the EVD with 20 cc of warm salineD.Start a phenylephrine dripE.Measure a CVPYour Notes: Expand/Contract ExplanationThe correct answer is: D: Start a phenylephrine dripThe patient is likely not adequately perfusing his brain secondary to high ICP (intracranial hypertension). ICP can rise from an increase of any of the three main components within the cranial vault: 1) CSF (obstruction, overproduction, decreased clearance); 2) Blood volume (increased perfusion as with hypertension or decreased vascular resistance, obstruction to venous return as with very high CVPs); and 3) Brain tissue (cerebral oedema). An EVD can be placed both to measure the ICP as well as drain fluid. When the ICP is greater than the EVD ‘pop-off’ pressure, CSF fluid is drained. In cases of rapid ICP increases, the CSF cannot drain as quickly as ICP increases. Other causes of an ICP being elevated with EVD in place include insufficient amount of CSF, restrictions on how much CSF can be drained per hour, and a kinked or obstructed catheter. Flushing 20 cc of saline into the ventricle with high ICPs is dangerous as it may further increase ICP. Applying suction to an EVD is idiotic, hopefully for obvious reasons. Decreasing the ‘pop-off’ of the EVD to 15 cm H20 will not help as the ICP is already greater than the level of the drain. Lowering the CVP would only help if it were greater than CSF, and there is no indication in the stem that the CVP would be greater than 28 cm H20 (which would likely be an error anyway if it read that high). Phenylephrine will raise the MAP to increase perfusion (MAP – ICP). Decrease the level of the drain to 15 cm H20 10 / 19% answers Apply intermittent suction to the EVD 1 / 2% answers Flush the EVD with 20 cc of warm saline 6 / 11% answers Start a phenylephrine drip 30 / 56% answers Measure a CVP 7 / 13% answers 15. Basic Card 8. Which of the following interventions will MOST LIKELY effectively treat a patient with left circumflex coronary artery stenosis having lateral wall st-depressions:A.Decreasing diastolic blood pressureB.Increasing left ventricular end diastolic volumeC.Decreasing heart rateD.Dilating coronary arteriesYour Notes: Expand/Contract ExplanationThe correct answer is: C: Decreasing heart rateThis is a tricky one to say the least. The point here is to make you think, not provide you the fairest of questions; although this does have two classic features of real board questions: it’s a bit ambiguous and may seem to have two correct answers!Coronary perfusion is a complex subject, but to simplify it can be thought of in terms of Ohm’s law where flow is dependent on the ratio of perfusion pressure to resistance. Perfusion pressure for the left ventricle (LV) is defined as aortic diastolic pressure minus LV end diastolic pressure (LVEDP) and only occurs during diastole. Resistance can be manipulated by coronary dilation. Coronary dilation occurs when the myocardium is not receiving enough oxygen, often from inadequate flow. When myocardial oxygen consumption outpaces delivery one can either:Increase aortic diastolic pressure that will increase coronary perfusion pressure. Potential downside: it will increase LV afterload and (depending on degree of increase in BP and the patient’s LV function) can decrease cardiac output and therefore coronary flow. Also increased afterload means increased LV wall tension, which means more O2 consumption.Decrease LVEDP, which will result in a greater proportion of time that aortic diastolic blood pressure is greater than LVEDP and therefore have perfusion (depending on coronary resistance). Downside: if associated with too great a reduction of LVED blood volume (and therefore pressure) it can also decrease cardiac output (by decreasing preload).Slowing heart rate, which will increase the time in diastole and lead to more time for perfusion. Also myocardial oxygen consumption will decrease (O2 consumption will fall greater by decreasing HR than decreasing afterload or contractility). Downside: hardly any assuming the HR is not so low cardiac output falls too far.Decreasing contractility, which will decrease LV wall tension and therefore myocardial oxygen consumption. Downside: can decrease cardiac output especially at its extremes. (Notice that beta blockers do a nice job of decreasing heart rate and LV wall tension!)Dilating coronary arteries can shift blood away from stenotic coronary distributions (LCx in this case) that are absolutely dependent on high perfusion pressures to overcome the resistance to normal areas. This is called coronary steal (you need to know this term) and it is a real thing…on the boards. In reality, in most cases there is plenty of pressure and blood for everyone (all coronary distributions), but this is the boards and that is why this choice would be the second best and not the best answer to the ambiguous question.Finally, we harp on this over and over, but it’s important: dealing with ambiguous questions requires a strategy. It’s important to not bring in any baggage to the stem with you. The stem did not tell you anything about the patient’s heart rate, blood pressure, etc. Therefore, when you read through the answer choices, for this question you should say, “Could, in some situations, decreasing diastolic BP lead to resolution of iscahemia?” The answer would be yes: in some, but not many situations. If you ask yourself this question you’ll find that there are three potential right answers, with decreasing diastolic BP requiring a very unique situation (increased myocardial strain due to hypertension) and the other two potentially correct choices (decreasing HR and increasing coronary dilation) being far better choices and generally correct in most situations. The final step is to tease through the two remaining choices. Note that the stem said there was coronary stenosis, not occlusion. Therefore there is a potential (or at least theoretical) downside of coronary dilation. Hang in there, you hate me now, but you’ll love me later. Decreasing diastolic blood pressure 5 / 9% answers Increasing left ventricular end diastolic volume 4 / 8% answers Decreasing heart rate 31 / 58% answers Dilating coronary arteries 13 / 25% answers 16. OB 52. A 28 year old G5P0 woman with severe mitral stenosis has expired during C-section. Review of the record shows that a spinal anesthetic was chosen and ACLS protocol was initiated 3 minutes following the neuraxial block. After 5 minutes of ACLS the fetus was emergently delivered. The record also demonstrates that the patient was unable to be intubated by the anesthesiologist and an LMA was used during the code. Which of the following describes the most likely cause of death for this patient:A.An increased pressure gradient across the mitral valveB.Decreased left atrial pressuresC.Bradycardia, leading to flash pulmonary oedemaD.Obstruction of venous return by the gravid uterusE.Chemical pneumonitis of alveoliYour Notes: Expand/Contract ExplanationThe correct answer is: B: Decreased left atrial pressuresThe combination of mitral stenosis and obstetrics is a boards classic, and even today it’s seen occasionally (often following rheumatic fever as a child). The most likely cause of death was decreased preload secondary to the sympathectomy generated from the spinal anesthetic. Decreased venous return to the left atrium decreases pressures. In mitral stenosis, high left atrial pressures are required for flow across the stenotic valve (see Cardiac Physiology 26). Decreased flow leads to a decreased (not increased) pressure gradient across the mitral valve (answer A). Tachycardia can precipitate flash pulmonary oedema in mitral stenosis (by requiring higher flows across the valve to maintain cardiac output, thereby generating higher left atrial pressures), not bradycardia (answer C). Also, the stem did not point towards pulmonary oedema or hypoxia being the underlying reason for the patient’s demise. Obstruction of the uterus on inferior vena caval flow can significantly impede cardiac resuscitation and delivery of the fetus should have occurred earlier, but this is not what caused the patient to crash. Although an LMA was used due to difficult airway, aspiration may have occurred (answer E), but again, was not the cause of the presentation. An increased pressure gradient across the mitral valve 20 / 37% answers Decreased left atrial pressures 23 / 43% answers Bradycardia, leading to flash pulmonary oedema 7 / 13% answers Obstruction of venous return by the gravid uterus 2 / 4% answers Chemical pneumonitis of alveoli 2 / 4% answers 17. Peds35. A 15 year old boy has masseter muscle spasm (MMS) and generalized rigidity following succinylcholine administration and the CRNA suggests rocuronium be given to break the spasm and improve surgical conditions, you reply:A.A succinylcholine gtt should be used insteadB.Cisatracurium would be a better choiceC.Diphenhydramine should be used insteadD.Rocuronium will not be effectiveE.Nitrous oxide may have contributed to the rigidityYour Notes: Expand/Contract ExplanationThe correct answer is: D: Rocuronium will not be effectiveThe patient is likely in the early stages of malignant hyperthermia (MH), as rigidity is the single most specific sign. Both non-depolarizing and depolarizing muscle relaxants such as rocuronium and answers A & C act at the muscle end plate. Acetycholine signals do not result in action potentials under blockade, therefore voltage gated calcium channels do not open, and calcium induced release of calcium (CIRC) does not occur (resulting in sarcoplasmic release of calcium and muscle contraction). However, in MH, the muscle endplate is circumvented as CIRC continues without any input from neuron signaling. Therefore, MH is unaffected by muscle relaxants (answer D). Nitrous oxide is not a triggering agent for MH (answer E), only succinylcholine and halogenated volatile agents. A succinylcholine gtt should be used instead 2 / 4% answers Cisatracurium would be a better choice 6 / 11% answers Diphenhydramine should be used instead 2 / 4% answers Rocuronium will not be effective 42 / 78% answers Nitrous oxide may have contributed to the rigidity 2 / 4% answers 18. REG 26. Which of the following is most true regarding intrathecal morphine:A.The late respiratory depression peak incidence occurs 24 hours after injectionB.Analgesia onset is similar to that of sufentanylC.Rostral spread is very similar to that of meperidineD.600 mcg reliably produces respiratory depression in most individualsE.Is a first line intrathecally delivered opioid for outpatient procedures.Your Notes: Expand/Contract ExplanationThe correct answer is: D: 600 mcg reliably produces respiratory depression in most individualsBy learning intrathecal fentanyl (regional anesthesia question 25) and morphine, you can essentially get a gauge of other opioids as they represent the two extremes: lipophilic (fentanyl, sufentanyl) and hydrophilic (morphine). Because morphine is hydrophilic (lipophobic), it crosses the dura slower and has a much longer lifespan within the CSF than fentanyl. Because of the slow clearance of the drug (and its hydrophilic properties) it has the greatest rostral spread among opioids. This means two important (board-worthy) things: First, a lumbar intrathecal injection will produce analgesia well into high thoracic levels. More lipophilic drugs like fentanyl will create a more narrow band around the site of injection. Drugs less lipophilic than fentanyl and less hydrophilic than morphine like hydromorphone or meperidine will have an intermediate level of rostral spread (answer C). Second, because of its long duration of action and high rostral spread, respiratory depression has two peaks, an early peak and a late peak. Like all opioids, soon after intrathecal injection, opioids can be detected in the CSF surrounding the brainstem, which can lead to respiratory depression. Unlike other opioids, morphine’s slow rostral spread leads to another peak of respiratory depression at about 6 hours after injection (answer A), but can occur later. A 600 mcg dose (less than 300 mcg is typical) leads to late respiratory depression in most people. Also, because of the late peak in respiratory depression, intrathecal morphine should not be used for outpatient procedures. Analgesia from intrathecal morphine has a slow onset (answer B) due to its hydrophilic nature and duration of action (in most cases) longer than 24 hours. Peak analgesic effects are typically at 6-12 hours after injection. The late respiratory depression peak incidence occurs 24 hours after injection 25 / 45% answers Analgesia onset is similar to that of sufentanyl 10 / 18% answers Rostral spread is very similar to that of meperidine 6 / 11% answers 600 mcg reliably produces respiratory depression in most individuals 11 / 20% answers Is a first line intrathecally delivered opioid for outpatient procedures. 4 / 7% answers 19. REA 14. A patient with congestive heart failure (CHF) is prescribed lisinopril and spirinolactone in addition to carvedilol, furosemide, and potassium supplements due to decreased ejection fraction (EF). What is the reason for lisinopril?A.Interruption of pathological increases in sodium retentionB.Decrease myocardial preloadC.Decrease plasma creatinineD.Prevent increases in potassiumE.To block angiotensin I receptorsYour Notes: Expand/Contract ExplanationThe correct answer is: A: Interruption of pathological increases in sodium retentionLisinopril is an angiotensin converting enzyme (ACE) inhibitor, which interrupts the conversion of angiotensin I to angiotensin II, and therefore the rennin angiotensin aldosterone (RAAS) (See renal question 6). Low cardiac output due to CHF with low EF decreases renal blood flow and thus glomerular filtration rate (GFR). Decreased GFR, as well as increased sympathetic discharge from low cardiac output causes increased rennin secretion from the juxtaglomerular apparatus, which causes stimulates the RAAS finally resulting in aldosterone release and increased sodium retention. Afterload increases from angiotensin II as well as fluid overload from sodium retention results in worsening cardiac function, decreasing cardiac output, and decreased GFR; which then further stimulates the RAAS. It is a pathological cycle that can be interrupted by ACE inhibitors or angiotensin II receptor blockers (ARBs). Interruption of pathological increases in sodium retention 30 / 58% answers Decrease myocardial preload 9 / 17% answers Decrease plasma creatinine 1 / 2% answers Prevent increases in potassium 4 / 8% answers To block angiotensin I receptors 8 / 15% answers 20. Resp 14. A patient has an elevated PaCO2 of 70 in the PACU following morphine administration for pain. She is breathing comfortably at a rate of 10, breath sounds are clear, CXR reveals normal lungs, and she is breathing room air. Her pulse oximeter reads 88%, what is the most likely reason for her hypoxaemia.A.Increased dead space lesion from residual anestheticB.Increased pACO2 in the alveoliC.Hypoxic inhaled gas mixtureD.Pulmonary oedemaE.Intracardiac shuntYour Notes: Expand/Contract ExplanationThe correct answer is: B: Increased pACO2 in the alveoliAccording to the alveolar gas equation PAO2 = (Pbarometric - PH2O) X [FiO2 – (PaCO2 / RQ)], high carbon dioxide levels can result in hypoxia at low FiO2s. The portion of the equation (Pbarometric - PH2O) is essentially fixed for a given atmospheric pressure and tends to be about 700. When FiO2 is low (21%); the portion of the equation (Pbarometric - PH2O) X FiO2 is about 150. Since RQ is typically 0.8, when the PaCO2 is 70, PaCO2 / RQ is almost 90. 150 – 90 = 60. Therefore the calculated PAO2 is 60, and if one is to assume a minimal A-a gradient (good lungs), PaO2 would be somewhat less than 60, easily corresponding to saturation such as 88%. Note that just by understanding the equation, actually calculating the numbers is unnecessary. Increased dead space lesion from residual anesthetic 9 / 16% answers Increased pACO2 in the alveoli 36 / 65% answers Hypoxic inhaled gas mixture 2 / 4% answers Pulmonary oedema 4 / 7% answers Intracardiac shunt 4 / 7% answers 21. VASO 16. Which of the following vasopressive agents would be the least likely to lead to increased intracellular cyclic adenosine monophosphate (cAMP):A.EpinephrineB.EphedrineC.PhenylephrineD.DobutamineE.MilrinoneYour Notes: Expand/Contract ExplanationThe correct answer is: C: PhenylephrineThis is a high yield question for the boards. You should be familiar with what receptors each vasopressor activates. The beta receptors (which answers A, B, & D activate) leads to a G-protein (Gs to be specific) mediated stimulation of adenylate cyclase which converts adenosine triphosphate (ATP) to cAMP, which has downstream effects as discussed in Vasopressor Question 17, ultimately leading to increased intracellular calcium concentrations. cAMP is metabolized by phosphodiesterases, which milrinone (answer E) inhibits the action of this enzyme. Therefore, beta-1 or -2 receptor activation increases cAMP production and phosphodiesterase inhibitors decrease the degradation of cAMP. In either case, cAMP levels rise. Phenylephrine has only very weak beta-1 agonism and is rather specific for the alpha-1 receptor. Alpha-1 receptor agonism also leads to increased intracellular levels, but not through cAMP. The alpha receptor, also a member of the g-protein receptor family, stimulates phospholipase C, splitting phospiatidyl inositol (into inositol triphosphate and 1,2-diacylglycerol), leading to release of calcium from the sarcoplasmic reticulum. Epinephrine 5 / 9% answers Ephedrine 10 / 18% answers Phenylephrine 20 / 36% answers Dobutamine 3 / 5% answers Milrinone 17 / 31% answers 22. TBO 1. A 25 year old man is tachycardic and hypotensive following a chest stab wound in the ED. Which of the following is true regarding this patient’s resuscitation:A.The patient likely has cardiac tamponade and should proceed to the OR prior to fluid resuscitationB.Normal saline is associated with better outcomes than with of lactated ringersC.Albumin is preferred over crystalloids in severe hypovolaemiaD.If administered prior to hospital arrival, hypertonic saline solution decreases mortality as compared to isotonic crystalloidsE.Resuscitating hypovolaemic patients with normal saline will typically result in a hyperchloraemic acidosisYour Notes: Expand/Contract ExplanationThe correct answer is: E: Resuscitating hypovolaemic patients with normal saline will typically result in a hyperchloraemic acidosisThe most important step in a patient’s resuscitation following establishing an airway, is fluid administration. Even in the setting of anaemia, adequate volume resuscitation (to increase cardiac output and therefore oxygen delivery) with crystalloid solutions can be life saving. If only normal saline is used, a hyperchloraemic acidosis can result due to the large chloride load (leading to bicarb spilling from the kidneys to maintain electroneutrality) and a resultant non-gap hyperchloraemic acidosis. The acidoisis is almost always of no clinical significance and resolves within a couple days (at most). The crystalloid versus colloid argument is forever unresolved and except in specific populations, no difference in meaningful outcome has been proven (answer C). Lactated ringers is slightly hypotonic, whereas normal saline is slightly hypertonic, but again, this has not led to a clinically significant outcome difference (answer B). The lactate in lactated ringers is converted to bicarbonate in the liver, thus preventing the hyperchloraemic acidosis seen with normal saline. Hypertonic saline (3%, 5%, 7.5%) is an inexpensive, easily stored and transported volume expander that has found significant use in the military (for those reasons). There are theoretical advantages to hypertonic solution (probably most importantly is decreased cerebral oedema), but again, no mortality difference has been found on numerous metaanalyses (answer D). Finally, there is not evidence for tamponade in this patient, and either way, immediate transfer to the OR would not be the first step. The patient likely has cardiac tamponade and should proceed to the OR prior to fluid resuscitation 7 / 13% answers Normal saline is associated with better outcomes than with of lactated ringers 4 / 7% answers Albumin is preferred over crystalloids in severe hypovolaemia 5 / 9% answers If administered prior to hospital arrival, hypertonic saline solution decreases mortality as compared to isotonic crystalloids 3 / 6% answers Resuscitating hypovolaemic patients with normal saline will typically result in a hyperchloraemic acidosis 35 / 65% answers 23. EYE 12. During a resection of a small tumor under direct laryngoscopy, a jet ventilator is attached to a side port of a laryngoscope for oxygenation. Which of the following is true:A.The patient is being oxygenated with an inspirational oxygen concentration of 100%B.The oxygen pressure inside the jet ventilator is higher than the attached supplying oxygen hoseC.The difference between capnography measured end tidal CO2 (ETCO2) and arterial CO2 (PaCO2) increasesD.The arterial O2 (PaO2) will decrease linearly with timeE.Spontaneous ventilation is required for effective oxygenationYour Notes: Expand/Contract ExplanationThe correct answer is: C: The difference between capnography measured end tidal CO2 (ETCO2) and arterial CO2 (PaCO2) increasesJet ventilation can be used during direct laryngoscopy to provide apneic oxygenation. A small side port is attached to the surgeon’s laryngoscope and high pressure (~50 psi) oxygen is directed towards the trachea in short bursts. The oxygen hose typically delivers about 40-50 psi, but looses pressure as it flows through the jet ventilator side port, but gains velocity. This principle is known as the venture effect (answer B). The high velocity stream of oxygen actually entrains room air, therefore lowering the overall FiO2 (answer A). In this setting, oxygenation is active, but ventilation is passive. Without patient effort, CO2 slowly diffuses out of the lung and consequently, CO2 is retained. Because ventilation (CO2 removal from the lungs) is passive (and ineffective), capnography underestimates the CO2 concentration in the alveoli (~ETCO2). Therefore the difference between the capnography value and PaCO2 value increases. Oxygenation, on the other hand, is well preserved, well over a half hour (assuming the jet ventilator is being used appropriately) (answer D). Jet ventilation is unnecessary if spontaneous ventilation is present (answer E). The patient is being oxygenated with an inspirational oxygen concentration of 100% 13 / 25% answers The oxygen pressure inside the jet ventilator is higher than the attached supplying oxygen hose 9 / 17% answers The difference between capnography measured end tidal CO2 (ETCO2) and arterial CO2 (PaCO2) increases 26 / 50% answers The arterial O2 (PaO2) will decrease linearly with time 1 / 2% answers Spontaneous ventilation is required for effective oxygenation 3 / 6% answers 24. NEU 25. Prior to clipping a large aneurysm, the surgeon requests an induced hypertension to a mean arterial pressure (MAP) of 85. Which of the following is most likely true:A.The surgeon is incompetent and should be reported to the medical boardB.Outcomes are improved when clipping large aneurysms at high MAPsC.The surgeon has placed a temporary clip on a feeding vesselD.There is uncontrolled bleeding on the fieldYour Notes: Expand/Contract ExplanationThe correct answer is: C: The surgeon has placed a temporary clip on a feeding vesselThere are (at least) two general strategies in clipping aneurysms. The traditional approach is placing the clips directly beside the aneurysm. In this case, a low MAP is associated with a decreased chance of bleeding, and it is even reasonable to induce hypotension with propofol, thiopental, nicardipine, nipride, or other drugs just prior to the clip placement. Even administration of adenosine to temporarily stop cardiac output is a reasonable option in some cases. The second strategy is to place a temporary clip on feeding vessel(s) so that the blood flow at the aneurysm is decreased (or even absent). In this case, induced hypertension may be needed to maintain perfusion pressure in collateral distributions to the feeding artery. The surgeon is incompetent and should be reported to the medical board 4 / 7% answers Outcomes are improved when clipping large aneurysms at high MAPs 11 / 20% answers The surgeon has placed a temporary clip on a feeding vessel 38 / 69% answers There is uncontrolled bleeding on the field 2 / 4% answers 25. VASO 25. Regarding the metabolism of sodium nitroprusside, which of the following is false:A.Haemoglobin (Hb) is converted into Met-HbB.Haeme is reduced from ferric (+3) to ferrous (+2)C.Cyamet-Hb is producedD.Thiocynate is producedE.Cyanide binds to cytochrome oxidaseYour Notes: Expand/Contract ExplanationThe correct answer is: B: Haeme is reduced from ferric (+3) to ferrous (+2)Everyone hates chemistry, but there are some things that have high potential of coming up on the boards, met-Hb and cyanide toxicity being two big ones. Nitroprusside produces both of these phenomenon. Nitroprusside is a nitrate that acts by a series of steps, first by entering red blood cells (RBCs). Inside the RBC, the chemical accepts an electron from the 2+ ferrous oxy-Hb and oxidizes it to a +3 Met-Hb. Before your eyes gloss over, lets go through this and simplify things. The haeme molecule incorporated in Hb has an iron atom which can have more electrons (Fe 2+), or fewer electrons (Fe 3+). Oxygen only likes haeme with more electrons, giving it a lower charge (+2), also known as ferrous state. When nitropruside is exposed to ferrous (2+) Hb, it takes an electron away, leaving the iron in the ferric (3+) state, which is called met-Hb. The nitroprusside molecule becomes unstable with the additional electron and breaks into five cyanide molecules (CN-) and nitric oxide. The nitric oxide goes on to stimulate guanylate cyclase, increasing cGMP (see Vasopressor question 20), producing vasodilation. The CN- molecules go on to bind one of three things. It can bind the met-Hb, producing cyamet-Hb (answer C), it can bind cytochrome oxidase in the electron transport chain (answer E) or bind with thiosulfate, producing thiocynate. The thiocynate is cleared by the kidney, but is moderately toxic in itself. Don’t worry, we have more questions to go over on this subject to get this concept down. Haemoglobin (Hb) is converted into Met-Hb 9 / 16% answers Haeme is reduced from ferric (+3) to ferrous (+2) 30 / 55% answers Cyamet-Hb is produced 5 / 9% answers Thiocynate is produced 8 / 15% answers Cyanide binds to cytochrome oxidase 3 / 5% answers Loading... JOIN THE M5