Sample Questions

The correct answer is: B: Lower extremity paralysis

Lower 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.

The correct answer is: B: Central sensitization involves receptor field expansion whereas peripheral sensitization does not

Peripheral 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.

The correct answer is: D: 5 cm H20 of CPAP to surgical lung

The 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.

The correct answer is: B: A transient, short lived leukopaenia

Transfusion 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.

The correct answer is: A: In the setting of high resistance, pressure does not guarantee sufficient flow

Ohms 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.

The correct answer is: C: The cardiac output (CO) has increased

Don’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 correct answer is: B: Decreased cardiac output

Make 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).

The correct answer is: D: Using a larger gauged catheter

This 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.

The 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.

The correct answer is: D: Delay the surgery for 2-3 months

Post-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).

The correct answer is: B: Increased gastric secretion

Opioids 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).

The correct answer is: B: Neostigmine

There 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.

The correct answer is: D: Interruption of sympathetic outflow

Propofol 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).

The correct answer is: D: Start a phenylephrine drip

The 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).

The correct answer is: C: Decreasing heart rate

This 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:

1. 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.
2. 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).
3. 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.
4. 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!)
5. 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.

The correct answer is: B: Decreased left atrial pressures

The 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.

The correct answer is: D: Rocuronium will not be effective

The 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.

The correct answer is: D: 600 mcg reliably produces respiratory depression in most individuals

By 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 correct answer is: A: Interruption of pathological increases in sodium retention

Lisinopril 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).

The correct answer is: B: Increased pACO2 in the alveoli

According to the alveolar gas equation PAO2 = (P_barometric - P_H2O) X [FiO2 – (Pa_CO2 / RQ)], high carbon dioxide levels can result in hypoxia at low FiO2s. The portion of the equation (P_barometric - P_H2O) is essentially fixed for a given atmospheric pressure and tends to be about 700. When FiO2 is low (21%); the portion of the equation (P_barometric - 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.

The correct answer is: C: Phenylephrine

This 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.

The correct answer is: E: Resuscitating hypovolaemic patients with normal saline will typically result in a hyperchloraemic acidosis

The 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 correct answer is: C: The difference between capnography measured end tidal CO2 (ETCO2) and arterial CO2 (PaCO2) increases

Jet 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 correct answer is: C: The surgeon has placed a temporary clip on a feeding vessel

There 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 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.