ICU Principles

The correct answer is: E: Hb X Sata X 1.34

Of the above answers, E is the most accurate. Oxygen content is essentially how much oxygen is held by the blood. Hb is the major carrier of blood and the saturation of Hb tells you what % of binding sites are occupied. The coefficient of 1.34 is a conversion factor because one gram of Hb can bind 1.34 ml of O2. Left out of the equation is the amount of oxygen dissolved in the blood (not bound to Hb) which equals: 0.003 X PaO2. Notice that a normal PaO2 is in the neighborhood on 100 and when multiplied by 0.003 = 0.3 ml O2. Assuming the Hb is 14 and the Sata is 100%, the oxygen content of the Hb portion of blood is almost 19.

Oxygen transport and consumption are major subjects on the boards and you HAVE to understand (as well as memorize) the equations. In fact, once you start thinking in terms of oxygen, numerous other concepts will start making a lot more sense. Here are some very important equations you MUST know

* not including the amount of O2 dissolved in blood for simplicity
^ a more common way memorized, but not my preference

The correct answer is: C: Decreased CO, Decreased Hb, and/or decreased Sata

Sat_mv is a measure of how much oxygen the body consumed (VO2) relative to how much was delivered (DO2). If more oxygen is delivered, and the VO2 stays the same, the Sat_mv will increase. Therefore, by increasing the Hb, increasing the Sat_a, or increasing the CO, more oxygen will be delivered to the organs. On the other hand, if VO2 decreases less oxygen will be consumed also rising the Sat_mv. Conversely if the Sat_mv decreases then either the VO2 increased, or the CO, Hb, and/or Sat_a decreased. This means that Satmv can be used a surrogate for how well the body is perfused, theoretically. In reality, organ specific deficits in perfusion and interruption in normal oxygen handling on the cellular level (especially in critically ill patients) can make this value less meaningful.

You will often see Sat_mv  expressed as Sv_o2, but here we use the term Sat_mv to not confuse the reader with ScV_O2 (central venous O2 saturation) 

The correct answer is: B: Hb is the principle determinant of oxygen content

A very easy question, but you have to have this concept down cold. The PaO2 evaluates the efficacy of gas exchange. As mentioned above (question 1), the amount of dissolved oxygen in blood is very little compared to that bound to Hb. Therefore Hb is the principle determinant of the ‘level’ or content of oxygen. Hb saturation curve is plotted against PaO2, because the PaO2 at various levels determines the % saturation of Hb.

The correct answer is: C: The 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 Sat_a.  If the extraction ratio increases then the mixed venous sat would be lower.  

The correct answer is: A: Hyperthermia

An increase in P50 means that it requires an increased PaO2 to saturate half the binding sites of Hb. This is also called a right shift which occurs with acidosis, increased 2,3 DPG, & hyperthermia. A left shift occurs with alkalosis, hypothermia, decreased 2,3 DPG, as well as abnormal Hb species such as metHb, carboxyHb, & foetal Hb.  So remember that a higher p50 means a right shift and a lower p50 means a left shift.  You should know what a normal p50 is.  You've seen this graph a million times, so don't let a little exam trick of giving you only the p50 miss an otherwise easy question.

The correct answer is: A: 1=D; 2=E; 3=C; 4=B; 5=A

These are all important values to know for the boards, as well as normal PA pressures, CVP, wedge pressures, cardiac indices, and ventilation parameters. Note that when VO2 is 250 and VCO2 of 200 the RQ is 0.8.

The correct answer is: C: This likely represents an example of dysoxia

The patient has a declining DO2 due to decreasing CO as well as worsening oxygenation (Sata), and therefore extracting more oxygen which decreases the Satmv. Satmv this low is indicative of very high oxygen extraction due to inadequate delivery of oxygen. The point where VO2 decreases due to the DO2 decreasing (no more oxygen can be extracted) is called dysoxia. In actuality it is probably not a simple as this stem makes it out to be. Organ specific dysoxia can occur with far higher Satmv than 60%.  

Dysoxia has been a buzzword as a way to understand shock.  Basically, when VO2 starts outpacing DO2, the mixed venous sat will start dipping below 70% (70-75% is around normal).  It is not uncommon to see very critically ill patients as well as those with low cardiac outputs ("heart patients") in the 50's (I've seen far lower as well, but on an exam you should be concerned about anything less than 70%).  So what do you do when your patient has a Satmv?  Consider if DO2 is ok: arterial saturation low (increase FiO2, PEEP), Hb low (transfusion), cardiac output low (inotrope, fluid bolus, etc).  If you have no further optimization options for DO2, start thinking about decreasing VO2 (decrease temperature, decrease nutrition (generally bad idea), paralyze (generally bad idea), etc).  

The correct answer is: C: The pH is low because there is insufficient oxygen in the final step in the electron transport chain

Oxygen is used for aerobic metabolism which produces 38 ATP molecules per molecule of glucose (although in reality it is likely less than that). Glucose byproducts are used to supply the citric acid cycle, which donates electrons to the electron transport chain (ETC). The ETC pumps H+ out of the mitochondria, creating a H+ gradient across the membrane. ATP synthase essentially allows H+ to re-enter the mitochondria and uses the energy to form ATP. When oxygen is not present, the ETC comes to a halt (O2 accepts the electrons donated by the citric acid cycle). In this situation cellular respiration is anaerobic and far fewer ATP molecules are produced. Additionally, lactic acid accumulates causing an anion gap metabolic acidosis.

The correct answer is: A: CO 8.2, Satmv 67%

The patient to most benefit from a blood transfusion is one who is anaemic; that is to say with a high CO and a low Satmv. The high CO is a compensatory mechanism to increase oxygen delivery in the absence of an ability to increase oxygen content. When the CO can no longer increase to overcome VO2 demands, the tissues will start to extract a greater percentage of oxygen from Hb, decreasing Satmv. Therefore, Satmv is a relatively good way to determine who truly needs blood transfusions when reasonable assumptions can be made about CO. Notice that Answer B also has a low Satmv, but because the CO is low, a blood transfusion alone is less likely to benefit the patient than the patient described in A. This is yet another example of a question with two potential right answers. Get used to it, it’s all over the boards.

The correct answer is: B: Nicardipine – decreased afterload, decreased myocardial wall tension and therefore myocardial O2 consumption

Of the available options, B makes the most sense. Decreasing myocardial wall tension decreases myocardial oxygen consumption, which in turn would decrease the overall VO2, therefore increasing Satmv. NTG primarily decreases preload, not afterload. A decrease in preload would also decrease myocardial O2 consumption and therefore VO2. A nipride gtt could in fact cause cyanide toxicity, decreasing oxygen consumption and increasing Satmv, but this is less likely than choice B given it has only been used for an hour. In the case of cyanide poisoning the Satmv would be elevated, but the patient would in fact be hypoxic at a cellular level, relying on anaerobic metabolism and developing a significant acidosis.

This is admittedly a strange question, but it integrates some basic principles of antihypertensives with their effects on VO2...not a concept one usually thinks about but an angle the ABA may want to "trick" you with.

The correct answer is: A: Cirrhosis, CI 5.2, arterial Sat 92%

This is a tough one, lets go through each in turn.  A cirrhotic patient tends to have high cardiac index (CI) as well as a propensity for peripheral AV shunting both of which cause an increased mixed venous sat (SVO2), since a lot of oxygen is delivered and with AV fistulas, less O2 will be consumed.  Low arterial saturations are common in ESLD patients due to an increased shunt fraction due to atalectasis and pulmonary AV fistulas which . This does limit DO2 (oxygen delivery), but the very high CO compensats for the low arterial saturation.

The septic patient tends to have an elevated Satmv (on exams!) because of high CO and decreased utilization of oxygen (sick mitochondria), but given the very low Hb and a PaO2 which correlates to a saturation in the low 90s, the oxygen delivery is still likely lower than the patient in choice A.

The patient in choice C has a lot of Hb, but a low CO in all likelihood.  Even though each cc of blood can carry more oxygen than the other patients, he is unable to substantially increase the DO2 due to the poor heart function.

A hyperbaric chamber can increase PaO2, but cannot make a Hb molecule more than 100% saturated which accounts for the great majority of oxygen content. This patient would likely have a high-normal Satmv, not an elevated one.

Finally in real life, nothing works quite this nicely (most cirrhotics do not have a very high mixed venous and most septic patients have a low mixed venous), but the point of this is how to analyze a stem, sort through clues, and pick the most likely answer.

The correct answer is: C: Sepsis

The other answers would be reasons that the Satmv would decrease. The LEAST likely reason would be sepsis as described above. Sepsis is classically thought of a reason for an elevated Satmv. It should be noted the reason for this is not entirely clear. Mitochondrial oxygen utilization is impaired, which would in that sense decrease the consumption of oxygen. However, there is a wide spread activation of the immune system, referred to as the ‘respiratory burst,’ where overall oxygen consumption is in fact increased. The increase in Satmv is most likely due to increased oxygen delivery primarily through increased CO.

The correct answer is: D: Increased stroke volume (SV) and heart rate

An increase in VO2 should cause a decrease in Satmv all other things being equal (at least on the boards).  By increasing DO2 in proportion to the increased VO2, we can achieve the original Satmv. Therefore, since the Stamp did not change, the DO2 must have increased.  You can increase the DO2 by increasing the cardiac output (stroke volume X HR), increasing the saturation of haemoglobin (Hb), or increasing the amount of Hb.   

Alkalosis and a left shift of the oxy-Hb curve would cause less oxygen to be made available to the tissues, slightly decreasing DO2. Increased PEEP may increase DO2 but if you are only increasing the saturation of Hb by 1% point, then the actual increase in DO2 would be great enough to counter the 20% increase in DO2 seen in this question.  Increased minute ventilation does not necessarily increase your arterial saturation.

The correct answer is: B: Bohr effect

This is a backwards stated question because Bohr effect essentially means that increasing CO2 binding to Hb (by increasing PaCO2) will cause an increased release of oxygen (in other words right shift). Therefore, the opposite must be true, that hypocarbia causes a left shift. Haldane effect is similar. This states that when deoxygenated, Hb can bind more CO2 (and therefore work as a buffer). Fick principle is what we’ve been talking about all along, relating oxygen delivery to consumption. LaPlace’s law relates pressure to wall tension [Pressure = (2 X Tension X Wall Thickness)/ Radius].

The correct answer is: D: Increase in carbohydrate proportion in TPN

The RQ is the balance between the production of CO2 and consumption of O2, or VCO2/ VO2. Nutrition can effect CO2 production in that carbohydrates, protein, and fat produce 1.0, 0.8, and 0.7 units of CO2 for every unit of O2 consumed. In patient’s nearing respiratory failure, decreasing carbohydrates and increasing lipids can decrease the overall RQ meaning the patient needs to expel LESS CO2 per O2 consumed. The other answers will not change the RQ.

The correct answer is: E: Decreased PaCO2

This is a simple respiratory question that is included in this section because the term VCO2 is used. Even though the pregnant patient is producing more CO2, her resting PaCO2 decreases due to increased minute ventilation. Also recall that this is a question about PAO2 (and PaO2), so the alveolar gas equation is important to understand: [(Patm – PH20) X FiO2] – PaCO2/ RQ. The term [(Patm – PH20) X FiO2 is fixed for this question, but when PaCO2 decreases, so does – PaCO2/ RQ. Therefore the PAO2 rises. This is the exact opposite question of Question 14 in the respiratory physiology section that you hopefully have reviewed prior to this specialty section. Answer C, an increased RQ would also cause this change, but RQ does not change with pregnancy, whereas PaCO2 does. Shunt and dead-space would affect the PaO2, but not really the PAO2. Haldane effect is discussed in ICU 14.

The correct answer is: B: Carbonic anhydrase (CA) is primarily found in the RBCs and endothelium, and is responsible for bicarbonate formation from CO2

CO2 is readily dissolvable and can be found throughout the body. CA helps catalyze the formation of bicarbonate from water and CO2, thus acting as a continual sink for CO2. CA is found in the endothelium and RBCs. Bicarbonate made in the RBC diffuses out, which continually favors the formation of bicarbonate proportional to how fast it diffuses out. The majority of blood CO2 is held as bicarbonate in the plasma and RBCs. In the pulmonary system, the bicarbonate re-enters the RBC, forms CO2 and diffuses out the lungs because the alveolus acts as a continual sink for CO2. CO2 itself can bind Hb which accounts for only a small portion of blood CO2.

The correct answer is: C: 46

The PmvCO2 is normally about 46 as it enters the lungs and is 40 as it exits (PaCO2).

The correct answer is: A: The patient was started on dobutamine

That was a very easy review question. If you got it wrong, stop and go back to the start. This is a huge concept on the boards and you have to have this down. Increased CO increases oxygen delivery (DO2) and therefore (assuming oxygen consumption (VO2) does not change) a lower ratio of oxygen needs to be extracted.  Dobutamine is primarily a B1 agonist and predictably increases CO.  Also note that if you were to give a blood transfusion and increase the Hb (without decreasing CO due to increased viscosity), the mixed venous saturation would also rise.  

The correct answer is: B: Pulmonary artery wedge pressure of > 18

ARDS is a result of an inflammatory response (often systemic) resulting in diffuse and inhomogeneous pattern of alveolar damage. Alveolar damage is often thought of occurring in two steps. First, the inflammatory response (cytokine release, etc) causes capillary leak syndrome, causing the capillary contents to extravasate to the lung. Second, immune cells (neutrophils, lymphocytes) enter the damaged alveoli leading to further damage and eventually fibrotic changes. Surfactant production in the lungs also decreases. On CXR this appears as bilateral ground glass to opaquely appearing opacities classically sparing the costophrenic angles. On CT one can see that the distribution of damage is very inhomogeneous with areas of extremely diseased lung next to areas of seemingly normal lung. P/F ratios are less than 200 for ARDS. The same picture with an increased P/F ratio from 200-300 is referred to as either acute lung injury (ALI) or more recently mild ARDS (which makes more sense since it is the same disease). ARDS is a disease of the lungs, so evidence of LV failure can complicate the presentation. Classically, the definition has included a wedge pressure < 18 to essentially rule out a cardiogenic cause of the pulmonary oedema. One of the problems of using wedge pressures in ARDS is that even patients with normally compliant hearts can suffer from ARDS-induced pulmonary hypertension causing a rightward bulge of the intraventricular septum, thus increasing left ventricular end diastolic pressures and wedge.

The correct answer is: D: Decreasing tidal volume when plateau pressures are greater than 30 cm H2O

As mentioned above, ARDS has an inhomogeneous distribution of diseased lung and more normal lung. The normal lung is more compliant, therefore air flow preferentially is directed there. This means that when large tidal volumes are used to ‘blow-up’ the diseased alveoli, it is more likely just causing barotraumas to the normal lung, worsening the disease. Therefore, new(er) ventilation strategies have been directed towards decreasing the ‘transpulmonary pressure gradient’ or more commonly thought of as its surrogate, the plateau pressure. Plateau pressures less than 30 are associated with improved outcomes. To make things easy for us simpletons, an algorithm was formed where tidal volumes are initially set at 6 cc/ kg of ideal weight ** and decreased if plateau pressures are elevated (> 30). PEEP is added for two reasons: First, and foremost, to improve oxygenation. By opening previously closed alveoli, gas exchange is improved. The second benefit is to reduce the trauma of continual opening and closing which is another story in and of itself. The concept of permissive hypercapnea means that so long as the patient is oxygenating, ventilation need not be increased to normalize the pH (answer A). You can think of addressing three concepts that make a ventilation strategy "lung protective:"

• Atelectrauma: lung injury and inflammation from repetitive opening and closing of alveoli - treatment is PEEP
• Volutrauma: lung injury and inflammation from alveolar stretch - treatment is small tidal volumes
• Barotrauma: lung injury and extra-alveolar air from high pressures - treatment is keeping plateau pressures under 30 and small tidal volumes

The correct answer is: B: Decrease PEEP

This is a very tricky question, and there are tricky questions on the boards. The most obvious thing wrong with the patient is the respiratory acidosis and secondly the low BP. Since PaO2 is good (for a patient with severe ARDS), the reflexive action would be to work on the respiratory acidosis. A lung protection strategy infers that keeping plateau pressures under 30 cm H20 improves outcomes (which is true), but its much more complicated than that…of course. The patient has the ‘ideal’ tidal volume producing a plateau pressure less than 30 cm H20, so the natural tendency would be to increase tidal volume in response to the low pH. However, the data from subsequent studies has shown that there is NO safe upper limit of tidal volumes or plateau pressures and the focus should be on maintaining small tidal volumes. When plateau pressures rise above 30 cm H20, this is reason to decrease tidal volumes, BUT the converse is not true: when plateau pressures are below 30 cm H2O, it is not a reason to increase tidal volumes. Therefore both answersIncrease and Decrease tidal volumes are incorrect. Since the patient has an acceptable PaO2 and mild hypotension, decreasing the PEEP may maintain an acceptable level of oxygenation while improving BP (due to its effects on cardiac preload by way of increased end expiratory intrathoracic pressures). Notice how ‘increasing the respiratory rate,’ was not an option, as that would be an acceptable thing to do to treat the mild acidosis.

The correct answer is: E: Small tidal volumes

Small tidal volumes have been proven to improve outcome in ARDS time and time again. Many data are pointing towards a less liberal fluid strategy for improved outcome as well (less fluid results in better pulmonary dynamics but overall outcome has not been proven beyond a reasonable doubt).  Exogenous surfactant is a hallmark treatment of respiratory distress syndrome (RDS) in premature newborns, but not adults. ARDS and RDS have many similarities and there is, in fact, a surfactant deficiency in ARDS. Nitric oxide can reduce shunt fraction by improving perfusion to well ventilated areas, but does not change outcome (it vasodilator those capillary beds near ventilated alveoli only with no systemic effect). High dose steroids was once popular, but also doesn’t seem to improve mortality (may be more helpful in some specific populations). Prone position studies have had mixed results in select populations but there does appear to be a real benefit.

The correct answer is: E: Pneumonia

Pneumonia and sepsis are the most common triggers for ARDS. Other major causes include those listed above as well as mechanical ventilation itself, aspiration, and drug overdose.

The correct answer is: A: Increase PEEP

The patient is hypoxic which can likely be overcome by either increasing PEEP or FiO2. Both have potential disadvantages. Increased FiO2, especially over 60% for > 48 hours may result in increased oxygen free radicals and oxygen toxicity, therefore worsening the underlying disease (ARDS)*. Increased PEEP increases mean airway pressures, decreases preload, and high levels can itself cause diffuse alveolar damage*. Additionally, PEEP can lead to pneumothorax, pneumopericardium, and subQ air. Between the two, PEEP is probably safer in the long term. There is no indication to decrease tidal volume as plateau pressures are less than 30 already. As discussed above, there probably is never a time to increase tidal volume. Changing from AC to SIMV makes no significant change in ventilation strategy as at high pressure supports, AC and SIMV are nearly indistinguishable.

As an aside, as an astute M5 member pointed out, strictly adhering to the ARDSnet protocol, the next move would be to increase FiO2, not PEEP. That being said, the ABA has steadfastly chosen increasing PEEP as the correct answer in this and similar situations, and I suggest you choose increasing PEEP provided you have room to go up on the plateau pressure. 

*Although oxygen toxicity is assumed, it is unclear what dose (how high of oxygen tension and for how long) and what patient factors (type of pulmonary edema, genetic, phenotypic) predispose to this phenomenon.

The correct answer is: A: A decrease in RR, minimal change in pH

The patient is tachypneic and failing what appears to be an early attempt near weaning (decreased RR, lack of PS). By increasing PS, spontaneous breaths now only supported with a PS of 5 cm H2O will have an increased tidal volume. Recall that PaCO2 level is a major determinate in ventilation levels; therefore to maintain the current PaCO2 level with an INCREASED tidal volume, RR will decrease. If RR did not decrease, then minute volume would increase and PaCO2 would decrease. With decreased PaCO2, the ventilatory drive will decrease (see Respiratory question 16), thus decreasing RR. If the patient was on an increased ventilator rate, the PaCO2 would no longer be controlling the additional amount of ventilation, it would now be the ventilator itself. In this setting, the minute volume can be increased and pH can rise significantly (respiratory alkalosis). If the patient had a respiratory acidosis (instead of a normal pH), increasing PS may, in fact, increase pH as well due to treatment of the respiratory failure.

The correct answer is: C: It is not as comfortable for patients as compared to inverse ratio ventilation

APRV is an increasingly utilized ventilatory strategy which employs two levels of continuously applied positive pressure (essentially two levels of CPAP), one very high, and one very low. During the high pressure time, alveoli are opened and oxygenation is improved. Just like increasing PEEP with traditional modes, increasing the high CPAP level can also improve oxygenation. A brief period (0.4-0.8 seconds) of low pressure (0-5 cm H2O) interrupts relatively long periods of high CPAP (4-8 seconds), allowing for CO2 removal (ventilation). The patient can spontaneously breathe at both levels of CPAP comfortably, unlike inverse ratio ventilation which is very distressing to patients. Pressure support can also be added to spontaneous breathing, but mean airway pressures (think plateau pressures) should be checked and ensure they stay below 30.

The correct answer is: C: Daily spontaneous breathing trial (SBT)

Patients who have favorable ventilatory dynamics, such as low PEEP (< 8 cm H20), FiO2 < 50%, PaO2 > 60, haemodynamically stable, etc should be given daily SBTs as it has been proven to liberate patients from the ventilator quicker than other methods including the physician’s best estimate. One of the most important measurements to be made is the rapid shallow breathing index (RSBI), which is respiratory rate divided by tidal volume. A RSBI under 100 (105 to be exact) is consistent with successful extubations. This is by no way random facts, but is standard of care now and on my oral boards.

The correct answer is: D: Venturi face mask at 8 L/ min adjusted to FiO2 of 35%

The patient requires supplemental oxygen but had CO2 narcosis with high FiO2 supplementation (see Respiratory question 17 for further explanation of this concept, long story short the supplemental O2 increases VQ mismatch and CO2 builds up). Therefore the FiO2 should be adjusted so that the lowest needed FiO2 is delivered for resolution of hypoxia (PaO2 > 60). The venturi face mask utilizes high flows of oxygen which entrain air into the mask through adjustable side holes by the Venturi effect. A simple mask can deliver relatively unpredictable FiO2 (30-60%) depending on the rate of oxygen flow, minute ventilation, and mask fit. High flows through nasal cannula are poorly tolerated and cause significant mucosal drying in the nose.

Here's some simplified rules of thumb:

• 2L nasal cannula: FiO2 ~25%
• 6L nasal cannula: FiO2 ~ 40%
• Simple face mask: FiO2 ~ 50%
• Venturi mask: can adjust accurately for FiO2 desired
• Non-rebreather: FiO2 >90%

The correct answer is: A: Tidal volumes are not guaranteed

In a theoretical sense, pressure control does not guarantee a tidal volume because decreased lung compliance can significantly decrease volume. Obviously in such a situation one would check the patient and machine, possibly increasing the level of pressure delivered to increase tidal volumes, but that was not part of the question and should not be assumed when answering this question. With pressure control, inspiratory times are commonly time cycled (pressure is delivered for a certain amount of time) until either a certain amount of volume has been given or not. When there is no cut-off on the amount of volume that can be delivered it is referred to as pressure limited (most common way PC is used in the OR), as tidal volume is purely a function of the pressure delivered. With VC, a certain volume is delivered and is typically limited by pressure to avoid volutrauma for noncompliant lungs or inappropriately large settings. Answers B and C are neither advantages or disadvantages, just simply descriptions of how the ventilator works. Both PC and VC can be synchronized.  Synchronized breaths are synchronized to either a change in pressure (the patient generates a certain negative pressure) or more commonly a certain flow rate (once a certain flow is achieved, the breath is initiated).  Pressure support is similar to pressure control except there are no control breaths (no minimal respiratory rate).

The correct answer is: A: Endotracheal tubes (ETTs) in place for more than 2 weeks is a risk factor for subglottic stenosis

Subglottic (not supraglottic) stenosis is a very serious risk factor when ETTs are left in for 3+ weeks, although even at 2 weeks can be a risk factor. If the patient were to be extubated soon, it may be wise to leave the ETT in, but this patient will require a long term artificial airway so a tracheostomy is favored. Its worth noting that the dogmatic practice of early trach stems from bygone days where different ETTs where used - but the dogma lives on in the boards. Modern ETTs have a lower and less defined rate of subglottic stenosis, and some authors believe that switching from ETT to trach is unnecessary. Other advantages of tracheostomy is increased mobilization, decreased ventilator associated pneumonia, patient comfort, and removal of mechanical ventilation (some patients need an airway, not a ventilator...think neuro-ICU).

The correct answer is: E: Lack of suspected infectious source

Yea, yea, yea, that was an easy one…but its harder then you might think to write challenging questions. I don’t think this has been a particularly highly tested subject on the boards, but it’s certainly on the list of things you should know, not only to pass the boards but understand sick patients as a consultant. Systemic inflammatory response syndrome (SIRS) is a constellation of signs which point towards….you guessed it, a systemic inflammatory response. You should know the diagnostic criteria of SIRS (even the surgery interns know this): Hyper or hypothermia, tachycardia, tachypnea or respiratory alkalosis, and a high or very low white count, or a significant left shift. Notice that specific numbers were not given so you can actually concentrate on understanding it, not memorizing stupid numbers. Sepsis occurs when SIRS coexists with a suspected or confirmed infection. Gram negatives are most common. The systemic inflammatory response and shock result in dysoxia (remember that…ICU question 7) and thus multiorgan failure, oliguria, ARDS, DIC, and generalized oedema.   Also of note, the cool kids no longer use the term SIRS and we talk about SOFA scores, and such.  For the purpose of your general anesthesiology boards, I wouldn't get too caught up in Sepsis-3 terminology.

The correct answer is: C: Wide spectrum antibiotics

The treatment of sepsis must focus on the underlying cause (perforated bowel and infection) as well as supportive therapies (respiratory failure, kidney failure, hypotension, etc). Antibiotics should be started wide spectrum in regards to the suspected source. Corticosteroids can help with refractory hypotension but also can cause worsening infection making it overall no benefit to outcome. Colloids have shown no superiority over crystaloids in this setting. Answers "Changed to prone position" and "Bircabonate gtt" are distracters.

The correct answer is: D: Immediately suctioned the oropharynx, intubated the patient, and suction the lungs prior to oxygenating

Aspiration pneumonia is often a relatively benign process when occurring to NPO outpatients because the serious risk factors are: particulate matter (food), high gastric volumes (diabetic, pregnant), low pH, or feculent (bowel obstruction). Particulate matter leads to (small) airway obstruction followed by necrosis. Acidic contents, especially large volumes, leads to a chemical pneumonitis with atelectasis and loss of surfactant. Feculent material can also leave a significant microbial load and infection. Bicitra when swallowed 30 minutes prior to aspirating leads to non acidic aspirate, avoiding the pneumonitis, but does not address particulate matter. H2 blockers and PPIs can decrease gastric acidity when given up to 2 hours before aspirating. Metoclopramide can increase gastric emptying, decreasing stomach volume. Whatever the case, the first priority following an aspiration is to establish an airway, which means suctioning the oropharynx (some sources say in the trendelenburg position), and place an ETT. Often, by the time this is done, the patient is desaturating and the natural reaction is to bag him. This causes the aspirate to be moved down into smaller airways; therefore additional suctioning should proceed ventilation.

The correct answer is: C: Extubation and observation

The patient meets extubation criteria and should be extubated and observed. If particulate matter was observed bronchoscopy may be warranted, but more helpful if done immediately. Corticosteroids has not been shown to help and might even hurt if there is an infection. Routine antibiotics are not indicated for aspiration pneumonia. The patient's metabolic acidosis is not a reason to keep her intubated.

The correct answer is: C: Illeus may present with increasing gastric residual volumes

Illeus will present with distention and increasing gastric residuals. Duodenal feeding (or lower in the GI tract) is not considered an increased risk for aspiration and should be continued. Gastric tube feeding should be stopped at least 6 hours prior to induction. Diarrhea is associated with hyperosmolar feeding, not hypoosmolar.

The correct answer is: D: Insulin is often added to TPN due to the high likelihood of hyperglycaemia

Don’t think TPN is on the boards, think again! TPN is used for patients that cannot tolerate enteral feeds or have an insufficient capacity to absorb nutrients. Patients coming to the OR should generally have their TPN continued as hypoglycaemia can occur due to the insulin added or be supplemented with a dextrose infusion. Insulin is added because hyperglycaemia is very common with TPN. Amino acid metabolism can result in worsening of encephalopathy (ammonia). High percentage of carbohydrates, not fat, can cause respiratory failure because the RQ for carbohydrates is 1.0 where as lipids is 0.7 (see ICU Question 15). Essential fatty acid deficiency can occur when lipids are not included in TPN at least once a week.

The correct answer is: E: Hypophosphataemia

All of the above can occur with TPN, but hypophosphataemia is most likely to result in respiratory failure. This concept has been tested on the anesthesia boards multiple times. NIF is a test of strength and the minimum is -20 to -25 cm H2O for extubation.

The correct answer is: D: Hand washing

Hand washing should occur before and after wearing gloves and should be lathered for at least 30 seconds. Alcohol based gels are a reasonable alternative in most cases where the hands are not visibly soiled or there is not concern for C. difficile spores (which are not killed with these agents).

The correct answer is: C: Coagulopathy

Regarding conditions requiring GI prophylaxisis, only two conditions are independent risk factors: mechanical ventilation for greater than 48 hours or coagulopathy (PLT < 50K, INR > 1.5, PTT > 2 X control). The following are also considered high risk conditions, but two of these must be present: Hypotension, severe head injury, > 30% burns, renal failure, or liver failure. The primary problem in stress related injury is decreased mucosa blood flow, and less so the problem of acidity. Other than H2 blockers, PPIs and sucralfate are also used effectively for prophylaxis. Other preventive strategies include reversing hypotension and enteral feedings.

The correct answer is: C: Gallbladder perforation can occur within 48 hours

Acalculous cholecystitis is an emergency as it can quickly progress to perforation and sepsis. Treatment includes surgical removal and percutaneous colostomy tube placement. Also note that the stem includes the three biggest risk factors for acalculous cholecystitis: surgery, trauma, and TPN.