2014

Question 1

1. Investigators have shown that the annual risk of stroke in elderly patients with untreated atrial fibrillation is 13%. Patients treated with coumadin however had an annual stroke risk of 3%. The annual risk of significant bleeding in the patients that where on coumadin was 6%, while those that where not on coumadin had an annual risk of bleeding of 0.5%. a. With your knowledge of statistical methods and equations (they actually say that in the exam), show us how an absolute risk reduction would be calculated and plug in the numbers without actually doing the calculation (1). b. How would you calculate the number needed to treat based on the information given in the stem? Please plug in the numbers without actually doing the calculation (1).

Answer 1

a. ARR = CER-EER = 13% - 3% = 10% (control and experimental event rate) b. NNT = 1/ARR NNT= 1/(EER-CER) = 1/(0.10) = 10

Question 2

2. They give you a long stem of a lady in her 60’s that presents with dysphagia, hematemesis and chest pain. She is admitted to the ICU with unstable vitals. They provide you with her saggital CT scan image, which we (the people who took the exam) largely disagreed on what it showed. In essence the image showed a bone window saggital cut CT image with an opacification extending all the way down to the diaphragm. Cephalad it extended up to the superior medastinum and encroached on the right lung apical region. Some of us thought it was a large ascending, transverse and descending thoracic aortic aneurysm (possibly a dissected aneurysm but you couldn’t really make out a dissection flap on the image). Some of my colleagues thought that it was an image of achalasia or an esophageal stricture with contrast dye filling up all her esophagus. Others thought it was a case of oesophageal rupture. They tell you she is now in distress and requires intubation. a) They ask you what the diagnosis is (1). b) During her intubation she has massive aspiration (Mendelson syndrome). In this patient specifically, how would this complicate things and worsen her outcome (3), yes they asked for 3 things! What steps would you take with intubation to minimize aspiration(3)?

Answer 2

a) ? achalasia vs. esophageal rupture b) -chemical pneumonitis (seems to be like Mendelson syndrome), can lead to ARDS -bacterial pneumonia -mechanical obstruction (airway obstruction or reflex airway closure) -difficult intubation The term chemical pneumonitis refers to the aspiration of substances that are toxic to the lower airways, independent of bacterial infection. The prototype and best studied clinical example is chemical pneumonitis associated with the aspiration of gastric acid first described by Mendelson in 1946 [25] and sometimes referred to as Mendelson’s syndrome. Classically occurs with aspiration of gastric contents followed by resp distress, cyanosis and infiltrates on CXR. Pts usually have rapid clinical recovery (24-36h) with radiographic resolution within 4-7d without the use of Abx. The following clinical features should raise the possibility of chemical pneumonitis [39]: ●Abrupt onset of symptoms with prominent dyspnea ●Fever, which is usually low grade ●Cyanosis and diffuse crackles on lung auscultation ●Severe hypoxemia and infiltrates on chest imaging involving dependent pulmonary segments. The dependent lobes in the upright position are the lower lobes. However, aspiration that occurs while patients are in the recumbent position may result in infection in the superior segments of the lower lobes and the posterior segments of the upper lobes. c) -Perform as a RSI (do not bag patients at high risk of aspiration - these were excluded from BVM-RSI study) -dedicated suction person -Perform intubation with head of bed elevated - +/-Decompress stomach prior to intubation (don’t put in NG if you think it’s ruptured) -+/-Cricoid pressure

Question 3

3. Bronchoscopy is an important skill for critical care physicians. Identify what the following images show. a. They show you an image with a circle around the RUL bronchus (1). b. They show you an image with a circle around the RML bronchus take-off from the bronchus intermedius (1). c. They show you an image with a circle around the LLL bronchus(1).

Answer 3

• https://www.youtube.com/watch?v=VLsXe5oB2W0&feature=player_embedded - https://www.youtube.com/watch?v=ThYHLG50pH0

Question 4

4. A younger gentleman was involved in an MVC and presents to the emergency department with polytrauma. They give you bunch of vitals and a bunch of CT images. His CT thorax transverse cut shows a left hemopneumothorax, his saggital CT chest shows sternal fractures and burst fracture in one of the thoracic vertebra and his pelvic CT scan shows a pelvic fracture. -Identify the injuries (4). o Hemopneumothorax o Sternal fracture o Thoracic vertebral fracture o Pelvic fracture -The patient is now in shock. Identify the different potential causes of shock in this gentleman and briefly describe their mechanism (4).

Answer 4

o Hemorrhagic - pelvis, chest o Obstructive - tension pneumothorax, cardiac tamponade o Neurogenic - high T-spine fracture above level of sympathetics o Cardiogenic - given sternal fracture patient at risk for cardiac contusion

Question 5

5. Your ICU is looking to implement a quality control system. -What steps would you take to implement a quality control system in the ICU (4)? -What components would you consider essential for any ICU quality control system (4)?

Answer 5

a) PDSA (plan, do, study, act) Plan - hypothesis and idea, questions and predictions Do - carry out the plan Study - analyze the data and compare to predictions Act - adapt, what changes can be made for next cycle? b) from previous answers…couldn’t find an official resource to support this o A system to flag issues o A comprehensive multidisciplinary team from all areas to develop new solutions o System to test the solution and transition into practice o System to assess the outcome of the new solution -?regular feedback to clinical teams?

Question 6

6. A middle aged lady has been receiving ovulation induction therapy to get pregnant. They are able to retrieve multiple ova for IVF. Later on she starts developing abdominal pain and respiratory distress. They show you a low cut in her pelvo-abdominal CT scan with multiple large follicles and some free fluid. They tell you she has developed ARDS and ask, what is the most likely cause of her ARDS (1)?

Answer 6

• Ovarian hyperstimulation syndrome Ovarian hyperstimulation syndrome (OHSS) occurs when the ovaries are hyperstimulated and enlarged due to fertility treatments (or rarely, mutations in the follicle-stimulating hormone [FSH] receptor), resulting in the shift of serum from the intravascular space to the third space, mainly to the abdominal cavity. In its severe form, OHSS is a life-threatening condition because it can cause venous or arterial thromboembolic events, including stroke and loss of perfusion of an extremity. Severe OHSS is characterized by an extraparenchymal restrictive type of pulmonary dysfunction, attributed to intraabdominal or pleural fluid accumulation, which limits descent of the diaphragm and expansion of the thoracic cage. This may induce uncoordinated lung ventilation and atelectasis with subsequent ventilation-perfusion mismatch and hypoxemia. The clinical picture may deteriorate further because of pulmonary infection, pulmonary thromboembolism, or ARDS, all of which have distinct clinical, radiographic, and blood gas characteristics.

Question 7

7. An elderly gentleman has had an aortic valve replacement and in the OR lead III is being monitored. He has a change in rhythm and they show you a rhythm strip showing sinus rhythm and then about 6 or 7 beats of wide complexes, which then goes back to normal sinus rhythm. They also show you underneath that rhythm strip, a print-out of the art. line trace. It shows that patient still has cardiac output throughout the wide complex rhythm but with a slightly lower pressure. - What is the rhythm change (1)? (some people thought it was a paced rhythm, others thought it was a non sustained VT, there were no clear pacing spikes) o Non-sustained VT What are 5 causes of WCT? Why did the pressure drop with that change (1)?

Answer 7

• What is the rhythm change (1)? (some people thought it was a paced rhythm, others thought it was a non sustained VT, there were no clear pacing spikes) o Non-sustained VT? A variety of definitions of NSVT have been published, but the most commonly used definition is [1]: ●Three or more consecutive ventricular beats ●Rate of >100 beats per minute ●Duration of less than 30 seconds 5 causes of WCT: 1) VT (look for AV dissociation, fusion beats, capture beats) 2) SVT with aberrhancy 3) SVT with pre-excitation 4) SVT with paced rhythm 5) artifact o Loss of atrial kick, given that the patient is having an aortic valve replaced likely has significant LVH and requires the atrial kick for optimal filling

Question 8

8. Non-invasive ventilation is a well established mode of treating respiratory failure of various etiologies. - How does non-invasive ventilation help patients with acute excarbations of COPD (2 mechanisms)? - How does NIV help patients with cardiogenic pulmonary edema (2 mechanisms)?

Answer 8

COPD -offloads respiratory muscles by providing inspiratory pressure augmentation to assist ventilation -applied PEEP can reduce work of breathing and assist in breath triggering/inspiratory initiation by reducing the pressure differential the pt’s diaphragm needs to generate in order to trigger a breath Cardiogenic pulm edema -increases intrathoracic pressure and thus decreases preload to heart causing less ventricular stretch and therefore in a more optimal position for force generation -increasing intrathoracic pressure decreases LV wall tension thereby decreasing myocardial workload -increases intrathoracic pressure which helps to move blood from aorta outside of thoracic cavity, thereby decreasing LV afterload -increases RV afterload decreasing RV output and leading to decreased LV preload -shift fluid from alveolar to interstitial tissue improving gas exchange and hypoxia

Question 9

9. List 5 pathogens associated with severe sepsis in patients 2 to 4 months after a solid organ transplant (5). BONUS: list common infections within the first month post transplant!

Answer 9

• Legionella - Mycoplasma In the period one to six months post-transplant, the nature of common infections changes. The effect of immunosuppression is often maximal, and patients are at greatest risk for the development of opportunistic infections. -PJP (pneumocystis jirovecii pneumonia) -aspergillus -viruses (CMV, EBV, HCV, HBV), including community acquired viruses (influenza, parainfluenza, RSV, adenovirus) -latent infections (strongyloidiasis, toxoplasmosis, Chagas) -geographic/endemic fungal infections: histoplasma capsulatum, coccidiodes -tuberculosis -NTB mycobatceria -GI parasites: cryptosporidium previous answers also listed: - Listeria - Norcardia - TB - CMV - HSV - Aspergillus - PJP - Cryptococcus - Influenza - Histoplasma - If still ventilated – MRSA, pseudomonas 1st month since transplant there are two major causes for infection: pre-existing infection from either the donor or recipient and infectious complication of the surgery/hospitalization…the major effects of exogenous immunosuppression are not yet evident! -VRE -MRSA -G neg bacteria -fluconazole resistant candida -HBV -HCV -colonizers that may cause infection (VRE) or organisms not covered by surgical prophylaxis

Question 10

10. Epiglottitis versus Ludwig’s angina. - What are the two most common pathogens that cause Epiglottitis (2)? - What are the two most common pathogens that cause Ludwig’s angina (2)? - What is the most important difference in management between the above conditions (1)?

Answer 10

Epiglottitis -Hemophilus influenza -B-hemolytic streptococci (ex. strep pyogenes) -+/-strep pneumoniae ***Mo says this one Ludwig’s angina (think oral flora) -Strep viridans (one of which is strep anginosus - formerly strep milleri -Polymicrobial (anaerobes: peptostreptococcus, fusobacterium, bacteroides, actinomyces) difference …after more thought I’m thinking Ludwig’s is different in that it is a deep neck space infection and can track down through fascial layers and into mediastinum/lungs…other option from prev answer was: o Ludwig’s angina more likely to need surgical or interventional drainage (look for infected teeth that can be extracted) o May need a trach -both however may need urgent and CAREFUL airway management/securing LUDWIGS Ludwig’s angina is a life-threatening cellulitis of the soft tissue involving the floor of the mouth and neck. It involves two compartments on the floor of the mouth namely sublingual and submaxillary space. It usually does not involve lymphatic system nor it forms abscess. Infection of the lower molars is the most common cause of Ludwig’s angina.[1] The infection is rapidly progressive leading to aspiration pneumonia and airway obstruction. The most common cause is dental disease in the lower molars mainly second and third which accounts for over 90% of cases.[2] Any recent infection or injury to the area may predispose the patient to develop Ludwig’s angina. Some common etiologies include injury or laceration to the floor of the mouth, mandible fracture, tongue injury, oral piercing, osteomyelitis, traumatic intubation, peritonsillar abscess, submandibular sialadenitis and infected thyroglossal cysts.[3] Predisposing factors include diabetes, oral malignancy, dental caries, alcoholism, malnutrition, and immunocompromised status. Since the infection does not spread via the lymphatic system, the infection is bilateral. The infection is usually polymicrobial involving the oral flora. The most common organisms are Staphylococcus, Streptococcus, Peptostreptococcus, Fusobacterium, Bacteroides and Actinomyces. The most common presenting symptoms include fever and chills with neck swelling, neck pain, odynophagia and dysphagia. People often describe the appearance as a “bull neck.” Less common symptoms include mouth pain, hoarse voice, drooling, tongue swelling, stiff neck and sore throat.[4] Stridor may indicate impending airway obstruction. Early airway management is critical to the treatment of Ludwig’s angina as the most common cause of death is sudden asphyxiation from airway obstruction. Flexible fiberoptic nasal intubation is clinician’s favored method of intubation. If the patient is not able to be intubated, the next step would be an emergency tracheotomy. Cricothyrotomy is very challenging because of the edema in the neck which can obscure the anatomy.

Question 11

11. A resident tried putting in a femoral central line in a 65 year old lady with septic shock and after poking the femoral artery a few times he/she was able to eventually cannulate the vein. The patient’s vitals stabilized with resuscitation but then her leg (with the line in place) started to become cold and mottled and showed signs of acute ischemia. Vascular surgery were consulted and they think the artery might have developed an intimal flap that caused the acute ischemia. They will operate and try to salvage that limb but an amputation is a strong possibility. -What are the 4 essential elements that need to be present in any disclosure of an adverse event (4)? -When do you disclose the adverse event (1)? -In general, who should be the one to disclose any adverse events to families(1)?

Answer 11

mine: attend to pt’s clinical care honesty documentation post analysis disclosure ?apology old answers: o Honest, open, and transparent disclosure of the facts o Empathetic expression of regret and apology o Comprehensive and timely investigation of the facts o The steps taken to manage the adverse patient safety event after providing care/stabilizing the patient and after preparing the known facts… o As soon as reasonably possible (as per CMPA) after ensuring the patient’s care needs have been met o The MRP Disclosure road map 1) attend to clinical care 2) plan the initial disclosure 3) attend disclosure meeting

Question 12

12. A patient with terminal COPD underwent a double lung transplant and the anesthesiologist inserted a pulmonary artery catheter in the OR that was confirmed to be in the right spot by the pressure waveform and by blood gases. The patient is now in the ICU and this is his chest X-Ray. They show you a left IJ line that doesn’t take the normal course. It comes down the left side of the heart before coursing medially half-way into the heart, then it goes back again and up pulmonary artery. Trace the pulmonary artery catheter course from it’s point of insertion in the IJ to the main pulmonary artery excluding the valves it passes through (i.e. no need to mention the valves it goes through) (4).

Answer 12

• Left internal jugular - Persistent left SVC - Coronary sinus - RA - RV - PA

Question 13

13. A post line insertion chest X-ray was done after insertion of a 7 Fr central line in the right internal jugular vein. They show you an image where the right “IJ” line courses down to the arch of the aorta (i.e. looks like a carotid line). - How would interpret this CXR (1)? - How would you deal with this situation (2)?

Answer 13

o Arterial cannulation o Leave the line insitu, labelled to ensure it is not used o Contract vascular surgery -later plan to disclose to patient/family

Question 14

14. A lady admitted to the medicine ward with an upper GI bleed, stated that she wanted nothing done and that if she were to worsen she wanted to be left to die in peace. After that she bleeds profusely and deteriorates. Her family arrive and want her intubated, and want her to get an upper GI scope and the works. - What ethical principle would be violated if you were to do as the family wants (1)? - What are 3 essential elements of any consent (3)?

Answer 14

o Autonomy -voluntary -pt must have mental capacity -pt must be properly informed

Question 15

15. Patient has a history of a single lung transplant 3 years ago. Now with a viral illness severe enough to require intubation in the ICU. They give you vent parameters that are relatively high from and airway pressure standpoint. They give you a CXR of a patient with a single lung (right) that is clearly quite big (likely due to compensatory emphysema plus the IPPV) and the medastinum is very slightly shifted to the left, with an empty (or fluid-filled) small left hemithorax. They tell you that the patient now is in obstructive shock (yes they actually say obstructive shock). Provided there is no pneumothorax, what single non-pharmacological maneuver could you do to help treat this hypotension (1)?

Answer 15

Decompress the trapped air

Question 16

16. • What is the most important physiotherapy intervention in the ICU (1)? What are three benefits of this intervention?

Answer 16

-Early progressive mobilization my answers: -shorter duration of MV -more likely to walk without assistance at hospital discharge -improved muscle strength -improved physical function -more days alive and out of hospital to day 180 -prevents delirium ***LOOK AT PADIS guideline https://www.ncbi.nlm.nih.gov/pubmed/27864615?dopt=Abstract old answers: o Improved muscle strength o Improved physical function o Improved quality of life o Decreased ICU LOS o Decreased duration of mechanical ventilation

Question 17

17. Fat embolism syndrome (FES) is common with long bone fractures. - What is the pathognomic sign of fat embolism syndrome (1)? - Name 3 non-traumatic causes of fat embolism syndrome (3)?

Answer 17

o Petechial/purpural rash that appears on the upper portion of the body Fat embolism syndrome (FES) typically manifests 24 to 72 hours after the initial insult, but may rarely occur as early as 12 hours or as late as two weeks after the inciting event [37]. Affected patients develop a classic triad: hypoxemia, neurologic abnormalities, and a petechial rash. None of these features are specific for FES. The characteristic red-brown petechial rash may be the last component of the triad to develop and occurs in only 20 to 50 percent (on average one third) of cases. It is found most often on the nondependent regions of the body including the head, neck, anterior thorax, axillae, and sub-conjunctiva.

1. o Acute pancreatitis
2. o Liposuction
3. -osteonecrosis
4. -bone marrow necrosis
5. -lipid based infusions or contrast agents
6. -IM injection of oil for cosmetic purposes
7. -sickle cell/thalassemia-related hemoglobinopathies (esp during crisis)

Question 18

18. Name 4 indications for hyperbaric oxygen therapy (4).

Answer 18

-Carbon monoxide poisoning -cyanide poisoning -Decompression sickness -Acute traumatic or thermal injury (compartment syndrome) -Necrotizing soft tissue skin infection -Non-healing ulcers -radiation injury

Question 19

20. A polytrauma patient with a closed head injury, rib fractures, pulmonary contusions, and some other injuries is intubated and has a right sided chest tube inserted before he is transferred by air ambulance. Before take off, his ETT cuff is filled with saline and his chest tube is clamped. He is put on board of a fixed wing aircraft and they mention that the ambient pressure on-board the aircraft is pressurized to 2500 metres high or 8000 feet altitude (as per the standards for pressurizing fixed-wing aircrafts, which usually fly much higher than that - they usually fly 10,000 metres altitude). The patient starts to desaturate and his oxygen requirement go up. The patient is now on an FiO2 of 0.8 with SpO2’s barely in the high 80’s. - What are 4 reasons for his desaturation (4)? - What would be the reason the ETT cuff was filled with saline (1)?

Answer 19

o Expansion of pneumothorax due to decreased ambient pressure o Decreased partial pressure of inspired oxygen o Progression of pulmonary contusion o Expansion of stomach gases compressing lungs -ETT displaced from position -?fat embolism o If air is used, as ambient pressure decreases the cuff would expand, this does not happen with saline

Question 20

21. You are trying to wean a patient off a ventilator but she keeps failing despite everything else heading in the right direction. You do a set of blood work to rule out metabolic causes of her failure and you find a very high TSH of 15 (normal is up to around 4), but her free T3, and free T4 are both normal. - What is the diagnosis (1)? - What lab test rules out non-thyroidal illness syndrome (1)?

Answer 20

recovering sick euthyroid (vs subclinical hypothyroidism) o Normal T3 and T4 o Elevated reverse T3 in sick euthyroid The most common hormone pattern in sick euthyroid syndrome is a low total T3 and free T3 levels with normal T4 and thyroid-stimulating hormone levels. The serum level of reverse T3 (rT3) is increased in euthyroid sick syndrome, except in renal failure. Low serum T3 is correlated with an increased length of hospital stay, intensive care unit admission, and the need for mechanical ventilation in patients with acute heart failure. The serum T4 value also correlates with outcome in critically ill patients; values under three microg/dL have been associated with mortality rates in excess of 85%. Two general guidelines are important in evaluating a critically ill patient. —First, measure TSH only if there is a high clinical suspicion of thyroid dysfunction. If TSH is abnormal, then further workup is done. If the TSH is greater than 20 microUnits/mL or is undetectable, euthyroid sick syndrome is less likely to be the cause, and overt thyroid dysfunction should be strongly considered. —When serum TSH is not elevated, euthyroid sick syndrome should be considered in patients with known thyroid disease and low serum-free T4. Thyroid function in non-thyroidal illness (UTD) TSH subnormal — Almost all patients who have a subnormal but detectable serum TSH concentration (greater than 0.05 mU/L and less than 0.3 mU/L) will be euthyroid when reassessed after recovery from their illness. In contrast, approximately 75 percent of patients whose TSH is undetectable (<0.01 mU/L) have thyrotoxicosis. ●In patients without a strong clinical suspicion of thyroid disease and minor TSH abnormalities (TSH between 0.05 and 0.3 mU/L with normal or low free T4), we reassess thyroid tests (TSH, free T4) after recovery. If true central hypothyroidism due to hypothalamic or pituitary disease remains in the differential diagnosis, measurement of serum cortisol can be helpful as it would be elevated in critical illness and low (or inappropriately normal) in patients with true central hypothyroidism. Measurement of serum rT3 is only rarely useful in hospitalized patients to distinguish between nonthyroidal illness (high values) and central hypothyroidism (low values); the values are low in the latter patients because of low production of the substrate (T4) for rT3. TSH high — As noted above, some hospitalized patients have transient elevations in serum TSH concentrations (up to 20 mU/L) during recovery from nonthyroidal illness [48]. Few of these patients prove to have hypothyroidism when reevaluated after full recovery from their illness. Patients with serum TSH concentrations over 20 mU/L usually have permanent hypothyroidism [50]. Our approach depends on the degree of TSH elevation and the clinical suspicion for underlying hypothyroidism: ●TSH between upper limit of normal and <10 mU/L – If the patient appears to be recovering from the underlying illness, we repeat the TSH in one to two weeks. Few of these patients prove to have hypothyroidism when reevaluated after recovery from their illness. ●TSH 10 to 20 mU/L – Treatment with levothyroxine may be appropriate depending on the free T4 level, clinical suspicion of hypothyroidism, and degree of nonthyroidal illness. If uncertain, repeat the TSH and free T4 in one to two weeks. Thyroid function tests may improve in patients recovering from nonthyroidal illness. ●TSH ≥20 mU/L – Assess the free T4 level. •Free T4 low – Hypothyroidism is likely. Initiate thyroid hormone. In the absence of suspected myxedema coma, repletion should be cautious, beginning with approximately half the expected full replacement dose of T4 (levothyroxine). In suspected myxedema coma, or in critically ill patients who cannot ingest or absorb oral medications, thyroid hormone should be given intravenously. •Free T4 normal – Repeat TSH and free T4 in one to two weeks. Thyroid function tests may improve in patients recovering from nonthyroidal illness.

Question 21

22. They show you diagrams of the the three set-ups of CRRT (hemofiltration, hemodialysis and hemodiafiltraton. - They ask you to label each mode of renal replacement therapy (3). - With regard to hemofiltration, state one advantage and one disadvantage of pre-filter replacement fluid substitution (2). State one advantage and one disadvantage of post- filter replacement fluid substitution (2).

Answer 21

This is how I would reason this question: pre and post fluid replacement - CVVH dialysate and fluid replacement - CVVHD dialysate - CVVD no dialysate and no replacement - SCUF (slow continuous ultrafiltration) overall review here aims of RRT are achieved through diffusion or convection, which are respectively referred to as hemodialysis or hemofiltration. Middle molecules are preferentially cleared by convective methods, rather than smaller molecules that are more reliably cleared by diffusion. Diffusion = hemodialysis Convection = hemofiltration CVVH = continuous veno-venous hemofiltration CVVHD = continuous veno-venous hemodialysis CVVHDF = continuous veno-venous hemodiafiltration​ majority of ICU RRT is CVVHF or CVVHDF HEMOFILTRATION Haemofiltration is a convective process whereby a hydrostatic pressure gradient is used to filter plasma, water, and solute across a membrane. This is analogous to the process within the renal corpuscle. The underlying mechanism is that of ‘solute drag’ where appropriately sized molecules are pulled along with the mass movement of solvent, traditionally termed ultrafiltration (UF). The convective transport is independent of solute concentration but determined by the direction and magnitude of the transmembrane pressure (TMP). Measures that result in a higher flow rate will increase UF production and in turn increase solute clearance. Equally, measures that increase the negative pressure across the membrane, including the pump on the effluent line, can have a marked effect. This fluid, known as effluent, is discarded. Owing to the high volumes produced, the circulating volume of the patient is replaced with a balanced crystalloid buffer solution. HEMODIALYSIS In haemodialysis, solute clearance is achieved by diffusion across the membrane. The space outside the blood-containing fibres within the ‘filter’ is filled with dialysate, which is pumped in a counter-current fashion to the flow of blood. Dialysate is reconstituted to include a buffer (which may be either acetic acid or bicarbonate) and essential electrolytes dissolved in ultrapure water rendered devoid of toxins and impurities. Diffusion occurs down concentration gradients allowing rapid equilibration of solutes across the membrane. The purpose of this counter-current flow system is to maintain a waste-solute concentration gradient (i.e. always lower on the dialysate side of the membrane, similar to solute movement within the Loop of Henle). RRT Membrane Two types of RRT membrane exist: cellulose based or synthetic. Exposure to an extracorporeal circuit and the interaction between blood and the membrane is known as biocompatibility. Less biocompatible membranes increase the likelihood of harmful side-effects associated with RRT. Cellulose-based membranes trigger activation of inflammatory pathways, which may increase the longevity of AKI. Studies suggest that the use of more biocompatible membranes may lead to faster restoration of renal function and improved patient outcomes.3 In short, it can be assumed that the most biocompatible membrane available should be used for RRT. Filter Fluid During haemofiltration, bicarbonate ions are freely filtered and therefore need to be replaced. Previously, standard lactate-based fluids were used as buffers, with the lactate subsequently being metabolized in the liver. In the context of critical illness, impaired hepatic function can lead to lactic acid accumulation. To compensate for this, bicarbonate-based buffer solutions have become commercially available. These fluids may be added to the circuit before the haemofilter (pre-dilution) or mixed with the blood in the venous drip chamber (post-dilution). Pre-dilution replacement reduces the incidence of filter clotting but reduces the effective clearance of solutes. Post-dilution replacement is, therefore, the ideal, but a compromise is often made to maintain the integrity and lifespan of the filter. Although there is no mortality benefit associated with the use of bicarbonate-based fluids, there is evidence for improved control of acidosis and cardiovascular instability. RRT Dosing For continuous techniques, dose is the sum of all effluent fluids expressed as millilitres per kilogram body weight per hour. It is important to note that the addition of dialysate and the targeting of negative fluid balance both add to the summative dose. Dosing of intermittent techniques is difficult because of urea kinetics and fluid shifts in the critically ill: because of this, most studies assessing IHD measure dose in relationship to frequency and duration of sessions. o Pre-filter  Advantage • Less clot, longer filter life  Disadvantage • Less removal of solute as you have a dilute solution o Post-filter  Advantage • More solute removal  Disadvantage • Shorter filter lifespan

Question 22

23. What properties of a molecule or toxin, govern whether it would be dialysable or not (4)? B. What are the mechanisms of drug and toxin removal with hemofiltration, i.e. how does it work to clear toxins (3)?

Answer 22

• Size - Protein bound - Volume of distribution - Water solubility - +/-charge - +/- interaction with the dialysis membrane? - Blood passed through filter with large pores - Ultrafiltrate passes through the pores, drags toxins with it (CONVECTION = Convection is bulk-flow of solute across a semi-permeable membrane together with a solvent in a manner that is dependent on transmembrane pressure and membrane characteristics.) - Rate of fluid is equal to drug clearance

Question 23

24. When using inotropes or pressers in the ICU, what are the considerations for using each of the following. - Milrinone (3 considerations) - Dobutamine (3 considerations)

Answer 23

• Milrinone (3 considerations) = phosphodiesterase 3 inhibitor which decreases the rate of cAMP degradation –> increases Ca influx into cell o Renal function o Fluid status o Cardiac function o Presence/absence of pulmonary hypertension o Concurrent beta-blockade -slower onset and clearance - Dobutamine (3 considerations) = primarily beta-1 adrenergic o Cause of current shock (cardiogenic) o Heart rate, arrhythmia -can increase O2 demand in pts with pre-existing MI -hypotension o Fluid status -more rapid onset

Question 24

25. A lady after a prolonged delivery develops respiratory distress, hypoxemia, RV dilation and failure and DIC (disseminated intravascular coagulopathy). What is the diagnosis (1)? What are the diagnostic criteria for this condition?

Answer 24

-Amniotic fluid embolism Amniotic fluid embolism is a clinical diagnosis. The diagnosis should be suspected in pregnant or recently postpartum women who experience sudden cardiovascular collapse, severe respiratory difficulty and hypoxia, and/or seizures, particularly when followed by disseminated intravascular coagulopathy (DIC). The condition generally arises during labor or soon after delivery, in the absence of other explanations for these findings. In many cases, the diagnosis is made retrospectively, after all investigative data, including autopsy data, have been collected. ●Sudden onset of cardiorespiratory arrest OR hypotension (systolic blood pressure <90 mmHg) with evidence of respiratory compromise (eg, dyspnea, cyanosis, or peripheral oxygen saturation <90 percent). ●Documentation of overt DIC using the scoring system of the Scientific and Standardization Committee on DIC of the International Society on Thrombosis and Haemostasis (ISTH), modified for pregnancy [8]: •Platelet count >100,000/mL = 0 points, <100,000 = 1 point, <50,000 = 2 points •Prolonged prothrombin time or international normalized ratio <25 percent increase = 0 points, 25 to 50 percent increase = 1 point, >50 percent increase = 2 points •Fibrinogen level >200 mg/L = 0 points, <200 mg/L = 1 point A score ≥3 is compatible with overt DIC. Coagulopathy must be detected before hemorrhage itself can account for dilutional or shock-related consumptive coagulopathy. ●Clinical onset during labor or within 30 minutes of placental delivery. ●Absence of fever (≥38°C) during labor.

Question 25

26. A short obese lady undergoes cardiac surgery (CABG) with a size 8 endotracheal tube. The anesthesiologist documents an atraumatic, easy intuition inserted on the first pass. She is doing really well in the ICU and has passed her SBT, is awake, and fits all the criteria for extubation. The respiratory therapist however, tells you she has no cuff leak. - What would you do (1)? - Explain why you would do that (1)?

Answer 25

o Extubate o There is no strong evidence that a lack of a cuff leak implies failure to extubate, and given the large size ETT in a short woman it is very likely that she’ll never have a cuff leak. Also given the report from the anesthesiologist it is unlikely that there was significant trauma during intubation causing severe swelling from MV guidelines: Risk factors for PES include: traumatic intubation, intubation longer than 6 days, large endotracheal tube, female sex, and reintubation after unplanned extubation

Question 26

27. A gentleman is recovering from his critical illness in the ICU quite well. He is now awake and cooperative, feeding well, and looking good, except that he keeps failing his SBT’s. - What are the advantages of proceeding tracheostomy (4)? - His tracheostomy procedure goes well. The next day however, upon turning the patient, the tracheostomy is dislodged, and you are unable to pass it in again. His SpO2 is now 50’s. What do you do now?

Answer 26

o Decrease resistance to airflow with a shorter airway allowing for weaning in ventilation o Allow for reduced sedation o Allow for secretion management o Improved patient comfort (speech, mobility, swallowing enhanced) -can be nursed outside of ICU -ease of replacement once tract has formed o Cover the trach site and bag from above, then intubate from above o Have trach replaced in OR

Question 27

28. A. What are two different ways of performing an spontaneous breathing trial (2)? B. What parameters would indicate failure of a spontaneous breathing trial (4)?

Answer 27

- T-piece - PS ventilation -CPAP - Tachypnea, inc WOB, diaphoresis - Tachycardia, cardiac arrhythmia - ST changes - Desats -abrupt change in LOC from my paper -gas exchange (i.e. oxygenation: SpO2 ≥85-90%, PO2 ≥ 50-60mm Hg, and ventilation: pH≥7.32, increase in PCO2 ≤10mm Hg) -hemodynamic stability (HR \<120-140bpm, HR not changed \>20%, SBP \<180-200mm Hg and \>90mm Hg, BP not changed \>20%, no vasopressor use) -respiratory pattern (RR≤30-35 breaths/min, RR not changed \>50%) -Subjective variables showing success included the absence of: change in mental status, onset/increase in discomfort, diaphoresis, and signs of increased work of breathing.

Question 28

29. A lady had underwent a mitral valve replacement in and is now in the ICU. Other than the surgical wires and mitral valve, what other anomalies do you observe in this chest X ray (2)? Her right IJ line was going outward into her right subclavian and her right pleural base looked thickened i.e. had a pleural plaque. Her gastric air bubble was quite big, and some of my colleagues said she had some air under her right hemidiaphragm but, I’m not really sure that was the intended anomaly. To me it looked like the calcified pleura at the right lung base gave an impression of some air under the diaphragm that didn’t quite exist. In addition to that, in the OR chest tubes go from underneath anyways and a little bit of air under the diaphragm immediately postop in the setting of a benign exam, is usually not a big deal. That is if we were to say that she had free air...(which as I said, she might not have had). The chest X-ray showed sternal wires, so it was a conventional MVR via a sternotomy.

Answer 28

?nothing to add

Question 29

30. Several authors have investigated the use of PA catheters and have always concluded that their use increases mortality rate. Other than lack of power and lack of blinding, name 3 other methodological limitations of their analyses (3)?

Answer 29

-Lack of standardization of response to hemodynamic values -groups not balanced in terms of severity of illness -interpretative of PA catheter was not uniform o FACTT was done in ARDS/ALI patients only - Delayed insertion of PAC (PAC-Man trial) - Unclear control group (PAC-Man control group had a large number with some form of measured cardiac output)

Question 30

31. You are managing a trauma patient in emerg. that has a widened mediastinum on CXR, and you suspect an aortic tear. a. What other CXR findings (other than a widened mediastinum) make you suspect an aortic tear? List four (4). b. What site is most commonly affected in traumatic aortic injury i.e. where does the aorta usually tear (1)?

Answer 30

a. - left Apical capping - Pleural effusion - Loss of aortic knuckle - Deviated NG or paratracheal stripe - 1st rib fracture b.- aortic isthmus: Just distal to the ligamentum arteriosum (near left subclavian) Most blunt injuries of the thoracic aorta occur at the aortic isthmus just distal to the left subclavian artery [17]. A number of theories are used to explain the mechanism of thoracic aortic injury at the isthmus. It is likely that most injuries probably involve a combination of forces. ●The isthmus is thought to be a transition zone between the more mobile ascending aorta and arch and the relatively fixed descending thoracic aorta that allows for stretching with rapid deceleration [15]. ●The isthmus may be intrinsically weaker than the remainder of the aorta as evidenced by a series of tensile strength tests conducted on aortic samples [20]. ●Blunt aortic injury may be the result of a "water hammer" effect in which compression of the abdomen due to a sudden impact occludes the aorta, leading to rupture of the proximal, intrinsically weak isthmus or other susceptible portion of the aorta

Question 31

32. A patient with a brain tumour and a brainstem bleed (or tumour, I can’t remember) is now intubated, ventilated and unresponsive. He has lost all cranial nerve reflexes. How would you proceed to diagnose brain death (1)?

Answer 31

- Ensure no confounders - Proceed with apnea test o CO2 should increase to above \>/=60 and by greater than \>/=20mmHg above baseline and pH =7.28 ???

Question 32

33. A gentleman who is postop. day 3 from a liver transplant, is currently still encephalopathic, with an elevated INR and bilirubin levels. He is still intubated. He now develops infiltrates on his CXR and he fits criteria for ARDS. Besides an infectious process, what are the the top 3 reasons he might have ARDS (and they do say other than infectious causes) (3)?

Answer 32

- Primary non-function - Hepatic artery thrombosis - Acute rejection - Pancreatitis - TRALI -ischemia reperfusion syndrome -gastric aspiration -TACO

Question 33

34. An obese 35-year-old gentleman with cervical spine degenerative disc disease underwent spinal surgery and his myelopathy symptoms where improving. 7 days later he starts developing symptoms of sepsis and is found to have surgical site infection (and they give you an image of horribly big neck abcess/infection that is posterior in location and clearly where the surgery was, and somewhat close to the spinal cord). He undergoes surgical drainage and all is well. Then 10 days later he develops chest pain, hemoptysis, desaturation and he is now on a face mask of oxygen with borderline saturations, a BP of 100/60 and a HR of 110. He gets a CT chest and they show you the images. - What are the abnormalities that you see, be specific (2)? He clearly had bilateral large pulmonary emboli with filling defects on the CT angio. And then on the lung windows, it looks like he had a left sided wedge shaped opacity i.e. a pulmonary infarct, and right sided consolidation that is not so wedge shaped but rather looks more diffuse.The lung window they show you is at the level of the trachea/aortic arch so the consolidation is higher up in the lung. Then they give you a saggital view on the same page that just shows small lung volumes and confirms the bilateral pulmonary emboli. - Give three reasons or three arguments against administering thrombolytics in this gentleman (3). - Give two reasons or arguments for administering thrombolytics in him(2).

Answer 33

o He has had recent spinal surgery and is it risk for bleeding at the surgical site which could lead to neurologic involvement o Based on his current hemodynamics he does not have a massive PE and as such it is unclear if he has a mortality benefit from thrombolytics o Given that he already has infarcted lung there is concern that that area of lung may bleed significantly (he also already has hemoptysis) -cardiac arrest -significant shock unresponsive to usual care (including iv heparin) ...I had put these ones but I think Mo's are better o Based on the CT scan he appears to have a submassive PE and could benefit from thrombolytics and have a decrease in development of right sided dysfunction over the next year o In recent studies of submassive PE’s treated with thrombolytics less patients went on to have a cardiac arrest that received treatment Thrombosis Canada Harm with thrombolysis outweighs the benefit in most patients with PE except in those who present with massive PE. Massive PE is defined as anatomically extensive PE plus persistent hypotension or overt right heart failure, where the short-term mortality is \>15%. Therefore, IV thrombolysis should be reserved for patients with persistent hypotension (SBP \<90 mmHg or a 40 mmHg drop from baseline) refractory to a small fluid challenge or clinical right heart failure and who do not have a contraindication. Thrombolysis is NOT routinely indicated in submassive (intermediate-risk) PE (normotensive with right ventricular dysfunction), as it increases major bleeding and stroke (~12%) without survival benefit. For select patients with submassive PE who are not at high risk of bleeding AND who have severe persistent symptoms and signs of right heart failure or cardiopulmonary deterioration, thrombolysis may be considered after discussion with a thrombosis expert. Thrombolysis is given as follows: recombinant tissue plasminogen activator (rt-PA) 100 mg over 2 hours or 0.6 mg/kg as a bolus; or weight-adjusted tenectaplase (TNK) as a bolus. Intravenous UFH should be used initially after thrombolytic therapy, followed by anticoagulation with warfarin or a DOAC.

Question 34

35. Malignant causes of spinal cord compression, are best diagnosed with what test (1)? - Upon making that diagnosis what medication would you give and what would be your reason for giving it (1)?

Answer 34

- MRI o Dexamethasone to help reduce swelling/size of the mass and restore neurologic function

Question 35

36. They tell you about a depressed lady who is on clomipramine and then comes in for an appy and then for some reason, she is also on selegiline. And then the surgeons give her some dilauded. She gets an acute bout of irritability, fever (temperature 41 degrees), and they even tell you she has clonus, and has a CK of 50,000. - What is your diagnosis (1)? - What 3 things would you do to treat this (3)? - list ten drugs that can cause this condition?

Answer 35

Serotonin syndrome. o Stop the offending agents o Active cooling o Administer benzos o Consider cyproheptadine -see list Serotonin syndrome is often misdiagnosed as NMS, but the two can readily be distinguished on the basis of history, examination findings, and clinical course (table 3) [10]. NMS develops over days to weeks [10], whereas serotonin syndrome develops over 24 hours [3]. Serotonin syndrome is characterized by neuromuscular hyperreactivity (tremor, hyperreflexia, myoclonus), while NMS involves sluggish neuromuscular responses (rigidity, bradyreflexia). Hyperreflexia and myoclonus are rare in NMS [10]. In addition, resolution of NMS typically requires an average of nine days, compared with less than 24 hours (usually) for resolution of serotonin syndrome [10]. Hyperthermia, altered mental status, muscle rigidity, leukocytosis, elevated creatine phosphokinase, elevated hepatic transaminases, and metabolic acidosis are seen in severe cases of both conditions, which highlight the necessity of a thorough history and physical examination.

Question 36

37. An elderly gentleman on dabigatrin for atiral fibrillation develops a nasty GI bleed. - What is the mechanism of action of dabigatrin (1)? - What is the antidote (1)? - Other than upper GI endoscopy for control of GI bleeding and blood transfusion, what are two other things you could do to control the bleeding (2)?

Answer 36

o Direct thrombin inhibitor o Idarucizumab o Insertion of blackmore tube o PPI o Angiographic embolization o Surgery o Idarucizumab list from uptodate on life-threatening bleeding from dabigatran -Idarucizumab -Activated PCC\* (eg, FEIBA) -Antifibrinolytic agent (eg, tranexamic acid, epsilon-aminocaproic acid) -Anticoagulant discontinuation -Oral activated charcoal (if last dose within prior two hours) -Hemodialysis -RBC transfusions if needed for anemia -Platelet transfusions if needed for thrombocytopenia or impaired platelet function (eg, due to aspirin) -Surgical/endoscopic intervention if appropriate

Question 37

38. A guy swallows around 15 grams of acetaminophen. He presents jaundiced and encephalopathic. They give you labs showing his ALT and AST to be in the 2000’s range with a high INR (1.6) and high bilirubin. - What is your diagnosis (1)? - In addition to encephalopathy and coagulopathy what 4 other things should you watch for and monitor closely in this patient (4)?

Answer 37

Acute Liver failure secondary to acetaminophen toxicity. o King’s college criteria -Acidosis and lactate -Renal function -Glucose -hypothermia -cerebral edema -electrolyte disturbances -acute lung injury -infection …? -Bilirubin (not on the acetaminophen kings college criteria) -Phosphate (not on kings college criteria)

Question 38

39. SVC syndrome may have a variety of causes. - Other than tumours, name one other cause of SVC syndrome (i.e. a non-neoplastic cause)(1)? - List two manifestations of SVC syndrome (2)? - Upon making that diagnosis, how would you treat it(1)?

Answer 38

o Thrombosis o Fungal infection o Fibrosing mediastinitis (histoplasmosis, TB, actiniomycosis, aspergillosis, blastomycosis) o Postradiation fibrosis -Aortic aneurysm/vasculitis/fistula -pericarditis o Head and neck edema o Stridor, hoarseness, dysphagia o Cerebral edema (headache, confusion, coma) -compartment syndrome of arms -head of bed elevation -steroids -?thrombolysis if clot o If medical emergency (stridor, coma) radiation therapy o endovascular recanalization +/- stent - +/- glucocorticoids but careful in setting of undiagnosed malignancy as this can obscure the Dx

Question 39

40. A previously well nourished Crohn’s patient, is now fresh postop., and has ileus. He is expected to have a protracted recovery and will likely require TPN. - A. What are 4 reasons for not starting early TPN in him and just attempting enteral feeds according to the Canadian nutrition guidelines (4)? To clarify the question, they are asking about the reasons for not doing simultaneous TPN with enteral feeds in patients that are previously well nourished and expected to eventually require TPN eventually anyways.

Answer 39

old answer: o Based on the critical care guidelines enteral nutrition is still associated with decreased infections, trend towards reduced hospital stay, decreased ICU LOS, early enteral nutrition is associated with decreased hospital mortality. When looking at the results of the 2014 Harvey trial have to take into account that a low number of patients remained on PN after 5 days, as such the conclusion that there was no harm associated with early PN may be due to short duration. No benefit suggested in combined PN+EN start Given increased cost and concern of harm with PN, this is not recommended from Mo: increased risk of infections ICU LOC duration of MV my answer: I think the guidelines suggest doing PN only when you have exhausted all options for EN (SB feeding tubes, motility agents). Recommendation 2013: Based on one level 1 study and seven level 2 studies, for critically ill patients starting on enteral nutrition we recommend that parenteral nutrition not be started at the same time as enteral nutrition. In the patient who is not tolerating adequate enteral nutrition, there are insufficient data to put forward a recommendation about when parenteral nutrition should be initiated. Practitioners will have to weigh the safety and benefits of initiating PN in patients not tolerating EN on an individual case-by-case basis. We recommend that PN not be started in critically ill patients until all strategies to maximize EN delivery (such as small bowel feeding tubes, motility agents) have been attempted. Recommendation: We strongly recommend that early supplemental PN and high IV glucose not be used in unselected critically ill patients (i.e. low risk patients with short stay in ICU). In the patient who is not tolerating adequate enteral nutrition, there are insufficient data to put forward a recommendation about when parenteral nutrition should be initiated. Practitioners will have to weigh the safety and benefits of initiating PN in patients not tolerating EN on an individual case-by-case basis. 2015 Recommendation: Based on 6 level 2 studies, in critically ill patients with an intact gastrointestinal tract, we recommend that parenteral nutrition not be used routinely, but early PN should be considered in nutritionally high-risk patients with a relative contraindication to early EN.

Question 40

41. A patient with an anterior mediastinal mass that is compressing the trachea and the great vessels, is currently in respiratory distress. - Besides intubating, is there anything else you can do to relieve the distress (1)? - Anesthesia is not available and you end up being the one that will intubate this patient, what will be your primary goal during the intubation procedure (1)?

Answer 40

sit the patient up  Lateral or prone  Place patient upright, if still ongoing can attempt prone positioning +/- heliox? -keep pt awake and breathing -Perform an awake fiberoptic intubation to avoid collapse of the airway

Question 41

42. With regards to Ringers lactate and normal saline (0.9%), they ask you about their composition and pH. They actually give you a table to fill in for both with the columns labeled: sodium, potassium, calcium, glucose, chloride, magnesium, lactate and pH.

Answer 41

see table---

Question 42

43. Each of these drugs has been shown to worsen outcome in certain critically-ill patient populations. Outline the implicated mechanism for worsening outcome and the critical care population affected. -etomidate (1 point for it’s mechanism, and 1 point for the patient population) -dopamine (1 point for it’s mechanism, and 1 point for the patient population)

Answer 42

etomidate = imidazole-derived, sedative-hypnotic agent o Adrenal suppression o Septic patients dopamine = dopamine receptors o Increased arrhythmias and SVT o Patients with cardiogenic shock

Question 43

44. Name 3 things that cryoprecipitate contains (3)?

Answer 43

-Fibrinogen (factor I) -Factor VIII -Factor XIII -vWF

Question 44

45. The retrospecitve data looking at early FFP administration in trauma patients improving mortality is limited by which type of bias (1)?

Answer 44

-Survivorship bias oPatients who survive have time to get more FFP, therefore more FFP may not be associated with survival

Question 45

46. An elderly lady was recently started on metformin, enalapril and something else by her family doctor. They give you a long story where she develops a fever, chills and presents to the emergency department with a pH: 6.9, HCO3: 5, CO2: 15, blood glucose: 15 mmol/L, urine ketones: +1. - Based on this blood work, what is the diagnosis (1)? - What is the most important intervention to correct her acid base disturbance (1)? What are the indications for dialysis in this condition?

Answer 45

metformin induced lactate acidosis o Hemodialysis with bicarbonate buffer o Fluid resuscitation UTD: - NaHCO3 for acidosis with pH \<7.15 - hemodialysis in the following situations: RECOMMENDED * lactate \>20 mmol/L * Severe metabolic acidosis (pH ≤7.0) * Failure to improve (as determined by pH, lactate concentration, or clinical status) with supportive care and bicarbonate therapy within two to four hours. SUGGESTED * lactate 15 to 20 mmol/L * Metabolic acidosis (pH of 7.0 to 7.1) * Comorbidities: * Shock or persistent hemodynamic instability requiring vasopressor therapy despite acute administration of IV boluses of isotonic crystalloid totalling 30 mL/kg * Kidney injury – Creatine \>2 mg/dL (adults), or \>1.5 mg/dL (elderly), or 2 times upper limit of normal (children), or chronic kidney disease (stage 3b or higher with eGFR \<45 mL/min/1.73 m2, oliguria, or anuria) * Liver failure – liver injury with coagulopathy (INR \>1.5) and any degree of encephalopathy * Decreased level of consciousness

Question 46

47. They give you a case of a gentleman with baseline renal impairment (but not requiring dialysis). He needs to get a CT with contrast for some reason. - What are the risk factors for contrast nephropathy (4)? 
 - What are the strategies to prevent it (3)? - Now his creatinine triples (from 150 to 450) and his urine output is \<0.5ml/kg/hr. How would you describe his kidney injury according to the RIFLE (risk, injury failure, loss, end-stage renal disease) classification, and according to some other kidney society (I think it was the Acute Kidney Injury Network) (2)?

Answer 46

o Factors that increase risk of contrast-induced nephrotoxicity -CKD -diabetic nephropathy -CHF -increased age \>75yrs -hypovolemia -high osmolarity contrast media -larger amounts of contrast media -sepsis/acute hypotension -previous chemo -organ transplant -vascular disease (HTN, CHF, CAD, PVD) -nephrotoxic meds Prevention strategies -avoid dehydration -use alternative imaging is able to answer diagnostic question -avoid high osmolar contrast media -avoid nephrotoxic meds 48h prior to contrast administration -FLUID is the most important thing see: https://radiology.queensu.ca/source/Radiology/Consensus\_Guidelines.pdf 
 o RIFLE - Failure o AKIN - Stage 3 https://ccforum.biomedcentral.com/articles/10.1186/cc7759/figures/1

Question 47

48. List four antiseizure medications that can be used to control status epilepticus other than benzodiazepines (4)? Then they tell you not to specify the exact drug nor the exact receptor subtypes, but they ask you to name two types of receptors that these drugs work on (2). What do the drugs do to the membrane potential? Then they ask what effect does this have on the ability of the neuronal cells to reach the threshold for an action potential (1)?

Answer 47

- Dilantin - Valproatic acid - Keppra - Carbamazepine - Phenobarbital - Ketamine - Propofol phenytoin: Stabilizes neuronal membranes and decreases seizure activity by increasing efflux or decreasing influx of sodium ions across cell membranes in the motor cortex during generation of nerve impulses. valproic acid: Intravenous valproic acid is increasingly used in the treatment of status epilepticus. It is preferred over phenytoin in patients with primary generalized epilepsies, although these patients represent a relatively small proportion of those with GCSE. Causes increased availability of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, to brain neurons or may enhance the action of GABA or mimic its action at postsynaptic receptor sites. Also blocks voltage-dependent sodium channels, which results in suppression of high-frequency repetitive neuronal firing. levetiracetam: The precise mechanism by which levetiracetam exerts its antiepileptic effect is unknown. However, several studies have suggested the mechanism may involve one or more of the following central pharmacologic effects: inhibition of voltage-dependent N-type calcium channels; facilitation of GABA-ergic inhibitory transmission through displacement of negative modulators; reduction of delayed rectifier potassium current; and/or binding to synaptic proteins which modulate neurotransmitter release. phenobarbital: Phenobarbital is a very effective anticonvulsant, especially in the acute management of seizures, but it was not the best initial treatment in the VA comparative trial [3]. Various studies have shown a rate of seizure control of approximately 60 percent when phenobarbital is used alone, similar to that with lorazepam alone or the combination of phenytoin and diazepam [3,60]. High doses of phenobarbital will control almost any seizure [61], but at the cost of substantial sedation and potential reduction of blood pressure and respiration. Despite its efficacy, phenobarbital is generally not used as a first-line treatment in adults because administration is slow, it causes prolonged sedation, and it may involve a higher risk of hypoventilation and hypotension than either benzodiazepines, phenytoin, valproate, or levetiracetam. Long-acting barbiturate with sedative, hypnotic, and anticonvulsant properties (?receptor?). propofol: Propofol is a short-acting, lipophilic intravenous general anesthetic. The drug is unrelated to any of the currently used barbiturate, opioid, benzodiazepine, arylcyclohexylamine, or imidazole intravenous anesthetic agents. Propofol causes global CNS depression, presumably through agonism of GABAA receptors and perhaps reduced glutamatergic activity through NMDA receptor blockade. - GABA -Na channel - Glutamate -NMDA - They cause hyperpolarization (increased GABA tone allows more chloride to flow into the cell) - Make it more difficult for the neuronoal cells to reach threshold potential

Question 48

49. Lady with recent diagnosis of systemic lupus has been prescribed an ACE inhibitor and another antihypertensive recently. She stops taking her medications for 2 days and now presents with a BP of 224/131 and papilledema, but is otherwise neurologically intact. - What BP would you target in the first 6 hours of trying to control her blood pressure (1) and they give you 3 lines to explain. - Name 3 drugs (available in Canada) of different classes that you would use to control 
her blood pressure (3). 


Answer 48

o Decrease by no more than 25%, and target to decrease the diastolic BP to 100-105 would target SBP of 180 UTD: In malignant hypertension, the initial aim of treatment is to lower the diastolic pressure to approximately 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in blood pressure not exceeding 25 percent of the presenting value. More aggressive blood pressure lowering is generally unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to cerebral ischemia, as well as increasing the risk of coronary and renal ischemia. ...which seems different from the recommendations for hypertensive emergency/retinopathy: The initial aim of treatment in patients with moderate to severe hypertensive retinopathy and/or hypertensive encephalopathy is to rapidly lower the mean arterial pressure by about 10 to 15 percent in the first hour, and by no more than 25 percent compared with baseline by the end of the first day of treatment [12,13]. This level of blood pressure (BP) control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce BP below the autoregulatory range, possibly leading to ischemic events (such as stroke or myocardial infarction) o Labetalol o Nicardapine o Nitroprusside o Hydralazine -? captopril?

Question 49

50. They show you a pressure-time graph showing the peak pressure, plateau pressure and the peak to plateau difference. - Name one lung disease that would increase your peak to plateau difference (1) 
 - Name one lung disease that would decrease your peak to plateau difference (1). [
Note that the question did ask for a lung disease that would decrease the peak to plateau difference (rather than a disease that would increase both the peak and the plateau without affecting the difference like for example ARDS)]

Answer 49

o Asthma o ?ARDS but this would increase both peak and plateau pressures...unsure

Question 50

51. A 30 year old gentleman is now intubated and and ventilated on an assist control mode with a Vt of 600 ml, Vt 600, RR 22, PEEP of 10. They give you his blood gas, and it looks pretty normal for a 30 year old. His pCO2 on the blood gas is 40 mmHg. They tell you his end-tidal CO2 is 30 mmHg. - How do you calculate dead space? Please show us the equation you used and plug in the numbers without actually performing the calculation (1). - Give us two reasons that he might have a large amount of deadspace (2)?

Answer 50

o Dead space = Vd/Vt = (PaCO2-PeCOS)/(PaCO2) o Vd/600 = (40-30)/(40) o Vd = 10/40\*600 o = 150 a) Bohr Equation: dead space = tidal volume X [(PaCO2 – PeCO2) / PaCO2] b) -decreased cardiac output -pulmonary embolism (or air, fat, amniotic fluid) -COPD/emphysema (less alveolar walls for gas exchange) -ARDS (protein rich fluid leaks from capillaries into alveoli causing development of hyaline membranes which impair gas exchange) -increasing PEEP might increase deadspace by impairing perfusion of overdistended regions -hypovolemia ...ETT (but I guess technically this would only increase anatomic deadspace, not alveolar) Anatomic dead space specifically refers to the volume of air located in the segments of the respiratory tract that are responsible for conducting air to the alveoli and respiratory bronchioles but do not take part in the process of gas exchange itself. These segments of the respiratory tract include the upper airways, trachea, bronchi, and terminal bronchioles. Alveolar dead space, on the other hand, refers to the volume of air in alveoli that are ventilated but not perfused, and thus gas exchange does not take place. Physiologic dead space is the sum of the anatomic and alveolar dead space. Breaking down this equation, there is tidal volume which is the normal amount of inspired and expired gas equivalent to 500 mL. This inspired air is assumed to contain relatively zero amount of carbon dioxide. The second half of the equation is representative of the fractional amount of dead space. Simply translating to the amount of carbon dioxide (CO2) exchanged for oxygen (O2). The exchange of gases through the respiratory membrane is so rapid that we can assume the arterial CO2 partial pressure is equal to that in the alveoli. The exchanged CO2 will now become PeCO2. PeCO2 will always have a smaller value than arterial CO2 due to the mixture and dilution of CO2 gases with the 150 mL of anatomical dead space sitting in the conductive airway that is assumed to be free of CO2. Thus, by subtracting PeCO2 from PaCO2 and dividing by the PaCO2 one has you have determined a fractional equivalent of the lung is not contributing to gas exchange. Multiply that value by the normal amount of air inspired (VT) you achieve a value for physiologic dead space. Increase in dead space is usually seen in an abrupt decrease in cardiac output, hypotension or pulmonary embolism, due to fat, air, or amniotic fluid. While obstruction can cause decreased perfusion in PE, the greatest decrease in pulmonary blood flow is due to vasoconstriction caused by locally released vasoactive substances. In these situations, a lack of gas exchange at the alveolar level results in a decrease of PaCO2 gas being exchange by the remaining healthy alveoli and ultimately a lower PeCO2. Looking back at the equation, a lower PeCO2 will result in an increase in the physiologic dead space value for that individual.

Question 51

52. An elderly patient arrested on the ward after an orthopaedic procedure. What is the role of an end-tidal CO2 monitor in the arrest (2)? 


Answer 51

- Help determine quality of CPR - Act as an indicator of ROSC - confirm ETT placement? -help prognosticate poor outcome at 20mins if no ROSC

Question 52

53. A patient has decided on withdrawal of life support. You remove the tube and he is now dysgenic and looks distressed. 
 - What pharmacologic intervention has the most evidence in palliative care for relief of respiratory distress (1)? 
 - In addition to the medication above and non-invasive ventilation, list 3 other interventions that you could do to relieve the dyspnea (3). Note that medications of the same class will be counted as one answer. 


Answer 52

morphine o Promethazine o Fan with cool air blowing on face o Benzos o Bronchodilators -oxygen if hypoxic -pursed lip breathing -relaxation techniques

Question 53

54. A trauma patient with pelvic fracture and pelvic bleed requires embolization in interventional radiology to control the bleeding. Now the patient is left with a pelvic hematoma. Name two potential complications of pelvic hematoma (2)?

Answer 53

- Infection - Ileus - High risk of DVT from pelvis vein compression -abdo compartment syndrome -ureteric obstruction

Question 54

55. Measuring intra-abdominal pressures is part of the skills required of an intensivist. - According to some important surgical society, what are the 4 conditions that have to 
apply to obtain an accurate intrabdominal pressure measurement (4). - With regards to the practical aspect of measuring intrabdominal pressures, outline the 
steps of measuring intraabdominal pressure (4).

Answer 54

o Supine o absent abdominal muscle contractions o Measured at end expiration o Transducer leveled at mid-axillary line https://link.springer.com/article/10.1007%2Fs00134-013-2906-z 2. The reference standard for intermittent IAP measurements is via the bladder with a maximal instillation volume of 25 mL of sterile saline 3. IAP should be expressed in mmHg and measured at end-expiration in the supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line 4. IAP is approximately 5–7 mmHg in critically ill adults 5. IAH is defined by a sustained or repeated pathological elevation in IAP C 12 mmHg 6. ACS is defined as a sustained IAP[20 mmHg (with or without an APP\60 mmHg) that is associated with new organ dysfunction/failure 7. IAH is graded as follows Grade I, IAP 12–15 mmHg Grade II, IAP 16–20 mmHg Grade III, IAP 21–25 mmHg Grade IV, IAP[25 mmHg o Clamp drainage tube of urinary catheter o Instill up to 25mL of sterile saline into the bladder o Connect pressure transducer to aspiration port o Take measurement at end expiration leveled at mid-axillary line

Question 55

56. Elderly lady with peripheral vascular disease has abdominal pain after meals, has significant weight loss and is diagnosed with intestinal angina. - Name the three arteries that supply the gastrointestinal tract and describe what parts of 
the gut they supply (3 for the names of the arteries, and 3 of their region of supply). 
 - In this lady, what artery is likely involved (1)? - 
She is now doing very poorly and you are called to assess her. She has severe 
abdominal pain, is tachypnic, and has a lactate of 3.5. They show you a saggital CT image of her abdomen with a horribly calcified aorta and stool & air though-out her abdomen, all the way to the rectum but she doesn’t appear to have frank air-fluid levels. Then they show you a CT angiogram image of her mesenteric vessels, but I have no clue how they would normally look and whether or not she had SMA obstruction. By the flow of the question however, I think she had SMA obstruction and bowel ischemia. Then they ask you what is the most important finding that you see on the imaging studies (1)
 - Then they ask what is the treatment is for this condition(1)? (
A colleague of mine thought there was extravastion of dye from one of the mesenteric vessels on the angiogram they showed (i.e. thought she was bleeding into her belly). Not really sure that was the case though. Regardless both would require an exploratory laparotomy.) What are indications for surgical vs endoscopic management?

Answer 55

o Celiac trunk  Foregut • Lower one-third of esophagus to second part of duodenum o SMA  Midegut • Middle of second part of duodenum to distal one-third of transverse colon o IMA  Hindgut • Distal one-third of transverse colon to halfway down anal canal o SMA o SMA occlusion Surgical exploration due to presence of bowel ischemia and instability...? ●Some patients (eg, acute-on-chronic occlusion) who are hemodynamically stable and do not have clinical signs of advanced bowel ischemia can be observed while on heparin anticoagulation, if there is evidence of good collateral blood flow on vascular imaging studies. Antiplatelet therapy may be justified in this setting if the risk of progressive ischemia appears to be greater than the risk of bleeding [32,34]. The patient should have serial clinical assessment (laboratory, physical examination) with a low threshold to repeat abdominal imaging studies or, if abdominal symptoms progress, surgical or endovascular intervention. ●A palliative approach may be the best option for poor-risk surgical candidates with extensive transmural infarction (eg, small bowel up to the midtransverse colon). Extensive bowel resection would be inappropriate for these patients and may also be inappropriate for a subset of patients who might otherwise be expected to tolerate the procedure but for whom lifelong parenteral nutrition would be unacceptable. ●Patients who are good-risk surgical candidates with indications for immediate laparotomy such as peritonitis or radiologic features of advanced bowel ischemia (free air, extensive pneumatosis) should be taken directly to the operating room for exploration. Resection of bowel should ideally be delayed until after mesenteric arterial revascularization can be performed to salvage as much bowel as possible; however, in practice, this sequence does not commonly occur. In situations where an individual with appropriate vascular expertise is not immediately available, resection of grossly necrotic or perforated bowel (leaving any questionable bowel) while awaiting intraoperative consultation is appropriate, or, alternatively, following resection, abdominal closure and transfer is also a reasonable option when required. •The traditional treatment for mesenteric embolism is open surgical embolectomy, which, in addition to expeditiously clearing the thrombus, allows direct assessment of bowel viability. •Open surgical treatment of mesenteric artery thrombosis is treated principally with mesenteric bypass. Thrombectomy alone is unlikely to offer a durable solution due to the presence of thrombogenic atherosclerotic plaques. Intraoperative retrograde superior mesenteric artery angioplasty and stenting is another option, particularly in the presence of gross contamination where bypass is more problematic. ●Patients who are hemodynamically stable and who do NOT have clinical or radiologic signs of advanced intestinal ischemia may be candidates for a primary endovascular approach. •Although we prefer open surgical thrombectomy for patients with acute embolism, percutaneous aspiration of the clot or catheter-directed thrombolytic therapy is another approach that has been used successfully with reasonable outcomes. •For patients with acute mesenteric thrombosis, a primary endovascular approach is a reasonable option with close clinical monitoring.

Question 56

57. What is the differential of wide complex tachycardias, besides VT (2)? - What findings on ECG would favour VT (they ask for only 2 findings?

Answer 56

-VT -SVT with aberrancy -SVT with pre-excitation -paced rhythm -artifact -AV dissociation -capture or fusion beats

Question 57

58. An elderly gentleman underwent a CABG & AVR and was “excessively oozy” in the OR. He is now stable in the CVICU. He had been looking good and they had stopped all the sedation when all of a sudden he starts seizing. List 4 potential causes for seizures in this gentleman (4)?

Answer 57

-TXA -ICH -ischemic stroke -air embolism

Question 58

59. Label the following with correct precautions to be taken in the ICU (contact, droplet or airborne). - Infulenza A - seasonal - Nisseria meningitides - Mycobacterium tuberculosis - Clostridium difficile

Answer 58

- Influenza A - seasonal (1) 
 o Droplet plus STANDARD - Nisseria meningitides (1) 
 o Droplet plus STANDARD - Mycobacterium tuberculosis(1) 
 o Airborne plus STANDARD - Clostridium difficile o Contact plus STANDARD

Question 59

60. A critically ill lady is found to have C diff colitis with pseudomembranes on endoscopy. - Name 3 risk factors for developing C diff colitis (3). 
 - A certain strain of C diff is associated with severe C diff outbreaks. What is the 
characteristic of this strain (1). 
 - What are four ways of treating recurrent C diff collitis(4).

Answer 59


o Recent antibiotic exposure o Hospitalization o Advanced age o Severe illness o Gastric acid suppression o Enteral feeding o GI surgery o Obesity o Cancer chemotherapy o Hematopoietic stem cell transplant 
 o NAP1/BI/027  Produces binary toxin  Produces larger quantities of toxin A and B in vitro than other strains  Partial deletion of tcdC, a gene that is responsible for down regulation of toxin production  Resistant to fluoroquinolones in vitro -vanco in tapered and pulsed regimen -fidaxomicin -vanco followed by rifaximin -Fecal transplantation (fpr pts with multiple recurrences) IDSA guidelines: XXXI. What are the best treatments for recurrent CDI? 1. Treat a first recurrence of CDI with oral vancomycin as a tapered and pulsed regimen rather than a second standard 10-day course of vancomycin (weak recommendation, low quality of evidence), OR 2. Treat a first recurrence of CDI with a 10-day course of fidaxomicin rather than a standard 10-day course of vancomycin (weak recommendation, moderate quality of evidence), OR 3. Treat a first recurrence of CDI with a standard 10-day course of vancomycin rather than a second course of metronidazole if metronidazole was used for the primary episode (weak recommendation, low quality of evidence). 4. Antibiotic treatment options for patients with \>1 recurrence of CDI include oral vancomycin therapy using a tapered and pulsed regimen (weak recommendation, low quality of evidence), a standard course of oral vancomycin followed by rifaximin (weak recommendation, low quality of evidence), or fidaxomicin (weak recommendation, low quality of evidence). 5. Fecal microbiota transplantation is recommended for patients with multiple recurrences of CDI who have failed appropriate antibiotic treatments (strong recommendation, moderate quality of evidence). 6. There are insufficient data at this time to recommend extending the length of anti–C. difficile treatment beyond the recommended treatment course or restarting an anti–C. difficile agent empirically for patients who require continued antibiotic therapy directed against the underlying infection or who require retreatment with antibiotics shortly after completion of CDI treatment, respectively (no recommendation).

Question 60

61. A gentleman with an open skin wound is admitted to the ICU with tetanus. What would your care for this gentleman comprise (4)?

Answer 60

* debride wound * metronidazole * human tetanus immune globulin * tetanus vaccine * benzos +/- NMB for spasms * MgSO4 +/- labetalol for autonomic instability * supportive care - **wound debridement** (to eradicate spores and necrotic tissue) - **antibiotics** (metronidazole is first line) - **human tetanus immune globulin**: Neutralization of unbound toxin — Since tetanus toxin is irreversibly bound to tissues, only unbound toxin is available for neutralization. Unbound toxin has been demonstrated in 10 percent of serum samples and 4 percent of cerebrospinal fluid (CSF) samples of cases upon presentation [39]. The use of passive immunization to neutralize unbound toxin is associated with improved survival, and it is considered to be standard treatment. manage autonomic instability. - **active immunization**: Since tetanus is one of the few bacterial diseases that does not confer immunity following recovery from acute illness, all patients with tetanus should receive active immunization with a full series (eg, three doses in adults and children \>7 years old) of tetanus and diphtheria toxoid-containing vaccines, commencing immediately upon diagnosis. **Control of muscle spasms** — Generalized muscle spasms are life threatening since they can cause respiratory failure, lead to aspiration, and induce generalized exhaustion in the patient.---BENZOs +/- NMB -**Management of autonomic dysfunction** — Several drugs have been used to produce adrenergic blockade and suppress autonomic hyperactivity; only treatment with magnesium sulfate has been studied in a randomized clinical trial in tetanus [47] because of its use in clinical series for the management of autonomic dysfunction and as adjunctive treatment for controlling spasms [47-50]. ---**Magnesium sulfate** — Magnesium sulfate acts as a presynaptic neuromuscular blocker, blocks catecholamine release from nerves, and reduces receptor responsiveness to catecholamines [51]. It has the advantage of worldwide experience in the treatment of eclampsia. ---**Beta blockade** — Labetalol (0.25 to 1.0 mg/min) has frequently been administered because of its dual alpha- and beta-blocking properties.

Question 61

62. A 35-year-old gentleman is diagnosed with meningitis. - What factors would determine your antibiotic choice for meningitis treatment (2). - Would you recommend giving anything else in addition to antibiotics? Justify your 
answer (1).

Answer 61

-Patient age (\>50yrs) -Immune status -alcoholism -debilitating illness -pregnancy -post trauma/post operative -shunt/EVD ventriculitis o Steroids Corticosteroids have been shown to decreaes mortality and hearing loss in adult pts with S. pneumonie meningitis...they are not recommended if Abx have already been administered!!!

Question 62

63. With regards to ventilator associated pneumonia. - Indicate 5 ways of preventing VAP (5). 
 - Name two risk factors for multi-drug resistant VAP (2). 


Answer 62

VAP prevention (specific guideline, see table 2 pg 920): http://www.inicc.org/media/docs/StrategiestoPreventVAPinAcuteCareHospitals-2014Update.pdf -use NIPPV (minimize invasive MV) -manage pts without sedation whenever possible -interrupt sedation daily -assess readiness to extubate daily -perform SBTs with sedatives turned off -facilitate early mobility -utilize ETT with supraglottic suction for pts expected to require \>48-72hrs of MV -change vent circuit ONLY if visibly soiled or malfunctioning -elevate head of bed 30-45degrees evidence that intervention improves outcomes but insufficient data on possible risks: -selective oral/digestive decontamination -???regular oral care with chlorhexidine no impact on VAP rates/average duration of MV/LoS/mortality: -stress ulcer prophylaxis -early tracheostomy -monitoring gastric residuals -early parenteral nutrition VAP Rx duration: 7 day course recommended for both HAP and VAP. o IV antibiotics in the past 90 days o Hospital stay \>/= 5 days prior to occurrence of VAP o septic shock at time of VAP -ARDS before VAP -acute RRT prior to VAP

Question 63

64. How are post pyloric feeds beneficial (4).
That was part of a question that I forget the rest of.

Answer 63

- Minimize aspiration risk - Decreased gastric distension (avoiding interference with respiratory function) - Minimize pancreatic stimulation in acute pancreatitis - Higher rates of adequate nutrition

Question 64

65. What are the diagnostic criteria for catheter-related blood stream infections (4)?

Answer 64

A CLABSI is a primary BSI in a patient that had a central line within the 48-hour period before the development of the BSI and is not bloodstream related to an infection at another site. CVC and peripheral cultures meeting either: Quantitative BCx criteria: Catheter BCx ≥ 3-fold higher CFU/ml compared to peripheral BCx or 2nd CVC lumen BCx) OR Differential time to positivity (DTP): Catheter BCx sample grows first ie ≥ 2 hours before the growth of peripheral BCx or 2nd CVC lumen BCx) CVC and second port CVC meeting either of: Quantitative BCx criteria: Catheter BCx ≥ 3-fold higher CFU/ml compared to peripheral BCx or 2nd CVC lumen BCx) OR Differential time to positivity (DTP): Catheter BCx sample grows first ie ≥ 2 hours before the growth of peripheral BCx or 2nd CVC lumen BCx) CVC tip and peripheral blood culture: Same organism from catheter tip (meet significant growth criteria) and peripheral BCx. Significant growth criteria: Quantitative method: 102 CFU/ml (intraluminal sonication/flushing of the catheter) OR Semi-quantitative method: ≥ 15 CFU/Plate (roll plate technique)

Question 65

66. A certain treatment was being proposed and patient consent was being obtained, and then they asked how you would determine if this patient is competent (2)?

Answer 65

- Semi-structured patient interview using a validated tool (i.e. MacCAT-T) - Assess understanding, reasoning, ability to express a choice, and an appreciation of the situation There is a legal presumption that a patient is capable of consenting to investigation and treatment unless there is reason to believe otherwise. Although the wording of the legal tests may differ, an individual who is able to understand the nature and anticipated effects of the proposed investigation or treatment and available alternatives, including the consequences of refusing, is typically considered mentally capable to give consent. Because incapacity can be temporary, it may be necessary to reassess capacity to consent at appropriate intervals.

Question 66

67. You are on the phone with another doctor in a peripheral hospital. He is dealing with a burn patient, that has burns to his head, chest and arms. What would you ask him to do before transferring the patient over to your hospital (2)?

Answer 66

- Intubate - If available give hydroxycobalamine on spec for cyanide toxicity (+/- sodium thiosulfate 25%) - Fluid resuscitate - Analgesia and sedation - Maintain on 100% FiO2 +/- consider escarotomy (should be performed within six hours for extremities with full-thickness burns as these eschars will be excised in the coming days)

Question 67

68. A lady collapsed at home, and they showing you her CT head, her CXR which shows pulmonary edema, and her EKG with some precordial ST elevation. They ask if a unifying diagnosis could explain all this, or they say how would you link all these findings pathophysiologally and they ask you to explain (3).

Answer 67

SAH --\> Takotsubo’s --\> CHF o Catecholamine excess induces coronary artery vasospasm leads to stress induced cardiomyopathy, leads to decreased LV function allowing for pulmonary edema The pathogenesis of this disorder is not well understood. It is not known why this disorder affects postmenopausal women disproportionately or why the left ventricular (LV) mid-cavity and apex are predominantly affected. Studies comparing LV systolic and diastolic function in patients with stress cardiomyopathy with function in patients with acute myocardial infarction (MI) have reached differing conclusions [21,22]. Initial systolic function may be similar [21] or worse [22] with stress cardiomyopathy compared with acute MI, while diastolic function may be similar [21] or better [22] with stress cardiomyopathy. Postulated mechanisms include catecholamine excess [8,23], microvascular dysfunction, and coronary artery spasm. Also, dynamic mid-cavity or LV outflow tract obstruction has been documented in some patients and may contribute to apical dysfunction. A number of features of stress cardiomyopathy, including its association with physical or emotional stress [4,5,7-10,16,20,24], suggest that this disorder may be caused by diffuse catecholamine-induced microvascular spasm or dysfunction, resulting in myocardial stunning [18], or by direct catecholamine-associated myocardial toxicity.

Question 68

69. List 5 mechanisms for hypotension in sepsis (5).

Answer 68

vasodilation from vasoactive mediators (eg NO) vasoplegia/vasodilation from impaired release of endogenous vasopressin redistribution of vascular fluid increased endothelial permeability redistribution of vascular fluid reduced arterial vascular tone (thereby increasing capillary pressure) decreased ventricular systolic and diastolic performance Hypotension due to diffuse vasodilation is the most severe expression of circulatory dysfunction in sepsis. It is probably an unintended consequence of the release of vasoactive mediators, whose purpose is to improve metabolic autoregulation (the process that matches oxygen availability to changing tissue oxygen needs) by inducing appropriate vasodilation. Mediators include the vasodilators prostacyclin and nitric oxide (NO), which are produced by endothelial cells. NO is believed to play a central role in the vasodilation accompanying septic shock, since NO synthase can be induced by incubating vascular endothelium and smooth muscle with endotoxin [50,51]. When NO reaches the systemic circulation, it depresses metabolic autoregulation at all of the central, regional, and microregional levels of the circulation. In addition, NO may trigger an injury in the central nervous system that is localized to areas that regulate autonomic control [52]. Another factor that may contribute to the persistence of vasodilation during sepsis is impaired compensatory secretion of antidiuretic hormone (vasopressin). This hypothesis is supported by a study that found that plasma vasopressin levels were lower in patients with septic shock than in patients with cardiogenic shock (3.1 versus 22.7 pg/mL), even though the groups had similar systemic blood pressures [53]. It is also supported by numerous small studies that demonstrated that vasopressin improves hemodynamics and allows other pressors to be withdrawn [54-57]. Vasodilation is not the only cause of hypotension during sepsis. Hypotension may also be due to redistribution of intravascular fluid. This is a consequence of both increased endothelial permeability and reduced arterial vascular tone leading to increased capillary pressure. In addition to these diffuse effects of sepsis on the circulation, there are also localized effects: ●In the central circulation (ie, heart and large vessels), decreased systolic and diastolic ventricular performance due to the release of myocardial depressant substances is an early manifestation of sepsis [58,59]. Despite this, ventricular function may still be able to use the Frank Starling mechanism to increase cardiac output, which is necessary to maintain the blood pressure in the presence of systemic vasodilation. Patients with preexisting cardiac disease (eg, elderly patients) are often unable to increase their cardiac output appropriately.

Question 69

70. In general, the immune system is divided into innate and acquired immunity. - What class of proteins is responsible for humoral immunity (1)? - What type of cells produce these proteins (1)? - What are the two cell types responsible for innate immunity (2)?

Answer 69

o Antibodies o B lymphocytes -\> plasma cells o Neutrophils o Monocytes and macrophages o NK cells o Epithelial cells o Mast cells o Platelets o Innate lymphoid cells

Question 70

71. You perform a pleural tap on a patient where it is clinically indicated. - How would you differentiate between an exudative and a transudative effusion (2)? - You do the tap and it is bloody. What is the differential of a bloody pleural tap (4)?

Answer 70

Light’s criteria Exudative if any of: • Pleural fluid PROtein/serum PROtein ratio \>0.5 • Pleural fluid LDH/serum LDH ratio greater than 0.6 • Pleural fluid LDH \> 2/3rds the upper limit of the lab’s normal serum LDH o Traumatic tap o Malignancy o Benign asbestos pleural effusion o Post cardiac injury syndrome o Pulmonary infarction (PE) -bleeding diathesis -aortic dissection/rupture -Infections such as dengue hemorrhagic fever, pulmonary tuberculosis

Question 71

72. You are in the hospital elevator with other people. A medical team - a staff person, the resident and the student are discussing a case that they are caring for. They are careful enough not to mention his name but keep referring to him as the “pneumonia guy”. They mention where he is located and lot of detail regarding his case. - What is happening here (1)? - What would you do in this situation (1)?

Answer 71

o Breach of confidentiality o In a polite manner inform the staff person that the information they are discussing about this patient provides enough detail that I would be able to easily identify this patient, and as such represents a breach of confidentiality. And remind him that even though I am a physician I am not within the patient’s circle of care.

Question 72

73. You are the medical director of the ICU, and two of your staff are arguing loudly inside the unit, to the degree that the nurses are starting to get uncomfortable. You ask them to take this discussion outside the ICU and to come talk about this in your office. But they just ignore you and walk away. What three things can you do to deal with this situation? The question states that they are normally very polite and professional people (3).

Answer 72

- Institute a time-out - Act as a mediator - Inform them that their actions are being disruptive and that they must leave the unit, but they are more than welcome to use your office - Attempt to identify the cause of the argument - Organize a conference/mediation with all players involved, including yourself, the nurse manager, and the two staff involved to address this situation as well as its impact - determine if other personal issues at play that may be causing them to be upset/burnt out/irritable

Question 73

74. What are the features of HELLP syndrome (3)? What obstetric condition can develop HELLP syndrome (1)?

Answer 73

●Hemolysis, established by at least two of the following: •Peripheral smear with schistocytes and burr cells •Serum bilirubin ≥1.2 mg/dL (20.52 micromol) •Low serum haptoglobin (≤25 mg/dL) or lactate dehydrogenase (LDH) ≥2 times the upper level of normal (in the local laboratory) •Severe anemia, unrelated to blood loss ●Elevated liver enzymes: •Aspartate aminotransferase (AST) or alanine aminotransferase (ALT) ≥2 times the upper level of normal (in the local laboratory) ●Low platelets: \<100,000 cells/microL oPre-eclampsia

Question 74

75. A lady with chronic long-standing pulmonary hypertension develops respiratory distress and is intubated at home and brought to hospital. In the ICU she is hypotensive, and hypoxic. Her PA catheter shows a pulmonary systolic pressure of 80. Her CI is 1.8. (N=2.8-4.2) - Why do you think she is hypotensive (1)? - What interventions could you do to improve her hypotension (3)? - Why would administering intravenous fluids in this patient lead to more hypotension i.e. be harmful (1)?

Answer 74

o Right heart failure o Improve oxygenation (decrease hypoxic vasoconstriction) o Inhaled nitric oxide o Milrinone ? PEEP titration to minimize RV afterload o Lead to further dilation of RV, which would impede LV

Question 75

76. You are called to help intubate a patient with tongue cancer. Your colleagues have tried to intubate multiple times and attempts with the layngoscope, glidesope, and fiberoptic bronchoscope have all been unsuccessful. It is now becoming difficult to bag mask ventilate this patient. What would you do (1)?

Answer 75

- Have one operator continue to bag from above and proceed with a surgical airway, cricothyroidotomy

Question 76

77. List 4 different conditions that could cause hypercapnic respiratory failure. Please make sure the different diseases/conditions have distinctly different mechanisms of causing hypercapnea (4).

Answer 76

mechanistically causes are: 1) decreased global minute ventilation 2) increased dead space 3) increased CO2 production (rarely primary cause) 1) decreased drive (WONT BREATH): Opioid overdose from decreased central drive to breath 2) Decreased respiratory nerve and muscle function and/or decreased thoracic cage function (CANT BREATH): ALS from respiratory muscle weakness 3) increased dead space COPD 4) asthma from decreased expiratory flow? 5) increased dead space from acute large PE? - PE: patients with acute PE, total dead space increases because lung units continue to be ventilated despite diminished or absent perfusion. Complete obstruction of a pulmonary artery by an embolus causes an increase in anatomic dead space. In contrast, incomplete obstruction of a pulmonary artery increases physiological dead space, ie, ratios of ventilation to perfusion increase. Increased dead space impairs the efficient elimination of carbon dioxide. However, medullary chemoreceptors sense any increase in arterial PCO2, and they will increase the total minute ventilation, thereby lowering the arterial PCO2 to normal and often below normal. Thus, most patients with PE present with a lower than normal arterial PCO2 and respiratory alkalosis because of an increased total minute ventilation. Limited data suggest that the increased total minute ventilation occurs because of reflex stimulation of irritant and juxta capillary sensors in the lung.

Question 77

78. Severe hemodynamic instability precludes organ donation in around 20% of patients diagnosed with brain death. In addition to the the development of diabetes insipidus causing excessive fluid loss, list two other causes of hemodynamic instability in brain dead patients (2).

Answer 77

- low preload --\> DI (already in answer), cerebral salt wasting, treatment for ICP with mannitol, vasodilation on rewarming (relative hypovolemia from increased vascular capacitance) -thyroid deficiency -low afterload --\> Loss of sympathetic tone from catecholamine depletion after surge -low afterload --\> Adrenal insufficiency (failure of pituitary axis) -low contractility --\> LV dysfunction (Takotsubo’s)

Question 78

79. List four pharmacological lines of treatment for calcium channel blocker toxicity other than catecholamine infusions (4).

Answer 78

-Calcium -High dose insulin (plus dextrose) -Intra-lipid -Glucagon -consider atropine for bradycardic patients but often not effective in CCB overdose pts