2018

Question 1

List 3 interventions that decrease mortality during variceal bleeding in cirrhotics

Answer 1

1. Antibiotic prophylaxis (broad-spectrum for 7d, Ceftriaxone or cipro if PO needed), they reduce risk of mortality, infections (SBP, UTI) and rebleeding. Ceftriaxone has been shown to be more effective than oral norfloxacin likely due to high rates of quinolone resistant organisms.
2. Vasoactive agents are associated with lower 7d all-cause mortality and lower transfusion requirements. Three most commonly used are somatostatin, octreotide and terlipressin. Terlipressin a synthetic analogue of vasopressin that has a longer biological activity and significantly fewer side effects, is effective in controlling acute variceal hemorrhage and has been associated with a decreased mortality. Given 2mg IV q4H and can be titrated down to 1mg q4H once hemorrhage is controlled.
3. Restrictive transfusion strategy for threshold of 70-90, rather than 90-110, was observed to lead to lower mortality and rebleeding rates. —this may be due to increase in hepatic venous pressure gradient (=wedged hepatic venous pressure - IVC pressure).

correction of coagulopathy (from guidelines): Regarding correction of coagulopathy, RCTs of recombinant factor VIIa have not shown a clear benefit, and therefore correcting the international normalized ratio (INR) by the use of fresh frozen plasma or factor VIIa is not recommended, particularly given that INR is not a reliable indicator of coagulation status in cirrhosis. No recommendations can be given regarding platelet transfusion in patients with variceal hemorrhage.

Endoscopy should be done ASAP and no more than 12hrs after presentation. If variceal source is confirmed banding should be performed but no mention on whether this actually affects mortality.

EGD should be performed within 12 hours of admission and once the patient is hemodynamically stable.

If a variceal source is confirmed/suspected, EVL should be performed.

In patients at high risk of failure or rebleeding (CTP class C cirrhosis or CTP class B with active bleeding on endoscopy) who have no contraindications for TIPS, an “early” (preemptive) TIPS within 72 hours from EGD/EVL may benefit selected patients.

For patients in whom an early TIPS is not performed, intravenous vasoactive drugs should be continued for 2-5 days and NSBBs initiated once vasoactive drugs are discontinued. Rescue TIPS is indicated in these patients if hemorrhage cannot be controlled or if bleeding recurs despite vasoactive drugs+EVL.

In patients in whom TIPS is performed successfully, intravenous vasoactive drugs can be discontinued.

Question 2

what are features of decompensated cirrhosis?

Answer 2

hepatic encephalopathy

variceal hemorrhage

ascites

Question 3

What are 3 factors that contribute to coagulopathy in a severe trauma patient?

Answer 3

1. acidosis from inadequate tissue perfusion (lactic acidosis), shown in vitro at pH<7.2
2. hypothermia (mild 34-36, moderate 32-34, severe <32), from exposure/examination, cold IV fluids. Causes platelet dysfunction and impaired enzyme function
3. resuscitation-associated (aka. dilutional) coagulopathy due to large volumes of unbalanced IV fluids or unbalanced component blood administration
4. DIC is a systemic process producing consumptive coagulopathy in concert with diffuse microvascular thrombosis. In trauma patients, tissue-injury-induced exposure of tissue factor and activation of the extrinsic coagulation cascade leads to thrombin generation proportional to injury severity. In addition, systemic embolism of tissue-specific thromboplastins from sites of injury (including bone marrow lipid material, amniotic fluid, and brain phospholipids) may predispose patients to DIC.
5. Acute traumatic coagulopathy (ATC) is an impairment of hemostasis and activation of fibrinolysis that occurs early after injury and is biochemically evident prior to, and independent of, the development of significant acidosis, hypothermia, or hemodilution.

Question 4

32. A patient has a new diagnosis of acute promyelocytic leukemia. She is admitted to the ICU with pulmonary hemorrhage which is ongoing. Four days after admission the patient has bilateral, symmetric, non-blanchable lesions on both hands (figure below). Relevant hematology: INR 4, aPTT 72 seconds, Platelet count 30 x 109/L and fibrinogen <1 g/L. HIT testing is negative and cultures are also negative.

Please outline the diagnosis of this condition.

Name one contraindication to therapy of the underlying condition.

Answer 4

Please outline the diagnosis of this condition

M3 associated DIC (M3 ?=acute promyelocytic leukemia)

Treated with all-trans retinoic acid + arsenic trioxide (7+3 = 7days cytarabine + 3 days daunorubicin or doxorubicin)

Name one contraindication to therapy of the underlying condition

TXA is contra-indicated: blockade of fibrinolysis can enhance thrombotic complications

PCC is contra-indicated: can enhance thrombosis

Give Cryop or Plts or FFP

is this refering to DIC?

from uptodate:

the administration of antifibrinolytic agents such as tranexamic acid (TXA), epsilon-aminocaproic acid (EACA) or aprotinin is generally contraindicated since blockade of the fibrinolytic system may increase the risk of thrombotic complications. However, these agents may be appropriate in patients who have severe bleeding associated with a hyperfibrinolytic state. There are no data regarding the use of prothrombin complex concentrates (PCC) in DIC. In the author’s opinion, PCCs are also contraindicated in DIC, since administration may trigger more thrombotic complications in the setting of an already hypercoagulable state.

In pts with DIC who have serious bleeding are at high risk of bleeding or require invasive procedures treatment is justified (don’t be afraid of fueling the fire).

• in pts with serious bleeding or need for emergent surgery give plts to target >50
• in pts with plts <10, give plts
• pts with serious bleeding and a signficantly prolonged INR or PTT or a fibrinogen level <0.5g/L and serious bleeding, give factor replacement. Options include: FFP, cryoprecipitate. From uptodate:
  
  • If the plasma fibrinogen level is <1 g/L, we administer cryoprecipitate to increase it to >1 g/L.
  • If the plasma fibrinogen level is >1 g/L and the PT or aPTT remains significantly elevated, we administer FFP or PF24. The goal is to reduce bleeding, not to normalize the coagulation tests. Dosing is provided in the table.

Question 5

Patient with non-necrotizing pneumonia. Abruptly worsens two days later with hypotension and hypoxemia. CXRs from ICU day #0 and day #2 show new large pneumothorax on right side.

a. What is the new diagnosis explaining his worsening?
b. What two necessary things must be done before air transport?
c. The RT at your center indicates that the patient has a 200 ml discrepancy between the inhaled and exhaled tidal volumes. What are 3 ventilator strategies to utilize to minimize this issue?

Answer 5

a) pneumothorax
b) insertion of chest tube and put to underwater suction +/- intubate
c) When any type of pulmonary barotrauma is detected, immediate attempts should be made at the bedside to lower the plateau airway pressure.

1. minimize tidal volume and PEEP
2. minimize chest tube suction
3. use negative pressure (i.e. spontaneous breathing) rather than positive pressure ventilation (or minimize positive pressure ventilated breaths)

Guidelines for ventilator management in the patient with airleak from barotrauma and alveolopleural fistula

• Reduce both mean airway pressure and the number of positive-pressure breaths, using the lowest number of mechanical breaths that permits acceptable alveolar ventilation
  
  • Wean patient completely if possible
  • Partial ventilatory support (eg, low-rate SIMV or pressure support) is preferable to total ventilatory support (eg, assist/control, high-rate SIMV, or pressure control ventilation)
  • Avoid or correct respiratory alkalosis (to minimize minute ventilation)
  • Consider use of permissive hypercapnia (reducing minute ventilation and allowing arterial PCO2 to rise)
• Limit effective (returned) tidal volume to 5 to 8 mL/kg
• Minimize inspiratory time, and hence mean airway pressure:
  
  • Keep inspiration-to-expiration ratio low (eg, 0.33)
  • Use high inspiratory flow rate (eg, 70 to 100 L/min)
  • Avoid inflation hold (end-inspiratory pause) and inverse-ratio ventilation
  • Use low-compressible-volume (non-disposable) ventilator circuit
• Minimize PEEP (both dialed-in and auto-PEEP)
• Use least amount of chest tube suction that maintains lung inflation
• If spontaneous movement exacerbates leak, keep patient heavily sedated (in unusual circumstances neuromuscular blockade may also be necessary)
• Explore position differences, and avoid patient positions that increase the leak
• Treat bronchospasm and other causes of expiratory airflow obstruction
• Consider specific or unconventional measures (eg, independent lung ventilation, high-frequency jet ventilation, PEEP to chest tubes, etc) only if the air leak per se is clinically felt to be worsening the patient’s condition (eg, intractable hypotension or arrhythmias in association with respiratory acidosis)
• Treat underlying cause of respiratory failure, maintaining nutritional and other support, with goal of discontinuing mechanical ventilation as soon as possible

Question 6

ventilator management in bronchopleural fistula, 10 things:

Answer 6

Guidelines for ventilator management in the patient with airleak from barotrauma and alveolopleural fistula:

• Reduce both mean airway pressure and the number of positive-pressure breaths, using the lowest number of mechanical breaths that permits acceptable alveolar ventilation
  
  • Wean patient completely if possible
  • Partial ventilatory support (eg, low-rate SIMV or pressure support) is preferable to total ventilatory support (eg, assist/control, high-rate SIMV, or pressure control ventilation)
  • Avoid or correct respiratory alkalosis (to minimize minute ventilation)
  • Consider use of permissive hypercapnia (reducing minute ventilation and allowing arterial PCO2 to rise)
• Limit effective (returned) tidal volume to 5 to 8 mL/kg
• Minimize inspiratory time, and hence mean airway pressure:
  
  • Keep inspiration-to-expiration ratio low (eg, 0.33)
  • Use high inspiratory flow rate (eg, 70 to 100 L/min)
  • Avoid inflation hold (end-inspiratory pause) and inverse-ratio ventilation
  • Use low-compressible-volume (non-disposable) ventilator circuit
• Minimize PEEP (both dialed-in and auto-PEEP)
• Use least amount of chest tube suction that maintains lung inflation
• If spontaneous movement exacerbates leak, keep patient heavily sedated (in unusual circumstances neuromuscular blockade may also be necessary)
• Explore position differences, and avoid patient positions that increase the leak
• Treat bronchospasm and other causes of expiratory airflow obstruction
• Consider specific or unconventional measures (eg, independent lung ventilation, high-frequency jet ventilation, PEEP to chest tubes, etc) only if the air leak per se is clinically felt to be worsening the patient’s condition (eg, intractable hypotension or arrhythmias in association with respiratory acidosis)
• Treat underlying cause of respiratory failure, maintaining nutritional and other support, with goal of discontinuing mechanical ventilation as soon as possible

Question 7

A patient post-carotid endarterectomy is brought to the ICU post-op, extubated. Patient initially doing well. Acutely develops pulsatile neck swelling. Currently stable, good sats. Surgeon currently on the way. What one thing should you do now while waiting for the surgeon?

Answer 7

?consider opening incision at the bedside?

A postoperative neck hematoma can be catastrophic and result in abrupt loss of the airway. When a significant neck hematoma develops in the postoperative period, immediate return to the operating room and re-exploration of the neck wound is necessary and can be lifesaving.

Reversal of intraoperative anticoagulation with protamine has reduced the incidence of serious bleeding that would require reoperation without a significant increase in other complications (eg, stroke, coronary events).

Uncontrolled hypertension while awakening from anesthesia or in the postoperative period can also lead to hematoma formation.

Question 8

What is a screening test that has been used in studies to assess for delirium in the ICU?
What are four characteristics of delirium?

Answer 8

Question 9

What are four factors associated with unplanned extubation?

Answer 9

oral intubated (rather than nasally intubated)

if ETT is not secured

if patients are agitated

low levels of sedation (in one study: lack of IV sedation)

physically restraints

Question 10

Patient in your ICU has large left pleural effusion. You wish to place a percutaneous drain. Goes in easily, but immediately drains 800ml of frank blood.

a. What do you do immediately?
b. Attached CT scan shows drain in LV. What is the diagnosis?
c. Patient is very upset. Says he was not warned of that potential complication. According to the CMPA, what 3 patient prerequisites must be present for informed consent?
d. What are four elements that need to be discussed in a discussion around informed consent

Answer 10

a) clamp drain, get emergent CT chest
b) iatrogenic cardiac injury from chest tube insertion

c)

1. voluntary (free of coercion or duress)
2. mental capacity to consent (pt understands proposed Rx/Ix, anticipated effect of the Rx and alternatives, and consequences of refusing Rx)
3. properly informed (discuss: material risks include risks that occur frequently as well as those that are very serious, such as death or permanent disability. A patient’s special circumstances might require discussion of potential but normally uncommon risks of the investigation or treatment, when typically these might not be seen as material.)

d) ******

The physician is required to provide information that the “reasonable” patient would want or need to make a decision.

Elements of informed consent are:

• diagnosis
• proposed treatment
• chances of success
• risks (material and special)
• alternative treatments
• consequences of no treatment
• answers to questions

The consent discussion should be documented in the medical record.

Question 11

What are Henry’s, Dalton’s, Boyle’s laws (defined in the question stem for you). List one medical contraindication to air transport that relates to each law?

Answer 11

Henry’s law -mass of gas absorbed by a liquid is directly proportional to the partial pressure of the gas above the liquid. Henry’s law has its most familiar applications in diving medicine, in which the increased pressure exerted on gases in the body at depth forces the gases into solution in the bloodstream. Rapid ascent from depth causes the gas to come out of solution within the bloodstream, resulting in decompression sickness. Henry’s law does not carry the same weight in aviation medicine because the degree of change in atmospheric pressure per unit of distance is considerably less than the degree of change in water. However, sudden decompression at altitude may result in dysbarism.

—> medical contraindication relating to Henry’s law: recent/current decompression illness or recent diving/rapid ascent from depth???

Dalton’s Law** - the total barometric pressure at any given altitude equals the sum of the partial pressures of gases in the mixture (Pt = P1 + P2 + P3 … Pn). Whereas oxygen still constitutes 21% of the atmospheric pressure at altitude, Boyle’s law notes that each breath brings fewer oxygen molecules per breath to the lungs, and hypoxia results (Table 191-1). The clinical effect of Dalton’s law is manifested as a decrease in arterial oxygen tension with increasing altitude.—> medical contraindication to Dalton’s law: severe refractory hypoxemia, mayeb recent severe TBI_???_**

Another thought: with recent extremity fracture that is casted: the hypoxic environment causes venodilation, leading to increased venous pooling and increasing the risk of swelling and compartment syndrome. For this reason, any cast (lower or upper extremity) applied for a fracture that is less than 48 hours old must be bivalved before flight.

Patients with COPD often have lower baseline oxygen saturation, particularly during an exacerbation of their disease. Even those who are asymptomatic with a baseline saturation of 93% will encounter difficulties in flight. Breathing air at 8000 ft (ie, the cabin pressure in flight) is equivalent to breathing 15% oxygen at sea level.4 This hypoxic aircraft environment will cause a decrease in your patient’s PaO2. A normal, healthy adult will desaturate to approximately 92% to 93% in flight. This COPD patient will desaturate to approximately 82% in flight and is likely to experience symptoms of hypoxia.

Boyle’s Law - the volume of a unit of gas (“unit” defined as a specific number of molecules) is inversely proportional to the pressure on it. In concrete terms, Boyle’s law means that as altitude increases and atmospheric pressure decreases, the molecules of gas grow apart, and the volume of the gas expands. With descent (increasing atmospheric pressure), the molecules are condensed, and gas volumes contract.

—> medical contraindication to Boyle’s law: simple pneumothorax can become a tension pneumothorax, but also consider other areas of trapped gas (otitis media with a blocked eustachian tube, rupture of a hollow viscus by expansion of intestinal gas, medical equipment with closed air spaces such as ventilator, ETT cuffs, IV tubing and pumps).

Boyle’s law is predominantly responsible for the presence of hypoxia at altitude as there are fewer molecules of oxygen present per volume of inhaled gas at altitude. Similarly, dispersion of molecules of water vapor within a gas volume is seen at height, and “dry air” results.

Question 12

Previously well 70 yo woman presents with 4 days of fever, new petechial rash and one day of fever. Hgb 65, platelets 80. Attached picture shows:

a. What is the most likely diagnosis?
b. What is the underlying pathology?
c. She begins to seize but settles after 2 doses of Ativan. Intubated for airway protection. Will be transferred to specialized ICU in 6 hours. What are two therapies you can do now while awaiting transfer?

Answer 12

a) Thrombotic thrombocytopenic purpura

Blood smear shows schistocytes. Schistocytes are fragmented red blood cells that can take on different shapes. They can be found as triangular, helmet shaped, or comma shaped with pointed edges. Schistocytes are most often found to be microcytic with no area of central pallor.

Schistocytes are split red blood cells that indicate microangiopathic hemolytic anemia. Their presence in a peripheral smear is the hallmark for diagnosing thrombotic thrombocytopenic purpura (TTP). Schistocytes may also be seen in healthy individuals and in patients with other diseases such as preeclampsia, eclampsia, chronic renal failure, solid organ or bone marrow transplantation, and diabetic microangiopathy as well as in patients with a prosthetic heart valve.

b) pathogenesis of TTP

TTP is caused by severely deficient activity of the ADAMTS13 protease, clinically defined as an activity level <10 percent [1]. ADAMTS13 is a plasma protease that was initially defined by its function as a von Willebrand factor (VWF)-cleaving protease. It cleaves the ultralarge, string-like molecules of VWF that are synthesized by endothelial cells and secreted into the plasma but remain attached to the endothelial surface. This normal cleavage to smaller sized multimers prevents ultralarge multimers from accumulating, especially in areas of high shear stress (eg, small arterioles and capillaries). Shear stress leads to a conformational change in the large VWF multimers that exposes the ADAMTS13 cleavage site. When protease activity is reduced, ultralarge VWF multimers accumulate on the endothelial surface, where platelets attach and accumulate.

A severe reduction in ADAMTS13 activity (eg, to less than 10 percent of normal) is present in most patients with acute TTP, although diagnosis is always made using a combination of clinical and laboratory findings. In contrast, modest reductions may occur in a variety of medical conditions such as sepsis or liver disease and are not thought to cause clinical disease.

The major cause of severe ADAMTS13 deficiency is an acquired autoantibody; inherited gene mutations account for a small additional number of cases. Additional conditions may further reduce ADAMTS13 activity, including sepsis, cardiac surgery, pancreatitis, and liver disease [15-19]. However, these additional conditions are extremely unlikely to lower ADAMTS13 activity to a level likely to cause disease.

ADAMTS13 activity also appears to decrease during the last two trimesters of pregnancy, declining to the lowest levels at 36 to 40 weeks of gestation and the early puerperium [18,20]. Higher levels of VWF also appear to reduce ADAMTS13 activity, as illustrated by kinetic studies in healthy individuals treated with desmopressin, which causes release of VWF from endothelial cells, with a concomitant reduction of ADAMTS13 activity, likely due to consumption [21]. These further reductions in ADAMTS13 activity and/or inflammatory stimuli in a patient with an underlying anti-ADAMTS13 autoantibody or hereditary ADAMTS13 deficiency may act as triggers for an acute episode of TTP.

The vast majority of cases of TTP (approximately 95 percent) are acquired due to formation of an inhibitory autoantibody to ADAMTS13 [1,23]. Risk factors for development of the autoantibody are not clearly defined, although acquired TTP is more common in young women, and the relative incidence is increased in blacks [24]. The incidence of acquired TTP also may be increased in individuals with other autoimmune conditions such as systemic lupus erythematosus (SLE) or certain human leukocyte antigen (HLA) types, but most affected patients do not have an underlying rheumatologic or immunologic condition

c) Thrombotic thrombocytopenic purpura (TTP) is a medical emergency that is almost always fatal if appropriate treatment is not initiated promptly. Plasma exchange (PEX) is the mainstay of treatment for all individuals with a presumptive diagnosis of TTP based on a PLASMIC score (calculator 1) in the intermediate- to high-risk range (5 to 7 points) and supported by a finding of severe ADAMTS13 deficiency. Additional therapies include glucocorticoids, rituximab, and caplacizumab; we risk-stratify patients to determine the glucocorticoid dose and to decide whether to use caplacizumab as part of initial therapy.

Therapies to initiate before transfer:

1. FFP, from uptodate:

Plasma infusion is not an adequate substitute for PEX in the treatment of acquired TTP, and PEX should not be delayed to allow for plasma infusion or because plasma infusion has been administered. Plasma infusion does not remove the inhibitor (autoantibody) to ADAMTS13, and the volume of plasma (and thus the amount of ADAMTS13) that can be delivered is significantly less than in PEX.

However, PEX may not be immediately available to all patients, and plasma infusion may provide temporary benefit in some patients.

2. glucocorticoids, from uptodate:

We routinely add glucocorticoids to PEX for initial treatment of patients with a presumptive diagnosis of acquired TTP. Our practice is consistent with that of most hematologists, despite the lack of randomized trials. The rationale is that the potential benefits in reducing inhibitor production and number of required PEX treatments outweigh the risks, which are relatively minor for the limited duration of therapy given.

Glucocorticoids are thought to hasten recovery because they reduce production of the ADAMTS13 inhibitor (autoantibody), by mechanisms similar to those in other autoimmune diseases. Other effects such as reduced cytokine production or decreased autoantibody-mediated clearance of ADAMTS13 may also contribute.

The dose and route of glucocorticoid administered may vary according to the severity of presentation:

●Standard risk – A typical dose for a patient who is alert and awake without neurologic abnormalities or elevated troponin is prednisone 1 mg/kg per day orally.

●High risk – For a more severely affected patient, intravenous methylprednisolone 1000 mg daily for three days or 125 mg two to four times daily may be appropriate. This is continued as long as the patient remains at high risk, and is followed by a dose of prednisone 1 mg/kg per day orally.

The intravenous route is also appropriate for individuals with gastrointestinal symptoms who may not be able to take or absorb oral medications.

Question 13

Laryngospasm during conscious sedation procedure. List 3 things to treat.

Answer 13

Laryngospasm is a prolonged exaggeration of the glottic closure reflex due to stimulation of the superior laryngeal nerve. Although the cords are adducted, the primary obstruction is caused by tonic contraction of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet.

1. constant positive pressure by BVM
2. apply pressure to the “laryngospasm notch.” Place the long finger of each hand into the most superior part of the depression behind the pinna of each ear. The fingertip should press against the ascending mandibular ramus anteriorly, the mastoid process posteriorly, and the base of the skull superiorly. Press very firmly inward toward the base of the skull while lifting the mandible to perform a “jaw thrust.”
3. lidocaine topically to vocal cords
4. paralysis and intubation +/- cricothyrotomy
5. clear secretions suction airway…may be bad as it could be a stimulus that can induce laryngospasm

Question 14

What are four confounders that prevent a determination of neurological determination of death?

Answer 14

1. unresuscitated shock
2. hypothermia (core temp <34)
3. severe metabolic disorders capable of causing a potentially reversible coma
4. severe metabolic abnormalities, including glucose, electrolytes (PO4, Mg, Ca), inborn errors of metabolism, and liver and renal dysfunction
5. peripheral nerve or muscle dysfunction or neuromuscular blockade potentially accounting for unresponsiveness
6. clinically significant drug intoxications (eg alcohol, barbiturates, sedatives hypnotics), however, therapeutic levels/dosing of anticonvulsants, sedatives and analgesics do not preclude the diagnosisNDD paper in CMAJ

Question 15

Rhythm strip showing weird paced rhythm with pacing spikes sometimes on top of QRS, sometimes no capture. Peaked T-waves.

a. What is the underlying rhythm?
b. What is the problem with the pacemaker?
c. What are two other diagnoses you can make based on T-wave abnormality?

Answer 15

a) unable to answer
b) sounds like it’s not sensing and not capturing
c) ?ishcemia, ?hyperkalemia

Differential diagnosis of tall (peaked) T waves

• Ischemic causes
  
  • Hyperacute phase of myocardial infarction
  • Acute transient transmural ischemia (Prinzmetal’s angina)
  • Chronic (evolving) phase of myocardial infarction (tall positive T waves reciprocal to primary deep T wave inversions)
• Nonischemic causes
  
  • Normal variants (“early repolarization” patterns)
  • Hyperkalemia
  • Acute hemopericardium
  • Cerebrovascular hemorrhage (more commonly T wave inversions)
  • Left ventricular hypertrophy
  • Right precordial leads, usually in conjunction with left precordial ST depressions and T wave inversions
  • Left precordial leads, particularly in association with “diastolic” volume overload conditions
  • Left bundle branch block (right precordial leads)
  • Acute pericarditis (occasionally)

Question 16

Rhythm strip showing V Fib

a. What is the rhythm?
b. What are 3 drugs that can be used to treat this rhythm?
c. CPR continues for 20 minutes. What is the EtCO2 cutoff below which patients are at increased risk of poor prognosis/neurological injury?

Answer 16

a) VF

b)

• amiodarone
  
  • for Unresponsive to cardiopulmonary resuscitation, defibrillation, and epinephrine: IV push, Intraosseous: Initial: 300 mg rapid bolus; if pulseless VT or VF continues after subsequent defibrillation attempt or recurs, administer supplemental dose of 150 mg
• magnesium sulfate
  
  • for VF/pulseless VT associated with torsades de pointes: IV/IO: 1 to 2 g (diluted in 10 mL D5W) administered as a bolus
• lidocaine
  
  • for VF or pulseless VT (after defibrillation attempts, CPR, and vasopressor administration), alternative to amiodarone: IV, intraosseous (IO): Initial: 1 to 1.5 mg/kg bolus. If refractory VF or pulseless VT, repeat 0.5 to 0.75 mg/kg bolus every 5 to 10 minutes (maximum cumulative dose: 3 mg/kg).

references seem to stress that lidocaine and amio should only be considered once defibrillation and epi have been given. There was one study comparing lidocaine, amio and placebo that did not find a significant difference between both drug groups.

c) In several prospective, observational studies, EtCO2 levels of ≤10 mmHg measured 20 minutes after the initiation of advanced cardiac life support accurately predicted death in adult patients with cardiac arrest. It has also been used by some to not go on to ECLS in pts with ETCO2 ≤10.

from ILCOR: we recommend that a specific end-tidal CO2 value at any time during CPR should not be used alone to stop CPR efforts. End-tidal CO2 values should be considered only as part of a multi-modal approach to decision-making for prognostication during CPR.

Question 17

Patient on percutaneous fem-fem V-A ECMO. Sats of 70% from pulse ox on R hand. PaO2 of 300 from L femoral art line.

a. What is the pathophysiology causing this?
b. Where would you draw ABGs to assess cerebral oxygenation?

Answer 17

a) Harlequin syndrome - the cardiac function recovers and thus is able to compete with the extracorporeal flow thereby causing upper body to be perfused by hear (and in context of bad lung function) can cause hypoxia in the upper limbs and head…the lower body is perfused by the ECMO circuit and there is no hypoxia. May need to change to VV ECMO (if lungs still sick).

Strategies to deal with this include:

• Change to VV ECMO ± inotropes, IAB/ pVAD
• Advance IVC cannula to RA/SVC
• VAV :Return oxygenated blood to RA
• VVA: additional SVC drainage cannula
• Upper body arterial return: subclavian
• Central VA ECMO
• LVAD/BiVAD configurations with oxygenator in circuit

b) ABG, SpO2 should be drawn from right radial side (or right ear lobe)

Question 18

Post-partum patient with heart failure, needing to be intubated

a. List two physiologic changes that make laryngoscopy more difficult
b. List two physiologic changes that make her desat quicker

Answer 18

a)

1. fluid retention and edema in pregnancy can affect upper airway (could also be worse in heart failure, eclampsia or iatrogenic fluid/blood administration)
2. breast engorgement may hinder insertion of laryngoscope (may need shorter handle)
3. +/- heart failure decreasing CO thereby making it take longer for drugs to get from peripheral vein to central circulation and site of action (I made this one up)

b)

1. decreased FRC
2. increased oxygen consumption

Question 19

Weird diagram clearly made on Microsoft Paint showing 6 different positions for intubating (1. pt supine, 2. supine w/ pillow under head, 3. w/ pillow under head and shoulders. 4. Pt ramped 5. pt ramped with pillow under head 6. ramped with pillow under head+shoulders)

a. What is the one best position for intubating a non-obese patient?
b. What is the one best position for intubating an obese patient?

Answer 19

a) ?supine with pillow under head and shoulders

In most patients, the best position for direct laryngoscopy with a Macintosh-style blade is achieved with the neck flexed and the head extended at the atlanto-occipital joint; the classic ‘sniffing’ position.

In the obese patient, the ‘ramped’ position should be used routinely to ensure horizontal alignment of the external auditory meatus and the suprasternal notch because this improves the view during direct laryngoscopy. This position also improves airway patency and respiratory mechanics and facilitates passive oxygenation during apnoea.

b) ramped with pillow under head+shoulders?

From uptodate: In preparation for intubation, the obese patient should be placed in an upright or semi-upright position (eg, reverse Trendelenburg), depending upon the degree of respiratory distress. An upright position improves respiratory function by allowing the diaphragm to fall downward and reducing the weight on the chest wall. Even in trauma patients requiring cervical spine stabilization, the stretcher can be tilted with the head elevated to improve breathing while preparations are made for intubation.

If there is no contraindication (eg, cervical spine precautions), the obese patient should be placed in a ramped or head-elevated position for direct laryngoscopy. In the ramped position, blankets or commercially available beds are used to elevate the head and torso such that the external auditory meatus and the sternal notch are horizontally aligned.

The sniffing position has traditionally been recommended to optimize glottic visualization during direct laryngoscopy, but the ramped position appears to be more effective in the obese patient. Several studies have compared the positions used to optimize the glottic view and improve intubation success:

●In a blinded, randomized trial, 60 morbidly obese patients were assigned to either the ramped or to the sniffing position (7 cm head elevation) for direct laryngoscopy and endotracheal intubation prior to surgery. The authors reported that the ramped position provided a significant improvement in the glottic view.

●A randomized trial of direct laryngoscopy in 40 anesthetized patients found that the glottic view improved by over 50 percent when the head-elevated position was used compared with supine positioning.

●A retrospective study of 528 intubations performed outside the operating room found that a backup and head elevated (ie, ramp) position was associated with significant reductions in multiple airway complications, including hypoxia, esophageal intubation, and intubation failure, compared with supine, neutral head positioning.

●A study using fresh cadavers found significant improvement in the glottic view during direct laryngoscopy with the head in a fully elevated position compared with either a supine or partially elevated position

Question 20

List four reasons that proning will improve oxygenation

Answer 20

1. improved V/Q matching - smaller volume of dependent lung (therefore less shunting and increased FRC) from off-loading of the heart
2. improved V/Q matching - smaller volume of dependent lung (therefore less shunting and increased FRC) from off-loading of the diaphragm/abdomen
3. improved V/Q matching - more homogeneous distribution of plateau pressure gradient in ventrodorsal and craniocaudal planes therefore improved distribution of ventilation
4. secretion mobilization - improves ventilation
5. improved aerosol delivery thereby increased effect - improves ventilation
6. more homogeneous distribution of perfusion due to less dependent perfusion - improved V/Q matching (less shunt)
7. decreases right heart afterload and therefore can increase cardiac output

Question 21

Patient with severe ARDS, on 100% FiO₂, PEEP 20 parasternal long axis view shown of a severely dilated RV/RVOT. List two things that can be done to treat this.

Answer 21

1. reduce RV afterload
   
   • pulmonary vasodilators
     
     • It is strongly recommended that inhaled rather than systemic pulmonary vasodilators be used when systemic hypotension is anticipated. iNO increases intracellular cyclic guanosine monophosphate and has been shown to transiently improve the PaO₂ to FiO₂ ratio and cardiac output in patients with ARDS and RVD. It is recommended that iNO be used as a short-term therapy to improve oxygenation indices in ARDS, as it does not improve mortality regardless of ARDS severity and has also been associated with acute kidney injury. Inhaled prostanoids such as prostaglandin I₂ (prostacyclin) and its analogues such as iloprost reduce PVR and improve RV performance. Use of nebulized iloprost in patients with ARDS and pulmonary hypertension has been associated with an improvement in gas exchange without causing hemodynamic instability
   • RV-protective ventilation strategies
     • minimze lung stress by limiting plateau and driving pressure
     • prevention or reversal of pulmonary vasoconstriction by improving oxygenation and strict CO₂ control
     • prone positioning to unload the RV
2. optimize preload (diuresis or fluid challenge)
   
   • consider mini fluid challenge: 100 mL of colloid or crystalloid fluid over 1 min) has been shown to predict fluid responsiveness in patients with circulatory failure receiving low tidal volume ventilation and may be a safer, yet rational, approach in patients with suspected RVD, as a small rise in cardiac filling pressures may lead to a greater increase in stroke volume during administration of a “mini fluid bolus” (steep portion of the Frank-Starling curve)
3. optimize RV contractility
   
   • ensure appropriate heart rate and rhythm (Right atrial contraction contributes up to 40% of RV filling and is of more importance when RV compliance is poor)
   • consider vasoative meds as hypotension can lead to RV ischemia and further RV impairement. Target systolic pressure higher than pulmonary pressure
     
     • Maintenance of an appropriate systemic pressure while not excessively increasing or even decreasing PAP are the traits of an ideal vasopressor. Norepinephrine has been shown in both animal models and humans to increase SVR while reducing PAP. Norepinephrine at high doses was shown to increase PVR over SVR preferentially and thus at high doses should be used cautiously. Phenylephrine has been shown to be not as effective as norepinephrine and in certain situations to actually worsen RV function. Vasopressin is also another vasopressor that preferentially increases SVR over PVR and thus can be useful to maintain systemic pressure without worsening RV afterload. At low doses (<0.03 units/min), vasopressin causes pulmonary vasodilation, but at higher doses it increases PVR and causes coronary vasoconstriction and should therefore

be used with caution.

* consider **_inodilators_** (dobutamine, milrinone)
    * Because of the profound systemic vasodilating capabilities of these agents, systemic hypotension can result, and thus they often need to be paired with a vasoconstrictor. Vasopressin, in contrast to norepinephrine, has been shown to be more beneficial at reducing PAP. When comparing dobutamine and milrinone, although there are equivalent reductions in PVR and improvements in cardiac output between the agents, there appears to be a greater reduction in SVR and pulmonary capillary wedge pressure when using milrinone. Levosimendan, a calcium sensitizing agent with inotropic and vasodilatory properties, has been shown to improve RV performance in patients with ARDS and septic shock. As an inodilator, it could potentially improve right ventricle/pulmonary vascular coupling, but it does not have a proven mortality benefit in the treatment of patients with ARDS and RVF

Question 22

Post-AVR patient with dynamic LVOT obstruction, pre-op EF 40%. Intrinsic rhythm 40, paced at 90. Started on 0.5mcg/kg/min milrinone. Pre and post PA cath measurements after a 1 litre bolus show higher CVP+wedge, worsening hypotension, worsening mixed venous O2, worsening cardiac index. Echo shows hyperdynamic LV.

a. List 3 physiologic reasons for dynamic LVOT.
b. List 3 treatments to improve the dynamic LVOT

Answer 22

a)

1. hypovolemia decreasing preload and therefore LVESV
2. increased inotropy from milrinone
3. decreased afterload from milrinone
4. maybe decreased LVESV from arrhythmia, ie. that its paced and therefore doesnt have atrial kick***
5. narrow LVOT diameter from hypertrophic LV septum
6. abnormal length or position of mitral valve anterior leaflet
7. hyperdynamic state which increases flow through LVOT thereby worsening Bernoulli effect on septum and mitral valve anterior leaflet

b)

1. decrease HR and inotropy with beta-blockers
2. increase preload with fluid bolus
3. increase afterload without inotropy (i.e. phenylephrine or vasopressin)
4. decrease or stop inotropic agents

Question 23

Post-MVR patient with rapid irregular rhythm on a strip (?afib). Cardioversion, adenosine, amiodarone didn’t work. List ONE bedside intervention you can do to treat this.

Answer 23

Valsalva maneuver technique — Various descriptions of the technique of performing a Valsalva maneuver exist.

● Valsalva maneuver: Most commonly, the patient is placed in a supine or semirecumbent position and instructed to exhale forcefully against a closed glottis after a normal inspiratory effort (ie, at tidal volume). Signs of adequacy include neck vein distension, increased tone in the abdominal wall muscles, and a flushed face. The patient should maintain the strain for 10 to 15 seconds and then release it and resume normal breathing.

● Modified Valsalva maneuver, which involves the standard strain (40 mmHg pressure for 15 seconds in the semirecumbent position) followed by supine repositioning with 15 seconds of passive leg raise at a 45 degree angle, has been shown to be more successful in restoring sinus rhythm for patients with SVT.

In the largest randomized trial of vagal maneuvers for the treatment of SVT, patients performing the modified Valsalva maneuver with supine repositioning and passive leg raise were significantly more likely to have restoration of sinus rhythm at one minute (43 versus 17 percent in the standard Valsalva group; adjusted odds ratio 3.7; 95% CI 2.3-5.8).

Indeed, in the operating room, a VM can be induced by the prevention of expiration while fresh gas flow continues to enter a circle system circuit with an adjustable pressure-limiting valve that is partially or fully closed.

Question 24

Septic shock patient on vasopressors. BP 80/50, HR 130. Echo shows severe mitral stenosis. List one drug you will use to treat this.

Answer 24

phenylephrine or vasopressin so as not to increase HR with other inopressors

Key points for management of MS:

• target HR 60-70bpm (Avoid tachycardia. Any tachyarrhythmia (eg, sinus tachycardia or atrial fibrillation [AF] with rapid ventricular response) can result in sudden severe hypotension and pulmonary edema due to inadequate time during diastole for blood in the LA to empty into the LV through the stenotic mitral valve. The sudden decrease in LV filling, stroke volume (SV), and cardiac output (CO) causes hypotension, while the sudden increase in LA pressure causes pulmonary edema.)
• sinus rhythm preferable over afib (although Afib very common in pts with MS)
• maintain adequate preload
• maintain adequate afterload (SBP>100, MAP>70 or both within 20% of baseline) because MS impairs normal compensatory responses to hypotension (SV cannot be substaintially increased and a slow HR must be maintained). Treat hypotension due to a presumed decrease in SVR with an alpha-adrenergic vasoconstrictor such as phenylephrine, administered as bolus doses or as an infusion. If phenylephrine is ineffective, norepinephrine or vasopressin may be administered.
• maintain contractility - Avoid doses of drugs that might cause significant depression of myocardial contractility (eg, high doses of propofol or volatile inhalation anesthetic agents).
• maintain RV function (which can often be impaired in MS) consider milrinone, low dose epi, and avoid hypoxemia and hypercarbia which can increase PVR

Question 25

Woman admitted with community acquired pneumonia, day 4 on vasopressors, steroids, antibiotics. Still hypotensive. HR 50. Na 124. Glucose 3. Temp 35.

a. List ONE blood test to confirm the diagnosis
b. List THREE medications to treat this condition

Answer 25

oops I initially didn’t realize the pt was already on steroids…

Now I’m thinking they are referring to myxedema coma for which we would give:

1. levothyroxine
2. triiodothyronine
3. hydrocortisone

a) The task force was unable to reach agreement on a single test that can reliably diagnose CIRCI, although:

• delta cortisol (change in baseline cortisol at 60 min of < 9 μg/dL) after cosyntropin (250 μg) administration
  
  • do not use plasma free or salivary cortisol for diagnosis of CIRCI
  • use high dose (250ug) rather than low dose (1ug) ACTH stim test for Dx of CIRCI
  • do not use response to hydrocortisone over 250ug ACTH stim test in diagnosing CIRCI
• a random plasma cortisol of < 10 μg/dL may be used by clinicians.

b)

• hydrocortisone
• methylprednisolone (suggested if using in ARDS due to better lung penetration)
• ???fludrocortisone

If using corticosteroids for septic shock, we suggest using long course and low dose (e.g., IV hydrocortisone < 400 mg/day for at ≥ 3 days at full dose) rather than high dose and short course in adult patients with septic shock
(conditional recommendation, low quality of evidence).

A network meta-analysis of 22 trials suggested no clear evidence for the superiority of one type of corticosteroids over another in adult patients with septic shock (43). However, hydrocortisone boluses and infusions were more likely than methylprednisolone boluses and placebo to reverse shock.

The latest Cochrane systematic review of the use of low-dose hydrocortisone for treating septic shock, including 33 RCTs with a total of 4,268 patients (42), showed that corticosteroids significantly reduced the risk of death at 28 days
compared with placebo. Three of these RCTs included children and the other 30 trials included only adults. Survival benefits were dependent on the dose of corticosteroids, with lower doses (< 400 mg of hydrocortisone or equivalent per day) for a longer duration of treatment (3 or more days at the full dose) found to be better, and on the severity of the sepsis. Furthermore,
corticosteroids did not cause harm except for an increased incidence of hyperglycemia and hypernatremia; there was no increased risk of superinfection or gastrointestinal bleeding.

Other CIRCI guideline recommendations:

• We suggest against corticosteroid administration in adult patients with sepsis without shock.
• We suggest using corticosteroids in patients with septic shock that is not responsive to fluid and moderate- to high-dose vasopressor therapy (conditional recommendation, low quality of evidence).
• We suggest use of corticosteroids in patients with early moderate to severe acute respiratory distress syndrome (PaO2/FiO2 of < 200 and within 14 days of onset) (conditional recommendation, moderate quality of evidence).

Clinical Signs and Symptoms of Critical Illness-Related Corticosteroid Insufficiency (CIRCI)
General

• Fever, asthenia

Neurological

• Confusion
• Delirium
• Coma

Cardiovascular

• Hypotension refractory to fluid resuscitation
• Decreased sensitivity to catecholamines
• High cardiac index

Digestive

• Nausea
• Vomiting
• Intolerance to enteral nutrition

Respiratory

• Persistent hypoxia

Laboratory

• Hypoglycemia
• Hyponatremia
• Hyperkalemia
• Metabolic acidosis
• Hypereosinophilia

Imaging

• Hemorrhage or necrosis in hypothalamus, pituitary gland or adrenal gland

Question 26

Patient presents to your ICU with a tunneled line. What are two organisms that mandate removal of the line?

Answer 26

Long-term catheters should be removed from patients with CRBSI associated with any of the following conditions: severe sepsis; suppurative thrombophlebitis; endocarditis; bloodstream infection that continues despite >72 h of anti-microbial therapy to which the infecting microbes are susceptible; or infections due to S. aureus**, **P. aeruginosa, fungi, or mycobacteria (A-II).

This is different than for short-term catheters:

Short-term catheters should be removed from patients with CRBSI due to gram-negative bacilli, S. aureus, enterococci, fungi, and mycobacteria (A-II).

Question 27

Patient in your ICU with pneumonia, on mechanical ventilation, PEEP 8, Pressure regulated to 28, FiO2 50%, RR set at 22, patient breathing at 27, Minute ventilation 12L/min. RT attempts SBT, RR is 30 and VT is 250cc. She feels the patient is not ready for extubation.

a. List two reasons that the patient is not ready for extubation
b. List two interventions with RCTs that demonstrated a reduction in duration of mechanical ventilation.

Answer 27

a)

• RSBI 120
  
  • Patients with RSBI <105 (“positive”):

If the patient otherwise meets criteria for liberation from the ventilator, a positive RSBI means they are likely to have successful extubation. Clinicians can use the positive RSBI as an additional supporting data point for the decision to extubate.

Patients with RSBI >105 (“negative”):

These patients are more likely to fail extubation. However, there are multiple confounding factors that make a patient more likely to have a negative RSBI, including female gender, smaller endotracheal tube size, and active suctioning during spontaneous breathing.

If a patient has a negative RSBI, but in all other respects is ready for extubation, consider potential confounding factors at play resulting in an inflated RSBI value (i.e., a negative RSBI should not necessarily deter clinicians from deciding to extubate).

• Minute Ventilation:
  
  • Normal minute ventilation is approximately 6 L/min. Based on an initial report of Sahn and Lakshminarayan, of less than 10 L/min became one of the standard weaning predictors. When interpreting these data, it is essential to recognize the influence of test-referral bias, because clinicians are reluctant to initiate weaning attempts in patients with a high.

b)

• protoclolized rehabilitation aimed at early mobilization
• ventilator liberation protocol
• this was NOT shown in RCTs of weaning duration in protocols attempting to minimize sedation

Question 28

Patient in shock with renal failure, need to start CRRT.

a. What is a relative contraindication to use of regional citrate for anticoagulation?
b. What are 3 laboratory tests that may indicate a rising citrate level?

Answer 28

a)

KDIGO:

• severely impaired liver function
• shock with muscle hypoperfusion

uptodate:

• acute liver failure with transaminases >1000, because they are unlikely to metabolize citrate and it could cause severe acidosis and hypocalcemia
• cardiogenic shock with blood lactate >8

From KDIGO guidelines:

The anticoagulant effect of sodium citrate relies on forming a complex with ionized calcium, thus removing an essential component of the coagulation cascade. Part of the citrate is removed in the extracorporeal circuit. Citrate reaching the systemic circulation is rapidly metabolized in the liver, muscle, and kidney, liberating the calcium and producing bicarbonate. The buffering effect of sodium citrate is proportional to the sodium ions it contains: a mole of trisodium citrate produces the same buffering effect as 3 moles of sodium bicarbonate; whereas preparations of citrate, including hydrogen citrate, have proportionally less buffering effect. Extracorporeal losses of calcium have to be compensated by an exogenous infusion.

5. 3.2: For patients without an increased bleeding risk or impaired coagulation and not already receiving effective systemic anticoagulation, we suggest the following:
6. 3.2.1: For anticoagulation in intermittent RRT, we recommend using either unfractionated or low-molecular-weight heparin, rather than other anticoagulants.(1C)
7. 3.2.2: For anticoagulation in CRRT, we suggest using regional citrate anticoagulation rather than heparin in patients who do not have contraindications for citrate. (2B)
8. 3.2.3: For anticoagulation during CRRT in patients who have contraindications for citrate, we suggest using either unfractionated or low-molecular-weight heparin, rather than other anticoagulants.(2C)
9. 3.3: For patients with increased bleeding risk who are not receiving anticoagulation, we suggest the following for anticoagulation during RRT:
10. 3.3.1: We suggest using regional citrate anticoagulation, rather than no anticoagulation, during CRRT in a patient without contraindications for citrate. (2C)
11. 3.3.2: We suggest avoiding regional heparinization during CRRT in a patient with increased risk of bleeding. (2C)

Regional citrate anticoagulation decreases the rate of clotting and may be used in all CRRT modalities. Compared with systemic heparin, RCA reduces the risks of bleeding. Multiple randomized trials and meta-analyses have shown that RCA is better than heparin at preserving filter patency and has a lower risk of adverse events, including bleeding. There does not appear to be a survival benefit of either heparin or RCA.

During RCA, sodium citrate is infused into the inflow (“arterial”) limb of the extracorporeal circuit, chelating calcium and inhibiting clotting. The majority of the calcium citrate complex is removed across the hemofilter. Any calcium citrate complex that remains postfilter is returned to the patient and metabolized to bicarbonate by the liver, kidney, and skeletal muscle. Regional anticoagulation is reversed by dilution of citrate in the extracellular compartment and by its rapid metabolic clearance.

A systemic calcium infusion is required to replace the calcium that is lost in the effluent in order to maintain a normal ionized serum calcium concentration.

The use of RCA may require modification of the composition of dialysate or replacement fluid. The concentration of buffers (eg, bicarbonate, lactate) is usually reduced to prevent alkalosis since citrate provides alkali.

Ideally, the dialysate and replacement fluids should also be calcium free to prevent reversal of the citrate effect in the extracorporeal circuit, although this is not absolutely necessary. If calcium-containing replacement fluid is used, more citrate is required to chelate calcium in both the blood and replacement fluid. Calcium chloride or calcium gluconate is infused into the venous return line at an initial rate of 2 to 3 mmol/hour to replace calcium lost in the effluent when using calcium-free dialysate and replacement fluids. The rate is adjusted according to measurements of plasma calcium concentration to prevent hypocalcemia or hypercalcemia.

b) citrate accumulation is suggested by:

• worsening metabolic acidosis with increasing anion gap
• decreasing ionized calcium requiring escalating calcium infusion rates
• increasing total calcium
• ratio of total calcium to ionized calcium >2.5

Question 29

Diagram showing flow-time diagram for patient on ventilator on pressure support mode. Showed a shaded area underneath the inspiratory flow portion on the breath cycle. Expiratory flow does not go back to zero before new breath initiated.

a. What does the shaded area represent?
b. What is the trigger for cycling to exhalation?
c. The patient feels inhalation happening for too long. What changes can be made on the ventilator to make the patient more comfortable? Assume pressure support will remain at 15.

Answer 29

a) inspired tidal volume
b) “E sens” (aka expiratory trigger sensitivity, flow cycle) which is a percentage (typically 5-75%) of peak flow at which the pressure support augmentation is stopped
c) increase E sensitivity

A typical ETS setting in a patient with normal lung mechanics undergoing NIV is 25%. With obstructive patients, for example, in a patient with chronic obstructive pulmonary disease (COPD), ETS should be set higher to increase the expiratory time and thus avoid air-trapping and intrinsic PEEP. Incorrect ETS settings leading to expiratory asynchrony may be recognized from either delayed or premature cycling leading to double triggering.

Delayed cycling can be recognized from an end-inspiratory peak in the pressure curve caused by an active expiratory effort, as well as a change in the slope of inspiratory flow towards the baseline. This is typically described in patients with COPD. The reduction in inspiratory flow is smaller, probably due to dynamic hyperinflation and airway resistance.

more info here: https://www.hamilton-medical.com/it/News/Newsletter-articles/Article~2018-02-15~Bedside-tip%3A-How-to-set-expiratory-trigger-sensitivity-%28ETS%29~fd2e3a48-1f6a-4a90-bf3e-befbe7fad210~.html

Question 30

Patient who was in ICU with severe ARDS. Discharged months ago. Has chronic dyspnea and exercise limitation.

a. What is the PF ratio criteria for severe ARDS?
b. List two reasons for his dyspnea besides pulmonary fibrosis.

Answer 30

a)

• mild P:F 200-300
• moderate P:F 100-200
• severe P:F <100

b)

• muscle weakness
• bronchiectasis
• low diffusing capacity

uptodate:

Lung function following ARDS is commonly compromised for as long as five years. However, it is uncertain whether decreased lung function results in physical impairment. The degree of compromise depends on which parameter of lung function is measured (spirometry, lung volumes, diffusing capacity). For example, upon discharge, approximately 80 percent of patients will have a reduction in diffusing capacity and a smaller percentage will have airflow obstruction (20 percent) or restriction (20 percent) on spirometry and lung volumes. In most patients, lung volumes and spirometry will normalize (ie, measure within 80 percent of predicted values) by six months, and diffusion capacity should normalize by five years. A small percentage of patients are left with residual deficits and supplemental oxygen is rarely required.

Herridge’s 1 yr follow up NEJM paper:

Second, muscle weakness may account for the restrictive changes on pulmonary-function testing and symptoms of dyspnea, but we did not measure maximal inspiratory or expiratory efforts.

From Herridge’s 5yr follow up NEJM paper:

Patients had normal or near-normal volumetric and spirometric test results between 3 and 5 years. Forty percent of the participants were seen at a home visit, during which pulmonary assessment was limited to spirometry. After ICU discharge, 25 patients underwent computed tomography (CT) of the chest at least once between the 2-year and 5-year follow-up visits. The most common finding was minor, nondependent pulmonary fibrotic changes that were consistent with ventilator-induced lung injury. Less common findings included bronchiectasis, bullae, pleural thickening, and pulmonary fibrosis. Only patients with bronchiectasis, pulmonary fibrosis, or both on CT imaging had clinically important pulmonary symptoms, including cough, sputum production, and exertional dyspnea.

Question 31

Patient who is being worked up for organ donation including heart.

a. What is the ONE important test to do for heart donation?
b. Donor heart has EF<40%. What are THREE non-inotrope drugs to improve chance of being able to successfully transplant the heart?

Answer 31

a) Echocardiography is required for potential heart donors; a cardiac catheterization may be required for older heart donors (>40 years) or those with significant risk factors for coronary heart disease. (uptodate)

b)

• thyroid hormone replacement
• methylprednisolone
• vasopressin

In a retrospective analysis of data on 66,629 donors, thyroid hormone therapy was associated with increased procurement of hearts, lungs, kidneys, pancreases, and intestines, but not livers.

from 2006 Canadian guidelines: Weight of currently available evidence in a large retrospective cohort study by the United Network for Organ Sharing (UNOS)10 in the United States suggests a substantial benefit of triple hormone therapy with minimal risk. A multivariate logistic regression analysis of 18 726 brain-dead donors showed significant increases in kidney, liver and heart utilization from donors receiving 3 hormonal therapies. Significant improvements in 1-year kidney graft survival and heart transplant patient survival were also demonstrated. A prospective randomized trial has not been performed.

Question 32

Patient with malnutrition admitted to your ICU. Assuming high risk of refeeding syndrome and normal renal function:
a. What are two changes you can make to your TPN prescription to minimize the risk of refeeding syndrome?

b. What are 3 clinical manifestations of severe hypophosphatemia?

Answer 32

a)

• ???permissive underfeeding (≤20 kcal/kg/d or 80% of estimated energy needs)
• ???use current weight as initial dosing weight

For patients who are underweight (body mass index [BMI] <18.5 kg/m2), we suggest using the current weight as the initial dosing weight. The reason is that calculation of caloric intake based on ideal body weight could lead to the administration of excess initial calories and induce refeeding syndrome.

Aspen guidelines: Attention to refeeding syndrome is especially important for the patient with risk factors (alcoholism, weight loss, low body mass index [BMI], prolonged periods NPO). Although refeeding syndrome can occur with EN, the risk is higher with initiation of PN. In those patients, advancement of feeding should be slower, taking 3–4 days to reach goal. Use of protocols and nutrition support teams have been shown to decrease PN-associated complications. Permissive underfeeding has also been shown to be a potential shortterm approach to avoid some of these complications.

b)

• encephalopathy, seizures
• myocardial dysfunction
• diaphragm weakness, respiratory failure/prolonged ventilation
• proximal myopathy, ileus, dysphagia
• rhabdomyolysis
• hemolysis
• thrombycytopenia (rare)
• reduced phagocytic and granulocyte function (of WBCs)

In significantly malnourished patients, the initial stage of oral, enteral, or parenteral nutritional replenishment causes electrolyte and fluid shifts that may precipitate disabling or fatal medical complications. The refeeding syndrome is marked by:

• Hypophosphatemia (HALLMARK)
• Hypokalemia
• Congestive heart failure, myocardial dysfunction
• Peripheral edema
• Rhabdomyolysis
• respiratory failure and diaphragm weakness
• Seizures, encephalopathy
• Hemolysis

The risk of hypophosphatemia during refeeding appears to be greater in patients who are more severely malnourished and at lower percent of ideal body weight. The pathogenesis of hypophosphatemia begins when stores of phosphate are depleted during episodes of anorexia nervosa and starvation. When nutritional replenishment starts and patients are fed carbohydrates, glucose causes release of insulin, which triggers cellular uptake of phosphate (and potassium and magnesium) and a decrease in serum phosphorous levels. Insulin also causes cells to produce a variety of depleted molecules that require phosphate (eg, adenosine triphosphate and 2,3-diphosphoglycerate), which further depletes the body’s stores of phosphate. The subsequent lack of phosphorylated intermediates causes tissue hypoxia, myocardial dysfunction, respiratory failure due to an inability of the diaphragm to contract, hemolysis, rhabdomyolysis, and seizures.

Question 33

Presented an ABG. pH 7.25, pCO2 25, HCO3 10. AG 19. Delta AG 7, delta HCO3 14. What is the nature of the abnormal ABG?

Answer 33

anion gap metabolic acidosis with appropriate respiratory compensation

anion gap=Na-Cl-HCO₃

delta/delta gap= increase in anion gap / decrease in bicarb

ANION GAP

normal AG typically 10-12 but needs to be corrected for high or low albumin

Albumin, which has a net negative charge, is the single largest (in mEq/L) contributor to the AG. As a result, the baseline AG must be adjusted downward in patients with hypoalbuminemia. The expected AG will fall by approximately 2.5 mEq/L for every 10 g/L reduction in the serum albumin concentration. Thus, the value for the expected baseline AG must be interpreted with this correction factor when metabolic acidosis increases the AG. Conversely, the expected baseline value for the AG must be adjusted upward using the same correction factor in patients with hyperalbuminemia.

DELTA GAP

If the extracellular space were an isolated compartment and none of the lactate or hydrogen ions were lost into the urine, then the increase in serum lactate concentration (L) and the increase in serum AG would exactly match the decrease in serum HCO3 caused by buffering of hydrogen ions. These opposite changes in the serum AG and HCO3 concentration would result in a delta AG/delta HCO3 ratio of 1:1, and perfect reciprocity would exist between the increase in AG and the decrease in HCO3.

However, several important factors that influence the delta AG/delta HCO3 ratio frequently alter this 1:1 relationship:

●The buffering reaction is not limited to the ECF, and the space of distribution of hydrogen ions is different from that of lactate (or other acid anions). Usually, the acid anions that remain in the body (eg, not excreted in the urine) are largely restricted to the extracellular space and thereby raise the AG. By contrast, more than 50 percent of the hydrogen ions released from the acids are buffered within the cells and in bone. The proportion of hydrogen ions that are buffered in compartments other than the extracellular space increases as the serum HCO3 falls. When hydrogen ions are buffered within cells and in bone, the serum HCO3 concentration does not fall. Thus, to the extent that this occurs, the serum AG will rise more than the HCO3 concentration will fall. This increases the delta AG/delta HCO3 ratio above 1:1.

●The renal excretion of the acid anions and hydrogen ions can occur at different rates. To the extent that acid anions are excreted with sodium or potassium, but not with hydrogen ions or ammonium, the serum AG will decrease without a concomitant increase in the serum HCO3, and this will reduce the delta AG/delta HCO3 ratio below 1:1.

Interpretation:

<0.4 hyperchloremic normal AG met acidosis

<1 high AG and normal AG metabolic acidosis (ratio is often <1 in met acidosis associated with renal failure)

1-2 Pure anion gap acidosis; Lactic acidosis: average value 1.6; DKA more likely to have a ratio closer to 1 due to urine ketone loss

>2 suggests a pre-existing elevated HCO₃ so consider concurrent metabolic alkalosis or pre-existing compensated respiratory acidosis

from uptodate:

A delta AG/delta HCO3 ratio below 1 suggests one of the following

• A coexisting normal (or hyperchloremic) AG metabolic acidosis (eg, due to diarrhea).
• A high AG acidosis in which both renal function is preserved and the acid anion is readily excreted into the urine (eg, ketoacidosis, toluene ingestion, or D-lactic acidosis).
• Patients with renal tubular acidosis of early renal insufficiency can also have a delta AG/delta HCO3 ratio below 1. Such patients have a type 4 renal tubular acidosis due to impaired renal tubule acid (mainly ammonium) excretory function, in addition to the accumulation of acid anions and other unmeasured anions that results from a declining glomerular filtration rate (GFR). However, the ratio will usually increase as renal function progressively deteriorates.

Question 34

Patient has AAA repair, prolonged case with massive transfusion. In the presence of elevated bladder pressures, list 4 clinical (non lab) features suggestive of abdominal compartment syndrome.

Answer 34

• elevated ICP
• hypoventilation/high airway pressures/low respiratory system (more specifically chest wall) compliance
• hypotension/shock/hemodynamic collapse
• oliguria/anuria
• bowel ischemia

Question 35

Patient is diagnosed with a Type B aortic dissection:

a. Define a type B dissection
b. List four complications from a Type B dissection other than death

Answer 35

a) The Stanford system classifies aortic dissections that involve the ascending aorta as type A, regardless of the site of the primary intimal tear, and all other dissections as type B.

b)

• dissection extension
• malperfusion or end-organ ischemia
• pain
• aortic rupture

Question 36

Young patient with confirmed bacterial meningitis, GCS still 5 on day 4, CT head normal. List 4 potential causes of decreased LOC in this patient.

Answer 36

• non-convulsive status epilepticus
• ischemic stroke
• superior sagital or cortical vein thrombosis
• medication-related (sedatives?)
• sensorineural hearing loss (i.e. they can’t hear the commands for GCS test?)
• high ICP (but this would have been shown on CT)
• brain abscess or focal cerebritis

Question 37

What are four reasons why a patient on V-V ECMO may desaturate?

Answer 37

1. recirculation
2. pulmonary shunt (i.e. actual lung disease or hypoxemia from native lungs has worsened)
3. low ECMO blood flow to cardiac output ratio (Some authors have recognized an ECMO blood flow to cardiac output ratio greater than 0.6 as an index for ECMO efficiency)
4. oxygenator dysfunction (blood clots or water drops inside membrane)

Question 38

What sort of precautions (contact, droplet, airborne) are needed for the following infections?

a. Influenza A
b. C. difficile
c. N. meningitidis (first 24 hours of antimicrobial therapy)
d. Tuberculosis

Answer 38

a) influenza A - DROPLET plus standard
b) C diff - CONTACT plus standard
c) N meningitidis - DROPLET plus standard (until 24hrs after initiation of appropriate antimicrobial therapy)
d) TB - AIRBORNE plus standard if pulmonary/laryngeal disease (use AIRBORNE+CONTACT+standard if extrapulmonary draining lesion, and use stanard if extrapulmonary and no draining lesion like meningitis)

STANDARD

• perform hand hygiene
• use PPT whenever there is expectation of possible exposure to infectious material
• follow respiratory hygiene/cough etiquette principles
• ensure appropriate pt placement
• properly handle and properly clean and disinfect pt care equipment and instruments/devices
• handle textiles and laundry carefully
• follow safe injection practices
• wear a surgical mask when performing LPs
• ensure healthcare worker safety including proper handling of needles and other sharps

CONTACT

• Ensure appropriate patient placement in a single patient space or room if available in acute care hospitals
• Use personal protective equipment (PPE) appropriately, including gloves and gown. Wear a gown and gloves for all interactions that may involve contact with the patient or the patient’s environment.
• Limit transport and movement of patients outside of the room to medically-necessary purposes.
• Use disposable or dedicated patient-care equipment (e.g., blood pressure cuffs).
• Prioritize cleaning and disinfection of the rooms

DROPLET

• source control
• ensure appropriate pt placement
• use PPE appropriately (Don mask upon entry into the patient room or patient space)
• limit transport and movement of pts

AIRBORNE

• source control (put a mask on the pt)
• ensure appropriate pt placement in an airborne infection isolation room
• restrict susceptible healthcare personnel from entering the room
• use PPE appropriately including N95 or high level respirator
• limit transport and movement of pts
• immunize susceptible persons ASAP following unprotected contact

Question 39

Patient is 2 days post-resuscitation in the cath lab. Attached X ray shows left IJ in right atrium and IABP in position (? too high).

a. What 2 abnormalities can be identified on this CXR?
b. Name 1 potential complication for each of the above abnormalities.

Answer 39

b)

CVC

• cardiac dysrhythmias
• cardiac perforation

IABP

• too high: obstruction of L subclavian artery
• too low: obstruction of splanchnic arteries

CVC placement:

The traditionally preferred position of the catheter tip is in the distal third of the SVC to minimize complications such as catheter migration, extravasation of irritant agents, vascular perforation, local vein thrombosis, catheter malfunction and cranial retrograde injection. The junction of the SVC and RA was considered to be located at the intersection of the right lateral margin of the SVC and the superior border of the RA (cardiac silhouette).

uptodate: To minimize the likelihood of cardiac complications, some guidelines recommend catheter tip position outside the right atrium and above the pericardial reflection. The right superior heart border on chest radiography is not a reliable determinant of right atrial position. The carina and right tracheobronchial angle represent reliable landmarks for the pericardial reflection, and right-sided catheters should generally be positioned above this point.

Nontunneled central venous catheters positioned deep into the right atrium or catheters placed in the right ventricle increase the risk for dysrhythmias and cardiac perforation, although cardiac perforation appears to be a rare event.

IABP placement:

The balloon should be located in the proximal descending aorta, just below the origin of the left subclavian artery. On CXR it should be at the level of the AP window (which is just below the aortic knuckle). This ideally results in the balloon terminating just above the splanchnic vessels.

Question 40

18 yo admitted to ICU with status asthmaticus. Managed in Emerg and intubated with fentanyl, midazolam and rocuronium. Becomes more hypotensive, more tachycardiac (HR 165 to 190). What four physiologic factors led to his hypotension.

Answer 40

1. dynamic hyperinflation
2. loss of sympathetic drive/endogenous catecholamines
3. midazolam, fentanyl causing peripheral vasodilation and loss of preload
4. ???hypovolemia, ???tension pneumo

interestingly: Rapid administration of midazolam (<2 minutes) has been reported to cause severe hypotension especially if administered concurrently with fentanyl. For procedural sedation (eg, intubation) or intermittent sedation dosing, administration over at least 2 to 5 minutes has been used, monitor for hypotension

Question 41

Older adult with severe COPD. Initial gas 7.10. Intubated and started on mechanical ventilation with RR 16, Vt 600 mL. Initially sats improve, but 5 mins later becomes more hypotensive and has a PEA arrest. What are four reasons to explain her worsening?

Answer 41

1. dynamic hyperinflation/breath-stacking
2. hypovolemia from presentation
3. ?tension pneumothorax
4. tube migration and mainstem vs esophageal intubation

Question 42

Patient admitted to ICU with progressive liver failure. Despite normal CXR, negative CT for PE, normal echo, is hypoxic (sats 85% on FiO2 1.0 and PEEP 10). What are four potential interventions to improve her oxygenation?

Answer 42

1. lay pt supine
2. increase PEEP (to decrease flow through aorto-venous shunts
3. ???inhaled pulmonary vascular dilators
4. ???liver transplantation
5. ???coil embolization

Hepatopulmonary syndrome (HPS) is characterized by the triad of abnormal arterial oxygenation caused by intrapulmonary vascular dilatations (IPVDs) in the setting of liver disease, portal hypertension, or congenital portosystemic shunts.

• Chronic liver disease – Chronic liver disease (CLD) of virtually any etiology including congenital liver disease that limit venous flow to the lung (eg, cavopulmonary shunt) can be associated with HPS, particularly when CLD is complicated by portal hypertension.
• Portal hypertension – HPS is most commonly seen in patients with portal hypertension in association with chronic liver disease but can also occur in those who have portal hypertension without underlying liver disease.

Pathogenic processes that have been proposed include:

• Increased bacterial translocation and toxin release (intestinal endotoxemia) from portal hypertension may stimulate the release of vasoactive mediators including nitric oxide (NO), heme-oxygenase-derived carbon monoxide and tumor necrosis factor alpha. Such mediators may result in pulmonary vasodilation or angiogenesis.
• Failure of the damaged liver to clear circulating pulmonary vasodilators, production of circulating vasodilators by the damaged liver, and inhibition of circulating vasoconstrictive substances by the damaged liver have also been proposed.

Platypnea and orthodeoxia are classic manifestations that are more specific for HPS, but not pathognomonic:

• Platypnea – Platypnea is an increase in dyspnea that is induced by moving into an upright position and relieved by recumbency.
• Orthodeoxia – Orthodeoxia refers to a decrease in the arterial oxygen tension (by more than 4 mmHg [0.5 kPa]) or arterial oxyhemoglobin desaturation (by more than 5 percent) when the patient moves from a supine to an upright position, which is improved by returning to the recumbent position.

It is hypothesized that platypnea and orthodeoxia in HPS are caused by preferential perfusion of intrapulmonary vascular dilatations (IPVDs; which disproportionately occur in the lung bases) when the patient is upright.

The only definitive therapy for patients with HPS is liver transplantation, which is reserved for those with severe or very severe HPS.

Question 43

Lineman sustained accidental electrical injury while working on power line. No LOC, no fall. Lowered gently to the ground. Contact points on right hand and left foot. Aside, from death, what are four major complications of electrical burns?

Answer 43

are these considered four major complications of electrical burns?

• rhabdomyolysis causing renal injury
• cardiac arrhythmias (The overall estimate of arrhythmia following electrical injury is approximately 15 percent; most of these are benign and occur within the first few hours of hospital admission. However, acute electrical cardiac injury can result in sudden cardiac arrest due to asystole (usually with DC current or lightning) or ventricular fibrillation (AC current) prior to hospitalization. Ventricular fibrillation is the most common fatal arrhythmia.)
• skin/surface burns: Superficial, partial-thickness, and full-thickness thermal burns can occur following electrical injury
• weakness, decreased LOC, respiratory depression, autonomic dysfunction, memory disturbances. Damage to both the central and peripheral nervous systems can occur after electrical injury. Manifestations may include loss of consciousness, weakness or paralysis, respiratory depression, autonomic dysfunction, and memory disturbances. Sensory and motor findings due to peripheral nerve damage are common.
• bone destruction: Because bone has the highest resistance of any body tissue, it generates the greatest amount of heat when exposed to an electrical current. Thus, the areas of greatest thermal injury are often the deep tissue surrounding long bones, potentially resulting in periosteal burns, destruction of bone matrix, and osteonecrosis.
• compartment syndrome, electrical coagulation of small blood vessels

Question 44

US screenshot of neck. Had to label 5 structures.

a. Sternocleidomastoid
b. IJ
c. Carotid artery
d. Thyroid gland
e. Trachea

Answer 44

see website for answers

Question 45

Capnography traching with ETCO2. Asked to match four blanks with either a letter or segment between letters (ex. A, or A-B)

a. Alveolar ventilation
b. Dead space ventilation
c. ETCO2 on monitor
d. Inspiration

Answer 45

weird if the question was truly a CO2-time (and not CO2-flow) graph

see figure from uptodate

NEED to discuss which graph it was

Question 46

Middle-aged alcoholic presents to hospital intubated for decreased LOC with point of care lactate >20. CT head normal. Not hypotensive. Not on metformin. No osmolar gap. CT angio abdomen shows no ischemic bowel. No abdo/extremity compartment syndrome. INR and Bili normal, AST 220 ALT 100.

a. What is the most likely cause of the lactic acidosis?
b. What one test will make the diagnosis?

Answer 46

a) lab inaccuracy where it cannot differentiate between lactate and glycolate (metabolite of ethylene glycol)…initially osmolar gap would be positive but as it gets metabolized it can normalize and thus leave only anion gap

The development of osmolal and anion gaps varies as a function of time from ingestion. As metabolism progresses, increasing amounts of these alcohols are converted to their metabolites. The contribution of the parent compounds to the osmolal gap decreases, whereas the contribution of the metabolites to the anion gap increases. Therefore, early in the course of poisoning, an anion gap may be absent in the presence of an osmolal gap, and an anion gap may exist without an osmolal gap as metabolism progresses.

b) ethylene glycol level testing

Patients with ethylene glycol poisoning can have elevations in their serum lactate concentration. In some cases, such elevations (usually minor) can be caused by actual increases in lactate. However, in other cases such elevations may be substantial and are likely to an error caused by some laboratory instruments that cannot differentiate between lactate and glycolate, a metabolite of ethylene glycol that is structurally similar to lactate.

A markedly elevated lactate concentration may be the first test result reported in a severely acidotic patient, now that lactate testing has become readily available, and traditionally suggests alternative diagnoses (eg, tissue hypoxia, metformin poisoning). However, it is important NOT to exclude ethylene glycol as a possible cause of acidosis merely because of a reportedly elevated lactate.

An unexplained, large osmolal gap is presumptive evidence of a recent methanol, ethylene glycol, or isopropyl alcohol exposure in the appropriate clinical setting, provided a significant ethanol ingestion has been excluded.

The osmolal gap is the difference between the measured osmolality and the calculated plasma osmolality, using standard units (mmol/L):

Calculated Posm = (2 x plasma [Na]) + [glucose] + [urea]

Question 47

Patient admitted and intubated for intracerebral bleed. List 6 radiographic or clinical findings that are significant for prognostication.

Answer 47

1. increasing age
2. decreased GCS
3. increasing ICH volume
4. presence of intraventricular hemorrhage
5. keep or infratentorial ICH location
6. preceding oral anticoagulation therapy

Question 48

Patient with confusion presents to ED, ABG shows pH 7.15 pCO2 25 HCO3 15 Sodium 135 Potassium 2.2 Chloride 100.

a. What is the most likely drug intoxication?
b. Besides IV fluid resuscitation, what are the three initial treatments for this patient?

Answer 48

a) ASA

A variety of acid-base disturbances can occur with salicylate intoxication. Salicylates stimulate the respiratory center directly, resulting in an early fall in the PCO2 and respiratory alkalosis. An anion-gap metabolic acidosis then follows, due primarily to the accumulation of organic acids, including lactic acid and ketoacids.

b)

• Administer supplemental glucose in patients with altered mental status, even if serum glucose concentration is normal: IV dextrose 50 g as 100 mL of 50 percent dextrose
• Administer multiple doses of activated charcoal (first dose: 1 g/kg orally up to 50 g)
• Alkalinize with sodium bicarbonate (The usual initial dose of sodium bicarbonate is 1 to 2 mEq (or mmol) per kg given as an intravenous bolus. This is followed by a sodium bicarbonate infusion of 100 to 150 mEq (or mmol) in one liter of sterile water with 5 percent dextrose)
  
  • The rate of the infusion is titrated to a urine pH of 7.5 to 8, but is usually 1.5 to 2 times the maintenance dose for intravenous fluids. Hypokalemia must be corrected or prevented for alkalinization to be effective. Enteral or parenteral potassium supplementation should be initiated even in patients with serum potassium concentrations in the low normal range, as alkalinization will further lower the serum potassium.
• +/- dialysis

-dont forget ABCs

Aspirin intoxication may decrease cerebral glucose concentrations despite a normal serum glucose.

Hypokalemia, if present, must be treated aggressively. Hypokalemia promotes the absorption of potassium in the distal tubule; this absorption occurs via a K+/H+ exchange pump (figure 1). The secretion of protons involved in this pump interferes with efforts at urinary alkalinization, which are a mainstay of therapy

Indications for hemodialysis include any of the following findings in the setting of salicylate poisoning:

• Altered mental status
• Pulmonary edema associated with respiratory distress and/or requiring supplemental oxygen
• Cerebral edema
• Acute or chronic kidney injury sufficient to impair salicylate elimination. A number of thresholds may be used to determine such kidney injury, including the following:
  
  • Serum creatinine >176 micromol/L (2 mg/dL) in average adult; or, serum creatinine >132 micromol/L (1.5 mg/dL) in elderly or patients with low muscle mass
  • Estimated glomerular filtration rate (GFR) <45 mL/minute per 1.73 m2
• Fluid overload that prevents the administration of sodium bicarbonate
• A markedly elevated serum salicylate concentration in acute overdose:
  
  • In patients with normal renal function: 90 mg/dL (7.2 mmol/L)
  • In patients with impaired renal function: 80 mg/dL (6.5 mmol/L)
• Severe acidemia: systemic pH ≤7.20
• Clinical deterioration despite aggressive and appropriate supportive care

Question 49

Post-op CABG patient with abdo pain, vomiting, distension. Previous hx of cholecystectomy. AXR shown with labels A (in RUQ) , B and C (around dilated loops of bowel). Asked to identify the abnormalities at A,B,C and give a diagnosis.

Answer 49

Although there is no universally agreed upon cut-off for what constitutes dilatation of the large bowel, 6cm is a reasonable value for the colon, with the cecum having an upper limit of 9cm 1. This is known as the 3-6-9 rule.

The 3-6-9 rule is a simple aide memoire describing the normal bowel caliber:

• small bowel: <3 cm
• large bowel: <6 cm
• cecum: <9 cm

Proximal bowel dilation with distal bowel collapse – Small bowel obstruction can be diagnosed if the more proximal small bowel is dilated more than 2.5 cm (outer wall to outer wall) and the more distal small bowel is not dilated.

Question 50

Which alcohol is directly toxic before it is metabolized? What are the two drugs to inhibit conversion?

Answer 50

isopropyl alcohol (as per UWO toxicologist)…but I wonder if could also be ethanol?

Ethanol decreases the rate of fomepizole elimination by ~50%; conversely, fomepizole decreases the rate of elimination of ethanol by ~40%.

Isopropyl alcohol is a sedative-hypnotic agent whose toxicity closely resembles that of ethanol, with which it shares strong structural similarity. Isopropyl alcohol does NOT cause an elevated anion gap acidosis, unlike the toxic alcohols methanol and ethylene glycol. Since acetone (the primary metabolite) is less toxic than isopropyl alcohol (the parent alcohol), there is no indication for ADH inhibition with fomepizole or ethanol following isopropyl alcohol exposure. Suspected methanol or ethylene glycol exposures should be managed accordingly.

Methanol and ethylene glycol are both primary alcohols, which are oxidized (via alcohol dehydrogenase and then aldehyde dehydrogenase) to carboxylic acids (formic acid in the case of methanol and glycolic, glyoxylic, and oxalic acids in the case of ethylene glycol). These acid metabolites cause the severe toxicity (ie, blindness, renal failure, and death) characteristic of methanol and ethylene glycol poisoning.

All alcohol poisonings are associated with an increased osmolal gap, if the patient presents soon after the ingestion.

The “parent alcohols” methanol and ethylene glycol are relatively nontoxic, and cause mainly central nervous system (CNS) sedation. However, profound toxicity can ensue when these parent alcohols are metabolized in vivo (ie, oxidized, primarily by alcohol dehydrogenase and aldehyde dehydrogenase).

The methanol metabolite formate and the ethylene glycol metabolites glycolate, glyoxylate, and oxalate accumulate following large ingestions. Above plasma levels of approximately 20 mg/dL (approximately 6 mmol/L of methanol or 3 mmol/L of ethylene glycol), these metabolites can cause specific end-organ damage:

• Formate causes retinal injury with optic disc hyperemia, edema, and eventually permanent blindness, as well as ischemic or hemorrhagic injury to the basal ganglia. These changes are postulated to result from disruption of mitochondrial function.
• Ethylene glycol metabolites target the kidney and lead to reversible oliguric or anuric acute kidney injury (acute renal failure), which in turn slows elimination of ethylene glycol.

Question 51

Patient is admitted comatose after acetaminophen ingestion of unknown time period.

a. What drug can be given right now
b. What one test result will predict need for liver transplant
c. What are two scoring tools for mortality prognostication in acute liver failure

Answer 51

NAC??? based on ?fulminant liver failure despite unknown time of ingestion…because uptodate says not to give activated charcoal if pts are sedated or unable to protect their airway or if pt is asymptomatic it’s been >4hrs since ingestion

N-acetylcysteine is the accepted antidote for acetaminophen poisoning and is given to all patients at significant risk for hepatotoxicity. Indications for N-acetylcysteine therapy include:

• Serum acetaminophen concentration drawn at four hours or more following acute ingestion of an immediate-release preparation is above the “treatment” line of the treatment nomogram for acetaminophen poisoning.
• A suspected single ingestion of greater than 150 mg/kg (7.5 g total dose regardless of weight) in a patient for whom the serum acetaminophen concentration will not be available until more than eight hours from the time of the ingestion.
• Patient with an unknown time of ingestion and a serum acetaminophen concentration >10 mcg/mL (66 micromol/L).
• Patient with a history of APAP ingestion and any evidence of liver injury.
• Patients with delayed presentation (>24 hours after ingestion) consisting of laboratory evidence of liver injury (ranging from mildly elevated aminotransferases to fulminant hepatic failure) and a history of excessive acetaminophen ingestion.

Adult patients who present soon after a potentially toxic ingestion of acetaminophen (single dose ≥7.5 g) are likely to benefit from gastrointestinal (GI) decontamination. We suggest treatment with activated charcoal (AC), 1 g/kg (maximum dose 50 g) by mouth in all patients who present within four hours of a known or suspected acetaminophen ingestion, unless there are contraindications to its administration.

Charcoal should be withheld in patients who are sedated and may not be able to protect their airway, unless endotracheal intubation is performed first. However, endotracheal intubation should not be performed solely for the purpose of giving charcoal. Asymptomatic patients who present more than four hours after a reported ingestion are unlikely to benefit from AC, and we do not recommend routine treatment in these patients.

b)

• hypoglycemia??? (one paper I found looked at glucose, lactice acid and PT, and hypoglycemia had the highest odds ratio for a composite end point of death or transplant)…but it’s not included in either King’s College or MELD

As a general rule, the most important factors for predicting the outcome in acute liver failure are the degree of encephalopathy, the patient’s age, and the cause of the acute liver failure.

c)

• King’s College Criteria
• Model for End-Stage Liver Disease (MELD) score

Question 52

Diagram of pressure time, flow time and esophageal pressure time curves

a. What is the mode of ventilation?
b. Described what is occurring to flow just after the dashed vertical lines?
c. Why is the ventilator delivering two breaths at a time?

Answer 52

a) pressure control
b) flow increases due to activation of the diaphragm and thus a decrease in pleural (and therefore alveolar) pressure
c) reverse triggering where the first breath in the couplet triggers the diaphragm to contract which creates a negative pleural (and therefore alveolar pressure) which then decreases the pressure measured by the ventilator which triggers a second breath.

Question 53

Patient has variceal bleed. Clinically stable, oxygenating well, mentating well. Is fully sedated, paralyzed. Failed intubation attempt 3 times via DL, DL with bougie, then VL. Patient is easy to ventilate and oxygenate.

a. List three things you will do now
b. Patient has recurrent hematemesis and you now cannot intubate cannot oxygenate. What one thing will you do right now?

Answer 53

a)

1. call for help
2. attempt to insert supraglottic device
3. raise head of bed, maintain cricoid pressure (decrease risk of aspiration)

b)

scalpel cricothyroidotomy

Question 54

LV Pressure-Volume curve shown. Label the following points:

a. Aortic valve closure
b. Isovolumetric contraction

Answer 54

aortic valve closure is top left corner

isovolumetric contraction is line on the right side

Question 55

LV Pressure-Volume curve shown. Draw a new curve showing the effects of increasing contractility, assuming afterload and preload remain constant.

Answer 55

ESPVR becomes steeper and so the aortic valve closure moves leftward increasing the area of encircled by the loop and thus increases stroke volume.

Question 56

Three Guyton vascular and cardiac function curves shown with low, normal, high MCFP and low, normal, high contractility. Intersection A is shown. Label the hemodynamic/clinical change at three labeled points, which correlated to heart failure, hypovolemia, and vasoplegia.

Answer 56

ok explanation here

online lectures here

Question 57

List 3 features that you have noticed in yourself or colleagues associated with ICU burnout.

Answer 57

Hallmarks of Burnout:

• depersonalization
• emotional exhaustion
• loss of sense of achievement

The clinical symptoms and signs of burnout are often non-specific and can include depression, irritability, insomnia, tiredness, and anger.

Stress vs burnout

Stress:

• Characterized by overengagement
• Emotions are overactive
• Produces urgency and hyperactivity
• Loss of energy
• Leads to anxiety disorders
• Primary damage is physical

Burnout:

• Characterized by disengagement
• Emotions are blunted
• Produces helplessness and hopelessness
• Loss of motivation, ideals, and hope
• Leads to detachment and depression
• Primary damage is emotional

Burnout can cause:

• PTSD and other psychological symptoms
• decreased pt satisfaction and quality of care
• increased job turnover

Question 58

28 year old woman with glioblastoma multiforme. Persistently comatose for weeks. No further chemotherapy, surgical or radiation options. Has been to ICU previously for respiratory failure and trached. Now has worsening respiratory distress and family wants you to take her to ICU. List 4 reasons why the family would want this.

Answer 58

• uncomfortable, guilt
• hope, religious belief
• disbelief of medical prognosis
• overburdened and paralyzed by their role
• family thought “pt wanted everything done”

The family may also insist on aggressive treatment because it is their understanding that the patient may have “wanted everything done.” In such cases, it may be appropriate to say “No.” True autonomy is not about offering patients to pick from a proverbial shopping list of what medicine can do, but about clarifying reasonable goals of care and offering only the treatments that can realistically achieve them. Providing a treatment when it is unlikely to lead to an acceptable outcome for the patient does not promote autonomy, but only false hope and confusion. While medicine does not have a crystal ball to know any outcome for certain, it is not entirely ignorant either, and it is important to counsel and guide patients and families in the decision-making process.

Question 59

Patient with non-small cell carcinoma with mets is now comatose. SDM states they would not want to live like this and are requesting MAID.

a. Medicolegally can you offer MAID?
b. What are three of the five criteria for MAID
c. What one thing will you offer to the patient/family at this point?

Answer 59

a) no

b)

A person may receive medical assistance in dying if and only if they:

• are eligible for publicly funded health services in Canada;
• are at least 18 years of age and capable of making health care decisions;
• have a grievous and irremediable medical condition;
• have made a voluntary request for medical assistance in dying; and
• give informed consent to receive medical assistance in dying after having been informed of the means that are available to relieve their suffering, including palliative care.

c) palliative care

the Act lays out protective measures and safeguards to protect against coercion or impulse. It requires that:

• requests for medical assistance in dying are in writing and witnessed by two independent witnesses;
• individuals seeking medical assistance in dying obtain a second opinion from an independent physician or nurse practitioner; and
• there are at least 10 clear days between the date that the request is signed by or on behalf of the person and the day on which the medical assistance in dying is provided or — if they and the other medical practitioner or nurse practitioner referred are both of the opinion that the person’s death, or the loss of their capacity to provide informed consent, is imminent — any shorter period that the first medical practitioner or nurse practitioner considers appropriate in the circumstances.

Question 60

List one advantage and disadvantage of external ventricular drain over other forms of ICP monitoring.

Answer 60

advantage:

accurate

allow drainage of CSF

disadvantages:

infection risk

risk of hemmorhage during insertion

Intraventricular monitors are considered the “gold standard” of ICP monitoring catheters. They are surgically placed into the ventricular system and affixed to a drainage bag and pressure transducer with a three-way stopcock. Intraventricular monitoring has the advantage of accuracy, simplicity of measurement, and the unique characteristic of allowing for treatment of some causes of elevated ICP via drainage of cerebrospinal fluid (CSF).

The primary disadvantage is infection, which may occur in up to 20 percent of patients. This risk increases the longer a device is in place [31,32]. Prophylactic catheter changes did not appear to reduce the risk of infection.

A further disadvantage of intraventricular systems includes a small (approximately 2 percent) risk of hemorrhage during placement.

Question 61

List 5 causes of hypotension in sepsis

Answer 61

• 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]. (See “Use of vasopressors and inotropes”, section on ‘Vasopressin and analogs’.)

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 62

***What is the risk of unsynchronized cardioversion over cardioversion? What is the pathophysiology?

Answer 62

***do we need to draw the electrical potential diaphragm and the ion channels here???

If an electrical shock is provided during the relative refractory period (corresponding to the latter part of the T wave), it is possible to induce VF (the so-called “R-on-T Phenomenon”). This would result in a patient who originally had a pulse being put into cardiac arrest.

To avoid inducing cardiac arrest in a patient with a pulse, synchronized cardioversion is performed instead of defibrillation when a patient is in an SVT with a pulse but is considered unstable according to the definition above.

During repolarization, heart cells prepare for the next impulse. During the contraction and early repolarization phases of the cardiac cycle, cardiac cells can’t respond to a stimulus, no matter how strong. Called the absolute refractory period, this phase protects the heart and allows cells to prepare for the next impulse. The absolute refractory period starts from the end of the P wave and extends to approximately the middle of the T wave.

The remaining portion of the T wave is the relative refractory period. During this period, the heart isn’t quite ready to respond, but a stimulus that’s strong enough can cause a contraction. However, the cardiac cells are irritable and commonly respond by causing a life-threatening rhythm, such as ventricular tachycardia or ventricular fibrillation.

R-on-T phenomenon — The term “R-on-T phenomenon” is largely only of historic interest and has little prognostic importance in most clinical situations. VPBs that begin at or near the apex of the T wave (termed the vulnerable period, which is a time when the energy threshold for ventricular fibrillation [VF] is reduced) are said to illustrate the “R-on-T” phenomenon. Although VPBs exhibiting the R-on-T phenomenon were originally felt to carry a grave prognosis (being associated with VF), subsequent studies found that late coupled VPBs were equally as likely as R-on-T VPBs to initiate repetitive ventricular arrhythmia (particularly VT) in humans [28-30]. In addition, the lack of significance of the R-on-T phenomenon is well illustrated during invasive electrophysiology studies during which programmed ventricular stimulation is routinely carried out, applying VPBs at the vulnerable period of the cardiac cycle, without producing malignant ventricular arrhythmias in normal hearts.

The R-on-T VPB may be of importance, however, in subsets of patients at risk for polymorphic VT or VF, such as those with acute myocardial ischemia, the Brugada syndrome, the malignant form of early repolarization, and idiopathic VF

Question 63

List four ways to improve oxygenation in severe ARDS.

Answer 63

By definition, patients with ARDS are severely hypoxemic. Options available for improving arterial oxygen saturation (SaO2) include:

• Use of high fractions of inspired oxygen (FiO2)
• Decrease oxygen consumption
• Improve oxygen delivery
• Manipulate mechanical ventilatory support

…actual answers here:

• conservative fluid strategy to reduce/minimize pulm edema (citation)
• prone positioning (P:F <150 with FiO2 0.6 as per PROSEVA)
• decrease O2 consumption by treating fever, anxiety, pain
• neuromuscular blockade (ACURASYS?now controversial since ROSE trial)
• inhaled vasodilators (NO, prostacyclin) but these have not been shown to reduce mortality/morbidity
• high PEEP strategy (unclear effect on mortality)

Question 64

Woman is admitted with alcoholic pancreatitis. Post-op from surgical resection, has been on meropenem, vancomycin for quite awhile now with persistent fever and WBC. CT scan shows no drainable collections. What one antimicrobial class would you add now?

Answer 64

antifungal coverage

Candida frequently contribute to polymicrobial infections that occur following gastrointestinal tract perforation, anastomotic leaks after bowel surgery, or acute necrotizing pancreatitis. Discrete abscesses with or without peritonitis can occur.

For critically ill pts initial treatment with an echinocandin (e.g. micafungin) instead of a trizole is recommended.

Question 65

List the two types of critical illness acquired weakness. List two risk factors.

Answer 65

• sepsis, SIRS
• multi-organ failure
• neuromuscular blockade
• +/- IV glucocorticoids
• +/- COPD/status asthmaticus/ARDS
• +/- high severity of illness
• +/- hyperglycemia
• +/- hyperthyroidism

Critical Illness myopathy (CIM)

• more common than CIP
• major histopathologic finding is relatively selective loss of myosin, identified as a lack of reactivity to myosin ATPase in non-necrotic fibers

Critical Illness polyneuropathy (CIP)

• common complication of severe sepsis, thought to be a neurologic manifestation of SIRS
• mechanism unknown

*can have combined CIM and CIP, termed critical illness polyneuromyopathy

Neuromuscular weakness due to critical illness myopathy (CIM) or critical illness polyneuropathy (CIP) is a common occurrence in patients who are critically ill, developing in ≥25 percent of patients who are mechanically ventilated in the intensive care unit (ICU) for at least seven days. Risk factors include sepsis, multiorgan failure, and the systemic inflammatory response syndrome.

possible risk factors:

• COPD, status asthmaticus, ARDS
• IV glucocorticoids (now somewhat controversial)
• NMB, recent meta-analysis shows modest association
• high illness severity, hyperglycemia, hyperthyroidism

Management:

Treatment of both critical illness myopathy (CIM) and critical illness polyneuropathy (CIP) is directed toward aggressive management of medical conditions, avoidance of additional complications such as venous thrombosis, and rehabilitation. Minimizing sedation, limiting or avoiding use of neuromuscular blockers, and early mobilization of critically ill patients may help to prevent or mitigate neuromuscular weakness, although supporting data are limited. Despite controversy regarding causality, it still seems reasonable to discontinue or reduce glucocorticoids as soon as possible.

Although not established, two studies have reported that intensive insulin therapy (target blood glucose 4.4 to 6.1 mmol/L) may lower the incidence of CIM and CIP among critically ill patients who remain in the intensive care unit for seven or more days.

Question 66

List four routine ICU labs that would suggest a patient has critical illness related corticosteroid insufficiency (CIRCI).

Answer 66

• Hypoglycemia (usually mild)
• Hyponatremia (rare and usually mild)
• Hyperkalemia (rare and usually mild)
• Metabolic acidosis
• Hypereosinophilia

CIRCI is characterized by dysregulated systemic inflammation
resulting from inadequate intracellular glucocorticoid-mediated
anti-inflammatory activity for the severity of the patient’s critical
illness.

Question 67

Patient with Parkinson disease admitted with severe gastroenteritis, unable to take PO meds. Becomes agitated and receives ativan and haloperidol. Now rigid, febrile, tachycardic, hypercapnic, essentially showing signs of NMS.

a. What two things led to him developing this?
b. What is the pathophysiology?
c. What is the one treatment you will start?

Answer 67

a)

• haldol
• L-dopa/dopamine agonist withdrawal/missed dose

b) unknown exactly but likely related to dopamine blockage/antagonism, where in the hypothalamus can cause fever and autonomic changes
c) Treatment:

• stop causative agent
• supportive care (hydration, electrolyte mgmt, watch for severe complications including MI, AKI, arrhythmias, resp failure, cardiomyopathy, VTE, DIC, Szs, hepatic failure)
• admit to ICU
• medical Rx: Recommendations for specific medical treatments in NMS are based upon case reports and clinical experience, not upon data from clinical trials. Their efficacy is unclear and disputed. Commonly used agents are dantrolene, bromocriptine, and amantadine. We are more likely to use these agents in more severe cases and escalate treatment if there is no effect or the patient worsens. A reasonable approach is to start with benzodiazepines (lorazepam or diazepam) along with dantrolene in moderate or severe cases, followed by the addition of bromocriptine or amantadine

Neuroleptic malignant syndrome (NMS) is a life-threatening neurologic emergency associated with the use of antipsychotic (neuroleptic) agents and characterized by a distinctive clinical syndrome of mental status change, rigidity, fever, and dysautonomia.

Mortality results directly from the dysautonomic manifestations of the disease and from systemic complications. Mortality has declined from the earliest reports in the 1960s of 76 percent and is more recently estimated between 10 and 20 percent.

Associated Meds:

Antipsychotic and antiemetic agents — NMS is most often seen with high-potency first-generation antipsychotic agents, formerly called neuroleptic agents (eg, haloperidol, fluphenazine). However, every class of antipsychotic drug has been implicated, including the low-potency (eg, chlorpromazine) and second-generation antipsychotic drugs (eg, clozapine, risperidone, olanzapine) as well as antiemetic drugs (eg, metoclopramide, promethazine, and domperidone).

While symptoms usually develop during the first two weeks of antipsychotic therapy, the association of the syndrome with drug use is idiosyncratic. NMS can occur after a single dose or after treatment with the same agent at the same dose for many years. It is not a dose-dependent phenomenon, but higher doses are a risk factor. Case-control studies implicate recent or rapid dose escalation, a switch from one agent to another, and parenteral administration as risk factors.

Antiparkinson medication withdrawal — NMS is also seen in patients treated for parkinsonism in the setting of withdrawal of L-Dopa or dopamine agonist therapy, as well as with dose reductions and a switch from one agent to another. Infection and surgery are possible precipitants as well.

Pathogenesis:

The cause of NMS is unknown. Current theories are limited in their ability to explain all clinical manifestations and in supporting data. An animal model for NMS has been developed, but it does not fully correspond with the human syndrome.

Because of the class of agents with which NMS is associated, dopamine receptor blockade is central to most theories of its pathogenesis. Central dopamine receptor blockade in the hypothalamus may cause hyperthermia and other signs of dysautonomia. Interference with nigrostriatal dopamine pathways may lead to parkinsonian-type symptoms such as rigidity and tremor.

Clinical Manifestations:

1. fever
2. rigidity
3. mental status changes
4. autonomic instability

Question 68

Patient with previous ASIA-A C7 spinal injury admitted with septic shock on vasopressors. Weaned off pressors and getting better. Suddenly has HTN 180/100 and severe headache. Urine output overnight was only 10cc, previously 1000cc.

a. What is the cause of HTN/headache?
b. What one thing would you do for treatment?

Answer 68

a) autonomic dysreflexia
b) insert foley and also attempt disimpaction then consider rapid onset, short-acting anti-hypertensives

Autonomic dysreflexia — SCI above T6 may be complicated by a phenomenon known as autonomic dysreflexia, a manifestation of the loss of coordinated autonomic responses to demands on heart rate and vascular tone. Uninhibited or exaggerated sympathetic responses to noxious stimuli below the level of the injury lead to diffuse vasoconstriction and hypertension. A compensatory parasympathetic response produces bradycardia and vasodilation above the level of the lesion, but this is not sufficient to reduce elevated blood pressure. SCI lesions lower than T6 do not produce this complication, because intact splanchnic innervation allows for compensatory dilatation of the splanchnic vascular bed.

The estimated frequency of this complication is quite variable, ranging from 20 to 70 percent of patients with SCI lesions above T6 [7,8]. Autonomic dysreflexia is unusual within the first month of SCI but usually appears within the first year [9,10].

Typical stimuli include bladder distention, bowel impaction, pressure sores, bone fracture, or occult visceral disturbances [7,8]. Sexual activity can be a trigger. Autonomic dysreflexia can also complicate medical procedures, as well as labor and delivery. (See “Neurologic disorders complicating pregnancy”, section on ‘Spinal cord injury’.)

Common clinical manifestations are headache, diaphoresis, and increased blood pressure [9]. Flushing, piloerection, blurred vision, nasal obstruction, anxiety, and nausea may also occur. Bradycardia is common; however, some patients have tachycardia instead. The severity of attacks ranges from asymptomatic hypertension to hypertensive crisis complicated by profound bradycardia and cardiac arrest or intracranial hemorrhage and seizures. The severity of the SCI influences both the frequency and severity of attacks.

Management of acute attacks includes:

• Measuring and monitoring blood pressure.
• Immediately sitting the patient upright to orthostatically lower blood pressure.
• Removal of tight-fitting garments.
• Searching for and correcting noxious inciting stimuli. Bladder distension and fecal impaction are the most common precipitants. Bladder catheterization and evaluation for urinary tract infection (UTI) should be undertaken; indwelling catheters should be checked for obstruction, and a rectal examination should be performed.
• Prompt reduction of blood pressure with a rapid-onset/short-duration agent, depending on the severity of attack and response to above measures. Medications often used in this setting include nitrates (1 inch, 2 percent nitropaste), nifedipine (10 mg oral or sublingual), intravenous hydralazine (10 mg), and intravenous labetalol (10 mg). Nitrates should be avoided in patients who may be using sildenafil for erectile dysfunction.

Question 69

Patient in ICU intubated with pneumonia. On ceftriaxone, azithromycin, norepinephrine, heparin for DVT prophylaxis and ranitidine for ulcer prophylaxis. ICU day 6 platelets go from 150->50. List two causes of thrombocytopenia in this patient other than sepsis/DIC.

Answer 69

• ceftriaxone
• heparin-induced thrombycytopenia

The most common cause of new-onset thrombocytopenia in a cohort of 329 medical and surgical ICU patients was sepsis, accounting for one-half of the cases. More than one cause of thrombocytopenia was found in 26 percent. The frequency of specific causes of thrombocytopenia included the following:

• Sepsis, all (48 percent)
• Sepsis with documented bacteremia (28 percent)
• Liver disease/hypersplenism (18 percent)
• Overt DIC (14 percent)
• Unknown cause (14 percent)
• Infection, other (11 percent)
• Primary hematologic disorder (9 percent)
• Medications, non-cytotoxic (9 percent)
• Medications, cytotoxic (7 percent)
• Massive transfusion (7 percent)
• Other causes (7 percent)
• Alcoholism (5 percent)

Beta-lactam antibiotics are among the most commonly prescribed drugs, grouped together based upon a shared structural feature, the beta-lactam ring. Beta-lactam antibiotics include:

• Penicillins
• Cephalosporins
• Cephamycins
• Carbapenems
• Monobactams
• Beta-lactamase inhibitors

Beta-lactam antibiotics may be associated with immune-mediated destruction of polymorphonuclear leukocytes, which is characterized by an abrupt onset of neutropenia with fever, rash, and eosinophilia. Similarly, beta-lactam antibiotics may cause immune-mediated hemolytic anemia, characterized by a positive non-gamma Coombs’ test or by subacute extravascular hemolysis with a positive gamma Coombs’ test. This latter reaction generally requires prolonged, high-dose therapy and signs of hypersensitivity are usually absent.

Acute immune thrombocytopenia has been associated with beta-lactam antibiotic administration. The platelet count generally normalizes within two weeks after the drug is stopped. Platelet dysfunction may be caused by high doses of ticarcillin; the newer anti-pseudomonal penicillin, piperacillin, has less of an effect on platelet function.

Heparin-induced thrombocytopenia (HIT) is a life-threatening complication of exposure to heparin (unfractionated or low molecular weight [LMW] heparin) that occurs in up to 5 percent of patients exposed. HIT is caused by autoantibodies to platelet factor 4 (PF4) complexed with heparin. These antibodies cause thrombocytopenia and thrombosis by peripheral platelet consumption and platelet activation, respectively.

Question 70

Given the following pacemaker codes describe how they pace: AAI, VVI, VOO, DDD, DVI.

Answer 70

Five position code:

I - chamber paced

O = none

A = atrium

V = ventricle

D = dual (A+V)

II - chamber sensed

O = none

A = atrium

V = ventricle

D = dual (A+V)

III - response to sensing

O = none

T = triggered

I = inhibited

D = dual (T+I)

IV - rate modulation, aka rate responsive, rate adaptive pacing

O = none

R = rate modulation

V - multisite pacing (rarely used)

Question 71

26yo M TBI ICU day 4 with new RLL airspace disease, increased secretions, increased O₂ requirements, febrile. You suspect he has developed a VAP. List 3 things you could have done to prevent this. Cultures grow MSSA and you switch to cloxacillin. What will your duration of treatment be?

Answer 71

VAP prevention (specific guideline, see table 2 pg 920):

• 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 duration:

• 7 day course recommended for both HAP and VAP.
• I couldn’t find any difference in treatment duration for MSSA VAP so assume it’s also 7d

Question 72

Based on the Monroe-Kelly doctrine list the components that make up intracranial pressure. List two ways in which compensation of these components occurs to lower an elevated ICP.

Answer 72

a)

• brain tissue: 80%
• CSF: 10%
• arterial blood volume (together with venous, 10%)
• venous blood volume

b) compensation by decrease in CSF volume and venous blood volume..once these mechanisms are exhausted the ICP increases…not sure if the question asks for ways we can lower ICP for which I would put:

• insertion of EVD to drain CSF
• osmotic diuresis (mannitol, 3% saline can help dehydrate brain tissue but requires intact BBB)
• elevate head of bed (?assist in draining venous blood and thus reducing its component in cranial vault)

Since the overall volume of the cranial vault cannot change, an increase in the volume of one component, or the presence of pathologic components, necessitates the displacement of other structures, an increase in ICP, or both. Thus, ICP is a function of the volume and compliance of each component of the intracranial compartment, an interrelationship known as the Monro-Kellie doctrine.

Normally, the intracranial components are in equilibrium as shown in chamber 1. Initially, the volume of a space-occupying lesion is compensated for by displacement of blood and CSF and ICP remains normal (chamber 2). When the limits of this compensation is reached; any additional increase in the volume of the mass lesion is accompanied by a corresponding increase in ICP (chamber 3, decompensated phase).

Question 73

There has recently been an error in your ICU where a patient who was supposed to receive dobutamine, accidentally received dopamine. Please provide one change to medication labelling you would implement to prevent this error from occurring again.

Answer 73

It has been proposed that patients in an ICU may have greater risk for ADEs compared with non-ICU patients because of :

1. The intensity of the work environment,
2. The greater exposure to medications, including high-alert and IV medications, and
3. The nature of the critical illness resulting in decreased physiologic reserve and organ dysfunction

Use of tall man lettering for medications sound-alike or look-alike (SALAD) (eg DOPamine – DOBUTamine), independent double checking in the dispensing process, and safe medication concentration practice (using premixed IV infusions)

Ideal patient safety culture in an ICU setting should incorporate multiple ME prevention strategies (prescribing, dispensing, administration, and monitoring) and educational materials

Prescribing:

1. computerized prescriber order entry (CPOE),
2. clinical decision support systems (CDSS) (eg in antibiotics administration)
3. Computerized drug dosing software (specific for insulin)
4. The use of protocols/bundles
5. medication reconciliation (no recommendation made)

Dispensing:

1. Automated dispending methods
2. Medication labeling practices for SALAD using tall man lettering
3. Compliance with safe medication concentration practice (premade IV preparation and requirement of pharmacist to prepare all IV medications)
4. Independent double checking during dispensing high risk medications

Administration:

1. bar-code medication administration (BCMA) systems
2. Double checking prior to administration
3. smart IV infusion pumps
4. Use of subjective assessment tool to titrate medication to effect (eg RASS)
5. standardized IV medication concentration practices may reduce MEs

Monitoring:

1. The use of automatic (reflex) ordering of lab test (eg heparin) or alerts prompting laboratory ordering

Patient safety surveillance:

1. Patient and family interview at discharge
2. Non-targeted chart review
3. Trigger initiated target chart review in addition to voluntary reports to improve the rates for identifying ADEs
4. Direct observation

Followed by evaluation with ICU specific surveillance and evaluation