2015 Flashcards

Question

26. List 5 risk factors for invasive candidiasis

Answer 1

* TPN * CVC * broad spectrum Abx * high APACHE scores * acute renal failure (especially if requiring hemodialysis) * prior surgery (especially abdominal surgery) * I think ICU admission is in and of itself a risk factor too * burn injury * candida colonization immunocompromised pts * hematologic malignancies * recipients of solid organ or hematopoietic cell transplants * those given chemotherapeutic agents, especially those associated with extensive GI mucosal damage

Answer 2

* sepsis/hemodynamic instability * presence of endocarditis/evidence of metastatic infection * presence of suppurative thrombophlebitis * presence of bacteremia after 72hrs of appropriate antimicrobial therapy * subcutaneously tunnelled CVC tunnel tract infection or subcutaneous post resevoir infection\ * candida * staph aureus Catheter removal (in addition to administration of systemic antimicrobial therapy) is warranted in the following circumstances, given high likelihood of severe and/or progressive infection with antibiotic therapy alone: * Sepsis * Hemodynamic instability * Presence of concomitant endocarditis or evidence of metastatic infection * Presence of suppurative thrombophlebitis * Presence of a propagating clot * Persistent bacteremia after 72 hours of appropriate antimicrobial therapy * Subcutaneously tunneled central venous catheter tunnel tract infection or subcutaneous port reservoir infection In addition, catheter removal is warranted in the setting of infection with the following pathogens, given relatively high virulence and relatively low likelihood of treatment response with antibiotic therapy alone: * S. aureus * P. aeruginosa * Drug-resistant gram-negative bacilli * Candida spp ***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).**

Answer 3

**a) CVC insertion bundle** * perform hand hygiene before insertion * adhere to aseptic technique * use maximal sterile barrier precautions (mask, cap, gown, gloves, full body drape) * choose the best insertion site to minimize infections and noninfectious complications based on individual patient characteristics (avoid femorals in obese pts) * \>0.5% chlorhexidine with alcohol * sterile gauze dressing or sterile transparent semipermeable dressing over site * For patients 18 years of age or older, use a chlorhexidine impregnated dressing with an FDA cleared label that specifies a clinical indication for reducing CLABSI for short term non-tunneled catheters unless the facility is demonstrating success at preventing CLABSI with baseline prevention practices **b) CVC care bundle** * Comply with hand hygiene requirements * Bathe ICU patients over 2 months of age with a chlorhexidine preparation on a daily basis * Scrub the access port or hub with friction immediately prior to each use with an appropriate antiseptic (chlorhexidine, povidone iodine, an iodophor, or 70% alcohol) * Use only sterile devices to access catheters * Immediately replace dressings that are wet, soiled, or dislodged * Perform routine dressing changes using aseptic technique with clean or sterile gloves. * Change gauze dressings at least every two days or semipermeable dressings at least every seven days. * For patients 18 years of age or older, use a chlorhexidine impregnated dressing with an FDA cleared label that specifies a clinical indication for reducing CLABSI for short-term non-tunneled catheters unless the facility is demonstrating success at preventing CLABSI with baseline prevention practices. * Change administrations sets for continuous infusions no more frequently than every 4 days, but at least every 7 days. * If blood or blood products or fat emulsions are administered change tubing every 24 hours. * If propofol is administered, change tubing every 6-12 hours or when the vial is changed c) * Catheter-related blood stream infection per 1000 catheter days [http://cmajopen.ca/content/5/2/E488.full.pdf+html](http://cmajopen.ca/content/5/2/E488.full.pdf+html) * pharmacist on rounds * appropriate transfusion practices * VAP bundle (HOB 30deg, SAT+SBT) * US-guidance for CVC insertion * pt centered care: documentation of goals of care * maintain adequate glycemic control

Answer 4

Laplace - The larger the vessel radius, the larger the wall tension required to withstand a given internal fluid pressure Bernoulli - an increase in the speed of a fluid occurs simultaneously with a decrease in pressure or a decrease in the fluid's potential energy Poiseuille - It states that the flow (Q) of fluid is related to a number of factors: the viscosity (n) of the fluid, the pressure gradient across the tubing (P), and the length (L) and diameter(r) of the tubing. Henry - the amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid. (relevant in nitrogen gas in diving I suppose) Boyle - pressure of a given mass of an ideal gas is inversely proportional to its volume at a constant temperature. Charles - volume of a gas proportional to temperature (i.e. when temperature of a gas increases so does volume). Charles’ law explains why the ambient temperature decreases with increased altitude. 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.

Answer 5

I guess first line for fulminant is PO Vanco plus IV Metronidazole **FULMINANT CDI defined as having hypotension, shock, ileus, or megacolon** 1. For fulminant CDI\*, vancomycin administered orally is the regimen of choice (strong recommendation, moderate quality of evidence). If ileus is present, vancomycin can also be administered per rectum (weak recommendation, low quality of evidence). The vancomycin dosage is 500 mg orally 4 times per day and 500 mg in approximately 100 mL normal saline per rectum every 6 hours as a retention enema. Intravenously administered metronidazole should be administered together with oral or rectal vancomycin, particularly if ileus is present (strong recommendation, moderate quality of evidence). The metronidazole dosage is 500 mg intravenously every 8 hours.\* \*Fulminant CDI, previously referred to as severe, complicated CDI, may be characterized by hypotension or shock, ileus, or megacolon. 2. If surgical management is necessary for severely ill patients, perform subtotal colectomy with preservation of the rectum (strong recommendation, moderate quality of evidence). Diverting loop ileostomy with colonic lavage followed by antegrade vancomycin flushes is an alternative approach that may lead to improved outcomes (weak recommendation, low quality of evidence)

Answer 6

MILRINONE - causes more systemic arterial vasodilation than dobutamine - causes more pulmonary vascular vasodilation than dobutamine - renally cleared so needs to be adjusted/avoided in renal impairment - does not significantly increase myocardial oxygen consumption - no tachyphylaxis (as can occur with dobutamine) - lusitropic properties DOBUTAMINE - more rapidly titratable (milrinone has longer half-life and is slower onset and offset) - less potent vasodilation (may be preferable in mixed shock) - can be used in renal failure \*The response to beta adrenergic agonists is more likely to be attenuated due to desensitization of the beta adrenergic receptor pathway, a common occurrence in severe HF. The PDE inhibitors act distal to the beta receptor and are thus somewhat less susceptible to this problem.

Answer 7

* don't give anything and instead should test with TEG then treat accordingly * target plts \>50 000 * fibrinogen \>1.2 * ...also the old answer said FFP but the INR of FFP is 1.5-1.7 so not very helpful here **uptodate:** **Indications for plasma products** – We do not routinely administer FFP or Cryoprecipitate to "correct" the PT/INR value prior to a procedure, because several large reviews of available evidence have shown no clinical benefit [3,8,72-75]. The underpinnings of INR as a target and measure of bleeding risk (outside of warfarin therapy) do not apply to patients with cirrhotic coagulopathy, which has a completely different pathophysiology than that seen in warfarin anticoagulation. Additional risks and disadvantages of giving FFP include transfusion reactions, volume overload (and associated increases in portal pressure, especially in individuals with varices), and infection. Administration of FFP also may create a significant delay while awaiting ABO typing, thawing of FFP, administration, and repeated laboratory testing of the PT/INR. **Thoracentesis** – Thoracentesis may be slightly more dangerous than paracentesis. Our approach is similar to that in liver biopsy and includes addressing comorbidities, using platelet transfusions to increase the platelet count to \>50,000/microL, transfusing Cryoprecipitate to raise the fibrinogen level to \>120 mg/dL, optimizing renal function, and controlling infection. **Assessment of hemostasis** – We rely on global measures of clot formation if available, or fibrinogen and platelet count if not. The value of using a measure of global clot formation to guide blood product use was demonstrated in a trial that randomly assigned 60 patients with cirrhosis who were undergoing an invasive procedure to be managed using thromboelastography (TEG) or according to standard hospital protocol [47]. Patients assigned to the TEG arm received FFP if the reaction time (r) was \>40 minutes (normal range for this study, 12 to 26 minutes) and platelets if the maximum amplitude (MA) was \<30 mm (figure 1 and table 4). Those assigned to standard protocol received FFP for INR \>1.8 and platelets for a count \<50,000/microL. The overall use of blood products was lower in the TEG group (17 versus 100 percent). There was no bleeding in the TEG group and one episode of bleeding in the control group (hemoperitoneum following large-volume paracentesis). This study highlights the difficulty in assessing need for prophylactic therapy without a standardized and accurate measure of in vivo hemostasis.

Answer 8

o Measures deoxygenated and oxygenated blood at two wavelengths (660 and 940 nm) through this difference establishes a percentage of bound oxygen o 3 factors that interfere with the apparatus  Low flow states  Hypothermia  Ambient light  Methylene blue Pulse oximetry uses spectrophotometry to determine the proportion of hemoglobin that is saturated with oxygen (ie, oxygenated hemoglobin; oxyhemoglobin) in peripheral arterial blood. Light, at two separate wavelengths, illuminates oxygenated and deoxygenated hemoglobin in blood. The ratio of light absorbance between oxyhemoglobin and the sum of oxyhemoglobin plus deoxyhemoglobin is calculated and compared with previously calibrated direct measurements of arterial oxygen saturation (SaO2) to establish an estimated measure of peripheral arterial oxygen saturation (SpO2) [4]. The microprocessors of pulse oximeters are calibrated using reference tables of actual SaO2 measurements performed using co-oximetry and compiled using data from exposing healthy volunteers to decreasing fraction of inspired oxygen (FiO2) to yield SaO2 ranging from **100 to 75 percent. Because it would be unethical to intentionally generate lower saturations in volunteers, values for an SaO2 less than 75 percent are obtained by extrapolation from these volunteer data.** Pulse oximeter manufacturers claim that reported values between 70 and 100 percent are accurate to within ± 2 percent of the true value, while those between 50 and 70 percent are within ± 3 percent. a) **motion/noise artifact** (siezure, shivering, pt transport) **hypoperfusion** (shock, vasoconstriction, PVD, In adults, the accuracy of standard pulse oximeters decreases dramatically when systolic blood pressure falls below 80 mmHg, generally resulting in underestimation of the actual arterial oxygen saturation) **hypothermia** occasionally **skin pigment** results in poor amplitude readings falsely normal/high readings **carboxyhemoglobin** (Carboxyhemoglobin absorbs at approximately the same amount of 660 nm light as oxyhemoglobin. Thus, the pulse oximetry reading represents an inexact summation of oxyhemoglobin and carboxyhemoglobin. Due to the interference of high levels of carboxyhemoglobin in carbon monoxide (CO) poisoning, or in chronic, heavy smokers, a falsely reassuring normal pulse oximetry reading may mask life-threatening arterial desaturation. Arterial oxygen tension (PaO2) measurements tend to be normal because PaO2 reflects O2 dissolved in blood, and this process is not affected by CO. In contrast, hemoglobin-bound O2(which normally comprises 98 percent of arterial O2 content) is profoundly reduced in the presence of carboxyhemoglobin.) In such cases, whenever carboxyhemoglobinemia is suspected, co-oximetry (not pulse oximetry) is recommended for the measurement of carboxyhemoglobin levels. **Glycohemoglobin A1c** — Glycohemoglobin A1c levels greater than 7 percent in type 2 diabetics with poor glucose control have been shown to result in overestimation of arterial oxygen saturation (SaO2) by pulse oximetry. Falsely low readings **Methemoglobin** — Methemoglobin absorbs at both 660 and 940 nm [7]. Methemoglobinemia should be suspected in those with cyanosis and normal PaO2. Up to a methemoglobin level of 20 percent, SaO2 drops by about one-half of the methemoglobin percentage. At higher methemoglobin levels, SaO2 trends toward 85 percent regardless of the true percentage of oxyhemoglobin, thus leading to over- or under-estimation of the true SaO2 [4,9,71,72]. When methemoglobinemia is suspected, co-oximetry should be used to accurately determine the methemoglobin level. **Sulfhemoglobin** — Sulfhemoglobin absorbs at 660nm, similar to oxyhemoglobin, and its absorbance at 940 nm is unknown. Sulfhemoglobinemia is most commonly caused by the ingestion of oxidizing drugs (eg, dapsone, sulfonamides, metoclopramide, nitrates) and patients present in a similar fashion to methemoglobinemia (cyanosis and normal PaO2). **Sickle hemoglobin** — Sickle hemoglobin generally produces pulse oximeter readings similar to normal hemoglobin, but rare cases of falsely elevated and falsely low readings have been reported especially during vaso-occlusive crises (perhaps due to hypoperfusion). Inherited forms of abnormal hemoglobin — Inherited forms of abnormal hemoglobin (Hb) are rare but have been reported to in falsely low SpO2 readings. **Severe anemia** — In vitro and animal studies suggest that pulse oximetry readings may be affected by profoundly decreased hemoglobin concentration. **Venous congestion** — Venous congestion due to tricuspid valve incompetence or cardiomyopathy may yield falsely low SaO2 readings, due to the generation of venous pulsations. This results from the instrument detecting less oxygenated, pulsatile venous blood as part of the arterial sample, thereby underestimating the actual SaO2. **Ambient light** — Intense daylight, fluorescent, incandescent, xenon, and infrared light sources have been reported to cause spurious pulse oximetry readings. **Nail polish** — The use of nail polish can potentially affect pulse oximeter readings if the polish absorbs light at 660 nm and/or 940 nm. **Vital dyes** — Vital dyes, such as methylene blue (used to treat methemoglobinemia, or during endoscopic polypectomy), indocyanine green (used for measuring cardiac output, for ophthalmic angiography, or for measuring liver blood flow), fluorescein (ophthalmic angiography) and isosulfan blue (used intraoperatively to mark breast and melanoma tumors), can cause erroneously low pulse oximetry readings due to absorption of light at 660 nm or 940 nm [20,100-105]. Methylene blue has the greatest impact, as it absorbs significantly at 670 nm. However, these effects tend to be transient, and resolve rapidly as the dyes are diluted and metabolized

Answer 9

* Limb ischemia * Mesenteric ischemia * Stroke * Dissection of iliacs * Bleeding early deflation leads to decreased benefits of the IABP: * suboptimal diastolic augmentation * suboptimal afterload reduction * can lead to coronary steal/retrograde flow * can lead to cerebral steal both from sucking blood back into aorta/lower body * assisted systolic pressure may be equal or greater than unassisted (?) 2 contraindications: * Aortic dissection or clinically significant aortic aneurysm * Aortic regurgitation * uncontrolled sepsis * uncontrolled bleeding disorder

Answer 10

a) cholinergic meds (organophosphates) muscarinic signs: **SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia** It should be noted that these mnemonics do NOT take into account the critical CNS and nicotinic effects of these toxins. The nicotinic effects include **fasciculations, muscle weakness, and paralysis** via acetylcholine stimulation of receptors at the neuromuscular junction. This mechanism is analogous to the depolarizing effects of succinylcholine in producing neuromuscular blockade. Nicotinic and muscarinic receptors also have been identified in the brain, and may contribute to central respiratory depression, lethargy, seizures, and coma Medication Causes: Organophosphates have been used as insecticides worldwide for more than 50 years. The use of these agents has declined in the last 10 to 20 years, in part due to the development of carbamate insecticides, which are associated with similar toxicities [1]. Medical applications of organophosphates and carbamates include reversal of neuromuscular blockade (neostigmine, pyridostigmine, edrophonium) and treatment of glaucoma, myasthenia gravis, and Alzheimer disease (echothiophate, pyridostigmine, tacrine, and donepezil). **RBC acetylcholinesterase assay** – provides a measure of the degree of toxicity (I guess you would expect the levels to be low in cholinergic toxicity) Other test is – pseudocholinesterase more easily performed Of note for the seizing patient with cholinergic toxicity – diazepam has been shown to decrease neurocognitive issues. No evidence for phenytoin. Rx: ATROPINE AND PRALIDOXIME Reactivates cholinesterase that had been inactivated by phosphorylation due to exposure to organophosphate pesticides and cholinesterase-inhibiting nerve agents (eg, terrorism and chemical warfare agents such as sarin) by displacing the enzyme from its receptor sites; removes the phosphoryl group from the active site of the inactivated enzyme

Answer 11

Decompress the lumen of the bowel with NG and/or rectal tube Evacuate intra-abdominal space occupying lesions: Drain ascites Improve abdominal wall compliance: * Increase sedation * Remove constrictive dressing * Reverse trendelenburg * Paralysis Optimize fluid administration Optimize systemic/regional perfusion

Answer 12

a) severe acute liver injury with encephalopathy and impaired synthetic function (INR\>/=1.5) b) complications: * hepatic artery thrombosis * right heart failure * bleeding * acute graft dysfunction * biliary leak/stricture * pulmonary: acute respiratory failure, pleural effusion, atelectasis * infections * malignancy (non melanoma skin, non-hodgkins) * ***does Mo agree with the answers from previous year?*** Acute liver failure refers to the development of severe acute liver injury with encephalopathy and impaired synthetic function (INR of ≥1.5) in a patient without cirrhosis or preexisting liver disease; time course typically defined as \<26wks c) King's College criteria uses encephalopathy grade III or IV but I think acidosis warrants discussion here As a general rule, the most important factors for predicting the outcome in acute liver failure are the degree of encephalopathy (table 1), the patient's age, and the cause of the acute liver failure. Spontaneous recovery is more likely with lower grades of encephalopathy [68]: * Grade I to II – 65 to 70 percent * Grade III – 40 to 50 percent * Grade IV – \<20 percent old answer o 4 complications of acute liver failure  Encephalophathy  Coagulopathy  Cerebral edema  Hepatorenal Syndrome  Hepatopulmonary syndrome/shunt  Hypoglycemia  Ascites  Hyperbillirubinemia o Best prognosticator and what level of this prognosticator would you guide to transplantation?  Grade of encephalopathy  Probability of spontaneous recovery: • Degree of encephalopathy • Age • Cause of acute liver failure

Answer 13

* normocapneia * head of bed elevation * hyperosmolar therapy (hypertonic saline, mannitol) * paralysis * cooling * EVD for CSF drainage * barbiturates * ensure no neck ties or trach ties * don't over PEEP pt Decompressive craniectomy Level IIA * Bifrontal DC is not recommended to improve outcomes as measured by the GOS-E score at 6 mo post-injury in severeTBIpatients with diffuseinjury(without mass lesions),andwith ICP elevationtovalues.20 mmHg for more than 15 min within a 1-h period that are refractory to first-tier therapies. However, this procedure has been demonstrated to reduce ICP and to minimize days in the ICU. * A large frontotemporoparietal DC (not less than 12 x 15 cm or 15 cm diameter) is recommended over a small frontotemporoparietal DC for reduced mortality and improved neurologic outcomes in patients with severe TBI. * \*The committee is aware that the results of the RESCUEicp trial2 were released soon after the completion of these Guidelines. The results of this trial may affect these recommendations and may need to be considered by treating physicians and other users of these Guidelines. We intend to update these recommendations if needed. Updates will be available at https://braintrauma.org/coma/guidelines. Prophylactic hypothermia Level IIB * Early (within 2.5 h), short-term (48 h post-injury), prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury. Hyperosmolar therapy * Recommendations from the prior (Third) Edition not supported by evidence meeting current standards. Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg body weight. Arterial hypotension (systolic blood pressure ,90 mm Hg) should be avoided. Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes. Cerebrospinal fluid drainage Level III * An EVD system zeroed at the midbrain with continuous drainage of CSF may be considered to lower ICP burden more effectively than intermittent use. * Use of CSF drainage to lower ICP in patients with an initial GCS ,6 during the first 12 h after injury may be considered. Ventilation therapies Level IIB * Prolonged prophylactic hyperventilation with PaCO2 of #25 mm Hg is not recommended. Recommendations from the prior (Third) Edition not supported by evidence meeting current standards. Hyperventilation is recommended as a temporizing measure for the reduction of elevated ICP. Hyperventilation should be avoided during the first 24 h after injury when CBF often is reduced critically. If hyperventilation is used, SjO2 or BtpO2 measurements are recommended to monitor oxygen delivery. Anesthetics, analgesics, and sedatives Level IIB * Administration of barbiturates to induce burst suppression measured by EEG as prophylaxis against the development of intracranial hypertension is not recommended. * High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Hemodynamic stability is essential before and during barbiturate therapy. * Although propofol is recommended for the control of ICP, it is not recommended for improvement in mortality or 6-month outcomes. Caution is required as high-dose propofol can produce significant morbidity. Steroids Level I * The use of steroids is not recommended for improving outcome or reducing ICP. In patients with severe TBI, highdose methylprednisolone was associated with increased mortality and is contraindicated. Nutrition Level IIA * Feeding patientsto attain basal caloric replacement at least by the fifth day and at most by the seventh day post-injury is recommended to decrease mortality. Level IIB * Transgastric jejunal feeding is recommended to reduce the incidence of ventilator-associated pneumonia. Infection prophylaxis Level IIA * Early tracheostomy is recommended to reduce mechanical ventilation days when the overall benefit is thought to outweigh the complications associated with such a procedure. However, there is no evidence that early tracheostomy reduces mortality or the rate of nosocomial pneumonia. * The use of PI oral care is not recommended to reduce ventilator-associated pneumonia and may cause an increased risk of acute respiratory distress syndrome. Level III * Antimicrobial-impregnated catheters may be considered to prevent catheter-related infections during external ventricular drainage. Deep vein thrombosis Prophylaxis Level III * LMWH or low-dose unfractioned heparin may be used in combination with mechanical prophylaxis. However, there is an increased risk for expansion of intracranial hemorrhage. * In addition to compression stockings, pharmacologic prophylaxis may be considered if the brain injury is stable and the benefit is considered to outweigh the risk of increased intracranial hemorrhage. * There is insufficient evidence to support recommendations regarding the preferred agent, dose, or timing of pharmacologic prophylaxis for deep vein thrombosis. Seizure prophylaxis Level IIA * Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS. * Phenytoin is recommended to decrease the incidence of early PTS (within 7 d of injury), when the overall benefit is thought to outweigh the complications associated with such treatment. However, early PTS have not been associated with worse outcomes. * At the present time there is insufficient evidence to recommend levetiracetam compared with phenytoin regarding efficacy in preventing early post-traumatic seizures and toxicity.

Answer 14

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

Answer 15

solubility increases as temperature decreases and therefore partial pressure decreases (think soda cans when warmed - they lose their CO2) **pH-Stat** During pH-stat acid-base management, the patient’s pH is maintained at a constant level by managing pH at the patient’s temperature. pH-stat pH management is temperature-corrected. Compared to alpha-stat, pH stat (which aims for a pCO2 of 40 and pH of 7.40 at the patient’s actual temperature) leads to higher pCO2 (respiratory acidosis), and increased cerebral blood flow. Often CO2 is deliberately added to maintain a pCO2 of 40 mm Hg during hypothermia. **Alpha-Stat** During alpha-stat acid-base management, the ionization state of histidine is maintained by managing a standardized pH (measured at 37C). Alpha-stat pH management is not temperature-corrected – as the patient’s temperature falls, the partial pressure of CO2 decreases (and solubility increases), thus a hypothermic patient with a pH of 7.40 and a pCO2 of 40 (measured at 37C) will, in reality, have a lower pCO2 (because partial pressure of CO2 is lower), and this will manifest as a relative respiratory alkalosis coupled with decreased cerebral blood flow. During alpha-stat management you have no idea what the patient’s pCO2 is, your goal is to maintain a constant dissociation state of histidine. Arguments for using pH-stat management include increased cerebral blood flow to decrease the duration of cooling as hypothermia is induced and to potentially decrease the duration of rewarming [79]. However, cerebrovascular disease may decrease vascular reactivity in response to arterial CO2 concentration leading to impaired cooling of brain regions supplied by diseased vessels if pH-stat management is used. for every degree C below 37... pH increases by 0.12 pao2 drops 5 PCO2 drops by 2

Answer 16

a) * high dose (\>4mg/kg/hr) * prolonged infusion (\>48h) * young age * critical illness * high fat and carbohydrate intake * inborn errors of mitochondiral fatty acid oxidation * concominant catecholamine infusion * concominant steroid therapy * traumatic brain injury b) * metabolic acidosis (combination of lactate and renal failure) * rhabdomyolosis (increased CK and myoglobin) from direct muscle necrosis of both skeletal and cardiac muscle * renal failure * hypertriglyceridemia * hyperkalemia * lipemia

Answer 17

* venous dilation * arterial dilation (to a lesser extent) * reduces cardiac oxygen demand by decreasing LVEDP (decreased DEMAND) * may have slight decrease in afterload (decreased DEMAND) * dilates coronary arteries and improves collateral flow to ischemic regions (increased SUPPLY) Nitroglycerin forms free radical nitric oxide. In smooth muscle, nitric oxide activates guanylate cyclase which increases guanosine 3’5’ monophosphate (cGMP) leading to dephosphorylation of myosin light chains and smooth muscle relaxation. Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure); may modestly reduce afterload; dilates coronary arteries and improves collateral flow to ischemic regions

Answer 18

o HR – with short acting esmolol to decrease wall stress o Pain – decrease catecholamine release and sympathetic drive o BP – with nitro * Anti-impulse therapy aims to reduce the velocity of left ventricular contraction, thereby decreasing shear stress and minimizing lesion progression * **beta blockers** (esmolol, labetalol) target HR \<60bpm * can use **diltiazem, verapamil** in pts not tolerant of beta blockers * once HR controlled to 60bpm or less, start vasodilator therapy with **nitroprusside** or nicardipine as long as BP \>120 * avoid inotropic agents and hydralazine * \*careful in cocaine overdose (in which case you would use benzos and avoid beta blockers) * pain control with **opioids**

Answer 19

To fulfill the Hunter Criteria, a patient must have taken a serotonergic agent and meet ONE of the following conditions: * Spontaneous clonus * Inducible clonus PLUS agitation or diaphoresis * Ocular clonus PLUS agitation or diaphoresis * Tremor PLUS hyperreflexia * Hypertonia PLUS temperature above 38ºC PLUS ocular clonus or inducible clonus Five principles are central to the management of serotonin syndrome: * Discontinuation of all serotonergic agents * Supportive care aimed at normalization of vital signs * Sedation with benzodiazepines * Administration of serotonin antagonists: If benzodiazepines and supportive care fail to improve agitation and abnormal vital signs, give cyproheptadine * Assessment of the need to resume use of causative serotonergic agents after resolution of symptoms * ... * Treat patients with temperature \>41.1°C with immediate sedation, paralysis, and endotracheal intubation; treat hyperthermia with standard measures; avoid antipyretics such as acetaminophen...In hyperthermia associated with serotonin syndrome, there is no role for antipyretic agents, such as acetaminophen; the increase in body temperature is not due to an alteration in the hypothalamic temperature set point, but rather an increase in muscular activity

Answer 20

o Acute onset with fluctuating over the day o Inattention o Disorganized thinking o Altered conciousness (old answer) DSM 5 A. Disturbance in **attention** (i.e., reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment). B. The disturbance develops over a **short period of time** (usually hours to a few days), represents an acute change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day. C. An additional disturbance in **cognition** (e.g.memory deficit, disorientation, language, visuospatial ability, or perception). D. The disturbances in Criteria A and C are **not better explained** by a pre-existing, established or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of arousal such as coma. E. There is evidence from the history, physical examination or laboratory findings that the disturbance is a **direct physiological consequence of another medical condition**, substance intoxication or withdrawal (i.e. due to a drug of abuse or to a medication), or exposure to a toxin, or is due to multiple etiologies.

Answer 21

**Persistent vegetative state** — Patients in a persistent vegetative state (PVS) represent a subgroup of patients who suffer severe anoxic brain injury and progress to a state of wakefulness without awareness. A vegetative state may represent a transition between coma and recovery or between coma and death. The term was first used in 1972 and is defined as [4,6,9-12]: * No evidence of awareness of self or environment and an inability to interact with others * No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli * No evidence of language comprehension or expression * Intermittent wakefulness manifested by the presence of sleep-wake cycles * Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and nursing care * Bowel and bladder incontinence * Variably preserved cranial nerve reflexes and spinal reflexes PVS is judged to be permanent after three months if induced nontraumatically. For traumatic brain injury, a year in this state is generally required to be considered permanent. **Minimally conscious state** — The term minimally conscious state (MCS) has been proposed to describe patients who do not meet criteria for persistent vegetative state [23]. As with PVS, these patients have a severe alteration in consciousness. In contrast to PVS, they may intermittently demonstrate limited interaction with the environment by visually tracking, following simple commands, signaling yes or no (not necessarily accurately), or having intelligible verbalization or restricted purposeful behavior.

Answer 22

o Most sensitive assay for HITT diagnosis?  Elisa test against PF4 o What is the gold standard  Mix serum of patient with a pool of normally functioning platelets and demonstrate activation of test platelets o Name two drugs that could be used for treatment?  Argatroban  Billivirudin **4Ts HIT Score** Thrombocytopenia ***Platelet count fall \>50 percent and nadir ≥20,000/microL – 2 points*** Platelet count fall 30 to 50 percent or nadir 10 to 19,000/microL – 1 point Platelet count fall \<30 percent or nadir \<10,000/microL – 0 points Timing of platelet count fall ***Clear onset between days 5 and 10 or platelet count fall at ≤1 day if prior heparin exposure within the last 30 days – 2 points*** Consistent with fall at 5 to 10 days but unclear (eg, missing platelet counts), onset after day 10, or fall ≤1 day with prior heparin exposure within 30 to 100 days – 1 point Platelet count fall at \<4 days without recent exposure – 0 points Thrombosis or other sequelae Confirmed new thrombosis, skin necrosis, or acute systemic reaction after intravenous unfractionated heparin bolus – 2 points ***Progressive or recurrent thrombosis, non-necrotizing (erythematous) skin lesions, or suspected thrombosis that has not been proven – 1 point*** None – 0 points Other causes for thrombocytopenia None apparent – 2 points Possible – 1 point Definite – 0 points Interpretation — The sum of the point values gives a total from 0 to 8. Pretest probabilities for HIT are as follows (table 5) [114]: * 0 to 3 points – Low probability (risk of HIT \<1 percent) * 4 to 5 points – Intermediate probability (risk of HIT approximately 10 percent) * 6 to 8 points – High probability (risk of HIT approximately 50 percent) Most sensitive assay = Immunoassay (eg ELISA) of PF4 complexes is probably the most sensitive Gold Standard = serotonin release assay Treatment options STOP ALL HEPARIN containing products **Argatroban** **Bivalirudin** **Danaparoid** **apixaban, dabigatran, rivaroxaban** **fondaparinux**

Answer 23

Canadian guidelines recommend early enteral nutrition within 24-48hrs of admission to ICU Contraindications from European guidelines include: overt bowel ischemia, ongoing UGIB, severe uncontrolled life-threatening hypoxemia, uncontrolled shock, abdominal compartment syndrome

Answer 24

* **PA rupture** * pulmonary infarction * RBBB * atrial and ventricular arrhythmias * infection * thrombus PA catheter on CXR * On the Xray, the tip should appear 3 -5 cm from the midline, no more than 2cm from the hilum (having it further increases risk of PA rupture/infarction) * On lateral CXR, the tip of the catheter is at or below the left atrium

Answer 25

Torsades des Pointes with long QT * hypoK * hypoMg * hypoCa * bradycardia * antiarrhythmic drugs (procainamide, sotalol, amiodarone) * antihistamines * antibiotics (macrolides, fluoroquinolones) * haldol * methadone * impaired renal function * impaired liver function * female sex * advanced age * heart failure * LVH HF and LVH are common risk factors for drug-induced TdP. Antiarrhythmic drugs and hypokalemia and/or hypomagnesemia associated with diuretic therapy may all contribute to proarrhythmia. It is not clear if there is an increased risk of LQTS or TdP with either type of heart disease alone. QTc prolongation may be common during the early phase of ischemia.

Answer 26

**_Critical illness myopathy Risk factors:_** * **sepsis** * **multiorgan failure** * **systemic inflammatory response syndrome (SIRS)** * **paralytic agents** * Associated and perhaps triggering factors may include a **higher illness severity index**, **hyperglycemia**, and **hyperthyroidism** * Earlier studies suggested that the main risk factor for CIM was the use of intravenous glucocorticoids in the ICU setting [5,35-38]. However, the glucocorticoid association is now controversial, and critically ill patients may develop CIM in the absence of exposure to intravenous glucocorticoids. **_Long-term complications of ARDS_** * **psychiatric**: depression, PTSD * **cognitive impairment** (memory, attention, concentration) * Pulmonary function outcomes may be heterogeneous after an episode of ARDS, but most young patients without documented preexisting lung disease regain normal or near-normal function with a persistent mild **reduction in diffusion capacity**. Most outcome studies found that ARDS survivors are often unable to resume their prior physical function, but the degree of pulmonary dysfunction documented across studies does not solely explain this degree of functional limitation. * **neuromuscular dysfunction** (critical illness myopathy, critical illness polyneuropathy) * **functional disability**, decreased physical quality of life

Answer 27

**Opioid via epidural complications** * respiratory depression * CNS depression * pruritis * nausea * urinary retention **Local Anesthetic via epidural complications** * **Local anesthetic systemic toxicity** — Local anesthetic systemic toxicity (LAST) can occur with any route of administration of local anesthetics, but is much less likely with spinal than with epidural anesthesia, because such a small dose of local anesthetic (LA) is injected for spinal anesthesia. LAST is a rare but potentially lethal event, that may consist of central nervous system and/or cardiovascular effects ranging from minor manifestations (eg, perioral numbness, tinnitus, twitching), to major events, including **seizures**, **coma**, **severe hypotension, arrhythmias, and asystole**. LAST occurs most commonly with inadvertent intravascular injection of LA with almost immediate onset of signs and symptoms, but delayed onset may also occur with epidural infusion after systemic absorption of LA or migration of the catheter into a blood vessel. * **hypotension from decreased SVR** **Technical complications** * **high or total spinal anesthesia** - The signs and symptoms include a rapid ascending sympathetic, sensory, and motor block with associated bradycardia, hypotension, dyspnea, and difficulty with swallowing or phonation. Symptoms can progress to unconsciousness (due to brainstem hypoperfusion and/or brainstem anesthesia), and respiratory depression (secondary to respiratory muscle paralysis and brainstem hypoperfusion). If a large dose of local anesthetic is unintentionally injected into the subarachnoid space, unconsciousness and respiratory depression may be the initial signs of a total spinal anesthesia. * **Subdural injection** — The subdural space is a potential space between the dura and arachnoid mater. Unintentional injection of local anesthetic solution into this space (usually intended for the epidural space) may cause a patchy block that results in more extensive cranial anesthesia than expected after epidural injection, with an onset intermediate between spinal and epidural anesthesia * **Nerve injury** * **Back pain** * **Post-dural puncture headache** * **urinary retention** * **local anesthetic systemic toxicity** * **spinal-epidural hematoma** * **infection**

Answer 28

o Two conditions that would benefit from lung isolation: * Prevention of soiling of countralateral lung * massive hemoptysis * Unilateral pulmonary infections such as bronchiectasis, lung abscess, or an infected cyst can produce copious amounts of purulent material necessitating lung isolation to protect the contralateral lung from contamination * Unilateral lung lavage — A DLT is required for whole lung lavage of each lung (eg, for treatment of pulmonary alveolar proteinosis) * thoracic surgery other ways to isolate lungs * bronchial blocker * advance ETT down one mainstem bronchus

Answer 29

* rebound pulmonary HTN causing RV failure * hypoxemia o Name 4 ways to manage RV failure * optimize preload * optimize afterload (PEEP, pulm vasodilation) * Maintain sinus rhythm * Increase inotropy with milrinone * Optimize RV coronary perfusion by ensuring systemic BP is \> pulmonary artery BP * Rate 80-100 mechanical support: * VA ECMO * RVAD

Answer 30

* Diffuse alveolar hemorrhage * ARDS * Reconstitution syndrome due to engrafting * GVHD * Cardiogenic pulmonary edema * aspiration pneumonitis (from difficulty swallowing due to mucositis) * drug toxicity (cyclophosphamide) * veno-occlusive disease

Answer 31

***pt probably has nephrogenic DI from chronic lithium and was unable to ask for water or had impaired thirst postoperatively (or was NPO) and thus became hypernatremic.*** ***I think the sodium continued to rise likely because they did not receive enough free water, may have had osmolar diuresis from too much dextrose, and/or the 1/2 NS was hyposomolar compared to urine thereby leading it to cause worsened hypernatremia since it effectively led to a sodium load with the free water being excreted.???*** ***Rx: of note polyuria is rarely harmful and uptodate suggests treatment for symptoms only but in this case with ++ hypernatremia I would think we should treat*** * ***low solute diet (low salt, low protein)*** * ***thiazide diuretic*** * ***add amiloride if still polyuric*** * \*thiazide and/or amiloride can increase lithium level so need to watch carefully * ***if polyuria persists add indomethacin (NSAID)*** * ***if polyuria persists do trial of desmopressin*** Patients with moderate to severe nephrogenic or central DI typically present with polyuria, nocturia, and polydipsia. Polyuria is arbitrarily defined as a urine output exceeding 3 L/day in adults of dilute urine (\<300mosm/kg). Causes of polyuria other than DI include primary polydipsia and increased solute excretion due to one or more of the following: glucosuria in uncontrolled diabetes mellitus, urea with a high-protein diet or after urea administration to treat hyponatremia [3], or sodium chloride and urea in a postobstructive diuresis. In addition, glucosuria can contribute to polyuria in patients with severe DI when hyperglycemia is induced by the administration of large volumes of intravenous dextrose in water. The serum sodium in untreated patients with DI is often in the high normal range to provide the stimulus for thirst to replace the urinary water losses. Moderate to severe hypernatremia can develop when thirst is impaired or cannot be expressed. This can occur in patients with central nervous system lesions who also have hypodipsia or adipsia, in infants, young children, and neurologically impaired adults who cannot independently access free water, and in the postoperative period in patients with unrecognized DI.

Answer 32

Ppeak is high due to narrowed and highly resistive airways but also consider kinked/soiled ETT Pplat is high due to dynamic hyperinflation for dynamic hyperinflation: quick bedside confirmation: end-expiratory hold **Mgmt of autopeep/dynamic hyperinflation** decrease tidal volume (i.e. Insp pressure in PCV) decrease I-time decrease RR ?technically you could decrease the inspiratory rise time to slightly decrease the tidal volume treat possible bronchoconstriction? Treatment of autoPEEP - Steps should be taken to correct auto-PEEP as soon as it is identified. Initial efforts should focus on determining and treating the underlying cause. When auto-PEEP persists despite management of its underlying cause, applied PEEP may be helpful if the patient has an expiratory flow limitation. When a high minute ventilation is the presumed cause of auto-PEEP, the minute ventilation should be decreased by lowering the tidal volume or respiratory rate. This frequently requires a strategy of permissive hypercapnia. When an expiratory flow limitation due to obstructive airways disease is the presumed cause of auto-PEEP, the duration of expiration should be prolonged. This can be accomplished by increasing the inspiratory flow, decreasing the tidal volume, or decreasing the respiratory rate. When increased expiratory resistance is the presumed cause of auto-PEEP, the source of increased resistance should be identified and corrected. This may require sedation, pharmacologic paralysis, or replacement of the endotracheal tube or ventilator tubing. Applied PEEP — Small amounts of applied PEEP can decrease auto-PEEP in patients who have an expiratory flow limitation [52-54]. This can be conceptualized as the applied PEEP holding open the narrowed airways during expiration, improving expiratory airflow, and allowing more complete expiration prior to the onset of the next breath. Additional benefits of using applied PEEP to offset auto-PEEP include decreased oxygen consumption and improved gas exchange. The latter is due to opening the small airways in the dependent lung zones and distributing inspired gas more homogeneously [55-57]. Applied PEEP should always be less than the measured auto-PEEP [58]. Otherwise, alveolar pressure may increase, placing the patient at increased risk for complications such as pulmonary barotrauma or hypotension (figure 5). One study even suggested that applied PEEP does not need to exceed the measured auto-PEEP for this to occur. Rather, it can occur if the applied PEEP is greater than 85 percent of the measured auto-PEEP [59]. Given the potential inaccuracy of auto-PEEP measurements, it is prudent to set applied PEEP to a level that is less than 50 percent of the measured auto-PEEP. Research has shown that mechanical ventilation with PEEP induces longitudinal atrophy by displacing the diaphragm in caudal direction and reducing the length of fibers. As a result, muscle fibers generate less force causing diaphragm weakness [60]. This may exacerbate diaphragm weakness in critically ill patients thus prolonging mechanical ventilation. This advocates for maintaining the lowest required PEEP setting. Applied PEEP should not be used to counter auto-PEEP in patients who do not have an expiratory flow limitation. Applied PEEP may increase alveolar pressure and increase the risk of both barotrauma and hemodynamic compromise in this setting [61].

Answer 33

o Valvular involvement leading to acute CHF symptoms o Heart block o Progression of disease regardless of appropriate antibiotic therapy o Large mobile mass (more than 10 mm) o Difficult to treat infection – fungal infection Early surgery in IE has been broadly defined as surgery performed before completion of a full course of antibiotics [9]. The following recommendations are similar to those in guidelines established by United States and European cardiology societies and the American Association for Thoracic Surgery [3,5,10,11]. Referral for early surgery is indicated in patients with left-sided native valve IE in the following clinical settings. * For patients with IE-associated valve dysfunction (usually aortic or mitral regurgitation) causing **symptoms or signs of heart failure (HF)**, we recommend referral for early valve surgery. * For patients with paravalvular extension of infection with development of annular or aortic abscess, destructive penetrating lesion (eg, **fistula), and/or heart block**, we suggest referral for early valve surgery. * For patients with infection due to a **difficult-to-treat pathogen**, we suggest referral for early valve surgery. Difficult-to-treat pathogens include fungi and multidrug-resistant organisms. We do not consider S. aureus IE alone an indication for early surgery. * For patients with persistent infection (manifested as **persistent bacteremia or fever lasting more than seven days** after initiation of appropriate antibiotic therapy, provided other sites of infection and causes of fever have been excluded), we suggest referral for early valve surgery. * Early surgery (within the first week of antibiotic therapy) may reduce the risk of embolism in patients with **large vegetations (\>10 mm)** but criteria for referral for surgery in this setting are controversial, and guideline recommendations have varied [3,5,11,12]. For patients with large vegetations, we perform an individualized risk-benefit assessment comparing early surgery with expectant management based upon multiple factors including the diameter and volume of the vegetation, change in size of the vegetation on appropriate antibiotic therapy, history of prior systemic embolization, likelihood that the patient will soon require valve surgery (eg, due to severe valve dysfunction), and patient age and life expectancy (which impacts prosthetic valve choice and exposure to long-term risks of prosthetic valve replacement).

Answer 34

* venous dilation * arterial dilation (to a lesser extent) * reduces cardiac oxygen demand by decreasing LVEDP (decreased DEMAND) * may have slight decrease in afterload (decreased DEMAND) * dilates coronary arteries and improves collateral flow to ischemic regions (increased SUPPLY) Nitroglycerin forms free radical nitric oxide. In smooth muscle, nitric oxide activates guanylate cyclase which increases guanosine 3’5’ monophosphate (cGMP) leading to dephosphorylation of myosin light chains and smooth muscle relaxation. Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure); may modestly reduce afterload; dilates coronary arteries and improves collateral flow to ischemic regions

Answer 35

1. increased uptake and usage of phosphate by regenerating liver 2. hyperphosphaturia post liver transplant 3. ?refeeding syndrome in this pt who likely malnourished * 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)

Answer 36

* patient autonomy * non-maleficence * seek second opinion * offer alternative mgmt (ie. palliative care) **SCCM guidelines** **Futile Interventions** Unlike potentially inappropriate treatments, futile treatments are deﬁned as treatments that have no chance of achieving the intended physiologic goal. By using this narrow deﬁnition of the term “futile,” there is a distinction between interventions that cannot work and those that might accomplish a physiologic goal, but raise ethical concerns; that is, potentially inappropriate treatments discussed previously here. Clinicians should not provide futile interventions. Administering ineffective interventions is contrary to the ethical obligation of clinicians to avoid harm. Physicians are also responsible for using medical resources responsibly, and should not administer costly interventions that cannot produce the desired response. **Responding to Requests for Futile Interventions** When responding to requests for futile interventions, physicians should try to understand why these requests are being made, provide emotional support to surrogate decision makers, and explain why such interventions will not be provided. If there is continued disagreement, clinicians should seek expert consultation to provide assistance in communication, but it is important to note that, although involving experts, physicians are not required to provide futile interventions (4). The committee recommends the following approach to manage such cases: 1. 1. Enlist expert consultation to continue negotiation during the disputeresolution process 2. 2. Give notice of the process to surrogates 3. 3. Obtain a second medical opinion 4. 4. Obtain review by an interdisciplinary hospital committee 5. 5. Offer surrogates the opportunity to transfer the patient to an alternate institution 6. 6. Inform surrogates of the opportunity to pursue extramural appeal 7. 7. Implement the decision of the resolution process

Answer 37

***using a fan with cool air blowing on face (has evidence)*** ***opioids for dyspnea*** - Systemic administration of opioid agonists is the most well-established pharmacologic treatment strategy for the symptomatic management of dyspnea in patients with advanced illness. ***(has evidence)*** ***relaxation techniques and psychosocial support (has evidence)*** ***breathing techniques, pursed lip, diaphragm breathing, tripoding (has evidence)*** NIV may be considered as a palliative measure in dying patients who have severe dyspnea and have decided to forego life-prolonging therapies and focus only on comfort measures Studies of supplemental oxygen for relief of dyspnea have shown mixed results in hypoxemic patients with cancer and severe lung disease. Widespread prescription of oxygen is not warranted for relief of dyspnea [63], even in the dying phase [64]. However, based upon moderate quality evidence, we suggest a therapeutic trial of oxygen supplementation for relief of dyspnea in hypoxemic patients. BUT OVERALL the evidence does not seem to support this... Systematic reviews of a small number of trials have concluded that the evidence does not support a role for benzodiazepines as a routine management strategy for dyspnea in the absence of anxiety

Answer 38

* transfer out of declassed pts * transfer stable pts from ER to another hospital's ICU * send some patients to PACU * send some pts to alternate ICU within same institution * call department head/nursing manager for overtime nursing coverage * "borrow" nurses from other ICUs

Answer 39

unless they are getting at toxic alcohols (in which case I would consider bicarbonate + fomepizole) **thiamine before dextrose in alcoholic patients** **Dextrose and saline solutions** — In patients with alcoholic or fasting ketoacidosis, at least partial correction of the metabolic acidosis can usually be achieved by the administration of dextrose and saline solutions [4,5,17,18,22,23,28,31,40]. These benefits are mediated by the following mechanisms: * Dextrose administration will increase insulin secretion and reduce glucagon secretion. The resulting increase in the insulin/glucagon ratio slows hepatic fatty acid oxidation and ketoacid generation. Higher insulin levels also inhibit hormone-sensitive lipase in adipose tissue, which reduces fatty acid release from peripheral fat. Both effects slow ketone body synthesis. Simultaneously, metabolism of beta-hydroxybutyrate and acetoacetate, largely in the brain and muscle regenerates bicarbonate and partially corrects the metabolic acidosis. The mechanism of partial correction is described above * Saline (or a near isotonic balanced electrolyte solution) will repair extracellular fluid deficits, which are most often due to vomiting (present in 73 percent of patients in a series of 74 patients cited above) [17] and the loss of sodium (and potassium) in the urine with beta-hydroxybutyrate and acetoacetate anions to maintain electroneutrality. In addition, extracellular volume repletion will reduce the secretion of hormones stimulated by hypovolemia, such as catecholamines and glucagon, that promote ketogenesis.

Answer 40

* physicians have an ethical, legal and professional obligation to disclose harm from healthcare delivery to pts * If the patient were to learn of the incident from someone other than you, it could cause further distress and irreparably harm your doctor-patient relationship. * Disclosure discussions should be documented in the medical record, and the information disclosed should be shared with the entire care team. In some cases, there may be a duty to report an adverse event or near miss. [https://www.cmpa-acpm.ca/serve/docs/ela/goodpracticesguide/pages/quick\_answers/quick\_answers-e.html#adverse\_events](https://www.cmpa-acpm.ca/serve/docs/ela/goodpracticesguide/pages/quick_answers/quick_answers-e.html#adverse_events) * Seek advice from CMPA

Answer 41

??? reverse triggering ???

Answer 42

???shorten inspiratory rise time???

Answer 43

* optimize preload * increase inotropy if in shock (dopamine and dobutamine according to uptodate) * reduce afterload (stop drugs that worsen it, treat hypoxia, MV/optimize PEEP, * optimize HR 80-100 * optimize systemic BP (should be \> pulm artery blood pressure to allow RV perfusion) * ensure optimal rhythm (ideally sinus) to maximize RV filling * coronary reperfusion (lytic/PCI if STEMI) * ACS medical treatment (antiplatelet drugs/beta blockers/statins etc)

Answer 44

**EEG AHA 2015 Recommendations—Updated** In comatose post–cardiac arrest patients who are treated with TTM, it may be reasonable to consider persistent absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest, and persistent burst suppression on EEG after rewarming, to predict a poor outcome (FPR, 0%; 95% CI, 0%–3%; Class IIb, LOE B-NR). Intractable and persistent (more than 72 hours) status epilepticus in the absence of EEG reactivity to external stimuli may be reasonable to predict poor outcome (Class IIb, LOE B-NR). In comatose post–cardiac arrest patients who are not treated with TTM, it may be reasonable to consider the presence of burst suppression on EEG at 72 hours or more after cardiac arrest, in combination with other predictors, to predict a poor neurologic outcome (FPR, 0%; 95% CI, 0%–11%; Class IIb, LOE B-NR). **Imaging** some evidence that reduced grey-white ratio and diffuse edema are poor prognostic markers but no mention about "normal CT head" which I suspect means it is not sensitive in general. **2015 Recommendations—New** In patients who are comatose after resuscitation from cardiac arrest and not treated with TTM, it may be reasonable to use the presence of a marked reduction of the GWR on brain CT obtained within 2 hours after cardiac arrest to predict poor outcome (Class IIb, LOE B-NR). It may be reasonable to consider extensive restriction of diffusion on brain MRI at 2 to 6 days after cardiac arrest in combination with other established predictors to predict a poor neurologic outcome (Class IIb, LOE B-NR). Acquisition and interpretation of imaging studies have not been fully standardized and are subject to interobserver variability.163 In addition, the recommendations for brain imaging studies for prognostication are made with the assumption that images are performed in centers with expertise in this area. **Persistent vegetative state** — Patients in a persistent vegetative state (PVS) represent a subgroup of patients who suffer severe anoxic brain injury and progress to a state of wakefulness without awareness. A vegetative state may represent a transition between coma and recovery or between coma and death. The term was first used in 1972 and is defined as [4,6,9-12]: * No evidence of awareness of self or environment and an inability to interact with others * No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli * No evidence of language comprehension or expression * Intermittent wakefulness manifested by the presence of sleep-wake cycles * Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and nursing care * Bowel and bladder incontinence * Variably preserved cranial nerve reflexes and spinal reflexes PVS is judged to be permanent after three months if induced nontraumatically. For traumatic brain injury, a year in this state is generally required to be considered permanent. **Minimally conscious state** — The term minimally conscious state (MCS) has been proposed to describe patients who do not meet criteria for persistent vegetative state [23]. As with PVS, these patients have a severe alteration in consciousness. In contrast to PVS, they may intermittently demonstrate limited interaction with the environment by visually tracking, following simple commands, signaling yes or no (not necessarily accurately), or having intelligible verbalization or restricted purposeful behavior.

Answer 45

search warrant and subpeona gunshot cases of abuse All provinces and territories have legislation that requires anyone (including physicians) to report certain deaths, including those that the person has reason to believe are violent, suspicious, or unexplained.

Answer 46

from PADIS guidelines Ungraded Statements: **Positive delirium screening in critically ill adults is strongly associated with cognitive impairment at 3 and 12 months after ICU discharge and may be associated with a longer hospital stay.** Delirium in critically ill adults has consistently been shown **NOT** to be associated with PTSD or post-ICU distress. Delirium in critically ill adults has **NOT** been consistently shown to be associated with ICU LOS, discharge disposition to a place other than home, depression, functionality/dependence , or mortality.

Answer 47

**Bias**: experimental error which deviates the research from a true finding **Confounders**: unaccounted for variables which may bias and deviate research from the truth **Type I Error**: false positive * - leads someone to conclude that relationship between two things exists, when in fact it doesn't * - alpha: p \< 0.05 * - Superiority studies **Type II Error**: False negative * - leads someone to conclude that no relationship between two things exists, when in fact it does * - Beta: 20% (0.2) * - Power = 1 - beta = 0.8 (typical studies need power of at least 0.8) * - Non-inferiority studies

Answer 48

**RIFL** see image in q **AKIN** A report by the AKIN proposed the following criteria for AKI [8, 9] : 1. Abrupt (within 48 h) reduction in kidney function currently defined as an absolute increase in serum creatinine of 0.3 mg/dL or more (≥26.4 μmol/L) or 2. A percentage increase in serum creatinine of 50% or more (1.5-fold from baseline) or 3. A reduction in urine output (documented oliguria of \< 0.5 mL/kg/h for \>6 h) The AKIN criteria differ from the RIFLE criteria in several ways. The RIFLE criteria are defined as changes within 7 days, while the AKIN criteria suggest using 48 hours. The AKIN classification includes less severe injury in the criteria and AKIN also avoids using the glomerular filtration rate as a marker in AKI, as there is no dependable way to measure glomerular filtration rate and estimated glomerular filtration rate are unreliable in AKI.