- How long after thrombolytics should we still give reversal agents?
Critical Care Questions
(If anyone knows the attribution of this list, please write me)
- Explain the mechanics of dependent lung consolidation in ARDS as seen on CT or MRI. Why does the consolidation shift within minutes of the patient being turned and then re-imaged? Is fluid moving through the lung to the lowest levels under the force of gravity? Draw a schematic model of what is happening that includes the bronchi, alveoli, and pulmonary parenchyma. (Hint: discussion of Gattinoni’s work and “little bambino lungs” in adults is good preparation for answering this question). What are the implications for respiratory management of such patients?
- Explain the pathophysiology of systemic edema in the setting of SIRS/MSOF/D. This discussion must include the effects of edema starting at the intracellular level, and progress through discussion of the gross hemodynamic and mechanical effects on the patient. (Hint: see the “Darwin Chronicles” on the CCM-L web-page).
- Explain the physiology and clinical consequences of “vascular steal” in the setting of arterio-venous fistula creation for hemodialysis. Generalize this concept to at least one other procedure used in critical care medicine.
- List 6 pathophysiological mechanisms involved in cerebral ischemia-reperfusion injury, one of which must be unique to the brain/CNS. Describe how at least two of these mechanisms interact to increase the severity of the injury and subsequent neuronal death. (Some known mechanisms: excitotoxicity, endothelial and astrocyticic edema resulting in compromised capillary perfusion, hemoconcentration and blood sludging at the capillary level due to water extraction from blood secondary to water translocation to cerebral parenchyma due to failure of ion pumping, patchy, failed, microcirculatory perfusion due to the no-reflow phenomenon, iron delocalization and Fenton-reactuion driven free radicals as a source of injury, other species of free radicals such as the hydroxyl radical, peroxynitrite, superoxide, peroxide, and others, the role of PARS in depleting neuronal high energy reserves and preventing neuronal recovery from ischemia-reperfusion injury,mitochondrial dysfunction due to poration and accumulation of long-chain acyl-coAs, and apoptosis to name a few).
- Explain apoptosis and its significance in critical care medicine. In which pathologies is apoptosis likely to be a major source or morbidity? How does apoptosis occur; explain the pathways by which apoptosis is both triggered and ultimately causes the cell to die. explain the difference between apoptosis and necrosis.
- What are the principal reasons patients with chronic renal failure, and especially patients on hemodialysis experience dramatically increased mortality and morbidity from atherosclerosis, infection, and cancer?
- Explain the cascade of oxygen tension from ambient air (~150 kPa) to the final ~3 kPa delivered to the mitochondria. Start with reduction in pO2 due to humidification of air in the upper airways and describe the decreases in pO2 every step of the way. Explain the importance of the oxy-hemoglobin dissociation curve in this process. Relate this cascade to the critical care setting in a patient with SIRS and explain the role of manipulation of the patient’s FiO2 in achieving the ultimate therapeutic goal of increasing mitochondrial pO2.
- Explain why the injured, hypoxic or compromised gut is a primary initiator or sepsis/SIRS. Explain what physiological fact makes the microvilli of the intestine so exquisitely susceptible to hypoxia/ischemia. Discuss three interventions to protect and to restore gut integrity in SIRS.
- Explore the pathophysiology of “shock-liver” and differentiate it from hypovolemic and septic shock.
- Give two major reasons why the kidneys require ~20% of the resting cardiac output? Discuss the forces that determine renal blood flow. Discuss the pathophysiology of acute renal ischemia and list at least two drugs which have been shown clinically or experimentally to protect the kidney against ischemia if administered prior to the insult. Be prepared to discuss the putative mechanisms by which the drug you choose are thought to work (i.e., xanthine oxidase inhibitors such as allopurinol). Give one clinical example of where such pre-insult drug treatment might be indicated.
- Discuss the pathophysiology of extracorporeal circulation. Explain why extracorporeal surfaces initiate pulmonary and systemic edema. Discuss the causes of CNS compromise due to extracorporeal circulation in CABG, open heart procedures (i.e., valve replacement, septal defect repair) and suggest at least three ways these complications can be minimized or avoided.
- Discuss the pathophysiology of alveolar flooding and relate it to inhalation of salt and fresh water in drowning. Explain the mechanism by which alveolar surfactant functions to maintain alveolar patency and maintain normal alveolar structure. Relate this to PEEP.
- Explain the pathophysiological mechanisms that may come into play during surface and core rewarming of profoundly hypothermic patients. Be prepared to discuss critical physiological milestones in hypothermia such as the temperature at which endogenous heat production is suppressed, the temperatures at which consciousness is significantly impaired and ultimately lost, the temperature at which respiratory arrest occurs and the temperature at which cardiac fibrillation occurs. Discuss two methods of surface rewarming. Discuss four methods of core re-warming.
- Discuss the likely clinical significance of mild pyrexia (0.5 to 1.0 degrees C) in previously alert elderly patients who present with confusion or obtundation to the ED.
- Explain the Gibbs-Donnan equilibrium and describe the effect, if any, of severe shock on the Gibbs-Donnan equilibrium. If there is an effect, what are the resulting histopathological consequences? How do the kidneys interact with the Gibbs-Donnan equilibrium? What is the role of idiogenic osmoles and what hazard do they represent, if any, in rapid rehydration after prolonged periods of hypernatremia and/or dehydration? Why?
- Explain the two major theories by which conventional closed-chest CPR (CC-CPR) is thought to facilitate systemic perfusion? What is the typical MAP achieved during CC-CPR? What is the minimum MAP generally thought to be necessary to maintain cerebral viability? Why does pulmonary edema develop rapidly during CC-CPR and what relationship does this have to difficulty in administering medications via a central venous line during CC-CPR?
- What is the most important acute physiological factor in successful cardiac defibrillation during CC-CPR?
- Explain the physiology of Active Compression-Decompression CPR (ACDC-CPR). Suggest one airway intervention which could greatly improve the efficacy of ACDC-CPR in increasing preload and improving cardiac output.
- Explain the physiological basis of left ventricular volume reduction surgery (the Batista Procedure). Would inflating a catheter-tethered balloon of sufficient volume in the left ventricle of patients in acute cardiac decompensation, who would likely benefit from the Batista procedure, be effective as a rescue or bridging technique to improve CO acutely so that surgery could be undertaken? Whether your answer is “yes” or “no,” cite and explain the underlying physiological principles on which you base your answer. If your answer was “yes” explain why balloon reduction of left intraventricular volume is not used in cases of acute heart failure?
- Explain what the physiological basis is for elevated levels of BNP being predictive of high risk for acute MI.
- Explain how the gastric mucosa is protected from gastric HCl- by a thin layer of mucous. Why is proton-mediated ulceration of the gastric mucosa almost an immediate consequence of the interruption of perfusion of the gastric mucosa despite the continued patency of the protective mucus layer? (Hint: this is the same question asked in different ways).
- Be able to explain the differences and relationship between intravscular volume (expansion or depletion), water balance (deficit or excess), and serum sodium levels (hyper or hypo). And subsequently, how to diagnose, treat, and correct each of the variable disorders. Salt and water balance are something every ICU patient has that intensivists deal with everyday. But, its amazing how many often I see other MD’s (primarily during CCM consults on the floor) bolusing with .45NS at 200cc/hr for hypotension, correcting severe (or not so severe) hyponatremia with 0.9NS at 60cc/hr, and using D5W at 100cc/hr as “maintenance” fluid when the serum sodium is 130 meq/L.