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critical care medicine review notes

141Critical Care Board Study Notes 2014


Jon-Emile S. Kenny M.D.2014


Esteemed reader,

I compiled these notes while studying for the ABIM Critical Care Medicine Board examination. These notes were made from a number of fairly recent resources including SCCM lectures, SEEK questions, ACCP study guides and, of course, pulmccm.org. I cannot guarantee their correctness in content, grammar, and spelling; nor are these notes peer-reviewed. They absolutely should not be used as a resource for patient care. They should be used for board exam preparation; that is all I will use them for as well. This is not my heart-lung physiology text. Please share these review notes freely. #FOAMccHappy Studies,


1Critical Care Board Study Notes 2014

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3Critical Care Board Study Notes 2014

hThe quality of CPR is associated with survival to discharge for in-house arrest. It is not the application of an AED, which has been studied. 40% of chest compressions in house are of insufficient depth, there is a long period of time during codes when health care providers are not actually on the chest. Compressions should be hard and fast [to Bee Gees stayn alive] 100 per minute, 2 inch depth. There should be minimization of time off the chest even for pulse checks and defibrillation. It is CPR that matters, 2 minutes of CPR interspersed with defibrillation, 1 mg epinephrine every 3-5 minutes or 40 U of vasopressin. Atropine is no longer a part of PEA.Avoid hyperventilation as this can reduce cerebral perfusion via alkalemia and more importantly cause dynamic hyperinflation.Previously, the brain injury [apoptosis, excitability, edema, etc.] induced by ischemia re- perfusion was thought to be treatable. The Feb. 2002 NEJM article with 137 patients in each arm, enrolled witnessed, shockable cardiac arrest patient s with ROSC but still not following commands. Patients were randomized to therapeutic hypothermia target 32 to 34 celsius over 8 hours, held at that temp for 24 hours and then passively re-warmed over 8 hours. A meta- analysis of the three largest trials [380 patients] showed an odds ratio of 1.7 for favourable neurological outcome. The largest of the three trials selected patients who were resuscitated within 60 minutes with a shockable rhythm, comatose, and not in shock. Cooling was done within 2 hours of the event.Therapeutic hypothermia [TH] is commonly associated with coagulopathy, hyperglycemia, bradycardia and hypovolemia the latter on

CARDIAC RESUSCITATION1.CRITICAL CARE CARDIOLOGYaccount of the cold diuresis. There is an increased risk of infection following TH and altered drug metabolism.However, skeptics noted the lack of blinding to treatment allocation in the above studies.Further, in the biggest of those hypothermia studies, a large number of patients in the usual care group developed fever which is associated with worse outcomes after cardiac arrest. So it was thought that perhaps TH simply had to accomplish fever reduction to improve outcome.So the big one came out in NEJM November 17, 2013 [950 patients in 3 years, 80% vfib, 12% asystole, 8% PEA, and randomized the patients to celsius 33 or 36 ASAP for 28 hours and then fever reduction for 72 hours]. After 72 hours, a neurologist blinded to initial treatment allocation recommended withdrawal or continued care based on standardized criteria, with withdrawal recommended only for known predictors of a terrible outcome [e.g., refractory status epilepticus; Glasgow motor score 1-2 with bilateral absence of N20 peak on median nerve SSEP]. CPC more than 2 or Rankin more than 3 was defined as severe disability. There was no difference in death or disability between the two groups [i.e. 33 versus 36 degrees] even in the 80% shockable group.Temperature should be maintained at 36 C or below after out-of-hospital cardiac arrest.Despite its physiologic rationale and evidence of benefit in prior smaller studies, targeted temperature management below 36 probably does not improve outcomes after out-of-hospital cardiac arrest of any type. Because average human core temperature is 37 C, maintaining temperature continuously at or below 36 C still would require cooling in almost all patients.

hIn a related vein, in 2013 JAMA, 100 patients with bacterial meningitis were randomized to 32-34 degrees or standard care and this trial was stopped early for a 20% absolute risk increase in mortality!What about the prognosis following cardiac arrest? What is the false positive rate for diagnosis of poor neurological outcome? We should strive for zero. Pupillary reaction to light has a false positive rate of 0-31% at day one. At day three, no pupillary reaction has a false positive rate for poor outcome of zero. So absent pupillary response at day three is important information. The absence of corneal reflex is similar at 72 hours. What about posturing?Similar at 72 hours. All of this data was generated during an era of no therapeutic hypothermia and the reason why neurological assessment for continued care in the aforementioned trial took place at 72 hours.So what has a perfect specificity for determining poor neurological outcome? There is a review in the Lancet day 3 absent motor, absent pupillary response and abnormalities in somatosensory evoked potentials. SSEP occurs when the median nerve is stimulated. Bilateral absence is poor neurological prognosis from NEJM article in 2009. Day 1-3 there is nothing great to help. You must wait at least 72 hours and you must wait for analgesia to wear off. This is important with TH because there is alteration of sedation and analgesia metabolism with hypothermia it will stay longer. There is no clear answer as to when the patient may wake up, but anecdotally up to one week as the effects of hypothermia wear off and sedation is cleared, though this will be less important as TH is used less with the results of the Nov. 2013 NEJM trial.Prognosis after a first cardiac arrest occurring in the ICU is poor. An observational study of almost 50,000 such arrests showed an overall survival to hospital discharge of 16%. Requiring vasopressors

prior to the arrest was a major discriminator in outcome:Only 10% of patients on pressors prior to arrest survived to discharge, and only 4% overall were discharged home [the others went to rehab or long-term acute care].Among those with PEA/asystole despite pressors, only 1.7% were able to perform their own activities of daily living at the time of discharge.People with ventricular fibrillation or tachycardia not requiring pressors prior to arrest did much better: 40% survived, 20% went home, and17% had good neuro outcomes.

CONGESTIVE HEART FAILUREAbout 50% of the mortality with heart failure is sudden, the other half is slow progression. There are stages of heart failure described in 2001 [ACC/AHA] where stage A is those patients at risk, B [structural disease without symptoms] is NYHA I, stage C [current or prior symptoms] corresponds to NYHA II and III and stage D is NYHA IV.NYHA Class IV heart failure has a 60% mortality at one year. In acute, severe heart failure a poor prognosticator is: hypotension. Hypernatremia and polycythemia are not. Hypotension is defined as a systolic below 115 mmHg. Other bad prognoses: hyponatremia, CAD, high BUN or creatinine, low EF, elevated BNP or troponin, anemia, diabetes.Precipitants of ADHF? 25% excess salt and fluid intake, 25% noncompliance with medications, and 16% from adverse medication effects [e.g. new CCB, NSAID, steroids, glitazones and ethanol, new anti-arrhythmics]. The rest are acute medical causes such as ischemia, PE, HTN, valve dysfunction, arrhythmia. There are extra-cardiac causes as well sepsis, infection, renal failure, thyroid, new anemia.

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Critical Care Board Study Notes 2014

FLAVORS OF MYOCARDIAL DYSFUNCTIONThere are different kinds of myocardial dysfunction to consider hibernating, stunned myocardium, sepsis, myocarditis, etc. Stunned myocardium occurs when there is ischemia that relates to a wall motion abnormality, but when blood flow resumes, there is a persistent WMA that lasts from hours to days. The patient must be supported during these time consider stress cardiomyopathy as an example of stunned myocardium. The patient may present with all the signs and symptoms of ischemia and heart failure with stress cardiomyopathy. There must be no coronary stenosis to explain the disease and WMA do not correspond to single coronary distribution. There may be STE and big T wave inversions.Recognize Takotsubo cardiomyopathy the major complications of this are mechanical in nature, heart failure, shock and arrhythmia. It presents exactly like a STEMI, or at least it can, but angiogram is normal and there is apical hypokinesis on the LV gram, this invariably resolves by 2 months. Some argue against the use of inotropes or catecholamines in these patients as they catechols be the cause; they argue that IABPs should be used. This disease usually happens in post-menopausal women and has a mortality rate of 0-8% in house.Hibernating myocardium is due to chronic ischemia without infarction. There will be a WMA that lowers ejection fraction. If the occlusion is reversed, the ejection fraction will return to normal. What kind of revascularization? In the CAST trial, those with a low ejection fraction who got CABG did better. The STITCH April 2011 NEJM looked at chronic heart failure patients [EF less than 35%] with bypass surgery [versus medical therapy] and there was improved death from cardiac causes, hospitalization [not