Thursday, September 16, 2010

SICU Rounds Report - Sept 16th 2010

From Brent (PharmD Student)
Acetazolamide use and outcomes in the ICU.  Acetazolamide (Diamox) reversibly inhibits carbonic anhydrase which results in a decrease in hydrogen ion secretion at the renal tubule and increased renal excretion of sodium, potassium, bicarbonate, and water.  This action can help correct alkalosis and fluid overload.
In a placebo-controlled study of intubated COPD patients on mechanical ventilation in the ICU, one dose of Diamox 500mg was shown to reverse metabolic alkalosis, but did not have a benefit from weaning patients from the ventilator or improving PaCO2.  The PaCO2/FiO2 ratio was increased, but no other respiratory markers were improved.
Diamox does significantly decrease serum bicarbonate and blood pH.  There is some concern with overcorrecting metabolic alkalosis with multiple doses, but side effects are uncommon with conventional dosing.  Of note, a trial comparing one dose of 500mg to multiple doses of 250mg of Diamox showed similar efficacy in reversing nonchloride responsive metabolic alkaloses in MICU patients.  Using the single 500mg dose would further reduce risk of side effects from use.  Also, avoiding repeat dosing for 3 to 5 days is recommended to reduce pH overcorrection and risk of hyperchloremic, hypokalemic metabolic acidosis
Currently, there is not enough data to state that the time to vent wean is decreased by using acetazolamide, but risk of poor outcomes from acetazolamide use are relatively rare when dosed in moderation.
Faisy, Christophe, et al. "Effectiveness of acetazolamide for reversal of metabolic alkalosis in weaning COPD patients from mechanical ventilation." Intensive care medicine 36.5 (2010):859-863.
Mazur, J. E., et al. "Single versus multiple doses of acetazolamide for metabolic alkalosis in critically ill medical patients: a randomized, double-blind trial." Critical care medicine 27.7 (1999):1257-1261.
From Patrick
AIVR.   Accelerated Idioventricular Rhythm (AIVR) is in the middle of the spectrum of ventricular rhythms that includes on one end of the spectrum the normal intrinsic ventricular escape rhythm (<40bpm) and on the other end ventricular tachycardia (>100-120bpm).  However, rate alone is not sufficient to differentiate AIVR (40bpm - 120bpm) from vtach (> 100-120bpm), because some slow vtach's can have overlapping rates with AIVR.
AIVR is generally transient and rarely causes hemodynamic instability or requires treatment.  In fact, AIVR has been extensively studied in STEMI patients and has been shown to be a marker of reperfusion or of reopening of occluded coronary arteries.  The underlying mechanism of AIVR appears to be enhanced automaticity (due to ischemia, reperfusion, hypoxia, drugs, or  electrolyte abnormalities, all of which accelerate phase 4 action potential depolarization rates leading to faster spontaneous cell depolarization enhanced automaticity) of the His-Purkinje fibers or the myocardium itself.
Diagnosing AIVR.  Pts typically have a history of myocardial ischemia with recent reperfusion through drugs or coronary artery interventions, hx of cardomyopathy or myocarditis, and occasionally pts will have a history of digoxin use, anesthetic agents, or even cocaine.  AIVR rarely occurs in pts without apparent heart disease or triggers.  Again, the most common cause of AIVR is myocardial ischemia - reperfusion.  Other common causes are digoxin toxicity (a possibility in our SIMU patient), cocaine toxicity, various anesthesia agents (desflurane and
halothane), cardiomyopathies, electrolyte abnormalities, and postresuscitation.  Other arrhythmias to consider on the differential are slow ventricular tachycardia, complete heart block, SVT with aberrancy, or junctional rhythm with aberrancy.  Characteristics that distinguish
AIVR from the others is that AIVR starts off gradually, with the ectopic ventricular focus firing gradually and gradually faster until it surpasses the rate of the sinus node; as a result, it is not
uncommon to see ventricular fusion beats (partial ventricular capture from two different rhythms) as a result of the sinus rhythm and ectropic ventricular rhythm overlapping in rate.  Similarly, AIVR usually ends gradually as a result of the AIVR rate decreasing or sinus rate increasing.  In contrast, ventricular tachycardia has a sudden onset and termination.  AIVR is different from SVT or junctional rhythms with aberrancy in that it is a wide QRS complex arrhythmia, whereas arrhythmias from above the SA node are normally narrow complex.
Work-up. Tests to perform in pts with suspected AIVR include Troponins (or CK / CK-MB), BUN and creatinine (to assess renal function in pts with suspected dig toxicity), digoxin levels, electrolytes, and echo / nuclear perfusion scan / coronary angiogram to assess cardiac disease
/ ischemia.  EKG is the most important test to obtain because it can be used to distinguish AIVR from other malignant arrhythmias such as Vtach or complete heart block.
Treatment.  Rarely requires treatment because it is usually self-limited and hemodynamically tolerated.  If treatment is performed, it is usually aimed at the underlying cause of the AIVR (treating ischemia, digoxin toxicity, electrolyte abnormalities, etc.).  Rarely, AIVR may lead to
intolerated rapid ventricular rate or even degenerate into vtach / vfib, in which case atropine can be used to increase the sinus rate and inhibit AIVR.
Pezeshkian NG, Yang Y.  Accelerated Idioventricular Rhythm.  Emedicine cardiology site -  Updated Apr 2010.
Hohnloser SH, Zabel M, Kasper W, Meinertz T, Just H. Assessment of coronary artery patency after thrombolytic therapy: accurate prediction utilizing the combined analysis of three noninvasive markers. J Am Coll Cardiol. Jul 1991;18(1):44-9.
Erkelsen CJ, Sørensen JT, Kaltoft AK, Nielsen SS, Thuesen L, Bøtker HE, et al. Prevalence and significance of accelerated idioventricular rhythm in patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. Am J Cardiol. Dec 15 2009;104(12):1641-6.
From Max
"Orthopedic" Bowel Regimen for Opioid-related Constipation.  Almost universally, if you are on an opioid you will have constipation. Defined: Fewer than 3 bowel movements per week, along with symptoms such as small or hard stools, abdominal bloating or pain, straining, need for digital manipulation, and nausea. ICU patients of course have limited mobility, which makes things worse. According to Max, some of these patients may also suffer from depression which, apparently, is a strong risk factor for constipation. Also, decrease in oral intake, especially fluid and fiber, furthers the problem. So here's how we attack it:
Bulking Agents. Psyllium, calcium polycarbophil, methylcellulose. Work by retaining water in the stool. However, psyllium has been associated with anaphylactic reactions and bloating is noted in patients receiving large quantities. Mechanical obstruction of the esophagus and colon has also been reported with the use of bulking agents.
Osmotic Laxatives. Polyethylene glycol, lactulose, and milk of magnesia. These agents contain poorly absorbed ions or molecules, which create an osmotic gradient and lead to water retention within the intestinal lumen. Adverse effects with osmotic laxatives may include electrolyte abnormalities, hypovolemia, and diarrhea.
Stool Softeners. Docusate sodium and docusate calcium. Soap like compounds that allow more interaction between water and solid stool to form "softened" stool. Safe with minimal side effects.
Stimulant Laxatives. These are the most exciting. Senna or bisacodyl-containing laxatives. They stimulate colon mucosal sensory nerve endings on contact and to inhibit water absorption via epithelial transport alteration. Adverse effects include abdominal discomfort, electrolyte imbalances, allergic reactions, hepatotoxicity, cathartic colon, and melanosis coli.
Maintain a high index of suspicion for the possibility of bowel obstruction or fecal impaction. If things are bad, Max believes rectal disimpaction must occur before treating constipation with an oral laxative regimen.
If a patient has not been on a bowel regimen, the STEP 1 regimen should be started. If there is no response in 24 hours, move to the next step. At any given time, if there has been no bowel movement in 3 or more days, a sodium phosphate or mineral oil enema should be administered. If this is not effective, a high colonic tap water enema should be administered.
Morrison S. et al. A Novel Interdisciplinary Analgesic Program Reduces Pain and Improves Function in Older Adults After Orthopedic Surgery. J Am Geriatr Soc. 2009;57(1):1-10
Ho J. et al. Update on Treatment Options for Constipation. ORTHOSuperSite. 2008
Bowel Regimen in Chronic Narcotic Use. Family Practice Web access on sept 14th, 2010.

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