Tag Archive for: Cardiac Arrest

Can We Agree on Cardiac Standstill?

18 Sep
September 18, 2017

Background: Point of Care Ultrasound (POCUS) has gained wider use in resuscitation of patients presenting with cardiac arrest. POCUS can play an important role in determining the etiology of arrest as well as being used to determine the presence or absence of mechanical activity. The REASON study demonstrated that patients with PEA or asystole without cardiac activity on POCUS are extremely unlikely to survive to hospital discharge though this study did not investigate the more important question of a survival with a good neurologic outcome. (Gaspari 2016). In light of this as well as other evidence, some have proposed that the absence of cardiac activity may be adequate to declare resuscitation futility and stop resuscitative efforts. However, there is a lack of agreement on what defines cardiac activity (see table 1). Due to this, and other factors, the level of agreement between physicians in interpretation of cardiac standstill is unknown. Read more →

Impact of POCUS During Cardiac Arrest Resuscitation on Compression Pauses

03 Aug
August 3, 2017

The provision of high-quality compressions with minimal interruptions is central to the management of cardiac arrest. Along with defibrillation, high-quality compressions are the only interventions proven to improve patient-oriented outcomes. Recently, point-of-care ultrasound (POCUS) has gained greater use in cardiac arrest care for determination the cause of arrest as well as guiding the resuscitation and interventions. Performance of POCUS during cardiac arrest can be challenging particularly in terms of obtaining cardiac windows. Among these challenges is obtaining images of the heart during compressions. As a result, cardiac POCUS is often performed during rhythm checks when there is a scheduled pause in compressions. Despite the potential benefit from POCUS, prolonged interruptions in compressions while attempting to get optimal windows is unlikely to benefit the patient and, may be harmful. Read more →

Is Amiodarone Dead?

12 Jun
June 12, 2017

Background: Amiodarone is a class III antidysrhythmic first released for human use in 1962. As with other drugs in this class, amiodarone acts by blocking potassium channels thus prolonging the action potential. This, in turn, leads to a lengthening of depolarization of the atria and ventricles. The drug spread rapidly through US hospitals as it was touted as “always works, and no side effects,” by it’s pharmaceutical manufacturer (Bruen 2016).

Of course, nothing comes free and soon after the drug became widely used, a multitude of adverse effects became apparent. These included minor issues – sun sensitivity and corneal deposits – to major ones – thyroid dysfunction (hypo- and hyperthyroidism), pulmonary toxicity and liver damage. Additionally, the medication’s mechanism of action wasn’t clean and simple – amiodarone is no known to have sodium-channel blocking (Class I), beta-blocking (Class II) and calcium-channel blocking (Class IV) effects.

Despite the multitude of issues, the drug continued to be used extensively because of it’s purported benefits. The drug was most commonly applied in the Emergency Department (ED) for conversion of atrial fibrillation, conversion of stable ventricular tachycardia and in refractory VF/VT cardiac arrest.

This post dives into the three most common places amiodarone is employed in the ED: cardioverion of atrial fibrillation, cardioversion of VT and in refractory VF/VT cardiac arrest and demonstrates that superior evidence points to better options for management. Read more →

In-Hospital Cardiac Arrest: The First 15 Minutes

27 Apr
April 27, 2017

Background: Over the past few years there has been a shift in cardiac arrest from the mantra of ABC (Airway, Breathing, Circulation) to CAB (Circulation, Airway, Breathing).  There has been increased emphasis on circulation and a de-emphasis of airway management in cardiac arrest.  Physiologically, this makes sense as the only two interventions in cardiac arrest that have been shown to make a difference in neurological outcomes are early, high quality CPR and defibrillation.  The reason for this is increased coronary and cerebral perfusion pressure, which improve oxygenation to ischemic tissue.  The less ischemic cardiomyocytes are the more likely they will convert to a perfusing rhythm.  Similarly, the less ischemic neurons are, the more likely we will have a better neurologic outcome for our patients.  It has been fairly well established in the peer reviewed literature that advanced airway management in the prehospital setting is associated with decreased survival with good neurologic outcome.  There is considerably less literature exploring this area in in-hospital cardiac arrest. Read more →

Cardiac Arrest, Return of Spontaneous Circulation (ROSC) With No ST-Segment Elevation on ECG. Now What?

15 Dec
December 15, 2016

cardiac-arrestBackground: The American Heart Association/American College of Cardiology (AHA/ACC) give a Class I recommendation for activation of the cardiac catheterization lab in patients with out-of-hospital cardiac arrest (OHCA) whom ST-segment elevation myocardial infarction (STEMI) is present.  The evidence for early cardiac catheterization in patients after cardiac arrest, with ROSC and no STEMI is a bit more controversial.  The most recent 2015 AHA/ACC guidelines recommend, “it may be reasonable,” to perform an emergent cardiac catheterization in select patients without STEMI. Read more →

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