Background: In 2016 the annual incidence of out-of-hospital cardiac arrest (OHCA) in the United States was roughly 360,000 and 209,000 for in-hospital cardiac arrest (IHCA) (Mozaffarian 2016). Though survival rates are relatively dismal, arrests in the setting of shock amenable rhythms – ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT) – have an overall better rate of return of spontaneous circulation (ROSC). While cardiac defibrillation may be effective in terminating VF/VT, defibrillation does not prevent recurrence of VF/VT. According to the advanced cardiovascular life support (ACLS) algorithm, amiodarone is still the recommended first-line medication for shock refractory VF/VT. These recommendations stem from two hallmark studies which demonstrated improved ROSC and survival rates to admission after amiodarone was administered (Dorian 2002, Kudenchuk 1999). However, ROSC does not represent a clinically meaningful endpoint. Subsequent studies have questioned the utility of amiodarone in cardiac arrest from the perspective of improving survival to hospital discharge or survival with a good neurological outcome. Read more →
Author Archive for: Swami
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 →
Intro: Vasoactive substances are powerful therapeutic medications that can boost a patient’s blood pressure and perfusion to target organs. They are often used in resuscitation to support tissue perfusion though their benefits are mostly unproven and may be harmful in certain circumstances (i.e. hypovolemia, hemorrhage). The cognitive response to hypotension should not be reaching for a pressor. The primary therapy for any sick hypotensive patient is treatment of the underlying pathology.
While many patients will respond to these medications, we occasionally encounter non-responder-patients who despite substantial doses do not show hemodynamic parameter improvements. Absence of response can result from a number of causes including misidentification of the underlying pathology (i.e. I missed the massive PE or pericardial tamponade thinking the patient was in septic shock). Premature diagnostic closure can lead us to simply push on with higher doses of pressors and adding additional pressors. However, there should be a cognitive pause at this point where the clinician reassesses the situation, considers alternate causes and therapeutics. Below is a list of pathologic conditions that complicate other diagnoses and are frequently missed as causes of non-response to vasopressors. This is the list I consider during my cognitive pause. Read more →
Angiotensin Converting Enzyme Inhibitors (ACE-I) are prescribed to millions of patients in the US. Though they are relatively safe, upper airway angioedema is one of the life-threatening adverse effects that we see frequently in the Emergency Department. Though this disorder is routinely treated with medications for anaphylaxis (i.e. epinephrine, histamine blockers, corticosteroids) the underlying mechanism of action predicts that these medications will fail. There is no well established treatment algorithm other than airway control if the angioedema is severe and appears to be causing a mechanical obstruction and cessation of the medication. A 2015 phase 2 study published in the NEJM touted the role for Icatibant in the treatment of these patients. Despite being heralded as “the cure,” the data set in this article was small questioning the validity of the findings. Enter the CAMEO study which attempts to further elucidate the benefits of this medication. Read more →
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 →