November 18, 2019

Background Information: Therapeutic hypothermia is the use of targeted temperature management to reduce neurologic sequelae resulting from the severe ischemia-reperfusion injury that occurs during cardiac arrest primarily from shockable rhythms.1 Although a mainstay treatment in the Advanced Cardiac Life Support (ACLS) guidelines, its use has been widely debated as beneficial in improving neurologic outcomes in post-cardiac arrest patients with non-shockable rhythms.2-7 Recent studies have also questioned the exact temperature at which patients should be cooled.8 The authors of this study sought to assess whether moderate therapeutic hypothermia, compared with targeted normothermia would improve neurologic outcomes in post-cardiac arrest patients who had a non-shockable rhythm.

August 5, 2019

Background: Epinephrine (adrenaline) remains a central part of management of OHCA in ACLS guidelines. Recent studies (i.e. PARAMEDIC-2) have raised concerns about the efficacy and possible deleterious effects of epinephrine on both overall survival and long-term neurological outcomes. Other observational trials have suggested that there may be a time dependent effect of epinephrine on survival, with earlier timing of epinephrine improving outcomes, and later timing of epinephrine causing deleterious effects[2]. This trial attempts to analyze the association between timing and dose of epinephrine given on survival and neurologic outcomes of patients with OHCA.

March 28, 2019

Pulse Checks Background: In an older study published in Resuscitation 1998 [1], ED physicians, ICU physicians, and nurses tried to identify a carotid pulse in a healthy male volunteer with normal blood pressure. 43.1% of the health professionals required >5 seconds to detect the carotid pulse and another 4.3% required >10 seconds.  Something I have advocated for in cardiac arrest is the death of pulse checks, as our fingers are poorly sensitive for detecting which patients have a pulse in a shock state.  A visible rhythm on the monitor, along with the absence of a pulse with digital palpation, does not always indicate the presence of true pulseless electrical activity (PEA).  Our reflexive action when we don’t feel a pulse is to begin CPR and give 1mg epinephrine which may not be beneficial in these patients.  Patients in profound shock don’t necessarily need cpr and 1mg of epinephrine, they need augmentation of cardiac output with either push dose pressors or hemodynamically driven epinephrine drips.  Now another study published in Resuscitation looked to compare the efficiency of cardiac ultrasonography (CUSG), doppler ultrasonography (DUSG) and manual pulse palpation to check the pulse in cardiac arrest patients [2].

July 13, 2018

Background: Focused use of ultrasound in resuscitation of patients with shock and cardiac arrest has become increasingly embraced in both the emergency department (ED) as well as in the prehospital setting. Application of ultrasound, particularly of echocardiography, has the potential to identify treatable causes of shock and arrest, identify shockable rhythms and identify the presence of mechanical activity. All of these can affect management decisions and, potentially effect outcomes. Recent studies have led to concerns that integration of point of care ultrasound (POCUS) in cardiac arrest increases pauses in compressions. Thus, it is important to establish what POCUS adds to shock and arrest management.

June 15, 2018

Background: As with all medications in cardiac arrest (i.e. epinephrine, amiodarone) the benefits of sodium bicarbonate administration have been discussed and debated for decades. While it is clear that sodium bicarbonate can play a role in resuscitation of arrest due to hyperkalemia, it’s role in patients with acidemia resulting from or causing arrest is unclear. In theory, raising the pH may be beneficial but the use of bicarbonate increases serum CO2 which may be deleterious as it creates a respiratory acidosis. Despite the absence of good evidence, sodium bicarbonate continues to be used in non-hyperkalemic cardiac arrest management.

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