#29 Cardiac Arrest

We all know BLS and even ACLS like the back of our hands so now it’s time to understand *why*. Why are VF and VT under the arrest algorithms? Why epi? Why are survival rates so low, even in the hospital?

Former paramedic and current BLS and ACLS instructor, Al Gook, answers some basic yet honest questions we all have about cardiac arrest and what we can do to improve our stubbornly low survival rates.

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Q: Why do we include VT, VF, and PEA under the banner of cardiac arrest in BLS/ACLS when the heart is still moving?

A: Perfusion is so poor in these rhythms that vital organs are not adequately perfused. If not converted, these rhythm will lead to asystole.

Q: What is the survival rate of cardiac arrest in the hospital? Outside of the hospital?

A: While difficult to measure, out of hospital survival rate is ~9% while in-hospital survival rate is ~20% (AHA).

Q: What is the pathophysiology of PEA?

A: PEA in patients who have organized cardiac electrical activity but the absence of mechanical contractions (no pulse). This is caused by factors that deplete myocyte high-energy phosphate stores and inhibit myocardial fiber shortening, including hypovolemia, hypoxia, and electrolyte abnormalities (particularly with potassium and calcium) (Paradis et al).

Q: Why is epinephrine given during cardiac resuscitation?

A: Epinephrine (Epi) binds to alpha-1 receptors in the blood vessels which cause vasoconstriction and this improve perfusion to the heart and brain. It also binds to beta-1 adrenergic receptors in the heart and this effect improves cardiac output by increasing HR, contractility, and conductivity through the AV node. The efficacy of epinephrine in cardiac resuscitation is being debated (RebelEM).