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Although numerous medications may be used during treatment of cardiac arrest, the primary agents are vasopressors (e.g., epinephrine and vasopressin) and antiarrhythmics (e.g., lidocaine and amiodarone). ACLS algorithms provide specific guidelines for the use and doses of these agents [1].

The majority of studies suggest no drug in isolation improves outcome following cardiac arrest in humans [63–66]. The continued use of these drugs is based on tradition, theory, and animal research, and the selection of specific agents in each class is largely a matter of individual choice. EMS physicians must be aware that the only medications evaluated by randomized clinical trials are epinephrine, amiodarone, lidocaine, vasopressin, and magnesium [64, 67, 68]. However, these studies are mostly confounded by drug administration at prolonged times after onset of cardiac arrest.

Vasopressors serve two intended purposes during cardiac arrest: vasoconstriction, and exerting positive inotropy and chronotropy. Alpha‐agonists increase peripheral resistance, shunting blood flow to the brain and heart. Beta‐agonists increase inotropy and chronotropy. In clinical context, these agents are used to help to sustain coronary and cerebral perfusion before restoration of pulses. AHA guidelines suggest administering 1 mg of IV epinephrine every 3‐5 minutes [1]. Vasopressin may be administered alone or in combination with epinephrine.

Compelling animal data indicate increased ROSC with the early delivery of epinephrine or vasopressin [69–72]. Although several small clinical series have reported increases in ROSC and survival to admission for patients treated with vasopressin, a randomized trial comparing vasopressin with epinephrine versus epinephrine alone did not demonstrate additional benefit from vasopressin use [67,73–75]. Recent studies have demonstrated improved ROSC and survival to hospital discharge in patients receiving epinephrine. Also, the point estimate number of survivors (with both good and poor neurologic outcome) at 90 days was higher in those receiving epinephrine [76, 77].

With vasopressors, there is a trade‐off between increased coronary perfusion and reduced cerebral perfusion (possibly via increased cerebral vasoconstriction). A once‐popular ACLS approach was the use of high‐dose epinephrine (5–7 mg IV) [63]. Although clinical trials using high‐dose epinephrine demonstrated increased rates of ROSC, this did not translate into survival to discharge [63].

Antiarrhythmics are commonly used in cases of VT/VF cardiac arrest. They may increase the likelihood of conversion to a perfusing rhythm. Lidocaine and amiodarone are currently recommended antiarrhythmics for shock‐refractory VF [1]. EMS physicians may choose between an IV bolus of 300 mg of amiodarone or 1–1.5 mg/kg of lidocaine for patients suffering pulseless VT/VF. The largest randomized controlled trial comparing amiodarone, lidocaine, and placebo demonstrated higher survival to hospital admission in the amiodarone and lidocaine arms (when compared to placebo), but no difference in survival to hospital discharge. However, in the subgroup of bystander‐witnessed cardiac arrest, amiodarone demonstrated a 5% increase in survival to hospital discharge when compared with placebo (p = 0.04), and lidocaine demonstrated a 5.2% increase in survival to hospital discharge when compared with placebo (p = 0.03) [78]. This phenotype of patient may derive additional benefit from antiarrhythmic medication.

Epidemiologic studies suggest that pulseless electrical activity (PEA) and asystole are increasingly common in out‐of‐hospital cardiac arrests [79–82]. Atropine is a vagolytic and reverses cholinergic‐mediated decreases in heart rate, blood pressure, and vascular resistance [1]. Although traditionally it has been used in bradycardic PEA or asystolic cardiac arrest, the limited available research does not suggest any benefit, and this drug is no longer recommend for routine use. Epinephrine should be administered, and potentially treatable causes (the “5 Hs and 5 Ts” of ACLS) should be considered (Table 13.1).

An additional drug worth comment is sodium bicarbonate. For years, sodium bicarbonate was administered routinely during cardiac arrest to reverse the metabolic acidosis of cardiac arrest and, it was hoped, increase the effectiveness of vasopressors and antiarrhythmics. In formal trials, this drug did not improve survival [83]. Sodium bicarbonate may be reasonable in scenarios of suspected hyperkalemic arrest (such as individuals with known renal failure) and in prolonged resuscitations with adequate ventilation. Calcium (chloride or gluconate), however, is the most effective medication in cases of severe hyperkalemia affecting cardiac conduction.

Table 13.1 The potentially treatable Hs and Ts of cardiac arrest

Hs:

Hypovolemia/Hemorrhage Hypoxia Hyper‐/hypokalemia Hydrogen ion (acidosis) Hypothermia

Ts:

Toxins Tamponade (cardiac) Tension pneumothorax Thrombosis (coronary) Thrombosis (massive pulmonary)