- Author: Sandy N Shah, DO, MBA, FACC, FACP, FACOI; Chief Editor: Barry E Brenner, MD, PhD, FACEP more...
Parasympathetic influences during cardiopulmonary arrest have not been elucidated fully, and clinical benefits of atropine have never been confirmed.
Atropine is no longer recommended by the American Heart Association (AHA) for asystole and pulseless electrical activity (PEA).
High-dose epinephrine (0.20 mg/kg) may improve the hemodynamics of cardiopulmonary resuscitation (CPR), thereby increasing the rate of return to spontaneous circulation; however, this agent has not been demonstrated to influence the final clinical outcome. Therefore, high doses are no longer are recommended for children or adults.
Adenosine antagonists, such as aminophylline, have been investigated but have not been shown to be clinically useful.
The goal in using anticholinergic agents is to enhance sinoatrial (SA) activity and to improve conduction through the SA or atrioventricular (AV) node by reducing vagal tone via muscarinic receptor blockade. This is effective only if the site of the block is within the SA or AV node. For patients with infranodal block, anticholinergic therapy is ineffective, and it may increase a Mobitz II second-degree block to a higher degree of block or a third-degree block.
Atropine is a parasympatholytic agent used to eliminate vagal influence on the SA and AV nodes. This agent is not effective for infranodal third-degree heart block, PEA, and asystole.
Adrenergic agents can produce constriction of skeletal and vascular muscle.
Epinephrine is considered the single most useful drug in cardiac arrest; however, some authorities question its clinical effectiveness in humans This agent is used to increase coronary and cerebral blood flow during cardiopulmonary resuscitation (CPR) and may enhance automaticity during asystole. In addition, epinephrine can be used for bradycardia in adult and pediatric patients.
Vasopressin has vasopressor and antidiuretic hormone (ADH) activity. This agent increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed via stimulation of V1 receptors (vasopressor effect). Vasoconstriction is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.
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