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Clin Pharm. 1987 Feb;6(2):118-39.

Advances in drug therapy of cardiopulmonary arrest.

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School of Pharmacy, University of Wisconsin-Madison 53706.

Erratum in

  • Clin Pharm 1987 May;6(5):369.


Advances in the selection and use of drugs during cardiopulmonary resuscitation (CPR) are reviewed. In 1985, the American Heart Association and the National Academy of Sciences-National Research Council revised standards and guidelines for CPR and emergency cardiac care. Algorithms were developed for treatment of (1) ventricular fibrillation and pulseless ventricular tachycardia, (2) ventricular tachycardia with pulse, (3) asystole, (4) electromechanical dissociation, (5) paroxysmal supraventricular tachycardia, (6) bradycardia, and (7) ventricular ectopy. Vasoconstriction, aortic diastolic arterial pressure, and coronary perfusion pressure are the most important determinants of the success of resuscitation. Because coronary perfusion occurs only during diastole, it is essential to maintain an adequate diastolic pressure. Arterial and central venous lines are needed for estimating coronary perfusion pressure, but end-tidal carbon dioxide measurement appears promising as a noninvasive alternative. Arterial blood gas measurements indicate respiratory alkalosis during CPR, but underlying tissue acidosis persists; venous blood gases appear to provide more useful information. A large catheter in a central vein above the diaphragm is the preferred route for drug administration during CPR, but an antecubital venipuncture site can be used to avoid interrupting CPR. Peak drug concentrations are higher and are achieved sooner with central venous than with peripheral venous injection. The endotracheal route can be used safely for administration of epinephrine, lidocaine, or atropine; an adequate volume (5 or 10 mL) of diluent is needed, and several insufflations should follow instillation. Drug distribution during CPR is greater to the brain and myocardium than to peripheral tissues. Epinephrine is administered to all patients in cardiopulmonary arrest; its beneficial effect is due to alpha-mediated vasoconstriction. Epinephrine increases cerebral as well as myocardial blood flow. The currently recommended dose of epinephrine hydrochloride is 0.5 to 1.0 mg i.v. at five-minute intervals. For endotracheal administration, an initial 1.0-mg dose is recommended, and subsequent doses are determined by patient response. Epinephrine has a beta-adrenergic-stimulating effect that may increase myocardial oxygen demand, but pure alpha agonists such as phenylephrine, methoxamine, and metaraminol have not been found superior to epinephrine. Epinephrine has not been proven to make ventricular fibrillation more susceptible to direct-current countershock. (ABSTRACT TRUNCATED AT 400 WORDS)

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