Pharmacologic Therapy

(Table 58-6: Adult Advanced Cardiac Life Support Drugs and Doses).

Establishing IV access and pharmacologic therapy should come after other interventions have been instituted. Of the drugs given during CPR, only epinephrine is acknowledged as being useful in helping to restore spontaneous circulation. Asystole and pulseless electrical activity (electromechanical dissociation) are circumstances in which drugs are most frequently given.

Routes of Administration
1. The preferred route of administration of all drugs during CPR is IV. (Central injection produces a higher drug level and more rapid onset than peripheral injection.) Because of poor blood flow below the diaphragm during CPR, drugs administered into the lower extremity may not reach sites of action.
2. If venous access cannot be established, the endotracheal tube is an alternative route of administration for epinephrine, lidocaine, and atropine (not sodium bicarbonate). Doses 2 to 2.5 times the established IV dose administered in 5- to 10-mL volumes are recommended when the tracheal route of administration is used.
Catecholamines and Vasopressors
1. Mechanism of Action. The efficacy of epinephrine lies entirely in its α-adrenergic actions. (Peripheral vasoconstriction leads to an increase in aortic diastolic pressure, causing an increase in coronary perfusion pressure and myocardial blood flow.)
  1. It is commonly believed that the ability of epinephrine to increase the amplitude of ventricular fibrillation (α-adrenergic effect) makes defibrillation easier. There is no proof, however, that epinephrine improves the success or decreases the energy necessary for successful defibrillation.
  2. When added to chest compressions, epinephrine helps develop the critical coronary perfusion pressure necessary to provide myocardial blood flow for restoration of spontaneous circulation.
2. Epinephrine is given 1 mg IV every 3 to 5 minutes in adults. If this dose remains ineffective, higher doses (3–7 mg IV) should be considered.
3. Vasopressin is recommended as an alternative to epinephrine in a dose of 40 U IV as a one-time injection. If additional vasopressor doses are need, epinephrine should be administered.
Amiodarone and Lidocaine
1. These drugs are used during cardiac arrest to aid in defibrillation when ventricular fibrillation is refractory to electrical countershock or when ventricular fibrillation recurs. Amiodarone may be considered the first drug for treatment of ventricular fibrillation that is resistant to electrical countershock.
  1. Lidocaine has few hemodynamic effects when given IV.
  2. Amiodarone can cause hypotension and tachycardia, especially with rapid IV administration.
2. The ventricular fibrillation threshold is decreased by acute myocardial ischemia or infarction, and this effect is partially reversed by lidocaine and amiodarone.
3. To rapidly achieve and maintain therapeutic blood levels during CPR, relatively large doses of lidocaine or amiodarone are necessary (see Table 58-6: Adult Advanced Cardiac Life Support Drugs and Doses).
Atropine
1. Atropine (1 mg IV repeated every 3 to 5 minutes to a total dose of 0.04 mg/kg, which is totally vagolytic) is commonly administered during cardiac arrest associated with a pattern of asystole or slow, pulseless electrical activity on the electrocardiogram (ECG). Atropine enhances sinus node automaticity and atrioventricular conduction via its vagolytic effects.
  1. Excessive parasympathetic tone probably contributes little to asystole or pulseless electrical activity in adults (most often caused by myocardial ischemia).
  2. Even in children, it is doubtful that parasympathetic tone plays a significant role during most cardiac arrests.
2. Full vagolytic doses of atropine may be associated with fixed mydriasis after successful resuscitation confounding neurologic evaluation.
Sodium Bicarbonate
1. The use of sodium bicarbonate during CPR is based on theoretical considerations that acidosis lowers the ventricular fibrillation threshold and respiratory acidosis impairs the physiologic response to catecholamines.
2. Little to no evidence supports the efficacy of sodium bicarbonate treatment during CPR. The lack of effect of buffer therapy may be explained by the slow onset of metabolic acidosis during cardiac arrest. (Acidosis as measured by blood lactate concentrations does not become severe for 15–20 minutes of cardiac arrest.)
3. In contrast to the lack of evidence that buffer therapy during CPR improves survival, the adverse effects of excessive sodium bicarbonate administration are well documented and include metabolic alkalosis, hypernatremia, and hyperosmolarity.
  1. IV sodium bicarbonate combines with hydrogen ions to produce carbonic acid that dissociates into carbon dioxide and water. (PaCO₂ is temporarily increased until ventilation eliminates the excess carbon dioxide.)
  2. Tissue acidosis during CPR is caused primarily by low tissue blood flow and accumulation of carbon dioxide in the tissues. (Theoretically, there is concern that carbon dioxide liberated from sodium bicarbonate could worsen existing tissue acidosis.)
4. Current practice restricts the use of sodium bicarbonate (1 mEq/kg IV initially with additional doses of 0.5 mEq/kg every 10 minutes [better if guided by blood gas determinations]) primarily to cardiac arrests that are associated with hyperkalemia, severe pre-existing metabolic acidosis, and tricyclic antidepressant overdose.
Calcium
1. The only indications for administration of calcium during CPR are hyperkalemia, hypocalcemia, or calcium blocker toxicity.
2. When calcium is administered, the chloride salt (2–4 mg/kg of the 10% solution IV) is recommended because it produces higher and more consistent levels of ionized calcium than other salts. (Calcium gluconate contains one third as much molecular calcium as the chloride salt.)

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