The goals of management of post-resuscitation myocardial dysfunction are (i) improved myocardial systolic and diastolic functions with increases in stroke volume and reduction of ventricular filling pressures, and (ii) control of arrhythmias.
The drugs recommended for the reversal of post-resuscitation myocardial systolic and diastolic dysfunction in the current guidelines for cardiopulmonary resuscitation (AQonym.ous.1992) are summarized in Table..! together with dosage, rationale for use, and side-effects. They include inotropic agents (i.e. dobutamine and phosphodiesterase inhibitors), vasopressor agents (i.e. dopamine and levarterenol), and preload and afterload reducing agents (i.e. nitroglycerin, nitroprusside (glyceryl trinitrate), phosphodiesterase inhibitors, and angiotensin-converting enzyme inhibitors).
Table 1 Pharmacological agents available for the management of post-resuscitation myocardial dysfunction
Dobutamine acts primarily on b1- and b2-adrenergic receptors. Its hemodynamic effects include increases in cardiac output and stroke volume, and decreases in systemic and pulmonary vascular resistance, and therefore improvement in systemic and coronary blood flow. Although dobutamine improves post-ischemic myocardial dysfunction, it has the potential of increasing myocardial oxygen consumption owing to its b-adrenergic actions. Therefore it may increase myocardial ischemic injury in settings in which coronary blood flow is critically reduced ( [email protected]@L 19.9.5).
Phosphodiesterase inhibitors such as amrinone have a combination of inotropic and vasodilator effects. These agents increase the concentration of cyclic adenosine monophosphate (cAMP) and myocardial contractility. The therapeutic benefit in the setting of post-resuscitation myocardial dysfunction is not well established and thus amrinone serves as a third-line drug, to be used after other agents have failed.
Dopamine acts on a-adrenergic, b-adrenergic, and dopaminergic receptors. It also prompts norepinephrine (noradrenaline) release from cellular sites. Dopamine increases myocardial contractility, but a1-adrenergic actions predominate at larger doses (>10 g/kg/min). This induced peripheral vasoconstriction accounts for increased afterload and results in increases in the workload on the heart and myocardial oxygen requirements. Therefore its use in the post-resuscitation setting is restricted to treatment of systemic hypotension. The same considerations apply to the more potent arterial vasoconstrictor, norepinephrine.
Dopexamine is a synthetic analog related to dopamine with intrinsic activity at both dopamine and b 2-adrenergic receptors. It has shown favorable hemodynamic effects in patients with severe congestive heart failure. The potential role of dopexamine in the setting of post-resuscitation myocardial dysfunction remains to be determined.
Pharmacological interventions optimizing left ventricular afterload and preload remain the mainstay for the treatment of post-resuscitation myocardial dysfunction. Nitroglycerin and nitroprusside are the predominant vasodilator drugs in current use. At medium and high doses (5-10 g/kg/min) nitroglycerin relaxes both venous and arterial smooth muscle. The more selective coronary vasodilation produced by nitroglycerin also favors its use in the management of post-resuscitation myocardial dysfunction in which cardiac arrest was caused by ischemic heart disease. At low doses, nitroglycerin acts primarily as a venodilator which decreases preload. Intermittent treatment with nitroglycerin after 24 h mitigates tachyphylaxis which accounts for loss of hemodynamic efficacy.
Nitroprusside is a rapid acting venous and arteriolar smooth muscle dilator with a very short half-life. It may elevate plasma thiocyanate concentration, induce an anion gap acidosis, and lead to cyanide toxicity. However, its short-term use is not likely to be constrained by these side-effects, particularly if used in dosages below 10 g/kg/min. It is widely used because it is easily titrated in patients who have both arterial and pulmonary artery monitors.
In patients with coronary atherosclerosis, coronary vasodilation may reduce blood flow of partially occluded vessels (coronary steal). This may explain the increased frequency of angina in patients with ischemic heart disease despite the favorable hemodynamic response of nitroprusside.
The roles of other vasodilators such as angiotensin-converting enzyme inhibitors and calcium-channel blockers for the management of post-resuscitation myocardial dysfunction are less well defined. The relatively long half-lives of these drugs and the need for intravenous formulations limit their roles in post-resuscitation settings.
Lidocaine (lignocaine) remains the drug of choice for the management of post-resuscitation ventricular arrhythmia. Adenosine has emerged as a first-line drug for treatment of atrial tachyarrhythmia with a short duration of action and absence of prolonged systemic hypotension. When tachyarrhythmias lead to hemodynamic instability, prompt d.c. cardioversion (100-360 J) is preferred. The initial therapy for bradyarrhythmia is atropine and a temporary transvenous pacemaker if the bradycardia is persistent and symptomatic. Both hypokalemia and hypomagnesemia must be excluded as causes of post-ischemic arrhythmias and treated appropriately.
No data are currently available to guide the use of buffer agents, and particularly sodium bicarbonate, for the management of post-resuscitation myocardial dysfunction. Recent animal studies indicate that buffer agents administered during cardiopulmonary resuscitation may ameliorate post-resuscitation myocardial dysfunction. Carbon-dioxide-consuming buffers, such as trimethamine (TRIS) and Carbicarb, improve post-resuscitation survival after prolonged cardiac arrest ( Sun et_ al 1996).
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