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Myocardial oxygen consumption

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2). [Pg.121]

Verapamil. Verapamil hydrochloride is a pbenyl alkyl amine and is considered the prototype of the Class I calcium channel blockers. Verapamil is also a potent inhibitor of coronary artery spasm and is useful in Prinzmetal s angina and in unstable angina at rest. Verapamil produces negative chronotropic and inotropic effects. These two actions reduce myocardial oxygen consumption and probably account for the effectiveness of verapamil in chronic stable effort angina (98,99). Moreover, verapamil is an effective antihypertensive agent. [Pg.126]

MV02, myocardial oxygen consumption SNS, sympathetic nervous system. [Pg.36]

The pharmacological mechanisms of action of NO donors that contribute to their benefit in coronary artery disease, congestive heart failure, and hypertension are listed in Table 11.1. These actions can be grouped into five categories vasodilation, decrease in myocardial oxygen consumption, improvement in hemodynamic performance,... [Pg.288]

Stable angina pectoris Decreased myocardial oxygen consumption -decreased LV end-diastolic dimension -decreased LV filling pressure -decreased LV systolic pressure -decreased PVR Increased coronary blood flow -epicardial coronary artery dilation -stenotic segment dilation -coronary collateral vessel dilation -increased subendocardial perfusion... [Pg.289]

Buxton DB, Nienaber CA, Luxen A, Ratib O, Hansen H, Phelps ME et al. Noninvasive quantitation of regional myocardial oxygen consumption in vivo with [1-1 ICjacetate and dynamic positron emission tomography. Circulation 1989 79 134-142... [Pg.34]

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. [Pg.85]

All of the aforementioned beneficial effects of the /3-blockers are caused by the blockade of /3i-adrenoceptors. The beneficial effect of /3-blockers in the treatment of angina is largely caused by the reduction of heart rate and the concomitant decrease in myocardial oxygen consumption, thus improving the imbalance between oxygen supply and consumption which underlies myocardial ischaemia. [Pg.325]

Verapamil and diltiazem as for the dihydropy-ridines. In addition reduction in heart rate reduced myocardial oxygen consumption. [Pg.333]

Esmolol is used in the treatment of supraventricular tachyarrhythmias for rapid control of ventricular rate and reduction of myocardial oxygen consumption. Discontinuation of administration is followed by a rapid reversal of its pharmacological effects because of es-molol s rapid hydrolysis by plasma esterases. [Pg.185]

The associated initial release of catecholamines may result in an excessive pressor response and stimulation of cardiac force and pacemaker activity. The resulting increase in myocardial oxygen consumption in a patient with ischemic heart disease may lead to ischemic pain (angina pectoris). Patients in a state of circulatory shock probably should not be administered bretylium because of its delayed sympatholytic action. [Pg.186]

Amiodarone relaxes vascular smooth muscle one of its most prominent effects is on the coronary circulation, reducing coronary vascular resistance and improving regional myocardial blood flow. In addition, its effects on the peripheral vascular bed lead to a decrease in left ventricular stroke work and myocardial oxygen consumption. Therefore, amiodarone improves the relationship between myocardial oxygen demand and oxygen supply. IV administration may be associated with profound hypotension requiring volume expansion therapy. [Pg.187]

The most prominent effect of halothane on the circulation is a dose-related decrease in arterial blood pressure. This is due mainly to reduced myocardial contractility and ventricular slowing. Cardiac output falls due to a decrease in stroke volume and bradycardia. Systemic vascular resistance also falls but this is less pronounced than with some other agents. Although halothane reduces myocardial oxygen consumption it also reduces oxygen demand and it is suitable for patients with myocardial ischaemia. [Pg.65]

Etomidate, when administered as the sole agent, produces little effect on cardiovascular function. It produces a slight reduction in systemic pressure and an increase in heart rate. Myocardial oxygen consumption is not significantly affected by etomidate. The drug does not release histamine and can be safely used in the presence of cardiorespiratory disease. [Pg.87]

Intracoronary, intravenous, or sublingual nitrate administration consistently increases the caliber of the large epicardial coronary arteries except where blocked by concentric atheromas. Coronary arteriolar resistance tends to decrease, though to a lesser extent. However, nitrates administered by the usual systemic routes may decrease overall coronary blood flow (and myocardial oxygen consumption) if cardiac output is reduced due to decreased venous return. The reduction in oxygen consumption is the major mechanism for the relief of effort angina. [Pg.258]

Many substituted benzofurans show marked pharmacological activity. 2-(4-Hydroxyben-zoyl)benzofuran exhibits a relaxant effect on histamine and acetylcholine spasm. 2-Ethyl-3 -(4-hydroxy-3,5-diiodobenzyl)benzofuran has been shown to be superior to khellin as a coronary dilator. 2-Butyl-3-benzoylfuranyl 4-diethylaminoethoxy-3,5-diiodophenyl ketone, an anginal drug which causes coronary dilation, depresses myocardial oxygen consumption (74HC(29)l). [Pg.708]


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