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Venous capacitance

Nicorandil. Nicorandil is a potassium channel opener that can lower blood pressure 21, 20, and 29 mm Hg after single oral doses of 10, 20, and 30 mg, respectively (250). There are no significant changes ia heart rate. Headache is the primary side effect. Nicorandil has potent coronary vasodilator effects. It causes sustained vasodilation of arteriolar resistance and venous capacitance blood vessels, thus reduciag cardiac preload and aftedoad. [Pg.143]

The answer is d. (Hardman, pp 794-795.) Hydralazine, minoxidil, diazoxide, and sodium nitroprusside are all directly acting vasodilators used to treat hypertension. Because hydralazine, minoxidil, nifedipine, and diazoxide relax arteriolar smooth muscle more than smooth muscle in venules, the effect on venous capacitance is negligible. Sodium nitroprusside, which affects both arterioles and venules, does not increase cardiac output, a feature that enhances the utility of sodium nitroprusside in the management of hypertensive crisis associated with MI. [Pg.126]

In heart failure, cardiac output rises again because ventricular afterload diminishes due to a fall in peripheral resistance. Venous congestion abates as a result of (1) increased cardiac output and (2) reduction in venous return (decreased aldosterone secretion, decreased tonus of venous capacitance vessels). [Pg.124]

In therapeutic doses, hydralazine produces little effect on nonvascular smooth muscle or on the heart. Its pharmacological actions are largely confined to vascular smooth muscle and occur predominantly on the arterial side of the circulation venous capacitance is much less affected. Because cardiovascular reflexes and venous capacitance are not affected by hydralazine, postural hypotension is not a clinical concern. Hydralazine treatment does, however, result in an increase in cardiac output. This action is brought about by the combined effects of a reflex increase in sympathetic stimulation of the heart, an increase in plasma renin, and salt and water retention. These effects limit the hypotensive usefulness of hydralazine to such an extent that it is rarely used alone. [Pg.228]

Alpha receptors are widely expressed in vascular beds, and their activation leads to arterial and venoconstriction. Their direct effect on cardiac function is of relatively less importance. A relatively pure agonist such as phenylephrine increases peripheral arterial resistance and decreases venous capacitance. The enhanced arterial resistance usually leads to a dose-dependent rise in blood pressure (Figure 9-... [Pg.182]

The primary direct result of an effective dose of nitroglycerin is marked relaxation of veins with increased venous capacitance and decreased ventricular preload. Pulmonary vascular pressures and heart size are significantly reduced. In the absence of heart failure,... [Pg.255]

Vascular smooth muscle tone is regulated by adrenoceptors consequently, catecholamines are important in controlling peripheral vascular resistance and venous capacitance. Alpha receptors increase arterial resistance, whereas 2 receptors promote smooth muscle relaxation. There are major differences in receptor types in the various vascular beds (Table 9-4). The skin vessels have predominantly receptors and constrict in the presence of epinephrine and norepinephrine, as do the splanchnic vessels. Vessels in skeletal muscle may constrict or dilate depending on whether ffor 13 receptors are activated. Consequently, the overall effects of a sympathomimetic drug on blood vessels depend on the relative activities of that drug at and 8receptors and the anatomic sites of the vessels affected. In addition, Di receptors promote vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels. Activation of the Di receptors in the renal vasculature may play a major role in the natriuresis induced by pharmacologic administration of dopamine. [Pg.181]

With large doses, thiopental causes dose-dependent decreases in arterial blood pressure, stroke volume, and cardiac output. This is due primarily to its myocardial depressant effect and increased venous capacitance there is little change in total peripheral resistance. Thiopental is also a potent respiratory depressant, lowering the sensitivity of the medullary respiratory center to carbon dioxide. [Pg.600]

In CHF, the impaired contractile function of the heart is exacerbated by compensatory increases in both preload and afterload. Preload is the volume of blood that fills the ventricle during diastole. Elevated preload causes overfilling of the heart, which increases the workload. Afterload is the pressure that must be overcome for the heart to pump blood into the arterial system. Elevated afterload causes the heart to work harder to pump blood into the arterial system. Vasodilators are useful in reducing excessive preload and afterload. Dilation of venous blood vessels leads to a decrease in cardiac preload by increasing venous capacitance arterial dilators reduce systemic arteriolar resistance and decrease afterload. [Pg.166]

Maintenance of an adequate oxygen supply is the first priority. A systolic blood pressure of 80 mmHg can be tolerated in a young person but a level below 90 mmHg will imperil the brain or kidney of the elderly. Expansion of the venous capacitance bed is the usual cause of shock in acute poisoning and blood pressure may be restored by placing the patient in the head-down position to encourage venous return to the heart, or by the use of a colloid... [Pg.156]

Sinus tachycardia (due to vagal blockade) is a common feature but abnormalities of cardiac conduction accompany moderate to severe intoxication and may proceed to dangerous tachy- or bradyarrhythmias. Hypoterrsion may result from a combination of cardiac arrhythmia, reduced myocardial contractility and dilatation of venous capacitance vessels. [Pg.376]

Dilatation of venous capacitance vessels reduced venous return to the heart (preload) leads to reduced cardiac output, especially in the upright position... [Pg.461]

In the treatment of acute myocardial failure with associated pulmonary oedema, the objectives are to improve gas exchange, increase myocardial contractility and reduce the workload of the left ventricle. Dobutamine, a somewhat selective pi -adrenoceptor agonist, produces a pronounced inotropic effect that results in an increased cardiac output (where contractility is the limiting factor) and an elevation of arterial blood pressure. The drug preparation, following appropriate dilution, is administered by continuous intravenous infusion at a rate of 1-5 (ig/kg min. An intravenous dose (0.5 mg/kg) of furosemide (loop diuretic) increases venous capacitance by redistributing venous blood from the lungs to the peripheral circulation, which... [Pg.143]

CO is the major determinant of SBP, whereas TPR largely determines DBP. In turn, CO is a fnnction of stroke volume, heart rate, and venous capacitance. Table 13-2 lists physiologic causes of increased CO and TPR and correlates them with potential mechanisms of pathogenesis. [Pg.187]

Intravenons nitroglycerin dilates both arterioles and venous capacitance vessels, thereby reducing both cardiac afterload and preload, which can decrease myocardial oxygen demand. It also dilates collateral coronary blood vessels and improves perfusion to ischemic myocardium. These properties make intravenous nitroglycerin ideal for the management of hypertensive emergency in the presence of myocardial ischemia. Intravenous nitroglycerin is associated with tolerance when used over 24 to 48 hours and can canse severe headache. [Pg.212]

Similar to diuretics, nitrates can provide symptom-targeted therapy by acting to decrease LV volume by increasing venous capacitance. In addition, nitrates can provide disease-targeted therapy by providing anti-ischemic effects in patients with DHF owing to CAD. [Pg.363]

Direct vasodilator agents T Renal vascular resistance (hydralazine, minoxidil) Arterial vasodilation plus dilatation of venous capacitance vessels (nitroprusside) Increase in RBF and no effect on GFR Decrease in GFR and RBF (acute effect)... [Pg.809]


See other pages where Venous capacitance is mentioned: [Pg.123]    [Pg.913]    [Pg.58]    [Pg.107]    [Pg.308]    [Pg.162]    [Pg.314]    [Pg.198]    [Pg.204]    [Pg.229]    [Pg.254]    [Pg.256]    [Pg.551]    [Pg.182]    [Pg.269]    [Pg.173]    [Pg.252]    [Pg.166]    [Pg.324]    [Pg.913]    [Pg.94]    [Pg.515]    [Pg.1455]    [Pg.145]    [Pg.253]    [Pg.365]    [Pg.480]    [Pg.98]    [Pg.70]    [Pg.391]   
See also in sourсe #XX -- [ Pg.226 ]




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