Cardiac output exercise effects

Mechanism of Action An antihypertensive that possesses nonselective beta-blocking and alpha-adrenergic blocking activity. Causes vasodilation. Therapeutic Effect Reduces cardiac output, exercise-induced tachycardia, and reflex orthostatic tachycardia reduces peripheral vascular resistance. 

Carvedilol (1) reduces cardiac output, (2) reduces exercise- or isoproterenol-induced tachycardia, and (3) reduces reflex orthostatic tachycardia. Significant -blocking effect is usually seen within 1 hour of drug administration. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

The hemodynamic effects of sotalol are related to its 3-adrenoceptor antagonist activity. Accordingly, decreases in resting heart rate and in exercise-induced tachycardia are seen in patients receiving sotalol. A modest reduction in systolic pressure and in cardiac output may occur. The reduction in cardiac output is a consequence of lowering the heart rate, since stroke volume is unaffected by sotalol treatment. In patients with normal ventricular function, cardiac output is maintained despite the decrease in heart rate because of the simultaneous increase in the stroke volume. 

Mechanism of Action AnACE inhibitor that suppresses the renin-angiotensin-aldos-terone system and prevents conversion of angiotensin I to angiotensin 11, a potent vasoconstrictor may also inhibit angiotensin II at local vascular and renal sites. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion. Therapeutic Effect Reduces peripheral arterial resistance, pulmonary capillary wedge pressure improves cardiac output and exercise tolerance. Pharmacokinetics ... 

Clinical effects In HF patients, digoxin has been proven to reduce symptoms, improve NYHA class, increase exercise time, modestly increase LVEE enhance cardiac output, and decrease HF hospitalizations (56,57). The Randomized Assessment of Digoxin on Inhibitors of the Angiotensin-Converting Enzyme (RADIANCE) (58) and Prospective Randomized study Of Ventricular Failure and the Efficacy of Digoxin (PROVED) (59) trials demonstrated that these beneficial effects are lost when digoxin is withdrawn from the medical therapy. Digoxin withdrawal has been associated... 

Clinical benefits and effects on mortality and hospitalization Whether used alone or in combination, hydralazine and isosorbide dinitrate decrease the preload and afterload, decrease mitral regurgitation, improve cardiac output, increase exercise capacity, modestly increase LVEF and prolong survival in patients with HF (63,64). V-Heart Failure Trial (HeFT) II (64) showed that enalapril had a major benefit on survival when compared with the combination of hydralazine-isosorbide dinitrate with enalapril in patients with predominantly NYHA class ll-lll. The African Americans in Heart Failure Trial (A-HeFT) (65) showed a beneficial effect of adding vasodilator therapy to African-American patients already treated with ACE inhibitors, (3 blockers, and spironolactone. There are no results with the same strategy in other patient groups. 

Heart failure is due to defects in cardiac contractility (the vigor of heart muscle), leading to inadequate cardiac output. Signs and symptoms include decreased exercise tolerance and muscle fatigue, coupled with the results of compensatory responses (neural and humoral) evoked by decreases in mean BP. Increased SANS activity leads to tachycardia, increased arteriolar tone T afterload, 4- output, 4 renal perfusion), and increased venous tone (T preload, T fiber stretch). Activation of the renin-angiotensin system results in edema, dyspnea, and pulmonary congestion. Intrinsic compensation results in myocardial hypertrophy. These effects are summarized in Figure IH-4-1. 

Intravenous diuretics, particularly furosemide and ethacrynic acid, effectively mobilize liquid from the lungs. The dual mode of action (i.e., initial venodilation and subsequent diuresis) results in effective reduction of venous return however, caution must be exercised in patients with low cardiac output because a further reduction may precipitate shock even after the pulmonary edema has subsided. 

The major hemodynamic effect of nadolol is a decrease in sinus node frequency causing a reduction in the heart rate and cardiac output, and the said effects are more pronounced during exercise. Nadolol decreases sinoatrial impulse formation but does not impair atrial conduction or that of accessory pathways. Similar to propranolol, nadolol causes a mild increase in plasma volume. 

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