Cardiac preload and afterload

These potent diuretic agents interact with almost the entire nephron, including Henle s loop (Fig. 7). Their primary effect is probably the inhibition of the active reabsorption of chloride ions, which then leads to the enhanced excretion of sodium ions and water. Plasma volume is reduced as a result of these effects, whereas in the long-term both cardiac preload and afterload will diminish. The metabolic side-effects of the loop diuretics are globally the same as those of the thiazides, with some incidental differences. Plasma renin activity increases by loop diuretic treatment and it can be well imagined that this effect is noxious in the long-term management of heart failure. The loop diuretics provoke a clearly... 

Furosemide Loop diuretic Decreases NaCI and KCI reabsorption in thick ascending limb of the loop of Henle in the nephron (see Chapter 15) Increased excretion of salt and water reduces cardiac preload and afterload reduces pulmonary and peripheral edema Acute and chronic heart failure severe hypertension edematous conditions Oral and IV duration 2-4 h Toxicity Hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy... 

Calcium channel blockers also cause some degree of systemic vasodilation, and some of their antianginal effects may be related to a decrease in myocardial oxygen demand caused by a decrease in cardiac preload and afterload that is, they may exert some of their... 

Calcium channel blockers can also be given to treat stable angina, especially if beta blockers are not tolerated or are contraindicated in specific patients.13 These drugs decrease cardiac workload directly by limiting calcium entry into myocardial cells and indirectly by producing peripheral vasodilation, thus decreasing cardiac preload and afterload.47 Hence, cal-... 

FIGURE 69 Nitroglycerin relaxes vascular smooth muscle of both the venous and arterial beds, resulting in a net decrease in myocardial oxygen consumption. The mechanism underlying the therapeutic actions of nitrates and nitrites may be their ability to relax vascular smooth muscle and consequently reduce cardiac preload and afterload. 

The intrinsic ability of cardiac muscle fibres to do work with a given preload and afterload. 

Mechanism of Action Adirect-acting inotropic agent acting primarily on beta,-adrenergic receptors. Therapeutic Effect Decreases preload and afterload, and enhances myocardial contractility, stroke volume, and cardiac output. Improves renal blood flow and urine output. 

Mechanism of Action A potent vasodilator used to treat emergent hypertensive conditions acts directly on arterial and venous smooth muscle. Decreases peripheral vascular resistance, preload and afterload improves cardiac output. Therapeutic Effect Dilates coronary arteries, decreases oxygen consumption, and relieves persistent chest pain. 

It has a brief duration of action. It relaxes directly arteriolar and venous smooth muscle. It decreases both preload and afterload thus both cardiac output and peripheral resistance are reduced. 

Combined arteriolar and venodilator Releases NO spontaneously activates guanylyl cyclase Marked vasodilation reduces preload and afterload Acute cardiac decompensation hypertensive emergencies (malignant hypertension) IV only duration 1-2 min. Toxicity Excessive hypotension, thiocyanate and cyanide toxicity Interactions Additive with other vasodilators... 

Promote dilation in the peripheral vasculature, which decreases the amount of blood returning to the heart (cardiac preload] and decreases the pressure the heart must pump against (cardiac afterload]... 

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. 

Vasodilators such as nitrates, ACE inhibitors, and hydralazine have been discussed previously. These agents are used to decrease arteriolar (afterload) or venous resistance (preload). A discussion of cardiodynamics is beyond the scope of this book. However, by decreasing preload and afterload these drugs decrease the work that the heart has to do to increase cardiac output this improves perfusion pressure on the arterial side and venous return on the venous side, which contributes to reduced peripheral edema. 

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. 

The hemodynamic effects of compounds supposed to affect the cardiovascular system are evaluated by measuring preload and afterload of the heart, contractility, heart rate, cardiac output and peripheral or coronary flow. To measure these cardiovascular parameters accurately, the use of larger animals such as dogs or pigs is necessary. This experimental model allows the classification of test drugs according to their action as having ... 

The workload of the heart is modified by using medication that increases or decreases preload and afterload, thereby adjusting stroke volume and cardiac output. Vasodilators decrease the preload and afterload, resulting in a decrease in blood pressure (arterial pressure) and cardiac output. Vasopressors increase the preload and afterload, causing in an increase in blood pressure cardiac output. 

Vasopressors increase the preload and afterload, resulting in an increase in blood pressure cardiac output. 

Anemia has both direct and indirect effects on left ventricular function and growth. Cardiac output increases because of a combination of increased cardiac preload and a reduction in afterload. Such changes lead to ventricular remodeling, with initial left ventricular dilation followed by subsequent hypertrophy. In ESRD other factors also contribute to LVH, including hypertension, volume expansion, and the metabolic consequences of uremia, to which maybe added the effects of diabetes. By the time patients with diabetes reach ESRD, they are more likely to have concentric LVH, more likely to have had ischemic heart disease, and more likely to have experienced cardiac failure than nondiabetic subjects. ... 

Isolated working heart preparation Perfusion of the heart ex vivo through the left atrium and ejection via the aorta resembling physiological conditions. Measurement of cardiac output. Preload and afterload can be adjusted. Other characteristics similar to Langendorff preparation. 

In a study using isolated guinea pig hearts, phthalide 20 exhibited negative chronotropic and inotropic responses and attenuated the decrease in coronary flow induced by pituitrin. This demonstrated the preload- and afterload-reducing properties of 20, which may contribute to its anti-anginal effect in vivo [305], This speculation, however, was challenged by the results in that 20 decreased the heart rate in renal hypertensive anesthetized rats [302] but its Z-isomer 22 did not affect the heart rate in normotensive conscious rats [303]. The impacts of phthalides 20 and 22 on cardiac function and angina pectoris/myocardial ischemia remain uncertain. 

In patients with elevated systemic vascular resistance and normal-to-elevated systemic blood pressure, afterload reduction with nitroprusside is logical it should be emphasized that nitroprus-side also increases venous capacitance, thereby also decreasing preload. In the context of myocardial dysfunction, afterload reduction will typically lead to improved forward cardiac output. Nitroprusside may also be effective when the systemic vascular resistance is elevated and systemic blood pressure is reduced the caveat in this more complex hemodynamic setting is that the load reduction produced by nitroprusside must be counterbalanced by an increase in stroke volume. This derivative increase in stroke volume may not occur in the patient with advanced heart failure rather, the result will be a further reduction in mean arterial pressure and the potential risk of peripheral organ hypoperfusion. An alternative approach would be the use of an inotropic-dilator drug such as milrinone, which will provide both preload and afterload reduction its concurrent positive inotropic effect may offset the reduction in mean arterial pressure that can occur from vasodilation alone. 

Treatment for heart failure focuses on decreasing volume to decrease preload and afterload and increasing cardiac function, as well as improving cardiac function. 

It provides detailed information on cardiac structure (atrial and ventricular cavity dimensions, areas, volumes, wall thickness, and mass), cardiac function (systolic and diastolic, right and left ventricular wall motion, fractional shortening and ejection fraction, global and regional, and preload and afterload), valvular disease (structure, function, and degree of regurgitation or stenosis), vascular structures, and hemodynamic data. 

The four factors that determine the cardiac output are the preload, afterload, heart rate, and myocardial contractility. The heart rate and contractility are intrinsic characteristics of the cardiac tissues per se. The preload and afterload, on the other hand, refleet the characteristics of both the heart and the vascular system. The preload and afterload influence cardiac performance, but at the same time, the magnitudes of both these factors are determined by the cardiac function and vascular characteristics. 

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