Hypertension cardiac output

The pathophysiology of primary hypertension is heterogeneous, but ultimately exerts its effects through the two primary determinants of blood pressure cardiac output and peripheral resistance. 

Cardiac output is an important determinant of blood pressure. Factors which elevate cardiac output may, in theory, contribute to the development of primary hypertension. Increases in cardiac output and subsequent blood pressure may arise from factors that increase preload (fluid volume) or contractility... 

Blood pressure = Cardiac output Hypertension = Increased CO... 

P-blocker therapy was ineffective in preventing coronary heart disease, cardiovascular mortality, and all-cause mortality when compared to diuretics for elderly patients (60 years of age or greater) treated for primary hypertension. Clearly, the effects of P-blockers on blood pressure are complex and difficult to ascribe to one or two mechanisms. Rather, the varied effects of negative chronotropic and inotropic properties along with reduced renin levels (Fig. 2-3) appear to result in an overall reduction in cardiac output and/or reduction in peripheral resistance. 

Only non-selective p-blockers reduce bleeding complications in patients with known varices. Blockade of P, receptors reduces cardiac output and splanchnic blood flow. 02-Adrenergic blockade prevents p2-receptor-mediated splanchnic vasodilation while allowing unopposed a-adrenergic effects this enhances vasoconstriction of both the systemic and splanchnic vascular beds. The combination of P, and P2 effects makes the non-selective p-blockers preferable to car-dioselective agents in treating portal hypertension.1,36,41... 

It is this reduction in preload that, in some cases, is beneficial to patients experiencing heart failure or hypertension. Unlike a healthy heart, a failing heart is unable to pump all of the blood returned to it. Instead, the blood dams up and overfills the chambers of the heart. This results in congestion and increased pressures in the heart and venous system and the formation of peripheral edema. Because the failing heart is operating on the flat portion of a depressed cardiac function curve (see Figure 14.2), treatment with diuretics will relieve the congestion and edema, but have little effect on stroke volume and cardiac output. 

Hypertension (blood pressure >140/90 mmHg) may be caused by an elevation in cardiac output or excessive vasoconstriction. Diuretics are used in these patients to reduce cardiac output. Assume that the hearts of these individuals are operating on the ascending portion of the cardiac function curve. As the plasma volume is reduced in response to treatment with diuretic drugs, venous return and preload are reduced, as are ventricular filling and stroke volume, and cardiac output, thus bringing blood pressure back within the normal range. 

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. 

Decreased cardiac output Heart failure Sepsis Pulmonary hypertension Aortic stenosis (and other valvular abnormalities) Anesthetics... 

It therefore seems likely that the anti-hypertensive action of the -blocking drugs is in some way associated with the decline in peripheral resistance which had initially been elevated as a response to a reduction in cardiac output. The precise mechanism responsible for the fall in total peripheral resistance is as yet unknown. We do know however that the majority of untreated hypertensives show an excessive sympathetic response to stimulae such as stress and exercise. It has been clearly shown that the substantial rise in blood pressure experienced by hypertensive patients following exercise is prevented by 8-blocking drugs (20). It could be therefore that it is simply the blockade of surges in cardiac output and blood pressure which leads to a relaxation of the vascular bed and the... 

With advancing age, the patient with essential hypertension progressively changes his hemodynamic pattern into one of normal cardiac output with increased peripheral arteriolar constriction and, finally, later in the natural course of the disease into one of lower cardiac output and further increase in peripheral vascular resistance ). 

Because of their reflex cardiac effect, vasodilators, if used alone in the treatment of hypertension, have not been a successful therapeutic tool. However, the reflex tachycardia and increase in cardiac output can be effectively blocked by the therapeutic association with a sympathetic blocker guanethidine, reserpine, methyldopa, or clonidine. More specifically, blockade of the cardiac beta-adrenergic receptors will also prevent the cardiac response to hydralazine. Thus, the therapeutic combination of hydralazine and propranolol can be successfully employed for effective blood pressure reduction(11). 

Figure 1. Cardiac output and blood pressure response in patient with hypertension...

Calcium-channel blockers interfere with the inward movement of calcium ions through the cell membrane channels. This results in reduction of myocardial contractility (hence negative inotropes), reduction of cardiac output and arteriolar vasodilatation. The dihydropyridine group, such as nifedipine and amlodipine, which may be used in the management of hypertension, are very effective as arterial vasodilators, whereas diltiazem and verapamil are very effective in reducing atrioventricular conduction. 

Hypertension infrequently results from another disease, such as a catecholamine-secreting tumor (pheochro-mocytoma) in most cases the cause carmot be determined essential (primary) hypertension. Antihypertensive drugs are indicated when blood pressure cannot be sufficiently controlled by means of weight reduction or a low-salt diet. In principle, lowering of either cardiac output or peripheral resistance may decrease blood pressure (cf p. 306,... 

In instituting single-drug therapy (monotherapy), the following considerations apply 3-blockers (p. 92) are of value in the treatment of juvenile hypertension with tachycardia and high cardiac output however, in patients disposed to bronchospasm, even 3i-se-lective blockers are contraindicated. 

Propranolol lowers blood pressure in the majority of patients with essential hypertension. These effects can be caused by a number of possible mechanisms, including lowering cardiac output, inhibiting the release of renin, lowering sympathetic release from the central nervous system, inhibiting the release of norepinephrine from sympathetic postganglionic nerves, and others. 

Prazosin is used for treating mid-to-moderate hypertension. When using this drug, blood pressure is reduced without any significant change in indicators of cardiac function such as frequency, coronary flow, or cardiac output. Synonyms of this drug are minipress and minizide. 

Cardiac insufficiency is a very common disease. It can be defined as an inability of the heart to pump a sufficient amount of blood to supply oxygen and nutrients to organs and tissue, which leads to fatigue, shortness of breath, and edema. Cardiac insufficiency is most often caused by arterial hypertension and ischemic heart disease. It can be manifested in severe form, as a sharp decline in cardiac output with symptoms of disrupted blood flow, and in chronic form, which is manifest as heart pain. 

The molecular mechanism of diuretics acting as antihypertensive agents is not completely clear however, use of diuretics causes a significant increase in the amount of water and electrolytes excreted in urine, which leads to a reduction in the volume of extracellular fluid and plasma. This in turn leads to a reduction of cardiac output, which is the main parameter responsible for a drop in arterial blood pressure and venous blood return. Cardiac output is gradually restored, but the hypotensive effect remains, possibly because of the reduced peripheral resistance of vessels. It is also possible that diuretics somehow lower vascular activity of noradrenaline and other factors of pressure in the organism. Methods of synthesizing thiazide diuretics used for hypertension are described in the preceding chapter. Chapter 21. 

Clonidine is a selective Oj-adrenergic agonist that exhibits pronounced hypotensive action that is associated with a reduction of overall peripheral vascular resistance, decline in frequency of cardiac contraction, and reduced cardiac output. Clonidine is the drug of choice for treating various degrees of hypertension when used in combination with oral diuretics. 

Prazosin is used to treat average or moderate hypertension. Upon taking this drug, blood pressure drops without substantial changes in indicators of heart work, such as rate, coronary flow, and cardiac output. 

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