Afterload increased

Mechanism of Action An antihypertensive that directly dilates pulmonary and systemic arterial vascular beds and inhibits platelet aggregation. Therapeutic Effect Reduces right and left ventricular afterload increases cardiac output and stroke volume. 

Increased hemodynamic load preload or afterload Increased heterogeneity Systemic neurohormones Pericardium... 

Pulmonary hypertension is a rare disorder, occurring with an approximate incidence of 1 to 2 cases per 1 milhon in the general population. With progression of the disease, right ventricular afterload increases, and the abihty to increase cardiac output with activity decreases. This progresses to right-sided heart failure and death. ... 

In addition to these direct cellular effects of Angll on cardiovascular structure, changes in cardiac preload (volume expansion owing to Na+ retention) and afterload (increased arterial blood pressure) probably contribute to cardiac hypertrophy and remodeling. Hypertension also contributes to hypertrophy and remodeling of blood vessels. 

A) Decreased heart rate Increased afterload Increased aldosterone Increased renin secretion Increased sympathetic outflow to the heart... 

Dmgs can be used to ease the workload of the heart by increasing or decreasing the preload and afterload resulting in adjusting the stroke volume and cardiac output. Vasodilators decrease the preload and afterload decreasing arterial pressure and cardiac output. Vasopressors increase the preload and afterload increasing the arterial pressure and cardiac output. 

Increase left ventricular myocardial function by decreasing afterload Increase electrical stability of the myocardium (38,51,55,69) Decrease regional ischemia following a regular program of submaximal exercise (51,55,69)... 

In the setting of a sustained loss of myocardium, a number of mechanisms aid the heart when faced with an increased hemodynamic burden and reduced CO. They include the following the Frank-Starling mechanism, tachycardia and increased afterload, and cardiac hypertrophy and remodeling (Table 3-2).5,7... 

Activation of both the RAAS and the SNS also contribute to vasoconstriction in an attempt to redistribute blood flow from peripheral organs such as the kidneys to coronary and cerebral circulation.7 However, arterial vasoconstriction leads to impaired forward ejection of blood from the heart due to an increase in afterload. This results in a decrease in CO and continued stimulation of compensatory responses, creating a vicious cycle of neurohormonal activation. 

Vasoconstriction Maintain blood pressure and perfusion in the face of reduced cardiac output Increased MV02 Increased afterload decreases stroke volume and further activates the compensatory responses... 

Higher vasopressin concentrations are linked to dilutional hyponatremia and a poor prognosis in HF. Vasopressin exerts its effects through vasopressin type la (Vla) and vasopressin type 2 (V2) receptors.5,7 Vasopressin type la stimulation leads to vasoconstriction, while actions on the V2 receptor cause free water retention through aquaporin channels in the collecting duct. Vasopressin increases preload, afterload, and myocardial oxygen demand in the failing heart. 

It has been proposed that NO mediates the myocardial depression associated with sepsis (F6, L14). NO synthesis induced by endotoxin blunts beta-adrenergic responsiveness (B2). In vivo, the use of NO synthase inhibitors led to conflicting results (M26), with a general decreased cardiac output and oxygen delivery being observed. NO synthase inhibition improved left ventricular contractility in endo-toxemic pigs but also increased ventricular afterloads, which ultimately is detrimental to cardiac function (H20). Possible sources of NO in the heart may be the vascular cells, the endothelial cells, and the cardiac myocytes (P6). 

The answer is a. (Hardman, pp 762-764.) Experimentally, nitrates dilate coronary vessels. This occurs in normal subjects, resulting in an overall increase in coronary blood flow. In arteriosclerotic coronaries, the ability to dilate is lost, and the ischemic area may actually have less blood flow under the influence of nitrates. Improvement in the ischemic conditions is the result of decreased myocardial oxygen demand because of a reduction of preload and afterload. Nitrates dilate both arteries and veins and thereby reduce the work of the heart. Should systemic blood pressure fall, a reflex tachycardia will occur. In pure coronary spasm, such as Prinzmetal s angina, the effect of increased coronary blood flow is relevant, while in severe left ventricular hypertrophy with minimal obstruction, the effect on preload and afterload becomes important. 

Again, increased afterload is non-physiological but it helps with understanding during discussion of the topic. 

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). 

Therapy of congestive heart failure. By lowering peripheral resistance, diuretics aid the heart in ejecting blood (reduction in afterload, pp. 132, 306) cardiac output and exercise tolerance are increased. Due to the increased excretion of fluid, EEV and venous return decrease (reduction in preload, p. 306). Symptoms of venous congestion, such as ankle edema and hepatic enlargement, subside. The drugs principally used are thiazides (possibly combined with K+-sparing diuretics) and loop diuretics. 

Factors determining oxygen demand. The heart muscle cell consumes the most energy to generate contractile force. O2 demand rises with an increase in (1) heart rate, (2) contraction velocity, (3) systolic wall tension ( afterload ). The latter depends on ventricular volume and the systolic pressure needed to empty the ventricle. As peripheral resistance increases, aortic pressure rises, hence the resistance against which ventricular blood is ejected. O2 demand is lowered by 3-blockers and Ca-antago-nists, as well as by nitrates (p. 308). 

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. 

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]. 

Taken together under physiological conditions the renin angiotensin system maintains volume and electrolyte homeostasis as well as the blood pressure. Under pathological conditions, like heart failure, it increases blood pressure and fluid retention, thereby enhancing pre- and afterload of the heart. 

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... 

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