Stroke Volume and Cardiac Output

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. 

During exercise when sympathetic stimulation to the heart is increased, the ejection fraction may increase to more than 80% resulting in greater stroke volume and cardiac output. 

Nitrates (e.g., ISDN) and hydralazine were combined originally in the treatment of HF because of their complementary hemodynamic actions. Nitrates are primarily venodilators, producing reductions in preload. Hydralazine is a direct vasodilator that acts predominantly on arterial smooth muscle to reduce systemic vascular resistance (SVR) and increase stroke volume and cardiac output. Evidence also suggests that the combination may provide additional benefits by interfering with the biochemical processes associated with HF progression. 

During IV administration, milrinone increases stroke volume (and cardiac output) with little change in heart rate. It also decreases PAOP by venodilation and thus is particularly useful in patients with a low cardiac index and an elevated LV filling pressure. However, this decrease in preload can be hazardous for patients without excessive filling pressure, leading to a decrease in cardiac index. 

Venous tone regulates the volume of blood returned to the heart, hence, stroke volume and cardiac output. The luminal diameter of the arterial vasculature determines peripheral resistance. 

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. 

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. 

The distribution of blood within the circulation is a function of vascular caliber. Venous tone regulates the volume of blood returned to the heart and, hence, stroke volume and cardiac output. The luminal diameter of the arterial vasculature determines peripheral resistance. Cardiac output and peripheral resistance are prime determinants of arterial blood pressure (p.324). 

Cardiovascular effects. Anaesthetic concentrations of isoflurane, i.e. 1-1.5 MAC, cause only a slight impairment of myocardial contractility and stroke volume and cardiac output is usually maintained... 

Injection into the left ventricle or the proximal aorta is likely to produce more marked effects. Cardiac rate, stroke volume, and cardiac output increase. There is a rise in right and left atrial pressures and left ventricular end-diastolic pressure. The pulmonary arterial pressure is also increased. The blood volume expands and peripheral blood flow increases and then decreases as systemic resistance falls. The hematocrit falls and venous pressure gradually rises. As the systemic arterial pressure falls, the heart rate increases. These responses are largely due to the injection of strongly hypertonic solutions, which promote a rapid expansion of the plasma volume water shifts from the extravascular fluid spaces to the blood and moves out of the erythrocytes, which shrink and become crenated. Blood viscosity rises, but plasma viscosity does not increase significantly. The erythrocytes give up potassium to the plasma and this might contribute to the observed reduction in peripheral vascular resistance. 

The hemodynamic effects of ritodrine have been assessed in 12 fetuses by cardiac and extracardiac Doppler sonography (1). Ritodrine significantly increased maternal and fetal heart rates, left cardiac stroke volume, and cardiac output. There was also an increase in the pulsatility index of the middle cerebral artery and a fall in the pulsatility index of the umbilical artery during ritodrine infusion. The authors suggested that ritodrine vasodilates fetal vessels in the placenta. 

Propane has been shown to have adverse effects on the cardiovascular system in the primate, dog, cat, and mouse. Guinea pigs exposed to 2.2-5.5% of the gas showed sniffing and chewing movements. In dogs, 1% caused hemodynamic changes, whereas 3.3% produced decreases in aortic pressure, stroke volume, and cardiac output and an increase in pulmonary resistance. Ten percent propane in the mouse and 15% in the dog did not produce arrhythmia but did produce weak cardiac sensitization. 

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. 

Activation of the SNS, the RAA system, AVP, and other mediators all cause vasoconstriction and increased SVR. In patients with heart failure, stroke volume varies inversely with SVR such that an increase in peripheral resistance leads to a severe decline in stroke volume and cardiac output (see Fig. 14—1). 

Hypertrophic cardiomyopathy (HCM) is a prototype for DHF The grossly thickened myocardium, structural changes, and interstitial fibrosis severely alter the passive elastic properties of the myocardium. Patients with HCM and LV outflow obstruction are sensitive to small changes in volume such that a small decrease in filling pressure can lead to a decrease in LV end-diastolic volume and a dramatic fall in stroke volume and cardiac output. 

The treatment of restrictive cardiomyopathy is complex becanse of the heterogeneity of the pathophysiologic abnormalities. Dinretics are used for the symptoms of venous congestion in the presence of restrictive cardiomyopathy, but caution is advised because these patients require high filling pressures to maintain an adequate stroke volume and cardiac output. Hypotension and hypoperfusion may occur as a result of the excessive use of diuretics. Because systolic function is often normal, digoxin is of little benefit and may be proarrhyth-... 

The decrease in blood pressure produced by the drug stimulates adrenergic activity and a concurrent increase in renin and angiotensin II. This promotes an increase in aldosterone and corresponding increase in sodium and water retention, which is not compensated for by an increase in GFR. These effects, together with the increase in stroke volume and cardiac output produced by the drug, tend to attenuate the hypotensive effects of the drug, with time. 

ACE inhibitors are more potent arterial than venous dilators. In response to ACE inhibition, mean arterial pressure (MAP) may decrease or be unchanged the change in MAP will be determined by the stroke volume response to afterload reduction. Heart rate typically is unchanged, even when there is a decrease in systemic arterial pressure, a response that hkely refiects a decrease in sympathetic tone in response to ACE inhibition. The decrease in left ventricular afterload results in increased stroke volume and cardiac output. Venodilation results in decreases in right and left heart filling pressures and end-diastolic volumes. 

A study found no pharmacokinetic interaction between nifedipine and famotidine, but the famotidine reversed the effects of nifedipine on systolic time intervals and significantly reduced the stroke volume and cardiac output. No adverse interaction was seen in 22 patients given calcium-channel blockers, including nifedipine, with famotidine for 6 to 8 weeks. ... 

Nitroxyl (HNO) donors and sodium nitroprusside (NaNP) decrease stroke volume and cardiac output in normals but increase both in heart failure patients (del Rio et al., 2014). They decrease dLYP/dt j but contractility is unchanged in normals but dLYP/dt is unchanged when heart failure is present. Studies of HNO donors conducted in normals would completely miss the therapeutic benefit that is demonstrated clearly in heart failure. 

The cardiac wall becomes thinner and weaker, with decreased stroke volume and cardiac output, resulting in decreased tissue perfusion, including the kidneys. 

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