Cardiac output, decreased

Hypotension is produced by sevoflurane as systemic vasodilation occurs and cardiac output decreases. Since it does not directly produce tachycardia, it is a useful alternative to consider in patients with myocardial ischemia. However, a concern for reflex-induced tachycardia remains. 

Mechanism of Action A betaj-adrenergic blocker that competitively blocks beta,-adrenergic receptors in cardiac tissue. Reduces the rate of spontaneous firing of the sinus pacemaker and delays AV conduction. Therapeutic Effect Slows heart rate, decreases cardiac output, decreases BP, and exhibits antiarrhythmic activity. Pharmacokinetics ... 

Mechanism of Action An antihypertensive that blocks betaj-adrenergic receptors at normal doses and betaj-adrenergic receptors at large doses. Predominantly blocks betaj-adrenergic receptors in cardiac tissue. Reduces aqueous humor production. Therapeutic Effect Slows sinus heart rate, decreases cardiac output, decreases blood pressure (BP), increases airway resistance, decreases intraocular pressure (lOP). Pharmacokinetics Well absorbed from the G1 tract. Protein binding unknown. Mini-mally metabolized in liver. Primarily excreted unchanged in urine. Not removed by hemodialysis. Half-life 6 hr (increased in decreased renal function). 

MecfMnism of Action An antihypertensive and antianginal agent that inhibits calcium movement across cardiacandvascular smooth-musclecell membranes. Potent peripheral vasodilator (does not depress SA or AV nodes). Therapeutic Effect Increases myocardial contractility, heart rate, and cardiac output decreases peripheral vascular resistance and BP. 

Mectianism of Action A cardiac inotropic agent that inhibits phosphodiesterase, which increases cyclic adenosine monophosphate and potentiates the delivery of calcium to myocardial contractile systems. Therapeutic Effect Relaxes vascular muscle, causing vasodilation. Increases cardiac output decreases pulmonary capillary wedge pressure and vascular resistance. 

Mechanism of Action An antianginal and antihypertensive agent that inhibits calcium ion movement across cell membranes, depressing contraction of cardiac and vascular smooth muscle. Therapeutic Effect Increases heart rate and cardiac output. Decreases systemic vascular resistance and BP. 

Mechanism of Action An antihypertensive that possesses nonselective beta-blocking. Has moderate intrinsic sympathomimetic activity. Therapeutic Effect Reduces cardiac output, decreases blood pressure (BP), increases airway resistance, and decreases myocardial ischemia severity. 

The net cardiovascular effects of moderate doses of cholinesterase inhibitors therefore consist of modest bradycardia, a fall in cardiac output, and an increased vascular resistance that result in a rise in blood pressure. (Thus, in patients with Alzheimer s disease who have hypertension, treatment with cholinesterase inhibitors requires that blood pressure be monitored to adjust antihypertensive therapy.) At high (toxic) doses of cholinesterase inhibitors, marked bradycardia occurs, cardiac output decreases significantly, and hypotension supervenes. 

Neurohumoral compensations. The body responds to the decreased cardiac pumping ability in a number of ways. In the early stages of failure, cardiac output decreases, and the delivery of oxygen and nutrients to tissues and organs is diminished. To compensate for this initial... 

Fluid retention A fall in cardiac output decreases blood flow to the kidney, prompting the release of renin, with a resulting increase in the synthesis of angiotensin II and aldosterone (see p. 181). This results in increased peripheral resistance and retention of sodium and water. Blood volume increases, and more blood is returned to the heart. If the heart is unable to pump this extra volume, venous pressure increases and peripheral edema and pulmonary edema occur (Figure 16.4). These compensatory responses increase the work of the heart and, therefore, can contribute to the further decline in cardiac function. 

However, if the ventricle is overly stretched, the effect of ventricular contraction is diminished. Q is the normal operating point to increased cardiac output. Decreased sympathetic reflexes and vascular tone cause decrease in ventricular end-diastolic pressure (B toQ). 

Rheumatic fever is now less common in developed countries, but in Hannah s youth it was an important cause of heart disease. The illness is due to infection with beta-haemolytic ( -haemolytic) streptococci, which cause a sore throat. In some young people, the bacterium induces antibody-mediated autoimmune responses, which initiate inflammatory changes in joints and heart valves, particularly in the mitral valve. Inflammation thickens and may partly fuse the cusps ofthe mitral valve, making it narrow and unable to close properly in ventricular systole. Eventually, cardiac output decreases and the ventricle begins to fail from overwork. Since blood is not pumped effectively from the left ventricle, pulmonary congestion develops. 

Q9 If the cardiac output decreases, the sympathetic nervous system is stimulated. What changes would you expect to observe in the circulation following stimulation of the sympathetic nervous system ... 

Despite the development of portosystemic collaterals, which ought to lead to a fall in portal hypertension, the hyperdynamic circulation accompanied by splanchnic vasodilation (= increased cardiac output, decreased systemic vascular resistance, hypervolaemia, systemic arteriolar vasodilation) maintains portal hypertension in both the splanchnic and systemic vascular systems. (10, 47, 87) The hyperdynamic circulation is either the cause... 

In CHF, increases cardiac output, decreases peripheral vascular resistance, B/P, pulmonary capillary wedge pressure, and heart rate. 

Halothane decreases cardiac output, decreases mean arterial pressure, and reduces atrial node firing, resulting in a decrease in heart rate. 

A) Decreased cardiac force Decreased cardiac output Decreased mean arterial blood pressure Increased systemic vascular resistance Tachycardia... 

Cardiac output decreased Harringtonine, homo Isoquinoline alkaloid 626... 

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