Anatomy & Physiology

Anatomy & Physiology Study Guide

19.11 Hormones Epinephrine, norepinephrine, and thyroid hormone increase heart rate by their effect on the SA node. The effects of epinephrine on the SA node are similar to those of norepinephrine. Epinephrine also affects the contractile cells; after massive sympathetic stimulation of the suprarenal medullae, the myocardium may become so excitable that abnormal contractions occur. Many hormones affect the contractility of the heart. For example, epinephrine, norepinephrine, and thyroid hormones all have positive inotropic effects. Glucagon also has a positive inotropic effect. Before synthetic inotropic agents were available, glucagon was used to create cardiac function. It is still utilized in cardiac emergencies and to treat some forms of heart disease. Many of the drugs used to treat hypertension (high blood pressure) have a negative inotropic action. Beta-blocking drugs, such as propranolol, timolol, metoprolol, atenolol, and labetalol, block beta receptors, alpha receptors, or both, and prevent sympathetic stimulation of the heart. Calcium channel blockers like nifedipine or verapamil, also have a negative inotropic effect. The afterload is the amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood. The greater the afterload, the longer the period of isovolumetric contraction, the shorter the duration of ventricular ejection, and the larger the ESV. Afterload is increased by any factor that restricts blood flow through the arterial system. For example, the constriction of peripheral blood vessels or a circulatory blockage will elevate arterial blood pressure and increase the afterload. If the afterload is too great, the ventricle cannot eject blood. Such a high afterload is rare in a normal heart, but damage to the heart muscle can weaken the myocardium enough that even a modest rise in arterial blood pressure can reduce stroke volume to dangerously low levels, producing symptoms of heart failure.

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