Anatomy & Physiology I and II

the SA node produces more rapid depolarization and an increase in the heart rate. The EDV The EDV is the amount of blood a ventricle contains at the end of diastole, just before a contraction begins. This volume is affected by two factors: the filling time and the venous return. Filling time is the span of ventricular diastole. As such, it depends entirely on the heart rate: The faster the heart rate, the shorter is the available filling time. Venous return is the rate of blood flow over this period. The ESV After the ventricle contracts, the amount of blood that remains in the ventricle at the end of ventricular systole is the ESV. Three factors that influence the ESV are the preload, the contractility of the ventricle, and the afterload. Contractility Contractility is the amount of force produced during a contraction, at a given preload. Under normal circumstances, contractility can be altered by autonomic innervation or circulating hormones. Under special circumstances, contractility can be altered by drugs or as a result of abnormal ion concentrations in the extracellular fluid. Factors that increase contractility are said to have a positive inotropic action ; those that decrease contractility have a negative inotropic action . Positive inotropic agents typically stimulate Ca 2+ entry into cardiac muscle cells, thus increasing the force and duration of ventricular contractions. Negative inotropic agents may block Ca 2+ movement or depress cardiac muscle metabolism. Positive and negative inotropic factors include ANS activity, hormones, and changes in extracellular ion concentrations.

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

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