Anatomy & Physiology

Anatomy & Physiology Study Guide When considering cardiac function over time, physicians are most interested in the cardiac output (CO) , the amount of blood pumped by the left ventricle in one minute. In essence, cardiac output is an indication of the blood flow through peripheral tissues—without adequate blood flow, homeostasis cannot be maintained. The cardiac output provides a useful indication of ventricular efficiency over time. The body precisely adjusts cardiac output such that peripheral tissues receive an adequate circulatory supply under a variety of conditions. When necessary, the heart rate can increase by 250 percent, and stroke volume in a normal heart can almost double. The Atrial Reflex The atrial reflex, or Bainbridge reflex, involves adjustments in heart rate in response to an increase in the venous return. When the walls of the right atrium are stretched, the stimulation of stretch receptors in the atrial walls triggers a reflexive increase in heart rate caused by increased sympathetic activity. Thus, when the rate of venous return to the heart increases, the heart rate, and hence the cardiac output, rises as well. Venous Return In addition to its indirect effect on heart rate via the atrial reflex, venous return also has direct effects on nodal cells. When venous return increases, the atria receive more blood, and the walls are stretched. The stretching of the cells of 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.

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