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BY : DR FARIHA RIZWAN Quantity of blood ejected by ventricle per minute. Quantity of blood ejected by left ventricle into aorta and from Rt.ventricle in pulmonary arteries is same. It is equal to venous return i.e, the amount of blood enters the right atrium per min. C.O= S.V x H.R =70 x 72 =5.5 L/min So the C.O is 5.5 L/min in male adults it is 10-20% less in young females. 1) Emotional state (anxiety, excitement) 2) Exercise ( In trained atheletes, it increases to 35 L/min). 3) Intake of meals. 4) Exposure to high environmental temp. 5) Pregnancy in later months. 6) Hyperthyroidism: Increase metabolic activity, increase oxygen consumption. 7) Anaemia 8) Injection of epinephrine Postural change: Sitting & standing from lying position. Myocardial diseases. Atrial fibrillation Complete heart block Cardiac failure CARDIAC OUTPUT Cardiac output (0) is the product of the heart rate (HR) and the stroke volume (SV) (amount of blood pumped per beat) CO=HR x SV Thus cardiac output can be increased due to a rise in either heart rate or stroke volume. During exercise in the upright position (e .g., running, cycling, etc. ),the increase in cardiac output is due to an increase in both heart rate and stroke volume. Regulation of Heart Rate During exercise, the quantity of blood pumped by the heart must change in accordance with the elevated skeletal muscle oxygen demand. Because the SA node controls heart rate, changes in heart rate often involve factors that influence the SA node. The two most prominent factors that influence heart rate are the parasympathetic and sympathetic nervous systems The parasympathetic fibers that supply the heart arise from neurons in the cardiovascular control center in the medulla oblongata and make up a portion of the vagus nerve. Upon reaching the heart,these fibers make contact with both the SA node and the AV node. When stimulated, these nerve endings release acetylcholine. It increases the permeability of K ions causes a decrease in the activity of both the SA and AV nodes due to hyperpolarization. The end result is a reduction of heart rate. Therefore the parasympathetic nervous system acts to slow down the heart rate. Studies have shown that the initial increase in heart rate during exercise, up to approximately 100 beats per minute, is due to a withdrawal of parasympathetic tone At higher work rates , stimulation of the SA and AV nodes by the sympathetic nervous system is responsible for increases in heart rate. Sympathetic fibers reach the heart by means of the cardiac accelerator nerves, which innervate both the SA node and the ventricles . Endings of these fibers release norepinephrine upon stimulation, which act on beta receptors in the heart and cause an increase in both heart rate and the force of myocardial contraction. At rest. a normal balance between parasympathetic tone and sympathetic activity to the heart is maintained by the cardiovascular control center in the medulla oblongata. For example, an increase in resting blood pressure above normal stimulates pressure receptors in the carotid arteries and the arch of the aorta, which in turn send impulses to the cardiovascular control center. In response, the cardiovascular control center increases parasympathetic activity to the heart to slow the heart rate and reduce cardiac output . This reduction in cardiac output causes blood pressure to decline back toward normal. Another regulatory reflex involves pressure receptors located in the right atrium. In this case, an increase in right atrial pressure signals the cardiovascular control center that an increase in venous return has occurred; hence, to prevent a backup of blood in the systemic venous system. The cardiovascular control center responds by sending sympathetic accelerator nerve impulses to the heart which increase heart rate and cardiac output. The end result is that the increase in cardiac output lowers right atrial pressure back to normal, and venous blood pressure is reduced. Finally, a change in body temperature can influence heart rate. An increase in body temperature above normal results in an increase in heart rate, whereas lowering of body temperature below normal causes a reduction in heart rate. Stroke volume, at rest or during exercise, is regulated by three variables ( I) the end-diastolic volume (EDV), which is the volume of blood in the ventricles at the end of diastole (2) the average aortic blood pressure; (3) the strength of ventricular contraction. EDV is often referred to as "preload," and it influences stroke volume in the following way Two physiologists, Frank and Starling, demonstrated that the strength of ventricular contraction increased with an enlargement of EDV (i.e , stretch of the ventricles) This relationship has become known as the FrankStarling law of the heart The increase in EDV results in a lengthening of cardiac fibers which improves the force of contraction in a manner similar to that seen in skeletal muscle. the influence of fiber length on cardiac contractility is that an increase in the length of cardiac fibers increases the number of myosin cross-bridge interactions with actin resulting in increased force production . A rise in cardiac contractility results in an increase in the amount of blood pumped per beat The principal variable that influences EDV is the rate of venous return to the heart. An increase in venous return results in a rise in EDV and therefore an increase in stroke volume. Increased venous return and the resulting increase in EDV play a key role in the increase in stroke volume observed during upright exercise. A second variable that affects stroke volume is the aortic pressure (mean arterial pressure) . In order to eject blood, the pressure generated by the left ventricle must exceed the pressure in the aorta. Therefore, aortic pressure or mean arterial pressure (called afterload) represents a barrier to the ejection of blood from the ventricles. Stroke volume is thus inversely proportional to the afterload; that is, an increase in aortic pressure produces a decrease in stroke volume. However, it is noteworthy that afterload is minimized during exercise due to arteriole dilation. This arteriole dilation in the working muscles reduces afterload and makes it easier for the heart to pump a large volume of blood . The final factor that influences stroke volume is the effect of circulating epinephrine norepinephrine and direct sympathetic stimulation of the heart by cardiac accelerator nerves Both of these mechanisms increase cardiac contractiIity by increasing the amount of calcium available to the myocardial cell In particular, epinephrine and norepinephrine both increase in entry of extracellular calcium into the cardiac muscle fiber. There are three principal mechanisms 1. VENOCONSTRICTION 2. MUSCLE PUMP pumping action of contracting skeletal muscle 3.RESPIRATORY PUMP (pumping action of the respiratory system) I. Venoconstriction increases venous return by reducing the volume capacity of the veins to store blood . The end result of a reduced volume capacity in veins is to move blood back toward the heart. Venoconstriction occurs via a reflex sympathetic constriction of smooth muscle in veins which is controlled by the cardiovascular control center 2. Muscle pump. is a result of the mechanical action of rhythmic skeletal muscle contractions. As muscles contracts they compress veins and push blood back toward the heart Between contractions, blood refills the veins and the process is repeated . Blood is prevented from flowing away from the heart between contractions by one-way valves located in large veins 3. Respiratory pump. The rhythmic pattern of breathing also provides a mechanical pump by which venous return is promoted During inspiration, pressure within the thorax (chest) decreases and abdominal pressure increases. This creates a flow of venous blood from the abdominal region into the thorax and therefore promotes venous return . the role of the respiratory pump is enhanced during exercise due to the greater respiratory rate recent evidence indicates that the respiratory pump is the predominant factor that promotes venous return to the heart during upright exercise. •Cardiac output is the product of heart rate and stroke volume (0 = HR X SV) The pacemaker of the heart is the SA node. SA node activity is modified by the parasympathetic nervous system (slows HR) and the sympathetic nervous system (increases HR). Heart rate increases at the beginning of exercise due to a withdrawal of parasympathetic tone. At higher work rates , the increase in heart rate is achieved via an increased sympathetic outflow to the SA nodes. Stroke volume is regulated via (I) end-diastolic volume (2) aortic blood pressure (3) the strength of ventricular contraction. Venous return increases during exercise due to (I) venoconstriction, (2) the muscle pump (3) the respiratory pump.