Porth's Essentials of Pathophysiology, 4e

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Circulatory Function

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stroke volume. The ejection fraction, which is the stroke volume divided by the end-diastolic volume, represents the fraction or percentage of the diastolic volume that is ejected from the heart during systole. One of the signs of heart failure is a decrease in the ejection fraction, which reflects the diminished function of the left ventricle. Atrial Filling and Contraction Because there are no valves between the junctions of the central veins (i.e., venae cavae and pulmonary veins) and the atria, atrial filling occurs during both systole and diastole. During normal quiet breathing, right atrial pressure usually varies between −2 and +2 mm Hg. It is this low atrial pressure that maintains the movement of blood from the systemic veins into the right atrium and from the pulmonary veins into the left atrium. Three main atrial pressure waves occur during the car- diac cycle (see Fig. 17-15). The first, or c wave, occurs as the ventricles begin to contract and their increased pres- sure causes the AV valves to bulge into the atria. The sec- ond, or v wave, occurs toward the end of systole when the AV valves are still closed and results from a slow buildup of blood in the atria. The third, or a wave, occurs during the last part of diastole and is caused by atrial contrac- tion. The right atrial pressure waves are transmitted to the internal jugular veins as pulsations. These pulsations can be observed visually and may be used to assess car- diac function. For example, exaggerated a waves occur when the volume of the right atrium is increased because of impaired emptying into the right ventricle. Right atrial pressure and filling is regulated by a balance between the ability of the right ventricle to move blood out of the right heart and the pressures that move blood from the venous circulation into the right atrium (venous return). When the heart pumps strongly, right atrial pres- sure is decreased and atrial filling is enhanced. Right atrial pressure is also affected by changes in intrathoracic pres- sure. It is decreased during inspiration when intrathoracic pressure becomes more negative, and it is increased dur- ing coughing or forced expiration when intrathoracic and right atrial pressures become more positive. Although the main function of the atria is to store blood as it enters the heart, these chambers also act as pumps that aid in ventricular filling. Atrial contraction occurs during the last third of diastole. Atrial contraction becomes more important during periods of increased activity when the diastolic filling time is decreased because of an increase in heart rate or when heart dis- ease impairs ventricular filling. In these two situations, the cardiac output would fall drastically were it not for the action of the atria. It has been estimated that atrial contraction can contribute as much as 30% to cardiac reserve during periods of increased need, while having little or no effect on cardiac output during rest. Regulation of Cardiac Performance The efficiency and work of the heart as a pump often is measured in terms of cardiac output or the amount of blood the heart pumps each minute. The cardiac output

(CO) is the product of the stroke volume (SV) or amount of blood that the heart ejects with each beat and the heart rate (HR) or number of times the heart beats each minute (i.e., CO = SV x HR). The cardiac output varies with body size and the metabolic needs of the tissues. It increases with physical activity and decreases during rest and sleep. The average cardiac output in normal adults ranges from 3.5 to 8.0 L/minute. In the highly trained athlete, this value can increase to levels as high as 32 L/minute during maximum exercise. The cardiac reserve refers to the maximum percent- age of increase in cardiac output that can be achieved above the normal resting level. The normal young adult has a cardiac reserve of approximately 300% to 400%. Cardiac performance is influenced by the work demands of the heart and the ability of the coronary circulation to meet its metabolic needs. The heart’s ability to increase its output according to body needs mainly depends on four factors: the preload or ventricular filling, the after- load or resistance to ejection of blood from the heart, cardiac contractility , and the heart rate . Heart rate and cardiac contractility are strictly cardiac factors, meaning they originate in the heart, although they are controlled by various neural and humoral mechanisms. Preload and afterload, on the other hand, are mutually depen- dent on the behavior of both the heart and blood vessels. Preload The preload represents the volume work of the heart. It is called the preload because it is the work or load imposed on the heart before the contraction begins. It is the amount of blood that the heart must pump with each beat and represents the volume of blood stretching the ventricular muscle fibers at the end of diastole (i.e., end-diastolic volume). It is determined by the amount of the blood that remains in the ventricle at the end of systole (end-systolic volume) plus the amount of venous blood returning to the heart during diastole. The increased force of contraction that accompa- nies an increase in ventricular end-diastolic volume is referred to as the Frank-Starling mechanism or Starling law of the heart (Fig. 17-16). The anatomic arrange- ment of the actin and myosin filaments in the myocar- dial muscle fibers is such that the tension or force of contraction is greatest when the muscle fibers are opti- mally stretched just before the heart begins to contract. The maximum force of contraction and cardiac output is achieved when the muscle fibers are stretched about two and one-half times their normal resting length. When the muscle fibers are stretched to this degree, there is optimal overlap of the actin and myosin fila- ments needed for maximal contraction. The Frank-Starling mechanism allows the heart to adjust its pumping ability to accommodate various levels of venous return. Cardiac output is less when decreased filling causes excessive overlap of the actin and myosin filaments or when excessive filling causes the filaments to be pulled too far apart. The Frank-Starling mecha- nism also plays an important role in balancing the out- put of the two ventricles.