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Heart Failure Fundamentals

Physiology of the Heart
Now that the anatomy has been reviewed, it is time to review the normal physiological characteristics of the heart. This module contains many highlighted terms. Your degree of understanding of these terms will directly relate to the ease with which you will understand the physiologic interactions involved with heart failure and its treatment. A cardiac cycle is the contraction and relaxation of the cardiac chambers that occur with one complete heart beat. At the beginning of the cardiac cycle, venous blood has been returned to the heart via the superior and inferior vena cava to the right atrium, while the left atrium has received re-oxygenated blood from the lungs. During this phase of the cardiac cycle, the tricuspid valve (right side) and mitral valve (left side) are open which allows passive filling of both the atria and the ventricles. Passive filling of the ventricles slowly increases the pressure in the ventricles due to increased blood volume. The SA node sends out an electrical signal which spreads throughout the atria causing depolarization and atrial contraction or systole. Atrial systole, or atrial kick, pushes the blood out of the atria and forces more blood into the ventricles. At a normal heart rate, the atrial kick can increase ventricular blood volume by approximately 30%. Following atrial systole, the atria relax and begin to passively fill with blood for the next cardiac cycle. During this relaxation period also called diastole, the electrical properties of the cardiac cells of the atria repolarize or return to a normal resting state. Following atrial systole, the pressure in the ventricles is greater than that in the atria causing the mitral valve and tricuspid valve to close. At this point, all of the valves are closed and pressure continues to increase in the ventricles. The electrical signal, initiated by the SA node, has now passed through the AV node and down through the His Bundle to the Purkinje fibers. Ventricular depolarization occurs as a result of the electrical impulse activating the cellular structure of the cardiac cells and ventricular systole results. When ventricular pressure is greater than the pressure in the aorta (left side) or the pulmonary artery (right side), the aortic and pulmonary valves open. The squeeze of the ventricles forces the blood into the pulmonary and arterial vasculature. Following systole, ventricular muscle relaxes and pressure in the ventricles begin to drop. When the pressure in the ventricles is lower than that in the aorta and pulmonary artery, the aortic and pulmonary valves close and a new cardiac cycle begins. The ventricles reach their end-systolic volume when these valves close. Cardiac output refers to the amount of blood pumped out the heart as a result of the cardiac cycle. Cardiac output is measured in liters per minute and is the product of the heart rate (beats per minute) and stroke volume (amount of blood ejected with each contraction). Heart rate and stroke volume are discussed below.

Cardiac Output = Heart Rate x Stroke Volume

Heart rate (HR) is the number of times per minute the cardiac cycle occurs and is affected by many factors. These factors include exercise, activity, the sympathetic and parasympathetic nervous systems, temperature, illness, and physical conditioning. HR will increase under conditions where the bodys demand for oxygen is increased, such as during exercise. An increased HR means more oxygenated blood is being pumped and delivered to vital organs and muscles. Normally, the heart spends one third of its time in systole and the Heart Failure Fundamentals Physiology of the Heart Module #3 Page 1 Copyright 2003 St. Jude Medical Cardiac Rhythm Managment Division Previous Presentation | Next Presentation | Quiz | Back to Index

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other two-thirds in diastole. With increased heart rates, the contraction time remains nearly unchanged. However, the resting or filling time becomes shortened. Increased heart rates in a diseased heart can result in inadequate ventricular filling and an inadequate blood supply to the muscle for its oxygen demand and workload. Heart rate can also increase in patients with HF as a mechanism to compensate for reduced stroke volume. Compensatory mechanisms will be discussed further in Module Seven. Stroke volume (SV) is the amount of blood ejected with each cardiac cycle or contraction. The normal heart ejects approximately 70 cc of blood with each contraction. If the stroke volume is 70 cc and the heart is beating 72 times per minute, the Cardiac Output is (72 bpm x 70 cc) 5040 cc of blood (5 liters) of blood per minute. With exercise, where heart rates reach 150 beats Figure 1 per minute and stroke volume increases due to increased contractility, cardiac output can reach 20 liters per minute or higher (Figure 1). There are three factors that influence and control stroke volume: Preload, Afterload, and Contractility. These factors are adjusted and manipulated in the treatment of heart failure. Preload is the amount of stretch on the cardiac muscle fibers (myocytes) produced by the volume of blood in the ventricles at the end of ventricular diastole or filling. Preload depends on the volume of venous return to the heart which is influenced by the actual volume of blood within the venous system and by venous tone or compliance. Preload is measured by the End Diastolic Index or EDI. The normal range for a resting adult is 60-110 ml/m2. The Frank -Starling Mechanism The greater the stretch or volume on the myocytes, the greater the ability to generate the force of the contraction. Increased Contractility Frank-Starlings Law (Figure 2) describes this stretchstrength relationship and shows that, up to a point, the Normal cardiac output is increased in proportion to the amount of diastolic stretch of the heart muscle fibers. Heart Failure There is a limited range of stretch in which the myocytes can perform effectively. Too little volume or stretch, as in dehydration, results in poor cardiac output due to the lack of Left ventricular end-diastolic prossure (or blood volume and lack of stretch. Too much stretch or volume) volume also results in poor cardiac output. The myocytes are Figure 2 unable to return to the pre-stretched state, resulting in less forceful contractions. In order to treat heart failure, diuretics (fluid pills) are utilized to decrease the volume of blood and thus the stretch on the myocytes. This is adjusting the preload. Afterload, the second component of stroke volume, addresses the amount of resistance that the left ventricle must overcome in order to pump or eject Determinants of Ventricular Function blood. Afterload also influences the amount of Contractility blood discharged into the systemic circulation. The greater the afterload, the harder the myocardium Preload Afterload will have to pump to overcome the increased resistance. Stroke Volume Systolic blood pressure and the Synergistic LV contraction vascular properties of the arteries Heart LV wall integrity (constricted or dilated) determine what Valvular competence Rate force the heart is working against in order to pump. To control afterload in Cardiac Output Figure 3 Heart Failure Fundamentals Physiology of the Heart Module #3 Page 2 Copyright 2003 St. Jude Medical Cardiac Rhythm Managment Division Previous Presentation | Next Presentation | Quiz | Back to Index
Stoke volume (Cardiac Output)

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the treatment of heart failure, it is important to address the resistance that the heart is working against. Thus, blood pressures are kept low, arteries are dilated to decrease resistance and the hearts workload is reduced. The third factor determining stroke volume is Contractility (Figure 3 on page 2 ). Contractility refers to the ability of the heart muscle fibers to contract or shorten. The degree of filling stretch of the fibers (preload), the resistance (afterload) which the fibers must work against to eject blood, and the ability of the fibers to contract to produce the force of ejection (contractility) have been identified as the factors in determining stroke volume. A cardiac output of 5 liters may be adequate in a small person, but just marginal in a very larger person. Cardiac Index is a term used to standardize the cardiac output measurement and depends on the size of the individual. The cardiac index,used in determining adequate tissue perfusion, is determined by dividing cardiac output by body surface area. A normal cardiac index is 2.5 to 4.0 liters/min. A cardiac index of anything less than 2.5 liters/min. means that the tissues are not being perfused adequately. Ejection Fraction, a term frequently used in the evaluation of the cardiac patient, refers to the percentage of blood ejected with each contraction. The ventricles do not eject all of their blood volume during each contraction; rather, some blood is kept in reserve for times of increased demand. For this reason, a normal Ejection Fraction is 55-70%. Ejection Fraction is calculated by dividing the stroke volume by the left ventricular end diastolic volume (LVED) or preload (the volume in the ventricle at the end of diastole). In order to further understand the hearts workload it is necessary to take a more in-depth look at pressure and blood flow through the body (hemodynamics). There are multiple factors affecting blood flow: resistance, viscosity, volume, vessel diameter, and pressure. The most influential factor is pressure. Blood flows from areas of higher to lower pressure. Intracardiac Ventricular Systole (Contraction) pressures are measured through invasive catheters which are placed in the heart to determine the force of pressure, a technique known as hemodynamic monitoring. Pulmonary Capillary Wedge Pressure is obtained by wedging a small balloon catheter in a branch of the pulmonary artery, reflecting the pressure in the pulmonary capillaries. This measurement represents the pressure in the left atrium. If the mitral valve is normal, the wedge pressure at the end of diastole can be thought to be the same as left ventricular end diastolic pressure, and can be used to calculate preload or left ventricular function. Arterial pressures are measured and used to calculate cardiac workload. Systolic blood pressure (Figure 4) represents the highest pressure against the walls of the arteries at the peak of systole Ventricular Diastole (Relaxation) (contraction). Diastolic blood pressure (Figure 5) refers to the lowest Figure 4 pressure on the arteries during diastole or relaxation. One additional term used in reference to pressure is the term pulse pressure. Pulse pressure is the difference in the systolic and diastolic values. With the aging process, pulse pressures tend to increase. Rather than a pulse pressure of 40mmHg due to blood pressure of 120/80, one would find a pulse pressure of 70mmHg due to the elderly patients blood pressure of 160/90. In the setting of heart failure, the pulse pressure will decrease. The heart failure patient may present with a pulse pressure of 30mmHg due to a blood pressure of 90/60. Pulse pressure may be useful in determining the severity of heart failure. Another factor in the equation of blood flow is the resistance in the circulatory system. As vessel diameter decreases due to constriction Figure 5 Heart Failure Fundamentals Physiology of the Heart Module #3 Page 3 Copyright 2003 St. Jude Medical Cardiac Rhythm Managment Division Previous Presentation | Next Presentation | Quiz | Back to Index

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(becomes smaller) the resistance to flow inscreases. Dilatation (becoming larger) on the other hand, decreases the resistance to flow. As heart failure education continues, more discussion will follow on the vasoconstriction that occurs due to the sympathetic nervous system response that occurs in order to maintain cardiac output, a process that actually increases cardiac workload. The third component affecting blood flow is viscosity, the thickness or stickiness of the blood itself. Just as with any liquid, thick blood moves more slowly than thin blood. Slower-moving blood results in increased resistance and increased work for the heart. The viscosity is determined by the number of red blood cells (hematocrit) and plasma proteins. If the HF patient is given diuretics and too much fluid is removed, the hematocrit will elevate. This elevation indicates that the viscosity of the blood is now thick, increasing the workload of the heart. This explains why a test called a blood count is ordered on the HF patient receiving diuretics. Volume is therefore a very important factor in hemodynamics and the balance of heart failure management. An increase in volume causes the chambers of the heart or the walls of the blood vessels to stretch in order to accommodate the extra blood, and dilatation or increased pressures result. Too little volume circulating in the chambers or vessels results in constriction and an increase in resistance. Constriction is the bodys pathological attempt at keeping pressures adequate to support circulation and blood pressure. Either too large or too small a blood volume can cause added work for the heart. A basic understanding of normal cardiac anatomy and physiology will give you a basis for understanding the progression of heart failure. Next weeks module of Heart Failure Fundamentals will discuss some of the causes of HF and will describe how normal cardiac anatomy and physiology are affected by this disorder.

Reference: Jaski, Brian. Basics of Heart Failure- A Problem Solving Approach. Kluwer Academic, Boston 2000. p.25-36. Heart Failure Fundamentals Physiology of the Heart Module #3 Page 4 Copyright 2003 St. Jude Medical Cardiac Rhythm Managment Division Previous Presentation | Next Presentation | Quiz | Back to Index