Anatomy and Physiology of Heart1

After fertilization the heart begins develop from mesoderm on 18 or 19 day. In the head end of the embryo, the heart develops from a group of mesodermal cells called the cardiogenic area. In response to signals from the underlying endoderm, the mesoderm in the cardiogenic area forms a pair of elongated strands called cardiogenic cords. Shortly after, these cords develop a hollow center and then become known as endocardial tubes. With lateral folding of the embryo, the paired endocardial tubes approach each other and fuse into a single tube called the primitive heart tube on day 21 following fertilization (Fig. 1.1). On 22 day the primitive heart tube develops into five distinct regions and begins to pump blood. From tail end to head end (the direction of blood flow) they are:

The remnant of the foramen ovale is the fossa ovalis. Formation of the interventricular septum partitions the ventricular region into a right ventricle and a left ventricle. Partitioning of the atrioventricular canal, atrial region, and ventricular region is basically complete by the end of the fifth week. The atrioventricular valves form between the fifth and eighth weeks. The semilunar valves form between the fifth and ninth weeks.

Heart is a roughly cone shaped hollow muscular organ. It measures about 12 cm in length, 8 to 9 cm in breadth at the broadest part, and 6 cm in thickness. Its weights is 280 to 340 g in male and 230 to 280 g in female.

The heart wall is composed mainly of a muscular layer, the myocardium. The epicardium and the pericardium cover the external surface. Internally, the endocardium covers the surface (Fig. 1.3).

The epicardium is a layer of mesothelial cells that forms the visceral or heart layer of the serous pericardium. Branches of the coronary blood and lymph vessels, nerves, and fat are enclosed in the epicardium and the superficial layers of the myocardium.

This continuous membrane thus forms the pericardial sac and encloses a potential space, the pericardial cavity. The serous parietal pericardium lines the inner surface of the thicker, tougher fibrous pericardial membrane. The pericardial membrane extends beyond the serous pericardium and is attached by ligaments and loose connections to the sternum, diaphragm, and structures in the posterior mediastinum.

The myocardial layer is composed of cardiac muscle (Fig. 1.4) cells interspersed with connective tissue and small blood vessels. Some atrial and ventricular myocardial fibers are anchored to the fibrous skeleton. The thin-walled atria are composed of two major muscle systems—one that surrounds both of the atria, and another that is arranged at right angles to the first and that is separate for each atrium.

The endocardium is composed of a layer of endothelial cells and a few layers of collagen and elastic fibers. The endocardium is in continuation with the tunica intima of the blood vessels.

The heart has four chambers. The two superior receiving chambers are the atria and the two inferior pumping chambers are the ventricles. On the anterior surface of each atrium is a wrinkled pouchlike structure called an auricle, so named because of its resemblance to a dog's ear. Each auricle slightly increases the capacity of an atrium so that it can hold a series of grooves, called sulci, that contain coronary blood vessels and a variable amount of fat. Each sulcus marks the external boundary between two chambers of the heart. The deep coronary sulcus encircles most of the heart and marks the external boundary between the superior atria and inferior ventricles. The anterior interventricular sulcus is a shallow groove on the anterior surface of the heart that marks the external boundary between the right and left ventricles. This sulcus continues around to the posterior surface of the heart as the posterior interventricular sulcus, which marks the external boundary between the ventricles on the posterior aspect of the heart.

The right atrium forms the right border of the heart and receives blood from three veins—the superior vena cava, inferior vena cava, and coronary sinus (veins always return blood to the heart). The right atrium is about 2–3 mm (0.08–0.12 in.) in average thickness. The anterior and posterior walls of the right atrium are very different. The posterior wall is smooth; the anterior wall is rough due to the presence of muscular ridges called pectinate muscles which also extend into the auricle. Between the right atrium and left atrium is a thin partition called the interatrial septum. A prominent feature of this septum is an oval depression called the fossa ovalis, the remnant of the foramen ovale, an opening in the interatrial septum of the fetal heart that normally closes soon after. Blood passes from the right atrium into the right ventricle through a valve that is called the tricuspid valve because it consists of three leaflets or cusps. It is also called the right atrioventricular valve. The valves of the heart are composed of dense connective tissue covered by endocardium.

The right ventricle is about 4-5 mm (0.16-0.2 in.) in average thickness and forms most of the anterior surface of the heart. The inside of the right ventricle contains a series of ridges formed by raised bundles of cardiac muscle fibers called trabeculae carneae. Some of the trabeculae carneae convey part of the conduction system of the heart. The cusps of the tricuspid valve are connected to tendonlike cords, the chordae tendineae which in turn are connected to cone shaped trabeculae carneae called papillary muscles. Internally, the right ventricle is separated from the left ventricle by a partition called the interventricular septum. Blood passes from the right ventricle through the pulmonary valve (pulmonary semilunar valve) into a large artery called the pulmonary trunk, which divides into right and left pulmonary arteries. Arteries always take blood away from the heart.

The left atrium is about the same thickness as the right atrium and forms most of the base of the heart. It receives blood from the lungs through four pulmonary veins. Like the right atrium, the inside of the left atrium has a smooth posterior wall. 8Because pectinate muscles are confined to the auricle of the left atrium, the anterior wall of the left atrium also is smooth. Blood passes from the left atrium into the left ventricle through the bicuspid (mitral) valve, which, as its name implies, has two cusps. The term mitral refers to the resemblance of the bicuspid valve to a bishop's miter (hat), which is two-sided. It is also called the left atrioventricular valve.

The left ventricle is the thickest chamber of the heart, averaging 10–15 mm (0.4–0.6 in.) and forms the apex of the heart. Like the right ventricle, the left ventricle contains trabeculae carneae and has chordae tendinae that anchor the cusps of the bicuspid valve to papillary muscles. Blood passes from the left ventricle through the aortic valve (aortic semilunar valve) into the ascending aorta. Some of the blood in the aorta flows into the coronary arteries, which branch from the ascending aorta and carry blood to the heart wall. The remainder of the blood passes into the arch of the aorta and descending aorta (thoracic aorta and abdominal aorta). Branches of the arch of the aorta and descending aorta carry blood throughout the body.

The tricuspid and bicuspid (mitral) valve (Fig. 1.7) complexes are composed of six components that function as a unit—the atria, the valve rings or annuli fibrosi of the fibrous skeleton, the valve cusps or leaflets, the chordae tendineae, the papillary muscles, and the ventricular walls. The mitral and tricuspid valve cusps are composed of fibrous connective tissue covered by endothelium. They attach to the fibrous skeleton valve rings. Fibrous cords called chordae tendineae connect the free valve margins and ventricular surfaces of the valve cusps to papillary muscles and ventricular walls. The papillary muscles are trabeculae carneae muscle bundles oriented parallel to the ventricular walls, extending from the walls to the chordae tendineae. The chordae tendineae provide many cross-connections from one papillary muscle to two valve cusps or from trabeculae carneae in the ventricular wall directly to valves.

Two coronary arteries, the right and left coronary arteries, branch from the ascending aorta and supply oxygenated blood to the myocardium (Figs 1.9 and 1.10).

The left main coronary artery arises from the aorta in the ostium behind the left cusp of the aortic valve. This artery passes between the left atrial appendage and the pulmonary artery and then typically divides into two major branches: the left anterior descending artery and the left circumflex artery.

The left anterior descending artery supplies portions of the left and right ventricular myocardium and much of the interventricular septum. The left anterior descending artery appears to be a continuation of the left main coronary artery. It passes to the left of the pulmonic valve region, courses in the anterior interventricular sulcus to the apex, then courses around the apex to terminate in the inferior portion of the posterior interventricular sulcus. Occasionally, the posterior descending branch of the right coronary artery extends around the apex from the posterior surface; the left anterior descending artery ends short of the apex.

The first diagonal branch is usually a large artery. It originates close to the bifurcation of the left main coronary artery and passes diagonally over the free wall of the left ventricle. It perfuses the high lateral portion of the left ventricular free wall.

Several smaller diagonal branches may exit from the left side of the left anterior descending artery and run parallel to the first diagonal branch. The one referred to as the second diagonal branch takes its origin approximately two-thirds of the way from the origin to the termination of the left anterior descending artery. This second diagonal branch perfuses the lower lateral portion of the free wall to the apex.

A variable number of septal branches occur. The first septal branch is the first to exit the left anterior descending artery. The others are referred to as minor septal branches. The septal branches exit at a 90 degree angle and course in the septum from the front to the back and caudally. Together, the septal branches perfuse two-thirds of the upper portion of the septum and most of the inferior portion of the septum. The remaining superoposterior section of the septum is supplied by branches from the posterior descending artery, which usually derives from the right coronary artery.

One or more right ventricular branches may exist. One runs toward the conus branch of the right coronary artery and may anastomose into the circle of Vieussens.

The final branches are the apical branches. These perfuse the anterior and diaphragmatic aspects of the left ventricular free wall and apex.

The circumflex artery supplies blood to parts of the left atrium and left ventricle. In 45% of cases, it supplies the major perfusion of the sinus node; in 10% of cases, it supplies the AV node. The circumflex artery exits from the left main coronary artery at a near right angle and courses posteriorly in the AV groove toward, but usually not reaching, the crux. If the circumflex reaches the crux, it gives rise to the posterior descending artery. In the 15% of cases in which this occurs, the left coronary artery supplies the entire septum and possibly the AV node. The branches of the circumflex artery, in order of origin, are as follows:

The atrial circumflex branch is usually small in caliber but may be as wide as the remaining portion of the circumflex. It runs along the left AV groove and perfuses the left atrial wall.

In 45% of cases, the sinus node artery originates from the initial portion of the circumflex; it runs cranially and dorsally, to the base of the superior vena cava in the region of the sinus node. This artery perfuses portions of the left and right atria as well as the sinus node.

From one to four obtuse marginal branches may be seen. These vary greatly in size. They run along the ventricular wall laterally and posteriorly, toward the apex, along the obtuse margin of the heart. The marginal branches supply the obtuse margin of the heart and the adjacent posterior wall of the left ventricle above the diaphragmatic surface.

The posterolateral branches arise from the circumflex artery in 80% of cases. These branches originate in the terminal portion of the circumflex artery and course caudally and to the left on the posterior left ventricular wall, supplying the posterior and diaphragmatic wall of the left ventricle.

The right coronary artery supplies the right atrium, right ventricle, and a portion of the posterior and inferior surfaces of the left ventricle. It supplies the AV node and bundle of His in 90% of hearts, and the sinus node in 55% of hearts. It originates behind the right aortic cusp and passes behind the pulmonary artery, coursing in the right AV groove laterally to the right margin of the heart and then posteriorly. The major branches of the right coronary artery, in order of origin, are as follows:

The conus branch is small and exits within the first 2 cm of the right coronary artery in 60% of cases. It sometimes originates as a separate vessel with an ostium within a millimeter of the right coronary artery. The branch proceeds centrally to the left of the pulmonic valve. It supplies the upper part of the right ventricle, near the outflow tract at the level of the pulmonic valve. When the conus branch anastomoses with a right ventricular branch of the left anterior descending artery, the resulting structure is called the circle of Vieussens, an important collateral link between left and right coronary arteries.

The sinus node artery arises from the right coronary artery in 55% of cases. It proceeds in the opposite direction from the conus branch, coursing cranially and to the right, encircling the superior vena cava. It usually has two branches–one supplies the sinus node and parts of the right atrium, and the other branches to the left atrium.

Right ventricular branch arises from the right coronary artery courses along the AV groove and supplies ventricular wall.

The right atrial branch proceeds cranially toward the right heart border and perfuses the right atrium.

The acute marginal branch is a fairly large branch of the right coronary artery. It originates at the acute margin of the heart near the right atrial artery and courses in the opposite direction, toward the apex. It perfuses the inferior and diaphragmatic surfaces of the right ventricle and occasionally the posterior apical portion of the interventricular septum.

The AV nodal branch is slender and straight. It originates at the crux and is directed inward toward the center of the heart. It perfuses the AV node and the lower portion of the interatrial septum.

The posterior descending branch is an important branch of the right coronary artery. It supplies the posterosuperior portion of the interventricular septum. It exits at the crux and courses in the posterior interventricular sulcus.

The left ventricular branch originates just beyond the crux. It runs centrally in the angle formed by the left posterior AV groove and the posterior interventricular sulcus. It perfuses the diaphragmatic aspect of the left ventricle.

A left atrial branch may course along the posterior left AV groove and perfuse the left atrium.

After blood passes through the arteries of the coronary circulation, it flows into capillaries, where it delivers oxygen and nutrients to the heart muscle and collects carbon dioxide and waste, and then moves into coronary veins. Most of the deoxygenated blood from the myocardium drains into a large vascular sinus in the coronary sulcus on the posterior surface of the heart; called vascular sinus. It is a thin walled vein that has no smooth muscle to alter its diameter. The deoxygenated blood in the coronary sinus empties into the right atrium. The principle tributaries carrying blood into the coronary sinuses are the following:

The resting coronary blood flow in the human being averages about 225 mL/min, which is about 4 to 5 percent of the total cardiac output. During strenuous exercise, the heart in the young adult increases its cardiac output fourfold to sevenfold, and it pumps this blood against a higher than normal arterial pressure. Consequently, the work output of the heart under severe conditions may increase sixfold to ninefold. At the same time, the coronary blood flow increases threefold to fourfold to supply the extra nutrients needed by the heart. This increase is not as much as the increase in workload, which means that the ratio of energy expenditure by the heart to coronary blood flow increases. Thus, the “efficiency” of cardiac utilization of energy increases to make-up for the relative deficiency of coronary blood supply.

Blood flow through the coronary system is regulated mostly by local arteriolar vasodilation in response to cardiac muscle need for nutrition. That is, whenever the vigor of cardiac contraction is increased, regardless of cause, the rate of coronary blood flow also increases. Conversely, decreased heart activity is accompanied by decreased coronary flow. This local regulation of coronary blood flow is almost identical to that occurring in many other tissues of the body, especially in the skeletal muscles all over the body.

Blood flow in the coronaries usually is regulated almost exactly in proportion to the need of the cardiac musculature for oxygen. Normally, about 70 percent of the oxygen in the coronary arterial blood is removed as the blood flows through the heart muscle. Because not much oxygen is left, very little additional oxygen can be supplied to the heart musculature unless the coronary blood flow increases. Fortunately, the coronary blood flow does increase almost in direct proportion to any additional metabolic consumption of oxygen by the heart. However, the exact means by which increased oxygen consumption causes coronary dilation has not been determined. It is speculated by many research workers that a decrease in the oxygen concentration in the heart causes vasodilator substances to be released from the muscle cells and that these dilate the arterioles.

Stimulation of the autonomic nerves to the heart can affect coronary blood flow both directly and indirectly. The direct effects result from action of the neurotransmitter substances acetylcholine from the vagus nerves and norepinephrine and epinephrine from the sympathetic nerves on the coronary vessels themselves.

The distribution of parasympathetic (vagal) nerve fibers to the ventricular coronary system is not very great. However, the acetylcholine released by parasympathetic stimulation has a direct effect to dilate the coronary arteries. There is much more extensive sympathetic innervations of the coronary vessels. The sympathetic transmitter substances norepinephrine and epinephrine can have either vascular constrictor or vascular dilator effects, depending on the presence or absence of constrictor or dilator receptors in the blood vessel walls. The constrictor receptors are called alpha receptors and the dilator receptors are called beta receptors. Both alpha and beta receptors exist in the coronary vessels. In general, the epicardial coronary vessels have a preponderance of alpha receptors, whereas the intramuscular arteries may have a preponderance of beta receptors. Therefore, sympathetic stimulation can, at least theoretically, cause slight overall coronary constriction or dilation, but usually constriction. In some people, the alpha vasoconstrictor 15effects seem to be disproportionately severe, and these people can have vasospastic myocardial ischemia during periods of excess sympathetic drive, often with resultant anginal pain. Metabolic factors—especially myocardial oxygen.

Vascular resistance is the opposition to blood flow due to friction between blood and the walls of blood vessels.

Vascular resistance depends on:

The smaller the lumen of a blood vessel, the greater its resistance to blood flow. Resistance is inversely proportional to the fourth power of the diameter (d) of the blood vessel's lumen (R=1/d⁴). The smaller the diameter of the blood vessel, the greater the resistance it offers to blood flow. For example, if the diameter of a blood vessel decreases by one-half, its resistance to blood flow increases 16 times. Vasoconstriction narrows the lumen, and vasodilation widens it. Normally, moment-to-moment fluctuations in blood flow through a given tissues are due to vasoconstriction and vasodilation of the tissue's arterioles. As arterioles dilate, resistance decreases, and blood pressure falls. As arterioles constrict, resistance increases, and blood pressure rises.

The viscosity (thickness) of blood depends mostly on the ratio of red blood cells to plasma (fluid) volume, and to a smaller extent on the concentration of proteins in plasma. The higher the blood's viscosity, the higher the resistance. Any condition that increases the viscosity of blood, such as dehydration or polycythemia (an unusually high number of red blood cells), thus increases blood pressure. A depletion of plasma proteins or red blood cells, due to anemia or hemorrhage, decreases viscosity and thus decreases blood pressure.

Resistance to blood flow through a vessel is directly proportional to the length of the blood vessel. The longer a blood vessel, the greater the resistance.

The volume of blood flowing back to the heart through the systemic veins occurs due to the pressure generated by contractions of the heart's left ventricle. The pressure difference from venules (averaging about 16 mm Hg) to the right ventricle (0 mm Hg), although small, normally is sufficient to cause venous return to the heart. If pressure increases in the right atrium or ventricle, venous return will decrease. One cause of increased pressure in the right atrium is an incompetent (leaky) tricuspid valve, which lets blood regurgitate (flow backward) as the ventricles contract. The result is decreased venous return and build-up of blood on the venous side of the systemic circulation. When you stand-up, for example, the pressure pushing blood up the veins in your lower limbs is barely enough to overcome the force of gravity pushing it back down. Besides the heart, two other mechanisms “pump” blood from the lower body back to the heart— The skeletal muscle pump, the respiratory pump.

An inherent and rhythmical electrical activity is the reason for the heart's lifelong beat. The source of this electrical activity is a network of specialized cardiac muscle fibers called autorhythmic fibers because they are self-excitable. Autorhythmic fibers repeatedly generate action potentials that trigger heart contractions. They continue to stimulate a heart to beat even after it is removed from the body for example, to be transplanted into another person and all of its nerves have been cut. Surgeons do not attempt to reattach heart nerves during heart transplant operations. For this reason, it has been said that heart surgeons are better “plumbers” than they are “electricians.” During embryonic development, only about 1% of the cardiac muscle fibers become autorhythmic fibers; these relatively rare fibers have two important functions.

The action potential initiated by the SA node travels along the conduction system and spreads out to excite the “working” atrial and ventricular muscle fibers, called contractile fibers. An action potential occurs in a contractile fiber as follows:

Unlike autorhythmic fibers, contractile fibers have a stable resting membrane potential that is close to 90 mV. When a contractile fiber is brought to threshold by an action potential from neighboring fibers, its voltage gated fast Na⁺ channels open. These sodium ion channels are referred to as “fast” because they open very rapidly in response to a threshold-level depolarization. Opening of these channels allows Na⁺ inflow because the cytosol of contractile fibers is electrically more negative than interstitial fluid and Na⁺ concentration is higher in interstitial fluid. Inflow of Na⁺ down the electrochemical gradient produces a rapid depolarization. Within a few milliseconds, the fast Na⁺ channels automatically inactivate and Na⁺ inflow decreases.

The next phase of an action potential in a contractile fiber is the plateau, a period of maintained depolarization. It is due in part to opening of voltage-gated slow Ca²⁺ channels in the sarcolemma. When these channels open, calcium ions move from the interstitial fluid (which has a higher Ca²⁺ concentration) into the cytosol. This inflow of Ca²⁺ causes even more Ca²⁺ to pour out of the sarcoplasmic reticulum into the cytosol through additional Ca²⁺ channels in the sarcoplasmic reticulum membrane. The increased Ca²⁺ concentration in the cytosol ultimately triggers contraction.

The recovery of the resting membrane potential during the repolarization phase of a cardiac action potential resembles that in other excitable cells. After a delay (which is particularly prolonged in cardiac muscle), additional voltage-gated K⁺ channels open. Outflow of K⁺ restores the negative resting membrane potential (–90 mV). At the same time, the calcium channels in the sarcolemma and the sarcoplasmic reticulum are closing, which also contributes to repolarization.

As action potentials propagate through the heart, they generate electrical currents that can be detected at the surface of the body. An electrocardiogram, abbreviated either ECG or EKG is a recording of electrical signals. The ECG is a composite record of action potentials produced by all the heart muscle fibers during each heartbeat. The instrument used to record the changes is an electrocardiograph.

The atria and ventricles depolarize and then contract at different times because the conduction system routes cardiac action potentials along a specific pathway. The term systole refers to the phase of contraction; the phase of relaxation is diastole dilation or expansion.

A single cardiac cycle includes all the events associated with one heartbeat. Thus, a cardiac cycle consists of systole and diastole of the atria plus systole and diastole of the ventricles.

In each cardiac cycle, the atria and ventricles alternately contract and relax, forcing blood from areas of higher pressure to areas of lower pressure. As a chamber of the heart contracts, blood pressure within it increases. Each ventricle expels the same volume of blood per beat, and the same pattern exists for both pumping chambers. When heart rate is 75 beats/min, a cardiac cycle lasts 0.8 sec.

During atrial systole, which lasts about 0.1 sec, the atria are contracting. At the same time, the ventricles are relaxed:

During ventricular systole, which lasts about 0.3 sec, the ventricles are contracting. At the same time, the atria are relaxed in atrial diastole.

During the relaxation period, which lasts about 0.4 sec, the atria and the ventricles are both relaxed. As the heart beats faster and faster, the relaxation period becomes shorter and shorter, whereas the durations of atrial systole and ventricular systole shorten only slightly.

Auscultation the act of listening to sounds within the body is usually done with a stethoscope. The sound of the heartbeat comes primarily from blood turbulence caused by the closing of the heart valves. Smoothly flowing blood is silent. Compare the sounds made by white water rapids or a waterfall with the silence of a smoothly flowing river. During each 23cardiac cycle, there are four heart sounds, but in a normal heart only the first and second heart sounds (S₁ and S₂) are loud enough to be heard through a stethoscope. The first sound (S₁), which can be described as a lubb sound, is louder and a bit longer than the second sound. S₁ is caused by blood turbulence associated with closure of the AV valves soon after ventricular systole begins. The second sound (S₂), which is shorter and not as loud as the first, can be described as a dupp sound. S₂ is caused by blood turbulence associated with closure of the semilunar valves at the beginning of ventricular diastole. Although S₁ and S₂ are due to blood turbulence associated with the closure of valves, they are best heard at the surface of the chest in locations that are slightly different from the locations of the valves. This is because the sound is carried by the blood flow away from the valves. Normally not loud enough to be heard, S₃ is due to blood turbulence during rapid ventricular filling, and S₄ is due to blood turbulence during atrial systole.

Although the heart has autorhythmic fibers that enable it to beat independently, its operation is governed by events occurring throughout the body. All body cells must receive a certain amount of oxygenated blood each minute to maintain health and life. When cells are metabolically active, as during exercise, they take-up even more oxygen from the blood. During rest periods, cellular metabolic need is reduced, and the workload of the heart decreases.

A healthy heart will pump out the blood that entered its chambers during the previous diastole. In other words, if more blood returns to the heart during diastole, then more blood is ejected during the next systole. At rest, the stroke volume is 50–60% of the end diastolic volume because 40–50% of the blood remains in the ventricles after each contraction (end systolic volume).

The second factor that influences stroke volume is myocardial contractility, the strength of contraction at any given preload. Substances that increase contractility are positive inotropic agents; those that decrease contractility are negative inotropic agents. Thus, for a constant preload, the stroke volume increases when a positive inotropic substance is present. Positive inotropic agents often promote Ca²⁺ inflow during cardiac action potentials, which strengthens the force of the next contraction. Stimulation of the sympathetic division of the autonomic nervous system (ANS), hormones such as epinephrine and norepinephrine, increased Ca²⁺ level in the interstitial fluid, and the drug digitalis all have positive inotropic effects. In contrast, inhibition of the sympathetic division of the ANS, anoxia, acidosis, some anesthetics, and increased K⁺ level in the interstitial fluid have negative inotropic effects. Calcium channel blockers are drugs that can have a negative inotropic effect by reducing Ca²⁺ inflow, thereby decreasing the strength of the heartbeat.

Ejection of blood from the heart begins when pressure in the right ventricle exceeds the pressure in the pulmonary trunk (about 20 mm Hg), and when the pressure in the left ventricle exceeds the pressure in the aorta (about 80 mm Hg). At that point, the higher pressure in the ventricles causes blood to push the semilunar valves open. The pressure that must be overcome before a semilunar valve can open is termed the afterload. An increase in afterload causes stroke volume to decrease, so that more blood remains in the ventricles at the end of systole. Conditions that can increase afterload include hypertension (elevated blood pressure) and narrowing of arteries by atherosclerosis.