Layer Upon Layer

The heart’s wall is made up of three layers: the epicardium, myocardium, and endocardium. (See Layers of the heart wall.) The epicardium, the outer layer (and the visceral layer of the serous pericardium), is made up of squamous epithelial cells overlying connective tissue. The myocardium, the middle layer, makes up the largest portion of the heart’s wall. This layer of muscle tissue contracts with each heartbeat. The endocardium, the heart’s innermost layer, contains endothelial tissue with small blood vessels and bundles of smooth muscle.

A layer of connective tissue called the pericardium surrounds the heart and acts as a tough, protective sac. It consists of the fibrous pericardium and the serous pericardium. The fibrous pericardium, composed of tough, white, fibrous tissue, fits loosely around the heart protecting it. The fibrous pericardium attaches to the great vessels, diaphragm, and sternum. The serous pericardium, the thin, smooth, inner portion, has two layers:

• the parietal layer, which lines the inside of the fibrous pericardium
• the visceral layer, which adheres to the surface of the heart

Between the Layers

The pericardial space separates the visceral and parietal layers and contains 10 to 20 mL of thin, clear pericardial fluid that lubricates the two surfaces and cushions the heart. Excess pericardial fluid, a condition called pericardial effusion, compromises the heart’s ability to pump blood.

Pump Up the Volume

The right and left ventricles serve as the pumping chambers of the heart. The right ventricle receives blood from the right atrium and pumps it through the pulmonary arteries to the lungs, where it picks up oxygen and drops off carbon dioxide. The left ventricle receives oxygenated blood from the left atrium and pumps it through the aorta and then out to the rest of the body. The interventricular septum separates the ventricles and also helps them to pump.

The chamber wall’s thickness depends on the amount of high-pressure work the chamber does. Because the atria collect blood for the ventricles and don’t pump it far, their walls are considerably thinner than the walls of the ventricles. Likewise, the left ventricle has a much thicker wall than the right ventricle because the left ventricle pumps blood against the higher pressures in the body’s arterial circulation, whereas the right ventricle pumps blood against the lower pressures in the lungs.

One-Way Valves

The heart contains four valves—two atrioventricular (AV) valves (tricuspid and mitral) and two semilunar valves (aortic and pulmonic). The valves open and close in response to changes in pressure within the chambers they connect. They serve as one-way doors that keep blood flowing through the heart in a forward direction.

When the valves close, they prevent backflow, or regurgitation, of blood from one chamber to another. The closing of the valves creates the heart sounds that are heard through a stethoscope.

The two AV valves, located between the atria and ventricles, are called the tricuspid and mitral valves. The tricuspid valve is located between the right atrium and the right ventricle. The mitral valve is located between the left atrium and the left ventricle.

Cardiac Cords

The mitral valve has two cusps, or leaflets, and the tricuspid valve has three. The cusps are anchored to the papillary muscles in the heart wall by fibers called chordae tendineae. These cords work together to prevent the cusps from bulging backward into the atria during ventricular contraction. If damage occurs, blood can flow backward into a chamber, resulting in a heart murmur.

Under Pressure

The semilunar valves are the pulmonic valve and the aortic valve. These valves are called semilunar because the cusps resemble three half-moons. Because of the high pressures exerted on the valves, their structure is much simpler than that of the AV valves.

They open because of pressure within the ventricles and close because of the back pressure of blood in the pulmonary arteries and aorta, which pushes the cusps closed. The pulmonic valve, located where the pulmonary artery meets the right ventricle, permits blood to flow from the right ventricle to the pulmonary artery and prevents blood backflow into that ventricle. The aortic valve, located where the left ventricle meets the aorta, allows blood to flow from the left ventricle to the aorta and prevents blood backflow into the left ventricle.

Circuit City

The right ventricle pumps blood through the pulmonic valve into the pulmonary arteries and then into the lungs. From the lungs, blood flows through the pulmonary veins and empties into the left atrium, which completes a circuit called pulmonary circulation.

When pressure rises to a critical point in the left atrium, the mitral valve opens and blood flows into the left ventricle. The left ventricle then contracts and pumps blood through the aortic valve into the aorta, and then throughout the body. Blood returns to the right atrium through the veins, completing a circuit called systemic circulation.

Getting into Circulation

Like the brain and all other organs, the heart needs an adequate supply of blood to survive. The coronary arteries, which lie on the surface of the heart, supply the heart muscle with blood and oxygen. Understand ing coronary blood flow can help you provide better care for a patient with a myocardial infarction (MI) because you’ll be able to predict which areas of the heart would be affected by a blockage in a particular coronary artery. Damaged heart tissue, once thought irreparable, may now be repaired, according to recent research. The “Singheart” RNA molecule may stimulate damaged cells to regenerate or “self-heal.” This could be especially helpful to those with heart failure.

Open that Ostium

The coronary ostium, an opening in the aorta that feeds blood to the coronary arteries, is located near the aortic valve. During systole, when the left ventricle is pumping blood through the aorta and the aortic valve is open, the coronary ostium is partially covered. During diastole, when the left ventricle is filling with blood, the aortic valve is closed and the coronary ostium is open, enabling blood to fill the coronary arteries.

With a shortened diastole, which occurs during periods of tachycardia, less blood flows through the ostium into the coronary arteries. Tachycardia also impedes coronary blood flow because contraction of the ventricles squeezes the arteries and lessens blood flow through them.

That’s Right, Coronary

The right coronary artery as well as the left coronary artery (also known as the left main artery) originate as a single branch off the ascending aorta from the area known as the sinuses of Valsalva. The right coronary artery supplies blood to the right atrium, the right ventricle, and part of the inferior and posterior surfaces of the left ventricle. In about 50% of the population, the artery also supplies blood to the SA node. The bundle of His and the AV node also receive their blood supply from the right coronary artery.

What’s Left, Coronary?

The left coronary artery runs along the surface of the left atrium, where it splits into two major branches: the left anterior descending and the left circumflex arteries. The left anterior descending artery runs down the surface of the left ventricle toward the apex and supplies blood to the anterior wall of the left ventricle, the interventricular septum, the right bundle branch, and the left anterior fasciculus of the left bundle branch. The branches of the left anterior descending artery—the septal perforators and the diagonal arteries—help supply blood to the walls of both ventricles.

Circling Circumflex

The circumflex artery supplies oxygenated blood to the lateral walls of the left ventricle, the left atrium and , in about half of the population, the SA node. In addition, the circumflex artery supplies blood to the left posterior fasciculus of the left bundle branch. This artery circles the left ventricle and provides blood to the ventricle’s posterior portion.

Circulation, Guaranteed

When two or more arteries supply the same region, they usually connect through anastomoses, junctions that provide alternative routes of blood flow. This network of smaller arteries, called collateral circulation, provides blood to capillaries that directly feed the heart muscle. Collateral circulation commonly becomes so strong that even if major coronary arteries become clogged with plaque, collateral circulation can continue to supply blood to the heart.

Veins in the Heart

The heart has veins just like other parts of the body. Cardiac veins collect deoxygenated blood from the capillaries of the myocardium. The cardiac veins join to form an enlarged vessel called the coronary sinus, which returns blood to the right atrium, where it continues through the circulation.

Atrial Kick

The atrial contraction, or atrial kick, contributes about 30% of the cardiac output—the amount of blood pumped by the ventricles in 1 minute. (See Quick facts about circulation.) Certain arrhythmias, such as atrial fibrillation, can cause a loss of atrial kick and a subsequent drop in cardiac output. Tachycardia also affects cardiac output by shortening diastole and allowing less time for the ventricles to fill. Less filling time means less blood will be ejected during ventricular systole and less will be sent through the circulation.

A Balancing Act

The cardiac cycle produces cardiac output, which is the amount of blood the heart pumps in 1 minute. It’s measured by multiplying heart rate times stroke volume. (See Understand ing preload, afterload, and contractility.) The term stroke volume refers to the amount of blood ejected with each ventricular contraction.

Normal cardiac output is 4 to 8 L/min, depending on body size. The heart pumps only as much blood as the body requires. Three factors affect stroke volume—preload, afterload, and myocardial contractility. A balance of these three factors produces optimal cardiac output.

Preload

Preload is the stretching of muscle fibers in the ventricles and is determined by the pressure and amount of blood remaining in the left ventricle at the end of diastole.

Afterload

Afterload is the amount of pressure the left ventricle must work against to pump blood into the circulation. The greater this resistance, the more the heart works to pump out blood.

Contractility

Contractility is the ability of muscle cells to contract after depolarization. This ability depends on how much the muscle fibers are stretched at the end of diastole. Over-stretching or under-stretching these fibers alters contractility and the amount of blood pumped out of the ventricles. To better understand this concept, imagine you are trying to shoot a rubber band across the room. If you don’t stretch the rubber band enough, it won’t go far. If you stretch it too much, it will snap. However, if you stretch it just the right amount, it will go as far as you want it to go.

Braking the Heart

The parasympathetic nervous system, on the other hand , serves as the heart’s brakes. One of this system’s nerves, the vagus nerve, carries impulses that slow heart rate and the conduction of impulses through the AV node and ventricles. Stimulating this system releases the chemical acetylcholine, slowing the heart rate.

The vagus nerve is stimulated by baroreceptors, specialized nerve cells in the aorta, and the internal carotid arteries. Conditions that stimulate the baroreceptors also stimulate the vagus nerve.

For example, a stretching of the baroreceptors, which can occur during periods of hypertension or when applying pressure to the carotid artery, stimulates the receptors. In a maneuver called carotid sinus massage, baroreceptors in the carotid arteries are purposely activated in an effort to slow a rapid heart rate.

Memory jogger To help you remember the difference between depolarization and repolarization, think of the R in repolarization as stand ing for REST. Remember that repolarization is the resting phase of the cardiac cycle.

“de”-Cycle and “re”-Cycle

As impulses are transmitted, cardiac cells undergo cycles of depolarization and repolarization. (See Depolarization–repolarization cycle) Cardiac cells at rest are considered polarized, meaning that no electrical activity takes place. Cell membranes separate different concentrations of ions, such as sodium and potassium, and create a more negative charge inside the cell. This is called the resting potential. After a stimulus occurs, ions cross the cell membrane and cause an action potential, or cell depolarization. Researchers have discovered a “calcium-sensing-gate,” which initiates calcium waves responsible for calcium-triggered arrhythmias. This discovery may aid in the development of new drug treatments. When a cell is fully depolarized, it attempts to return to its resting state in a process called repolarization. Electrical charges in the cell reverse and return to normal.

A cycle of depolarization–repolarization consists of five phases—0 through 4. The action potential is represented by a curve that shows voltage changes during the five phases. (See Action potential curve)

Many Phases of the Curve

During phase 0, the cell receives an impulse from a neighboring cell and is depolarized. Phase 1 is marked by early, rapid repolarization. Phase 2, the plateau phase, is a period of slow repolarization.

During phases 1 and 2 and at the beginning of phase 3, the cardiac cell is said to be in its absolute refractory period. During that period, no stimulus, no matter how strong, can excite the cell.

Phase 3, the rapid repolarization phase, occurs as the cell returns to its original state. During the last half of this phase, when the cell is in its relative refractory period, a very strong stimulus can depolarize it.

Phase 4 is the resting phase of the action potential. By the end of phase 4, the cell is ready for another stimulus.

All that electrical activity is represented on an electrocardiogram (ECG). Keep in mind that the ECG represents electrical activity only, not actual pumping of the heart.

Setting the Pace

The SA node is located in the upper right corner of the right atrium, where the superior vena cava joins the atrial tissue mass. It’s the heart’s main pacemaker, generating impulses 60 to 100 times per minute. When initiated, the impulses follow a specific path through the heart. They usually can’t flow backward because the cells can’t respond to a stimulus immediately after depolarization.

Bachmann’s Bundle of Nerves

Impulses from the SA node next travel through Bachmann’s bundle, tracts of tissue extending from the SA node to the left atrium. Impulses are thought to be transmitted throughout the right atrium through the anterior, middle, and posterior internodal tracts. Impulse transmission through the right and left atria occurs so rapidly that the atria contract almost simultaneously.

AV: The Slow Node

The AV node, located in the inferior right atrium near the ostium of the coronary sinus, is responsible for delaying the impulses that reach it. Although the nodal tissue itself has no pacemaker cells, the tissue surrounding it (called junctional tissue) contains pacemaker cells that can fire at a rate of 40 to 60 times/min.

The AV node’s main function is to delay impulses by 0.04 seconds to keep the ventricles from contracting too quickly. This delay allows the ventricles to complete their filling phase as the atria contract. It also allows the cardiac muscle to stretch to its fullest for peak cardiac output.

Branch Splitting

The bundle of His, a tract of tissue extending into the ventricles next to the interventricular septum, resumes the rapid conduction of the impulse through the ventricles. The bundle eventually divides into the right and left bundle branches.

The right bundle branch extends down the right side of the interventricular septum and through the right ventricle. The left bundle branch extends down the left side of the interventricular septum and through the left ventricle.

The left bundle branch then splits into two branches, or fasciculi: the left anterior fasciculus, which extends through the anterior portion of the left ventricle, and the left posterior fasciculus, which runs through the lateral and posterior portions of the left ventricle. Impulses travel much faster down the left bundle branch (which feeds the larger, thicker-walled left ventricle) than the right bundle branch (which feeds the smaller, thinner-walled right ventricle).

The difference in the conduction speed allows both ventricles to contract simultaneously. The entire network of specialized nervous tissue that extends through the ventricles is known as the His–Purkinje system.

Those Perky Purkinje Fibers

Purkinje fibers extend from the bundle branches into the endocardium, deep into the myocardial tissue. These fibers conduct impulses rapidly through the muscle to assist in its depolarization and contraction.

Purkinje fibers can also serve as a pacemaker and are able to discharge impulses at a rate of 20 to 40 times/min, sometimes even more slowly. (See Pacemakers of the heart) Purkinje fibers usually aren’t activated as a pacemaker unless conduction through the bundle of His becomes blocked or a higher pacemaker (SA or AV node) doesn’t generate an impulse. (See Pediatric pacemaker rates)

Ages and stages

Pediatric pacemaker rates In children younger than age 3, the AV node may discharge impulses at a rate of 50 to 80 times/min; the Purkinje fibers may discharge at a rate of 40 to 50 times/min.

When the Heart Goes on “manual”

Automaticity is a special characteristic of pacemaker cells that generate impulses automatically, without being stimulated to do so. If a cell’s automaticity is increased or decreased, an arrhythmia can occur. Tachycardia, for example, is commonly caused by an increase in the automaticity of pacemaker cells below the SA node. Likewise, a decrease in automaticity of cells in the SA node can cause the development of bradycardia or an escape rhythm (a compensatory beat generated by a lower pacemaker site).

Out of Synch

Impulses that begin below the AV node can be transmitted backward toward the atria. This backward, or retrograde, conduction usually takes longer than normal conduction and can cause the atria and ventricles to beat out of synch.

Coming Back for More

Sometimes impulses cause depolarization twice in a row at a faster-than-normal rate. Such events are referred to as reentry events. In reentry, impulses are delayed long enough that cells have time to repolarize. In these cases, the active impulse reenters the same area and produces another impulse.

That’s a wrap!

Cardiac anatomy and physiology review The Heart’s Valves Tricuspid: AV valve between the right atrium and right ventricle Mitral: AV valve between the left atrium and left ventricle Aortic: Semilunar valve between the left ventricle and the aorta Pulmonic: Semilunar valve between the right ventricle and the pulmonary artery Blood Flow Deoxygenated blood from the body returns to the right atrium and then flows to the right ventricle The right ventricle pumps blood into the lungs where it’s oxygenated. Then the blood returns to the left atrium and flows to the left ventricle Oxygenated blood is pumped to the aorta and the body by the left ventricle Coronary Arteries and Veins Right coronary artery: Supplies blood to the right atrium and ventricle and part of the left ventricle Left anterior descending artery: Supplies blood to the anterior wall of the left ventricle, interventricular septum, right bundle branch, and left anterior fasciculus of the left bundle branch Circumflex artery: Supplies blood to the lateral walls of the left ventricle, left atrium, and left posterior fasciculus of the left bundle branch Cardiac veins: Collect blood from the capillaries of the myocardium Coronary sinus: Returns blood to the right atrium Cardiac Cycle Dynamics Atrial kick: Atrial contraction, contributing about 30% of the cardiac output Cardiac output: The amount of blood the heart pumps in 1 minute, calculated by multiplying heart rate times stroke volume Stroke volume: The amount of blood ejected with each ventricular contraction (it’s affected by preload, afterload, and contractility) Preload: The passive stretching exerted by blood on the ventricular muscle at the end of diastole Afterload: The amount of pressure the left ventricle must work against to pump blood into the aorta Contractility: The ability of the heart muscle cells to contract after depolarization Innervation of the Heart Two branches of the autonomic nervous system supply the heart: Sympathetic nervous system: Increases heart rate, automaticity, AV conduction, and contractility through release of norepinephrine and epinephrine Parasympathetic nervous system: Vagus nerve stimulation reduces heart rate and AV conduction through release of acetylcholine Transmission of Electrical Impulses Generation and transmission of electrical impulses depend on the following cell characteristics: Automaticity: A cell’s ability to spontaneously initiate an impulse, such as found in pacemaker cells Excitabilit: How well a cell responds to an electrical stimulus Conductivity: The ability of a cell to transmit an electrical impulse to another cardiac cell Contractility: How well the cell contracts after receiving a stimulus Depolarization–repolarization Cycle Cardiac cells undergo the following cycles of depolarization and repolarization as impulses are transmitted: Phase 0: Rapid depolarization—the cell receives an impulse from a nearby cell and is depolarized Phase 1: Early repolarization—early rapid repolarization occurs Phase 2: Plateau phase—a period of slow repolarization occurs Phase 3: Rapid repolarization—the cell returns to its original state Phase 4: Resting phase—the cell rests and readies itself for another stimulus Cardiac Conduction The electrical impulse begins in the SA node and travels through the internodal tracts and Bachmann’s bundle to the AV node From the AV node, the impulse travels down the bundle of His, along the bundle branches, and through the Purkinje fibers Intrinsic Firing Rates SA node: 60 to 100/minute AV junction: 40 to 60/minute Purkinje fibers: 20 to 40/minute Abnormal Impulses Automaticity: The ability of a cardiac cell to initiate an impulse on its own Retrograde conduction: Impulses that are transmitted backward toward the atria Reentry: When an impulse follows a circular, rather than the normal, conduction path

Repeating Itself

An injured pacemaker (or nonpacemaker) cell may partially depolarize, rather than fully depolarizing. Partial depolarization can lead to spontaneous or secondary depolarization, which involves repetitive ectopic firings called triggered activity.

The resultant depolarization is called afterdepolarization. Early afterdepolarization occurs before the cell is fully repolarized and can be caused by hypokalemia, slow pacing rates, or drug toxicity. If it occurs after the cell has been fully repolarized, it’s called delayed afterdepolarization. These problems can be caused by digoxin toxicity, hypercalcemia, or increased catecholamine release. Atrial or ventricular tachycardia may result. You’ll learn more about these and other arrhythmias in later chapters.