The heart is located in the mediastinum of the thoracic cavity.

The heart is located inside the pericardial sac, which is itself located in the lower (supradiaphragmatic) part of the mediastinum. The heart occupies the central portion of the mediastinum, extending slightly to the right from the midline and projecting with its apex toward the left lateral side (Fig. 4-3). The great vessels (i.e., the superior and inferior vena cava, the aorta, the pulmonary artery, and the pulmonary veins) are attached to the heart at its “base,” which is located cranially and to the right of the apex. The contours of the heart are clearly visible in anteroposterior (AP) radiographic films.

Figure 4-3 Anatomic location of the heart in the thorax. In a radiograph the right border is made of the contours of the right atrium (RA) and right ventricle (RV). The inferior border is made of right ventricle and on the left lateral side of the apex of the left ventricle (LV). The left border is made of the contours of left atrial appendage and left ventricle, and along the upper margin the aortic arch.

In adults the anterior mediastinum contains the remnants of the thymus, which does not affect the function of the heart unless enlarged due to thymoma or lymphoma. The posterior side of the heart is in anatomic contact with the esophagus and the thoracic aorta. Transesophageal echocardiography may be used to assess the left atrium lying on the esophagus, but it may also provide data on the entire heart.

The heart has four chambers and can be functionally divided into a right and a left part.

The heart has two atria and two ventricles (Fig. 4-4). The right atrium and ventricle contain unoxygenated (“venous”) blood, which has an oxygen saturation between 72% and 80%. The contracting right heart pumps the blood into the lungs, where is it oxygenated. The left atrium and ventricle contain oxygenated (“arterial”) blood with an oxygen saturation of 95% or more. The left ventricle propels the oxygenated blood into the periphery through the aorta and the arteries.

Figure 4-4 Cross section through the right and left heart and the great vessels. The range of systolic and diastolic pressures in each chamber is indicated. The oxygen saturation of blood in the right heart ranges from 72% to 80%, and is 95% or more in the left heart.

The atria and the ventricles and the great arteries are separated one from another by valves. These valves open and close during the cardiac contraction cycle, thus allowing the orderly flow of blood from one compartment to another. The closure and opening of the valves and the cardiac contractions account for the pressure gradients that develop differentially in each chamber.

The right atrium receives the venous blood from the upper and the lower venae cavae. The venous blood enters the right ventricle through the right atrioventricular (AV) orifice, which is tricuspid. The blood is pumped by the ventricle through a tricuspid pulmonary orifice into the pulmonary artery. The oxygenated blood returns to the heart through the pulmonary veins, which convey it to the left atrium. From the left atrium the blood passes through the left AV orifice, which is bicuspid and called mitral, and enters the left ventricle. The left ventricle pumps the blood into the aorta through the aortic valve.

The entire heart, except the endocardium, receives oxygenated blood through two coronary arteries.

Most human hearts have two coronary arteries, which originate from the coronary sinuses in the initial part of the thoracic aorta (Fig. 4-5).

Figure 4-5 Coronary arteries. Cross sections of the heart show the typical blood supply areas of each of the three major coronary arteries.

The right coronary artery provides the blood for the entire right ventricle, the posterior side of the left ventricle, and the posterior side of the interventricular septum. In 90% of people it gives rise to the posterior descending coronary artery and is therefore by convention considered to be the dominant artery. It also provides the blood to the sinoatrial (SA) node in 60% and to the AV node in 90% of people.

The left coronary artery branches within 2.5 cm of its origin, giving rise to the left anterior descending (LAD) and left circumflex artery (LCX). The LAD provides blood to the anterior wall of the left ventricle, the apex of the heart, and the anterior part of the interventricular septum. The LCX provides the blood for the lateroposterior wall of the left ventricle.

The coronary arteries are located subepicardially on the external surface of the heart. The major veins follow the arteries. Because of their location these major vessels are not compressed by the contracting myocardium during the systole—a period of the cardiac cycle when the coronaries actually dilate to accommodate the influx of oxygenated blood. Coronary arteries have β₂-adrenergic receptors, which react to stimuli from sympathetic nerves, thereby causing coronary vasodilatation. Parasympathetic stimulation also causes mild coronary vasodilatation.

Due to their location in the epicardial fat tissue the coronary arteries are at a distance from the endocardium. The nourishment of the endocardium is, however, not affected by this distance because the endocardium receives oxygen and nutrients from the ventricular blood. The zone that is at risk for hypoxia, however, is the subendocardial myocardium, which is beyond the supply zone from the ventricles and is the last to receive the blood from the coronary arteries.

The coronary arteries and their major branches are considered to be functionally terminal arteries. Although there are 40-μm or smaller caliber anastomoses between the major coronary arteries, these anastomoses are not sufficient to compensate for the occlusion of one coronary artery or its major branches. If a coronary artery become progressively stenotic these anastomoses can increase in size and become functional and provide blood to the relatively ischemic portion of the heart supplied normally by the other coronary.

The heart is composed of three layers: endocardium, myocardium, and pericardium.

The inside of the heart is covered with endocardium, which is a layer continuous with the endothelium of blood vessels. The endocardium also covers the surface of the valves. The myocardium, or the muscle layer, is the primary contractile component of the heart. The pericardium forms the pericardial sac and also covers the external surface of the heart as epicardium.

The myocardium is composed of two types of cells called cardiac myocytes: conducting cells and contractile cells.

Contractile function of cardiac myocytes depends on the proper functioning of sarcomeres and supporting structures in the cytoplasm.

Contractile units in the cytoplasm of cardiac myocytes are called sarcomeres (Fig. 4-6). They are composed of thick myosin filaments interdigitating with thinner actin filaments and a number of contraction-regulating proteins, such as tropomyosin and troponins (C, I, and T). During contraction the myosin filaments slide along one another, whereas during relaxation they slide in the opposite direction.

Figure 4-6 Sarcomeres. These basic contractile units consist of thick myosin and thin actin filaments that slide along each other in one direction in systole and the other in diastole.

(Modified from Boon NA, Colledge NR, Walker BR [eds]: Davidson’s Principles and Practice of Medicine, 20th ed. Churchill-Livingstone, Edinburgh, 2006.)

The overlapping of actin and myosin filaments accounts for the striation of cardiac myocytes. Three regions are recognized by light microscopy: two lighter regions called I (isotropic), and a darker region called A (anisotropic). By electron microscopy the central part of the I region contains the Z line. Normal sarcomeres, measured from one Z line to another, vary in length from 1.5 μm in contracted muscle cells in systole to 2.2 μm in stretched muscle fibers in diastole.

The cell membrane of myocytes, also known as sarcolemma, invaginates into the cytoplasm, forming the so-called transverse tubular system (T tubules). The T system is an important regulator for the flux of calcium ions from outside into the cells and from one cellular compartment to another (Fig. 4-7). The T tubules are closely linked to the sarcoplasmic reticulum, a system of cisterns that serve as the main intracellular store of calcium. The sarcoplasmic reticulum and the T tubules form an integral system essential for the rapid transmission of electrical stimuli and the contraction–relaxation of myocytes.

Figure 4-7 Transverse tubular system and sarcoplasmic reticulum. The T tubules represent invaginations of the sarcolemma.

Cardiac contractions depend on the interaction of the external innervation and the endogenous conduction system of the heart.

The heart receives parasympathetic innervation from the vagus and sympathetic innervation from sympathetic ganglia. The cholinergic parasympathetic stimuli, which are under normal circumstances predominant, stimulate the heart through the AV and SA node. Vagal stimulation has a negative chronotropic and inotropic effect; that is, it slows down the heartbeat and reduces the strength of the cardiac contraction. Sympathetic stimuli transmitted mostly through β₁-adrenergic receptors have a positive chronotropic and inotropic effect. Sensory nerves, important for the cardiac reflexes, exit the heart through the vagus nerve.

The automatic contractility of the heart is regulated through the SA and AV node and the conduction system of the myocardium. The SA node is the source of initial impulses and accounts for the normal “sinus rhythm.” The depolarization wave is transmitted from the SA node to the internodal and interatrial fibers, which causes depolarization of the right and left atrium. The electric impulses cannot freely pass into the ventricle because the annulus fibrosus blocks their propagation. The only way that the impulses can get into the ventricle is by reaching first the AV node located on the atrial side of the annulus fibrosus. From the SA node the electric impulses enter the bundle of His, which penetrates the annulus fibrosus and allows the stimuli to pass from the atrium to the ventricle. Then they reach the Purkinje fibers and are transmitted to cardiac myocytes, causing their depolarization. These electrical events can be traced externally and if superimposed on one another can be recorded as an electrocardiographic tracing (Fig. 4-8).

Figure 4-8 Electric currents generated by depolarization of various parts of the conduction system and the myocardium. Superimposed one over another these electric impulses can be registered as the normal electrocardiographic (ECG) tracing. AV, atrioventricular; SA, sinoatrial.

(Modified from Boron WF, Boulpaep EL [eds]: Medical Physiology. Saunders, Philadelphia, 2003.)

Cardiac myocyte contraction begins with the depolarization of the sarcolemma.

The contraction of cardiac myocytes is closely related to changes in the plasma membrane. Sarcolemma, the plasma membrane of cardiac myocytes, is selectively permeable to ions. The differential distribution of ions inside and outside the myocytes accounts for the electric charge of the cells membrane, which in a resting cell is approximately -90 mV. If the cell is stimulated, the potential is reduced to a critical level, called threshold potential, whereupon the cell membrane undergoes depolarization, which is completed spontaneously according to the all-or-none law. The cell membrane is then repolarized by several mechanisms, and the cycle is repeated automatically.

The cardiac myocyte’s action potential, or the change in the membrane potential that occurs after the cell has been adequately stimulated, can be divided into five phases (Fig. 4-9):

Figure 4-9 Action potential of cardiac myocytes. Each of the five phases is characterized by an influx or efflux of Na⁺, K⁺, and Ca²⁺.

Contraction of sarcomeres requires a marked increase of cystosolic calcium concentration so that it could start binding to troponin C.

During phase 2 of the myocyte action potential Ca²⁺ enters into the cytoplasm through the calcium channels and is transferred into the sarcoplasmic reticulum (Fig. 4-10). The entry of extracellular Ca²⁺ acts as a trigger for discharge of large amounts of Ca²⁺ stored inside the cisterns of the sarcoplasmic reticulum and to a lesser degree in mitochondria. Once the concentration of cytosolic calcium has risen 10-fold Ca²⁺ binds to troponin C, which inactivates troponin I, allowing it to induce conformational changes in tropomyosin, the principal regulator of actin–myosin interaction. Tropomyosin deblocks actin, allowing it to interact with myosin. This interaction is a multistep process that ultimately leads to contraction of the sarcomeres.

Figure 4-10 The role of calcium (Ca²⁺) in mediating the contraction of sarcomeres. The entry of Ca²⁺ from outside the cell triggers the release of Ca²⁺ from the sarcoplasmic reticulum and to a lesser extent from mitochondria. Free cytoplasmic Ca²⁺ binds to troponin C, which interacts with other troponins and tropomyosin enabling the contraction of sarcomeres. At the end of the contraction Ca²⁺ is released from the sarcomeres and returned to the sarcoplasmic reticulum. Tn-C, troponin C.

After the contraction occurs the calcium dissociates from tropomysin, which inhibits actin–myosin interaction, leading to relaxation of the sarcomeres. Free Ca²⁺ is pumped by Adenosine triphosphate (ATP)-dependent calcium pumps back into the sarcoplasmic reticulum and mitochondria, where it is stored. It is also exchanged for Na⁺ across the plasma membrane and extruded from the cell cytoplasm into the interstitial space. During the next action potential the entire cycle is repeated.

Contraction of the myocytes results in systole and the expulsion of the blood from the ventricles, whereas during diastole the ventricles dilate and fill with blood.

The cardiac cycle has two phases: systole, during which the myocardium of the ventricles contracts, and diastole, during which the ventricles dilate. The force of cardiac contraction is influenced by several factors, the most important of which are the preload, contractility of the myocytes, and the afterload (Fig. 4-11).

Figure 4-11 Cardiac output depends on the preload, the afterload, and the contractility of the heart.

(Modified from Price AS, Wilson LM: Pathophysiology. Clinical Concepts of Disease Processes, 6th ed. Mosby, St. Louis, 2003.)

Preload refers to the end-diastolic volume (i.e., the amount of blood in the ventricles just before the contraction). The contraction of the ventricles increases in proportion to the increased preload (i.e., the venous return to the heart). This is in keeping with the Frank-Starling law of the heart, which states that “volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole.” Many years after Frank and Starling defined their law, it was shown that the increased end-diastolic pressure leads to lengthening of the sarcomeres, which thereupon contract more forcefully (Fig. 4-12). In other words the energy of contraction is proportional to the initial length of the cardiac muscles. The Frank-Starling law works only within limits: if the optimal lengthening of sarcomere is exceeded, the contractions become less powerful.

Figure 4-12 Ventricular performance curve according to the Frank-Starling law of the heart. The cardiac output. The left ventricular (LV) stroke increases proportionately to the end-diastolic pressure (i.e., the length to the sarcomere). If the maximum permissible length is exceeded, the LV stroke decreases. Positive inotropic stimuli increase the LV stroke. Negative inotropic stimuli decrease contractility and reduce the LV stroke. CAD, coronary artery disease.

Increased contractility (positive inotropic effect) refers to faster contraction of myocytes or increased velocity of shortening at a constant preload. It can be achieved by sympathetic stimulation or with drugs that have, like digitalis, a positive inotropic effect. Sympathetic stimulation also has a positive chronotropic effect; that is, it increases the heart rate, which also contributes to increased cardiac output.

Decreased contractility (negative inotropic effect) is encountered under pathologic conditions, such as coronary heart disease, hypoxia, and acidosis. In such conditions the heart cannot increase cardiac output in response to increased end-diastolic pressure.

Afterload refers to the pressure and resistance against which the ventricles work. In the left ventricle, afterload may be caused by narrowing of the arteries or arterial hypertension, as well as by narrowing of the aortic valves by rheumatic disease or calcification. Afterload to the right ventricle results from various conditions causing pulmonary hypertension or left ventricular failure. Afterload must be overcome by increased cardiac work, but ultimately the heart fails.

The action of the heart occurs in repetitive cycles, which include coordination of myocardial contractility and opening and closing of valves.

The cardiac cycle can be monitored by recording the pressure in various chambers or in the aorta, by measuring the volume of blood in various chambers, by recording the electric potential in electrocardiographic (ECG) tracings, and by monitoring the opening and closing of valves using a cardiac phonograph (Fig. 4-13).

Figure 4-13 Electrical and mechanical events during the cardiac cycle.

(Modified from Guyton AC, Hall JE, Textbook of Medical Physiology, 10th ed. Saunders, Philadelphia, 2000, p. 99.)

The cardiac cycle begins with the formation of an action potential inside the sinus node. This occurs during diastole when the muscle is relaxed and the ventricles dilated. Through the opening of the mitral and tricuspid valves the ventricles fill until the pressure inside the ventricles reaches the pressure in the atria. This part of the heart cycle is called diastasis. The impulses generated in the SA node are transmitted to the atrial musculature. Spreading of the depolarization through the atria is seen in ECG as the P wave. The impulses also reach the AV node from which they enter into the ventricles. The 0.10-second delay in the relay of the impulses to the atrial muscles and the entry of the electric current into the ventricles allows enough time for the atrial contraction, which typically precedes ventricular contraction before the arteriovenous (A-V) valves close.

The depolarization of the ventricles shows up in the ECG as the QRS complex, which leads to systolic contraction of the ventricles. At the beginning of systole the A-V valve closes to prevent the reflux of blood into the atrium once the ventricle begins contracting. The closure of the A-V valve is heard as the first heart sound (S₁). It is low in pitch and continues relatively long after the closure. Initially the ventricular contraction is isovolumic, but then the aortic valve opens and the blood ejection phase begins. During this phase the blood is ejected into the aorta from the left ventricle and into the lungs from the right ventricle. At the end the volume of the blood in the ventricles decreases dramatically.

At the end of systole the aortic valve closes and diastole begins with isovolumic relaxation of the ventricles. The closure of the aortic valve is heard as the second heart sound (S₂). At the end of the isovolumic relaxation the A-V valve opens and the rapid filling (inflow) phase of diastole begins; the cycle is then repeated. The third cardiac sound (S₃) can be heard during the period of rapid filling in young persons; in older persons S₃ is a sign of ventricular dysfunction. The fourth cardiac sound (S₄) is produced by atrial contraction. These phases of the systole and diastole are presented in Figure 4-14. Heart sounds are shown in Figure 4-15.

Figure 4-14 Phases of ventricular filling and contraction.

Figure 4-15 Cardiac sounds. S₁ is produced by opening of the atrioventricular valves. S₂ is produced by closure of the aortic valve. S₃ is heard during rapid filling in diastole in young persons. S₄ is the result of atrial contraction before the A-V valves close.

The four phases of the ventricular systole and diastole can be best presented as a pressure–volume loop.

Changes in the ratio of left ventricular volume and intraventricular pressure during the four periods of the cardiac cycle are shown in Figure 4-16. This pressure–volume loop has four parts, as follows:

Figure 4-16 Pressure–volume loop of the heart during the contraction–relaxation cycle. The left ventricular pressure (ordinate) is plotted against the left ventricular volume (abscissa). A, Mitral valve opens and diastolic filling of the ventricles begins. A–B corresponds to diastolic filling. B, Mitral valve closes at the end of diastole and isovolumic contraction of the ventricles begins. B–C corresponds to isovolumic contraction of the ventricle. C, Aortic valve opens and the ejection of blood from the ventricle begins. C–D corresponds to the ejection phase of systole. D, Aortic valve closes and end-systolic volume is reached, whereupon the ventricles relax. D–A corresponds to isovolumic ventricular relaxation.

The ejection fraction is usually about 60% of the total blood volume in the ventricle.

At the end of diastole each ventricle contains approximately 110 to 120 mL of blood, known as end-diastolic volume. Stroke volume output during systole equals 70 mL, and the remaining 40 to 50 mL is called the end-systolic volume. The ejection fraction is calculated as the percentage of end-diastolic volume that is ejected from the ventricle. In normal healthy persons it is in the range of 60%. Stroke volume output can be increased during strong cardiac contractions, which reduce the end-systolic volume to 10 to 20 mL, as well as by increasing the end-diastolic volumes of the ventricle (Fig. 4-17).

Figure 4-17 Increased stroke volume. Left part of the figure shows the effects of stronger ventricular contraction reducing the end-systolic ventricular volume (D–d). The right part of the figure shows the effects of increased diastolic filling, which also increase the stroke volume.

Chest discomfort and pain are common symptoms that may be of cardiac or noncardiac origin.

Chest discomfort and pain are closely related sensations that vary in intensity. Minor pain may be perceived as discomfort, and pain often begins as discomfort that gradually intensifies. Clinically it is customary to subdivide chest pain into two groups: cardiac and noncardiac. The most common causes of acute chest discomfort and pain are listed in Table 4-2.

Table 4-2 Major Causes of Chest Discomfort and Pain

Cardiac pain may be classified as ischemic or pericardial.

Cardiac pain is transmitted to the cerebral sensory cortex through the sympathetic and parasympathetic autonomic nerve fibers. The parasympathetic fibers are part of the vagus nerve. The sympathetic sensory fibers enter the upper five to six thoracic and lower cervical ganglia and from there interconnect with afferent fibers leading the sensations into the sensory cortex. Because these sensory fibers communicate with other sensory nerves it is not always possible to determine the exact origin of pain. Accordingly it is important to remember that pain originating from many other organs may be perceived as cardiac, and conversely, pain of cardiac origin may be misinterpreted as stemming from other organs.

Ischemic cardiac pain originates from the myocardium that is not receiving enough oxygen for its needs. Typically this kind of pain is characteristic of ischemic coronary heart disease and is found in patients who have angina pectoris or who have had or are having a myocardial infarction (MI). Similar pain is experienced by patients who have aortic stenosis preventing normal perfusion of the coronary arteries.

Ischemic cardiac discomfort and pain are described as heaviness or pressure or squeezing behind the sternum (retrosternal pain). The pain has an epicenter over the sternum radiating to the arm, neck, and lower jaw. Most often it radiates into the left arm along the ulnar side (Fig. 4-18). Less commonly it may be bilateral, and occasionally it may radiate to the back, usually along the left scapula. The pain is usually related to exercise, but in MI it may be of sudden onset and occur during sleep or rest. The pain of angina is usually short-lived and can be relieved by nitroglycerine, in contrast to the pain of MI, which is often crushing and of longer duration.

Figure 4-18 Ischemic cardiac pain. A, The pain most often radiates to the ulnar side of the left arm. B, Less often the pain radiates to the right side, the neck, and the face, or to the dorsal side of the chest.

Pericardial pain is caused by pericarditis and is typically most intense behind the sternum or at the apex of the heart. It is described as stabbing, burning, or piercing. It lasts longer than ischemic pain and is unrelated to exercise. It may be aggravated by lying down, coughing, deep inspiration, or movement. It can be partially relieved by leaning forward or preventing chest movements. Pericardial pain is usually not radiating outside the chest.

Palpitation is a subjective feeling of heartbeating.

Patients typically complain that they feel their “heart beating fast” or “skipping beats.” This very common symptom may be correlated with irregularities of the pulse. It may be caused by the following functional irregularities of heartbeat:

Cardiac dyspnea results from increased respiratory effort aimed at compensating for hypoxia.

Dyspnea is a sense of difficulty in breathing or shortness of breath. Note that it is a subjective feeling and reflects the patients’ consciousness of increased respiratory effort. Furthermore, the sensation of shortness of breath is very common, and accordingly dyspnea is also a physiological phenomenon that occurs whenever there is a “hunger for air” due to strenuous exercise, a sudden rush of activity (e.g., a fast sprint), adjusting to high altitudes (“mountain sickness”), and even in anxiety states.

An important aspect of cardiac dyspnea is the sensation of chest tightness and shortness of breath. These symptoms result from impulses emanating from mechanoreceptors in the lungs, sensory stimuli from the chest wall, and those generated by the chemoreceptors reacting to the reduced concentration of oxygen in the blood. All these afferent signals act on the respiratory center to generate an adequate ventilatory response, perceived by the individual as a “respiratory effort” or “labored breathing” (Fig. 4-19).

Figure 4-19 Cardiac dyspnea caused by left heart failure. CNS, central nervous system; PCO₂, partial pressure of carbon dioxide.

Cardiac dyspnea must be distinguished from noncardiac dyspnea.

When a patient presents with dyspnea it is most important to establish whether it is acute or chronic and to decide whether it is of cardiac or noncardiac origin. The most common form of noncardiac dyspnea is respiratory dyspnea caused by a variety of bronchopulmonary diseases, such as bronchial asthma, chronic obstructive pulmonary disease, and pneumonia (Fig. 4-20). Systemic diseases such as acidosis or neuromuscular diseases such as myasthenia gravis also may affect breathing and cause dyspnea. All these diseases can be excluded from the differential diagnosis by taking a thorough history, performing a complete physical examination, and conducting any necessary additional testing.

Figure 4-20 Differentiation of cardiac from noncardiac dyspnea. CHF, congestive heart failure.

Once the pulmonary dyspnea has been excluded and cardiac dyspnea is suggested, it is important to decide whether the symptom is related to high-, normal-, or low-output heart failure. This determination allows the physician to decide whether the dyspnea is related to intrinsic heart failure presenting usually as low-output heart failure or some other condition, such as anemia or hyperthyroidism, which present with high-output failure. Obesity typically manifests with dyspnea with normal cardiac output.

Cardiac dyspnea is traditionally divided into two forms: dyspnea on effort and dyspnea at rest.

Stay updated, free articles. Join our Telegram channel

Join