A hollow, muscular organ, the pump of the circulatory system. Its wall has three layers: the outer epicardium, a serous membrane; the middle myocardium, made of cardiac muscle; and the inner endocardium, endothelium that lines the chambers and covers the valves. The heart is enclosed in the pericardium, a fibroserous sac; the potential space between the parietal pericardium and the epicardium is called the pericardial cavity, which contains serous fluid to prevent friction as the heart beats.
STRUCTURES OF THE HEART (A) Anterior view of the heart; (B) Frontal section of the heart; SEE: circulation, coronary for illus.; SEE: cardiomyopathy, hypertrophic
The upper right and left atria are thin-walled receiving chambers separated by the interatrial septum. The lower right and left ventricles are thick-walled pumping chambers separated by the interventricular septum; normally the right side has no communication with the left. The right side receives deoxygenated blood via the venae cavae from the body and pumps it to the lungs; the left side receives oxygenated blood from the lungs and pumps it via the aorta and arteries to the body. Contraction of the heart chambers is called systole; relaxation with accompanying filling with blood is called diastole. The sequence of events that occurs in a single heartbeat is called the cardiac cycle, with atrial systole followed by ventricular systole. For a heart rate of 70 beats per minute, each cycle lasts about 0.85 sec.
In the healthy state, all four cardiac valves prevent backflow of blood. The atrioventricular valves are at the openings between each atrium and ventricle; the tricuspid valve, between the right atrium and ventricle; and the bicuspid or mitral valve, between the left atrium and ventricle. The pulmonary semilunar valve is at the opening of the right ventricle into the pulmonary artery; the aortic semilunar valve is at the opening of the left ventricle into the aorta.
In adults, the cardiac output varies from 5 L/min at rest to as much as 20 L/min during vigorous exercise. At the rate of 72 times each minute, the adult human heart beats 104,000 times a day, 38,000,000 times a year. Every stroke forces approx. 5 cu in (82 ml) of blood out into the body, amounting to 500,000 cu in (8193 L) a day. In terms of work, this is the equivalent of raising 1 ton (907 kg) to a height of 41 ft (12.5 m) every 24 hr.
The myocardium receives its blood supply from the coronary arteries that arise from the ascending aorta. Blood from the myocardium drains into several cardiac veins.
The heart initiates its own beat, usually from 60 to 80 beats per minute, but the rate may be changed by impulses from the cardiac centers in the medulla oblongata. Accelerator impulses are carried by sympathetic nerves. Preganglionic neurons in the thoracic spinal cord synapse with postganglionic neurons in the cervical ganglia of the sympathetic trunk; their axons continue to the heart. Sympathetic impulses are transmitted to the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, and myocardium of the ventricles and increase heart rate and force of contraction. Inhibitory impulses are carried by the vagus nerves (parasympathetic). Preganglionic neurons (vagus) originating in the medulla synapse with postganglionic neurons in terminal ganglia in the wall of the heart. Parasympathetic impulses are transmitted to the SA and AV nodes and decrease the heart rate. Sensory nerves from the heart serve for the sensation of pain, which is caused by an insufficient supply of oxygen to the myocardium. The vagus and glossopharyngeal are the sensory nerves for reflex changes in heart rate. These nerves arise from pressoreceptors or chemoreceptors in the aortic arch and carotid sinus, respectively.
Listening to the heart with a stethoscope reveals the intensity, quality, and rhythm of the heart sounds and detects any adventitious sounds, e.g., murmurs or pericardial friction. The two separate sounds heard by the use of a stethoscope over the heart have been represented by the syllables “lubb,” “dupp.” The first sound (systolic), which is prolonged and dull, results from the contraction of the ventricle, tension of the atrioventricular valves, and the impact of the heart against the chest wall and is synchronous with the apex beat and carotid pulse. The first sound is followed by a short pause, and then the second sound (diastolic) is heard, resulting from the closure of the aortic and pulmonary valves. This sound is short and high pitched. After the second sound there is a longer pause before the first is heard again. A very useful technique for listening to the variation in sounds between one area and another is to move the stethoscope in small steps from site to site.
The patient should be recumbent when the examination begins. After all possible signs have been elicited, the examination should be repeated with the patient sitting, standing, or leaning forward, and any variations from this change of position should be noted. Auscultation is performed first while the patient is breathing naturally, next while he holds the breath in both deep inspiration and expiration, and finally while the patient takes three or four forced inspirations. By listening over the entire thoracic cavity, the examiner should try to localize the points at which heart sounds, both normal and abnormal, are heard with the greatest intensity. The examination should proceed from below upward and from left to right.
The normal location of valves should be noted for auscultation. The aortic valve is in the third intercostal space, close to the left side of the sternum; the pulmonary valve is in front of the aorta, behind the junction of the third costal cartilage with the sternum, on the left side. The tricuspid valve is located behind the middle of the sternum about the level of the fourth costal cartilage. Finally, the mitral valve is behind the third intercostal space about 1 in (2.5 cm) to the left of the sternum.
Both heart sounds either are heard better or are actually accentuated in increased heart action from any cause, normal or abnormal, e.g., anemia, vigorous exercise, cardiac hypertrophy, thin chest walls, and lung consolidation as found in pneumonia. Accentuation of the aortic second sound results from hypertrophy of the left ventricle, increased arterial resistance (as in arteriosclerosis with hypertension), or aortic aneurysm. Accentuation of the pulmonary second sound results from pulmonary obstruction (as in emphysema, pneumonia, or hypertrophy of the right ventricle). Both heart sounds are poorly heard or are actually decreased in intensity in general obesity, general debility, degeneration or dilatation of the heart, pericardial or pleural effusion, and emphysema.
The reduplication of heart sounds is probably due to a lack of synchronous action in the valves of both sides of the heart. It results from many conditions but notably from increased resistance in the systemic or the pulmonary circulation (as in arteriosclerosis and emphysema). It is also frequently noted in mitral stenosis and pericarditis.
A murmur (an abnormal sound heard over the heart or blood vessels) may result from obstruction or regurgitation at the valves following endocarditis; dilatation of the ventricle or relaxation of its walls rendering the valves relatively insufficient; aneurysm; a change in the blood constituents (as in anemia); roughening of the pericardial surfaces (as in pericarditis); and irregular action of the heart. Murmurs produced within the heart are called endocardial; those outside, exocardial; those produced in aneurysms, bruits; those produced by anemia, hemic murmurs.
Hemic murmurs, which are soft and blowing and usually systolic, are heard best over the pulmonary valves. They are associated with symptoms of anemia.
An aneurysmal murmur (bruit) is usually loud and booming, systolic, and heard best over the aorta or base of the heart. It is often associated with an abnormal area of dullness and pulsation and with symptoms resulting from pressure on neighboring structures.
Pericardial friction sounds are superficial, rough, and creaking, to and fro in tempo, and not transmitted beyond the precordium. These sounds may be modified by the pressure of the stethoscope.
Murmur intensity and configuration: The intensity (loudness) of murmurs may be graded from I to VI as follows: (1) Grade I-faint, audible only with intense listening in a quiet environment; (2) Grade II-quiet but immediately audible; (3) Grade III-moderately loud; (4) Grade IV-quite loud; a thrill (like the purring of a cat) usually felt over the heart; (5) Grade V-loud enough to be heard with the stethoscope not completely in contact with the chest wall; and (6) Grade VI-loud enough to be heard with the stethoscope close to but not actually touching the chest.
The configuration of sound intensity of a murmur may begin low and rise in intensity (crescendo) or be relatively loud and then decrease in intensity (decrescendo) or some combination of those features or may exhibit the same intensity from beginning to end.
This process not only determines position, force, extent, and rhythm of the apex beat but also detects any fremitus or thrill. A thrill is a vibratory sensation like that when the hand is placed on the back of a purring cat. Thrills at the base of the heart may result from valvular lesions, atheroma of the aorta, aneurysm, and roughened pericardial surfaces (as in pericarditis). A presystolic thrill at the apex is almost pathognomonic of mitral stenosis. In children especially, a precordial bulge, substernal thrust, or apical heave suggests cardiac enlargement.
This procedure determines the shape and extent of cardiac dullness. The normal area of superficial or absolute percussion dullness (the part uncovered by the lung) is detected by light percussion and extends from the fourth left costosternal junction to the apex beat; from the apex beat to the juncture of the xiphoid cartilage with the sternum; and thence up the left border of the sternum. The normal area of deep percussion dullness (the heart projected on the chest wall) is detected by firm percussion and extends from the third left costosternal articulation to the apex beat; from the apex beat to the junction of the xiphoid cartilage with the sternum; and thence up the right border of sternum to the third rib. The lower level of cardiac dullness fuses with the liver dullness and can rarely be determined. The area of cardiac dullness is increased in hypertrophy and dilation of the heart and in pericardial effusion; it is diminished in emphysema, pneumothorax, and pneumocardium.
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