Introduction to cardiac anatomy and physiology

Chapter 1 Introduction to cardiac anatomy and physiology

An appreciation of the anatomy of the heart and great vessels is central to the understanding of cardiac function and disease and for optimal interpretation of diagnostic techniques such as auscultation, echocardiography and radiography. This chapter also reviews cardiovascular physiology focusing on impulse conduction within the equine heart and on the heart as a muscular pump. Although clinically important parameters such as stroke volume, cardiac output and blood pressure are emphasized, these haemodynamic parameters are actually the ultimate functional expression of the biochemical and biophysical processes of myocyte excitation, contraction and relaxation.


The heart can be regarded as a parallel pump system: deoxygenated blood returning from the body enters the right side from where it is directed via the pulmonary arterial system to the lungs for oxygenation. Oxygenated blood returns to the left side of the heart via the pulmonary veins and is then pumped to the body via the systemic arterial system. Deoxygenated blood returns via the systemic veins to the right side. The heart is located within the middle mediastinal space where its long axis is orientated at approximately 10° to vertical with its base lying dorsal and cranial to the apex. The apex is located above the last sternebra cranial to the sternal portion of the diaphragm. The heart consists of two atria and two ventricles, blood entering via the atria and leaving via the ventricles. The right atrium (RA) occupies the cranial part of the heart base and consists of two main parts, the larger part, the sinus venarum cavarum, into which the veins empty, and a conical out-pouching, the auricle. The auricle is triangular and broad-based and curves around the base of the heart towards the left ending cranial to the origin of the main pulmonary artery (Figs. 1.1 and 1.2). The cranial vena cava (draining structures of the head and neck) enters the most dorsal part of the RA, the caudal vena cava (draining abdominal structures) opens into the caudal part and the azygous vein (draining the caudal thorax) enters between the two cavae. The coronary sinus (draining the coronary circulation) opens into the RA ventral to the caudal vena cava. There are also several smaller veins that drain directly into the RA (see Figs. 1.1 and 1.2). On the internal surface of the RA there are pronounced ridges formed by extensive bands of pectinate muscles and dorsally these form the terminal crest at the base of the auricle (Fig. 1.3). The oval fossa is a diverticulum at the point of entrance of the caudal vena cava that is a remnant of the foramen ovale, the communication that exists between the two atria in the fetus.

The right atrioventricular (AV) or tricuspid valve forms the ventral floor of the RA and the entrance to the right ventricle (RV) (see Figs. 1.1 and 1.2). As its name suggests, the tricuspid valve is composed of three large leaflets: one is septal, one lies on the right margin (parietal) and the third lies between the AV opening and the right outflow tract (angular). The leaflets are anchored to the papillary muscles of the RV by a series of chordae tendineae. The RV is a crescent-shaped structure in cross-section and triangular when viewed from its inner aspect (see Fig. 1.2). It wraps around the cranial aspect of the heart and, in this respect, the convention derived from human anatomy ascribing the terms right and left to the heart, is rather misleading. In the horse, the heart would be better defined as having cranial and caudal components. The internal surface of the RV is trabeculated and moderator bands cross the lumen of the RV from the septum to the opposite wall carrying conduction tissue (see Fig. 1.3). These moderator bands vary in size greatly among individuals. Ventrally, the RV does not reach the heart’s apex. It extends dorsally and to the left to form the right outflow tract leading to the main pulmonary artery (PA) via the pulmonary valve (right semilunar valve) valve (see Fig. 1.3). The pulmonary valve consists of three half-moon-shaped cusps, the right, left and intermediate, which occasionally have small fenestrations along their free edges and are attached to a fibrous ring at the base of the pulmonary artery. The PA arises from the left side of the RV and curves dorsally, caudally and medially to run under the descending aorta where it branches into left and right. The right PA passes over the cranial part of the left atrium and under the trachea while the left PA is in contact with the bulk of the dorsal surface of the left atrium (LA) (see Fig. 1.2).

The LA forms the caudal part of the base of the heart and also has an auricle, extending laterally and cranially on the left side. The left auricle is more pointed than the right auricle and lacks a terminal crest (see Fig. 1.2). The LA lacks the extensive pectinate muscles that characterize the RA. Seven or eight pulmonary veins enter the LA around its caudal and right aspects. A depression may be appreciated on the septal surface, corresponding with the site of the fetal foramen ovale. The ventral floor of the LA consists of the left AV, mitral or bicuspid valve (see Figs. 1.1 to 1.3). This consists of two large leaflets, the septal and parietal leaflets which are larger and thicker than those of the tricuspid valve. The left ventricle (LV) is conical with walls approximately three times thicker than those of the RV, and it forms the bulk of the caudal aspect of the heart including the apex. The portion of the wall that forms the division between the LV and RV is called the interventricular septum while the remainder is termed the free wall. Arising from the free wall are two large papillary muscles that are symmetrically located to the left and right sides of the free wall and anchor the chordae tendineae of the mitral valve (see Fig. 1.2). The interventricular septum (IVS) is mainly composed of muscular tissue, but at its most dorsal extent the membranous or nonmuscular septum is thinner and composed of more fibrous tissue. The left ventricular outflow tract lies in the centre of the heart and the aortic (left semilunar) valve consists of three half-moon-shaped cusps that are stronger and thicker than those of the pulmonary valve. The free edges often contain central nodules of fibrous tissue but may also have fenestrations. The cusps are attached to the fibrous and cartilaginous tissues that comprise the aortic annulus. The proximal segment of the aorta is the ascending aorta; it sweeps dorsally and cranially between the main PA on the left and the RA on the right. It then continues caudally and to the left as the descending aorta. The base of the aorta is bulbous in shape, and this bulbous portion is the sinus of Valsalva. The sino-tubular junction marks the point where the vessel becomes more tubular (see Figs. 1.1 and 1.3). To provide the blood to the myocardium, two coronary arteries arise from the right and left sinus of Valsalva. The most caudally located third part of the sinus lacks a coronary artery and is termed the septal (noncoronary) sinus. The same terminology is applied to the cusps of the aortic valve (see Fig. 1.2). The ligamentum arteriosum can be found in the site corresponding to the remnant of the ductus arteriosus, a vessel joining the PA to the descending aorta in the fetus (see Fig. 1.3).

The heart lies within the pericardial cavity that is comprised of the parietal pericardium and visceral pericardium (epicardium). The parietal pericardium attaches to the tunica externa of the proximal aorta, pulmonary artery, vena cavae and pulmonary veins. Between the parietal pericardium and visceral pericardium (epicardium) is a thin film of free serous fluid (pericardial fluid). The ventricular myocardium consists of muscle layers arranged both longitudinally and also spiralling circumferentially. The muscular tissue of the atria is separated from that of the ventricles by a fibrous skeleton that surrounds the atrioventricular orifices. The myocardium receives its blood supply from the coronary arteries and veins. There is an extensive autonomic nervous supply to the heart from the vagus nerve and sympathetic trunk (see Chapter 2).


Contraction of cardiac myocytes occurs only in response to generation of action potentials in the cell membranes. Thus, normal mechanical function of the heart requires an orderly sequence of action potential generation and propagation through the atrial and ventricular myocardium. Spontaneous generation of an action potential without an external stimulus (automaticity) occurs normally as an inherent property of myocytes within the sinoatrial (SA) node, the atrioventricular (AV) node and the specialized conduction fibres of the His Purkinje system. However, cells of the SA node normally have the fastest rate of spontaneous action potential generation; consequently, the SA node is the site of impulse formation in the normal heart. The SA node is richly innervated by the parasympathetic and sympathetic nervous systems that provide stimuli to alter heart rate.

From the SA node, the impulse spreads over the atria to the AV node producing electrical potentials that inscribe a P wave on the surface electrocardiogram (ECG). Since spread of the cardiac impulse through the atria is in an overall direction that is dorsal to ventral, P waves are typically positive in a base apex ECG recording (see Chapter 6). The impulse is then conducted slowly through the AV node producing a delay recognized by an isoelectric segment (PR segment) on the ECG. The degree of AV conduction delay is influenced by autonomic tone with vagal tone reducing and sympathetic tone increasing rate of conduction. Autonomic tone, therefore, becomes an important determinant of heart rate in horses with dysrhythmias such as atrial fibrillation.

After relatively slow conduction through the AV node, the cardiac impulse is rapidly conducted over the bundle of His and Purkinje system to the terminal Purkinje fibres and the working ventricular myocytes. The equine Purkinje system is widely distributed throughout the right and left ventricular myocardium, penetrating the entire thickness of the ventricular walls. This vast distribution of the Purkinje system is physiologically important because the conduction velocity of working ventricular myocytes is approximately 6 times slower than conduction velocity of the Purkinje cells. Consequently, the time duration and sequence of ventricular activation and, ultimately, the surface ECG is affected. Specifically, the earliest phase of ventricular activation in horses consists of depolarization of a small apical region of the septum (Fig. 1.4). This early depolarization is often in an overall left to right and ventral direction. The electrical potentials generated from this early phase of ventricular activation may produce the initial portion of the QRS complex on the surface ECG. However, there is significant variation in the direction of this early phase of ventricular activation, and in some horses the vectors of local electrical activity effectively cancel each other thereby eliminating any deflection on the surface ECG. Thus, the duration of QRS complexes in normal horses may vary from 0.08 to 1.4 seconds. Immediately after early ventricular activation of the apical portion of the septum, the major masses of both ventricles and the middle portion of the septum are depolarized with a single “burst” of activation that results from the vast distribution and penetration of the Purkinje fibres. Since this depolarization occurs without a spread of the impulse in any specific direction it contributes negligibly to genesis of the QRS complex on the ECG. The final phase of equine ventricular activation consists of depolarization of the basilar third of the septum, which occurs in an apical to basilar direction. This final phase of activation is responsible for generating most of the QRS complex and normally produces a negative deflection in a base apex recording (see Fig. 1.4).2,3


The cardiac cycle describes and relates temporally the mechanical, electrical and acoustical events that occur in the heart and great vessels. The cardiac cycle is usually described from onset of systole to end of diastole. It is helpful to describe the cardiac cycle with a diagram showing time on the horizontal axis (Fig. 1.5). An understanding of the cardiac cycle is essential for understanding function of the normal heart and for an appreciation of how various diseases disturb normal function.

The cardiac cycle is divided into ventricular systole and ventricular diastole. Systole is comprised of the isovolumic contraction phase and ventricular ejection. Diastole consists of the isovolumic relaxation phase, the rapid filling phase, diastasis and atrial contraction. It is helpful to recall that mechanical events are stimulated by electrical depolarization, and, thus, the mechanical events occur slightly after the electrical events on the cardiac cycle diagram.


Ventricular diastole begins at aortic valve closure. The left ventricular pressure, which has been declining due to relaxation of the myocytes, continues to decline rapidly during early diastole, but ventricular volume remains constant because all of the cardiac valves are closed. This initial phase of diastole is, therefore, isovolumic relaxation, and the rate of intraventricular pressure decline during this phase of the cardiac cycle is determined by the rate of active relaxation of the myofibres. When left ventricular pressure drops below left atrial pressure, the mitral valve leaflets open and ventricular filling begins. Opening of the mitral valve marks the onset of the rapid filling phase of diastole during which filling occurs passively due to a difference in pressure between the ventricle and atrium that results largely from myocyte relaxation. The velocity of left ventricular inflow and the volume of blood transferred from the atrium to the ventricle during this early filling phase are largely determined by the increasing pressure gradient created by the continuing decline in tension in the ventricular myocytes at this time. As left ventricular pressure decline slows and ventricular filling progresses the atrioventricular pressure difference approaches zero and ventricular volume reaches a plateau. This phase of diastole is known as diastasis because minimal changes in intraventricular pressure and volume are occurring at this time. The duration of diastasis varies inversely with heart rate, and at resting heart rates in horses diastasis is the longest phase of diastole. Diastasis becomes progressively shorter as heart rate increases, but the shortening of diastasis from physiological increases in heart rate has a negligible effect on ventricular filling. Atrial systole is the final phase of ventricular diastole. This phase begins slightly after the P wave of the ECG. Atrial contraction recreates an atrioventricular pressure gradient that produces augmented LV filling. In healthy resting horses atrial systole has minimal effects on ventricular filling and cardiac performance. However, absence of atrial contraction or loss of atrioventricular synchrony in exercising horses has a considerable adverse effect on ventricular filling and cardiac output.

Although this discussion of the cardiac cycle has focused on events occurring on the left side of the circulation, events on the right side are nearly simultaneous and analogous. The main difference between the two sides of the heart is that the right ventricular and pulmonary artery peak systolic pressures are lower than the comparable left-sided pressures.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Introduction to cardiac anatomy and physiology
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