The Cardiovascular System

The Cardiovascular System

Narciso Rodriguez

Functional Anatomy


Anatomy of the Heart

The heart is a hollow, four-chambered muscular organ approximately the size of a fist. It is positioned obliquely in the middle compartment of the mediastinum of the chest, just behind the sternum (Figure 9-1). Approximately two-thirds of the heart lies to the left of the midline of the sternum between the points of attachment of the second through the sixth ribs. The apex of the heart is formed by the tip of the left ventricle and lies just above the diaphragm at the level of the fifth intercostal space to the left. The base of the heart is formed by the atria and projects to the patient’s right lying just below the second rib. It is level with the second rib below the sternum. Posteriorly, the heart rests on the bodies of the fifth to the eighth thoracic vertebrae. Because of its position between the sternum and the spine, rhythmic compression of the heart can maintain blood flow during cardiopulmonary resuscitation.

Externally, surface grooves called sulci mark the boundaries of the heart chambers. Compared with the ventricles, the atria are small, thin-walled chambers that contribute little to the total pumping activity of the heart.

The heart is enclosed in a double-walled sac called the pericardium. The outer fibrous layer consists of tough connective tissue. The inner serous layer is thinner and more delicate. The structure of the pericardium can be summarized as follows:

A thin layer of fluid called the pericardial fluid separates the two layers of the serous pericardium. This layer of fluid helps minimize friction as the heart contracts and expands within the pericardium. Inflammation of the pericardium results in a clinical condition called pericarditis. An abnormal amount of fluid can accumulate between the layers resulting in a pericardial effusion. A large pericardial effusion may affect the pumping function of the heart resulting in a cardiac tamponade. A cardiac tamponade compresses the heart muscle leading to a serious decrease in blood flow to the body, which ultimately may lead to shock and death.

The heart wall consists of three layers: (1) outer epicardium, (2) middle myocardium, and (3) inner endocardium. The myocardium composes the bulk of the heart muscle and consists of bands of involuntary striated muscle fibers. The contraction of these muscle fibers creates the pumplike action needed to move blood throughout the body.

Support for the four interior chambers and valves of the heart is provided by four atrioventricular rings, which form a fibrous “skeleton.” Each ring is composed of dense connective tissue termed anulus fibrosus cordis. This connective tissue, besides providing an anchoring structure for the heart valves, electrically isolates the atria from the ventricle. No impulses can be transmitted through the heart tissue from the atria to the ventricles.

The two atrial chambers are thin-walled “cups” of myocardial tissue, separated by an interatrial septum. On the right side of the interatrial septum is an oval depression called the fossa ovalis cordis, which is the remnant of the fetal foramen ovale, the shunt that allowed blood to enter the left atrium from the right atrium before birth. In addition, each atrium has an appendage, or auricle, the function of which is unknown. In the presence of cardiac dysrhythmias, blood flow can become stagnant on these appendages leading to the formation of thrombi.

The two lower heart chambers, or ventricles, make up the bulk of the heart’s muscle mass and do most of the pumping that circulates the blood (Figure 9-2). The mass of the left ventricle is normally about two-thirds larger than the mass of the right ventricle and has a spherical appearance when viewed in anteroposterior cross section. The right ventricle is thin-walled and oblong, forming a pocket-like attachment to the left ventricle. Because of this relationship, contraction of the left ventricle pulls in the right ventricular wall, aiding its contraction. The effect, termed left ventricular aid, explains why some forms of right ventricular failure are less harmful than might be expected. The right and left ventricles are separated by a muscle wall termed the interventricular septum (see Figure 9-2).

The valves of the heart are flaps of fibrous tissue firmly anchored to the anulus fibrosus cordis (Figure 9-3). Because they are located between the atria and ventricles, they are called atrioventricular valves. The valve between the right atrium and ventricle is called the tricuspid valve. The valve between the left atrium and ventricle is the bicuspid, or mitral, valve. The atrioventricular valves close during systole (contraction of the ventricles), preventing backflow of blood into the atria. Closure of these valves provides a critical period of isovolemic contraction, during which chamber pressures quickly increase just before ejection of the blood.

The free ends of the atrioventricular valves are anchored to papillary muscles of the endocardium by the chordae tendineae cordis (see Figure 9-2). During systole, papillary muscle contraction prevents the atrioventricular valves from swinging upward into the atria. Damage to either the chordae tendineae cordis or the papillary muscles can impair function of the atrioventricular valves and cause leakage upward into the atria.

Common valve problems include regurgitation and stenosis. Regurgitation is the backflow of blood through an incompetent or a damaged valve. Stenosis is a pathologic narrowing or constriction of a valve outlet, which causes increased pressure in the proximal chamber and vessels. Both conditions affect cardiac performance. In mitral stenosis, high pressures in the left atrium back up into the pulmonary circulation. This can cause pulmonary edema and a diastolic murmur (see Chapter 15).

A set of semilunar valves separates the ventricles from their arterial outflow tracts, the pulmonary artery and the aorta (see Figure 9-3). Consisting of three half-moon–shaped cusps attached to the arterial wall, these valves prevent backflow of blood into the ventricles during diastole (or when the chambers of the heart fill with blood). The pulmonary valve is at the outflow tract of the right ventricle. During the cardiac contraction (systole), blood is ejected out of the heart and to the lungs through the right valves and to the body through the left valves. Similar to the atrioventricular valves, the semilunar valves can leak (regurgitation) or become obstructed (stenosis).

Similar to the lungs, the heart has its own circulatory system, which is called the coronary circulation. However, in contrast to the lungs, the heart has a high metabolic rate, which requires more blood flow per gram of tissue weight than any other organ except the kidney. To meet these needs, the coronary circulation provides an extensive network of branches to all myocardial tissue (Figure 9-4).

Two main coronary arteries, a left and a right, arise from the root of the aorta. Because of their position underneath the aortic semilunar valves (see Figure 9-4), the coronary arteries get the maximal pulse of pressure generated by contraction of the left ventricle. Blood flows through the coronary arteries only during ventricular diastole (relaxation). A healthy heart muscle requires about image of the blood supply of the body to function properly. As might be expected, partial obstruction of a coronary artery may lead to tissue ischemia (decreased oxygen [O2] supply), a clinical condition called angina pectoris. Complete obstruction may cause tissue death or infarct, a condition called myocardial infarction.

Mini Clini

Mitral Stenosis, Poor Oxygenation, and Increased Work of Breathing

The mitral valve lies between the left atrium and left ventricle. A stenotic mitral valve is one that is narrowed and offers high resistance to the blood flowing into the left ventricle from the left atrium. Pulmonary edema is a condition in which fluid collects in the spaces between the alveolar and capillary walls, known as the interstitial spaces.


Blood flows from the lungs into the left atrium, where it may encounter high resistance through a narrowed, stenotic mitral valve; this causes high pressure to build in the left atrium. Pressure in the pulmonary veins and eventually in the pulmonary capillaries also increases. This high pressure within the capillaries engorges them and forces fluid components of the blood plasma out of the vessels into the interstitial spaces of the lungs, creating pulmonary edema. This collection of fluid interferes with O2 diffusion from the lung into the blood. Engorged capillaries surrounding the alveoli create a stiff “web” around each alveolus, which makes expanding the lungs difficult. Some areas of the lung expand more easily than others; this causes inhaled air to be preferentially directed into these compliant regions, whereas “stiffer,” more noncompliant regions are underventilated. The underventilated regions do not properly oxygenate the blood as perfusing them. Mitral stenosis, a cardiac problem, has significant pulmonary consequences.

For a description of the major branches of the coronary arteries and their areas of vascularization, see Table 9-1 and Figure 9-4. After passing through the capillary beds of the myocardium, the venous blood is collected by the coronary veins that closely parallel the arteries (see Figure 9-4). These veins gather together into a large vessel called the coronary sinus, which passes left to right across the posterior surface of the heart. The coronary sinus empties into the right atrium between the opening of the inferior vena cava and the tricuspid valve.

In addition to these major routes for return blood flow, some coronary venous blood flows back into the heart through the thebesian veins. The thebesian veins empty directly into all the heart chambers. Any blood coming from the thebesian veins that enters the left atrium or ventricle mixes with arterial blood coming from the lungs. Whenever venous blood mixes with arterial blood, the overall O2 content decreases. Because the thebesian veins bypass, or shunt, around the pulmonary circulation, this phenomenon is called an anatomic shunt. When combined with a similar bypass in the bronchial circulation (see Chapter 8), these normal anatomic shunts account for approximately 2% to 3% of the total cardiac output.

Properties of the Heart Muscle

The performance of the heart as a pump depends on its ability to (1) initiate and conduct electrical impulses and to (2) contract synchronously the heart’s muscle fibers quickly and efficiently. These actions are possible only because myocardial tissue possesses four key properties:

Excitability is the ability of cells to respond to electrical, chemical, or mechanical stimulation. The myocardial property of excitability is the same as that exhibited by other muscles and tissues. Electrolyte imbalances and certain drugs can increase myocardial excitability and produce abnormalities in electrical conduction that may lead to cardiac arrhythmias.

Inherent rhythmicity, or automaticity, is the unique ability of the cardiac muscle to initiate a spontaneous electrical impulse. Although such impulses can arise from anywhere in the cardiac tissue, this ability is highly developed in specialized areas called heart pacemaker, or nodal tissues. The sinoatrial node and the atrioventricular node are good examples of specialized heart tissues that are designed to initiate electrical impulses (see Chapter 17). An electrical impulse from any source other than a normal heart pacemaker is considered abnormal and represents one of the many causes of cardiac arrhythmias.

Conductivity is the ability of myocardial tissue to spread, or radiate, electrical impulses. This property is similar to that of smooth muscle in that it allows the myocardium to contract without direct neural innervation (as required by skeletal muscle). The rate at which electrical impulses spread throughout the myocardium is extremely variable. These differences in conduction velocity are needed to ensure synchronous contraction of the cardiac chambers. Abnormal conductivity can affect the timing of chamber contractions and decrease cardiac efficiency.

Contractility, in response to an electrical impulse, is the primary function of the myocardium. In contrast to the contractions of other muscle tissues, however, cardiac contractions cannot be sustained or tetanized because myocardial tissue exhibits a prolonged period of inexcitability after contraction. The period during which the myocardium cannot be stimulated is called the refractory period, and it lasts approximately 250 msec, nearly as long as the heart contraction or systole.

Microanatomy of the Heart Muscle

Understanding how cardiac muscle contracts requires knowledge of the microanatomy of the heart. In contrast to the long, cylindrical, multinucleated skeletal muscle fibers, cardiac cells are short, fat, branched, and interconnected. As seen under the microscope, myocardial muscle fibers are approximately 15 µm wide × 100 µm long. Individual fibers are enclosed in a membrane called the sarcolemma, which is surrounded by a rich capillary network (Figure 9-5).

Cardiac fibers are separated by irregular transverse thickenings of the sarcolemma called intercalated discs. These discs provide structural support and aid in electrical conduction between fibers. Each muscle fiber consists of many smaller units called myofibrils, which contain repeated structures approximately 2 µm in size termed sarcomeres. Within the sarcomeres are contractile protein filaments responsible for shortening the myocardium during systole. These proteins are of two types: thick filaments composed mainly of myosin and thin filaments composed mostly of actin.

According to the sliding filament theory, myocardial cells contract when actin and myosin combine to form reversible bridges between these thick and thin filaments. These bridges cause filaments to slide over one another, shortening the sarcomere and muscle fibers as a whole.

In principle, the tension developed during myocardial contraction is directly proportional to the number of cross-bridges between the actin and myosin filaments. The number of cross-bridges is directly proportional to the length of the sarcomere. This principle underlies Starling’s law of the heart, also known as the Frank-Starling law. According to this law, the more a cardiac fiber is stretched, the greater the tension it generates when contracted.

The Frank-Starling law holds true up to a sarcomere length of 2.2 µm. Beyond this length, the actin and myosin filaments become partially disengaged, and fewer cross-bridges can be formed. With fewer cross-bridges, the overall tension developed during contraction is less. This relationship is extremely important and is explored later in the discussion of the heart as a pump.

Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on The Cardiovascular System
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