Cardiovascular System

Chapter 7

Cardiovascular System

Physiology of the cardiovascular system

The function of the cardiovascular system is to maintain an adequate supply of blood to all the tissues of the body. This is accomplished by the rhythmic contractions of the heart, the rate of which is controlled by the autonomic nervous system. The vagus nerve slows heart action by transmitting the chemical acetylcholine, whereas the sympathetic nervous system stimulates the release of epinephrine that accelerates the heart rate and increases the force of its contractions.

The heart consists of four chambers whose walls are composed of striated muscle (myocardium), and it is lined with a smooth delicate membrane (endocardium), which is continuous with the inner surface of the blood vessels (Figure 7-1). The heart consists of two atria and two ventricles, with a partition (the septum) separating the right and left sides of the heart. The ventricles are considerably larger and thicker walled than the atria because they have a substantially heavier pumping load. Between each atrium and its associated ventricle are the atrioventricular valves (one on the right and one on the left side of the heart), which

Radiographer Notes

Plain chest radiography and fluoroscopy of the cardiovascular system are used to identify abnormalities in the size and shape of the heart and to detect calcification of heart valves, coronary arteries, or the pericardium. The presence and extent of functional disorders are better demonstrated using angiography, computed tomography (CT), ultrasound, radionuclide imaging, and magnetic resonance imaging (MRI).

As for all chest radiographs, it is essential that the radiographer perform cardiovascular studies with the patient positioned correctly and using proper technical factors. To this end, it would be helpful for the reader to review the radiographer notes at the beginning of the chapter on the respiratory system. An abnormality identified on a chest radiograph may be the first evidence of cardiovascular disease in an asymptomatic patient.

Radiographers can specialize in invasive diagnostic and therapeutic cardiovascular procedures, gain advanced certification in cardiovascular interventional technology, and be employed by cardiac or vascular catheterization laboratories. Angiocardiography is a diagnostic procedure performed to identify the exact anatomic location of an intracardiac disorder. Coronary angioplasty is a therapeutic procedure in which a narrowed coronary artery is dilated by inflation of a balloon, which is attached to a catheter and manipulated fluoroscopically to the site of the stenosis. Because both angiocardiography and angioplasty involve the use of contrast material in patients who often have severe preexisting medical conditions, it is essential that the radiographer be always alert to the possibility of cardiac or respiratory arrest and prepared to immediately assist with basic and advanced life support.

The injection of contrast material into arteries (arteriograms) and veins (venograms) can be performed in almost any portion of the body. As in the heart, these invasive studies use potentially dangerous substances, so the radiographer must be alert for possible complications and prepared to assist in cardiorespiratory emergencies. In addition, these examinations require that the radiographer be trained in sterile technique, be able to use specialty equipment, and be familiar with the various types of catheters that are inserted into the vascular system for the delivery of contrast material.

Ultrasound, Doppler ultrasound, CT, and MRI are quickly becoming preferred initial modalities for imaging the vascular system.

permit blood to flow in only one direction (Figure 7-2). These valves consist of flaps (or cusps) of endocardium that are anchored to the papillary muscles of the ventricles by cordlike structures called the chordae tendineae. The mitral valve (bicuspid valve) (left atrioventricular) between the left atrium and the left ventricle has two cusps, whereas the tricuspid valve (right atrioventricular) between the right atrium and the right ventricle has three cusps. The semilunar valves separate the ventricles from the great vessels leaving the heart. The pulmonary valve lies between the right ventricle and the pulmonary artery, whereas the aortic valve separates the aorta from the left ventricle.

Deoxygenated venous blood is returned to the heart from the body through the superior and inferior venae cavae, which empty into the right atrium. Blood flows from the right atrium across the tricuspid valve into the right ventricle, which then pumps blood through the pulmonary valve into the pulmonary artery. Within the capillaries of the lungs, the red blood cells take up oxygen and release carbon dioxide. The freshly oxygenated blood then passes through the pulmonary veins into the left atrium, from which it flows across the mitral valve into the left ventricle. Contraction of the left ventricle forces oxygenated blood through the aortic valve into the aorta and the rest of the arterial tree to provide oxygen and nourishment to tissues throughout the body. The general circulation of the body is termed the systemic circulation (Figure 7-3), whereas the circulation of blood through the lungs is the pulmonary circulation. Because greater pressure is needed to pump blood through the systemic circulation than through the pulmonary circulation, the wall of the left ventricle is considerably thicker than that of the right ventricle.

The atria and ventricles alternately contract and relax. The contraction phase is called systole; the heart chambers relax and fill with blood during diastole (the relaxation phase). The normal cardiac impulse that stimulates mechanical contraction of the heart arises in the sinoatrial (SA) node, or pacemaker, which is situated in the right atrial wall near the opening of the superior vena cava. The impulse passes slowly through the atrioventricular (AV) node, which is located in the right atrium along the lower portion of the interatrial septum, and then spreads quickly throughout the ventricles by way of a band of atypical cardiac muscle fibers the bundle of His. The bundle of His terminates in Purkinje fibers, which can conduct impulses throughout the muscle of both ventricles and stimulate them to contract almost simultaneously. Specialized pacemaker cells in the SA node possess an intrinsic rhythm, so that even without any stimulation by the autonomic nervous system the node itself initiates impulses at regular intervals (about 60 to 75 beats per minute).

If the SA node for some reason is unable to generate an impulse, pacemaker activity shifts to another excitable component of the conduction system. These ectopic pacemakers also generate impulses rhythmically, although at a much slower rate. For example, if the AV node were to control pacemaker activity, the heart would beat 40 to 60 times per minute. If the conduction system of the heart is unable to maintain an adequate rhythm, the patient may receive an artificial pacemaker that electrically stimulates the heart, either at a set rhythm or only when the heart rate decreases below a preset minimum.

The heart muscle is supplied with oxygenated arterial blood by way of the right and left coronary arteries. These small vessels arise from the aorta just above the aortic valve. Unoxygenated blood from the myocardium drains into the coronary veins, which lead into the coronary sinus before opening into the right atrium.

The heart is surrounded by a double membranous sac termed the pericardium. The pericardium has a well-lubricated lining that protects against friction and permits the heart to move easily during contraction.

Congenital heart disease

Left-to-Right Shunts

The most common congenital cardiac lesions are left-to-right shunts, which permit mixing of blood in the systemic and pulmonary circulations. Because blood is preferentially shunted from the high-pressure systemic circulation to the relatively low-pressure pulmonary circulation, the lungs become overloaded with blood. The magnitude of the shunt depends on the size of the defect and the differences in pressure on the two sides. An increased load on the heart produces enlargement of specific cardiac chambers, depending on the location of the shunt. The size of the defect determines the hemodynamic consequence for the systemic cardiac output.

The most common congenital cardiac lesion is atrial septal defect, which permits free communication between the two atria as a result of either lack of closure of the foramen ovale after birth or its improper closure during gestation. Because the left atrial pressure is usually higher than the pressure in the right atrium, the resulting shunt is from left to right and causes increased pulmonary blood flow and overloading of the right ventricle. This produces the radiographic appearance of enlargement of the right ventricle, the right atrium, and the pulmonary outflow tract (Figure 7-4).


Figure 7-4 Atrial septal defect. Frontal projection of the chest demonstrates cardiomegaly along with an increase in pulmonary vascularity reflecting a left-to-right shunt. Small aortic knob (white arrow) and descending aorta (small arrows) are dwarfed by enlarged pulmonary outflow tract (open arrow).

In a patient with a ventricular septal defect, the resulting shunt is also from left to right because the left ventricular pressure is usually higher than the pressure in the right ventricle. The shunt causes increased pulmonary blood flow and consequently increased pulmonary venous return (Figure 7-5). This leads to diastolic overloading and enlargement of the left atrium and left ventricle. Because shunting occurs primarily in systole and any blood directed to the right ventricle immediately goes into the pulmonary artery, there is no overloading of the right ventricle and radiographically no right ventricular enlargement is seen.


Figure 7-5 Ventricular septal defect. Heart is enlarged and somewhat triangular, and there is increased pulmonary vascular volume. Pulmonary trunk is very large and overshadows the normal-sized aorta, which seems small by comparison.

The third major type of left-to-right shunt is patent ductus arteriosus. The ductus arteriosus is a vessel that extends from the bifurcation of the pulmonary artery to join the aorta just distal to the left subclavian artery. It serves to shunt blood from the pulmonary artery into the systemic circulation during intrauterine life. Persistence of the ductus arteriosus, which normally closes soon after birth, results in a left-to-right shunt. The flow of blood from the higher-pressure aorta to the lower-pressure pulmonary artery causes increased pulmonary blood flow, and an excess volume of blood is returned to the left atrium and left ventricle. Radiographically, there is enlargement of the left atrium, the left ventricle, and the central pulmonary arteries, along with a diffuse increase in pulmonary vascularity (Figure 7-6). The increased blood flow through the aorta proximal to the shunt produces a prominent aortic knob in contrast to the small- or normal-size aorta seen in atrial and ventricular septal defects.

All left-to-right shunts can be complicated by the development of pulmonary hypertension (Eisenmenger’s syndrome). This is caused by increased vascular resistance within the pulmonary arteries related to chronic increased flow through the pulmonary circulation. Pulmonary hypertension appears radiographically as an increased fullness of the central pulmonary arteries with abrupt narrowing and pruning of peripheral vessels (Figure 7-7). The elevation of pulmonary arterial pressure tends to balance or even reverse the left-to-right shunt, thus easing the volume overloading of the heart.

Radiographic Appearance

Chest radiographs provide an initial assessment of pulmonary vasculature, size of the main pulmonary arteries, size and position of the aorta, and size and contour of the cardiac silhouette. In the preceding paragraphs, specific descriptions appear with each septal defect.

Doppler echocardiography can identify atrial and ventricular defects and extent of blood flow to determine the severity of the left-to-right shunting (Figure 7-8). Pressures can be measured to determine cardiac output from both the atria and ventricles. Dilatation of the ventricles implies patent ductus arteriosus.

Spin-echo magnetic resonance imaging (MRI), breath-hold magnetic resonance angiography (MRA), and cine MRI studies are being used to demonstrate congenital heart disease in cases in which ultrasonography is not diagnostic or feasible. MRI demonstrates both the morphologic and the functional anomalies in multiple planes. Patent ductus arteriosus appears as a signal loss on cine MRI and MRA images.

Angiocardiography is the most definitive imaging technique for demonstrating the atria and ventricles of the heart, but it is also the most invasive.

Tetralogy of Fallot

Tetralogy of Fallot is the most common cause of cyanotic congenital heart disease. It consists of four (thus “tetra”) abnormalities: (1) high ventricular septal defect, (2) pulmonary stenosis, (3) overriding of the aortic orifice above the ventricular defect, and (4) right ventricular hypertrophy. Pulmonary stenosis causes an elevation of pressure in the right ventricle and hypertrophy of that chamber. Because of the narrow opening of the pulmonary valve, an inadequate amount of blood reaches the lungs to be oxygenated. The ventricular septal defect and the overriding of the aorta produce right-to-left shunting of unoxygenated venous blood into the left ventricle and then into the systemic circulation, thus increasing the degree of cyanosis.

Radiographic Appearance

Enlargement of the right ventricle causes upward and lateral displacement of the apex of the heart (Figure 7-9). This results in the classic coeur en sabot appearance, in which the heart resembles the curved-toe portion of a wooden shoe. In about one fourth of patients with tetralogy of Fallot, the aorta is on the right side.

Currently, echocardiography is the modality of choice to demonstrate the four abnormalities constituting tetralogy of Fallot. Spin-echo MRI best demonstrates the ventricular septal defect, right ventricular outflow (pulmonary stenosis), overriding aorta, and right ventricular hypertrophy. Cine MRI shows pulmonary stenosis as a flow void, for demonstrating it better than echocardiography.

Coarctation of the Aorta

Coarctation refers to a narrowing, or constriction, of the aorta that most commonly occurs just beyond the branching of the blood vessels to the head and arms. The blood supply and the pressure to the upper extremities are higher than normal. As a result, there is decreased blood flow through the constricted area to the abdomen and legs. Classically the patient has normal blood pressure in the arms, but very low blood pressure in the legs. Coarctation of the aorta is the most frequent cause of hypertension in children.

The relative obstruction of aortic blood flow leads to the progressive development of collateral circulation—the enlargement of normally tiny vessels in an attempt to compensate for the inadequate blood supply to the lower portion of the body.

Radiographic Appearance

Coarctation of the aorta is often seen radiographically as rib notching (usually involving the posterior fourth to eighth ribs) resulting from pressure erosion by dilated and pulsating intercostal collateral vessels, which run along the inferior margins of these ribs (Figure 7-10A). Notching of the posterior border of the sternum may be produced by dilation of mammary artery collaterals.

Coarctation of the aorta often causes two bulges in the region of the aortic knob that produce a characteristic figure-3 sign on plain chest radiographs (Figure 7-10B) and a reverse figure-3 (or figure-E) impression on the barium-filled esophagus (Figure 7-10C). The more cephalic bulge represents dilatation of the proximal aorta and the base of the subclavian artery (prestenotic dilatation); the lower bulge reflects poststenotic aortic dilatation.

With use of echocardiography to evaluate the aortic arch, the severity of the coarctation can be determined. Doppler echocardiography measures the gradient flow at the stenosis, and the diastolic runoff can be demonstrated.

Aortography can accurately localize the site of obstruction, determine the length of the coarctation, and identify any associated cardiac malformations. More recently, MRI has been used to demonstrate aortic narrowing (Figure 7-11) and to evaluate the appearance of the aorta after corrective surgery.

Acquired vascular disease

Coronary Artery Disease

Narrowing of the coronary arteries causes oxygen deprivation of the myocardium and ischemic heart disease. In most patients, narrowing of the lumen of one or more of the coronary arteries is attributable to the deposition of fatty material on the inner arterial wall (atherosclerosis). Factors predisposing to the development of coronary artery disease include hypertension, obesity, smoking, a high-cholesterol diet, and lack of exercise.

The speed and degree of luminal narrowing determine whether an atherosclerotic lesion causes significant and clinically evident ischemia. Temporary oxygen insufficiency causes angina pectoris, a feeling of severe chest pain that may radiate to the neck, jaw, and left arm (sometimes both arms) and that is often associated with the sensation of chest tightness or suffocation. Attacks of angina pectoris are often related to a sudden increase in the demand of the myocardium for oxygen, such as after strenuous exercise or a heavy meal or with emotional stress or exposure to severe cold. The placing of a nitroglycerin tablet under the tongue causes venous dilatation, thus decreasing preload and myocardial oxygen demand.

Occlusion of a coronary artery deprives an area of myocardium of its blood supply and leads to the death of muscle cells (myocardial infarction) in the area of vascular distribution. The size of the coronary artery that is occluded and the myocardium that it supplies determines the extent of heart muscle damage. The greater the area affected, the poorer the prognosis because of the increased loss of pumping function that may result in congestive heart failure (CHF). A favorable prognostic factor is the development of collateral circulation, through which blood from surrounding vessels is channeled into the damaged tissue. If the patient survives, the infarcted region heals with fibrosis. Long-term complications include the development of thrombi on the surface of the damaged area and the production of a local bulge (ventricular aneurysm) at the site of the weakness of the myocardial wall.

Radiographic Appearance

Radionuclide thallium perfusion scanning is the major noninvasive study for assessment of regional blood flow to the myocardium. Focal decreases in thallium uptake that are observed immediately after exercise but are no longer identified on delayed scans usually indicate transient ischemia associated with significant coronary artery stenosis or spasm. After exercise, focal defects that remain unchanged on delayed scans more frequently reflect scar formation. A normal thallium exercise scan makes the diagnosis of myocardial ischemia unlikely, although in about 10% of patients with significant obstructive disease, the presence of sufficient collateral vessels can prevent the radionuclide demonstration of regional ischemia.

Radionuclide CT scanning (single-photon emission computed tomography, or SPECT), using technetium pyrophosphate or other compounds that are taken up by acutely infarcted myocardium, is a new noninvasive technique for detecting, localizing, and classifying myocardial necrosis (Figure 7-12). Newer CT technology (spiral multidetector) provides visualization of the coronary arteries in a noninvasive approach. CT quantifies the artery calcification, evaluates stenosis, measures cardiac function, and analyzes plaque. To best demonstrate the coronary arteries, electrocardiography-synchronized scanning is completed in the diastolic phase (Figure 7-13, p. 260). On CT, areas of myocardial ischemia appear as regions of decreased attenuation because of the higher water content resulting from intramyocardial cellular edema. Multidetector helical CT scans provide calcium screening for detecting hard plaque. To evaluate soft plaque, CT angiography (CTA) is required. Studies have indicated that MRI is also of value in detecting early signs of muscular necrosis in myocardial infarction (Figure 7-14, p. 260) and may help determine whether the infarction is acute or remote.

Plain chest radiographs are usually normal or nonspecific in most patients with ischemic heart disease. Calcification of a coronary artery, although infrequently visualized on routine chest radiographs and usually requiring cardiac fluoroscopy, strongly suggests the presence of hemodynamically significant coronary artery disease (Figure 7-15, p. 260). Plain chest radiographs are also entirely normal in many, if not most, patients after myocardial infarction. The images are primarily of value in detecting evidence of pulmonary venous congestion in patients in whom CHF develops as a result of an inability of the remaining heart muscle to propel blood through the circulation adequately.

Coronary arteriography is generally considered the definitive test for determining the presence and assessing the severity of coronary artery disease. About 30% of significant stenoses involve a single vessel, most commonly the anterior descending artery. Another 30% involve two vessels, and significant stenosis of the three main vessels can be demonstrated in the remaining 40%. About 50% of coronary artery disease occurs in the left coronary artery, 35% in the right coronary artery, and 15% in the left circumflex artery (Figure 7-16, p. 261).

Intravascular ultrasound (IVUS) provides the most precise anatomic information to guide interventional procedures. The severity of arterial stenosis, measurement of lesion length, lumen dimension, and any unusual morphology can be determined. This modality is especially helpful in demonstrating the origin of the left main coronary artery, which may be obscured by the catheter in angiography. However, this equipment is not readily available in most institutions because of its expense.


Aortocoronary bypass grafting, usually using sections of saphenous vein, is an increasingly popular procedure in patients with ischemic heart disease. Arteriography has been the procedure of choice for demonstrating the patency and functional efficiency of aortocoronary bypass grafts. Patent functioning grafts demonstrate prompt clearing of contrast material and adequate filling of the grafted artery. Stenotic or malfunctioning grafts demonstrate areas of narrowing, filling defects, and slow flow with delayed washout of contrast material.

Percutaneous transluminal coronary angioplasty (PTCA) using a balloon catheter is now a recognized procedure for the treatment of patients with narrowing of one or more coronary arteries (Figure 7-17, p. 262). As in other types of PTA, a catheter is placed under fluoroscopic guidance into the affected coronary artery, and an arteriogram is performed for localization. The angioplasty balloon is then positioned at the level of the stenosis and inflated. After dilation, coronary arteriography is repeated to illustrate the resulting appearance of the stenosis and to detect any complications of the procedure. Symptomatic improvement occurs in 50% to 70% of dilations. About 3% to 8% of patients who undergo PTCA experience either persistent coronary insufficiency or sudden occlusion of a coronary artery at the site of dilation at the time of the procedure. Therefore, the procedure should be performed at a time when an operating room, an anesthetist, and a cardiac surgeon are available so that immediate coronary bypass surgery can be performed if necessary. The percentage of deaths from coronary angioplasty is less than 1%. In conjunction with PTCA, deployment of a drug-eluting stent helps in many cases to maintain the open lumen (Figure 7-18, p. 262). Other interventional procedures are endovascular stenting, atherectomy, and laser-assisted angioplasty.

Congestive Heart Failure

Congestive heart failure (CHF) refers to the inability of the heart to propel blood at a rate and volume sufficient to provide an adequate supply to the tissues. Causes of CHF include an intrinsic cardiac abnormality, hypertension, and any obstructive process that abnormally increases the peripheral resistance to blood flow. Intrinsic cardiac abnormalities include insufficient or defective cardiac filling and impaired contractions for emptying.

Radiographic Appearance

Left-sided heart failure produces a classic radiographic appearance of cardiac enlargement, redistribution of pulmonary venous blood flow (enlarged superior pulmonary veins and decreased caliber of the veins draining the lower lungs), interstitial edema, alveolar edema (irregular, poorly defined patchy densities), and pleural effusions (Figure 7-19, p. 263). In acute left ventricular failure resulting from coronary thrombosis, however, there may be severe pulmonary congestion and edema with very little cardiac enlargement. Pulmonary congestion and edema may require a change in radiographic technique to compensate for the increased fluid in the lungs. The major causes of left-sided heart failure include coronary heart disease, valvular disease, and hypertension.

In right-sided heart failure, dilatation of the right ventricle and right atrium is present (Figure 7-20, p. 263). The transmission of increased pressure may cause dilatation of the superior vena cava, widening of the right superior mediastinum, and edema of the lower extremities. The enlargement of a congested liver may elevate the right hemidiaphragm. Common causes of right-sided heart failure are pulmonary valvular stenosis, emphysema, and pulmonary hypertension resulting from pulmonary emboli.

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Apr 10, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Cardiovascular System

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