Figure 7. The myocardium in the left ventricle is significantly thicker than that of the right ventricle. Both ventricles pump the same amount of blood, but the left ventricle must generate a much greater pressure to overcome greater resistance in the systemic circuit. The ventricles are shown in both relaxed and contracting states.
Note the differences in the relative size of the lumens, the region inside each ventricle where the blood is contained. The innermost layer of the heart wall, the endocardium , is joined to the myocardium with a thin layer of connective tissue. The endocardium lines the chambers where the blood circulates and covers the heart valves.
It is made of simple squamous epithelium called endothelium , which is continuous with the endothelial lining of the blood vessels. Once regarded as a simple lining layer, recent evidence indicates that the endothelium of the endocardium and the coronary capillaries may play active roles in regulating the contraction of the muscle within the myocardium. The endothelium may also regulate the growth patterns of the cardiac muscle cells throughout life, and the endothelins it secretes create an environment in the surrounding tissue fluids that regulates ionic concentrations and states of contractility.
Endothelins are potent vasoconstrictors and, in a normal individual, establish a homeostatic balance with other vasoconstrictors and vasodilators. In order to develop a more precise understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail. The septa are physical extensions of the myocardium lined with endocardium.
Located between the two atria is the interatrial septum. Normally in an adult heart, the interatrial septum bears an oval-shaped depression known as the fossa ovalis , a remnant of an opening in the fetal heart known as the foramen ovale. The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the pulmonary circuit.
Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern. Between the two ventricles is a second septum known as the interventricular septum. Unlike the interatrial septum, the interventricular septum is normally intact after its formation during fetal development.
It is substantially thicker than the interatrial septum, since the ventricles generate far greater pressure when they contract. The septum between the atria and ventricles is known as the atrioventricular septum. It is marked by the presence of four openings that allow blood to move from the atria into the ventricles and from the ventricles into the pulmonary trunk and aorta.
Located in each of these openings between the atria and ventricles is a valve , a specialized structure that ensures one-way flow of blood. The valves between the atria and ventricles are known generically as atrioventricular valves. The valves at the openings that lead to the pulmonary trunk and aorta are known generically as semilunar valves. The interventricular septum is visible in the image below. In this figure, the atrioventricular septum has been removed to better show the bicupid and tricuspid valves; the interatrial septum is not visible, since its location is covered by the aorta and pulmonary trunk.
Since these openings and valves structurally weaken the atrioventricular septum, the remaining tissue is heavily reinforced with dense connective tissue called the cardiac skeleton , or skeleton of the heart. It includes four rings that surround the openings between the atria and ventricles, and the openings to the pulmonary trunk and aorta, and serve as the point of attachment for the heart valves.
The cardiac skeleton also provides an important boundary in the heart electrical conduction system. Figure 8. This anterior view of the heart shows the four chambers, the major vessels and their early branches, as well as the valves. The presence of the pulmonary trunk and aorta covers the interatrial septum, and the atrioventricular septum is cut away to show the atrioventricular valves.
One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum primum does not close at birth, and the fossa ovalis is unable to fuse.
As much as 20—25 percent of the general population may have a patent foramen ovale, but fortunately, most have the benign, asymptomatic version.
Patent foramen ovale is normally detected by auscultation of a heart murmur an abnormal heart sound and confirmed by imaging with an echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery to repair and seal the opening.
Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of the ligamentum arteriosum, the remnant of the fetal shunt called the ductus arteriosus. If severe, this condition drastically restricts blood flow through the primary systemic artery, which is life threatening.
In some individuals, the condition may be fairly benign and not detected until later in life. Detectable symptoms in an infant include difficulty breathing, poor appetite, trouble feeding, or failure to thrive. In older individuals, symptoms include dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to resect remove the affected region or angioplasty to open the abnormally narrow passageway.
Studies have shown that the earlier the surgery is performed, the better the chance of survival. A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close.
The condition may range from severe to benign. Failure of the ductus arteriosus to close results in blood flowing from the higher pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases pulmonary pressure and makes respiration difficult.
Symptoms include shortness of breath dyspnea , tachycardia, enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure ligation , manual closure using platinum coils or specialized mesh inserted via the femoral artery or vein, or nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an open position.
If untreated, the condition can result in congestive heart failure. Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes.
Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow into the left ventricle and mix with the blood that is relatively high in oxygen.
Symptoms include a distinct heart murmur, low blood oxygen percent saturation, dyspnea or difficulty in breathing, polycythemia, broadening clubbing of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most common cause of cyanosis following birth. Other heart defects may also accompany this condition, which is typically confirmed by echocardiography imaging.
Tetralogy of Fallot occurs in approximately out of one million live births. Normal treatment involves extensive surgical repair, including the use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60 percent by 4 years of age; 30 percent by 10 years; and 5 percent by 40 years. Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope.
In this case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart sounds may be detected. This is often followed by medical imaging to confirm or rule out a diagnosis.
In many cases, treatment may not be needed. Some common congenital heart defects are illustrated in Figure 9. Figure 9. The right atrium serves as the receiving chamber for blood returning to the heart from the systemic circulation. The two major systemic veins, the superior and inferior venae cavae, and the large coronary vein called the coronary sinus that drains the heart myocardium empty into the right atrium.
The superior vena cava drains blood from regions superior to the diaphragm: the head, neck, upper limbs, and the thoracic region. It empties into the superior and posterior portions of the right atrium. The inferior vena cava drains blood from areas inferior to the diaphragm: the lower limbs and abdominopelvic region of the body. It, too, empties into the posterior portion of the atria, but inferior to the opening of the superior vena cava.
Immediately superior and slightly medial to the opening of the inferior vena cava on the posterior surface of the atrium is the opening of the coronary sinus. This thin-walled vessel drains most of the coronary veins that return systemic blood from the heart. The majority of the internal heart structures discussed in this and subsequent sections are illustrated in Figure 8.
While the bulk of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface demonstrates prominent ridges of muscle called the pectinate muscles. The right auricle also has pectinate muscles. The left atrium does not have pectinate muscles except in the auricle.
The atria receive venous blood on a nearly continuous basis, preventing venous flow from stopping while the ventricles are contracting. While most ventricular filling occurs while the atria are relaxed, they do demonstrate a contractile phase and actively pump blood into the ventricles just prior to ventricular contraction.
The opening between the atrium and ventricle is guarded by the tricuspid valve. The right ventricle receives blood from the right atrium through the tricuspid valve.
They are composed of approximately 80 percent collagenous fibers with the remainder consisting of elastic fibers and endothelium. They connect each of the flaps to a papillary muscle that extends from the inferior ventricular surface.
There are three papillary muscles in the right ventricle, called the anterior, posterior, and septal muscles, which correspond to the three sections of the valves.
When the myocardium of the ventricle contracts, pressure within the ventricular chamber rises. Blood, like any fluid, flows from higher pressure to lower pressure areas, in this case, toward the pulmonary trunk and the atrium.
To prevent any potential backflow, the papillary muscles also contract, generating tension on the chordae tendineae. This prevents the flaps of the valves from being forced into the atria and regurgitation of the blood back into the atria during ventricular contraction. The image below shows papillary muscles and chordae tendineae attached to the tricuspid valve. Figure In this frontal section, you can see papillary muscles attached to the tricuspid valve on the right as well as the mitral valve on the left via chordae tendineae.
The walls of the ventricle are lined with trabeculae carneae , ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction.
It arises from the inferior portion of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle. When the right ventricle contracts, it ejects blood into the pulmonary trunk, which branches into the left and right pulmonary arteries that carry it to each lung.
The superior surface of the right ventricle begins to taper as it approaches the pulmonary trunk. At the base of the pulmonary trunk is the pulmonary semilunar valve that prevents backflow from the pulmonary trunk. After exchange of gases in the pulmonary capillaries, blood returns to the left atrium high in oxygen via one of the four pulmonary veins. While the left atrium does not contain pectinate muscles, it does have an auricle that includes these pectinate ridges.
Blood flows nearly continuously from the pulmonary veins back into the atrium, which acts as the receiving chamber, and from here through an opening into the left ventricle.
Most blood flows passively into the heart while both the atria and ventricles are relaxed, but toward the end of the ventricular relaxation period, the left atrium will contract, pumping blood into the ventricle. This atrial contraction accounts for approximately 20 percent of ventricular filling. The opening between the left atrium and ventricle is guarded by the mitral valve. Recall that, although both sides of the heart will pump the same amount of blood, the muscular layer is much thicker in the left ventricle compared to the right.
Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The mitral valve is connected to papillary muscles via chordae tendineae. There are two papillary muscles on the left—the anterior and posterior—as opposed to three on the right. The left ventricle is the major pumping chamber for the systemic circuit; it ejects blood into the aorta through the aortic semilunar valve.
With the atria and major vessels removed, all four valves are clearly visible, although it is difficult to distinguish the three separate cusps of the tricuspid valve. A transverse section through the heart slightly above the level of the atrioventricular septum reveals all four heart valves along the same plane Figure The valves ensure unidirectional blood flow through the heart.
Between the right atrium and the right ventricle is the right atrioventricular valve , or tricuspid valve. It typically consists of three flaps, or leaflets, made of endocardium reinforced with additional connective tissue.
The flaps are connected by chordae tendineae to the papillary muscles, which control the opening and closing of the valves. Emerging from the right ventricle at the base of the pulmonary trunk is the pulmonary semilunar valve, or the pulmonary valve ; it is also known as the pulmonic valve or the right semilunar valve. The pulmonary valve is comprised of three small flaps of endothelium reinforced with connective tissue. When the ventricle relaxes, the pressure differential causes blood to flow back into the ventricle from the pulmonary trunk.
This flow of blood fills the pocket-like flaps of the pulmonary valve, causing the valve to close and producing an audible sound. Unlike the atrioventricular valves, there are no papillary muscles or chordae tendineae associated with the pulmonary valve. Located at the opening between the left atrium and left ventricle is the mitral valve , also called the bicuspid valve or the left atrioventricular valve.
Structurally, this valve consists of two cusps, known as the anterior medial cusp and the posterior medial cusp, compared to the three cusps of the tricuspid valve.
In a clinical setting, the valve is referred to as the mitral valve, rather than the bicuspid valve. The two cusps of the mitral valve are attached by chordae tendineae to two papillary muscles that project from the wall of the ventricle. At the base of the aorta is the aortic semilunar valve, or the aortic valve , which prevents backflow from the aorta.
It normally is composed of three flaps. When the ventricle relaxes and blood attempts to flow back into the ventricle from the aorta, blood will fill the cusps of the valve, causing it to close and producing an audible sound. In the image above, the two atrioventricular valves are open and the two semilunar valves are closed.
This occurs when both atria and ventricles are relaxed and when the atria contract to pump blood into the ventricles. The image below shows a frontal view. Although only the left side of the heart is illustrated, the process is virtually identical on the right. The two atrioventricular valves are open; the two semilunar valves are closed. The atria and vessels have been removed. When the mitral valve is open, it allows blood to move from the left atrium to the left ventricle.
The aortic semilunar valve is closed to prevent backflow of blood from the aorta to the left ventricle. Image a above shows the atrioventricular valves closed while the two semilunar valves are open.
This occurs when the ventricles contract to eject blood into the pulmonary trunk and aorta. Closure of the two atrioventricular valves prevents blood from being forced back into the atria. This stage can be seen from a frontal view in image b above. The two atrioventricular valves are closed, but the two semilunar valves are open. What are the tiny hairs that are found in the cochlea.
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Trending Questions. It is used primarily as palliative treatment for neoplastic effusions with a poor prognosis. It may be performed in the catheterization laboratory under fluoroscopy using a balloon-dilating catheter. Cardiac tamponade occurs when fluid accumulation in the finite serous pericardial space causes an increase in pressure, with subsequent cardiac compression and hemodynamic compromise.
Elevated intrapericardial pressure leads to progressive limitation of diastolic ventricular filling, resulting in lowered cardiac output. Symptoms resulting from decreased cardiac output and congestion include dyspnea, chest discomfort, weakness, restlessness, agitation, drowsiness, oliguria, and anorexia.
If the tamponade develops acutely as a complication of an acute MI free wall rupture or trauma, the presentation is usually catastrophic, with shock or sudden death. Tachycardia and tachypnea are common.
Pulsus paradoxus is defined as an inspiratory decline in systolic blood pressure of more than 10 mmHg resulting from compression and poor filling of the left ventricle. Pulsus paradoxus is nonspecific and insensitive and can occur with extracardiac disease, such as severe chronic obstructive pulmonary disease or asthma. The ECG may be unremarkable. Abnormal findings on ECG include tachycardia, electrical alternans Figure 9 , low voltage, and may include changes associated with acute pericarditis Figure 6.
Usually, a moderate-size or large pericardial effusion is present and leads to increasing compression and subsequent diastolic compression of the cardiac chambers, usually in the sequence right atrium, right ventricle, left atrium with the lowest pressure chamber being affected first.
The most sensitive finding for tamponade physiology on the echocardiogram is inferior vena cava plethora, with absent inspiratory collapse; however this is not very specific.
Right ventricular diastolic inversion may also been seen. Absent diastolic flow from the hepatic views suggests tamponade physiology. The most typical finding on right heart catheterization is equalization of mean right atrial, right ventricular and pulmonary artery diastolic, and mean pulmonary capillary wedge pressures.
The symptoms of pericardial tamponade can mimic those of right-sided heart failure, right ventricular infarction, constrictive pericarditis, and pulmonary embolism. However, with the use of echocardiography and occasionally right heart catheterization, these may be distinguished. Patients with pretamponade and tamponade require immediate hospital admission and prompt pericardial drainage by pericardiocentesis. The drain catheter may be left in place for up to 48 hours if drainage is slow or reaccumulation likely.
If follow-up echocardiography documents fluid reaccumulation, a pericardial window should be considered, because the infection risk associated with a pericardial drain increases after 48 hours.
Constrictive pericarditis refers to an abnormal scarring and loss of elasticity of the pericardium, resulting in impaired ventricular filling and decreased cardiac output. The frequency of different causes of constrictive pericarditis depends on the population and geography in question.
In developed countries, cardiac surgery and idiopathic constriction are the leading cause, while in certain developing countries tuberculous remains the number one etiology. The initiating event results in a chronic inflammatory pericardial process, resulting in fibrinous scarring and occasionally calcification of the pericardium Figure As the heart becomes encased with a non-compliant pericardium, ventricular interdependance and dissociation between the intrathoracic and intracardiac pressure occurs.
In constriction, normal expansion of the right heart is restricted by the pericardium and the septum shifts to the left to accommodate the increase in venous return with inspiration; the opposite movement occurs with expiration. Normally, there is a reduction in intrathoracic and intracardiac pressure with inspiration.
The rigid pericardium impedes normal ventricular expansion and therefore venous return and pulmonary venous pressure. Because intrathoracic pressure drops but left ventricular pressure does not decrease with inspiration there is a reduction in the transpulmonary gradient. This leads to impaired ventricular filling and decreased cardiac output. Ultimately, right and then left ventricular heart failure develop. Distinguishing heart failure caused by constrictive physiology from diastolic restrictive physiology is a classic diagnostic dilemma.
Symptoms are often vague and their onset is insidious; they include malaise, fatigue, and decreased exercise tolerance.
With progression of constrictive pericarditis, symptoms of right-sided heart failure eg, peripheral edema, nausea, abdominal discomfort, ascites become apparent and usually precede signs of left-sided failure eg, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea. Increased ventricular filling pressures cause jugular venous distention and Kussmaul's sign paradoxical rise in jugular venous pressure on inspiration , which is sensitive but not specific for constrictive pericarditis.
Constrictive effusive pericarditis consists of a tense pericardial effusion in the presence of pericardial constriction, and both tamponade and constrictive signs and symptoms are present.
Brain natriuretic peptide BNP is a serum biomarker that can help distinguish constrictive pericarditis from restrictive cardiomyopathy. Despite elevated filling pressures in both conditions, levels of BNP are significantly higher in restrictive cardiomyopathy. Pericardial calcifications Figure 10 , pleural effusions, and biatrial enlargement may be noted on the chest radiograph.
Echocardiography is the best imaging modality for assessing hemodynamic parameters noninvasively. M-mode echocardiography is useful for looking for rapid motion followed by abrupt flattening of the left ventricular free wall in early and mid diastole respectively. Two-dimensional echocardiography may demonstrate a thickened pericardium about one third of cases , myocardial tethering, abrupt cessation of left ventricular and right ventricular diastolic filling, biatrial enlargement, tubular deformity of the left ventricle, respirophasic septal shift, septal bounce and inferior vena cava plethora with absent inspiratory collapse.
Doppler echocardiographic findings have the highest sensitivity and specificity for detecting constrictive physiology. Excessive respiratory variations in transmitral, transtricuspid, pulmonary venous, and hepatic vein flow are characteristic. Low tissue velocity at both medial and lateral annuli suggests restriction. More recently developed echocardiographic modalities such as strain imaging have enhanced the ability to discriminate between restriction and constriction.
Direct pressure measurements are performed if there is doubt about the diagnosis. Characteristic features in the right atrium include: elevated right atrial pressures, prominent x and y decents and Kussmaul's sign. Square-root or dip-and-plateau right ventricular pressure waveforms reflect impaired ventricular filling.
Because of the fixed and limited space within the stiff pericardium, end-diastolic pressure equalization typically within 5 mmHg occurs between these cardiac chambers. Pulmonary artery systolic pressures are usually normal in pericardial constriction; higher pulmonary pressures suggest a restrictive cardiomyopathy. The ratio of the right ventricular to left ventricular systolic pressure-time area during inspiration compared to expiration is a highly sensitive and specific means of differentiating constriction from restriction Figure Computed tomography is the imaging modality of choice to evaluate the thickness of the pericardium and for pericardial calcification.
While echocardiography is the first choice imaging modality for assesssment of constriction, for many patients CMR is becoming increasingly utilized in the initial evaluation, particularly if any ambiguity remains regarding the diagnosis, if there is suggestion of active inflammation, or if the duration of symptoms has been brief.
Cardiac magnetic resonance is very useful to differentiate a small pericardial effusion from pericardial thickening. The superior signal-to-noise and contrast-to-noise ratio of CMR allows precise evaluation of the morphological and hemodynamic changes seen in pericardial constriction.
Real-time cine sequences allow evaluation of the features described above in the 2D echocardiographic evaluation of pericardial constriction, which is useful if echocardiographic images are sub-optimal.
Phase encoding velocity imaging potentially provides similar data to Doppler echocardiography but is not yet generally employed in routine practice. The degree of constrictive physiology occurs along a spectrum of severity. Early forms may be difficult to diagnose without a high degree of clinical suspicion.
It is increasingly recognized that some of these patients may respond to medical therapy, without surgical intervention; this is referred to as transient constrictive pericarditis. Medical treatment is limited in chronic constrictive pericarditis in the absence of active inflammation. Diuretics and a low-sodium diet may be tried for patients with mild to moderate New York Heart Association Class I or II heart failure symptoms or contraindications to surgery.
For effusive-constrictive pericarditis therapy includes pericardiocentesis initially, followed by treatment with anti-inflammatory agents. Frequently, pericardiectomy is necessary for long-term management. Recurrence following surgery is caused mainly by incomplete resection of the pericardium.
Without surgical treatment, biventricular failure develops. Long-term survival after pericardiectomy is worse than matched controls but this is mainly related to the underlying etiology. Grimm, DO Published: July Summary Suggested Readings References. Figure 1: Click to Enlarge. Figure 2: Click to Enlarge. Figure 3: Click to Enlarge.
Figure 4: Click to Enlarge. Figure 5: Click to Enlarge. R and V 1 leads and PR depression elsewhere. Figure 7A: Click to Enlarge. Figure 7B: Click to Enlarge. Figure 8A: Click to Enlarge. Figure 8B: Click to Enlarge. Figure 9: Click to Enlarge. Figure Click to Enlarge.
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