Subcostal View

Fig. 7. Increased echogenicity within pericardial space. Subcostal view showing mobile echodensities (arrow) within the pericardial effusion (double arrow). The differential diagnosis includes hemopericardium, suppurative infection, and malignancy.

Constrictive Pericarditis

Constrictive Pericarditis Descent
Fig. 8. Pressure tracings in constrictive pericarditis (see "Chronic Constrictive Pericarditis" section). a, a wave; LA, left atrium; LV, left ventricle; RA, right atrium; v, v-wave; x, x descent; y, y descent.

abnormal rise in jugular venous pressure upon inspiration), hepatomegaly, ascites and peripheral edema. Occasionally, a pericardial knock can be auscultated as a low-pitched early diastolic sound. The ECG often reveals diffuse T-wave flattening. Atrial fibrillation is common.

Certain echocardiographic findings are consistent with the diagnosis of constrictive pericarditis (Table 2). Typically, ventricular chamber sizes and wall thicknesses are normal. Imaging may reveal a thickened pericardium (Fig. 9), although this is an insensitive finding (computed tomography and magnetic resonance imaging are often more useful in delineating abnormal pericardial thickness). Often, the inferior vena cava (IVC) and hepatic veins are dilated, owing to an elevated right atrial pressure. M-mode recordings may reveal multiple linear and parallel echoes posterior to the LV representing the thickened pericardium. More helpful is the finding of impaired outward movement of the posterior LV wall during mid- to late diastole, reflecting the filling limit of the stiffened pericardium (Fig. 10). This finding, known as posterior wall "flattening," is relatively sensitive, present in 85% of patients with constrictive pericarditis, but is nonspecific as up to 20% of normal individuals also demonstrate this pattern. Other echocardiographic features in constrictive pericarditis include paradoxical motion of the interventricular septum (septal "bounce") and premature opening of the pulmonic valve in diastole,

Bouncing Interventricular Septum
Fig. 9. Constrictive pericarditis. Parasternal long-axis (PLAX) view showing loculated pericardial effusion (arrow) and pericardial thickening with increased calcification (arrowhead).
Echocardiogram Pericarditis
Fig. 10. Constrictive pericarditis. M-Mode echocardiogram showing posterior wall diastolic flattening—a characteristic finding in constrictive pericarditis.

especially with inspiration (Fig. 11; please see companion DVD for corresponding video). Commonly, the normal respiratory variation of the diameter of the IVC is blunted.

Doppler evaluation provides further evidence of constrictive physiology. Pulsed Doppler interrogation of hepatic vein flow shows an accentuated A-wave. Pulsed Doppler of transmitral diastolic inflow shows

Constrictive Pericarditis Septal Bounce

Fig. 11. Mechanism of septal "bounce"/diastolic "checking"/ "shuddering" in constrictive pericarditis. Signs of ventricular interdependence are manifest in constrictive pericarditis. During inspiration, right heart filling proceeds at the expense of left ventricular filling (seen on spectral Doppler pattern)—shifting the interventricular septum to the left. This is followed by an abrupt cessation of diastolic filling (diastolic "checking") corresponding to a third heart sound or pericardial "knock." During expiration, increased left heart filling occurs at the expense of the right ventricle with reciprocal movement in the interventricular septum. (Please see companion DVD for corresponding video.)

Fig. 11. Mechanism of septal "bounce"/diastolic "checking"/ "shuddering" in constrictive pericarditis. Signs of ventricular interdependence are manifest in constrictive pericarditis. During inspiration, right heart filling proceeds at the expense of left ventricular filling (seen on spectral Doppler pattern)—shifting the interventricular septum to the left. This is followed by an abrupt cessation of diastolic filling (diastolic "checking") corresponding to a third heart sound or pericardial "knock." During expiration, increased left heart filling occurs at the expense of the right ventricle with reciprocal movement in the interventricular septum. (Please see companion DVD for corresponding video.)

Constrictive Pericarditis Septal Bounce

Fig. 12. Constrictive pericarditis. Sketch depicting exaggerated patterns of ventricular filling in inspiration and expiration in constrictive pericarditis. In inspiration, an exaggerated increase in right ventricular (tricuspid valve [TV]) inflow velocities occurs at the expense of left ventricular (mitral valve [MV]) inflow as manifest on pulsed Doppler tracings. During expiration, reciprocal changes occur. Similar respirophasic variations on pulsed Doppler can be seen in pulmonary embolism, right ventricular infarction, and chronic obstructive pulmonary disease.

Fig. 12. Constrictive pericarditis. Sketch depicting exaggerated patterns of ventricular filling in inspiration and expiration in constrictive pericarditis. In inspiration, an exaggerated increase in right ventricular (tricuspid valve [TV]) inflow velocities occurs at the expense of left ventricular (mitral valve [MV]) inflow as manifest on pulsed Doppler tracings. During expiration, reciprocal changes occur. Similar respirophasic variations on pulsed Doppler can be seen in pulmonary embolism, right ventricular infarction, and chronic obstructive pulmonary disease.

an increased E velocity with a shortened deceleration time and a reduced A-wave velocity, owing to impaired late diastolic filling. Marked respiratory variation may be noted in early diastolic right and left ventricular filling, with a more than 25% increase of transtricus-pid valve flow and more than 25% decrease of trans-mitral valve flow during inspiration (Fig. 12; see Chapter 9, Fig. 12).

Mitral Inflow With Respiratory Varience
Fig. 13. (See legend, next page)

Pericardial Effusions and Compressive Syndromes

Pericardial effusions develop as a response to injury of the pericardium. The clinical presentation of the effusion may vary depending on the etiology, but as intrapericardial pressure rises, cardiac chamber compression can occur with the development of the clinical syndrome of cardiac tamponade. The variability of cardiac compression from a pericardial effusion depends not only on the overall volume of effusion but also on the rate at which the fluid has accumulated. A very gradually developing pericardial effusion, as may be seen in chronic hypothyroidism, may enlarge to more than a liter in volume without evidence of cardiac compression, as the pericardium stretches over time. Conversely, acute

Subcostal Short Axis View

Fig. 13. Pericardial tamponade. (A) Two-dimensional parasternal long axis views (top panels), and M-mode taken from parasternal long axis (bottom left panel) and subcostal (bottom right panel) positions in a patient with cardiac tamponade. The arrows in the top right and bottom left panels indicate RV collapse. (B) Systolic and diastolic parasternal short axis views (PSAX) showing diastolic compression of right ventricular outflow tract. Respirophasic variation in flow across pulmonary valve on pulsed Doppler examination is shown (bottom panel). (C) Apical four-chamber views showing both right and left atrial inversion (collapse, curved arrows) during systole. Right atrial systolic collapse is a sensitive finding in pericardial tamponade, but left atrial systolic collapse is less commonly seen. (Please see companion DVD for corresponding video.)

Fig. 13. Pericardial tamponade. (A) Two-dimensional parasternal long axis views (top panels), and M-mode taken from parasternal long axis (bottom left panel) and subcostal (bottom right panel) positions in a patient with cardiac tamponade. The arrows in the top right and bottom left panels indicate RV collapse. (B) Systolic and diastolic parasternal short axis views (PSAX) showing diastolic compression of right ventricular outflow tract. Respirophasic variation in flow across pulmonary valve on pulsed Doppler examination is shown (bottom panel). (C) Apical four-chamber views showing both right and left atrial inversion (collapse, curved arrows) during systole. Right atrial systolic collapse is a sensitive finding in pericardial tamponade, but left atrial systolic collapse is less commonly seen. (Please see companion DVD for corresponding video.)

Tamponade With Doppler
Fig. 14. Cardiac tamponade: ventricular filling. Minor respirophasic variation in left ventricular filling (mitral valve inflow Doppler) was seen in the patient featured in Fig. 13A-D was seen, but right ventricular filling (tricuspid valve inflow) showed marked respirophasic changes.

hemorrhage into the pericardium could cause clinical tamponade with less than 100 cc of fluid accumulation.

The pathophysiology of pericardial tamponade relates to the elevation of intrapericardial pressure and the consequent compression of the cardiac chambers (Fig. 13A-C; please see companion DVD for corresponding video). As the intrapericardial pressure rises, there is a progressive increase, and eventually equalization of diastolic pressures of all four cardiac chambers. This leads to impairment of venous return and filling of the ventricles during diastole (Fig. 14). In distinction to pericardial constriction, impairment of ventricular filling in tamponade occurs throughout diastole, including the early phase. This is reflected by a blunted "y" descent on the atrial pressure tracings. The impairment of ventricular filling leads to elevated systemic and pulmonary venous pressures and reduced stroke volume and cardiac output. Pulsus paradoxus results when the inspiratory increase in venous return to the heart expands the RV and, because of ventricular interdependence, reduces LV filling such that LV stroke volume subsequently falls.

Fig. 15. Pericardial effusion: anatomical relationships. Images from two different patients showing anatomical relationships of anterior and posterior pericardial effusions (parasternal long axis view, A) and postero-lateral effusion (parasternal short axis view, B). Note the presence of marked left ventricular hypertrophy in A. Standard abbreviations apply; also PA, pulmonary artery, dtAo, descending thoracic aorta. (Please see companion DVD for corresponding video.)

Anatomical Subcoastal View Heart

Fig. 15. Pericardial effusion: anatomical relationships. Images from two different patients showing anatomical relationships of anterior and posterior pericardial effusions (parasternal long axis view, A) and postero-lateral effusion (parasternal short axis view, B). Note the presence of marked left ventricular hypertrophy in A. Standard abbreviations apply; also PA, pulmonary artery, dtAo, descending thoracic aorta. (Please see companion DVD for corresponding video.)

The etiologies of pericardial effusions are largely the same as those that cause acute pericarditis (Table 1). Large effusions are most commonly seen in malignancies, tuberculous pericarditis, myxedema, uremia, and connective tissue diseases. One important cause of a pericardial effusion unrelated to pericarditis is hemo-pericardium, e.g., owing to perforation of a cardiac chamber as may occur after chest trauma, or iatrogeni-cally during a cardiac catheterization procedure.

The clinical manifestations of a pericardial effusion may include the sharp, pleuritic chest pain of pericarditis, dyspnea, cough, or a dragging or heavy sensation in the chest. In the case of tamponade, the presentation may be more dramatic, including more pronounced dyspnea, hypotension, and/or shock.

Physical findings related to pericardial effusion are variable. Jugular venous distention is evident when the effusion is compressive such that there is elevation of right-sided filling pressures. The cardiac exam may be notable for a faint apical impulse, soft or muffled heart sounds, and if tamponade is present, hypotension and tachycardia. The classic sign of cardiac tamponade, pulsus paradoxus (>10 mmHg fall in systolic blood pressure with inspiration) is suggestive of tamponade in the appropriate clinical setting, although it can also be detected in other forms of intrathoracic pathology. Laboratory studies that suggest the presence of a peri-cardial effusion include an enlarged, globular heart on chest radiography, and low voltage and/or electrical alternans on the ECG.

Echocardiography imaging for evaluation of pericar-dial fluid is very sensitive and relies on the visualization of an echolucent space between the pericardial layers

Table 3 Pericardial Effusion: Echocardiography Differential Diagnosis

Pericardial fat pad Pleural effusion Pericardial cyst

Primary mesothelioma of the pericardium (rare)

(Fig. 15; please see companion DVD for corresponding video). Volumes as little as 15-50 mL of fluid can be detected. On two-dimensional (2D) imaging, an echofree space superior to the right atrium in the apical four-chamber view is the most sensitive finding.

Actual characteristics of pericardial fluid can be difficult to determine echocardiographically. Findings such as increased echogenicity of the fluid may suggest the nature and composition of the fluid but the correlative power of such findings is unreliable.

Other conditions can mimic the presence of a pericardial effusion (Fig. 3, Table 3). As previously described, epicardial fat is a common finding, usually located on the anterior surface of the heart, although it may also be observed posteriorly where it can be confused with an effusion. Distinguishing features include the more granular echogenic appearance of fat compared to effusion. Left-sided pleural fluid may also be confused with pericardial effusion, but the descending aorta provides a useful landmark in distinguishing the two (Fig. 16). In the parasternal long-axis view, pleural fluid extends posterior to the descending aorta, whereas pericardial fluid is usually limited anterior to it. Visualization of atelectatic lung tissue adjacent to pleural fluid is also helpful (Fig. 7; see Chapter 19).

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Herbal Remedies For Acid Reflux

Herbal Remedies For Acid Reflux

Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.

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Responses

  • franco
    Can anterior fat pad be seen in plan view on echocardiograms?
    2 years ago
  • Dina
    Can i see pericardial effusion around the LV in the subcostal view?
    10 months ago

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