each other (exaggerated ventricular interdependence) The left ventricular systolic pressure falls when the systolic pressure in the right ventricle rises during inspiration and the reverse happens during expiration (ventricular discordance).3,4,37–40 The presence of an atrial septal defect, ventricular dysfunction, and aortic regurgitation may mask the findings of ventricular interdependence by nullifying the effect of respiration on ventricular preload.3–5 Experimental41–44 and clinical studies38,45 have shown that cardiac tamponade is not an “all-or-none” phenomenon Instead, it represents a continuum from minimal hemodynamic impairment to a state of hemodynamic collapse Clinical examination is sufficient to recognize hemodynamic collapse but is inadequate in identifying milder hemodynamic compromise.39 Usually, left- and right-sided filling pressures are elevated to 20 to 25 mm Hg In cases with hypovolemia, filling pressure may be less than 10 mm Hg Occasionally, cardiac tamponade may be regional, resulting from localized clot or loculated effusion when typical physical, hemodynamic, and echocardiographic findings are absent Rarely, large pleural effusion46 and pneumopericardium can compress the heart mimicking tamponade physiology.3,47 Clinical Presentation The clinical presentation depends on the speed of accumulation of pericardial fluid Slowly accumulating effusion is often asymptomatic and detected incidentally Rapid accumulation of even small amounts of fluid can cause symptoms Initially, compensatory sympathetic stimulation causes tachycardia, diaphoresis, and peripheral vasoconstriction.3,4 With progressive accumulation of fluid, compensatory mechanisms prove inadequate and cardiac output declines Patients who are unable to mount a normal adrenergic response, such as those receiving β-blocking agents, are more susceptible to acute hemodynamic collapse Dyspnea is common though the exact mechanism remains unknown.3,5 The JVP is markedly elevated with blunted “y” and preserved “x” descent Unimpeded transmission of thoracic pressure to cardiac chambers and consequent preferential right ventricular filling permits normal inspiratory fall in JVP Pulsus paradoxus, characterized by an abnormally large (>10 mm Hg) decline in blood pressure during inspiration, is another distinctive clinical feature In reality, there is no paradox and it only reflects exaggerated ventricular interdependence.5,48,49 The fall in blood pressure provides an estimate of ventricular interdependence and is proportionate to the severity of cardiac tamponade Pulsus paradoxus is not unique to tamponade, and may be present in pericardial constriction, pulmonary embolism, and other pulmonary diseases with wide respiratory variation in thoracic pressures Clinical recognition of paradoxical pulse relies on respiratory variation in Korotkoff sounds and therefore cannot be measured by currently available oscillometric sphygmomanometers As such, the measurement of paradoxical pulse is difficult in children due to high heart and respiratory rates.50 Respiratory variations in plethysmography waveform on pulse oximetry correlates well with invasive assessment of pulsus paradoxus and can be used at the bedside to ascertain the diagnosis and severity of tamponade.50,51 The heart sounds are muffled Cardiac impulse is difficult to localize In some cases, compression of the lower part of the lungs causes bronchial breathing and dullness to percussion (Ewart's sign) In its severe form, cardiac tamponade is characterized by Beck's triad, which includes distant heart sounds, hypotension, and distended neck veins.52 Investigations Electrocardiogram shows compensatory sinus tachycardia, low QRS voltages, and electrical alternans (Fig 57.3) Low QRS voltages are a nonspecific sign and may be seen in patients with emphysema, pneumothorax, and infiltrative myocardial diseases Electrical alternans, on the other hand, is specific for large effusion albeit with poor sensitivity.3–5,39 Nonspecific ST-T changes may be present with coexisting pericarditis The chest radiograph may be normal in patients with mild pericardial effusion Large pericardial effusion present with a symmetrically enlarged cardiac silhouette with distinct margins assuming round, flask-like “water bottle” configuration Lateral view radiograph shows a linear lucency separating the posterior chest wall and epicardial fat (fat pad sign).3,4 FIG 57.3 Twelve-lead ECG from a child with large pericardial effusion showing sinus tachycardia and beat-to-beat change in QRS axis (electrical alternans) Echocardiography detects pericardial effusion with very high accuracy.6 In adults and adolescents, based on the width of echo-free space between visceral and parietal pericardium at end-diastole, circumferential pericardial effusion is classified as small (20 mm), and very large (>25 mm).4,53 There is no such standard for children Occasionally, left-sided pleural effusion can mimic pericardial effusion The presence of fluid between the heart and descending thoracic aorta in parasternal long-axis view localizes fluid to the pericardium (Fig 57.4; Video 57.1) Echocardiography also aids in the assessment of hemodynamic impact of pericardial effusion A dilated inferior caval vein with less than 50% inspiratory collapse is highly suggestive of cardiac tamponade This finding may be absent in patients with hypovolemia and low-pressure tamponade Echogenicity of pericardial fluid provides important information about the possible cause of effusion Fibrinous strands within the fluid suggest acute inflammation and are common with bacterial pericarditis.4,6