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Transcript
CARDIAC TAMPONADE Avi Patel, M.D. August 1, 2005 Introduction The pericardium is made of two layers: the inner visceral pericardium closely opposed to the heart and outer, fiberous parietal pericardium. About 20-50cc of fluid is usually present in the potential space between these two layers. Expansion of this space with hemodynamic compromise is a medical emergency known as cardiac tamponade. Cardiac tamponade is a syndrome caused by the accumulation of fluid under pressure in the pericardial space that results in decreased filling of the ventricle and ultimately to hemodynamic compromise and collapse. Tamponade can be acute or subacute. Pathophysiology Three phases of hemodynamic change are described in tamponade: 1. Phase 1: Accumulation of fluid increases ventricular stiffness requiring higher filling pressures. During this phase, left and right ventricular filling pressures are higher than the pressure in the pericardium. 2. Phase 2: As fluid accumulates, the pericardial pressure increases above the ventricular filling pressure, leading to reduction of cardiac output due to diminished diastolic filling of the ventricles. The increasing intrapericardial pressure cannot be overcome by the heart’s transmural distending pressure to allow for adequate filling. 3. Phase 3: Cardiac output falls further secondary to equilibration of pericardial and left ventricular filling pressures. Venous return is compromised as well since the heart is compressed throughout the cardiac cycle because of the pressure exerted by the expanding pericardial space. During inspiration, negative thoracic pressure leads to a decrease in the pressure of in both the right atrium and the pericardial space. The result is augmented venous return to the right heart and increased right ventricular volume. This increase in right volume causes bowing of the intraventricular septum since pressure cannot be transmitted through the effusion-encased free right ventricular walls. This decrease in blood pressure during inspiration causes an augmented pulsus paradoxus. The blood that expands the right heart accumulates in the vast pulmonary venous circulation further decreasing left ventricular filling and ultimately cardiac output. Not all expansions in the volume of pericardial fluid lead to acute tamponade. Rapid accumulation of 150-200 cc of fluid can lead to profound hemodynamic compromise while more chronic expansions of this space (even as much as a liter) may lead to few symptoms. Pericardial compliance also plays a role in the onset and severity of clinical presentation of expanding pericardial fluid volume. Etiology Any cause of pericarditis can cause tamponade. The most common cause, however is malignancy (subacute). Younger individuals more likely to have tamponade from HIV and trauma (acute), while more elderly patients more commonly have malignancy or uremic pericardial effusions (subacute). Clinical Manifestations/Physical Findings Dyspnea Orthopnea Syncope Tachycardia Tachypnea Peripheral vasoconstriction Hepatomegally Pericardial friction rub Classic findings: a. Beck’s Triad (in very acute tamponade as in rupture) i. Increase JVP ii. Hypotension iii. Diminished heart sounds b. Pulsus Paradoxus >10-12mmHg i. In a semirecumbent patient breathing normally ii. Inflate pressure cuff to 20mmHg above systolic pressure and deflate until first Korotkoff sound is heard only during expiration. iii. Further deflate the cuff until the first Korotkoff sound is audible during both inspiration and expiration. iv. The difference between the two is the measured pulsus. c. Kussmaul’s sign: paradoxical increase in JVD during inspiration. Usually inspiration decreased intrathoracic pressure leading to increased venous return and decrease in JVD during inspiration. With severe constrictive pericarditis or very acute tamponade, the non-compliant pericardium restricts the ability of the heart to accept this return resulting in paradoxical increase in JVD. d. Ewart Sign or Pins Sign: area of dullness with bronchial breath sounds below the angle of the left scapula. e. Absence of Y descent in JVP: marker or poor diastolic filling. Diagnostic studies ECG: low voltage, sinus tachycardia, PR segment depression, or electrical alternans CXR: water bottle shaped heart, enlarged cardiac silhouette Echocardiogram: Remember tamponade is a clinical diagnosis rather than an echocardiographic one. o Early diastolic collapse of the RV free wall o Late diastolic compression/compression of the right atrium o “swinging of the heart” in the pericardium o >40% inspiratory augmentation of Right sided flow o >25% decrease in mitral flow during inspiration o <50% reduction in diameter of dilated IVC during inspiration o Carotid respiratory variation Right Heart Catheterization o Near equalization of right atrial, right ventricular diastolic, pulmonary arterial diastolic, and wedge pressures. Atrial tracing with sudden x descent and absent or attenuated y descent. A brief reminder: NORMAL JVP v a c y x a= atrial contraction c=tricuspid valve closure x=atrial relaxation v=passive atrial filling (vent contract) y=atrial emptying Therapy Tamponade with mild compromise of hemodynamics can be treated conservatively with echocardiography, monitoring and avoidance of volume depletion while trying to correct the underlying cause of this syndrome. The mainstay of acute tamponade is fluid or other volume expanders to try to maintain filling pressures. Inotropes are also listed as a treatment, though seemingly only as a temporizing measure before drainage. PEEP is avoided. Drainage may be accomplished by several approaches: o Blind subxiphoid percutaenous drainage 16-18 gauge needle inserted at 30-45º to the skin near the left xiphocostal angle, aiming toward the left shoulder. Emergency only. Mortality 4% complication 17% o o o Echocardiographically guided placement of drainage catheter Percutaneous ballon pericadiotomy: Percutaneously creates a window Recurrent may require surgical window, shunt, sclerosing, or resection