Cardiac Tamponade Francesca N. Delling October 17, 2007

Tamponade Etiology Physiology - comparison with constrictive pericarditis Types of tamponade Diagnosis - clinical presentation, physical exam, EKG, CXR, echo Treatment

Etiologies Infectious Neoplastic Uremic Viral (coxsackie B, echovirus, influenza) Bacterial Others: TB, fungal, toxoplasmosis Neoplastic Uremic Trauma / cardiac surgery / aortic dissection / cardiac procedures Radiation Connective tissue disease (RA, SLE, scleroderma) Myocardial ischemia / infarct Myxedema Idiopathic

Physiology Exaggerated ventricular interaction During inspiration  greater RV inflow and outflow and concurrent decrease in LV size, outflow tract flow velocity profile and mitral valve inflow During expiration  LV filling and LV outflow augmented at the expense of reduced RV volume and Doppler flow velocities

Increasing pericardial Physiology Normal pericardium Increasing pericardial pressure Increasing filling pressures RVEDP = LVEDP Equalization of diastolic pressures

Comparison with constrictive pericarditis Features in common - diastolic dysfunction and preserved ventricular ejection fraction - heightened ventricular interaction - increased respiratory variation of ventricular inflow and outflow manifested clinically by pulsus paradoxus (less frequent in constrictive pericarditis) - equally elevated central venous, pulmonary venous, and ventricular diastolic pressures Distinctive features - tamponade  pericardial space is open and transmits respiratory variation in thoracic pressure to heart (pericardium does not see fluctuation in thoracic pressure in constrictive pericarditis) - constrictive pericarditis: venous return does not increase with inspiration. Diminished LV and increased RV volume are 2/2 lesser pressure gradient from the pulmonary veins

Types of tamponade Acute tamponade - Due to trauma, rupture of the heart or aorta or complication of an invasive diagnostic or therapeutic intervention - Sudden in onset - Hypotension common Subacute tamponade - Pericardial fluid accumulates slowly - Hypotension with a narrow pulse pressure, reflecting limited stroke volume. However, patients with preexisting hypertension may remain hypertensive due to increased sympathetic activity

Acute vs chronic tamponade Pericardial pressure-volume curves are shown. On the left, rapidly increasing pericardial fluid first reaches the limit of pericardial reserve, then exceeds the limit of pericardial strech, causing a steep rise in pressure which becomes even steeper as smaller increments in fluid cause a disproportionate increase in pericardial pressure. On the right, aslower rate of pericardial filling takes longer to exceed the limit of pericardial stretch, because there is more time for the pericardium to stretch.

Types of tamponade (continued) Low pressure tamponade - Severely hypovolemic pts (hemorrhage, hemodyalisis, or overdiuresis)  intracardiac and pericardial diastolic pressures are only 6 to 12 mmHg  fluid challenge usually elicits typical tamponade hemodynamics Regional tamponade - caused by a loculated, eccentric effusion - typical physical, hemodynamic, and echocardiographic signs of tamponade may be absent

Clinical Presentation Tachypnea and exertional dyspnea  rest air hunger Weakness Presyncope Dysphagia Cough Anorexia (Chest pain)

Physical Exam Findings Tachycardia Hypotension  shock Elevated JVP with blunted y descent Muffled heart sounds Pulsus paradoxus (Pericardial friction rub)

JVP and pulsus paradoxus in tamponade Prominent X descent (first deflectio of jugular pulse during systole due to atrial relaxation and TV descent) and blunted Y descent (second deflection of jugular pulse due to diastolic inflow of blood into the right ventricle) because of the limited or absent late diastolic filling of the ventricle. A fall in systolic pressure with inspiration in pulsus paradoxus is associated with decrease in LV filling Y descent blunted because of limited or absent lated diastolic filling of the right ventricle

Other causes of pulsus paradoxus Obstructive airway disease Acute and chronic Constriction Restriction Pulmonary embolism RV infarction Circulatory failure

EKG pericarditis Electrical alternans, low voltage, tachycardia

EKG tamponade Electrical alternans, low voltage, tachycardia

EKG electrical alternans Simply secondary to large pericardial effusion (swinging of the heart with variation of cardiac position within the pericardium from beat to beat)

Chest X-ray Enlarged cardiac silhouette

Echocardiography 2D and M-mode RV diastolic collapse RA collapse/inversion IVC plethora Doppler Exaggerated respiratory variation in mitral and tricuspid inflow velocities Phasic variation in right ventricular outflow tract/left ventricular outflow tract flow Exaggerated respiratory variation in inferior vena cava flow

Echocardiogram: RVDC Most commonly involves the RV outflow tract (more compressible area of RV) Occurs in early diastole, immediately after closure of the pulmonary valve, at the time of opening of the tricuspid valve When collapse extends form outflow tract to the body of the right ventricle, this is evidence that intrapericardial pressure is elevated more substantially

Parasternal long axis view

M-mode Beginning of systole ES DC

Short axis view

4 chamber view

Subcostal view

M-mode Beginning of systole ES DC

Echocardiogram: RA Inversion Right atrium normally contracts in volume with atrial systole In the presence of marked elevation of intrapericardial pressure, RA wall will remain collapsed throughout atrial diastole (early ventricular systole) Isolated RA inversion occurs during late diastole Very sensitive but specificity = 86% Positive predictive value = 50% RA Inversion Time Index (RAITI) - Calculated by dividing - Using 33% as the threshold Specificity = 100% Sensitivity = 94% Total # frames with inversion Total # frames in the cardiac cycle

M-mode across RA

Peak velocity of mitral inflow varies > 15% with respiration

Peak velocity of tricuspid inflow varies > 25% with respiration

IVC plethora

Predictable hierarchy of events Exaggerated respiratory variation of tricuspid inflow Exaggerated respiratory variation of mitral inflow Abnormal right atrial collapse Right ventricular free wall collapse

Instances when echo abnormalities are not seen Significant RV hypertrophy, usually due to PHTN Thickening of the ventricular wall due to malignancy, overlying inflammatory response or thrombus in hemorrhagic pericarditis Low-pressure tamponade (hypovolemic patients)

Echocardiogram: Additional roles Confirm size of the pericardial effusion Small defined as < 100 mL Moderate defined as 100 – 500 mL Large defined as > 500 mL Confirm location of the pericardial effusion Rule out loculated effusions Assist pericardiocentesis

Assessment of the patient Insignificant effusion Flat neck veins Normal BP, HR, RR, good perfusion Hemodynamically significant-Compensated Elevated JVP Mild paradox, No hypotension or tachycardia Good perfusion Mild RV collapse

Assessment of the patient Hemodynamically Severe-Max Compensation Elevated JVP Prominent paradox, Tachycardia No hypotension-adequate perfusion Chamber collapse on ECHO Hemodynamically Severe-Decompensated Tachycardia, tachypnea Hypotension with paradox Chamber collapse, swinging heart

Pericardiocentesis Usually performed if more than 1 cm effusion Also performed if effusion smaller in the setting of acute trauma and hemodynamic compromise Pericardial window if need for biopsies and if evidence of coaugulopathy

RB 74 yo male with recently diagnosed adenocarcinoma of undetermined primary who presented to ED on 10/6 with chest pain

RB BP 125/65, pulsus paradoxus of 12 JVP 12 cm PMI located in 5th ICS, distant heart sounds Faint crackles lung bases

RB CT chest consistent with large pericardial effusion and moderate compression of right ventricle Worsened metastatic disease including enlargement of subclavicular, mediastinal, right hilar lymph nodes and pulmonary nodules Stat echo showing…

10/6 TTE Large pericardial effusion. Effusion is loculated (4.6 anterior to the right atrium and RV). Stranding visualized within the pericardial space c/w organization. Sustained RA diastolic collapse c/w low filling pressures or early tamponade. RV diastolic collapse c/w impaired filling/tamponade physiology

10/6 TTE Large pericardial effusion. Effusion is loculated (4.6 anterior to the right atrium and RV). Stranding visualized within the pericardial space c/w organization. Sustained RA diastolic collapse c/w low filling pressures or early tamponade. RV diastolic collapse c/w impaired filling/tamponade physiology

10/6 TTE Large pericardial effusion. Effusion is loculated (4.6 anterior to the right atrium and RV). Stranding visualized within the pericardial space c/w organization. Sustained RA diastolic collapse c/w low filling pressures or early tamponade. RV diastolic collapse c/w impaired filling/tamponade physiology

10/6 pericardiocentesis Drainage of 400 cc of bloody fluid Pre-procedure: pulsus 20 mmHg, cardiac output 3.8 Post-procedure: pulsus < 10 mmHg, cardiac output 5.0

TTE post-procedure

Thank you