Francesca N. Delling October 17, 2007 Cardiac Tamponade.

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Transcript of Francesca N. Delling October 17, 2007 Cardiac Tamponade.

Francesca N. DellingOctober 17, 2007

Cardiac Tamponade

• Etiology • Physiology - comparison with constrictive pericarditis

• Types of tamponade• Diagnosis - clinical presentation, physical exam, EKG, CXR, echo

• Treatment

Tamponade

Etiologies• Infectious

– 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

Physiology

Normal pericardium

Increasing pericardialpressure

Increasing fillingpressures

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

(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

Types of tamponade

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

Y descent blunted because of limited or absent lated diastolicfilling 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

EKG tamponade

EKG electrical alternans

Chest X-ray

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

Beginning of systole

ESDC

M-mode

Short axis view

4 chamber view

Subcostal view

Beginning of systole

ESDC

M-mode

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 abnormalitiesare 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– Elevated JVP– 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

10/6 TTE

10/6 TTE

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