CARDIAC TAMPONADE

CARDIAC TAMPONADE - Keith Medeiros, MD
BASICS
DESCRIPTION
• Rapid or slow compression of cardiac chambers by pressure on the heart secondary to an increase in pericardial fluid.
• Tamponade can be acute or subacute depending on the etiology.
• As fluid accumulates, pressure primarily affects the compliant cardiac wall and transmits the pressure transmurally, resulting in increased ventricular pressure. This decreases ventricular filling and reduces cardiac output by reducing stroke volume.
• The compensatory mechanisms for tamponade are increased peripheral resistance, central venous pressure, and heart rate.
• In some patients, pulsus paradoxus (10 mm Hg drop in systolic blood pressure between inspiration and expiration) and equalization of pressures may not occur, the absence of which does not rule out tamponade.
• In patients with elevated left ventricular (LV) diastolic pressures (as with chronic hypertension), resistance to LV filling is constant. Throughout the cardiac cycle, equalization of pressures in these patients may only be noted in the right heart chambers, with LV pressures being higher than right ventricular (RV) pressures.
• Variants include low pressure and regional tamponade.
• System(s) Affected: Cardiovascular
RISK FACTORS
Cardiac tamponade should be suspected in the hemodynamically unstable patient
• With known pericarditis
• Following blunt or penetrating chest trauma
• Following open heart surgery or cardiac catheterization
• With known or suspected intrathoracic neoplasm
• With suspected dissecting aortic aneurysm
• With renal failure on dialysis
PATHOPHYSIOLOGY
Fluid accumulation in the pericardial space leading to compression of cardiac chambers as the heart has to compete with increased pericardial contents for the fixed intrapericardial space. Cardiac filling is reduced, limiting cardiac output and eventually causing hypotension and shock. This can occur rapidly in cases of acute tamponade, usually resulting from trauma or surgery, or over weeks to months with slowly developing effusions that allow the pericardial compliance to increase gradually (1)[A].
ETIOLOGY
• Uremia
• Neoplasm: Breast, lung, lymphoma, leukemia
• Occurs in 1% of fibrinolytic-treated acute MI and is associated with increased 30-day mortality (2)[A].
• Postoperative
• HIV
• Other viruses: Coxsackie group B, influenza, ECHO, herpes
• Bacterial infection: Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae (rare)
• Fungal infection: Histoplasmosis capsulatum
• Lupus and rheumatologic disease
• Trauma
• Placement of central venous catheter, pacer wires
• Hypothyroidism
• Drug effects
ASSOCIATED CONDITIONS
• Myocardial infarction
• Aortic aneurysm


DIAGNOSIS
SIGNS AND SYMPTOMS
• Acute
- Patients may complain of chest pain or dyspnea
- Markedly elevated JVP
- Signs of cardiogenic shock: Cyanosis, cool extremities, and oligouria
• Subacute
- Most common complaints are intolerance to minimal activity and dyspnea. Agitation, central nervous system depression, coma, and cardiac arrest may develop later.
History
History of renal failure, surgery, neoplasm, or trauma
Physical Exam
• Beck triad: Distant heart sounds, hypotension, distended neck veins
• Narrow pulse pressure
• Pulsus paradoxus: >10 mm Hg drop in systolic blood pressure between inspiration and expiration
• Neck veins may be distended and reveal a rapid systolic (X) descent and attenuated or absent diastolic (Y) descent
• Tachycardia: A compensatory mechanism to maintain output
• Right upper quadrant tenderness due to hepatic engorgement
• Increased area of cardiac dullness outside the apical point of maximum impulse
TESTS
ECG
• May show sinus tachycardia, low-voltage QRS complexes, diffuse ST segment elevation, and PR segment depression of pericarditis
• Electrical alternans (QRS and/or R wave variation from beat to beat) seen in 10-20% of cases of tamponade; 50-60% of these are neoplastic in origin
Lab
• CBC
• Sedimentation rate
• Cardiac enzymes to rule out acute myocardial infarction
• Antinuclear antibodies
• Rheumatoid factor
• BUN/creatinine
• Pericardial fluid for culture of bacteria, fungus, mycobacteria, Gram stain, hematocrit, cell count, cytology, glucose, protein, rheumatoid factors, complement levels
Imaging
• Chest radiograph: May show enlargement of cardiac shadow (if >200 mL fluid present)
• Echocardiogram:
- Diagnostic of cardiac compression
 RA collapse is a sensitive sign of increased intrapericardial pressure but, diastolic RV collapse is more specific for tamponade (3,4)[A].
- Doppler: May show respiratory variation in transvalvular flow velocities, LV ejection, and LV isovolumetric times (3,4)[A].
Diagnostic Procedures/Surgery
Right heart catheterization:
• Equalization (within 2-3 mm) of right atrial, pulmonary artery diastolic, pulmonary capillary wedge, left atrial, and left ventricular diastolic pressures
• The intracardiac diastolic pressure will approximate the intrapericardial pressure.
• The dip and plateau pattern of constriction or restriction pericardial disease is absent.
• Loss of Y descent on atrial waveform
Pathological Findings
Pericardial blood usually does not clot, but occasionally will.
DIFFERENTIAL DIAGNOSIS
• Tension pneumothorax
• Acute RV failure
• COPD
• Constrictive pericarditis
• Acute acceleration of chronic bronchitis
• Acute pulmonary embolus
• Fat embolus
• Excessive or rapid administration of fluids
• Abdominal distention from ascites or ileus
• Increased intrathoracic pressure from pneumothorax, hemothorax, airway obstruction, or mechanical ventilation
• Administration of vasopressors
TREATMENT
STABILIZATION
Inpatient
GENERAL MEASURES
• Maintain hemodynamic stability until definitive correction of the pericardial tamponade
• All patients should have BP, heart rate, and at a minimum, central venous pressure measurement every 15 minutes. Strong consideration should be given to placement of a Swan-Ganz catheter if time allows.
• Fluids may be of temporary benefit, but rising filling pressures may further compromise coronary perfusion
Diet
As tolerated
Activity
Bed rest
MEDICATION (DRUGS)
Inotropic support with or without vasodilators is controversial partly due to maximal endogenous inotropic stimulation present during acute tamponade (1)[A].
SURGERY
Pericardiocentesis:
• Indications
- Rapid deterioration of hemodynamic function
- A delay in operation for traumatic effusion
- Diagnosis
• If rapid reaccumulation is anticipated (as in malignancy), it may be helpful to insert a long-term drainage catheter. Also consider instillation of sclerosing agents.
• Surgery should be performed under the most optimal circumstances available, as the patient's condition allows.
• Blind pericardiocentesis should be performed only in life-threatening emergencies.
• Ideally, echocardiography can be brought to the bedside to assist in needle placement and progress of fluid removal.
• Invasive monitoring is also helpful to follow decrease in pericardial pressures.
• Fluoroscopy may also be used.
• ECG guidance using the "V" lead to avoid contact with the epicardium may be useful.
• 20% of patients with tamponade will have a negative tap because the pericardial sac contains coagulated material. Hemorrhagic pericardial effusions usually do not clot.
FOLLOW-UP
Follow-up echocardiography should be used to evaluate for recurrence of effusions (3,4)[A].
PROGNOSIS
Good results are expected with the appropriate treatment.
COMPLICATIONS
• Cardiac perforation and/or laceration at time of pericardiocentesis
• Pneumothorax at time of pericardiocentesis
• Constriction of pericardium
PATIENT MONITORING
Close monitoring until stable with telemetry to monitor for cardiac arrhythmia
REFERENCES
1. Spodck DH, Acute cardiac tamponade. N Engl J Med 2003 Aug 14;349(7):684-690.
2. Patel MR et al. Cardiac tamponade in the fibrinolytic era: Analysis of 100,000 patients with ST-segment elevation myocardial infarction. Am Heart J 2006 Feb;151(2):316-322.
3. Cheitlin MD, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: Summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines for the Clinical Application of Echocardiography, Circulation. 2003;108:1146.
4. Cheitlin MD, et al, ACC/AHA Guidelines for the Clinical Application of Echocardiography. Circulation 1997;95:1686-1744.