Cardiac Tamponade – Causes, Symptoms, Diagnosis, Treatment and Ongoing care
- A rapid or slow accumulation of fluid within the pericardium that causes compression of the chambers of the heart, impairing diastolic filling and ultimately leading to cardiovascular collapse.
- Tamponade can be acute or subacute, depending on the etiology:
- Acute: Rapid accumulation (usually blood) within a stiff, noncompliant pericardium
- Subacute: Gradual increase of a preexisting effusion, with limited accommodative pericardial stretch
- Variants include low-pressure and regional tamponade:
- Low-pressure: Occurs when left- and right-sided pressures equalize at lower pressures; occurs when a decrease in intravascular volume makes an unchanged preexisting effusion hemodynamically significant (1)
- Regional: Occurs when a loculation or hematoma limits diastolic filling
Difficult to assess due to absence of population-based studies
Difficult to assess due to absence of population-based studies
- As a pericardial effusion accumulates, it overcomes the pericardium’s intrinsic compliance yielding increased intrapericardial pressure. This pressure eventually exceeds intracardiac diastolic pressures, compresses the chambers of the heart, and limits diastolic filling with subsequent reduction of cardiac output.
- Diastolic filling is decreased first in the more compliant right-sided chambers (RA, then RV), followed by decrease of the left side. Tamponade is defined as the critical point at which diastolic equalization of the left and right ventricles occurs, total venous return drops, and cardiac output falls.
- The hemodynamic significance of the effusion depends on:
- Rate of accumulation
- Compliance of the pericardium to accommodate the enlarging effusion
- Acute tamponade (most commonly from a rapidly accumulating hemopericardium, with sometimes as little as 50–100 mL of fluid):
- Penetrating or blunt trauma
- Iatrogenic instrumentation (cardiac surgery, central lines, pacer wire migration, peripherally inserted central catheter lines)
- Aortic dissection
- Rupture of cardiac free wall, ventricular aneurysm, or coronary artery. These most commonly occur during the postmyocardial infarction (MI) period.
- Subacute tamponade (any condition that causes a pericardial effusion) (2):
- Idiopathic pericarditis (20%)
- Iatrogenic effusions (16%) (see above)
- Malignancy (13%): Breast, lung, lymphoma, leukemia, or radiation pericarditis
- Idiopathic effusion (9%)
- Acute MI (8%): Can complicate 15% of MIs and <1% of MIs treated with thrombolysis (2)
- End-stage renal disease (ESRD) (6%): Usually blood urea nitrogen >60 mg/dL, but hemodialysis is an independent risk factor
- Congestive heart failure (CHF) (5%): Effusions seen in 14% of CHF
- Collagen vascular disease (5%): Systemic lupus erythematosus, rheumatoid arthritis (RA)
- Infection (4%):
- Bacterial infection: Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae (rare)
- Fungal infection: Histoplasmosis capsulatum
- Viral infection: Coxsackie group B, influenza, enteric cytopathogenic human orphan, herpes
- Hypothyroidism with myxedema
- Massive fluid resuscitation
- Low-pressure tamponade:
- Patients with preexisting effusions who receive hemodialysis or diuretics thus reducing intravascular volume
- Regional tamponade:
- Localized hematomas after cardiac surgery or post-MI
- Dyspnea: Most sensitive symptom (88%) (2)
- Vague chest pain or an overall subjective sense of discomfort
- Syncope or presyncopal symptoms
- Altered mentation from poor perfusion
- Nausea or abdominal pain from hepatic venous engorgement
- In acute presentations, look for history of recent trauma, surgery, vascular instrumentation
- In subacute presentations, patients may have histories of known preexisting effusions with new or worsening exertional dyspnea.
- Only sign may be pulseless electrical activity
- Beck triad: Distant heart sounds, hypotension, distended neck veins:
- Pertains specifically to acute tamponade
- Subacute tamponade: Beck triad is often absent, and blood pressure (BP) may be normal or elevated (2).
- Most sensitive physical findings on exam (2):
- Pulsus paradoxus (82%).
- Tachypnea (80%)
- Tachycardia (77%)
- Jugular venous distention (76%)
- Pulsus paradoxus: Defined as an exaggerated drop in systolic blood pressure (SBP) (usually >10 mm Hg) during inspiration:
- This is due to the fact that the normal transmission of pressure from the intrapleural to intrapericardial cavity does not occur. Therefore, with inspiration, there is a relative decrease in the pressures across the pulmonary vascular bed with a relatively fixed left atrial pressure. This leads to decreased pulmonary venous drainage into the left atrium and therefore a decrease in left-sided stroke volume with inspiration (3).
- Likelihood ratio (LR) for >12 mm Hg: 5.9; likelihood ratio (LR) for >10 mm Hg: 3.3
- Can be absent in the settings of hypovolemia, severe AI, severe LV dysfunction, ASD, or in patients with positive-pressure ventilation (4)
- Can also be seen in the setting of acute pulmonary embolus, RV infarction, and COPD
- Can be false positive in severe lung disease
- Performed best via sphygmomanometer by the following steps:
- Insufflate cuff >20 mm Hg beyond systolic pressure.
- Slowly deflate cuff and record pressure at which Korotkoff sounds are slightly audible at expiration only.
- Further deflate cuff and record pressure at which Korotkoff sounds are equally audible at inspiration and expiration.
- If these 2 pressures differ by >10 mm Hg, pulsus paradoxus is present.
- Respiratory distress, but with surprisingly little or no pulmonary edema
- Jugular venous distention with a rapid systolic (X) descent and absent diastolic (Y) descent
- Narrow pulse pressure (due to limited stroke volume and increased peripheral vascular resistance)
- Signs of cardiogenic shock: Low BP with poor mentation and cool, poorly perfused extremities
- Kussmaul sign (elevation of jugular venous distention with inspiration caused by increased right-sided pressure)
- Increased peripheral (right-sided) edema due to impaired venous return
- Right upper quadrant tenderness due to hepatic engorgement
- Increased area of cardiac dullness outside the apical point of maximum impulse
Diagnostic Tests & Interpretation
- Sinus tachycardia
- Low-voltage QRS, defined as <5 mm in limb leads and <10 mm in precordial leads; sensitivity of 42%
- Signs of pericarditis (except in uremic pericarditis): Initially diffuse ST segment elevation and PR segment depression of pericarditis; later stages exhibit T-wave inversions that may be transient or permanent
- Electrical alternans (QRS and/or P-wave beat-to-beat variation in axis and/or amplitude) is only seen in 10–20% of cases of tamponade. However, it is the most specific ECG finding for tamponade (4).
Initial lab tests
- Acute tamponade (trauma and preoperative labs):
- Complete blood count (CBC), serum chemistries, coagulation panel, ethanol, drugs of abuse, UA
- Subacute tamponade (evaluate cause of the effusion):
- CBC, serum chemistries, erythrocyte sedimentation rate, cardiac enzymes, antinuclear antibodies, rheumatoid factor
- Fluid analysis of glucose, protein, cell count, lactate dehydrogenase, amylase, cholesterol, cytology, complement levels, Gram stain, and cultures (including bacterial, viral, acid-fast bacilli, and fungal cultures)
- Chest radiograph:
- May show enlargement of cardiac shadow (if >200 mL fluid present)
- Cardiomegaly is 89% sensitive.
- Echocardiography (5):
- Diastolic chamber collapse: RA collapse in late diastole (more sensitive 55–60%, less specific 50–68%) and RV collapse in early diastole (less sensitive 38–48%, more specific 84–100%) (3)
- Doppler flow: An exaggerated increase through tricuspid valve (>40% variation) and exaggerated decrease (>25% variation) through mitral valve. High sensitivity (75%) and specificity (91%).
- Inferior vena cava (IVC) distention with <50% collapse during inspiration (3)
- Compression of pulmonary trunk
- Paradoxical motion of interventricular septum
- Swinging heart
- CT: Helpful in evaluating cause (i.e., aortic dissection) and characterizing the effusion (i.e., blood, pus, serous). A pericardial effusion with any of the following is suggestive of tamponade (3):
- IVC diameter 2 × aorta
- Reflux of contrast into IVC and/or azygous vein
- Compression of coronary sinus
- Flattening of anterior surface of heart and concave chamber deformity
- Bowing of the IV septum into the LV
- MRI (3):
- Can detect fluid collection as small as 30 mL
- Highly effective in evaluating the composition of pericardial effusion
- Use is limited due to emergent nature of tamponade.
Right heart catheterization:
- Diastolic pressures of RA and RV are increased and eventually equalize with the left-sided chambers and the intrapericardial pressure (usually at 15–20 mm Hg) (4).
- The dip and plateau pattern of constriction or restriction pericardial disease is absent.
- Any condition causing obstructive or cardiogenic shock, such as massive pulmonary embolism, tension pneumothorax, anterior wall MI, MI with valve rupture or dysfunction, or constrictive/restrictive pericarditis
- Of note, effusive-constrictive pericarditis can be especially difficult to distinguish from tamponade because it involves an effusion that is present with chamber collapse but is not the reason for the collapse. Differentiation can be made on echo by close examination of the diastolic filling patterns:
- In tamponade, chamber filling is decreased but continuous throughout diastole.
- In constrictive pericarditis, there is a surge of filling at the beginning of diastole, but is minimal during the rest of the diastolic cycle.
- Fluid bolus is temporizing in acute setting.
- In subacute tamponade, most agree that while all patients do not universally benefit from fluid, those with hypotension do (6)[B].
- Vasopressors if necessary: Dobutamine thought to maintain better cardiac output and delivery of oxygen than does norepinephrine.
- Benefit of inotropes is unclear.
- High-dose anti-inflammatory medications for pericarditis
- Maintain hemodynamic stability until definitive drainage.
- ICU monitoring
- Consider Swan-Ganz catheter if time allows.
- Hemodialysis for ESRD if patient is not in extremis (volume overload can be a cause for increasing pericardial effusions in ESRD)
- Minimize positive end expiratory pressure and pressure support if mechanically ventilated to preserve cardiac filling (4)[A].
Drainage is the definitive treatment (7)[A]. For acute traumatic tamponade: Prepare operating room for definitive cardiac repair via subxiphoid pericardotomy or full surgical thoracotomy. Pericardiocentesis is NOT the definitive treatment, as coagulated blood within the pericardium makes aspiration limited and hemorrhage from the cardiac injury usually refills the sac immediately. However, if there is hypotension despite fluid, a pericardiocentesis can be attempted in the emergency room (ER). For subacute tamponade: Pericardiocentesis may be guided by CT (98% success rate), fluoroscopy (93%), or ultrasound (93% for effusions >10 mm; only 58% in smaller effusions). Blind approach may be necessary in sudden cardiovascular collapse (73% success rate). An 18-G spinal needle is used, and, with the aid of a guide wire, a pigtail catheter can be introduced into the pericardium to prevent reaccumulation (7)[A]. The catheter can usually be pulled once it is draining <50 mL/d (4)[A]. If pericardiocentesis is unsuccessful in the setting of cardiovascular collapse, an immediate thoracotomy in ER is indicated (8)[B].
Requires ICU-level monitoring
Follow-up echocardiogram may be used to evaluate for recurrence of effusions (7)[A].
Acute traumatic tamponade: 70–80% survival rate quoted for level-1 trauma centers (8).
- Chamber lacerations
- Ventricular tachycardia
1. Sagristà-Sauleda J, Angel J, Sambola A, et al. Low-pressure cardiac tamponade: clinical and hemodynamic profile. Circulation. 2006;114:945–52.
2. Roy CL, Minor MA, Brookhart MA, et al. Does this patient with a pericardial effusion have cardiac tamponade? JAMA. 2007;297:1810–8.
3. Restrepo CS, Lemos DF, Lemos JA, et al. Imaging findings in cardiac tamponade with emphasis on CT. Radiographics. 2007;27:1595–610.
4. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684–90.
5. Wann S, Passen E et al. Echocardiography in pericardial disease. J Am Soc Echocardiogr. 2008;21:7–13.
6. Sagristà-Sauleda J, Angel J, Sambola A, et al. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation.2008;117:1545–9.
7. Cheitlin MD, Armstrong WF, Aurigemma GP, 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 (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography).Circulation. 2003;108:1146–62.
8. Fitzgerald M, et al. Definitive management of acute cardiac tamponade secondary to blunt trauma. Emerg Med Australasia. 2005;17:494–9.
Hoit BD et al. Pericardial disease and pericardial tamponade. Crit Care Med.2007;35:S355–64.
423.3 Cardiac tamponade
35304003 Cardiac tamponade (disorder)
- Pericardial tamponade is a potentially reversible cause of pulseless electrical activity: Perform emergent pericardiocentesis as diagnostic and therapeutic maneuver.
- Checking for pulsus parodoxicus may be a useful bedside maneuver with reasonable sensitivity in most cases, although nonspecific.
- Acute tamponade from trauma or intrapericardial rupture presents with much more rapid clinical deterioration than does subacute tamponade due to sudden rises in pericardial pressure and inability of the pericardium to stretch to accommodate the effusion.