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Cardiac Tamponade

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Cardiac Tamponade

BASICS

DESCRIPTION

Difficult to assess due to absence of population-based studies

Initial Tests (lab, imaging)

Maintain hemodynamic stability until definitive drainage, ICU monitoring; may consider Swan-Ganz catheter if time allows

Vasopressors and/or inotropes if necessary; treat underlying cause if apparent.

Admission Criteria/Initial Stabilization

Follow-up echocardiogram may be used to evaluate for recurrence of effusions (8)[A].

Acute traumatic tamponade: 70-80% survival rate at Level 1 trauma centers

11 Roy CL, Minor MA, Brookhart MA, et al. Does this patient with a pericardial effusion have cardiac tamponade? JAMA. 2007;297(16):1810-1818.22 Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690.33 Hoit BD. Pericardial disease and pericardial tamponade. Crit Care Med. 2007;35(8)(Suppl):S355-S364.44 Wann S, Passen E. Echocardiography in pericardial disease. J Am Soc Echocardiogr. 2008;21(1):7-13.55 Restrepo CS, Lemos DF, Lemos JA, et al. Imaging findings in cardiac tamponade with emphasis on CT. Radiographics. 2007;27(6):1595-1610.66 Sagrist -Sauleda J, Angel J, Sambola A, et al. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation. 2008;117(12):1545-1549.77 Fitzgerald M, Spencer J, Johnson F, et al. Definitive management of acute cardiac tamponade secondary to blunt trauma. Emerg Med Australas. 2005;17(5-6):494-499.88 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(9):1146-1162.

Grecu L. Cardiac tamponade. Int Anesthesiol Clin. 2012;50(2):59-77.

  • An accumulation of fluid within the pericardium that causes compression of the chambers of the heart, impairing diastolic filling, reducing cardiac output, 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 pericardiumSubacute: gradual increase of a preexisting effusion, overwhelming normal accommodative pericardial stretch
  • Acute: rapid accumulation (usually blood) within a stiff, noncompliant pericardium
  • Subacute: gradual increase of a preexisting effusion, overwhelming normal accommodative pericardial stretch

EPIDEMIOLOGY

ETIOLOGY AND PATHOPHYSIOLOGY

  • As a pericardial effusion accumulates, it overcomes the pericardium's intrinsic compliance, yielding increased intrapericardial pressure. This pressure eventually exceeds intracardiac diastolic pressures, compressing the chambers of the heart and limiting diastolic filling, yielding a subsequent reduction of cardiac output.
  • Diastolic filling is decreased first in the more compliant right-sided chambers-right atrium (RA), then right ventricle (RV)-followed by a decrease of the left ventricle (LV). Tamponade is defined as the critical point at which diastolic equalization of the LV and RV occurs, total venous return drops, and cardiac output falls.
  • The hemodynamic significance of the effusion depends on the following:Rate of accumulationCompliance of the pericardium to accommodate the enlarging effusion
  • Acute tamponade (typically from a rapidly accumulating hemopericardium, with as little as 50 to 100 mL of fluid)Penetrating or blunt trauma (up to 10% of blunt trauma results in cardiac tamponade)IatrogenesisCardiac surgeryPacer wire migration or electrophysiologic studyCentral venous catheterizationAortic dissection: rupture of cardiac free wall, ventricular aneurysm, or coronary artery; these most commonly occur during the postmyocardial infarction (MI) period.
  • Subacute tamponadePericarditis (20% of subacute tamponade)Iatrogenic effusions (16%) (see above)Malignancy (13%): breast, lung, lymphoma, leukemia, or radiation pericarditisIdiopathic effusion (9%)Acute MI (8%)End-stage renal disease (ESRD) (6%): usually BUN >60 mg/dL; hemodialysis is an independent risk factor.Congestive heart failure (CHF) (5%)Collagen vascular disease (5%): systemic lupus erythematosus, rheumatoid arthritis (RA)Infection (4%)HIVBacterial infection: Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae (rare)Fungal infection: Histoplasma capsulatumViral infection: coxsackie group B, influenza, echoviruses (enteric cytopathogenic human orphan), herpesHypothyroidism with myxedemaMassive fluid resuscitationCoagulopathies
  • Low-pressure tamponadePatients with preexisting effusions who receive hemodialysis or diuretics, thus, reducing intravascular volumeA decrease in intravascular volume makes an unchanged preexisting effusion hemodynamically significant.
  • Regional tamponade (a loculation or hematoma limits diastolic filling)Loculations are often associated with tuberculosis.Localized hematomas are associated with cardiac surgery or post-MI.
  • Rate of accumulation
  • Compliance of the pericardium to accommodate the enlarging effusion
  • Penetrating or blunt trauma (up to 10% of blunt trauma results in cardiac tamponade)
  • IatrogenesisCardiac surgeryPacer wire migration or electrophysiologic studyCentral venous catheterizationAortic dissection: rupture of cardiac free wall, ventricular aneurysm, or coronary artery; these most commonly occur during the postmyocardial infarction (MI) period.
  • Cardiac surgery
  • Pacer wire migration or electrophysiologic study
  • Central venous catheterization
  • Aortic dissection: rupture of cardiac free wall, ventricular aneurysm, or coronary artery; these most commonly occur during the postmyocardial infarction (MI) period.
  • Pericarditis (20% of subacute tamponade)
  • Iatrogenic effusions (16%) (see above)
  • Malignancy (13%): breast, lung, lymphoma, leukemia, or radiation pericarditis
  • Idiopathic effusion (9%)
  • Acute MI (8%)
  • End-stage renal disease (ESRD) (6%): usually BUN >60 mg/dL; hemodialysis is an independent risk factor.
  • Congestive heart failure (CHF) (5%)
  • Collagen vascular disease (5%): systemic lupus erythematosus, rheumatoid arthritis (RA)
  • Infection (4%)HIVBacterial infection: Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae (rare)Fungal infection: Histoplasma capsulatumViral infection: coxsackie group B, influenza, echoviruses (enteric cytopathogenic human orphan), herpes
  • Hypothyroidism with myxedema
  • Massive fluid resuscitation
  • Coagulopathies
  • HIV
  • Bacterial infection: Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae (rare)
  • Fungal infection: Histoplasma capsulatum
  • Viral infection: coxsackie group B, influenza, echoviruses (enteric cytopathogenic human orphan), herpes
  • Patients with preexisting effusions who receive hemodialysis or diuretics, thus, reducing intravascular volume
  • A decrease in intravascular volume makes an unchanged preexisting effusion hemodynamically significant.
  • Loculations are often associated with tuberculosis.
  • Localized hematomas are associated with cardiac surgery or post-MI.

COMMONLY ASSOCIATED CONDITIONS

DIAGNOSIS

HISTORY

  • Dyspnea: most sensitive symptom (88%) (1)[A]
  • 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, and vascular instrumentation.
  • In subacute presentations, patients may have histories of known preexisting effusions with new or worsening exertional dyspnea.

PHYSICAL EXAM

  • Beck triad: distant heart sounds, hypotension, distended neck veinsTypically pertains specifically to acute tamponadeSubacute tamponade: Beck triad is often absent, and BP may be normal or elevated.
  • Most sensitive physical exam findings (1)[A]: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 inspirationIn normal physiology: With inspiration, there is a relative decrease in the pressures across the pulmonary vascular bed with a relatively fixed left atrial (LA) pressure. This leads to decreased pulmonary venous drainage into the LA and therefore, a decrease in left-sided stroke volume with inspiration.In cardiac tamponade physiology: Normal transmission of pressure from the intrapleural to intrapericardial cavity does not occur. Therefore, increased pressure in the RV with filling occurs at the expense of LV filling, causing a further reduction in cardiac output and a greater drop in SBP than usual.Likelihood ratio (LR) for >12 mm Hg: 5.9; LR for >10 mm Hg: 3.3Can be absent in the settings of hypovolemia, severe aortic insufficiency, severe LV dysfunction, atrial septal defect, or in patients with positive-pressure ventilationCan also be seen in the setting of acute pulmonary embolus, RV infarction, chronic obstructive pulmonary disease (COPD), asthma, and severe lung diseasePerformed best via sphygmomanometer by the following steps:Insufflate cuff >20 mm Hg beyond systolic pressureSlowly deflate cuff and record pressure at which Korotkoff sounds are audible at expiration only.Further deflate cuff and record pressure at which Korotkoff sounds are equally audible at inspiration and expiration.If these 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
  • Only sign may be pulseless electrical activity.
  • Typically pertains specifically to acute tamponade
  • Subacute tamponade: Beck triad is often absent, and BP may be normal or elevated.
  • Pulsus paradoxus (82%)
  • Tachypnea (80%)
  • Tachycardia (77%)
  • Jugular venous distention (76%)
  • In normal physiology: With inspiration, there is a relative decrease in the pressures across the pulmonary vascular bed with a relatively fixed left atrial (LA) pressure. This leads to decreased pulmonary venous drainage into the LA and therefore, a decrease in left-sided stroke volume with inspiration.
  • In cardiac tamponade physiology: Normal transmission of pressure from the intrapleural to intrapericardial cavity does not occur. Therefore, increased pressure in the RV with filling occurs at the expense of LV filling, causing a further reduction in cardiac output and a greater drop in SBP than usual.
  • Likelihood ratio (LR) for >12 mm Hg: 5.9; LR for >10 mm Hg: 3.3
  • Can be absent in the settings of hypovolemia, severe aortic insufficiency, severe LV dysfunction, atrial septal defect, or in patients with positive-pressure ventilation
  • Can also be seen in the setting of acute pulmonary embolus, RV infarction, chronic obstructive pulmonary disease (COPD), asthma, and severe lung disease
  • Performed best via sphygmomanometer by the following steps:Insufflate cuff >20 mm Hg beyond systolic pressureSlowly deflate cuff and record pressure at which Korotkoff sounds are audible at expiration only.Further deflate cuff and record pressure at which Korotkoff sounds are equally audible at inspiration and expiration.If these pressures differ by >10 mm Hg, pulsus paradoxus is present.
  • Insufflate cuff >20 mm Hg beyond systolic pressure
  • Slowly deflate cuff and record pressure at which Korotkoff sounds are audible at expiration only.
  • Further deflate cuff and record pressure at which Korotkoff sounds are equally audible at inspiration and expiration.
  • If these pressures differ by >10 mm Hg, pulsus paradoxus is present.

DIFFERENTIAL DIAGNOSIS

  • 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 patternsIn tamponade, chamber filling is decreased but continuous throughout diastole.In constrictive pericarditis, a surge of filling occurs at the beginning of diastole but is minimal during the rest of the diastolic cycle.
  • In tamponade, chamber filling is decreased but continuous throughout diastole.
  • In constrictive pericarditis, a surge of filling occurs at the beginning of diastole but is minimal during the rest of the diastolic cycle.

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.
  • Hypertension may be present in 27-43% of cases of tamponade and is more likely to be present in preexisting hypertension or advanced renal disease.
  • Acute tamponade (trauma and preoperative labs): CBC, serum chemistries, coagulation panel, ethanol level, drugs of abuse, urinalysis
  • Subacute tamponade (evaluate cause of the effusion)CBC, serum chemistries, ESR, cardiac enzymes, antinuclear antibodies (ANA), rheumatoid factor (RF)Fluid analysis of glucose, protein, cell count, lactate dehydrogenase (LDH), amylase, cholesterol, cytology, complement levels, Gram stain, and cultures (including bacterial, viral, acid-fast bacilli, and fungal cultures)
  • Chest radiograph: Use is limited. May show enlargement of cardiac shadow (if >200 mL fluid present). Cardiomegaly is 89% sensitive, with very poor specificity.
  • Echocardiography (3,4)[A]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%). Note that chamber collapse may be attenuated if right-sided intracardiac pressures are elevated.Doppler flow evidence of pulsus paradoxus: with inspiration, exaggerated increased flow 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 inspirationCompression of pulmonary trunkParadoxical motion of interventricular septumSwinging heart
  • CT (5)[A]: may be 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.IVC diameter ≥ aorta diameter — 2Reflux of contrast into IVC and/or azygous veinCompression of coronary sinusFlattening of anterior surface of heart and concave chamber deformityBowing of the interventricular septum into the LV
  • MRI (5)[A]: Use is limited due to emergent nature of tamponade. Can detect fluid collection as small as 30 mL; (highly) effective in evaluating the composition of pericardial effusion
  • CBC, serum chemistries, ESR, cardiac enzymes, antinuclear antibodies (ANA), rheumatoid factor (RF)
  • Fluid analysis of glucose, protein, cell count, lactate dehydrogenase (LDH), amylase, cholesterol, cytology, complement levels, Gram stain, and cultures (including bacterial, viral, acid-fast bacilli, and fungal cultures)
  • 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%). Note that chamber collapse may be attenuated if right-sided intracardiac pressures are elevated.
  • Doppler flow evidence of pulsus paradoxus: with inspiration, exaggerated increased flow 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
  • Compression of pulmonary trunk
  • Paradoxical motion of interventricular septum
  • Swinging heart
  • IVC diameter ≥ aorta diameter — 2
  • 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 interventricular septum into the LV
  • Diastolic pressures of RA and RV are increased and eventually equalize with the left-sided chambers and the intrapericardial pressure (usually at 15 to 20 mm Hg).
  • The dip and plateau pattern of constriction or restriction pericardial disease is absent.

TREATMENT

GENERAL MEASURES

MEDICATION

  • Fluid bolus is temporizing in acute setting.
  • In subacute tamponade, most agree that although all patients do not benefit from fluid, those with hypotension do.

ADDITIONAL THERAPIES

  • 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.

SURGERY/OTHER PROCEDURES

  • Acute tamponade: requires surgical intervention; pericardiocentesis may be performed as a temporizing measure in the setting of hypotension despite fluid resuscitation. However, 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.
  • Subacute tamponade: Pericardiocentesis is usually sufficient for definitive treatment; may be guided by CT (98% success rate), fluoroscopy (93%), or ultrasound (93% for effusions >10 mm). Blind approach may be necessary in sudden cardiovascular collapse (73% success rate). If pericardiocentesis is unsuccessful in the setting of cardiovascular collapse, an immediate thoracotomy may be indicated (7)[B].

INPATIENT CONSIDERATIONS

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

PROGNOSIS

COMPLICATIONS

  • Chamber lacerations
  • Pneumothorax
  • Ventricular tachycardia

REFERENCES

ADDITIONAL READING

CODES

ICD10

ICD9

SNOMED

CLINICAL PEARLS

  • Pericardial tamponade is a potentially reversible cause of pulseless electrical activity.
  • Checking for pulsus paradoxus 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.
  • Fluid resuscitation can be a temporizing measure until definitive therapy with pericardiocentesis can be performed.