Cardiac Tamponade Clinical Presentation

Symptoms vary with the underlying cause and the acuteness of the tamponade. Patients with acute tamponade may present with dyspnea, tachycardia, and tachypnea. Cold and clammy extremities from hypoperfusion are also observed in some patients.

A comprehensive review of the patient's history usually helps identify the probable etiology of a pericardial effusion, which may result in cardiac tamponade.

• Patients with systemic or malignant disease present with weight loss, fatigue, or anorexia.
• Chest pain may be the presenting symptom in patients with pericarditis or myocardial infarction.
• Musculoskeletal pain or fever may be present in patients with an underlying connective tissue disorder.
• A history of renal failure can lead to a consideration of uremia as a cause of pericardial effusion.
• Careful review of a patient's medications may indicate drug-related lupus leading to a pericardial effusion.
• Recent cardiovascular surgery, coronary intervention, or trauma can lead to the rapid accumulation of pericardial fluid and tamponade.^[3]
• Recent pacemaker lead implantation or central venous catheter insertion can lead to the rapid accumulation of pericardial fluid and tamponade.^[4]
• Consider HIV-related pericardial effusion and tamponade if the patient has a history of intravenous drug abuse or opportunistic infections.
• Inquire about chest wall radiation (ie, for lung, mediastinal, or esophageal cancer).
• Inquire about symptoms of night sweats, fever, and weight loss, which may be indicative of tuberculosis.

In a retrospective study, the most common symptoms noted by Roy et al are dyspnea, tachycardia, and elevated jugular venous pressure.{Ref34} Evidence of chest wall injury may be present in trauma patients. Tachycardia, tachypnea, and hepatomegaly are observed in more than 50% of patients with cardiac tamponade, and diminished heart sounds and a pericardial friction rub are present in approximately one third of patients. Some patients may present with dizziness, drowsiness, or palpitations. Cold, clammy skin and weak pulse due to hypotension are also observed in patients with tamponade.

• The Beck triad or acute compression triad

  • Described in 1935, this complex of physical findings refers to increased jugular venous pressure, hypotension, and diminished heart sounds.
  • These findings result from a rapid accumulation of pericardial fluid. However, this classic triad is usually observed in patients with acute cardiac tamponade.
• Pulsus paradoxus or paradoxical pulse

  • This is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in systemic blood pressure.
  • To measure the pulsus paradoxus, patients are often placed in a semirecumbent position; respirations should be normal. The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly deflated until the first Korotkoff sounds are heard only during expiration. At this pressure reading, if the cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff sound is not audible during inspiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present.
  • The paradox is that while listening to the heart sounds during inspiration, the pulse weakens or may not be palpated with certain heartbeats, while S₁ is heard with all heartbeats.
  • A pulsus paradoxus can be observed in patients with other conditions, such as constrictive pericarditis, severe obstructive pulmonary disease, restrictive cardiomyopathy, pulmonary embolism, rapid and labored breathing, and right ventricular infarction with shock.
  • A pulsus paradoxus may be absent in patients with markedly elevated LV diastolic pressures, atrial septal defect, pulmonary hypertension, and aortic regurgitation.
• Kussmaul sign

  • This was described by Adolph Kussmaul as a paradoxical increase in venous distention and pressure during inspiration.
  • This sign is usually observed in patients with constrictive pericarditis but occasionally is observed in patients with effusive-constrictive pericarditis and cardiac tamponade.
• Ewart sign

  • Also known as the Pins sign, this is observed in patients with large pericardial effusions.
  • It is described as an area of dullness, with bronchial breath sounds and bronchophony below the angle of the left scapula.
• The y descent

  • The y descent is abolished in the jugular venous or right atrial waveform.
  • This is due to an increase in intrapericardial pressure, preventing diastolic filling of the ventricles.
• Dysphoria: Behavioral traits such as restless body movements, unusual facial expressions, restlessness, sense of impending death were reported by Ikematsu in about 26% patients with cardiac tamponade.^[5]
• Low-pressure tamponade: In severely hypovolemic patients, classical physical findings such as tachycardia, pulsus paradoxus, and jugular venous distension were infrequent. Sagrista-Sauleda et al identified low-pressure tamponade in 20% of patients with cardiac tamponade.^[6] They also reported low-pressure tamponade in 10% of large pericardial effusions.

For all patients, malignant diseases are the most common cause of pericardial tamponade. Among etiology of tamponade, Merce et al reported malignant diseases in 30-60% of cases, uremia in 10-15% of cases, idiopathic pericarditis in 5-15%, infectious diseases in 5-10%, anticoagulation in 5-10%, connective tissue diseases in 2-6%, and Dressler or postpericardiotomy syndrome in 1-2%. Tamponade can occur as a result of any type of pericarditis.^[7]

• HIV infection
• Infection - Viral, bacterial (tuberculosis), fungal
• Drugs - Hydralazine, procainamide, isoniazid, minoxidil
• Postcoronary intervention (ie, coronary dissection and perforation)
• Acupuncture^[8]
• Postcardiac percutaneous procedures such as mitral valvuloplasty, atrial septal defect (ASD) closure, left atrial appendage occlusion
• Trauma to the chest
• Cardiovascular surgery (postoperative pericarditis)^[3]
• Postmyocardial infarction (free wall ventricular rupture, Dressler syndrome)
• Connective tissue diseases -Systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis
• Radiation therapy to the chest
• Iatrogenic^[9] - After sternal biopsy, transvenous pacemaker lead implantation, pericardiocentesis, or central line insertion
• Uremia
• Anticoagulation treatment
• Idiopathic pericarditis
• Complication of surgery at the esophagogastric junction such as antireflux surgery
• Pneumopericardium (due to mechanical ventilation or gastropericardial fistula)
• Other causes include hypothyroidism, Still disease, and Duchenne muscular dystrophy
• Type A aortic dissection