Cardiac tamponade: 12 pearls in diagnosis and management
ABSTRACTCardiac tamponade shares symptoms and signs such as dyspnea, edema, and low urine output with other, more-common diseases. Consider it when there is chest trauma or when the patient has a chronic medical illness that can involve the pericardium. Successfully treating it can be rewarding for both the patient and the physician.
KEY POINTS
- Slow accumulation of pericardial fluid can result in edema, whereas rapid accumulation leads to hypotension.
- Diuretics can worsen tamponade by removing enough volume from the circulation to lower the central venous pressure below the intrapericardial pressure.
- Try to determine why cardiac tamponade has occurred. Cardiac or aortic rupture requires surgery. If the gross appearance of the pericardial fluid does not match the presumed etiology, reconsider your diagnosis.
- Always review imaging studies before making the diagnosis of cardiac tamponade.
- When cardiac tamponade is considered, pulsus paradoxus must be measured, and if present, integrated with other physical findings and the echocardiogram. However, pulsus paradoxus can be present in the absence of cardiac tamponade, and vice versa.
- Consider the size and location of the pericardial effusion and the patient’s hemodynamic status when deciding between surgery and needle aspiration.
PEARL 4: CARDIAC OR AORTIC RUPTURE REQUIRES SURGERY
When the etiology of cardiac tamponade is cardiac or aortic rupture, the treatment is surgical.
Painful sudden causes of cardiac tamponade include hemopericardium due to rupture of the free wall after myocardial infarction, and spontaneous or posttraumatic dissection and rupture of the ascending aorta. Prompt diagnosis is necessary, but since these lesions will not close and heal spontaneously, the definitive treatment should be surgery. Moreover, needle removal of intrapericardial blood that has been opposing further bleeding is sure to permit bleeding to recur, often with lethal consequences.2
Causes of cardiac tamponade that have a less-acute onset are likely to be complications of medical problems. Medical illnesses known to be associated with cardiac tamponade include:
- Infectious disease (idiopathic or viral, associated with smallpox vaccination, mycobacterial, purulent bacterial, fungal)
- Metastatic cancer (lung, breast, esophagus, lymphoma, pancreas, liver, leukemia, stomach, melanoma)3
- Connective tissue disease (rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, scleroderma, Wegener granulomatosis, acute rheumatic fever)
- Endocrine disease (hypothyroidism)
- Drug side effects (procainamide, isoniazid, hydralazine, minoxidil, phenytoin, anticoagulants, methysergide)
- Inflammatory bowel disease (Crohn disease, ulcerative colitis)
- Congestive heart failure
- Uremia
- Radiation therapy
- Postmyocardial infarction syndrome (Dressler syndrome)
- Postpericardiotomy syndrome.
PEARL 5: REVIEW IMAGING BEFORE DIAGNOSING
What often brings a patient with cardiac tamponade to the attention of the physician is a finding on echocardiography, computed tomography, or magnetic resonance imaging of the chest.
Always review the imaging studies before making the diagnosis of cardiac tamponade. These tests must be reviewed to assess the anatomy and the size and location of the effusion. Particularly, one must look for atrial and right ventricular collapse and inferior vena caval plethora, which are echocardiographic signs of cardiac tamponade.4 Figures 1, 2, and 3 show imaging studies in a patient who presented with worsening cough 2 weeks after undergoing a cardiac procedure and who was found to have cardiac tamponade.
When the history and these imaging studies place cardiac tamponade high in the differential diagnosis as the cause of edema or dyspnea, it is time to reexamine the patient. The best first step is to measure pulsus paradoxus.
HOW PULSUS PARADOXUS OCCURS
To fully appreciate the subtleties of the next pearls, it is necessary to understand the pathophysiology of cardiac tamponade.
When pericardial fluid accumulation raises the pericardial pressure above the central venous pressure and pulmonary venous pressure (intravascular pressure), blood will not passively return to the right side of the heart from the venae cavae nor to the left side of the heart from the pulmonary veins unless it is influenced by the effects of respiration on intrathoracic pressure. During respiration, the right and left sides of the heart are alternately filled and deprived of their respective venous return.
During inspiration, as the intrathoracic pressure decreases, blood in the venae cavae empties into the right side of the heart, while blood in the pulmonary veins preferentially remains in the pulmonary veins, underfilling the left side of the heart. Since the right ventricle is more filled than the left ventricle during inspiration, the ventricular septum shifts from right to left, further opposing pulmonary venous return. As a result, during cardiac tamponade, the systemic blood pressure falls with inspiration.
During expiration the opposite occurs. Expiration decreases the intrathoracic volume, so the intrathoracic pressure rises. This tends to oppose vena caval return to the right side of the heart and to favor pulmonary venous return to the left side of the heart. The ventricular septum shifts from left to right, further accommodating left ventricular filling, raising stroke volume, and increasing blood pressure. This exaggerated alternate filling of the right and left sides of the heart during cardiac tamponade is what accounts for pulsus paradoxus, an inspiratory fall in systolic blood pressure of greater than 10 mm Hg.
If intravascular pressure is low (due to hemorrhage, dehydration, or diuretic therapy), the pressure in the pericardial space needed to oppose venous return is much less. In this low-pressure scenario, the results are low cardiac output and hypotension, which are treated by giving intravenous fluids to maintain intravascular volume.
