A 54-year-old man with atrial fibrillation underwent percutaneous pulmonary vein isolation under general anesthesia earlier in the day. In the recovery room, he became tachycardic, hypotensive, and short of breath and complained of chest tightness. Electrocardiogram (ECG) revealed low QRS complexes and electrical alternans. Cardiac tamponade is suspected.
What is cardiac tamponade?
Cardiac tamponade is defined as accumulation of fluid in the pericardial sac that interferes with cardiac filling and causes hypotension. The pericardial sac encloses the heart. It is composed of two membranes, an outer fibrous pericardium and an inner serous pericardium. The serous pericardium is composed of a visceral layer fused to the epicardium and a parietal layer fused to the fibrous pericardium. The pericardial sac normally contains 15–50 mL of straw-colored fluid.
Cardiac tamponade can be classified further as acute or subacute based on the time it takes to develop. Acute cardiac tamponade can occur with 150 mL of fluid in the pericardial space owing to poor compliance of the fibrous pericardium. In subacute cardiac tamponade, a large amount of fluid (>1000 mL) might be present if the pericardium has had time to stretch.
The progression of tamponade physiology as described by Reddy occurs in three phases. Initially, when fluid starts accumulating in the pericardial sac, the intrapericardial pressure begins to increase, but a compensatory increase in central venous pressure allows for maintenance of right ventricular and left ventricular filling. As more fluid accumulates, the intrapericardial pressure equalizes first with the right ventricular filling pressure, interfering with ventricular filling. The right ventricle is compromised first because it is more compliant than the left ventricle and has a lower filling pressure. At this phase, stroke volume is diminished, but cardiac output may be maintained by a higher heart rate. Last, as further fluid accumulates, intrapericardial pressure equalizes with left ventricular filling pressure, and cardiac output becomes severely compromised.
What are the etiologies of cardiac tamponade?
Acute tamponade can be caused by chest trauma, ascending aortic dissection, percutaneous coronary interventions, and intracardiac arrhythmia ablations. Indwelling central venous catheters have also been identified by the American Society of Anesthesiologists (ASA) Closed Claims Project as a cause of tamponade. Recent pericardiotomy, as performed during cardiac surgery, has also been implicated in the development of cardiac tamponade, even though the pericardial sac has been left open; in this situation, a localized hematoma can cause regional cardiac tamponade (i.e., a specific chamber is compressed).
Subacute cardiac tamponade can be caused by malignancy, renal failure, infections such as tuberculosis, and hypothyroidism.
What are the signs and symptoms of cardiac tamponade?
Depending on the severity and acuity of development of cardiac tamponade, shortness of breath, chest tightness, dizziness, distended neck veins, and shock are nonspecific signs and symptoms. Classic signs of cardiac tamponade include the following:
Pulsus paradoxus—an exaggerated decrease in systolic arterial blood pressure associated with inspiration (>10 mm Hg)
Beck triad—dilated neck veins, muffled heart tones, and hypotension
Low voltage in all leads
Electrical alternans—changing electrical axis caused by the heart swinging freely in the pericardial fluid
Equalization of central venous pressure (CVP), pulmonary artery diastolic pressure (PADP), and pulmonary artery capillary wedge pressure (PACWP) and absent y descent in right atrial and wedge pressure tracings are signs seen when a pulmonary artery catheter is present. Chest x-ray might show an enlarged cardiac silhouette if there is >250 mL of pericardial fluid ( Box 8-1 ).