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Adenike Odunmbaku, MD, PGY-3
Heart Failure after Pericardiocentesis and Pericardial Window
A 65yo male presented to the ED with shortness of breath, tachypnea, and tachycardia. His past medical history is significant for hypertension that is well controlled with nifedipine. He stated that he had shortness of breath for the past one week, but his breathing acutely worsened over the past 6hours. He denied chest pain, palpitations, fever, or cough.
In the ED, his ECG showed sinus tachycardia with a heart rate of 118, low voltage QRS complexes with alternating heights, and no ST changes. The patient appeared in moderate respiratory distress with accessory muscle use. Physical exam was significant for tachycardia, distant heart sounds, distended neck veins, breath sounds that were clear to auscultation bilaterally, a soft nontender abdomen, and no pedal edema. Chest xray showed cardiomegaly with small pleural effusions at bilateral lung bases. Bedside ultrasound showed a significantly large pericardial effusion with collapse of the right ventricle. The diagnosis of pericardial tamponade was made and emergency pericardiocentesis was performed in the ED. Patient’s respiratory status improved significantly and he was admitted to the CCU for further management.
In the CCU, official echocardiogram was obtained which showed moderate pericardial effusion, no collapse of right ventricle, and a left ventricle that was small and hyperdynamic with no wall motion abnormalities. Pericardial ftluid analysis showed malignant cells and patient was later diagnosed with small cell lung cancer. Although the patient initially remained stable in the CCU, he had another episode of acute decompensation requiring a second emergency pericardiocentesis due to recurrent tamponade physiology. Discussion took place regarding the risk/benefit of scheduling a pericardial window for the patient. There was concern due to numerous case reports citing spontaneous heart failure and marked deterioration after large drainage of fluid from a pericardial window. The decision was made to schedule patient for a pericardial window given the continuous accumulation of pericardial fluid. Immediately after the drainage of 950cc of pericardial fluid, the patient experienced cardiac arrest in the operating room. Patient was resuscitated with epinephrine, IV fluids, and open cardiac massage. He regained pulse, was stabilized, and he was transferred back to the CCU on mechanical ventilation. Repeat official echocardiogram showed trace pericardial effusion with now poor left ventricular function with general hypokinesia. ECG now showed T wave inversions and Q waves in anterolateral leads but cardiac markers were not elevated. He was treated aggressively in the CCU with ACE-I, diuretics, and inotropes but he ultimately died due to presumed cardiogenic shock.
Pericardiocentesis and pericardial window are commonly performed procedures which may lead to complications such as infection, bleeding, perforation of a ventricle, laceration of a coronary artery, pneumothorax, and death. Numerous case reports have described the development of cardiogenic shock, pulmonary edema, and acute respiratory distress syndrome following large drainage of fluid following pericardiocentesis and pericardial window. The development of heart failure and subsequent cardiogenic shock were all preceded by rapid evacuation of a large volume of pericardial fluid. One proposed mechanism is that the rapid removal of a large volume of fluid produces a mismatch between preload and afterload of the left ventricle. Removal of the large volume pericardial fluid causes for the right ventricle to no longer be compressed. As a result, there is a drastic increase in venous return producing rapid filling of the right ventricle, subsequent overfilling of the left ventricle, and pulmonary hypertension. The combination of the volume mismatch between ventricles and the vasoconstriction that is already present secondary to increased catecholamies could lead to increased left ventricle end diastolic pressure and left ventricle systolic failure.
Another proposed mechanism is that circulatory collapse following rapid evacuation of large volume pericardial fluid occurs because of a myocardial stunning. The idea is that regional hypokenesis and heart failure ensues because of a mismatch of oxygen supply along the myocardial wall. Following the evacuation of pericardial fluid, more blood flow and therefore more oxygen is distributed to the newly filled right ventricle. The left ventricle subsequently receives less oxygen and a stunning phenomenon occurs which is often reversible.
When comparing pericardiocentesis and pericardial window, there is no significant difference in mortality (19.8% surgical group vs 18.1% pericardiocentesis group; P=.8). Pericardial windows have a higher rate of complications such as perforation of myocardium and perforation of coronary artery (4.9% vs 26.4%; P<.0001; odds ratio [OR], 6.9; 95% confidence interval [CI], 2.6–18.2). Pericardiocentesis was more likely to require repeat procedure to drain recurrent pericardial effusion (28.9% vs 2.8%; P<.0001; OR, 14.2; 95% CI, 3.3–61.3).
Left ventricular dysfunction is a rare complication following large volume fluid removal from pericardial window or pericardiocentesis. The exact pathophysiological mechanism for the LV dysfunction is unknown. The rapid evacuation of large volumes of pericardial fluid is not recommended. It is unclear how much time should be taken to remove the pericardial fluid but some have reported that the rate should not exceed 50mL/min and pericardiocentesis with an indwelling pigtail catheter is preferred.
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