|Home | About | Journals | Submit | Contact Us | Français|
Paradoxical hemodynamic instability is defined as unexpected hemodynamic compromise that develops in a patient after pericardial fluid drainage. The overall incidence of the condition is about 5%, and it has a high in-hospital mortality rate. The condition has been reported to occur regardless of the approach that is used to drain the fluid or the underlying cause of the disease. The pathophysiology of paradoxical hemodynamic instability and the appropriate intervention are not very clear, and further studies are needed to identify appropriate preventive measures.
We report a rare manifestation of paradoxical hemodynamic instability in a 65-year-old woman who had a history of stage IV lung cancer. She presented with a one-week history of pleuritic chest pain and shortness of breath on exertion. Echocardiography revealed a large circumferential pericardial effusion with right atrial and ventricular collapse during diastole, suggesting a compressive effect of the pericardial fluid; however, left ventricular systolic function was well preserved. The patient underwent the scheduled creation of a subxiphoid pericardial window. Immediately after the pericardial fluid was evacuated, her heart began to beat more vigorously, but this was abruptly followed by an episode of asystole. Pacing and medical therapy were unsuccessful in preventing repeated episodes of asystole, and the patient died.
To our knowledge, this is the 2nd report of unexpected asystole after the creation of a subxiphoid pericardial window, and it is the first report of a takotsubo-like contractile pattern associated with paradoxical hemodynamic instability.
Malignant involvement of the pericardium has been detected on autopsy in up to 20% of cancer patients,1 and the most common metastatic tumor involving the pericardium is lung cancer.2 A pericardial effusion that arises in a patient with a known malignancy usually indicates metastasis.1 Cardiac tamponade, the most severe consequence of a pericardial effusion, occurs when accumulated fluid compresses the cardiac chambers. The result is reduced venous return and subsequently decreased cardiac output. Most patients who undergo evacuation of a clinically significant pericardial effusion experience rapid improvement in their symptoms and hemodynamic status. We describe the occurrence of an uncommon and frequently fatal3 postoperative sequela of pericardial drainage: paradoxical hemodynamic instability (PHI). Paradoxical hemodynamic instability is defined as unexpected hemodynamic compromise that develops in a patient after pericardial fluid drainage.
In February 2011, a 65-year-old woman presented with a one-week history of pleuritic chest pain and shortness of breath on exertion. Six months earlier, she had been diagnosed with stage IV non-small-cell lung cancer and bilateral pulmonary embolism. She was given anticoagulative therapy and was treated with palliative radiation and chemotherapy, including pemetrexed. She had recently undergone successful gamma-knife radiosurgery for cancer that had metastasized to the brain. The current physical examination revealed a heart rate of 116 beats/min, a blood pressure of 106/75 mmHg with a pulsus paradoxus of 20 mmHg, a respiratory rate of 16 to 18 breaths/min, and markedly distended jugular veins. Auscultation revealed distant heart sounds without murmurs or gallops, and no added respiratory sounds. A chest radiograph showed mild enlargement of the cardiac silhouette, a left mid-lung mass, and a new 4-cm mass in the left upper lobe. An electrocardiogram showed sinus tachycardia with low voltage. Echocardiography revealed a large circumferential pericardial effusion with right atrial and ventricular collapse during diastole, suggesting a compressive effect of the pericardial fluid; however, left ventricular systolic function was well preserved (Fig. 1). Because of the size of the pericardial effusion with right ventricular collapse, as well as an inferior vena cava that was plethoric with no inspiratory collapse seen on echocardiography, she was scheduled for subxiphoid pericardial window surgery.
At the time of surgery, the patient was placed supine in mild reverse Trendelenburg position because of her shortness of breath. After the placement of an arterial line and central access through her implanted chemotherapy port, she was placed under general endotracheal anesthesia. She tolerated induction moderately well, despite some atrial fibrillation, with heart rates from 100 to 120 beats/min and systolic blood pressures (SBP) above 120 mmHg. A transesophageal echocardiographic (TEE) probe was inserted. An incision of 6 to 8 cm was made over the xiphoid process and deepened until the xiphoid process was transected and removed. The palpable pericardial sac had minimal pericardium, which was stretched and thin. The sac was grasped with Allis clamps. An incision instantly released dark serosanguinous effluent. The fluid was suctioned and sent for culture and cytologic analysis. The patient's heart began to beat more vigorously, and the effusion, as seen on TEE, was almost completely drained. Asystole abruptly occurred, and no ventricular movement was seen through the window. The surgeon placed 2 fingers into the pericardial window and initiated cardiac compressions from the inferior side of the heart, yielding an SBP above 120 mmHg. Only 10 to 15 seconds of asystole were observed before cardiopulmonary resuscitation (CPR) was initiated. Epinephrine was administered, and, after approximately 1 minute of CPR, a spontaneous rhythm resumed, with the patient's SBP in the 200-mmHg range. After several minutes of slow decline in SBP, asystole again abruptly occurred. Cardiac massage was repeated as atropine and calcium were administered. The ensuing rhythm was wider and more abnormal than before, with discrete ST elevations. The pericardium and heart were examined to verify that no inadvertent injuries had occurred to cause this rapid decline in condition; no injury was identified. A 3rd episode of asystole occurred, despite adequate inotropic therapy. The patient had no electrolyte abnormalities, and her hemoglobin level was stable above 9 g/dL. She was adequately volume-resuscitated with over 2 L of crystalloid solution and 1 unit of packed red blood cells. The TEE probe, which had been in place throughout, showed minimal contractile motion in the right side of the heart. The left side, which initially had been moving vigorously, decreased to an ejection fraction of 0.25 and continued to decrease with each episode of asystole to approximately 0.10. An epicardial electrode lead was placed at the inferior aspect of the heart through the pericardial window, for capture and pacing. The lead was brought out elsewhere and the subxiphoid window was closed. After the heart was paced, epinephrine and dopamine drips were begun, to maintain the SBP in the 90- to 100-mmHg range.
The patient's surgical incision was closed, and she was taken to the cardiothoracic intensive care unit in morbid and guarded condition while being given several vasopressors. Despite intermittent pacing, tachycardia and an SBP of about 110 mmHg alternated. Transthoracic echocardiography with the use of DEFINITY® contrast agent (Lantheus Medical Imaging, Inc.; N. Billerica, Mass) revealed an ejection fraction of 0.10 to 0.15 and a takotsubo-like contractile pattern (Fig. 2). The basal segments contracted with akinesia elsewhere. In addition, the right ventricle was dilated with reduced function, and there was severe tricuspid regurgitation. The patient's condition continued to deteriorate, and increasing support was required. The family requested no further extraordinary measures, and, after another episode of asystole, the patient died.
Pericardial effusion is frequently associated with metastatic cancer, and it can also occur in some inflammatory and infectious diseases. In most cases, draining the pericardial fluid results in complete, asymptomatic recovery. However, sometimes the procedure leads to hemodynamic compromise.
To our knowledge, this is only the 2nd report of unexpected asystole after the creation of a subxiphoid pericardial window. In a report comparing subxiphoid and percutaneous pericardial drainage, Leung Wai Suen and colleagues3 described the case of a 23-year-old woman with systemic lupus glomerulonephritis and tamponade in whom 1 L of effusive fluid was drained via a subxiphoid surgical approach. The patient developed bradycardia and then asystole 30 minutes later. She responded initially to CPR but died of recurrent asystole in 1 hour. In the medical literature, this has been referred to as PHI or as low cardiac output syndrome.
To our knowledge, ours is the first report of a takotsubo-like contractile pattern in association with PHI. Although the cause of this characteristic wall-motion abnormality remains unclear, psychological stress and elevated sympathetic tone might play a role, and both are typically present in cancer patients. Burgdorf and colleagues4 showed a possible link between malignancies and the occurrence of takotsubo cardiomyopathy as either a paraneoplastic phenomenon or a result of increased sympathetic tones.
Wagner and colleagues5 described an overall incidence of about 5% and a high in-hospital mortality rate for PHI. They also identified evidence that tamponade, large amounts of effusion, and malignant cells identified upon cytologic or pathologic analysis increase the risk of PHI. The syndrome has been reported to occur irrespective of the drainage approach or underlying cause of the disease.
The pathophysiology of PHI is not clear. It is postulated that tamponade results in an unexpected, sudden increase in preload. This can lead to enlargement of the right ventricle and eventually to right-sided heart failure. In some instances, global ventricular failure has been noted. Another theory is that tamponade causes decreased coronary flow, which leads to decreased contractility and hypoperfusion of the myocardium and then to systolic dysfunction. Even after reversal of the tamponade, the myocardium will not revert to a normal state.
The appropriate intervention in PHI is also not defined. Some authors have recommended that drainage be gradual, to prevent PHI. There are no scientific studies to support this approach. Further studies are needed to identify the risk factors underlying PHI and the appropriate preventive measures.
We thank Nidhi Gupta, MD, Rathan Nair, MD, and Hilana Nashad, MD, for contributing to the content of this paper.
Address for reprints: Murad Abdelsalam, MD, Department of Internal Medicine, Harrisburg Hospital, 111 S. Front St., Harrisburg, PA 17101