Intracardiac shunt with hypoxemia caused by right ventricular dysfunction following pericardiocentesis

Abstract

Significant hypoxemia can result from right-to-left intracardiac shunting through a patent foramen ovale, an atrial septal defect or a ventricular septal defect. Pulmonary embolus, congenital heart disease and pericardial tamponade are well-recognized causes of right-to-left shunting. However, right-to-left shunting can also follow pericardiocentesis. A case of profound hypoxemia caused by right ventricular hypokinesis precipitated by pericardial tap is reported. This under-recognized entity can be responsible for significant morbidity in the critical care setting. The clinical presentation, natural history, diagnosis and treatment of hypoxemia caused by intracardiac shunt following pericardiocentesis are discussed.

CASE PRESENTATION

A 55-year-old woman presented with progressive shortness of breath on exertion over the previous one week. Her medical history was significant for breast cancer diagnosed seven years earlier (treated with mastectomy and chemotherapy), as well as hypertension and reflux esophagitis. Medication use included ramipril, domperidone and omeprazole.

In the emergency department, the patient’s temperature was 36.4°C, her blood pressure was 110/75 mmHg, her heart rate was 120 beats/min and her respiratory rate was 28 breaths/min, with an oxygen saturation of 90% on room air. The jugular venous pulse was elevated at 8 cm above the sternal angle. Her heart sounds were faint, but there were no clear gallop rhythms, rubs or murmurs. The lung fields were clear to auscultation, with dullness to percussion at the bases. No lymphadenopathy was palpated in the head and neck, axillary or inguinal areas. An abdominal examination revealed no ascites, and no enlargement of liver or spleen. There was no evidence of peripheral edema.

Blood work included normal complete blood count, electrolytes, urea, creatinine, international normalized ratio and partial thromboplastin time. Liver biochemistry was abnormal, with elevated aspartate aminotransferase 128 U/L, alanine aminotransferase 79 U/L, gamma-glutamyl transferase 233 U/L, alkaline phosphatase 130 U/L and conjugated bilirubin of 28 mmol/L. While still in the emergency department, her oxygen saturation fell to 84% despite the use of 100% inspired oxygen. An arterial blood gas performed shortly thereafter showed a pH of 7.39, partial pressure (Pa) of CO₂ 35 mmHg, PaO₂ of 57 mmHg and bicarbonate of 20 mmol/L. The alveolar-arterial oxygen gradient was markedly abnormal, at 612 mmHg.

An electrocardiogram showed sinus tachycardia with T wave flattening in leads V2 to V6, as well as low QRS voltage. A chest radiograph revealed bilateral pleural effusion, bibasilar atelectasis and an enlarged cardiac silhouette (Figure 1). Given the profound hypoxemia, a computed tomography scan was performed to rule out pulmonary embolus. This revealed a large pericardial effusion, and a subsegmental pulmonary embolus involving the left upper lobe (Figure 2).

Figure 1).

Chest x-ray demonstrating cardiomegaly and bilateral pleural effusion

Figure 2).

Computed tomography scan demonstrating pulmonary embolus in the left subsegmental pulmonary artery (arrows)

The patient was admitted to the intensive care unit. An echocardiogram was performed to further characterize the effusion seen on computed tomography. This indicated pericardial tamponade, with a collapse of the right ventricle (Figure 3). Right ventricular systolic pressure was estimated at 30 mmHg, and right ventricular systolic function appeared to be preserved. Needle pericardiocentesis removed 600 mL of hemorrhagic fluid, and a pericardial drain was left in situ. Cautious anticoagulation with intravenous heparin was started the next day for the pulmonary embolus.

Figure 3).

Echocardiography demonstrating tamponade with a collapse of the right ventricle and left atrium (arrow indicates compression of the right ventricle)

In intensive care, the patient’s blood pressure fell to 90/50 mmHg, requiring augmentation with intravenous dopamine. Her hypoxemia did not resolve as expected, despite relief of the tamponade and therapeutic anticoagulation for the pulmonary embolus over three days. Her PaO₂ on 65% inspired oxygen was 65 mmHg. The hypoxemia appeared out of proportion to the subsegmental pulmonary embolus noted, especially in the absence of pulmonary hypertension. Therefore, a transesophageal echocardiogram was performed to assess for the presence of intracardiac shunt. This revealed bidirectional flow across a patent foramen ovale (PFO) (Figure 4), with right-to-left shunting during systole (associated with severe right ventricular global hypokinesis). Vigorous fluid administration allowed for the discontinuation of intravenous dopamine. Due to ongoing hypoxemia, the PFO was closed percutaneously with an Amplatzer closure device (AGA Medical, USA) (Figure 5). Her hypoxemia resolved, and she was successfully weaned to tracheostomy and eventual discharge from hospital. Follow-up echocardiography one and three months later showed recovery of right ventricular function and no evidence of a shunt or recurrent significant effusion. Cytology of the pericardial fluid revealed adenocarcinoma cells. The patient’s oncologist was asked to re-evaluate her breast cancer in light of these findings. Warfarin therapy for a total of three months was arranged, with outpatient follow-up of international normalized ratio.

Figure 4).

Doppler echocardiography demonstrating right-to-left shunting in systole (left) and left-to-right shunting in diastole (right). LA Left atrium; RA Right atrium

Figure 5).

Deployment of the Amplatzer closure device (AGA Medical, USA) for a patent foramen ovale

DISCUSSION

A PFO can be found in 25% of the general population (1). A PFO functions as a one-way flap, so that, under normal conditions, higher pressures in the left heart prevent significant right-to-left shunting. However, conditions that raise right atrial pressure, such as significant tricuspid or pulmonic valve disease, tetralogy of Fallot, significant atrial and ventricular septal defects, pulmonary hypertension, right ventricular dysfunction, tamponade and positive pressure ventilation can cause right-to-left shunting and hypoxemia. Right-to-left shunting through a PFO or an atrial septal defect has also been described as a cause of hypoxemia in the postcardiac surgery setting.

Hypoxemia from intracardiac shunting following pericardiocentesis has been described (2). Some authors have postulated that the prompt removal of a large amount of pericardial fluid may increase right ventricular tension following re-expansion of the right ventricle (3). This causes global right ventricular dysfunction and elevates right atrial pressure, with consequent shunting through a previously asymptomatic PFO. Right ventricular dysfunction following tamponade is usually self-limited, but patients may be unable to tolerate hypoxemia over the period required for recovery. In our case, the pulmonary embolus may have also contributed to the right ventricular dysfunction, which became more clinically prominent after the pericardiocentesis.

Transthoracic echocardiography with injection of intravenous agitated saline echocontrast and the Valsalva manoeuvre has 63% sensitivity and 100% specificity to detect a shunt (4). Transesophageal echocardiography is the gold standard and can further characterize the degree and nature of shunt, as well as associated lesions.

The treatment course for right-to-left shunting through a PFO or atrial septal defect following the relief of pericardial tamponade remains unclear. Conservative measures include adequate hydration to maintain right-sided cardiac output, afterload reduction and proper oxygenation pending the recovery of right ventricular function. Some authors, however, have advocated early closure of the PFO with percutaneous closure devices to stop shunting and hypoxemia (5). This approach offers excellent closure rates without the associated risk of surgical closure.