Cardiac Tamponade Causing Predominant Left Atrial and Ventricular Compression After Left Ventricular Assist Device Placement

Background

Cardiac tamponade is a life-threatening condition that occurs when pericardial fluid accumulates in the pericardial sac, causing compression of the heart, which leads to a decrease in cardiac output and obstructive shock [1]. Malignancy, pericarditis, and iatrogenic causes (post-surgery and cardiovascular invasive procedures) are the most common etiologies of cardiac tamponade [2]. Pericardial effusion can occur following open-heart surgery due to the increased risk of intrapericardial inflammation and bleeding [3]. Patients undergoing left ventricular assist device (LVAD) placement are at particularly high risk of pericardial bleeding and cardiac tamponade because of the need for postoperative anticoagulation agents [3]. Cardiac tamponade typically affects right-sided cardiac chambers because of the lower pressures of the right atrium and right ventricle [4]. Cardiac tamponade of the left-sided cardiac chambers is rare and typically only seen in situations such as those in patients with severe pulmonary arterial hypertension (PAH) or loculated posterior pericardial effusion [4]. This case report describes a patient who developed left-sided cardiac tamponade after LVAD placement and his subsequent hospital course.

Case Report

A 47-year-old man with a past medical history of non-ischemic dilated cardiomyopathy requiring automatic implantable cardioverter defibrillator placement, hypertension, hyperlipidemia, atrial fibrillation, chronic kidney disease stage III, and hypothyroidism presented to an outside hospital with 2 weeks of worsening lower-extremity edema, dyspnea on exertion, and paroxysmal nocturnal dyspnea. The patient reported an unintentional 3.6-kg weight gain during this time despite taking extra doses of his prescribed furosemide. His initial blood pressure was 83/61 mmHg, troponin level was 0.03 ng/mL, B-type natriuretic peptide (BNP) was 2037 pg/mL, and creatinine was 4.28 mg/dL. He was negative for COVID-19 and his chest radiograph was within normal limits. Initially, a norepinephrine infusion was started and a total of 3 L of intravenous fluids and colloids were given during the outside hospital stay in an attempt to optimize volume status. Urine output remained low at approximately 10 mL/h; therefore, diuresis was initiated with a furosemide infusion. Transthoracic echocardiography (TTE) revealed a severely dilated left ventricle with severely depressed left ventricular function with estimated ejection fraction of 20%. A diagnosis of cardiogenic shock was made and dobutamine and vasopressin infusions were added to his medication regimen. A temporary dialysis catheter was placed on hospital day 6 to initiate continuous renal replacement therapy (CRRT). Improvements in his urine output and creatinine were noted; however, due to continued hypotension requiring inotropic and vasopressor support, he was transferred to our hospital for evaluation for LVAD and/ or heart transplantation.

On presentation to our facility, the patient’s blood pressure was 104/62 mmHg and he had a troponin level of 60 ng/mL, BNP of 3294 pg/mL, and creatinine of 2.81 mg/dL. He was weaned off of all vasoactive infusions upon admission, although the furosemide infusion was continued. TTE revealed a severely dilated left ventricle with global hypokinesis and ejection fraction of 20%, as well as a mildly dilated and depressed right ventricle with severe tricuspid regurgitation. Right heart catheterization revealed biventricular failure and a high mean right atrial pressure (23 mmHg) along with a low pulmonary artery pulsatility index (0.4). He was evaluated by an interdisciplinary team for LVAD Heartmate 3TM placement and was deemed to be a surgical candidate. He underwent successful LVAD placement several days later with no intraoperative complications and without need for additional mechanical right ventricular support. He was transferred to the intensive care unit (ICU) in stable condition on inhaled nitric oxide and intravenous epinephrine, vasopressin, and norepinephrine infusions with the LVAD speed at 5400 revolutions per minute (rpm) and flow at 4 L per minute (lpm).

The patient was extubated on postoperative day 1. Inotropic and vasopressor modifications were made based on evaluation of point-of-care cardiac ultrasound, pulmonary artery catheter assessment, LVAD settings, and hemodynamic evaluation. He was started on a milrinone infusion in the setting of moderate right ventricular dysfunction; the epinephrine infusion was maintained while norepinephrine and vasopressin infusions were weaned. On postoperative day 2, TTE illustrated dilated right and left ventricles with a midline interventricular septum. The LVAD flow was increased to 6000 rpm, but this caused significant bowing of the septum toward the left ventricle; therefore, the speed was decreased to 5800 rpm. Low-dose dobutamine eventually replaced epinephrine, as is standard practice at our institution. A heparin infusion was started on postoperative day 2, and a transition to warfarin was commenced on postoperative day 4. He remained hemodynamically stable and all inotropic and vasopressor infusions except low-dose dobutamine were stopped on postoperative day 5.

On postoperative day 6, He developed shortness of breath and lower back pain. He was tachycardic and hypotensive by Doppler-derived blood pressure assessment, with mean arterial pressure gradually declining to 50 mmHg, requiring reinitiation of the dobutamine infusion and then a low-dose epinephrine infusion, as well as inhaled nitric oxide. The patient’s central venous pressure was elevated at 21 mmHg, his mixed venous oxygen saturation was 41%, cardiac output using the Fick equation was 2.0 l pm, and systemic vascular resistance was 996 mmHg•min•mL–1. His LVAD flow had decreased to 2.7 l pm, pulsatility index had increased from 2 to 8, and speed and power remain unchanged. Point-of-care cardiac ultrasound showed a questionable pericardial effusion; however, the study was limited as it was difficult to visualize the cardiac structures and function in the setting of the patient’s body habitus and the LVAD. With initial concern for potential right ventricular failure in the setting of interventricular septum interdependence, the LVAD flow was decreased to 5600 rpm. Cardiac surgery was updated. Given the limited point-of-care ultrasound findings and the patient’s perceived relative hemodynamic stability, urgent computed tomography was ordered and revealed a moderate-to-large, dense pericardial effusion. The decision was made to perform emergent chest exploration and assessment of LVAD function.

The patient was alert and oriented, communicating appropriately, and lying supine on initial evaluation by the anesthesiologist. Intraoperatively, an arterial line was placed before induction and standard monitors were used. A judicious approach to general endotracheal anesthesia was instituted using ketamine and fentanyl, and then etomidate and rocuronium. The patient was placed in Trendelenburg positioning immediately after induction due to a decrease in mean arterial pressure. Transesophageal echocardiography (TEE) revealed near-complete collapse of the left atrium and left ventricle, with preservation of the right-heart chamber sizes in the setting of a large heterogeneous posterior pericardial effusion. There was no evidence of right atrial systolic free wall or right ventricular diastolic free wall collapse (Figures 1, 2). No significant deterioration in right ventricular function was noted, and the interventricular septum was undiscernible given the small left ventricular cavity size. The median sternotomy was reopened expeditiously, and posterior hemopericardium and thrombi were evident; therefore, a mediastinal washout was performed. Clinical findings were consistent with obstructive shock, and successful evacuation led to de-escalation of hemodynamic support. A specific source of bleeding was not discovered, and no active bleeding was seen. Postoperative TEE revealed an estimated left ventricular ejection fraction of 20–25% in the setting of the LVAD with interval resolution of the pericardial effusion and moderately depressed right ventricular function. The LVAD was programmed to a speed of 5200 rpm with a flow of 3.9 lpm, and the interventricular septum was noted to be midline. He was transferred to the ICU and remained hemodynamically stable for the next several days. He was discharged home postoperatively on day 13 with appropriate medications and follow-up.

Discussion

The decision to intervene surgically in this patient permitted evacuation of the hemopericardium and thrombi, as well as an opportunity to assess LVAD function using TEE under general anesthesia. Initially the differential diagnosis of this patient’s change in clinical status included pericardial effusion with developing cardiac tamponade, deterioration in right ventricular function, hypovolemia, pump thrombosis, or a combination of these etiologies. TEE was invaluable in further deciphering the exact etiology of the clinical picture.

Cardiac tamponade is a medical emergency due to the accumulation of blood, pus, other fluid, or gas within the pericardial space. As fluid accumulates, intrapericardial pressure increases, leading to compression of all cardiac chambers and subsequent equalization of diastolic pressures. This results in decreased venous return, cardiac filling, and cardiac output [5]. The rate of fluid accumulation relative to pericardial stretch is the key factor in determining the severity and speed of onset of cardiac tamponade with classic clinical signs described as Beck’s triad: hypotension, jugular venous distention, and muffled heart sounds [6]. Other clinical signs include dyspnea, hypoxia, pulsus paradoxus, tachycardia, electrical alternans on an electrocardiogram, and an enlarged cardiac silhouette on chest radiography [5].

Prompt diagnosis is critical in mitigating the mortality risk of patients with cardiac tamponade [6]. Although the diagnosis of cardiac tamponade is largely clinical, clinicians may consider chest radiography or computed tomography, electrocardiography, and especially point-of-care ultrasound or echo-cardiography to support or confirm the diagnosis, but only if time permits based on the acuity of the clinical presentation. TEE can be particularly useful when TTE is non-diagnostic and in post-cardiac surgery patients suspected of having localized effusions containing clots [6]. Treatment typically involves either emergent drainage via needle paracentesis or open surgical drainage, especially when a clot is evident [6]. Studies have shown that in general there is no significant difference in overall mortality between percutaneous pericardiocentesis and open surgical drainage for evacuating symptomatic pericardial effusions and cardiac tamponade [7]. The decision to proceed with one of these interventions is strictly based on the clinical setting. In this setting, pericardiocentesis would have likely proven inadequate given the posterior location and composition of the effusion. Video-assisted thoracoscopic surgery has also been shown to be efficacious in treating large pericardial effusions and cardiac tamponade [8]. However, further studies are required to evaluate the benefit in patients with posterior loculated pericardial effusions.

Cardiac tamponade is a potentially dangerous complication after implantation of LVADs [9]. Patients with LVADs are at increased risk of bleeding due to the risk of von Willebrand syndrome, platelet dysfunction, angiodysplasia, and arteriovenous malformation [10]. LVADs also pose a significant risk of pump thrombosis; therefore, patients require aggressive anticoagulation, further increasing bleeding risk. Studies report that 40% of patients with ventricular assist devices experienced early postoperative bleeding and 20% developed tamponade requiring surgical intervention [11]. Thus, early recognition and management in suspected patients is essential. The patient described in this report had multiple risk factors for developing cardiac tamponade, including recent LVAD surgery and initiation of heparin and warfarin therapies.

Isolated left-sided cardiac tamponade is a rare finding given the increased wall thickness and higher pressures of the left-sided chambers compared to the right [12]. Thus, cardiac tamponade usually affects the right side of the heart given its low chamber pressures and comparably thinner walls. However, after LVAD implantation and without significant valvular heart disease, there is an associated decrease in left atrial pressure, end-diastolic left ventricular pressure, and left ventricular diameter [13]. Most cases of isolated left-sided cardiac tamponade involve patients with severe pulmonary hypertension or posterior loculated effusions after cardiac surgery [14]. Common symptoms associated with cardiac tamponade may be masked in patients with LVADs [15]. Thus, high clinical suspicion of cardiac tamponade is warranted, not only if right atrial pressure quickly increases, but also if a LVAD pump flow decreases [15]. Studies have demonstrated that although right-sided cardiac compression tends to have more pronounced acute hemodynamic effects than left-sided cardiac compression, left-sided cardiac tamponade can also lead to significant hemo-dynamic instability [16]. While cases of cardiac tamponade in patients with recent LVAD placement exist, cases in the literature of isolated left-sided collapse in this patient population are scarce, but possible. Thus, it is imperative to be cognizant of a more indolent presentation of cardiac tamponade in patients with LVADs, especially when left-sided heart chambers are primarily involved.

Conclusions

This case presentation illustrates how a change in clinical status several days after LVAD implantation presents a clinical conundrum best deciphered through multiple data points, with TEE being an important resource in differentiating etiologies. Cardiac tamponade can have various presentations, and typically involves the right-sided cardiac chambers. However, the left atrium and left ventricle can also be affected. Isolated left-sided cardiac tamponade is rare but can occur in the setting of a posterior loculated pericardial effusion. Patients with recent cardiac surgery, especially LVAD placement, who start to show evidence of hemodynamic deterioration, require swift comprehensive evaluation and early management.