Acute right ventricular failure and pulseless electrical activity arrest following auto-transfusion of blood

Abstract

Air embolism is a rare but potentially catastrophic complication of interventional procedures. The occurrence of acute right ventricular dysfunction during intraoperative auto-transfusion of blood, presumably related to pulmonary embolism of agitated air microbubbles and microthrombi, is less commonly recognized. We report a case of auto-transfusion complicated by acute right ventricular failure and pulseless electrical activity arrest. Auto-transfusion of recovered blood is a practical solution to reduce need for post-procedure allogenic transfusions. Although such interventions are frequently performed without complications, they do have inherent risks that should be readily acknowledged. This case clearly describes a severe complication and sequelae of auto-transfusion.

<Learning objective: Auto-transfusion of recovered blood is commonly performed in surgical and interventional procedures to reduce the need for allogenic transfusion. Despite this benefit, the risks and complications of auto-transfusion can be severe and must be considered. We report a case of intraprocedural auto-transfusion resulting in introduction of air emboli and subsequent cardiac arrest. Additionally, we provide a brief review of air emboli and underlying pathophysiology that leads to cardiovascular decline.>

Introduction

Air embolism is an uncommon but life-threatening event that occurs when air is introduced into the vasculature [1]. Air emboli are most commonly described in the literature as a complication of cardiac surgery involving cardiopulmonary bypass, as well as neurosurgical and otolaryngologic operations [2]. They rarely occur with routine infusion of intravenous fluids and blood products. However, introduction of air emboli has been described during autologous blood transfusion with intraoperative blood salvage devices [3]. We present a case of acute right ventricular failure and pulseless electrical activity arrest, following auto-transfusion of aspirated blood from iatrogenic pericardial effusion.

Case report

The patient was a 78-year-old woman with past medical history of paroxysmal atrial fibrillation, transient ischemic attack (TIA), hypertension, and gastrointestinal bleeds who was admitted to our hospital for placement of Watchman left atrial appendage (LAA) closure device (Atritech, Inc., Minneapolis, MN, USA).

Preprocedure transthoracic echocardiogram (TEE) was performed which provided visualization of single-lobed “chicken-wing” shaped LAA. Femoral central venous access was obtained. Heparin 7000 units was administered and acute clotting time (ACT) was measured at 333 s and 303 s on repeat. Under fluoroscopic and TEE guidance, transseptal puncture was performed, and Watchman device was deployed in the LAA. Contrast extravasation into the pericardial space was noted, which was concerning for LAA laceration (Fig. 1A). Intra-procedure TEE confirmed an expanding pericardial effusion with hypotension (Fig. 1B). The patient received intravenous fluids and vasopressor support. The subxiphoid area was prepared and draped and emergent pericardiocentesis was performed resulting in improvement in blood pressure. Protamine sulfate was administered to reverse heparin anticoagulation, while a total of 1200 mL of blood was eventually aspirated from the pericardial space. As the pericardial space was being drained using 60 cc syringes, simultaneously, approximately 800 mL of aspirated blood were autotransfused via the femoral vein with care to prevent any obvious injection of air. Protamine 50 mg was administered and ACT corrected to 145 s.

Fig. 1.

Fluoroscopic image depicting deployed Watchman device in left atrial appendage (white arrow) with contrast extravasation (black arrow) into pericardial space (A). Intra-procedure transesophageal echocardiographic image of pericardial effusion (white arrow) following Watchman deployment (B).

LV, left ventricle.

Following auto-transfusion of blood, the patient acutely became hemodynamically unstable. TEE showed complete resolution of pericardial effusion but right ventricular enlargement and marked systolic dysfunction with septal flattening were noted, suggestive of right ventricular volume and pressure overload (Fig. 2A). A small underfilled left ventricular chamber due to loss of preload was also seen. The patient continued to decompensate and ultimately PEA arrested despite inotropic and vasopressor support. Cardiopulmonary resuscitation was performed with two minutes of chest compressions. The patient received bicarbonate, calcium gluconate, epinephrine, norepinephrine, and intravenous fluids. Return of spontaneous circulation was achieved and improvement in right ventricular systolic function with return of preload to the left ventricle (Fig. 2B). Based on the temporality of the hemodynamic decompensation, despite the volume resuscitation and evacuation of the pericardial space, immediately following the auto-transfusion of blood, the acute right ventricular failure was thought to be due to introduction of air microemboli, microthrombi, and/or other sediments in hemolyzed blood during reinfusion of aspirated pericardial blood.

Fig. 2.

Transesophageal echocardiographic (TEE) video clip during pulseless electrical activity (PEA) arrest showing right ventricle enlargement, interventricular septal flattening, and reduced left ventricle chamber volume (A). Post recovery TEE video clip with reduced right ventricle chamber volume and improved left ventricle filling (B). Thumbnail images represent diastolic still frames from corresponding video clips, described above. Yellow line within thumbnail images demarcates endocardial border of right and left ventricles, during PEA and post recovery.

LV, left ventricle; RV right ventricle.

Appropriate positioning of the Watchman device was reconfirmed, the device released and the remainder of the access/delivery apparatus removed from the left atrium. Right heart catheterization for hemodynamic evaluation showed right atrial pressure 19/16 mmHg (mean 13), right ventricular pressure 43/10 mmHg (end-diastolic 16), pulmonary capillary wedge pressure 15/16 mmHg (mean 15), and pulmonary artery pressure 43/23 mmHg (mean 29). Pulmonary arteriogram was performed that showed absence of obvious perfusion defects in the pulmonary circulation (Fig. 3). The patient remained hemodynamically stable and was quickly weaned off vasopressor support. She received a total of 3 L crystalloid and 3 units of cross-matched allogeneic packed red blood cells, in addition to the auto-transfused volume. After overnight observation in the intensive care unit, she was extubated the next morning. Colchicine was used to suppress pericarditis, the pericardial drain was removed after 48 h, and warfarin anticoagulation was reinitiated for 45 days. The patient continued to recover and transthoracic echocardiogram 1 week later showed normal biventricular function and no pericardial effusion.

Fig. 3.

Post-procedure pulmonary arteriogram demonstrating the absence of overt perfusion defects.

Discussion

We hypothesize that the patient suffered an acute air embolism with auto-transfusion of blood products. Echocardiographic evidence with volume-overloaded, dilated, and non-contractile right ventricle, and hyperdynamic but underfilled left ventricle suggests an obstructive process within the pulmonary vasculature. Introduction of micro-emboli/thrombi is also suspected given emergent auto-transfusion of recycled blood products immediately preceding the pulseless arrest. Without any specific intervention, there was gradual improvement in right ventricular function and restoration of left ventricular preload with return of spontaneous circulation, consistent with recovery from air embolism.

Air embolism is a rare but often fatal complication of various medical interventions and procedures. Air emboli can be classified into venous and arterial air emboli, the consequences of which differ greatly in severity. Arterial air emboli are typically more catastrophic as they directly enter the arterial system and can obstruct arterial circulation resulting in ischemia and subsequently infarction [1]. Air in the left heart can migrate to the right coronary with ST-elevation myocardial infarction and ventricular fibrillation. Ischemic stroke is widely acknowledged as a debilitating complication of arterial air embolism. Venous air emboli are generally less problematic, as circulating air is reduced to small inconsequential particles on route back to central circulation [2]. The potential consequences of venous air embolism range from transient hypoxemia, hypotension, and right heart strain to right heart failure, cardiac arrest, and death [1]. The extent of complications is based on the volume and rate at which air is introduced [1].

A gas air-lock phenomenon is thought to occur with introduction of large quantities of air and accumulation in the right ventricle preventing effective contraction [1]. Alternatively, small air bubbles lodged in pulmonary arterioles can impede pulmonary microcirculation and cause pulmonary vasoconstriction, leading to increased pulmonary artery and right ventricle pressures [4]. Air-blood interaction within the pulmonary microcirculation also triggers the formation of an air-fibrin matrix that leads to aggregation of platelets, red blood cells, and fat globules [5], [6]. This has been demonstrated in animal air embolism models with postmortem examination revealing fibrin plugs in the terminal branches of pulmonary arteries [5].

The risk of air embolism with transfusion of recovered blood has been considered since the onset of intra- and postoperative auto-transfusions in the 1970s [7]. Initially developed to reduce allogenic blood transfusions during coronary artery bypass surgery, auto-transfusion carries an increased intrinsic risk of air emboli due to the multiple sites of potential air entry with retrieval and reinfusion of scavenged blood [7], [8]. Air introduced into the blood collection and reinfusion circuits can result in air embolism, particularly with pressurizing reinfusion bags for rapid infusion [8], [9]. Although there are individual case reports of air embolism associated with perioperative blood recovery procedures, the true incidence of such events is not known. A large retrospective study conducted by the New York State Department of Health in the USA was initiated to determine the incidence of fatal air emboli with reinfusion of recovered blood products. The frequency of fatal air embolism among over 120,000 perioperative reinfusions over a 5-year period was found to be between 1:30,000–1:38,000 [3]. The rate of air emboli with reinfusion was significantly higher than that of conventional blood product transfusion, which yielded no cases of air emboli with over 8 million transfusions [3]. Thus, the incidence of air emboli with auto-transfusion is low but the morbidity and mortality associated with each event is high.

In a retrospective study of patients who emergently required pericardiocentesis due to complications from electrophysiology procedures, Venkatachalam et al. of the Mayo Clinic determined that autologous blood recovery and reinfusion provided a safe and practical alternative to allogenic transfusion [10]. The risk of air emboli was felt to be minimized in the Mayo study by incorporation of a vacuum to remove air from the cell-salvage reservoir [10]. Cell salvage devices can separate the red blood cells (RBC) by centrifugation from anticoagulated blood, and reinfuse the RBC. Cell processors can remove byproducts such as activated cytokines, activated platelets, clotting factors, other plasma proteins, free hemoglobin and other waste including air. In our case, cell salvage equipment was not used.

The risk of significant pericardial effusion requiring intervention with Watchman device placement is estimated to be between 2% and 4% [11]. In comparison, the prevalence of hemodynamically significant pericardial effusion following permanent pacemaker placement and catheter ablation for atrial fibrillation are both between 0.5% and 2% [12], [13]. The estimated complication risks following Watchman device placement are based on early randomized control trials and rates have decreased significantly with increased operator experience [11].

Caution must be exercised to prevent introduction of air by using a drainage sheath with a competent valve that can be further reinforced to avoid introduction of air in the aspirate. Further, it is imperative to use a closed system with a 3-way stopcock with ability to aspirate and transfuse blood without any unnecessary portal for introduction of air. An autologous blood recovery system to filter and wash the erythrocytes clear of free hemoglobin, serum proteins, and clotting factors with use of vacuum to clear any air from the aspirated blood reservoir prior to transfusion can be utilized. When such a system to wash the RBCs prior to auto-transfusion is not used, blood salvaged after reversal of anticoagulation may contain high concentrations of activated clotting factors, thrombin, fibrin, platelet clumps, and other sediment from hemolysis, and auto-transfusion of such blood should be avoided to prevent circulatory failure.

This case demonstrates the under-recognized risk of acute right ventricular failure with emergent auto-transfusion of recovered blood. Auto-transfusion was used over allogenic transfusion due to the acute onset of hemodynamic instability and need for emergent resuscitation. Pericardiocentesis was simultaneously being performed for tamponade and the reinfusion of aspirated blood was felt to be an efficient alternative to allogenic transfusion. In retrospect, appropriate cell saver and bubble filtration systems should have been implemented as well. Despite the published utility and efficacy of auto-transfusion, direct auto-transfusion and cell salvage and reinfusion systems provide a potential mechanism for air to be introduced into the vasculature. As previously discussed, large volumes of air can severely compromise cardiovascular function and precipitate cardiac arrest. Likewise, small emboli of air bubbles, fibrin, and other sediments in salvaged blood entering the pulmonary microcirculation can facilitate formation of microthrombi resulting in obstructed circulation and arrest. We hypothesize that our patient’s acute clinical decline was due to cardiovascular sequelae from microemboli in the auto-transfused blood including agitated air microbubbles. This case is novel in its depiction of cardiac arrest from auto-transfusion of recovered blood. Furthermore, it exposes a need for preventative measures to minimize the risk of air and thromboemboli with intra-procedure auto-transfusion of recovered blood.

Conflict of interest

The authors declare that there is no conflict of interest.

Appendix A. Supplementary data

The following is Supplementary data to this article: