Harbinger of Difficult Weaning from Cardiopulmonary Bypass in Aortic Valve Replacement Surgery: A Case Report

ABSTRACT

Failure to wean from cardiopulmonary bypass (CPB) is a rare but critical intraoperative challenge. Common causes include residual structural defects (causing intracardiac shunting, prosthetic valve leaks), left ventricle outflow tract obstruction, ventricular dysfunction, or vasoplegic syndrome. We present the case of a 56-year-old man with severe aortic stenosis who underwent surgical aortic valve replacement. Separation from CPB failed repeatedly due to acute right ventricular dysfunction detected on transesophageal echo. The patient was found to have a congenital anomalous high origin of the right coronary artery (RCA), likely compromised during surgery. Timely recognition and surgical revascularization of the RCA with a saphenous vein graft restored right ventricular function and facilitated successful weaning. This case highlights the importance of intraoperative echocardiography, awareness of anomalous coronary anatomy, and prompt multidisciplinary decision-making in managing difficult separation from CPB.

INTRODUCTION

Weaning from cardiopulmonary bypass (CPB) involves gradually transferring circulatory and respiratory support from the extracorporeal circuit to the patient’s heart and lungs. Successful weaning requires coordinated efforts among the surgeon, anesthesiologist, and perfusionist, supported by hemodynamic monitoring and transesophageal echo (TEE). Difficult separation occurs when high-dose inotropes or vasopressors are needed to maintain perfusion due to structural defects or ventricular dysfunction. We report a 56-year-old man with a high-origin right coronary artery undergoing aortic valve replacement who developed acute right ventricular failure during CPB separation, highlighting the importance of prompt intervention after diagnosis.

CASE REPORT

A 56-year-old hypertensive male presented with 2 months of exertional dyspnea (New York Heart association class II). He denied chest pain, palpitations, syncope, or orthopnea. Examination revealed a displaced apical impulse located 2 cm lateral to the midclavicular line and an ejection systolic murmur at the aortic area radiating to both carotids. Routine investigations were normal, and electrocardiogram showed sinus rhythm.

Transthoracic echocardiography demonstrated a bicuspid aortic valve with severe stenosis (mean gradient 62 mmHg, valve area 0.5 cm²), marked left ventricular (LV) hypertrophy (posterior wall thickness 14 mm), and preserved biventricular systolic function. Coronary angiography revealed normal epicardial coronaries with anomalous high origin of right coronary artery (RCA) [Figure 1a and b]. The patient was scheduled for surgical aortic valve replacement (AVR).

Figure 1.

(a) Coronary a ngiogram showing RCA with high anomalous origin. (b) Coronary angiogram showing normal RCA (for comparison)

Anesthesia induction was uneventful. Intraoperative TEE confirmed preoperative findings [Video 1].

Following midline sternotomy and aortic and venous cannulation, the aorta was cross-clamped and antegrade Delnido root cardioplegia (1.4 L) delivered. Topical cooling was used. The heart arrested well. After excision of diseased valve via transverse aortotomy, a 23 mm St Jude Regent bileafelet mechanical prosthesis was implanted. The patient was rewarmed to 36.0°C, and aortotomy closed. Adrenaline (0.05 → 0.1 mcg/kg/min) was initiated for bradycardia, followed by pacing at 90 bpm (VOO). The prosthetic valve function was confirmed. After deairing, sinus rhythm returned heart rate (HR) 80–85 bpm, with VVI at 65 bpm.

During weaning from CPB, blood pressure (BP) remained around 70/50 mmHg, CVP 15 cmH2O, and HR 80 bpm. Adrenaline increased to 0.15 mcg/kg/min. Differentials included (cardiogenic shock vs vasoplegia) were air in the coronaries, prosthetic dysfunction causing LV dysfunction, RV dysfunction due to coronary compromise, inadequate myocardial protection, and vasoplegia. TEE revealed acute RV dysfunction. Mid esophageal (ME) four chamber RV focused view and ME inflow–outflow view revealed hypokinesia of RV mid and basal free wall with bulging of interatrial septum (IAS) into the left atrium with each contraction suggesting elevated right atrial pressure [Video 2]. The LV contractility was good as seen in transgastric mid papillary view. This was immediately communicated to the surgical team.

Milrinone (0.375 → 0.5 mcg/kg/min) was started, but separation from CPB remained unsuccessful. Given the anomalous RCA origin and RV dysfunction, iatrogenic compromise was suspected. The decision was made to perform coronary artery bypass grafting (CABG) to RCA using saphenous vein graft. A second dose of Delnido root cardioplegia (1 L) was given. Heart was arrested. Reinfusion of root cardioplegia confirmed the absence of flow through opened RCA, thus establishing diagnosis of RCA occlusion. The temperature was allowed to drift to 35.3°C. Following grafting, the contractility recovered within minutes of cross clamp removal (HR 80–90 bpm), permitting smooth CPB separation on low-dose adrenaline (0.05 mcg/kg/min) [Video 3]. The total bypass duration was 4 hours, 19 minutes; the cross clamp times were 78 minutes for AVR and 13 minutes for CABG.

Post grafting, RV function normalized and extubated 2 hours later in ICU. The patient remained hemodynamically stable, with no LCOS. The patient was transferred to the high dependency unit (HDU) on POD 2 and discharged on POD 4 to ward. RV function was monitored in the ICU, and HDU was normal. Follow-up echocardiography at 1 month demonstrated mildly reduced RV function, with a tricuspid annular plane systolic excursion (TAPSE) of 14 mm, with good clinical recovery.

DISCUSSION

The goal of weaning is to transfer the CPB’s pumping action to the patient’s heart smoothly while maintaining hemodynamics. Successful weaning requires close coordination among anesthesiologists, surgeons, and perfusionists with rapid decision making regarding surgical corrections and inotropic support.[1] The use of standardized checklists before separation from CPB is a Class I recommendation to enhance team performance and patient safety.[2]

Difficult CPB separation, defined by increasing inotrope requirements or failure to wean despite adequate support, occurs in up to 45% of cardiac surgeries.[1] Common causes include surgical failure, ventricular dysfunction, LVOT obstruction, and vasoplegia. TEE is crucial in identifying the underlying cause. When TEE demonstrates good contractility without LVOT obstruction, vasoplegia should be suspected and treated with vasopressors such as norepinephrine, phenylephrine, or vasopressin. Conversely, poor ventricular contractility with adequate preload causing low cardiac output syndrome (LCOS) may benefit from inotropes such as adrenaline, Dobutamine, or non-catecholamine agents like Milrinone or Levosimendan. Nonpharmacological strategies include biventricular or atrio-ventricular pacing; refractory ventricular failure may require mechanical ventricular support including intra-aortic balloon pump, ventricular assist devices, or extracorporeal membrane oxygenation (ECMO).

Anomalous aortic origin of coronary artery (AAOCA) is an uncommon congenital variant, with an incidence of 1–5% and 0.28–1.3% in angiographic and autopsy series.[3,4,5,6] Most anomalies are asymptomatic but can present with chest pain, dyspnea, or syncope and are associated with myocardial ischemia or sudden cardiac death, particularly in young individuals.[5,6] There are multiple classification systems based on anatomy and function.[7] Anomalous high take-off RCA is particularly rare (0.04–0.15% of all reported coronary abnormalities) yet clinically significant.[6] The second most common cause for sudden cardiac death in young adults is AAOCA.[8] A known association exists between bicuspid aortic valve and AAOCA, more often involving left coronary artery. Postmortem studies suggest that both share a common embryological origin, explaining their coexistence.[9]

Most published cases of anomalous origin of RCA occur during AVR and describe the artery arising from or near the left sinus of Valsalva (SoV).[6,10,11,12,13] These patients frequently developed post-op myocardial infarction due to compression of the anomalous artery requiring PCI or CABG. Intraoperative RV dysfunction necessitating urgent CABG has also been reported.

In our case, RCA originated from the ascending aorta, traversed an intramural course, and appeared externally from the Right SoV, an extremely rare variant. The origin was likely just below the aortotomy (approximately 2.5 cm from the take-off of RCA from right aortic sinus) with an intramural course and was compromised during either clamping or aortotomy. RCA compromise was confirmed intraoperatively when cardioplegia infusion failed to produce flow. Preoperative CT angiogram which could have delineated the course was not performed.

Only one other article by Tarhan et al.[14] describes a similar RCA anomaly, originating 5 cm above right SoV with an intramural course, successfully managed by prompt CABG causing no problems while weaning from CPB.

Patients with unrecognized AAOCA are at risk aortic of coronary compromise during aortotomy manipulation. Recommended surgical options include direct implantation of coronary artery, unroofing, or CABG.[15] When performing a transverse aortotomy, particular care is essential to avoid injuring anomalous coronaries. Preoperative 3D multidetector CT angiography (MDCTA) and intraoperative imaging can aid surgical planning.[10] Hybrid operating rooms have been used to confirm coronary patency intraoperatively in patients undergoing AVR with coronary anomalies.[10,13]

This case underscores the need for vigilance in AAOCA, where unexplained RV dysfunction should raise suspicion of RCA compromise.

For anesthesiologists, difficulty in CPB separation, persistent hypotension, acute RV dysfunction, and escalating inotropic needs should prompt evaluation for coronary injury. TEE remains indispensable for real-time assessment of ventricular function, prosthetic valve integrity, and ischemia detection. Rising CVP, direct visualization of distending RV, and poor RV contractility confirm the diagnosis. Prompt reinstitution of CPB and revascularization, guided by effective communication between teams, can be life-saving.

Take home points

• Difficult CPB weaning warrants immediate evaluation for structural or ischemic causes.

• Preoperative coronary angiography and CT imaging help define coronary anatomy before surgery.

• Intraoperative TEE is vital for assessing ventricular function, prosthetic valve performance, and ischemia.

• Timely surgical revascularization can reverse ischemic RV dysfunction.

• Close coordination among anesthesiologists, surgeons, and perfusionists is crucial for successful CPB separation.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.