Introduction

Ventilator care following myocardial infarction often involves the management of multiple potential complications, including cardiogenic shock, pulmonary edema, and persistent hypoxemia [1]. When hypoxemia persists despite resolution of conventional causes, less common etiologies, such as an extracardiac shunt, should be considered [2]. Here, we present a case of uncorrectable hypoxemia in a patient with post-myocardial infarction that was ultimately found to be due to a pulmonary arteriovenous malformation (AVM). This case highlights the importance of considering extracardiac shunts in the differential diagnosis of persistent hypoxemia and demonstrates the critical role of bedside imaging in determining the cause.

Case

Ethics statement: This study was exempted from review by the Institutional Review Board (IRB) of Yeungnam University Hospital (IRB No: YUMC 2024-10-034). Written informed consent was obtained from the patient to participate in the study.

A 78-year-old man presented to the emergency department with severe squeezing chest pain. He had no significant medical history including cardiovascular risk factors. On arrival, he was hypotensive, with a blood pressure of 70/40 mmHg. The initial arterial blood gas analysis (ABGA) revealed an O₂ saturation of 89.6% and partial pressure of oxygen (PaO₂) of 62.8 mmHg. Chest radiography revealed mild pulmonary edema (Fig. 1). Electrocardiography demonstrated junctional rhythm with ST-segment elevation in the inferior leads (Fig. 2). Bedside transthoracic echocardiography (TTE) revealed severe hypokinesis of the left ventricular inferior wall and enlargement of the right atrium and right ventricle.

Emergent coronary angiography revealed complete occlusion of the right coronary artery, which was treated using balloon angioplasty and stent placement. Despite successful revascularization, a no-reflow phenomenon occurred, which led to ventricular fibrillation. Sinus rhythm was restored after appropriate defibrillation; however, cardiogenic shock persisted. The patient required inotropic support and ventilation in the coronary care unit (CCU).

After 2 days of CCU management, the patient's blood pressure normalized, and chest X-ray showed improvement in pulmonary edema. Ventilator weaning was attempted but was unsuccessful due to persistent hypoxemia (PaO₂, 46.1 mmHg; O₂ saturation, 88.6% with 100% fraction of inspired oxygen [FiO₂]), suggesting a right-to-left shunt or another extracardiac cause of the hypoxemia. The patient was further treated for 2 days with ventilator support and intravenous loop diuretics to completely exclude pulmonary edema due to left heart failure. Despite these efforts and additional reductions in pulmonary edema on chest X-ray, the hypoxemia persisted (PaO₂, 51.2 mmHg; O₂ saturation, 88.6% with 80% FiO₂).

Given the persistent hypoxemia despite the resolution of pulmonary edema, a differential diagnosis of intracardiac or extracardiac shunting was considered. Bedside TTE with a saline contrast test was performed to evaluate possible shunting, with appearance in the left atrium after six beats and complete opacification of the left ventricular endocardium after nine beats, consistent with a significant extracardiac shunt (Fig. 3). Subsequent chest computed tomography (CT) confirmed the presence of a large pulmonary AVM in the left lower lobe (Fig. 4). Despite ongoing hypoxemia, FiO₂ gradually decreased, and the patient was successfully weaned from the ventilator without further complications. After ventilator weaning, ABGA showed a PaO₂ of 51.2 mmHg and an O₂ saturation of 89%. The patient did not report dyspnea and maintained a similar O₂ saturation until discharge, suggesting a long-term adaptation to these PaO₂ and O₂ saturation levels.

Discussion

Pulmonary AVMs can lead to significant right-to-left shunting, resulting in refractory hypoxemia that is unresponsive to conventional management [3]. This case underscores the importance of considering extracardiac shunts such as pulmonary AVMs in patients with unexplained hypoxemia, particularly when conventional causes such as pulmonary edema have been excluded. Saline contrast echocardiography serves as a valuable bedside tool for identifying such shunts [4], especially in critically ill patients in whom transportation for CT imaging may be challenging.

While CT remains the gold standard for diagnosing pulmonary AVMs [5], saline contrast echocardiography can provide crucial diagnostic information and guide management decisions in a timely manner. Barzilai et al. [6] proposed a grade of left ventricular opacification on agitated saline contrast echocardiography, which can predict pulmonary AVMs. This grading system includes four grades: grade 1, minimal left ventricular opacity (<20 bubbles); grade 2, moderate opacity; grade 3, extensive opacity without outlining the endocardium; and grade 4, extensive opacity with an endocardial definition. Additionally, a study that simultaneously performed agitated saline contrast echocardiography and thoracic CT found that shunts of grades 2, 3, and 4 were associated with pulmonary AVMs in 25%, 80%, and 100% of cases, respectively [7]. Our patient was classified as grade 4, and such a significant degree of shunting strongly suggested the presence of a pulmonary AVM. Early recognition and appropriate management of pulmonary AVMs are essential to avoid unnecessary prolonged ventilator support and to improve patient outcomes.

This case report highlights the role of bedside imaging in diagnosing the cause of persistent hypoxemia in patients who are critically ill. Pulmonary AVMs should be considered in the differential diagnosis of unexplained hypoxemia. Saline contrast echocardiography can be an effective diagnostic tool to guide appropriate management.

Article information

Conflicts of interest

No potential conflict of interest relevant to this article was reported.

Funding

None.

Author contributions

Conceptualization: KUC, JWS; Writing-original draft: KUC; Writing-review & editing: KUC, JWS.

Fig. 1.

Chest radiography shows mild pulmonary edema. R, right; AP, anteroposterior.

Fig. 2.

Electrocardiography demonstrates a junctional rhythm with ST-segment elevation in the inferior leads (II, III, aVF). aVR, augmented vector right; aVL, augmented vector left; aVF, augmented vector foot.

Fig. 3.

Saline contrast echocardiography demonstrates agitated saline bubbles in the left ventricle, consistent with an extracardiac shunt (observed at zero, three, six, and nine cardiac beats).

Fig. 4.

Contrast-enhanced thoracic computed tomography reveals a 3.5-mm pulmonary arteriovenous malformation in the left lower lobe (arrow).

References

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Figure & Data

References

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