Refractory hypoxemia in right ventricular infarction: a case report.

Abstract: Right ventricular infarction has many clinical features. Although hypoxemia is a common presenting symptom with multiple causes in the setting of myocardial infarction, the authors present a case resulting from an acute right-to-left shunt secondary to a previously dormant patent foramen ovale. A 74-year-old male presented to the hospital after feeling unwell for the previous 2 days. Initial evaluation revealed marked hypoxemia without respiratory distress. Electrocardiographic findings and cardiac seromarkers revealed a completed inferior myocardial infarction. The patient's hypoxemia was refractory to 100% oxygen, indicating a right-to-left shunt. A transesophageal echocardiogram confirmed clinical suspicions for a right-to-left shunt through a patent foramen ovale. Despite sporadic reports in the literature, this still is a poorly recognized clinical condition. The authors review a case report that will enable the general internist to consider a right-to-left shunt in the setting of hypoxemia in myocardial infarction.

Key Words: hypoxemia, patent foramen ovale, right ventricular infarction

Introduction

Right ventricular infarction has many unique features on clinical presentation. Hemodynamic consequences include hypotension, bradycardia, supraventricular arrhythmias, and atrioventricular block. (1) Hypoxemia is another serious consequence that may result from acute right-to-left shunting through a previously dormant atrial septal defect or patent foramen ovale. (2) We present a patient with refractory hypoxemia caused by an intracardiac shunt in the setting of an acute right ventricular infarction.

Case Report

A robust 74-year-old male presented to the hospital after feeling unwell for the previous 2 days. He was an avid outdoorsman who had recently returned from his cabin located in the remote wilderness. During vigorous physical exertion, he became acutely diaphoretic, dizzy, and nauseated and fell to the ground, where he had two episodes of emesis and diarrhea. The patient stayed overnight in his cabin and drove 90 miles home the following day. Approximately 48 hours after the pri-mary event, the patient's daughter became concerned about his "dusky" appearance and overall poor physical condition and brought him to the hospital for further evaluation. The patient had no chest pain. On presentation, he was alert and oriented, with stable vital signs. Initial evaluation showed an elderly male with a cyanotic general appearance in no appreciable distress. Physical examination revealed no appreciable cardiac murmurs or ventricular heave and no jugular venous distension. The patient had clear lung fields with no ancillary respiratory muscles in use. Diagnostic studies included a normal chest radiograph, a hematocrit of 39%, and an electrocardiogram with sinus rhythm but prominent Q waves noted in leads II, III, and a VF consistent with a completed inferior myocardial infarction. Initial cardiac enzymes revealed a troponin I level of 51.8 ng/mL. Arterial blood gases obtained at admission while breathing room air showed a pH of 7.49, Pa[O.sub.2] of 45 mm Hg, and PaC[O.sub.2] of 33 mm Hg, with an oxygen saturation of 84%. Supplementation with 100% oxygen by 2.5 cm of continuous positive airway pressure only increased the Pa[O.sub.2] by 7 mm Hg, with an arterial to alveolar gradient of 508. A nuclear viability scan was obtained, revealing a static inferior myocardial defect without evidence of reperfusion. A ventilation/perfusion scan showed low probability for pulmonary embolism. An echocardiogram was obtained and showed a severely dilated right ventricle with depressed right ventricular function. Injection of agitated saline microbubbles revealed a prominent right-to-left interatrial shunt. A transesophageal echocardiogram further identified the defect as a large patent foramen ovale (PFO). The patient slowly improved, with overall good performance status, and was able to be discharged home on supplemental oxygen. He was referred for percutaneous closure of the existing defect. Follow-up arterial blood gases showed a pH of 7.42, PC[O.sub.2] of 39 mm Hg, P[O.sub.2] of 72 mm Hg, with 95% oxygen saturation on room air.

Right ventricular infarction is a commonly recognized complication of inferior myocardial infarction. (3) Its natural history and clinical presentation are distinct and require prompt recognition by the physician for appropriate therapeutic intervention. (1) Hypotension and cardiac arrhythmias are commonly encountered phenomena that may predispose the patient to acute clinical deterioration if not managed distinctly from the standard myocardial infarction paradigm. Arterial hypoxia is a common complication of acute myocardial infarction. Its origins are many and include left ventricular failure with pulmonary congestion, pulmonary embolism, coexisting chronic lung disease, and, less commonly, the development of an intracardiac shunt. (4,5) Hypoxemia in the paradoxical setting of a normal chest radiograph in our patient prompted further investigation for more subtle diagnoses, including pulmonary embolism and the remote possibility of an intracardiac shunt. A low probability V/Q scan suggested pulmonary embolism to be an unlikely culprit in the setting of this patient's persistent hypoxia. Furthermore, the severe hypoxia was not appropriately corrected with 100% supplemental oxygen, which strongly suggested the presence of an intracardiac shunt. (6)

Patent foramen ovale is being increasingly recognized and occurs in 20% of the general adult population. (7) Embryologically, PFO is a remnant of fetal circulation. The primum septum and secundum septum seal within the first 2 years of life, preventing the existence of the interatrial conduit noted in fetal circulation. (8) In the setting of right ventricular infarction, cardiac hemodynamics are often dramatically affected by the presence of a "probe" patent foramen ovale. The hypocontractile right ventricle that results causes an acute increase in right ventricular pressures that are ultimately transmitted to the right atrium. In right ventricular infarction, right atrial pressures may actually increase with inspiration and exceed left atrial pressures. (9) In this context, a previously asymptomatic PFO may create a large interatrial shunt, resulting in systemic hypoxemia refractory to supplemental oxygenation. Another serious consequence of right ventricular (RV) pump failure is severe hypotension as the result of a precipitous drop in left ventricular preload. (10) We believe that the large right-to-left atrial shunt, while causing severe hypoxemia, still maintained left ventricular preload and prevented life-threatening hypotension and cardiogenic shock. The increase in right-sided cardiac pressures in our patient opened the previously dormant PFO and created a spontaneous "atrial septostomy." Kernis et al (10) report a case supporting the salutary effects of percutaneous atrial septostomy for refractory cardiogenic shock caused by RV ischemic dysfunction.

Appropriate treatment of patients with RV infarction and PFO cannot be initiated until a timely diagnosis is made. Therapy is aimed at increasing oxygenation while maintaining hemodynamic parameters. Positive end expiratory pressure has been noted to cause an increase in right-sided cardiac pressures and thus must be avoided in this clinical scenario. (11) High inspired oxygen concentrations have not been demonstrated to be helpful and may result in increased oxygen toxicity. Afterload reduction with agents such as nitrates may also be harmful due to potential decreases in left atrial pressures, which would accentuate the shunt. (11)

Conclusion

Hypoxia caused by RV infarction complicated by a patent foramen ovale is becoming increasingly described in the literature but is still a poorly recognized clinical phenomenon. These patients may rapidly deteriorate without prompt evaluation and recognition. Persistent hypoxemia in the setting of an inferior infarction should prompt early and aggressive pursuit of a right-to-left shunt by way of a "probe" patent foramen ovale.

References

1. Pfisterer M. Right ventricular involvement in myocardial infarction and cardiogenic shock. Lancet 2003;362:392-394.

2. Laham RJ, Kalon KL, Douglas P, et al. Right ventricular infarction complicated by acute right to left shunting. Am J Cardiol 1994;74:824-826.

3. Bansal RC, Marsa RJ, Holland DJ, et al. Severe hypoxemia due to shunting through a patent foramen ovale: A correctable complication of right ventricular infarction. J Am Coll Cardiol 1985;5:188-192.

4. Rietveld AP, Merrman L, Essed C, et al. Right to left shunt, with severe hypoxemia, at the atrial level in a patient with hemodynamically important right ventricular infarction. J Am Coll Cardiol 1983;2:776-779.

5. Fedullo AJ, Swinburne AJ, Mathew TM, et al. Case report: Hypoxemia from right to left shunting through patent foramen ovale. Am J Med Set 1985;289:164-166.

6. Morris A, Dinen N. Hypoxia and intracardiac right to left shunt. Arch Intern Med 1978;138:1405-1406.

7. Mas JL, Arquizan C, Lamy C, et al. for the Patent Foramen Ovale and Atrial Septal Aneurysm Study Group. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm or both. N Engl J Med 2001;345:1740-1745.

8. Kerut EK, Norfleet WT, Plotnick GD, et al. Patent foramen ovale: A review of associated conditions and the impact of physiological size. J Am Coll Cardiol 2001;38:613-621.

9. Cox D, Taylor J, Nand N. Refractory hypoxemia in right to left shunting via a patent foramen ovale: Efficacy of contrast transesophageal echocardiography. Am J Med 1991;91:653-655.

10. Kernis SJ, Goldstein J, Yerkey M, et al. Percutaneous atrial septostomy for urgent palliative treatment of severe refractory cardiogenic shock due to right ventricular infarction. Cathet Cardiovasc Interv 2003;59:44-48.

11. Upstrom EL, Kern MJ, Mezei L, et al. Balloon catheter closure of patent foramen ovale complicating right ventricular infarction: Improvement of hypoxia and intracardiac venous shunting. Am Heart J 1998;116:1092-1096.

Lindsay C. Crawford MD, Mukta Panda MD, and Suresh Enjeti MD

From the Department of Medicine, Pulmonary Division, University of Tennessee College of Medicine-Chattanooga Unit, Chattanooga, TN.

Reprint requests to Dr. Lindsay C. Crawford, UTCOM-CU Department of Medicine, 960 East Third Street, Suite 208, Chattanooga, TN 37403. E-mail: [e-mail]

Accepted August 1, 2005.

RELATED ARTICLE: Key Points

* Patent foramen ovale is a frequently occurring phenomenon, existing in up to 20% of the population.

* Right ventricular infarction is a distinct clinical entity and must be managed separately from the standard myocardial infarction protocol.

* Refractory hypoxemia in the setting of a right ventricular infarction should prompt consideration of a right-to-left shunt.