Asian Cardiovasc Thorac Ann 1999;7:287-291
© 1999 Asia Publishing EXchange Pte Ltd
Intracardiac Right-to-Left Shunt Complicating Right Ventricular Failure
Hasanat Sharif, MD,
A Thomas Pezzella, MD,
Husam H Farah, MD,1,
Raj Baljepally, MD,1,
Dennis Maki, MD,1
Division of Cardiac Surgery
1 Division of Cardiology
St. Vincent Hospital
Worcester, Massachusetts, USA
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For reprint information contact: A Thomas Pezzella, MD Tel: 1 508 798 6318 Fax: 1 508 798 1621 email: thomas.pezzella{at}banyan.ummed.edu Division of Cardiac Surgery, St. Vincent Hospital, 25 Winthrop Street, Worcester, MA 01604, USA.
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Abstract
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Three cases of intracardiac right-to-left shunt at the atrial level complicating right ventricular failure (RV) are described. Severe hypoxemia resulted in 2 patients and stroke in the third. This was a consequence of right ventricular infarction causing right-sided heart failure resulting in high right-sided pressures. Echocardiography demonstrated the shunts. A review of the literature on this uncommon problem suggested management strategies based on the limited experience with this condition.
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Introduction
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Right ventricular (RV) failure is a well-recognized complication of inferoposterior myocardial infarction (MI). A rare presentation of this condition is hypoxemia refractory to adequate ventilation, indicating a ventilation-perfusion mismatch. In such instances, the possibilities of an extracardiac or intracardiac right-to-left shunt should be entertained. The intracardiac shunt can occur at the atrial level through a patent foramen ovale. This results from right atrial (RA) pressure exceeding left atrial (LA) pressure as a consequence of RV failure. Subsequent hypoxemia or paradoxical embolus can occur.
Case 1
A 74-year-old woman with a history of coronary artery disease presented with unstable angina. She was found at cardiac catheterization to have 80% ostial stenosis of the left main coronary artery, 80% stenosis of the right coronary artery, and total occlusion of the circumflex artery. Her left ventricular ejection fraction was 60%. RA pressure was 4 mm Hg, RV pressure 25/2 mm Hg, pulmonary artery pressure 22/8 mm Hg, and pulmonary capillary wedge pressure was 9 mm Hg. Oxygen saturation (SaO2) was 69% in the right atrium and 67% in the pulmonary artery. Catheterization was complicated by the onset of new left bundle branch block for which a temporary transvenous pacemaker was inserted. An intraaortic balloon was inserted because of hemodynamic instability. The following day, coronary artery bypass graft surgery was performed on the left anterior descending (LAD), right coronary artery, and obtuse marginal branch of the circumflex artery. She developed right-sided pneumothorax on the first postoperative day, for which chest tube thoracostomy was performed. There was new ST-segment elevation on her electrocardiogram and raised plasma creatine kinase levels. However, she improved hemodynamically and the intraaortic balloon was subsequently removed.
On the 3rd postoperative day while still intubated, she became cyanotic and progressively hypoxic and desaturated in spite of adequate ventilation. Her positive end-expiratory pressure was increased to 7.5 cm H2O and inhaled oxygen was increased to 100%. However, her arterial blood gas analysis revealed pH 7.44, PCO2 38 mm Hg, PO2 29 mm Hg, HCO3 30 meq•L–1, and SaO2 60%. Chest radiography was unrevealing and a ventilation-perfusion scan gave a low probability of pulmonary embolus. A transthoracic echocardiogram showed preserved LV function, a dilated right atrium, hypokinesia of the inferoposterior wall, and moderate tricuspid regurgitation. A contrast echocardiographic study using micro air bubbles showed a right-to-left shunt. Trans-esophageal echocardiography revealed severe tricuspid regurgitation with a jet of regurgitant blood across a patent foramen ovale to the left atrium (Figure 1
). Discontinuation of positive end-expiratory pressure im-proved her oxygenation, resulting in pH 7.5, PCO2 35 mm Hg, PO2 59 mmHg, HCO3 28 meq•L–1, and SaO2 of 93% on a fraction of inspired oxygen (FiO2) of 1. She continued to improve and after a few hours, the FiO2 was successfully reduced to 0.6 with SaO2 of 93%. She was extubated on the 5th postoperative day and discharged 5 days later with room-air SaO2 of 92% and an unremarkable chest radiograph. An echocardiogram performed 9 months postoperatively demonstrated good RV contractile function and both color-flow Doppler and a bubble study with agitated saline showed no evidence of shunting across the patent foramen ovale.
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Figure 1. Transesophageal echocardiogram showing a severe tricuspid regurgitant jet (TR) through a patent foramen ovale (PFO) in case 1. LA = left atrium, RA = right atrium, RV = right ventricle.
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Case 2
A 61-year-old man with known coronary artery disease presented with dyspnea on exertion. An exercise tolerance test was stopped early due to hypotension. The patient stabilized with no electrocardiographic changes. He had a history of hypertension, hyperlipidemia, previous angioplasty of the LAD, and uncomplicated inferior wall MI. A left ventriculogram showed anterior apical hypokinesis and inferior wall dyskinesis with an overall left ventricular ejection fraction of 30%. His right atrial pressure was 7 mm Hg, RV pressure 28/7 mm Hg, pulmonary artery pressure 29/10 mm Hg, and pulmonary capillary wedge pressure 10 mm Hg. SaO2 was 58% in the right atrium and 59% in the pulmonary artery. He underwent bypass grafting to the posterior descending artery, obtuse marginals 1 and 2, ramus intermedius, and LAD. An intraaortic balloon pump was placed post-operatively because of failure to wean from cardio-pulmonary bypass.
He was explored on the night of surgery for bleeding from a left internal mammary artery branch. A second exploration revealed diffuse mediastinal oozing. A left mediastinal hematoma and the left hemothorax were evacuated. The chest was left open and coagulopathy was treated with blood-component therapy. Postoperative electrocardiography showed deepened Q waves and creatine kinase levels were raised. He became pro-gressively hypoxic with arterial blood pH 7.49, PO2 41 mm Hg, PCO2 40 mm Hg, HCO3 24 meq•L–1, and SaO2 77% on FiO2 of 1. He had a blood pressure of 108/89 mm Hg, sinus tachycardia at 114 beats•min–1, central venous pressure 23 mm Hg, pulmonary artery pressure 38/28 mm Hg, and pulmonary capillary wedge pressure l0 mm Hg. It was thought that the patient had fluid overload resulting in high filling pressures and impaired oxygenation. Hemo-filtration was performed and 4 L of fluid were removed. However, there was no improvement in oxygenation. The chest radiograph was normal. At this stage, a right-to-left shunt was suspected. Transesophageal echocardiography showed significant tricuspid regurgitation, enlarged right atrium and ventricle, with a dyskinetic infero-apical wall. The interatrial septum bulged towards the left atrium and a patent foramen ovale was visualized with a right-to-left shunt. His left ventricular ejection fraction was 40% with mild mitral regurgitation. Despite aggressive resuscitative attempts, he expired the following day. Autopsy permission was denied.
Case 3
A 70-year-old woman with a history of hypercholes-terolemia, hypothyroidism, and diet-controlled diabetes mellitus presented with chest pain, diaphoresis, shortness of breath, and light-headedness. An electrocardiogram showed ST depression and plasma creatine kinase was elevated. Cardiac catheterization revealed 99% stenosis of a dominant right coronary artery, 95% stenosis of the LAD, and an occluded circumflex artery. Left ventricu-lography showed an ejection fraction of 45%, inferior wall hypokinesis, and grade 1+ to 2+ mitral regurgitation. Her RA pressure was 15 mm Hg, RV pressure 45/12 mm Hg, pulmonary artery pressure 45/19 mm Hg, and pulmonary capillary wedge pressure 29 mm Hg. SaO2 was 60% in the right atrium and 64% in the pulmonary artery. An intraaortic balloon pump was inserted for hemodynamic instability.
The following day, the patient underwent bypass grafting to the LAD, obtuse marginal, and distal right coronary arteries. There was a visible lateral left ventricular transmural MI and the right heart was noted to be full at the time of surgery. Prior to cardiopulmonary bypass, central venous pressure was 18 mm Hg and pulmonary artery pressure was 46/30 mm Hg. Following the operation, central venous pressure was 18 mm Hg and pulmonary artery pressure was 34/23 mm Hg. The patient did well and was extubated on the day after surgery. After weaning from the balloon pump, her central venous pressure was 4 mm Hg and pulmonary artery pressure was 28/15 mm Hg. Blood pH was 7.41, PCO2 37 mm Hg, PO2 107 mm Hg, HCO3 24 meq•L–1, and SaO2 98% on 6 L of inspired nasal oxygen. Postoperatively, the creatine kinase level was elevated but returned to baseline by the 2nd day. Electrocardiographic changes had resolved completely by the time of her discharge on the 7th postoperative day.
Sixteen days after discharge she was readmitted with a dense right-sided hemiplegia. An emergency computed tomography scan of the brain revealed no abnormality but a follow-up scan next day showed extensive infarction involving the left basal ganglia and the left temporoparietal regions. There were ST elevations on the electrocardio-gram, the creatine kinase level was raised, and SaO2 was 96%. She also had a swollen right leg and duplex scanning revealed extensive popliteal and iliofemoral thromboses. A transthoracic echocardiogram showed RA and RV dilation. There was a serpiginous thrombus in the right ventricle seen traversing a patent foramen ovale and continuous with a thrombus in the left atrium. There was reduced right and left ventricular systolic function with posterior wall hypokinesis. In view of the dense stroke and the patient's mental obtundation, her family opted for conservative management. Therefore, she was treated with anticoagulants only and transferred to a rehabilitation facility.
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Discussion
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Right ventricular infarction occurs in 24% of cases of transmural posteroinferior MI.1 This can result in RV failure, high RV and RA pressures, and varying degrees of tricuspid regurgitation. A patent foramen ovale was found in 27% of normal hearts in one postmortem study.2 However, a right-to-left intracardiac shunt through a patent foramen ovale does not occur until the RA pressure exceeds the pressure in the LA. These altered hemodynamics can be seen in RV failure secondary to RV infarction. The addition of positive end-expiratory pressure may worsen the shunt by increasing the end-expiratory lung volumes, thereby increasing pulmonary vascular resistance.3,4 This causes pulmonary hypertension, increased RV systolic pressure and consequently raised RA pressure.
An intracardiac right-to-left shunt manifests as hypoxemia refractory to conventional treatment or paradoxical embolism, as in our third case. Consideration should therefore be given to this condition in such a clinical setting. Other causes of hypoxemia include pulmonary embolism, adult respiratory distress syndrome, severe chronic obstructive pulmonary disease, tension pneumo-thorax, and cardiac tamponade. Hypoxemia may occur after pneumonectomy due to higher right-sided filling pressures and modification of the anatomic relationship between the inferior vena cava and the atrial septum and also following coronary bypass surgery. Diagnosis is based on electrocardiography and cardiac enzymes to rule out new or extending MI and chest radiography to exclude pneumothorax. A ventilation-perfusion scan may suggest the possibility of pulmonary embolism. Transesophageal echocardiography may reveal new regional wall-motion abnormalities and can also document a shunt with a bubble study.
Treatment of right-to-left shunt through a patent foramen ovale should be aimed at reducing the shunt fraction. This can be achieved by reducing RA pressure or increasing LA pressure. Positive end-expiratory pressure has an adverse effect by increasing RA pressure and should be discontinued. Inotropic agents are used to support RV systolic function.5 The importance of this cannot be stressed enough as improvement of RV function is the final determinant of a successful outcome. Other treatment modalities are still controversial. The use of nitrates to reduce RA pressure by venodilation has been advocated.6 It has also been suggested that nitrates can be used as a bedside diagnostic test in right-to-left shunt, showing an immediate increase in systemic oxygen saturation.5 However, despite encouraging results, the clinical use of nitrates has limited acceptance.6 Arterial vasodilators can exaggerate the shunt by lowering LA pressure and should not be used.7 Beta blockers have been used with favorable results.8 Their mechanism of action is not well understood but it is thought that they may improve RV function by reducing heart rate and oxygen consumption.
Closure of the patent foramen ovale by surgical or percutaneous means has been accomplished with limited clinical success.5,6,9,10–14 It has been suggested that closure of a patent foramen ovale can be detrimental to clinical status by reducing LV filling and increasing filling of the noncompliant RV. Five out of 8 patients who had closure of a patent foramen ovale died. In fact, creation of an atrial septal defect could conceivably improve RV function and can be useful in acute RV failure.15 Theoretically, in the setting of acute MI with RV involvement, early myocardial revascularization should improve RV function and thereby reduce the shunt fraction.16 Revascularization can be achieved by thrombolytic therapy, angioplasty or coronary bypass surgery. Atrioventricular sequential pacing may also reduce RA pressure by maintaining atrial contraction.5
Another modality is mechanical support of the right ventricle.15,17 This can be achieved by pulmonary artery balloon counterpulsation or RV assist devices but as far as we are aware, their use has not been reported in this setting. Extracorporeal membrane oxygenation would seem to be an ideal treatment for hypoxia while awaiting recovery of a stunned right ventricle; results are best in patients less than 60 years old and the need for systemic heparinization with consequent bleeding complications may preclude the use of this treatment postoperatively.18 We are not aware of any reports of its use in this situation.
A review of the literature from 1986 to 1998 revealed 18 cases of intracardiac right-to-left shunt through a patent foramen ovale complicating RV infarction (Table 1). Twelve of these 18 patients were female. The mean age at presentation was 63.4 years with a range of 35 to 78 years. The time of presentation ranged from 1 to 6 days (mean, 2.12 days). This correlates well with the clinical observation that RV function improves within 3 days after acute inferior MI.19 The mortality was high at 50% (9/18), with no gender difference. There were 5 deaths among 8 patients who had the patent foramen ovale closed; 5 of the other 10 patients died. Seven patients had some form of revascularization; 4 of these died. It is difficult to draw firm conclusions from the small numbers reported, although it would appear that mortality is higher in patients over the age of 60 years and age may be a factor in predicting outcome in this condition.
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Abstract
Introduction
