Severe Hypoxemia in 73-Year-Old Patient with Septal Defect

SEVERE HYPOXEMIA in 73-YEAR-OLD PATIENT WITH SEPTAL DEFECT

M. Haitham Bakir, MD, FCCP,
Southern Illinois University, School of Medicine.

Introduction
Case Presentation
Discussion
Conclusion

Introduction:

Atrial septal defects (ASD) account for almost a third of congenital heart defects in adults, usually causing symptoms in the fourth decade of life. It is less likely to present at the age of 73 for the first time. Our patient had severe hypoxemia with normal clinical radio graphical and physiological findings except hints on blood gases.

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Case Presentation:

The 73-year-old male with history of hypertension and mild hyperlipidemia, presented with a 6-week complaint of dyspnea on exertion.

He reported that he developed this dyspnea while working outdoors. Since its onset, it had become progressive affecting most all of his activities. However, the dyspnea was not present at rest.

He had never smoked, or been chronically exposed to any toxic fumes or dusts. Patient had no cough, chest pain, palpitations, orthopnea, playtpnea, fever or chills.

There is no history of congenital heart disease or pulmonary disease in the family.
Physical exam revealed a well- nourished gentleman. Cardiovascular exam revealed regular rate and rhythm of heart without murmur, gallop, or rub, point of maximal impulse in the 5th intercostal space, good peripheral pulses. Lungs were clear. No edema of the extremities.

Patient’s primary physician had sent him to a cardiologist for evaluation for the dyspnea. The cardiologist performed a treadmill exercise test that was prematurely aborted due to significant dyspnea after 2 minutes. There were not any EKG changes noted with this study.
Tran thoracic echocardiogram revealed borderline left atrial enlargement but otherwise normal.
After the cardiac work-up was negative patient was sent to a pulmonologist for further evaluation. The patient had a normal chest x-ray, ventilation/perfusion lung scan, and spiral CT.
Pulmonary function test revealed normal FVC, FEV1, FEV1/FVC, and DLCO. Blood gases revealed pH 7.47, pCo2: 29, pO2: 52, O2 saturation: 84% on room air.
Blood count revealed hemoglobin of 14.2 g/dl and hematocrit of 42%. Electrolytes, kidney and liver functions were normal.
There was no improvement in oxygen saturation with high flow oxygen administration.
Patient was next sent to Southern Illinois University School of Medicine for further evaluation for his hypoxemia e possibility of right to left shunt was entertained.
Shunt fraction was calculated to be 23.5% with placing patient on 100 % FiO2 in the clinic; oxygen saturation was between 74% and 82% on room air at rest.
The patient next had a transesophageal echocardiogram performed which revealed moderated left atrial enlargement, a small secundum atrial septal defect with moderated left to right shunting per color flow doppler, and severe right to left shunting as demonstrated by agitated contrast saline injection. Right-sided cardiac catheterization was performed which revealed normal pressures along with a “shoulder” on downslope of the cardiac output suggesting a right to left shunt.
The patient was then sent for surgical repair. On opening, the surgeon noted the pericardium to be thickened, particularly on the right side of the heart compatible with constrictive pericarditis.
The patient then underwent pericardiectomy and closure of the atrial septal defect. Pathological evaluation revealed pericarditis that was most likely idiopathic/viral as AFB; bacterial, fungal, and viral cultures were all negative. The patient tolerated the procedure well. He was discharged 7 days after the surgery. Oxygen saturations prior to discharge were consistently in the range of 96-100% with rest and above 92% with activity on room air.
On follow-up six months later, the patient had no dyspnea with oxygen saturations with activity above 92%.

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Discussion:

ASD could cause shunting left to right, right to left, or bi-directional. Shunting is generally left to right initially but as hemodynamics are altered the shunt becomes bi-directional or reversed. These hemodynamic alterations may be caused by increased right sided heart pressures secondary to volume overloading secondary to the left to right shunting over a period of time, right ventricular infarction, pulmonary embolism, or as in our case, constrictive pericarditis that is more prominent on the right side causing elevated right-sided pressures and shunt reversal and the hypoxemia that is therefore precipitated.

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Conclusion:

1-Right to left shunt should be considered in patients with hypoxemia when not corrected with high oxygen supplementation.
2-Transesophageal echo with agitated saline or right heart catheterization are diagnostic.

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