B50-27 Clearing the Air: Chronic Mitral Valve Stenosis Repair With Subsequent Resolution of Hypercapnia

Mitral Valve Stenosis is a well-recognized cause of pulmonary hypertension and right heart failure. Chronic mitral valve stenosis can lead to elevation of pulmonary venous pressure which can, overtime, lead to hemodynamic burden on pulmonary circulation manifesting as obstructive ventilator defects and ultimately CO2 retention later in the course of the disease. A64 year old woman with known severe pulmonary hypertension and moderate mitral stenosis for many years that had been suffering increasing shortness of breath with minimal activity. The patient was on oxygen and had been seen by a pulmonary hypertension specialist in the past who noted that some degree of her pulmonary hypertension is related to mitral stenosis. Patient subsequently underwent trans-esophageal echocardiogram and found to have severe mitral stenosis with mean gradient of 13 mmHg across the valve. Right heart catheterization was performed, supporting post capillary pulmonary hypertension. Concurrently, the patient had been noted to retain chronically retain CO2. She does have history of prior COPD and very severe obstruction per her pulmonary function tests despite minimal smoking history. She had worsening respiratory acidosis with pCO2 increasing to 120 mmHg and was subsequently intubated. Patient subsequently underwent Mitral Valve Replacement with 31mm St. Jude Epic Mitral Valve. The patient’s CO2 rapidly decreased towards normal, hovering around 50 mmHg after repair and remaining there without any other intervention. It has been long understood that chronic mitral valve stenosis can present with obstructive findings on spirometry in some patients in light of pulmonary vascular congestion and edema rather than obstructive airway disease as we traditionally understand it. There have been studies done showing that there is some reversibility of this obstructive defect after repair of the mitral valve. It is presumed that the mechanism underlying this is due to increased airway resistance and uneven ventilation-perfusion in the setting of chronic pulmonary congestion and vascular remodeling. In our patient with long standing pulmonary hypertension, she had a V/Q scan with heterogeneous distribution likely reflecting long standing pulmonary congestion and interstitial edema. This prolonged post capillary pulmonary hypertension seems to have led to a severe obstructive pattern on her pulmonary function tests and thus her chronic CO2 retention. Interestingly after the valve was replaced, her CO2 had normalized suggestive of reversible obstructive defect. This also implies possible airway obstruction and dead space that may have been contributing to CO2 retention as underlying pathophysiology.