SESSION TITLE: Pulmonary Vascular Disease Cases
SESSION TYPE: Case Reports
PRESENTED ON: Saturday, March 22, 2014 at 04:15 PM - 05:15 PM
INTRODUCTION: Data has been published suggesting that iNO can be utilized in a variety of situations, however, there is little literature on its use in the setting of acute decompensation in valvular disease.
CASE PRESENTATION: A previously healthy 32 year old female, 29 weeks of gestation, presented to an outside hospital with dyspnea progressing over two months and development of a rust-colored sputum. She required intubation hours after presentation, and a cardiac echo revealed critical aortic and mitral stenosis with valves characteristic of rheumatic heart disease. Upon transfer to our institution, the patient’s blood pressure was 60s/40s and she requiried an FiO2 of 100%. Cardiac cath revealed aortic and mitral valve areas of 0.47 cm2 and 0.67 cm2¬, respectively, and a PAP of 80/40. The. She continued to desaturate and inhaled nitric oxide was initiated with a brisk positive response. The patient’s aortic valve was successfully opened with balloon valvuloplasty, and her PA pressures settled around 50s/30s in the next 24 hours. The patient was titrated off pressors at 48 hours, titrated off iNO at 72 hours, and extubated at 96 hours. She left the hospital with close outpatient follow up, and returned two weeks later in labor. Her infant was successfully delivered by C section, and both were doing well at time of writing.
DISCUSSION: Typically, pregnant women experience an increase in cardiac output of about 30 to 50% - increasing blood flow and hydrostatic pressure in the pulmonary vasculature. This is particularly marked in the case of patients with mitral stenosis. Due to its extremely short half-life and inhaled delivery, NO acts in a highly localized fashion thereby improving ventilation-perfusion mismatch in patients with pulmonary edema. As as shown in a study of 18 women with mitral stenosis and pulmonary hypertension, NO decreases pulmonary arterial pressure and significantly reduces pulmonary vascular resistance without effecting left atrial pressure or cardiac output. In this patient, her pulmonary artery pressures were markedly decreased by the institution of iNO and markedly increased at times of discontinuation.
CONCLUSIONS: Whether by improving ventilation/perfusion mismatch or decreasing pulmonary vascular resistance, inhaled NO is effective in increasing oxygenation in a patient with pulmonary hypertension and critical mitral and aortic stenosis in the acute setting.
Reference #1: Mahoney PD, Loh E, Blitz LR, Herrmann HC. Hemodynamic effects of inhaled nitric oxide in women with mitral stenosis and pulmonary hypertension. Am J Cardiol 2001;87:188-192.
Reference #2: Gelson E, Gatzoulis M, Johnson M. Pregnancy and valvular heart disease. BMJ 2007; 335:1042-5.
Reference #3: Hayward CS, Macdonald PS, Keogh AM. Inhaled nitric oxide in cardiology. Expert Opin. Investig. Drugs (2001) 10(11):1947-1956.
DISCLOSURE: The following authors have nothing to disclose: Nicholas Juul
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