Sleep apnea syndrome as a cause of severe pulmonary hypertension
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FILIMON, Vlad. Sleep apnea syndrome as a cause of severe pulmonary hypertension. In: MedEspera: International Medical Congress for Students and Young Doctors, Ed. 7th edition, 3-5 mai 2018, Chişinău. Chisinau, Republic of Moldova: 2018, 7, pp. 19-20.
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MedEspera
7, 2018
Congresul "International Medical Congress for Students and Young Doctors"
7th edition, Chişinău, Moldova, 3-5 mai 2018

Sleep apnea syndrome as a cause of severe pulmonary hypertension


Pag. 19-20

Filimon Vlad
 
”Nicolae Testemițanu” State University of Medicine and Pharmacy
 
 
Disponibil în IBN: 31 octombrie 2020


Rezumat

Background. Sleep apnea is a disorder characterized by pauses in breathing or periods of shallow breathing during sleep. There are three forms of sleep apnea: obstructive (OSA), central (CSA), and a combination of the two called mixed. OSA affects 1 to 6% of adults and 2% of children, but CSA affects less than 1% of people. Case report. Patient X, 58 years old, of female, was admitted at the Institute of Cardiology with mixed (inspiratory and expiratory) dyspnea at minimal effort, ankle swelling, general weakness, dizziness. The patient suffers from arterial hypertension during 14-year with maximum levels 180/90 mmHg, working blood pressure being - 130/80 mmHg. At home regular treatment with tab. Bisoprolol 2.5 mg in the morning, tab. Aspirin 75 mg/day, tab. Losartan 50 mg in the evening, tab. Torasemidi 10 mg in the morning, over a day. The general condition worsened the last month when signs of congestive heart failure progressed. The echocardiographical examination revealed severe cardiomegaly (LA - 50 mm, LV - 60 mm, RA - 51 mm, RV - 40 mm), preserved left ventricular function (EF - 58%), reduced right ventricular function (TAPSE - 16 mm), severe pulmonary hypertension (PASP - 140 mmHg). To determine the cause of the pulmonary hypertension, a number of investigations were performed. Pulmonary artery angiography by computed tomography revealed pulmonary artery enlargement (40 mm) and dilated intrapulmonary arteries, but no data on thrombosis. Spirography has revealed severe changes in the function of external respiratory organs, being restrictive. Laboratory analyzes excluded the systemic sclerodermia (ANA-negative, Anti Scl-70 antibodies – 1.5 U/ml, Anti Centromer B antibodies – 0.3 U/ml) and normal values of D-dimers (0.24 ng/ml) excluded the presence of venous thrombosis. To exclude the presence of Sleep Apnea Syndrome, cardio-respiratory polygraphy was performed. A severe form of Sleep Apnea-Hypopnea Syndrome was recorded, with the Apnea-Hypopnea Index (AHI) – 84.3/hour, with severe intermittent and continue nocturnal hypoxemia in close correlation with respiratory events, having a Desaturation Index (DI) – 82 6/hour. Average SaO2 – 69.6%, SaO2 minimum – 42%, SaO2 <90% = 07 hours 50 min 48 sec. Conclusions. After 10 days of complex treatment with diuretics, direct and indirect anticoagulants, nitrates, angiotensin II receptor blockers, beta-adrenoblockers, continuous oxygen therapy, and CPAP + Oxygen therapy, the general condition improved: the mixed dyspnoea at minimal effort was reduced, general weakness , dizziness disappeared as well as the ankle swelling, and pulmonary artery systolic pressure decreased from 140 mmHg to 100 mmHg.

Cuvinte-cheie
sleep apnea-hypopnea syndrome, pulmonary hypertension