Abstract
OBJETIVO: O estudo consiste em verificar os efeitos da utilização do óxido nítrico inalatório (NOi) em pacientes no pós-operatório de cirurgia valvar mitral. MÉTODO: Os efeitos do NOi foram medidos principalmente por meio da verificação de alterações na pressão arterial pulmonar (PAP). Outras medidas realizadas incluíram: pressão arterial média (PAM), pressão venosa central média (PVC), pressão média de átrio esquerdo (PAE), saturação de oxigênio por oximetria de pulso, complacência pulmonar estática e gradiente transpulmonar (GTP). RESULTADOS: Nos 20 pacientes estudados, obteve-se tempo mediano de utilização do NOi de 19,1 horas. A PAP média reduziu significativamente de 33,8 ± 6,17 mmHg (pré-NOi) para 29,1 ± 6,46 mmHg, nos 30 minutos iniciais e para 28,4 ± 5,22 mmHg, considerando a média de todas as medidas pós-NOi (p< 0,05). O GTP também apresentou redução estatisticamente significativa. Não houve alterações significativas nas demais medidas hemodinâmicas. CONCLUSÃO: Os achados indicam que a utilização do NOi reduz a PAP sem efeitos sistêmicos, demonstrando efeito vasodilatador seletivo no sistema vascular pulmonar.
Highlights
Pulmonary hypertension (PH) is a clinical and hemodynamic syndrome that results in vaso-occlusive alterations of the micro circulation system, aggravated by pathologic interactions between the vascular wall and circulating elements [1]
The findings indicate that the use of inhaled nitric oxide (iNO), in post-operative period of mitral valve operation associated with pulmonary hypertension, reduces pulmonary artery pressure (PAP) without systemic effects, demonstrating a selective vasodilator effect on the pulmonary vascular system
The findings of the current study show this selective effect of nítrico inalatório (NOi), as no significant alteration was seen in the mean arterial pressure (MAP)
Summary
Pulmonary hypertension (PH) is a clinical and hemodynamic syndrome that results in vaso-occlusive alterations of the micro circulation system, aggravated by pathologic interactions between the vascular wall and circulating elements [1]. The disease constitutes a problem that can lead to substantial morbidity and mortality rates in the postoperative period of heart surgery [2,3]. Mitral valve lesions, such as stenosis and insufficiency, make the blood flow turbulent and may lead to progressive fibrosis and calcification of the valve apparatus, enlargement of the left atrium and calcification and obliterate changes of the pulmonary artery bed [4]. There is an increase in the retrograde pulmonary venocappilary pressure and the appearance of reactive arteriolar vasoconstriction that causes anatomic restrictions of the pulmonary vascular bed due to thickening of the media layers of small arteries and arterioles, by peripheral extension of the smooth musculature of these vessels and partial or complete obliteration of their lumens [5]. NO mediates several cellular phenomena including endothelium-dependent vasorelaxation, macrophage-mediated cytotoxicity, inhibition of the activation, adhesion and aggregation of platelets [7]
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