Avaliação do shunt intrapulmonar em pacientes com hipertensão pulmonar tromboembólica crônica
Data
2023-10-11
Autores
Loureiro, Camila Melo Coelho 
Orientadores
Ramos, Roberta Pulcheri
Tipo
Tese de doutorado
Título da Revista
ISSN da Revista
Título de Volume
Resumo
Introdução: A hipertensão pulmonar tromboembólica crônica (HPTEC) é desencadeada principalmente pela obstrução mecânica por trombos associada a remodelamento vascular pulmonar. A circulação colateral brônquica tem sido estudada como mecanismo protetor ou implicada na patogênese da doença microvascular, além de contribuir para alterações nas trocas gasosas em repouso e durante o exercício. Objetivos: Avaliar a relação entre o shunt intrapulmonar e correlatos com dados clínicos, hemodinâmicos, laboratoriais, ecocardiográficos, tomográficos e de exercício em pacientes com HPTEC. Métodos: Estudo prospectivo, transversal com intervenção diagnóstica em pacientes do ambulatório de Circulação Pulmonar da UNIFESP. Inicialmente, foram realizados ecocardiograma transtorácico, teste de caminhada de 6 minutos (TC6M) e teste de exercício cardiorrespiratório (TECR) incremental. Após o cateterismo cardíaco direito, os pacientes realizaram TECR de carga constante (50% da carga máxima do teste incremental) em ar ambiente e novamente com oxigênio a 100% via máscara facial acoplada ao saco de Douglas. Amostras de sangue arterial e venoso misto foram obtidas para análise dos gases e cálculo do shunt intrapulmonar pela seguinte equação: QS/QT = [(PAO2 - PaO2) x 0,0031] / {CavO2 + [(PAO2 - PaO2) x 0,0031]}. Resultados: Dados de quatorze pacientes (7 mulheres, 49 ± 15 anos) com HPTEC foram analisados. A pressão média da artéria pulmonar foi de 54 ± 17 mmHg, a pressão de oclusão da artéria pulmonar foi de 11 ± 3 mmHg e a resistência vascular pulmonar foi de 789 ± 372 dina.s.cm5. A distância média no TC6M foi de 458 ± 78 m, o V̇O2 no pico foi de 15 ± 2 mL/kg/min e a SpO2 no nadir foi 90 ± 4% no TECR. Todos os participantes apresentaram um aumento do volume/fração de shunt detectado pela respiração de oxigênio a 100% em repouso, o qual diminuiu durante o exercício (17,0 ± 3,6% versus 9,8 ± 3,0%; p <0,001). Houve diminuição da PvO2 (p <0,001) e aumento do espaço morto (p <0,05) no exercício em ar ambiente. A fração de shunt correlacionou-se negativamente com a gravidade hemodinâmica e os valores de troponina. Houve correlação positiva com a PvO2, a PaCO2 e a fração do venous admixture ao esforço. Conclusão: O shunt intrapulmonar parece ser um mecanismo adaptativo na HPTEC em repouso e durante o exercício, possivelmente associado à diminuição dos efeitos deletérios da alta pressão de perfusão pulmonar e ao incremento do débito cardíaco ao esforço.
Introduction: Chronic thromboembolic pulmonary hypertension (CTEPH) is mainly caused by mechanical obstruction by thrombi associated with pulmonary vascular remodeling. Bronchial collateral circulation has been studied as a protective mechanism or implicated in the pathogenesis of microvascular disease, in addition to contributing to changes in gas exchange at rest and during exercise. Objectives: To evaluate the relationship between intrapulmonary shunt and correlates with clinical, hemodynamic, laboratory, echocardiographic, image and exercise data of patients with CTEPH. Methods: Prospective, cross-sectional study with diagnostic intervention in patients from UNIFESP’s Pulmonary Circulation outpatient clinic. Initially, transthoracic echocardiography, 6-minute walk test and incremental cardiorespiratory exercise test were performed. After undergoing right heart catheterization, patients performed a 50% maximal workload steady-state exercise at room air and receiving100% oxygen with a face mask from a Douglas bag. Arterial and mixed venous blood samples were obtained for gas analysis and calculation of intrapulmonary shunt using the following equation: QS/QT= [(PAO2 - PaO2) x 0.0031] / {CavO2 + [(PAO2 - PaO2) x 0.0031]}. Results: Data from fourteen patients (7 women, 49 ± 15 years) with CTEPH were analyzed. Mean pulmonary artery pressure was 54 ± 17 mmHg, pulmonary artery occlusion pressure was 11 ± 3 mmHg and pulmonary vascular resistance was 789 ± 372 dina.s.cm5. The average 6-minute walk distance was 458 ± 78 m, V̇O2 at peak was 15 ± 2 mL/kg/min and nadir SpO2 was 90 ± 4%. All participants showed an increased shunt volume/ fraction detected by 100% oxygen breathing at rest that decreased during exercise (17,0 ± 3,6% versus 9,8 ± 3,0%; p <0,001). There was a decrease in PvO2 (p <0.001) and an increase in dead space (p <0.05) during exercise in room air. Shunt fraction was negatively correlated with hemodynamic severity and troponin values. There was a positive correlation with PvO2, PaCO2 and venous admixture fraction on exertion. Conclusion: Intrapulmonary shunt seems to be an adaptive mechanism in CTEPH at rest and during exercise, possibly associated with a decrease in the deleterious effects of high pulmonary perfusion pressure and an increase in cardiac output on exertion.
Introduction: Chronic thromboembolic pulmonary hypertension (CTEPH) is mainly caused by mechanical obstruction by thrombi associated with pulmonary vascular remodeling. Bronchial collateral circulation has been studied as a protective mechanism or implicated in the pathogenesis of microvascular disease, in addition to contributing to changes in gas exchange at rest and during exercise. Objectives: To evaluate the relationship between intrapulmonary shunt and correlates with clinical, hemodynamic, laboratory, echocardiographic, image and exercise data of patients with CTEPH. Methods: Prospective, cross-sectional study with diagnostic intervention in patients from UNIFESP’s Pulmonary Circulation outpatient clinic. Initially, transthoracic echocardiography, 6-minute walk test and incremental cardiorespiratory exercise test were performed. After undergoing right heart catheterization, patients performed a 50% maximal workload steady-state exercise at room air and receiving100% oxygen with a face mask from a Douglas bag. Arterial and mixed venous blood samples were obtained for gas analysis and calculation of intrapulmonary shunt using the following equation: QS/QT= [(PAO2 - PaO2) x 0.0031] / {CavO2 + [(PAO2 - PaO2) x 0.0031]}. Results: Data from fourteen patients (7 women, 49 ± 15 years) with CTEPH were analyzed. Mean pulmonary artery pressure was 54 ± 17 mmHg, pulmonary artery occlusion pressure was 11 ± 3 mmHg and pulmonary vascular resistance was 789 ± 372 dina.s.cm5. The average 6-minute walk distance was 458 ± 78 m, V̇O2 at peak was 15 ± 2 mL/kg/min and nadir SpO2 was 90 ± 4%. All participants showed an increased shunt volume/ fraction detected by 100% oxygen breathing at rest that decreased during exercise (17,0 ± 3,6% versus 9,8 ± 3,0%; p <0,001). There was a decrease in PvO2 (p <0.001) and an increase in dead space (p <0.05) during exercise in room air. Shunt fraction was negatively correlated with hemodynamic severity and troponin values. There was a positive correlation with PvO2, PaCO2 and venous admixture fraction on exertion. Conclusion: Intrapulmonary shunt seems to be an adaptive mechanism in CTEPH at rest and during exercise, possibly associated with a decrease in the deleterious effects of high pulmonary perfusion pressure and an increase in cardiac output on exertion.