Fundamento: Não há estudos que tenham descrito e avaliado a associação entre hemodinâmica, limitações físicas e qualidade de vida em pacientes com hipertensão pulmonar (HP) sem doença cardiovascular ou respiratória concomitante. Objetivo: Descrever o perfil hemodinâmico, a qualidade de vida e a capacidade física de pacientes com HP dos grupos I e IV e estudar a associação entre esses desfechos. Métodos: Estudo transversal em que foram incluídos pacientes com HP dos grupos clínicos I e IV e classes funcionais II e III, submetidos a avaliações hemodinâmica (cateterismo), de tolerância ao exercício e de qualidade de vida. Resultados: Foram avaliados 20 pacientes com idade média de 46,8±14,3 anos. Eles apresentaram pressão de encunhamento arterial pulmonar de 10,5±3,7 mmHg, distância percorrida no teste de caminhada de 6 minutos (DTC6M) de 463±78 m, consumo de oxigênio no pico do exercício de 12,9±4,3 mLO2.kg-1.min-1 e domínios de qualidade de vida com escores < 60%. Houve associação entre índice cardíaco (IC) e equivalente ventilatório de CO2 (r=-0,59; p<0,01), IC e equivalente ventilatório de oxigênio (r=-0,49; p<0,05), pressão atrial direita (PAD) e domínio 'estado geral de saúde' (r=-0,61; p<0,01), PAD e DTC6M (r=-0,49; p<0,05), resistência vascular pulmonar (RVP) e domínio 'capacidade funcional' (r=-0,56; p<0,01), RVP e DTC6M (r=-0,49, p<0,05) e índice de RVP e capacidade física (r=-0,51; p<0,01). Conclusão: Pacientes com HP dos grupos I e IV e classes funcionais II e III apresentam redução da capacidade física e dos componentes físico e mental de qualidade de vida. As variáveis hemodinâmicas IC, pressão arterial pulmonar diastólica, PAD, RVP e índice de RVP associam-se com a tolerância ao exercício e domínios da qualidade de vida.

Background: No studies have described and evaluated the association between hemodynamics, physical limitations and quality of life in patients with pulmonary hypertension (PH) without concomitant cardiovascular or respiratory disease. Objective: To describe the hemodynamic profile, quality of life and physical capacity of patients with PH from groups I and IV and to study the association between these outcomes. Methods: Cross-sectional study of patients with PH from clinical groups I and IV and functional classes II and III undergoing the following assessments: hemodynamics, exercise tolerance and quality of life. Results: This study assessed 20 patients with a mean age of 46.8 ± 14.3 years. They had pulmonary capillary wedge pressure of 10.5 ± 3.7 mm Hg, 6-minute walk distance test (6MWDT) of 463 ± 78 m, oxygen consumption at peak exercise of 12.9 ± 4.3 mLO2.kg-1.min-1 and scores of quality of life domains < 60%. There were associations between cardiac index (CI) and ventilatory equivalent for CO2 (r=-0.59, p <0.01), IC and ventilatory equivalent for oxygen (r=-0.49, p<0.05), right atrial pressure (RAP) and 'general health perception' domain (r=-0.61, p<0.01), RAP and 6MWTD (r=-0.49, p<0.05), pulmonary vascular resistance (PVR) and 'physical functioning' domain (r=-0.56, p<0.01), PVR and 6MWTD (r=-0.49, p<0.05) and PVR index and physical capacity (r=-0.51, p<0.01). Conclusion: Patients with PH from groups I and IV and functional classes II and III exhibit a reduction in physical capacity and in the physical and mental components of quality of life. The hemodynamic variables CI, diastolic pulmonary arterial pressure, RAP, PVR and PVR index are associated with exercise tolerance and quality of life domains.

OBJECTIVE: The respiratory ratio is a dimensional construct of the respiratory subtype of panic disorder (PD). The respiratory subtype has been correlated with an increased sensitivity to CO2 inhalation, positive family history of PD and low comorbidity with depression. The objective of our study was to determine whether the respiratory ratio is correlated with CO2-induced panic attacks and other clinical and demographic features. METHODS: We examined 91 patients with PD and submitted them to a double-breath 35% CO2 challenge test. The respiratory ratio was calculated based on the Diagnostic Symptom Questionnaire (DSQ) scores recorded in a diary in the days preceding the CO2 challenge. The scores of the respiratory symptoms were summed and divided by the total DSQ score. RESULTS: The respiratory ratio was correlated with CO2 sensitivity, and there was a non-statistically significant trend towards a correlation with a family history of PD. CONCLUSIONS: The positive correlation between the respiratory ratio and the anxiety elicited by the CO2 inhalation indicates that the intensity of respiratory symptoms may be proportional to the sensitivity to carbon dioxide.

Acute respiratory distress syndrome (ARDS) is characterized by diffuse alveolar damage, and evolves progressively with three phases: exsudative, fibroproliferative, and fibrotic. In the exudative phase, there are interstitial and alveolar edemas with hyaline membrane. The fibroproliferative phase is characterized by exudate organization and fibroelastogenesis. There is proliferation of type II pneumocytes to cover the damaged epithelial surface, followed by differentiation into type I pneumocytes. The fibroproliferative phase starts early, and its severity is related to the patient’s prognosis. The alterations observed in the phenotype of the pulmonary parenchyma cells steer the tissue remodeling towards either progressive fibrosis or the restoration of normal alveolar architecture. The fibrotic phase is characterized by abnormal and excessive deposition of extracellular matrix proteins, mainly collagen. The dynamic control of collagen deposition and degradation is regulated by metalloproteinases and their tissular regulators. The deposition of proteoglycans in the extracellular matrix of ARDS patients needs better study. The regulation of extracellular matrix remodeling, in normal conditions or in several pulmonary diseases, such as ARDS, results from a complex mechanism that integrate the transcription of elements that destroy the matrix protein and produce activation/inhibition of several cellular types of lung tissue. This review article will analyze the ECM organization in ARDS, the different pulmonary parenchyma remodeling mechanisms, and the role of cytokines in the regulation of the different matrix components during the remodeling process.