Pulmonary hypertension due to acute respiratory distress syndrome

Abstract

Our aims were to describe the prevalence of pulmonary hypertension in patients with acute respiratory distress syndrome (ARDS), to characterize their hemodynamic cardiopulmonary profiles, and to correlate these parameters with outcome. All consecutive patients over 16 years of age who were in the intensive care unit with a diagnosis of ARDS and an in situ pulmonary artery catheter for hemodynamic monitoring were studied. Pulmonary hypertension was diagnosed when the mean pulmonary artery pressure was >25 mmHg at rest with a pulmonary artery occlusion pressure or left atrial pressure <15 mmHg. During the study period, 30 of 402 critically ill patients (7.46%) who were admitted to the ICU fulfilled the criteria for ARDS. Of the 30 patients with ARDS, 14 met the criteria for pulmonary hypertension, a prevalence of 46.6% (95% CI; 28-66%). The most common cause of ARDS was pneumonia (56.3%). The overall mortality was 36.6% and was similar in patients with and without pulmonary hypertension. Differences in patients' hemodynamic profiles were influenced by the presence of pulmonary hypertension. The levels of positive end-expiratory pressure and peak pressure were higher in patients with pulmonary hypertension, and the PaCO2 was higher in those who died. The level of airway pressure seemed to influence the onset of pulmonary hypertension. Survival was determined by the severity of organ failure at admission to the intensive care unit.

Pulmonary hypertension and right ventricular involvement in hospitalised patients with COVID-19

“…As expected, the observed figures seem lower compared with previous studies exploring PH and RV failure among ARDS patients in ICU settings. 22 26 27 Although the absence of positive-pressure ventilation-mediated changes in pulmonary haemodynamics could be implicated in the observed prevalence of PH and RVD in our population, most included patients fulfilled criteria of ARDS even though outside the ICU setting (median PaO 2 /FiO 2 243 (132–314), bilateral lung infiltrates in 82.5% of patients). 12 18 Therefore, the observed findings refer to a population with moderate–severe COVID-19, without critical lung involvement (requiring ICU admission) but also without mild SARS-CoV-2 pneumonia (likely not determining hospital admission).…”

“…In terms of TTE findings, patients with PH had significantly higher basal RV end-diastolic diameter (42 (38-48) vs 36 (32-39) mm, p<0.001) and mid RV end-diastolic diameter (37 (31-40) vs 30 (26-32) mm, p<0.001), and lower TAPSE (20 (17)(18)(19)(20)(21)(22) vs 22 (20-25) mm, p=0.004) and S' wave (12 (9-13) vs 13 (11)(12)(13)(14)(15) cm/s, p=0.004) compared with patients without PH. The median estimated SPAP in the PH group was 42 (39-47) mm Hg.…”

“…Downloaded from The association between severe acute respiratory failure and PH has been demonstrated by several studies, mainly focusing on critically ill patients treated in ICU setting. [21][22][23][24] Secondary alterations of pulmonary vascular haemodynamics during acute respiratory distress syndrome (ARDS) are multifactorial, depending on hypoxia, vascular remodelling or compression by oedema or fibrosis, increased alveolar pressure, vasoconstriction, local thrombosis or pulmonary embolism, and reduced pulmonary compliance and use of PEEP. 4 5 7 25 While the advanced stages of COVID-19 are characterised by severe ARDS and need of mechanical ventilation (and the mentioned pathophysiological mechanisms could be directly translated to such scenario), whether a less-advanced SARS-CoV-2 pneumonia could determine a significant change in pulmonary vascular haemodynamics leading to PH and RV involvement was unknown.…”

Arrhythmias and COVID-19

“…Right myocardial strain can be seen as a result of pulmonary embolism, which has been reported as the most common thrombotic complication in COVID-19 patients ( 53 ), or due to pulmonary hypertension, causing increased right sided pressures secondary to severe ARDS, sepsis, or heart failure ( 54 ). On the one hand, increased right atrial pressure along with increased sympathetic tone in patients with pulmonary hypertension and hypoxia can predispose to increased risk of atrial tachyarrhythmias ( 55 ).…”

Hipertensión pulmonar en la unidad de terapia intensiva

“…Ñamendys y sus colaboradores abordan en su trabajo un grupo de dichos pacientes, manejados en la unidad de terapia intensiva (UTI) del Instituto Nacional de Ciencias Médicas y Nutrición «Salvador Zubirán», con una prevalencia de 46.6% y sin impacto particular sobre la mortalidad (36.6%) de esta dificultad respiratoria ya de por sí catastrófica; en ellos, el nivel de la presión de la vía aérea parece haber influenciado el inicio de la HP. 2 Hipertensión pulmonar en la unidad de terapia intensiva www.medigraphic.org.mx vés de la disminución de la presión de llenado del ventrículo izquierdo. La HP producida por neumopatía y/o hipoxia requiere el uso de O 2 suplementario (recomendación IC); en estos pacientes, el empleo de vasodilatadores puede producir un mayor grado de hipoxemia al romperse la vasoconstricción hipóxica.…”