Acta Anaesthesiol Scand. 2021 Mar 16. doi: 10.1111/aas.13819. Online ahead of print.
INTRODUCTION: Critically ill Covid-19 pneumonia patients are likely to develop the sequence of acute pulmonary hypertension, right ventricular (RV) strain, and eventually RV failure due to known pathophysiology (endothelial inflammation plus thrombo-embolism) that promotes increased pulmonary vascular resistance and pulmonary artery pressure. This study aimed to investigate the occurrence of acute pulmonary hypertension (aPH) as per established trans-thoracic echocardiography (TTE) criteria in Covid-19 patients receiving intensive care and to explore whether short-term outcomes are affected by the presence of aPH.
METHODS: Medical records were reviewed for patients treated in the intensive care units at a tertiary university hospital over a month. The presence of aPH on the TTE was noted, and plasma NTproBNP and troponin were measured as markers of cardiac failure and myocardial injury, respectively. Follow-up data were collected 21 days after the performance of TTE.
RESULTS: In total, 26 of 67 patients (39%) had an assessed systolic pulmonary artery pressure of >35 mm Hg (group aPH), meeting the TTE definition of aPH. NTproBNP levels (median [range]: 1430 [102-30300] vs. 470 [45-29600] ng L-1 ; p = 0.0007), troponin T levels (63 [22-352] vs. 15 [5-407] ng L-1 ; p = 0.0002), and the 21-day mortality rate (46% vs. 7%; p < 0.001) were substantially higher in patients with aPH compared to patients not meeting aPH criteria.
CONCLUSION: TTE-defined acute pulmonary hypertension was frequently observed in severely ill Covid-19 patients. Furthermore, aPH was linked to biomarker-defined myocardial injury and cardiac failure, as well as an almost 7-fold increase in 21-day mortality.