The Burden of Right ventricular dysfunction in Critically Ill COVID-19 illness
Numerous reports have confirmed a hypercoagulable state associated with severity of COVID-19 infection with multiple manifestations including a significantly increased risk of deep venous thrombosis and pulmonary embolism. While respiratory compromise in coronavirus was initially mostly attributed to ARDS, the contribution of embolic phenomena is now more appreciated. In our cohort of COVID 19 patients, while the median D-dimer level was significantly elevated at 7283 for the entire cohort, this was twice as high for patients who died. Previous work has demonstrated the RV involvement that occurs as a result of this increased right sided afterload. (11) This was confirmed in our cohort with 32% of patients experiencing RV dilatation and 21% experiencing reduction in RV systolic function. However, the diagnosis of pulmonary embolism in COVID 19 patients is difficult. First, many of them experience acute kidney injury as a result of their infection that is thought to be multifactorial and related to micro thrombi, endothelial dysfunction, volume status, etc. (2). This acute kidney injury precludes many patients from receiving diagnostic CT pulmonary angiograms. Second, many radiology departments attempt to limit the scanning of COVID 19 patients due to extensive decontamination required after each study. This highlights the additional role of bedside cardiac ultrasound in the management of these patients. At our institution, many patients with ongoing hypoxia received echocardiograms and were presumptively treated for PE with tPA if evidence of RV strain was found.
In a recently published report of 110 patients from New York City, undergoing echocardiographic evaluation the prevalence of RV dilation was 31% (out of 110 patients; 30% intubated and in-hospital mortality 20%).(11) Our findings are similar with 32% patients having evidence of RV dilation. Another recent publication from China demonstrated the added value of RV strain in predicting mortality in 120 COVID-patients (12.5% intubated and 15% in hospital mortality) (6). While strain analysis is a more sensitive marker of RV dysfunction, we were not able to assess that given significant differences between our cohort and Li et al’s report. Only 12.5% of their cohort was mechanically ventilated compared to 57% in our study. Furthermore, the median BMI in our cohort was 30 compared to 23 in Li et al study. This large percentage of intubated and obese patients limited the quality necessary for reliable strain imaging. Our study did demonstrate however that biomarkers could predict the presence of RV dilation/dysfunction. Patients with signs of RV involvement had significant higher pro BNP (4618 vs 2092) and D dimer (12553 vs 5570) compared to those normal right ventricles. This RV strain is presumably a manifestation of subclinical pulmonary embolism, hypoxemic vasoconstriction and other sequela of infection. While future studies are needed, this would seem to suggest that there exists a biomarker threshold over which a cardiac ultrasound should be performed to assess for RV dysfunction.