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.