ABSTRACT
Introduction: Patients with serious COVID infections frequently develop shock. Their right-sided hemodynamic profiles have not been well characterized. Method(s): In a prospectively collected database including 1997 patients hospitalized for COVID pneumonia from March 2020 to March 2021, 368 had shock requiring vasopressors. 327 had echocardiography to assess ventricular function and stroke volume based on clinical indications. LVEF (LV ejection fraction) and RVFAC (RV fractional area change) were measured using Simpson's rule, stroke volume (SV) by aortic Doppler, and RVSP (RV systolic pressure) from tricuspid regurgitation velocity;187 had evaluable data on all parameters. Patients were divided into groups with low or preserved RVFAC (RVFAC or RVFAC , cutoff <e35%), and low or normal cardiac index, (CI, CI or CI cutoff <e2.2 L/min/m2 ). Result(s): Mean age: 65+/-12, LVEF 59.5+/-12.8, RVFAC 35.3+/-10.6, CI 2.41+/-0.89. Overall hospital mortality in this cohort with shock was 80%. Mean RVSP was 38.8+/-12.2, PEEP 11.0+/-3.7. 43% of patients had low RVFAC (<35%), and RVFAC correlated with other measures of RV function such as tricuspid annular peak systolic excursion (TAPSE) and lateral tricuspid annulus peak systolic velocity (S'). Higher RVSP correlated with lower CI (r=0.134, p= 0.016) but not with PEEP (r=0.03, p=0.70). Mortality did not differ significantly among groups, (p=0.19 by ANOVA) but was highest in the group with low RVFAC and low CI. (Figure) Conclusion(s): RV dysfunction is common in patients with severe COVID-19 and shock. Although RV dysfunction is probably associated with a worse prognosis, outcome in COVID may be tied to pulmonary recovery. Whether treatment targeted at RV dysfunction will improve outcome remains uncertain.
ABSTRACT
Introduction: The cause of tachycardia and dyspnea on exertion (DOE) in the Post Acute Sequelae CoV-2 syndrome (PASC) has yet to be identified. While endothelial invasion of the virus is well documented, how that might explain PASC is unknown. Hypothesis: Covid induced changes in vascular signaling to autonomic regulatory centers can induce sinus tachycardia and DOE. Methods: In a prospective, observational study, we enrolled 18 PASC patients who reported DOE or inappropriate tachycardia. All patients had normal left ventricular function, CXR, Hgb and thyroid studies. None had preexisting autonomic dysfunction. Vascular resistance was assessed by echocardiographic measurement of aortic-vascular impedance (Zva)=(systolic BP + mean Ao valve gradient)/stroke volume index. Ambulatory heart rate monitoring and head-up tilt table testing (HUTT) were performed. Results: Consecutively enrolled patients (18) were studied (17 females, ages 27 to 64). None had a significant aortic valve gradient. Zva was elevated in 17 of 18 patients. Ambulatory monitoring revealed episodes of symptomatic sinus tachycardia. Higher average daily heart rates correlated significantly with higher Zva levels (fig1). The 14 patients with DOE trended to higher average Zva levels than the 4 patients without dyspnea (4.13 +- 0.85 vs 3.5 +- 0.24, P=0.14). Of the 17 patients who had HUTT, 16 demonstrated patterns of orthostatic intolerance consistent with excess sympathetic tone including both postural orthostatic tachycardia and neurogenic cardiac syncope. Conclusions: PASC associated sinus tachycardia and HUTT abnormalities result from excess sympathetic tone. Covid-19 vascular injury as evidenced by abnormal Zva values may result in abnormal vascular signaling to autonomic regulatory centers. Resultant increases in sympathetic output may produce inappropriate sinus tachycardia, vasomotor dysregulation and DOE via peripheral vasoconstriction.
ABSTRACT
Introduction: The response to COVID infection has been associated with intense inflammation, and some patients have cardiac involvement. In a group of patients with COVID infection and shock whose ventricular function was characterized by echocardiography, we examined the relationship between levels of ferritin, an inflammatory marker that is elevated in COVID, and LV ejection fraction (EF). Methods: Of 1275 patients hospitalized with COVID pneumonia, 215 had shock requiring vasopressors. 162 had echocardiography to assess ventricular function and stroke volume. EF was measured using Simpson's rule and stroke volume (SV) by Doppler. Patients were divided into groups with low or preserved EF (EF or EF , cutoff <e45%), and low or normal cardiac index, (CI, CI or CI , cutoff ≤<e2.2 L/min/m2). Ferritin within 7 days of the echo was available in 147/162 patients. We examined the association between ferritin levels and ejection fraction. Results: Mean age was 66.7, EF 58.7±13.9;CI 2.41±0.89 L/min/m2 , ferritin 3036±2318 ng/mL (normal <336). Five patients had obstructive shock from pulmonary embolism (normal LVEF, low SV, RV dysfunction) and were excluded. The other 157 patients were divided into groups based on EF and CI (Figure). High ferritin levels correlated with low EF (r=-0.18, p=0.02), and ferritin levels were greatly increased in patients with a hemodynamic profile of cardiogenic shock. (EF CI , Figure, p=0.017 by ANOVA) Conclusion: COVID-induced shock had a cardiogenic profile (EF CI ) in 10% of patients, and another 5% had low EF but normal CI. Ferritin correlated with low EF and was increased in patients with a profile of cardiogenic shock. This suggests that marked inflammation may depress myocardial function in COVID patients with shock-analogous to a similar myocardial depression seen with bacterial-associated septic shock.