New study characterizes cardiac function in severe COVID-19 patients

In a recently published study, Dr Journal of Critical CareResearchers assessed cardiac function in patients exposed to severe coronavirus disease 2019 (COVID-19).

Background

Cardiovascular changes have been associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in infected patients. Most Covid-19-infected patients have elevated troponin levels, which are associated with increased mortality. Additionally, case reports of fulminant myocarditis or cardiogenic shock have been published. Acute cor pulmonale (ACP), pulmonary embolism (PE), and right ventricular enlargement have also been documented.

There is not enough information about how the heart works in relation to the lungs and breathing mechanics during artificial ventilation. These features may also be important in severe COVID-19 because they are associated with cardiac dysfunction associated with adult respiratory distress syndrome (ARDS).

About the study

In the current study, the researchers characterized cardiac function in critically ill patients with severe COVID-19 disease.

Laboratory-confirmed COVID-19 patients hospitalized in the intensive care unit (ICU) between April and July 2020 at four university-affiliated hospitals in Chile were included in this prospective, multicenter study. All consecutive COVID-19 patients requiring invasive mechanical ventilation (MV) were eligible for the study. The critical care echocardiography (CCE) examination included collection of demographic data, Sequential Organ Failure Assessment (SOFA), Acute Physiology and Chronic Health Evaluation II (APACHE II), hemodynamic variables, respiratory system mechanics, biomarkers, and tissue perfusion parameters. An assessment at one year of follow-up was conducted by telephone interview or an online death registry.

Transthoracic echocardiography was performed by a medical operator under the supervision of the center’s principal investigator. The team also performed echocardiographic estimations. Lung-protective ventilation techniques were used to manage patients during their treatment. Echocardiogram examination was performed with adequate sedation. Measurements were obtained, and three consecutive cardiac cycles were averaged.

Left ventricular ejection fraction (LVEF), calculated using modified Simpson’s formula, was used to assess LV systolic function. Patients were classified as hyperkinetic with LVEF >60%, normokinetic with LVEF between 45% and 60%, and hypokinetic with LVEF less than 45%. LV outflow tract (LVOT) was used to determine cardiac output (CO). LVOT area and velocity time integral (VTI) were multiplied to determine stroke volume (SV). CO was determined as the sum of heart rate and SV. Tissue Doppler imaging (TDI) was used to capture the peak mitral annular myocardial velocity wave (s’).

Mitral inflow pulsed wave Doppler was used to determine atrial velocity (A) and initial peak velocity (E) in left ventricular diastole. Left and right ventricular end-diastolic areas (LVEDA and RVEDA) were assessed, and the ratio of LVEDA and RVEDA was calculated. RV dilatancy associated with a paradoxical septal motion was referred to as ACP. Peak tricuspid annular myocardial velocity wave (s’) and tricuspid annular plane systolic excursion (TAPSE) measurements were used to assess RV systolic function.

result

The study group included a total of 140 individuals with a mean age of 57 ± 11 years, of which 29% were female. Obesity, hypertension and diabetes mellitus were the three primary comorbidities. Approximately 65 patients were in the prone position during echocardiographic measurements. PaO2/FiO2 ratio was 155, and MV settings closely followed lung protective ventilation techniques.

Cardiac output was 5.1 L/min, while 86% of patients required a median dose of 0.05 g/kg/min of norepinephrine to maintain a mean arterial pressure above 65 mmHg. Most patients had normal perfusion parameters, including a lactate level of 1.7 mmol/L and a Pv-aCO2 gradient of 6. According to the parameters employed, 36 patients were fluid-responsive and seven patients showed signs of elevated LV filling pressure.

Compared to patients with RV dilatation, ACP patients showed more severe pulmonary morbidity such as lower compliance, greater driving pressure and the presence of respiratory acidosis associated with higher APACHE II and SOFA scores at admission. Compared to patients with TAPSE who had dilatation alone, subjects with ACP had significantly lower RV systolic function. ACP patients required more norepinephrine and had a lower stroke volume and higher heart rate, a longer capillary refill time, higher troponin levels, and higher lactate levels associated with a higher prevalence of LV systolic dysfunction.

Whereas 27 patients demonstrated LV or RV dysfunction, 82 patients showed signs of diastolic dysfunction, including 66 with grade I, 16 with grade II, and zero with grade III. LV systolic dysfunction and diastolic dysfunction showed no individual association with mortality. 44 patients died, including 40 who died in the ICU. ICU mortality was higher in ACP patients. During one year of follow-up, only one patient died. ACP and PaO2/FiO2 were independent predictors of mortality according to multivariate analysis.

Study results showed that mechanically ventilated patients diagnosed with COVID-19 ARDS typically experienced right ventricular enlargement. Only 40% of subjects with acute cor pulmonale had concurrent pulmonary embolism, which was also associated with decreased pulmonary function.