Table 1 The echocardiographic features of nCoV pneumonia

Hyperdynamic cardiac function

Increase of cardiac output (CO) and ejection faction (EF) of the left ventricular (LV), with/without the decrease of peripheral vascular resistance

Cardiac stress response to systemic inflammatory response, increase of LV preload by fluid resuscitation, decrease of LV afterload by reduced peripheral vascular resistance.

Acute stress-induced (takotsubo) cardiomyopathy

LV segmental contraction abnormalities and apical ballooning

Elevated levels of circulating plasma catecholamines and its metabolites, microvascular dysfunction, inflammation, estrogen deficiency, spasm of the epicardial coronary vessels, and aborted myocardial infarction.

Right ventricular (RV) enlargement and acute pulmonary hypertension

The end-diastolic area of right ventricular/left ventricular > 0.6. The interventricular septum protruded to the left ventricle, showing the “D-sign.” Decreased systolic and/or diastolic function of RV, changes in frequency and rhythm of pulmonary blood flow, tricuspid valve regurgitation.

The increase in pulmonary vascular resistance caused by hypoxia, pulmonary vasospasm, hypercapnia and inflammation; fluid overload; unsuitable mechanical ventilation parameter setting.

Diffuse myocardial inhibition

Decreased systolic and/or diastolic function of the whole heart.

Severe hypoxia, long term of anoxia and inflammation. The circulatory failure is often caused by diffuse cardiodepression after arrest and the decrease of vascular tension caused by lactic acidosis.