The role of cardiac dysfunction and post-traumatic pulmonary embolism in brain-lung interactions following traumatic brain injury

date, two theories have been developed to explain its occurrence: increased lung capillary permeability and increased pulmonary vascular hydrostatic pressure due to sympathetic overflow. It has been observed that catecholamine storms lead to a state of systemic vasoconstriction with strong venoconstriction, resulting in the induction of elevated pulmonary artery wedge pressure and hydrostatic PE. However, besides these two hypotheses, NPE can also result from cardiac dysfunction [2]. Therefore, we propose a new hypothesis that cardiac dysfunction is due to TBI rather than PE due to existing chronic heart failure.