Fig. 5

Systemic effect of cardiac arrest and clinical implications in the ventilator targets to achieve. Catecholamine release, with impaired mitochondrial metabolism, can activate immunology response. Neuronal and immune responses are rapidly activated during cardiac arrest and trigger a pathway of systemic neuroendocrine and immune responses which have important systemic consequences. Global cerebral ischemia and immunological disturbances induce microgliosis, damage of blood-brain barrier, and cerebrovascular system. Endothelial dysfunction and blood brain barrier permeability are crucial in above pathological processes. The brain-lung or brain-heart-lung couplings and their disturbances may be considered as modulator of post ischemic injury, peripheral inflammation, and multiorgan dysfunction, observed in post cardiac arrest patients. Post ischemic induction of necrosis, apoptosis, and systemic inflammation predisposes to neuronal damage and poor recovery. Pulmonary complications following cardiac arrest, through cerebral ischemia or immunological activation, can result in neurogenic pulmonary edema, ARDS, or pneumonia. The clinical consequences of these pathophysiological pathways are different according to three different phases: cardiac arrest, cardiopulmonary resuscitation, and post resuscitation. ARDS, acute respiratory distress syndrome