Central neurogenic hyperventilation

Specialty: Respiratory.

• central neurogenic hypernea
• rapid, deep breathing of cerebral origin

Why it occurs

• Invasive tumor lesions located in the midbrain or upper pons (astrocytomas, glioblastomas that destroy the mechanisms of cortical and diencephalic inhibition of respiration, inducing continuous, rapid and deep hyperventilation that persists even during sleep and anesthesia)
• Severe head trauma with diffuse axonal damage in the upper brain stem
• Ischemic or hemorrhagic cerebrovascular accident (CVA) affecting the upper pontine pathways
• Diffuse cerebral anoxic encephalopathy after cardiorespiratory arrest
• Incipient central transtentorial herniation (mechanical compression of mesencephalic structures).

Initial workup

Computed tomography (CT) or urgent high-resolution brain magnetic resonance imaging (MRI) focused on the posterior fossa and brain stem; Immediate analytical arterial blood gas (confirm severe respiratory alkalosis with marked hypocapnia and elevated PaO2); Continuous electroencephalographic monitoring; Monitoring intracranial pressure (ICP) if indicated.

Standard management

• There are no specific drugs that safely inhibit the damaged respiratory center without risk of abrupt ventilatory stop; Deep sedation with continuous intravenous infusion of Propofol (1-4 mg/kg/hour) or Midazolam (0.05-0.2 mg/kg/hour) associated with controlled mechanical ventilation is usually required to normalize PaCO2 and blood pH.