hypercapnia - or controlled mechanical hypoventilation - is a ventilation
strategy, whereby priority is given to the prevention or limitation of
severe pulmonary hyperinflation over the maintenance of normal alveolar
ventilation, provided oxygenation is preserved. Tidal volumes are adjusted
to prevent hyperinflation and increased airway pressures. Allowing alveolar
hypoventilation will invariably lead to hypercarbia and respiratory acidosis.
Several investigators have reported that hypoventilation is safe and may
improve outcome. The resulting acidosis is less severe and the elevation
in arterial PCO2 is generally well tolerated, when carbon dioxide levels
are allowed to increase gradually.
effects of hypercapnia:
diffuses across cell membranes and leads to the formation of carbonic
acid and generation of hydrogen ions. Fortunately, intracellular buffering
is rapid, reaching 90% completion within three hours after the onset of
hypercapnia increases sympathetic nervous system discharge. As a result,
plasma levels of epinephrine and norepinephrine rise, leading to increased
myocardial contractility and cardiac output but also increased risk for
on central nervous system
leads to cerebral vasodilation, increased intracranial pressure, and lowering
of the seizure threshold.
hypoventilation has the potential for lowering the arterial PO2. Although
the use of supplemental oxygen allows for substantial reduction of minute
ventilation without jeopardizing oxygenation. In addition, hypercapnic
acidosis shifts the oxyhemoglobin dissociation curve to the right, thereby
promoting oxygen release at the tissue level.
uncontrolled studies suggest that permissive hypercapnia is an acceptable
strategy for limiting airway pressures and avoiding volutrauma in patients
with acute lung injury. However, controlled randomized trials are lacking.
How low a pH and how high a pCO2 can be safely tolerated is unknown. A
pH >7.24 is widely accepted, but pHs as low as 7.05 have been accepted
without obvious adverse effects. Hypercarbia is generally not harmful,
provided that oxygenation is preserved and conditions of increased susceptibility
of respiratory acidosis are avoided. Because of its effect on cerebral
vascular tone and seizure threshold, permissive hypercapnia is contraindicated
in patients with cerebrovascular disease, trauma, space-occupying intracranial
lesions and seizure disorders. Further data are needed concerning the
safety of hypercapnia in patients with coronary artery disease and heart