Permissive hypercapnia is the deliberate limitation of ventilator support to avoid alveolar overdistension, allowing Paco2 levels greater than normal (50-100 mm Hg). Allowing the Paco2 to rise to these levels should be considered when the only alternative is a potentially dangerous increase in alveolar distending pressure or significant levels of auto-PEEP. The potential adverse effects of an elevated Paco2 are listed in Table 2-1. Most of the more important clinical problems occur at Paco2 levels above 150 mm Hg. However, even small increases in Paco2 increase cerebral blood flow and permissive hypercapnia is generally contraindicated when intracranial pressure is increased (eg, acute head injury). Elevated Paco2 also stimulates ventilation and may contribute to asynchrony, but patients are usually sedated when permissive hypercapnia is used.
Table 2-1Physiologic Effects of Permissive Hypercapnia ||Download (.pdf) Table 2-1 Physiologic Effects of Permissive Hypercapnia
• Shift of the oxyhemoglobin dissociation curve to the right
• Decreased alveolar
• Stimulation and depression of the cardiovascular system
• Central nervous system depression
• Increased ventilatory drive
• Pulmonary vasoconstriction (pulmonary hypertension)
• Systemic vasodilatation (systemic hypotension)
• Increased intracranial pressure
• Anesthesia ( > 200 mm Hg)
• Decreased renal blood flow ( > 150 mm Hg)
• Leakage of intracellular potassium ( > 150 mm Hg)
Permissive hypercapnia may adversely affect oxygenation in some patients. Elevated Paco2 and acidosis shift the oxyhemoglobin dissociation curve to right. This decreases the affinity of hemoglobin for oxygen, decreasing oxygen loading in the lungs but facilitating unloading of oxygen at the tissues. As illustrated by the alveolar gas equation, an increase in alveolar Pco2 results in a decrease in alveolar Po2. For each Paco2 rise of 1 mm Hg, the Pao2 decreases by about 1 mm Hg. When permissive hypercapnia is allowed, optimal efforts to maximize oxygenation should be used.
As illustrated in Figure 2-1, carbon dioxide stimulates or depresses some parts of the cardiovascular system, but opposite effects can occur via stimulation of the autonomic nervous system. It is thus difficult to predict the precise response of the cardiovascular system to permissive hypercapnia. An increase in Pco2 might cause pulmonary hypertension and it might affect cardiac output. Rarely, pharmaceutical agents might need to be adjusted in the presence of permissive hypercapnia, but this is usually the result of acidosis and not the elevated Pco2 per se.
This diagram illustrates the complexity of the mechanisms by which carbon dioxide influences the circulatory system. See text for details. (Reproduced with permission from Nunn JF. Carbon dioxide. In: Nunn JF, ed. Applied Respiratory Physiology. 2nd ed. London, UK: Butterworth and Co.; 1977:334–374.)
The primary factor limiting permissive hypercapnia is the acidosis that results. Patients without significant comorbid conditions usually tolerate a pH as low as 7.20, and previously healthy patients may tolerate an even lower pH. The specific acceptable pH needs to be determined on an individual patient basis. If Paco2 increases gradually, renal compensation can occur. Abrupt changes in ventilation that result in rapid and marked elevation of Paco2 are more poorly tolerated.
Whether buffers should be administered to manage the acidosis induced by permissive hypercapnia is debatable. The use of sodium bicarbonate in the setting of permissive hypercapnia has not been extensively studied. One might expect a short-term increase in carbon dioxide load when sodium bicarbonate is administered, which is exhaled over time if the level of ventilation is held constant. An alternative buffer is THAM, which does not generate CO2 and produces intracellular as well as extracellular buffering of pH. THAM can actually result in a decrease in Pco2.
Cautious use of permissive hypercapnia is recommended only when the VT and Pplat targets have been met and respiratory rate cannot be increased further. There does not seem to be any significant short-term adverse effect in the majority of patients. However, what is not known is if there are any long-term effects of permissive hypercapnia.