SUMMER 2010

Hypercapnia: The Changing Story

Myra Aultman CRNA and Gwendolyn Boyd MD
University of Alabama at Birmingham, Callahan Eye Foundation Hospital

Anesthesia providers have traditionally ventilated patients with 10-12 ml/kg tidal volumes resulting in a target EtCO2 ranging from 30-35 mm Hg. However, more recently, the beneficial effects of "permissive hypercarbia or hypercapnia" have been demonstrated to reduce acute lung injury (ALI) as well as to improve peripheral tissue oxygenation in morbidly obese patients. [1,2]

Hager et.al. [2] reported that maintaining an EtCO2 of 50 mm Hg, described as "mild hypercapnia", would reduce the risk of wound infection in morbidly obese patients. The risk of surgical infection increases as tissue oxygen partial pressures decrease because neutrophils, which contain an oxidase enzyme, can no longer function optimally as phagocytes in an environment of reduced oxygenation. [3] An environment of decreased tissue oxygenation can also occur during hypothermia or perioperative cigarette smoking. [2] Moreover, the tissue oxygenation in morbidly obese patients is much reduced as compared to that of lean individuals. [4] Therefore, morbidly obese patients are at less risk for surgical wound infection with an EtCO2 of 50 mmHg because of the beneficial effects of carbon dioxide on increasing cardiac output and causing peripheral vasodilation. [2]

A reduced risk of barotrauma (lung stretch or damage from shear forces) is accomplished in obese patients or patients with ARDS when patients are ventilated with tidal volumes of 6-8 mg/kg and a respiratory rate of 10 breaths per minute (bpm), while maintaining a peak inspiratory pressure (PIP) of less than 45 cm H2O. [5] This can also result in a favorable environment of mild hypercarbia (as indicated by an increased EtCO2) leading to better tissue oxygenation secondary to peripheral vasodilation and an increased cardiac index. [2] Although lung injury still occurs, lower peak pressure ventilation results in a reduction in mortality according to results from the ARDS Network study. [4] Barotrauma is also seen in COPD patients during ventilatory support which is associated with high peak pressures and variable transalveolar pressure and alveolar distention. [7] Moreover, there is unpredictable gas distribution as a result of positive pressure ventilation at high peak pressures which causes overdistention of some alveoli while allowing consolidation of other alveoli. [5, 8] This maldistribution of ventilation is most evident with lung diseases such as COPD and ARDS.

Another major disadvantage of hyperventilation occurs during cardiopulmonary resuscitation. The effectiveness of CPR is reduced when venous blood return to the right heart is prevented with the lack of chest wall recoil during hyperventilation and positive pressure ventilation. When negative intrathoracic pressure is not allowed, coronary perfusion pressure is reduced, leading to an increased likelihood of death. [9]

"Permissive hypercarbia is a technique that refers to a strategy of ventilation that allows the arterial carbon dioxide levels to rise in a controlled fashion in order to reduce lung injury at the expense of gas exchange. [10] Hypercapnic acidosis attenuates the inflammatory responses and barotrauma that sometime result from previously accepted tidal volumes during mechanical ventilation. [10]

The PaCO2 is the most effective regulator of the diameter of the blood vessels in the brain. It has been a traditional practice to hyperventilate neurosurgical patients (to an EtCO2 of 24 mm Hg or a PaCO2 of 30 mg Hg) for craniotomy in order to reduce the diameter size of those vessels allowing for a decrease in intracranial pressure. However, the reduction in the size of the arterioles, while reducing intracranial mass, also increases cerebral vasculature resistance causing a reduction in blood flow. Could the combination of positive pressure ventilation, which causes a decrease in venous return and cardiac output, and reduced cerebral blood flow as a result of hyperventilation, play a role in post-operative cognitive dysfunction? Hypocapnia as a result of hyperventilation has been shown to reduce cerebral blood flow during cognitive effort. [11] Moreover, specific to our practice of ophthalmic anesthesia, vasoconstriction and reduced blood flow may interfere with the perfusion of the retina, which is supplied by choroidal and central retinal arterial circulation. [12]

Finally, hyperventilation, with resultant reduction in arterial CO2, can diminish a patient's respiratory drive until "metabolic activity can replenish CO2 levels" as well as “trap” opioids in brain tissue. [13] This occurs because respiratory alkalosis, as a result of hyperventilation, alters the lipid solubility of a drug such as fentanyl. [14] Fentanyl becomes more lipid soluble with an increasing pH, so that it is not only better able to cross the blood-brain barrier but also more readily binds to brain tissue. [13] Increased fentanyl binding in addition to entry across the blood brain barrier can result in a reduced need for additional analgesia in the post-operative patient. Additional dosages of fentanyl during this period could place these patients at risk for respiratory arrest, even if they seem fully awake and alert.

A literature review by Hill and Joshi [15] evealed that mild hypercapnia, defined as EtCO2 of 40 mm Hg or higher, could be beneficial unless in an environment of elevated intracranial pressure or hypercapnic respiratory acidosis. The authors wrote that mild hypercapnia “should become a standard of care, except with the caveats previously described.” [15]

In summary:

• Hyperventilation can cause decrease coronary perfusion pressure which can be lethal during CPR.
• Hypocarbia and hyperventilation at high peak pressures in morbidly obese critically ill patients with ARDS or COPD can result in reduced tissue oxygenation and barotrauma.
• Hypocarbia and hyperventilation (due to increased cerebral arterial resistance) may be associated with cognitive dysfunction during the perioperative period.
• Hyperventilation and hypocarbia can result in decreased respiratory drive.
• Hyperventilation and hypocarbia can result in opioid trapping in brain tissue which can put a patient at risk for a respiratory arrest in the perioperative period.
• Mild hypercarbia (50 mm Hg) is beneficial in reducing wound infection in morbidly obese patients.
• Mild hypercarbia (50 mm Hg) results in improved lung function in critically ill patients.

References

1. Laffey J.G., O'Croinin, D., McLoughlin, P., Kavanagh, B.P. Permissive hypercapnia-role in protective lung ventilatory strategies. Intensive Care Med (2004).30:347-356.

2. Hager,H., Reddy, D., Mandadi,G., Pulley,D. Eagon,J.C., Sessler, D.I., Kurz, A. Hypercapnia improves tissue oxygenation in morbidly obese surgical patients. Anesth Analg (2006); 103(3): 677-681.

3. Roos, D., van Bruggen, R. Meischi, C. Oxidative killing of microbes by neutrophils. Microbes Infect November 2003; 5(14): 1307-1315.

4. Kabon, B., Nagele, A., Reddy,D. Eagon, C., Fleshman, J.W., Sessler,D.I., Kurz, A. Obesity decreases perioperative tissue oxygenation. Anesthesiology (Feb. 2004); 100(2): 274-280.

5. Lee WL Slutsky AS Ventilator induced lung injury and recommendations for mechanical ventilation of patients with ARDS (2001) Semin Resp Crit Care Med 22: 260-280

6. Soni, N., Williams, P. Positive pressure ventilation: what is the real cost? Br. J Anaesth, 2008; 101 (4): 446-57.

7. Gammon,B., Shin,M. S., Buchalter,S.E. Pulmonary barotrauma in mechanical ventilation: patterns and risk factors. Chest, 1992. 102(2): 568-575.

8. Gali, B., Goyal, D.G. Positive pressure mechanical ventilation. Emerg Med Clin North Am, 2003. 21: 453-473.

9. Aufderheide, T.P., Lurie, K.G. Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med., 2004; 32 (9 supplement): S345-S351.

10. Malhotra, A., Kacmarek, R.M. Mechanical Ventilation. Benumof's Airway Management, 2nd ed. (editor Carin A. Hagberg). Philadelphia, Mosby Elsevier, 2007; p. 1115.

11. Debreczeni,R. Amrein, I., Kamondi, A., Szirmai, I. Hypocapnia induced by involuntary hyperventilation during mental arithmetic reduces cerebral blood flow velocity. Tohoku J. Exp. Med., 2009, 217(2): 147-154.

12. Wang L., Cull G., Fortune,B., Cioffi, G.A.Retinal and choroidal vasoreactivity to altered PaCO2 in rat measured with a modified microsphere technique. Exp Eye Res (2008); 86: 908-913.

13. Coleman, L.S. Intraoperative hyperventilation may contribute to postop opioid hypersensitivity. APSF Newsletter Winter 2009-2010. Letter to the editor, p. 62.

14. Ainsile,S.G., Elsele,J.H., Corkill,G. Fentanyl concentrations in brain and serum during respiratory acid-base changes in the dog. Anesthesiology 1979; 51 p. 293-297.

15. Hill, G.E., Joshi, G.P. Intraoperative end tidal carbon dioxide concentrations: what is the target? American Society of Anesthesiologists Newsletter. April 2009;73(4):12-