Letters t» tk

Editor

The Apnea-PaCO,

Relationship-Unanswered

‘To the Editor: Though with some delay, we read with great interest the papers of Stock and coworkers’,’ and the additional editorial of Shapiro,” prompting US to give some additional remarks to the subject of rapid PaCO, increase at the start of hyperoxic apnea. Some years ago we observed the same phenomenon in our cardiac surgery patients and presented our observations in 1987 at the Centra1 European Congress of Anaesthesiology,” and at the 1988 10th Annual Meeting of the Society of Cardiovascular Anesthesiologists in New Orleans. The rapid initial increase of PaCO,, for example, during intubation apnea, is only the tip of the iceberg. What was much more fascinating for US was the in-

paC

Questions? creasing positive differente between arterial and mixed-venous PCOr: almost after 25 seconds of apnea PVCO, decreases PaC02! The corresponding behavior can be observed for the pH. In two subsequent publications”,” we described the Christiansen-Douglas-Haldane effect (CDH-effect) as the main reason for the initial fast increase of PaC02 during apnea-besides ongoing CO,-production in the tissue and veno-arterial equilibration of partial pressures-and as the only reason for the observed (Figures 1-4). PU),- and pH-reversal The CDH-effect describes the dependence of’ CO, absorption by blood on the degree of hemoglobin oxygenation: oxygenated hemoglobin as compared to deoxygenated hemoglobin has a reduced CO, binding capacity due to its increased acidity. During the condition of hyperoxic apnea, i.e., continuous oxygen uptake without CO, delivery by the lungs, the PaCO,

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Figure 1. Changes of PaCO, and PYCO, during the first 2 min of hyperoxic apnea. Arterial and mixed venous blood samples (1.5 ml each) were taken sequentially immediately before ( - 5) and during the first 2 min of apnea (12 samples, each withdrawn 10 sec). For more information, refer to references 6 and 8. (Reprinted with permission from Brandt L, Mertzlufft F, Dick W: Arterial and mixed venous blood gases during early intubation apnea. Clinical evidente of the Christiansen-Douglas-Haldane effect. Amesthes& 1989; 38: 167-73.)

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Figure 2. Changes of pHa and pHv during the first 2 min of hyperoxic apnea. (Reprinted with permission from Brandt L, Mertzlufft F, Dick W: Arterial and mixed venous blood gases during early intubation apnea. Clinical evidente of the Christiansen-Douglas-Haldane effect. Anuesthesi~t 1989; 38: 167-73.)

. I.elters

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the Editor

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Figure 3. ArteriaUmixed venous PCO, differente (avDPC0,) during the fïrst 2 min of hyperoxic apnea. (Reprinted with permission from Brandt L, Mertzlufft F, Dick W: Arterial and mixed venous blood gases during early

intubation apnea. Clinical evidente of the ChristiansenDouglas-Haldane effect. Anaesthesist 1989;38: 167-73.)

wil1 not only approximate the PYCO, but wil1 even exceed it. Without the CDH-effect, rapid adjustment of PaCO, to PVCO, would be expected during apnea due to the lack of CO, excretion. If, however, ongoing oxygenation (high PaO,) with concomitant lack of CO, remains delivery (apnea, i.e., the CO, concentration constant during lung passage of the blood) leads to a continuing sufficient oxygenation of blood during its passage through the lung capillaries, then this leads to a rightward shift of the CO, binding curve, the CDH-effect. The problem has already been recognized and solved, although documented mainly in German language journals. A knowledge of languages is always beneficial, as we find when studying American journals. But, as we know that the German language is very hard to learn, we published our results in English as well.7,x Ludwig

Brandt, MD, PhD

Klinik für Anaesthesiologie Johannes Gutenberg-Universität D-6500 Mainz, Germany Friedrich

Mertzlufft,

MD

Klinik für Anaesthesiologie Universitätskliniken des Saarlandes D-6650 Homburg-Saar, Germany

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Figure 4. Arterialimixed venous pH differente (avDpH) during the fitst 2 min of hyperoxic apnea. (Reprinted with permission from Brandt L, Mertzlufft F, Dick W: Arterial and mixed venous blood gases during early intubation apnea. Clinical evidente of the Christiansen-Douglas-Haldane effect. Anaesth~.~ist 1989;38: 167-73.)

References 1. Stock MC, DownsJB, McDonald JS: The carbon dioxide rate of rise in awake apneic humans. J Clin Anesth 1988;1:96-103. 2. Stock MC, Schisler JQ, McSweeney TD: The PaCO, rate of rise in anesthetized patients with airway obstruction. J Clin Anesth 1989;1:328-32. relationship: some clin3. Shapiro BA: The apnea-PaCO, ical and medico-legal considerations (Editorial). J Clin Anesth 1989; 1:323-7. 4. Mertzlufft FO, Rudlof B, Jantzen AH, Brandt L, Dick W: Christiansen-Douglas-Haldane-effect: also in vivo? (Abstract). Anaesthesist 1987;36(Suppl):374. FO, Rudlof B, Dick W: Christian.5. Brandt L, Mertzlufft sen-Douglas-Haldane effect under clinical conditions in vivo. Anaesthesist 1988;37:529-34. 6 Brandt L, Mertzlufft F, Dick W: Arterial and mixedvenous bloed gases during early intubation apnea. Clinical evidente of the Christiansen-Douglas-Haldane effect. Anaesthesist 1989;38: 167-73. 7 Mertzlufft FO, Brandt L, Stanton-Hicks M, Dick W: Arterial and mixed venous blood gas status during apnoea of intubation-proof of the Christiansen-Douglas-Haldane Effect in vivo. Anaesth Intensive Care 1989; 17:32531. F, Brandt L: Blood CO, and pH transients 8. Mertzlufft during apnoea after 0, breathing in patients. Adv Exp Mrd Bio1 1990;249 (in press).

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The apnea-PaCO2 relationship--unanswered questions?

Letters t» tk Editor The Apnea-PaCO, Relationship-Unanswered ‘To the Editor: Though with some delay, we read with great interest the papers of Sto...
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