Hyperoxic ventilation at the critical hematocrit: effects on myocardial perfusion and function.
BACKGROUND
Hemodilution reduces hematocrit (Hct) and blood oxygen content. Tissue oxygenation is mainly preserved by increased cardiac output. As myocardial O2-demands increase, coronary vasodilatation becomes necessary to increase myocardial blood flow. Myocardial ischemia occurs at a critical Hct-value (Hctcrit), with accompanying exhaustion of coronary reserve. Hyperoxic ventilation is known to both reverse peripheral tissue hypoxia at Hctcrit and also to induce coronary vasoconstriction. This study aimed to determine whether hyperoxic ventilation at Hctcrit further exacerbates myocardial ischemia and dysfunction.


METHODS
Nine anesthetized pigs ventilated on room air were hemodiluted by 1:1 exchange of blood with pentastarch (6%HES) to Hctcrit, defined as onset of myocardial ischemia (ECG changes). At Hctcrit, hyperoxic ventilation was started. Measurements were performed at baseline, at Hctcrit, and after 15 min of hyperoxic ventilation. We determined myocardial blood flow (microsphere method), arterial O2-content, subendocardial O2-delivery and myocardial function (left ventricular pressure increase).


RESULTS
At Hctcrit 7 (6;8)%, O2-content was reduced [3.7 (3.1;3.9) ml dl(-1)]. Despite a compensatory increase of myocardial blood flow [531 (449;573), ml min(-1)100 g(-1)], all pigs displayed myocardial ischemia and compromised myocardial function (P < 0.05). Hyperoxic ventilation produced increased coronary vascular resistance secondary to vasoconstriction, and reduced myocardial blood flow [426 (404;464), ml min(-1)100 g(-1); P < 0.05]. Myocardial oxygenation was found to be maintained by increased O2-content [4.4 (4.2;4.8), ml dl(-1); P < 0.05], the contribution of dissolved O2 to subendocardial O2-delivery increased (32 vs. 8%; P < 0.05), which preserved myocardial function.


CONCLUSIONS
Hyperoxic ventilation at Hctcrit is followed by coronary vasoconstriction and reduction of coronary blood flow. However, myocardial oxygenation and function is maintained, as increased O2-content (in particular dissolved O2) preserves myocardial oxygenation.
Institute for Surgical Research, Ludwig-Maximilians-University Munich, Germany. Gregor.Kemming@med.uni-muenchen.de
G I
GI
Kemming
F G
FG
Meisner
J
J
Meier
J
J
Tillmanns
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Thein
J
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Eriskat
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Habler
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D004562:Electrocardiography / Q000187:drug effects; D006321:Heart / Q000503:physiopathology*; D006334:Heart Function Tests; D006400:Hematocrit; D006438:Hemodilution; D006895:Hydroxyethyl Starch Derivatives / Q000627:therapeutic use; D018496:Hyperoxia / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000503:physiopathology; D010101:Oxygen Consumption / Q000502:physiology; D010102:Oxygen Inhalation Therapy / Q000009:adverse effects; D010952:Plasma Substitutes / Q000627:therapeutic use; D012121:Respiration, Artificial; D013552:Swine; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology
D006895:Hydroxyethyl Starch Derivatives; D010952:Plasma Substitutes