This study was designed to evaluate the sensitivity of changes in myocardial carbon dioxide and oxygen tensions as indicators of regional myocardial ischemia and also to determine to what extent these changes can be related to changes in intramyocardial ST segment voltage. Changes in ST segment voltage recorded in unipolar epicardial electrodes proved to be a less-sensitive indicator of underlying myocardial ischemia than were changes in ST segment voltage recorded in unipolar intramyocardial electrodes. In 9 dogs, regional ischemia was produced by placing a variable constrictor on the left circumflex coronary artery; circumflex flow was monitored. Myocardial carbon dioxide and oxygen tensions were measured using a mass spectrometer. Unipolar electrograms were recorded using a multicontact plunge electrode. With progressive degrees of proximal stenosis, ranging from a critical stenosis, which is associated with a decrease in mean flow of less than 15%, to a severe stenosis associated with and 80% decrease, ST voltage increased 21 mv and carbon dioxide tension increased 84 mm Hg, but oxygen tension decreased only 7 mm Hg. The study suggests that increases in intramyocardial ST segment voltage, an index of myocardial ischemia, are associated with parallel increases in myocardial carbon dioxide tension, each providing a more sensitive quantitative correlate of regional myocardial ischemia than do decreases in oxygen tension. The local accumulation of carbon dioxide may be an important pathophysiological mechanism in myocardial ischemia.

Changes in intramyocardial ST segment voltage and gas tensions with regional myocardial ischemia in the dog.

Oxygenated Fluosol-43 cardioplegia (CP), a perfluorocarbon with high oxygen solubility, was compared with crystalloid and oxygenated blood cardioplegia. Potassium in each CP was 25 mEq/l. Thirty perfused rabbit hearts in three groups of 10 hearts each underwent 100 minutes of global ischemia at 20 degrees C, followed by 45 minutes of reperfusion at 37 degrees C. During ischemia, CP was given every 20 minutes. With each CP injection, increases in myocardial oxygen tension were recorded using mass spectrometry and oxygen consumption (MVO2) was calculated. Left ventricular function was assessed before and after ischemia by measuring isovolumic developed pressure and dP/dt with an intraventricular balloon. Intramyocardial PO2 increased by 19.6 +/- 1.8 mm Hg in the Fluosol CP group, 0.4 +/- 0.1 mm Hg in the crystalloid CP group and 1.5 +/- 0.3 mm Hg in the blood CP group (p less than 0.001, Fluosol CP vs crystalloid CP and blood CP). MVO2 with each CP injection, expressed as ml O2/100 g dry weight, was 203.8 +/- 7.0 for Fluosol CP, 20.4 +/- 1.2 for crystalloid CP and 39.2 +/- 4.3 for blood CP (p less than 0.001 Fluosol CP vs crystalloid CP and blood CP). Recovery of maximal dP/dt after 45 minutes of reperfusion, expressed as a percentage of preischemic control, was 75.6 +/- 4.0% for Fluosol CP, 60.9 +/- 5.5% for crystalloid CP and 53.4 +/- 3.7% for blood CP (p less than 0.02 Fluosol CP vs blood CP and crystalloid CP). These data clearly show that the use of Fluosol cardioplegic solution enhanced oxygen delivery and use compared with blood and crystalloid cardioplegic solutions. The marked increase in intramyocardial oxygen and MVO2 with each injection of Fluosol CP shows that there is effective aerobic metabolic activity during ischemia, which may explain the improved functional recovery. The failure of blood CP to afford similar protection can be explained by a decreased oxygen release from hemoglobin due to the leftward shift of the oxygen-hemoglobin dissociation curve with hypothermia.

Superiority of perfluorocarbon cardioplegia over blood or crystalloid cardioplegia.

We have investigated the rate of rise of myocardial PCO2 (PmCO2) after coronary artery occlusion using a new method for this measurement. Previous studies of PmCO2 have been limited by the slow response of the only available method, and no increase in MmCO2 prior to 3 minutes after occlusion has been found. We have implanted a miniature PCO2 electrode, with a 63% response time of 14 seconds, into the left ventricle of 14 open-chest dogs. After abrupt coronary occlusion, PmCO2 began to rise in 13.6 +/- 1.1 seconds in heparinized dogs and in 7.5 +/- 0.7 seconds in unheparinized dogs. The subsequent magnitude of the increase in PmCO2 was 24, 88, 171, and 222 mm Hg at 2, 5, 10, and 15 minutes after occlusion. The rate of rise of PmCO2 was essentially linear from 1 minute to 10 minutes at a rate of 18.3 mm Hg/min. The rate of rise was slower during the first 30 seconds after occlusion (6.1 mm Hg/min) and also from 30 seconds to 1 minute (9.7 mm Hg/min). This rate of rise is much greater than that previously observed and reflects the severe myocardial acidosis developing during ischemia. A rise in PmCO2 is one of the earliest metabolic changes that has been observed during myocardial ischemia.

Rate of rise of myocardial PCO2 during early myocardial ischemia in the dog.

Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion An isolated, isovolumic, feline heart model was used to asses the effectiveness of nifedipine in both cardioplegic (100 microgram/10 ml) and noncardioplegic (10 microgram/10 ml) doses for providing myocardial preservation during 90 minutes of hypothermic ischemic arrest and 45 minutes of normothermic reperfusion Use of nifedipine was compared to hypothermia (27 degrees C) alone and to hypothermia with potassium cardioplegia Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured by mass spectrometry Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole The rates of rise of PCO were greatest in the group receiving 10 microgram nifedipine and in the control group The rates of rise in the 

Comparison of myocardial protection with nifedipine and potassium.

Intramyocardial pH as an index of myocardial metabolism during cardiac surgery.

The methodology for use of the mass spectrometer for the measurement of intramyocardial gas tensions in the canine preparation is described. Baseling studies were carried out initially in 36 animals, and control levels for myocardial oxygen tension and myocardial carbon dioxide tension were 19 mm Hg (S.D. 6 mm Hg) and 43 mm Hg (S.D. 10 mm Hg), respectively. Myocardial oxygen tension was not altered significantly by varying the arterial oxygen tension between 65 and 300 mm Hg. However, myocardial carbon dioxide tension increased linearly with increased arterial carbon dioxide tension. In 15 dogs placed on total cardiopulmonary bypass, a perfusion pressure 40-60 mm lower than the control mean arterial pressure resulted in myocardial ischemia with a decrease in myocardial oxygen tension and an increase in myocardial carbon dioxide tension. A subsequent increase in perfusion pressure to control levels resulted in resolution of ischemia and return of myocardial oxygen and carbon dioxide tensions to their control level. In another series of open-chest dogs on cardiopulmonary bypass, a proximal constriction applied to the left coronary circumflex artery resulted in a marked decrease in myocardial oxygen tensions and a marked increase in myocardial carbon dioxide tensions in the region supplied by the constricted vessel. In yet another series of open-chest dogs, it was found that incremental decreases in coronary flow established by constriction of the circumflex artery resulted in an exponential increase in both myocardial carbon dioxide tensions and ST-segment elevation as determined by a 25-gauge multi-contact plunge electrode placed in the posterior left ventricular wall. It appears that mass spectrometry techniques for evaluating myocardial ischemia have several advantages over myocardial biopsy techniques for assay of ATP and lactate, and also over the technique of coronary sinus lactate determination.

Mass spectrometry for the measurement of intramyocardial gas tensions: methodology and application to the study of myocardial ischemia.

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Mass spectrometry for the measurement of intramyocardial gas tensions: methodology and application to the study of myocardial ischemia.