title: Metabolic monitoring during continuous warm- and cold-blood cardioplegia by means of myocardial tissue pH and PO2.
abstract: OBJECTIVE
  To study the changes in myocardial tissue pH and PO2 during cold- and warm-blood cardioplegic arrests.
  
  
  METHODS
  An experimental study in dogs.
  
  
  METHODS
  Nine dogs underwent the following procedures: 30 minutes with an empty heart beating under cardiopulmonary bypass (control period); 30 minutes of warm (33 degrees C) cardioplegic arrest with a 1:4 mix of crystalloid in blood solution administered continuously at 150 mL/min; 30 minutes of cold (15 degrees C) cardioplegic arrest; and 30 minutes of myocardial reperfusion. The cardioplegic blood solution was administered antegradely through the ascending aorta.
  
  
  METHODS
  Tissue pH and PO2. Arterial and coronary sinus oxygen content and myocardial consumption calculated.
  
  
  RESULTS
  There was a modest but significant increase in the left anterior descending (LAD) and circumflex (Cx) tissue pH throughout the experiment. PmO2 in the LAD territory averaged 44 (7) mm Hg (mean and standard error of the mean) during the bypass period, 123 (23) mm Hg at the termination of warm cardioplegic arrest, 146 (28) mm Hg at the end of cold arrest and 66 (17) mm Hg after reperfusion. Oxygen consumption averaged 0.65 (0.15) mL/min during the bypass period, 0.3 (0.18) mL/min at the end of warm arrest, 0.25 (0.16) mL/min at the end of cold arrest and 0.45 (0.08) mL/min after reperfusion (p < 0.05). Oxygen delivery to the LAD territory was greater than myocardial oxygen consumption by an average of 2.02 (0.4) mL/min during bypass, 2.02 (0.62) mL/min after warm arrest, 2.12 (0.5) mL/min after cold arrest and 1.55 (0.25) mL/min after reperfusion (p > 0.05).
  
  
  CONCLUSIONS
  During cardioplegic arrest, tissue PO2 increased and oxygen consumption decreased significantly, whereas tissue pH remained normal, suggesting that continuous warm- and cold-blood cardioplegia maintained aerobic glycolysis during myocardial arrest. Thus, the increase in myocardial tissue PmO2 during cardioplegic arrest reflects the decrease in myocardial oxygen consumption while maintaining oxygen supply.
authors.affiliation: Department of Surgery, Université de Montréal, Que.
authors.forename: M
authors.initials: M
authors.lastname: Carrier
authors.forename: S
authors.initials: S
authors.lastname: Trudelle
authors.forename: A
authors.initials: A
authors.lastname: Khalil
authors.forename: L C
authors.initials: LC
authors.lastname: Pelletier
mesh_terms: D000818:Animals; D002314:Cardioplegic Solutions / Q000008:administration & dosage*; D002315:Cardiopulmonary Bypass; D003080:Cold Temperature; D004285:Dogs; D006324:Heart Arrest, Induced / Q000379:methods*; D006358:Hot Temperature; D006863:Hydrogen-Ion Concentration; D008991:Monitoring, Physiologic; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D010101:Oxygen Consumption
chemical_list: D002314:Cardioplegic Solutions