Systemic oxygen uptake during experimental closed-chest cardiopulmonary resuscitation using air or pure oxygen ventilation.
BACKGROUND
Although clinical cardiopulmonary resuscitation always includes ventilation with pure oxygen, this kind of ventilation has been reported to be associated with worse neurological outcome than ventilation with air in experimental cardiopulmonary resuscitation (CPR). The aim of the present investigation was to compare the systemic oxygen uptake during experimental closed-chest CPR including ventilation with pure oxygen or ambient air and, furthermore, to elucidate possible mechanisms of action in the regulation of pulmonary gas exchange.


METHODS
In 24 anesthetized piglets, 2 min of induced ventricular fibrillation and no ventilation was followed by 10 min of closed-chest CPR including i.v. administration of 0.5 mg adrenaline (at 8 min), and in one of the experimental groups alkaline buffer (at 5 min). The piglets were randomly divided into 3 groups: air ventilation during the entire CPR period with saline administration (n=8), air ventilation during the entire CPR period plus tris buffer mixture (n=8), and air ventilation for 3 min followed by 100% oxygen with saline administration (n= 8).


RESULTS
In the group ventilated with air and treated with tris buffer mixture, cardiac output was significantly greater than in the group ventilated with pure oxygen. The arterial-mixed venous oxygen content difference was approximately 25% greater with pure oxygen than with air ventilation; however, there was no difference in systemic oxygen uptake. Systemic oxygen uptake increased after administration of tris buffer mixture in the group ventilated with air.


CONCLUSIONS
Pulmonary hypoxic vasoconstriction appeared to be abolished during CPR including pure oxygen ventilation. Blood flow, not ventilation or pulmonary gas exchange, is the limiting factor during experimental closed-chest CPR.
Rubertsson
S
S
Department of Anesthesiology and Intensive Care, Uppsala University Hospital, Sweden.
Karlsson
T
T
Wiklund
L
L
D000322:Adrenergic Agonists / Q000008:administration & dosage / Q000627:therapeutic use; D000388:Air; D000704:Analysis of Variance; D000818:Animals; D001775:Blood Circulation / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002021:Buffers; D002302:Cardiac Output / Q000502:physiology; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D004837:Epinephrine / Q000008:administration & dosage / Q000627:therapeutic use; D000860:Hypoxia / Q000503:physiopathology; D007275:Injections, Intravenous; D009460:Neurologic Examination; D010100:Oxygen / Q000008:administration & dosage* / Q000009:adverse effects / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology*; D011651:Pulmonary Artery / Q000503:physiopathology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D011897:Random Allocation; D012121:Respiration, Artificial / Q000379:methods*; D012965:Sodium Chloride; D013552:Swine; D013566:Sympathomimetics / Q000008:administration & dosage / Q000627:therapeutic use; D016896:Treatment Outcome; D014325:Tromethamine; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014692:Ventilation-Perfusion Ratio / Q000502:physiology; D014693:Ventricular Fibrillation / Q000628:therapy
D000322:Adrenergic Agonists; D002021:Buffers; D013566:Sympathomimetics; D014325:Tromethamine; D012965:Sodium Chloride; D010100:Oxygen; D004837:Epinephrine