Hemodynamic effects of epinephrine in combination with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation.
OBJECTIVE
To evaluate the hemodynamic actions of epinephrine combined with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation (CPR).


METHODS
Prospective, randomized, controlled trial.


METHODS
Experimental animal laboratory in a university hospital.


METHODS
A total of 28 anesthetized piglets.


METHODS
After catheterization and application of a pulmonary artery flow probe (transit-time ultrasound flowmetry), the animals were stabilized. Induction of ventricular fibrillation was followed by a 15-min period of CPR, including manual heart compressions and mechanical ventilation with pure oxygen. On commencement of CPR, a 4-min alkaline buffer infusion began, with 50 mmol of sodium bicarbonate (n = 7), tris buffer mixture (n = 7), or tris buffer (n = 7), or, as a control (n = 7), the same volume of normal saline. After 8 mins of CPR, 0.5 mg of epinephrine was given intravenously; after 15 mins, direct current shocks were used to revert the heart to sinus rhythm.


RESULTS
Blood flow measured in the pulmonary artery during open-chest CPR was approximately 20% of normal cardiac output. Administration of epinephrine reduced pulmonary artery flow irrespective of buffer. Sodium bicarbonate alone resulted in higher systemic blood pressure than pure tris: tris buffer mixture and normal saline were intermediate. Sodium bicarbonate combined with epinephrine tended to produce lower systemic blood pressure than other combinations.


CONCLUSIONS
Experimental open-chest CPR generates pulmonary artery blood flows (20% of normal cardiac output) that are at best at the lower level of those blood flow rates previously reported (25% to 40% of normal cardiac output) from studies of closed-chest CPR. Different alkaline buffers influence circulatory and acid-base parameters differently before and after administration of epinephrine.
Rubertsson
S
S
Department of Anesthesiology and Intensive Care, Uppsala University Hospital, Sweden.
Wiklund
L
L
D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002021:Buffers; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000187:drug effects; D016887:Cardiopulmonary Resuscitation; D004837:Epinephrine / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects*; D006863:Hydrogen-Ion Concentration; D010100:Oxygen / Q000097:blood; D011446:Prospective Studies; D011651:Pulmonary Artery / Q000502:physiology; D011652:Pulmonary Circulation / Q000187:drug effects; D012964:Sodium / Q000494:pharmacology; D017693:Sodium Bicarbonate; D013552:Swine; D014325:Tromethamine / Q000494:pharmacology
D001639:Bicarbonates; D002021:Buffers; D014325:Tromethamine; D002245:Carbon Dioxide; D017693:Sodium Bicarbonate; D012964:Sodium; D010100:Oxygen; D004837:Epinephrine