Minimal coronary stenoses and left ventricular blood flow during CPR.
OBJECTIVE
To assess the effect of a 33% coronary stenosis on myocardial blood flow during normal sinus rhythm and CPR.


METHODS
Prospective, before and after cardiac arrest and CPR; before and after creation of a 33% stenosis.


METHODS
The University of Arizona Resuscitation Research Laboratory.


METHODS
Ten domestic closed-chest swine with patent coronary stenoses.


METHODS
A Teflon cylinder was placed in the mid-left anterior descending coronary artery to create a 33% stenosis. Myocardial blood flow was measured with colored microspheres both proximal and distal to the stenosis during normal sinus rhythm and during CPR.


RESULTS
During normal sinus rhythm, the stenosis did not alter the amount of myocardial blood flow distribution or quantity. Proximal to the stenosis the endocardial/epicardial flow ratio was 1.49 +/- 0.33, and distal to the stenosis it was 1.50 +/- 0.50. Likewise, during normal sinus rhythm, blood flow proximal and distal to the stenosis did not differ for either the epicardium (79 +/- 9 versus 66 +/- 13 mL/min/100 g) or the endocardium (111 +/- 27 versus 83 +/- 19 mL/min/100 g). However, the distribution of myocardial blood flow was markedly altered during CPR. The resultant endocardial/epicardial flow ratios were significantly less than during normal sinus rhythm, 0.49 +/- 0.11 (three minutes of CPR) and 0.74 +/- 0.07 (eight minutes of CPR) proximal to the stenosis and 0.39 +/- 0.15 (three minutes of CPR) and 0.49 +/- 0.14 (eight minutes of CPR) distal to the stenosis (P less than .05 versus normal sinus rhythm). In the presence of a 33% mid-left anterior descending coronary artery stenosis, endocardial blood flow at eight minutes of CPR was significantly lower distal to the stenosis compared with proximal to the stenosis (23 +/- 7 mL/min/100 g versus 74 +/- 18 mL/min/100 g; P less than .02).


CONCLUSIONS
Minimal coronary lesions that do not diminish myocardial perfusion during normal physiologic conditions appear to significantly decrease subendocardial blood flow during cardiac arrest and CPR.
Kern
K B
KB
Department of Internal Medicine, University of Arizona College of Medicine, University Medical Center, Tucson.
Ewy
G A
GA
D000818:Animals; D000829:Animals, Domestic; D001783:Blood Flow Velocity / Q000502:physiology; D016887:Cardiopulmonary Resuscitation; D003251:Constriction, Pathologic; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels; D006323:Heart Arrest / Q000503:physiopathology* / Q000628:therapy; D006439:Hemodynamics; D011446:Prospective Studies; D013552:Swine; D016277:Ventricular Function, Left / Q000502:physiology*