Limit to cardiac compensation during acute isovolemic hemodilution: influence of coronary stenosis

Abstract

We assessed limit to cardiac compensation during isovolemic hemodilution (HD) in 14 anesthetized dogs. Radioactive microspheres were used to evaluate myocardial blood flow (MBF) and its transmural distribution (endo/epi). Myocardial O2 consumption (MVO2) and percent lactate extraction were determined. Coronary vasodilator reserve was assessed from reactive hyperemic responses. Dogs were divided into group 1, with intact left anterior descending coronary artery (LAD), and group 2, with critical stenosis of LAD. Measurements were obtained at baseline and during graded HD (Hespan) until cardiac failure (CF). CF occurred at lower hematocrit in group 1 compared with group 2 (9 +/- 1 vs. 17 +/- 1%). In group 1, MBF increased during HD to maintain MVO2 constant; increases in MBF were transmurally uniform until CF, when decreased endo/epi and lactate production suggested subendocardial ischemia. Coronary vasodilator reserve decreased progressively during HD and was absent at CF. In group 2, stenotic LAD demonstrated constant MBF (resulting in decreased MVO2) during HD. At CF, these responses along with reduced endo/epi and lactate production indicated local myocardial ischemia. We conclude that 1) with normal coronary circulation, cardiac function was well maintained over a wide range of hematocrits because increases in MBF were transmurally uniform and sufficient to maintain myocardial oxygenation: CF occurred during extreme HD when MBF became maldistributed, resulting in subendocardial ischemia; 2) critical coronary stenosis impaired coronary vascular adjustment to HD and reduced significantly tolerance of left ventricle to HD; and 3) present findings underscore the importance of recruitment of coronary vasodilator reserve in preserving total and regional myocardial oxygenation during HD.

L’hémodilution ne modifie pas les effets vasodilatateurs coronariens de l’oxyde nitrique endogène ou exogène

“…Previous findings from our laboratory have demonstrated a remarkable capacity of the coronary circulation to increase its blood flow during ANH, as needed to maintain myocardial oxygen supply and contractile function. 17,18 Whereas previous studies have suggested a role for reduced viscosity in this response, 24,25 the finding of diminished coronary reactive hyperemic responses shown previously, 17,18 and confirmed herein, implies that coronary vasodilation is also prominently involved.…”

“…Under baseline conditions, the left ventricle extracts approximately 75% of the oxygen that is delivered to it; thus, it has a limited oxygen extraction reserve. 17,22,23 Consequently, to offset the induced decreases in arterial oxygen content, the myocardium is critically dependent on increases in CBF during ANH. Previous findings from our laboratory have demonstrated a remarkable capacity of the coronary circulation to increase its blood flow during ANH, as needed to maintain myocardial oxygen supply and contractile function.…”

“…Since the increases in MBF during ANH have been shown to be just sufficient to maintain coronary venous PO 2 (and presumably myocardial PO 2 ) constant, 17,18 a factor that is coupled to myocardial oxygen metabolism seems probable. Potential candidates include adenosine released from the cardiomyocytes 23 and an opening of the adenosine triphosphate-sensitive potassium channels in vascular smooth muscle.…”

“…In Group 2, coronary vasodilator reserve was evaluated in the LAD bed under baseline condition and following ANH; the ratio of the peak CBF was used during the reactive hyperemia following release of a 60-sec occlusion to the baseline (preocclusion) CBF. 17,18 series 2 effect of anh on ach-and snp-induced coronary vasodilation Additional studies were performed on six dogs to assess effect of ANH on ACh-and SNP-induced coronary vasodilation. An extracorporeal perfusion system containing an arterial blood reservoir was used to facilitate the intracoronary infusions of drugs and to ensure that coronary perfusion pressure was maintained constant at 80 mmHg.…”

Análise funcional do endotélio no perioperatório de operações vasculares

“…Nos leitos coronários onde há obstruções críticas, não ocorre o esperado aumento de fluxo sanguíneo, mecanismo responsável pela adaptação miocárdica à anemia. Desta forma, a anemia aguda determina em pacientes coronariopatas rápida instalação de isquemia miocárdica, conforme experimentalmente demonstrado em animais submetidos a hemodiluição normovolêmica (70) . O desbalanço entre a oferta e demanda miocárdica de oxigênio é agravado pelo fato dos próprios mecanismos sistêmicos para adaptação à anemia, anteriormente citados, determinarem maior consumo miocárdico de oxigênio.…”