The contribution of cardiac mechanics to isolated increases in peripheral blood flow (1073.4)

Abstract

The human heart responds to whole‐body increases in cardiovascular demand by enhancing heart rate (HR) and intrinsic cardiac muscle function. However, it is not known if enhanced left ventricular (LV) muscle function ('LV mechanics') also contributes to localized increases in peripheral blood flow and, if so, whether enhanced peripheral blood flow per se or other arterial hemodynamic signals are the mechanism for acutely adjusting LV mechanics. We performed cardiac and vascular ultrasonography in eight healthy individuals (4 women) during 1) Baseline, 2) Bilateral arm heating (BAH), and 3) BAH with partial brachial artery occlusion (BAH+OCC) at mean arterial pressure (MAP, 85±15 mmHg). BAH markedly increased skin temperatures (32.71±0.69 to 39.21±0.60 deg. C, p<0.0001) while rectal core temperature was unaltered (p=0.54). Brachial artery blood flow measured in the left arm increased almost threefold with BAH (98±46 to 266±96 mL/min, P<0.0001) and returned to baseline levels with BAH+OCC. Arterial wave reflection, as assessed by applanation tonometry, had a tendency to increase with BAH and remained elevated with BAH+OCC (p=0.07). Increased cardiac output (p=0.02) was entirely explained by increased HR of 3‐4 bpm (P=0.002). In contrast, LV mechanics ‐ evaluated by systolic longitudinal strain and diastolic untwisting velocity ‐ did not change with BAH but they declined significantly with BAH+OCC (both p<0.05), which was accompanied by a rise in MAP (P<0.0001).In conclusion, the heart contributes to isolated increases in peripheral blood flow by enhancing HR but not its intrinsic LV muscle mechanics. Because LV output was maintained during the period of enhanced blood flow demand and increased afterload (=BAH+OCC), reduced systolic and diastolic LV mechanics during this condition may reflect an intrinsic protection of LV myofibers from pressure stress rather than a decline in LV function.