Abstract

Alternation of heart rate between 2 values using a pacemaker generates oscillations in end-tidal CO(2) (et-CO(2)). This study examined (a) whether modulating atrioventricular delay can also do this, and (b) whether more gradual variation of cardiac output can achieve comparable changes in et-CO(2) with less-sudden changes in blood pressure. We applied pacemaker fluctuations by adjusting heart rate (by 30 bpm) or atrioventricular delay (between optimal and nonoptimal values) or both, with period of 60 s in 19 heart failure patients (age 73+/-11, EF 29+/-12%). The changes in cardiac output, by either heart rate or atrioventricular delay or both, were made either as a step ("square wave") or more gradually ("sine wave"). We obtained changes in cardiac output sufficient to engender comparable oscillations in et-CO(2) (P=NS) in all 19 patients either by manipulation of heart rate (14), or by atrioventricular delay (2) or both (3). The square wave produced 191% larger and 250% more sudden changes in blood pressure than the sine wave alternations (22.4+/-11.7 versus 13.6+/-4.5 mm Hg, P<0.01 and 19.8+/-10.0 versus 7.9+/-3.2 mm Hg over 5 s, P<0.01), but peak-to-trough et-CO(2) elicited was only 45% higher (0.45+/-0.18 versus 0.31+/-0.13 kPa, P=0.01). This study shows that cardiac output is the key to dynamically manipulating the respiratory system with pacing sequences. When manipulating respiration by this route, a sine wave pattern may be preferable to a square wave, because it minimizes sudden blood pressure fluctuations.

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