Left Ventricular Strain Rate is Reduced during Voluntary Apnea in Healthy Humans

During an apneic event, sympathetic nerve activity increases resulting in subsequent increases in left ventricular afterload and myocardial work. It is unknown how cardiac mechanics are acutely impacted by the increased myocardial work during an apneic event. 10 healthy individuals (23 ± 3 yrs) performed multiple voluntary end-expiratory apnea (VEEA) maneuvers exposed to room air, while a subset (n=7) completed multiple VEEA exposed to hyperoxic air (100% F_iO₂). Beat-by-beat blood pressure, heart rate and stroke volume were measured continuously. Effective arterial elastance (EA) was calculated as an index of cardiac afterload and myocardial work calculated as the rate pressure product (RPP). Tissue Doppler echocardiography was used to measure left ventricular (LV) tissue velocities, and deformation via strain, and strain rate (SR). Systolic blood pressure (18 ± 13 mmHg, p<0.01), EA (0.13 ± 0.10 mmHg/mL, p<0.01), and RPP (9 ±10 mmHg x bpm 10^-2, p<0.01) significantly increased with room air VEEA. This occurred in parallel with decreases in peak longitudinal systolic (-0.62 ± 0.41cm s^-1, p<0.01) and early LV filling (-2.81 ± 1.99 cm s^-1, p<0.01) myocardial velocities. Longitudinal SR (-0.30 ± 0.321/s, p=0.01) was significantly decreased during room air VEEA. VEEA with hyperoxia did not alter (p>0.18) EA or RPP and attenuated the systolic blood pressure response compared to room air. Myocardial velocities and LV strain rate response to VEEA were unchanged (p=0.30) with hyperoxia. Consistent with our hypotheses, VEEA-induced increases in EA and myocardial work impact left ventricular mechanics, which may depend, in part, on stimulation of peripheral chemoreceptors.

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