Decrease in left ventricular ejection time on digital arterial waveform during simulated hypovolemia in normal humans
Thomas Geeraerts1, Pierre Albaladejo, Adrien Descorps Declère
1Department of Anesthesiology and UPRES 3540, Hôpital de Bicêtre, Le Kremlin Bicêtre, France.
Insights
Peripheral left ventricular ejection time (LVET) can reflect central LVET changes during hypovolemia. This noninvasive measurement offers a reliable method for monitoring reduced blood volume.
Area of Science:
- Cardiovascular Physiology
- Hemodynamics
- Noninvasive Monitoring
Background:
- Left ventricular ejection time (LVET) is altered during hypovolemia.
- Central arterial pulse wave modifications during hypovolemia are not fully understood.
- Comparison of central and peripheral arterial pulse wave changes during hypovolemia is needed.
Purpose of the Study:
- To compare modifications of the pulse wave in central (carotid) and peripheral (digital) arteries during central hypovolemia.
- To assess the utility of peripheral LVET as a noninvasive indicator of hypovolemia.
Main Methods:
- Nine healthy volunteers underwent progressive lower body negative pressure (LBNP) to induce hypovolemia.
- Carotid arterial pressure waveforms were recorded using tonometry.
- Digital pulse waves and stroke volume were measured using volume-clamp and thoracic impedance methods, respectively.
Main Results:
- Mean arterial pressure remained stable.
- Heart rate increased and stroke volume decreased significantly with LBNP.
- Both carotid and digital LVET decreased significantly at -10 mm Hg LBNP.
Conclusions:
- Peripheral LVET variations correlate with central LVET changes during LBNP.
- Digital LVET is a potentially reliable noninvasive parameter for monitoring hypovolemia.
Background:
Left ventricular ejection time (LVET) measured in central arteries is modified during hypovolemia. We compared modifications of the pulse wave in a central artery (carotid) and in a peripheral artery (digital) during central hypovolemia induced by lower body negative pressure (LBNP) in conscious volunteers.
Methods:
Hypovolemia was simulated with progressive LBNP (baseline, -10, -20, and -30 mm Hg) in nine young healthy volunteers. The carotid arterial pressure waveform was recorded using a Millar tonometric method. The digital pulse wave was measured with a volume-clamp method (Finapres) and the stroke volume with a thoracic impedance method (Biomed).
Results:
Mean arterial pressure did not change during LBNP. Compared with baseline values, heart rate increased significantly at the -30 mm Hg level (68 +/- 13 beats/min vs. 59 +/- 11 beats/min), and stroke volume decreased as soon as -10 mm Hg was achieved (113 +/- 41 mL vs. 127 +/- 35 mL). Both carotid and digital LVET decreased significantly at the -10 mm Hg level (337 +/- 26 and 339 +/- 24 ms vs. 360 +/- 35 and 361 +/- 24 ms, respectively).
Conclusion:
Peripheral LVET could reflect variation of central LVET during LBNP and be a reliable noninvasive parameter for monitoring hypovolemia.
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