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A187
October 17, 2009 10:00 AM - 11:30 AM Room Room 356 |
| Changes in Middle Cerebral Artery and Forehead Microvascular Flow during Simulated Hypovolemia |
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Kathleen J. Samuels, B.A., Keith J. Ruskin, M.D., Awad A. El-Ashry, M.D., Kirk H. Shelley, M.D., Ph.D., David G. Silverman, M.D. Anesthesiology, Yale Univ School of Med., New Haven, Connecticut |
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Introduction:
With most hypovolemic challenges, causing hypoperfusion to the point of inducing a CNS symptom such as lightheadedness has the potential for causing persistent ischemia and development of ischemic injury. The present study employed lower body negative pressure (LBNP), a rapidly titratable and reversible means of inducing simulated hypovolemia (1), for a comparison of transcranial Doppler (TCD) ultrasound of the middle cerebral artery and laser Doppler (LD) flowmetry of the forehead microvasculature.
Methods: With IRB approval, 9 healthy subjects (mean age 26.3±2.7) were subjected to a rapidly progressive LBNP protocol (-70 mmHg in 1 min followed by progressive declines of ∼10 mmHg until they reported lightheadedness or had a BP decline >20% baseline BP). Monitoring included EKG, continuous noninvasive finger arterial blood pressure (BP), TCD positioned at the transtemporal window, and LD flowmetry of the forehead microvasculature. Each of these devices was recorded continuously at baseline and during progressive LBNP and compared to its value at Base at the following stages: Presympt (approx. 30 sec before the onset of symptoms), and Sympt (onset of symptoms). If the subject did not become lightheaded, then s/he was categorized as asymptomatic, and the Sympt phases was taken as the time at which the BP cutoff for discontinuation of LBNP was reached. Results: In the 6 subjects who subsequently became lightheaded, LD dec by 10.9±11.7% at Presympt (p=NS for interphase difference). It then dec by an additional 20.4±18.7% with the onset of lightheadedness (p=0.035 for Presympt vs. Sympt) (Fig. 1).[figure1]As shown in Fig. 2, peak TCD readings dec by 29.3±9.7% from Base to the time of the Presympt measurement (p=0.001); they then inc by 4.1±12.9% with the onset of Sympt (p=NS). (The relatively high SD reflect inter-subject, not intra-subject, variability.)[figure2]In the 2 subjects who remained asymptomatic, LD did not change significantly in the Presympt and Sympt phases (Fig. 1) where Sympt was the time when the study was terminated because the BP cutoff was reached. In these asymptomatic subjects, the TCD flow velocity declined progressively (Fig. 2). Discussion: The present findings suggest that monitoring of the microvasculature in the distribution of the carotid arteries provides a better indication of changes in perfusion associated with lightheadedness than measurement of velocity at the middle cerebral artery. The discordance between LD and TCD is consistent with autoregulatory mechanisms at the level of the forehead microvasculature that have been reported in the context of systemic administration of phenylephrine (2). Refs: 1. Crit Care Med 2008;36:1892-9 2. Microvasc Res 63:196-208, 2002. From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists. |
Figure 1
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