Abstract
Variability in arterial pressure and cerebral blood flow has traditionally been interpreted as a marker of cardiovascular decompensation, and has been associated with negative clinical outcomes across varying time scales, from impending orthostatic syncope to an increased risk of stroke. Emerging evidence, however, suggests that increased hemodynamic variability may, in fact, be protective in the face of acute challenges to perfusion, including significant central hypovolemia and hypotension (including hemorrhage), and during cardiac bypass surgery. This review presents the dichotomous views on the role of hemodynamic variability on clinical outcome, including the physiological mechanisms underlying these patterns, and the potential impact of increased and decreased variability on cerebral perfusion and oxygenation. We suggest that reconciliation of these two apparently discrepant views may lie in the time scale of hemodynamic variability; short time scale variability appears to be cerebroprotective, while mid to longer term fluctuations are associated with primary and secondary end-organ dysfunction.
Highlights
Traditionally, clinicians have assessed the cardiovascular status of their patients with static “snapshot” techniques, such as radial pulse for heart rate, brachial sphygmomanometry for arterial pressure, and chest excursions for respiration rate
Lucas et al (2013) observed a 15% increase in tolerance to combined head-up tilt and lower body negative pressure (LBNP) in subjects breathing at a fixed rate of 6 breaths/min (i.e., 0.1 Hz) vs. spontaneous breathing at 16–20 breaths/min (i.e., 0.27–0.33 Hz), thereby forcing a marked increase in low frequency (LF) power of mean arterial pressure and mean cerebral blood velocity; again, the reduction in cerebral blood velocity was similar between the two breathing conditions, so did not account for the improvement in tolerance
While these improvements in tolerance to central hypovolemia were not associated with the preservation of absolute cerebral blood flow, the effect of LF pulsatile cerebral blood flow on cerebral tissue oxygenation is a plausible underlying mechanism based on the animal and human clinical studies outlined above using pulsatile perfusion at higher frequencies
Summary
Clinicians have assessed the cardiovascular status of their patients with static “snapshot” techniques, such as radial pulse for heart rate, brachial sphygmomanometry for arterial pressure, and chest excursions for respiration rate. There is growing recognition that assessment of hemodynamic variability (e.g., heart rate and arterial pressure) across multiple time scales may provide important insight into acute and long-term clinical outcomes, such as risk of stroke (Shimbo et al, 2012), myocardial infarction (Kjellgren and Gomes, 1993), and end organ damage from hypertension (Mancia et al, 2007; Verdecchia et al, 2007; Leoncini et al, 2013) With advances both in monitoring technologies and data analysis capabilities, we have the capacity to capture dynamic changes in patient status by recording and analyzing non-invasive, high frequency hemodynamic waveform data, including ECG, arterial pressure, and most recently, cerebral blood flow and oxygenation. The potential role of increased variability in arterial pressure and cerebral blood flow on clinical outcome is somewhat disparate, with studies suggesting both protective (e.g. Sanderson et al, 1972; Allen et al, 2012; Koning et al, 2012), and www.frontiersin.org
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