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Positional circulatory control in the sleeping infant and toddler: role of the inner ear and arterial pulse pressure
Author(s) -
Cohen Gary,
Vella Silvano,
Jeffery Heather,
Lagercrantz Hugo,
KatzSalamon Miriam
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2012.229641
Subject(s) - blood pressure , circulatory system , heart rate , reflex , medicine , tachycardia , cardiology , pulse pressure , pulse (music) , anesthesia , physics , detector , optics
Key points• Fast‐acting reflexes fine‐tune heart rate and blood pressure as the push and pull of gravity changes from moment to moment. • Circulatory failure may occur if these mechanisms fail to develop normally. • Reactions to routine movements such as head‐up and sideways tilt show how two key reflexes involved develop during sleep, in early infancy. • Sensors that detect motion and arterial pulsations, located in the inner ear and arteries, respectively, produce carefully coordinated changes in heart rate and blood pressure as body position and the force/direction of gravity alters. • Both mechanisms are intact in infants exposed to tobacco, but a mild pulse pressure anomaly reflexively slows their heart and lowers their blood pressure on tilt to upright. • Circulatory dysfunction need not necessarily reflect abnormal development of key reflexes per se , but other factors that inappropriately trigger or inhibit them.Abstract Heart rate (HR) and arterial blood pressure (BP) are rapidly and reflexively adjusted as body position and the force/direction of gravity alters. Anomalies in these mechanisms may predispose to circulatory failure during sleep. We analysed the development of two key reflexes involved by undertaking a longitudinal (birth–1 year) comparison of instantaneous HR and BP changes evoked by abrupt upright, sideways or horizontal repositioning. Each manoeuvre triggered an identical rise in HR (tachycardia) followed by a slower rise in diastolic blood pressure (DBP)/systolic blood pressure (SBP) and variable pulse pressure (PP) change. We show that tachycardia is triggered by acceleration (vestibular) sensors located in the inner ear and slight changes in the pulsatile component of BP then signal to the arterial baroreceptors to reinforce or oppose these actions as needed. We also identified a PP anomaly in sleeping 1‐year‐olds of smokers that prematurely slows HR and is associated with mild positional hypotension. We conclude that positional circulatory compensation is initiated pre‐emptively in a feed‐forward manner and that feedback changes in vago‐sympathetic drive to the heart (and perhaps blood vessels) by PP exert a slower but powerful modulating effect. An anomaly in either or both mechanisms may weaken positional compensation in some sleeping infants.