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Relationship between breath‐synchronous arterial pressure and heart rate variations during orthostatic stress
Author(s) -
Sundblad Patrik,
Linnarsson Dag
Publication year - 2003
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1046/j.1475-097x.2003.00479.x
Subject(s) - medicine , supine position , heart rate , respiration , blood pressure , baroreflex , cardiology , orthostatic vital signs , respiratory rate , anesthesia , tidal volume , respiratory system , anatomy
Summary It has recently been shown that the phase relationship between respiration‐induced changes in arterial pressure (AP) and heart rate (HR) are different in supine and upright postures. We wanted to further analyse the coupling between respiration, arterial blood pressure and HR in the time domain, and how this coupling was altered during orthostatic stress. Nine healthy subjects were studied. Respiration‐induced changes in AP and HR were recorded during frequency‐ and volume‐controlled breathing. This was done during supine rest with and without lower body negative pressure (−50 mmHg) (LBNP). All experiments were performed after β 1 ‐blockade. Responses were averaged breath‐by‐breath to enhance the time resolution and to eliminate noise. The respiration‐induced changes in arterial pulse pressure (PP) were different between control and LBNP: The peak in PP during the respiratory cycle occurred 0·9 ± 0·8 (mean ± SD) s before the onset of inspiration during supine control and 0·8 ± 2·1 s after the onset of inspiration during LBNP ( P = 0·03). These changes in the timing of peak PP significantly distorted the cyclic systolic AP and mean AP fluctuations during LBNP. Despite the altered AP response with LBNP, HR fluctuations closely correlated in time with respiration in all conditions, albeit with a significantly reduced amplitude during LBNP (−49%, P = 0·01). The results points to a lack of coupling between AP and HR during paced breathing and thus suggest that respiratory sinus dysrhythmia at least, to a large extent, is independent of the arterial baroreflex.