Respiratory and non-respiratory sinus arrhythmia: implications for heart rate variability

The quantity of blood arriving at the left side of the heart oscillates throughout the breathing cycle due to the mechanics of breathing. Neurally regulated fluctuations in the length of the heart period act to dampen oscillations of the left ventricular stroke volume entering the aorta. We have reported that stroke volume oscillations but not spectral frequency variability stroke volume measures can be used to estimate the breathing frequency. This study investigated with the same recordings whether heart period oscillations or spectral heart rate variability measures could function as estimators of breathing frequency. Continuous 270 s cardiovascular recordings were obtained from 22 healthy adult volunteers in the supine and upright postures. Breathing was recorded simultaneously. Breathing frequency and heart period oscillation frequency were calculated manually, while heart rate variability spectral maximums were obtained using heart rate variability software. These estimates were compared to the breathing frequency using the Bland–Altman agreement procedure. Estimates were required to be \±10% (95% levels of agreement). The 95% levels of agreement measures for the heart period oscillation frequency (supine: -27.7 to 52.0%, upright: -37.8 to 45.9%) and the heart rate variability spectral maximum estimates (supine: -48.7 to 26.5% and -56.4 to 62.7%, upright: -37.8 to 39.3%) exceeded 10%. Multiple heart period oscillations were observed to occur during breathing cycles. Both respiratory and non-respiratory sinus arrhythmia was observed amongst healthy adults. This observation at least partly explains why heart period parameters and heart rate variability parameters are not reliable estimators of breathing frequency. In determining the validity of spectral heart rate variability measurements we suggest that it is the position of the spectral peaks and not the breathing

The effect of smoking nicotine tobacco versus smoking deprivation on motion sickness

BACKGROUND: The experienced smoker maintains adequate nicotine levels by 'puff-by-puff self-control' which also avoids symptomatic nauseating effects of nicotine overdose. It is postulated that there is a varying 'dynamic threshold for nausea' into which motion sickness susceptibility provides an objective toxin-free probe. Hypotheses were that: (i) nicotine promotes motion sickness whereas deprivation protects; and (ii) pleasurable effects of nicotine protect against motion sickness whereas adverse effects of withdrawal have the opposite effect. METHODS: Twenty-six healthy habitual cigarette smokers (mean±SD) 15.3±7.6cigs/day, were exposed to a provocative cross-coupled (coriolis) motion on a turntable, with sequences of 8 head movements every 30s. This continued to the point of moderate nausea. Subjects were tested after either ad-lib normal smoking (SMOKE) or after overnight deprivation (DEPRIV), according to a repeated measures design counter-balanced for order with 1-week interval between tests. RESULTS: Deprivation from recent smoking was confirmed by objective measures: exhaled carbon monoxide CO was lower (P<0.001) for DEPRIV (8.5±5.6ppm) versus SMOKE (16.0±6.3ppm); resting heart rate was lower (P<0.001) for DEPRIV (67.9±8.4bpm) versus SMOKE (74.3±9.5bpm). Mean±SD sequences of head movements tolerated to achieve moderate nausea were more (P=0.014) for DEPRIV (21.3±9.9) versus SMOKE (18.3±8.5). DISCUSSION: Tolerance to motion sickness was aided by short-term smoking deprivation, supporting Hypothesis (i) but not Hypothesis (ii). The effect was was approximately equivalent to half of the effect of an anti-motion sickness drug. Temporary nicotine withdrawal peri-operatively may explain why smokers have reduced risk for postoperative nausea and vomiting (PONV).