RSA magnitude is lower and mean arterial blood pressure variability is greater during IPPV than during metronome breathing. We conclude that in healthy humans, RSA stabilizes mean arterial blood pressure at respiratory frequency.
Cardiac stroke volume estimated by ultrasound Doppler and by arterial blood pressure curve showed parallel variations beat-to-beat during simulated hemorrhage, whereas impedance cardiography did not appear to track beat-to-beat changes in cardiac stroke volume. The variability in cardiac stroke volume was decreased during mild and moderate hypovolemia and could be used for early detection of hypovolemia.
Introduction The human temperature control within the thermoneutral zone (TNZ) depends on the regulation of skin blood flow to hands and feet (acral skin) [1]. The acral skin blood flow is regulated by absolute level and fluctuations in arterio‐venous anastomoses’ vasculature resistance. We hypothesized that a change in ambient temperature would not affect the hemodynamic responses within the TNZ in healthy humans. Methods Twenty‐four young healthy human subjects were exposed to three ambient temperatures (20°C, 26°C and 32°C) while supine and lightly dressed in a climate chamber. Each temperature plateau lasted for 40 minutes. The protocol either started at 20°C or 32°C, with a subsequent increase or decrease in temperature, respectively, and the order was randomized. Beat‐by‐beat blood flux from both index fingers and the left forearm were recorded simultaneously by laser Doppler flowmetry (DRT4, Moor Instruments, Devon, UK), together with heart rate (HR, from ECG). Non‐invasive finger arterial blood pressure (Finometer, Finapres Medical System, Netherlands; calibrated at each temperature plateau) was recorded continuously from the right middle finger, providing mean arterial pressure (MAP) and estimated beat‐to‐beat cardiac stroke volume (SV). The medians and their corresponding 95% confidence intervals were calculated by Hodges‐Lehmann’s estimates. Wilcoxon signed rank sum test for paired samples tested differences between states. Preliminary results Increasing ambient temperature from 20°C to 32°C caused a five‐fold increase in left fingertip flux (p<0.003) while left forearm flux doubled (p<0.008). The fluctuations in the bilateral fingertip flux were maximum correlated at 26°C (>0.82) and significantly higher than the correlation at 32°C (0.73, p<0.01 as compared to 26°C). The hemodynamic variables changed significantly within the TNZ. MAP decreased from 74 (70,77) mmHg at 20°C to 64 (60,68) mmHg at 32°C (p<0.0001). SV decreased from 102 (93, 113) ml at 20°C to 97 (86, 106) ml at 32°C (p<0.0004). HR increased minimally from 20°C (56 bpm (52, 59) to 32°C (58 bpm (56, 61) (p=0.01). Conclusions The marked changes in acral skin blood flow within TNZ affected the central hemodynamic variables, with the vasodilation reflected in MAP decrease coinciding with an increase in ambient temperature. HR and SV showed minimal changes within TNZ. Support or Funding Information The Research Council of Norway (grant no: 230354) Responses in acral and non-acral skin vasomotion and temperature during lowering of ambient temperatureMElstadLVanggaardAHLossiusLWalløeTK.BergersenJ Therm Biol.4516874
Increasing resistance to inspiration further decreases intrathoracic and intracranial pressures, leading to increases in venous return, stroke volume, and consequently, arterial pressure and cerebral perfusion pressure. Accordingly, inspiratory resistance breathing may be of therapeutic interest for clinical conditions associated with decreased delivery of blood and oxygen to the brain. Previous studies in healthy humans have investigated the effect of inspiratory resistance breathing on the cerebral circulation, by studying blood velocity within intracranial vessels (via transcranial Doppler (TCD) ultrasound), with equivocal results. The aim of this study was to investigate the effect of inspiratory resistance breathing on blood flow through the internal carotid artery (ICA), and cerebral tissue oxygenation during hypoxia. We hypothesized that inspiratory resistance breathing would increase ICA blood flow, and improve cerebral tissue oxygenation during a mild hypoxic stimulus. Methods Six healthy human subjects (5M/1F) completed two 10‐min protocols in randomized order: 1) breathing a hypoxic gas mix (16% O2, balance N2), and 2) breathing a hypoxic gas mix (16% O2, balance N2) with inspiratory resistance of −7 cmH2O. ICA blood flow was derived from simultaneous measurements of blood velocity and diameter measured by duplex ultrasound, middle cerebral artery velocity (MCAv) was recorded continuously by TCD ultrasound, and cerebral tissue oxygenation (ScO2) was recorded by near‐infrared spectroscopy. Arterial oxygen saturation (SpO2) was measured by pulse oximetry, and end‐tidal O2 (etO2) was measured by a gas analyzer. Data were analyzed from the last 1‐min of baseline and each protocol with a linear mixed model. Results The hypoxic stimulus decreased SpO2 and etO2 (P<0.0001), and inspiratory resistance breathing did not protect against these responses (P≥0.21). ICA diameter increased with hypoxia under both conditions (P=0.002), regardless of resistance breathing (P=0.56). ICA velocity (23.6 ± 1.6 cm/s vs. 25.7 ± 1.1 cm/s) and flow (298.8 ± 36.6 ml/min vs. 328.8 ± 39.5 ml/min) were lower with hypoxia and inspiratory resistance breathing compared with hypoxia alone (P≤0.07), while mean MCAv was not affected by either hypoxia or resistance breathing (P≥0.15). ScO2 decreased under both conditions (P=0.0009; hypoxia: −2.7 ± 0.9 %; hypoxia + resistance breathing: −3.6 ± 0.8 %), with no effect of inspiratory resistance breathing (P=0.90). Conclusion These preliminary data demonstrate that, contrary to our hypothesis, inspiratory resistance breathing did not increase ICA blood flow, nor improve cerebral tissue oxygenation during a mild hypoxic stimulus. Rather, ICA blood flow decreased with inspiratory resistance breathing during hypoxia, primarily due to a reduction in ICA blood velocity. Further studies are required to elucidate whether inspiratory resistance breathing may be of therapeutic interest for clinical conditions affecting cerebral blood flow and tissue oxygenation.
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