Aortic pressure wave reconstruction during exercise is improved by adaptive filtering: a pilot study

Reconstruction of central aortic pressure from a peripheral measurement by a generalized transfer function (genTF) works well at rest and mild exercise at lower heart rates, but becomes less accurate during heavy exercise. Particularly, systolic and pulse pressure estimations deteriorate, thereby underestimating central pressure. We tested individualization of the TF (indTF) by adapting its resonance frequency at the various levels of exercise. In seven males (age 44–57) with coronary artery disease, central and peripheral pressures were measured simultaneously. The optimal resonance frequency was predicted from regression formulas using variables derived from the individual’s peripheral pressure pulse, including a pulse contour estimation of cardiac output (pcCO). In addition, reconstructed pressures were calibrated to central mean and diastolic pressure at each exercise level. Using a genTF and without calibration, the error in estimated aortic pulse pressure was −7.5 ± 6.4 mmHg, which was reduced to 0.2 ± 5.7 mmHg with the indTFs using pcCO for prediction. Calibration resulted in less scatter at the cost of a small bias (2.7 mmHg). In exercise, the indTFs predict systolic and pulse pressure better than the genTF. This pilot study shows that it is possible to individualize the peripheral to aortic pressure transfer function, thereby improving accuracy in central blood pressure assessment during exercise

Hemodynamic mechanisms underlying prolonged post-faint hypotension

During hypotension induced by tilt-table testing, low presyncopal blood pressure (BP) usually recovers within 1 min after tilt back. However, in some patients prolonged post faint hypotension (PPFH) is observed. We assessed the hemodynamics underlying PPFH in a retrospective study. Seven patients (2 females, aged 31-72 years) experiencing PPFH were studied. PPFH was defined as a systolic BP below 85 mmHg for at least 2 min after tilt back. In 6 out of 7 presyncope was provoked by 0.4 mg sublingual NTG, administered in the 60° head-up tilt position following head-up tilt for 20 min. Continuous BP was monitored and stroke volume (SV) was computed from pressure pulsations. Cardiac output (CO) was calculated from SV × heart rate (HR); and total peripheral resistance (TPR) from mean BP/CO. Left ventricular contractility was estimated by dP/dt (max) of finger pressure pulse. Systolic BP (SYS), diastolic BP (DIAS) and HR during PPFH were lower compared to baseline: SYS 75 ± 14 versus 121 ± 18 mmHg, DIAS 49 ± 9 versus 71 ± 9 mmHg and HR 52 ± 14 versus 67 ± 12 beats/min (p < 0.05). Marked hypotension was associated with a 47% fall in CO 3.1 ± 0.6 versus 5.9 ± 1.3 L/min (p < 0.05) and decreases in dP/dt, 277 ± 77 versus 759 ± 160 mmHg/s (p < 0.05). The difference in TPR was not significant 1.1 ± 0.3 versus 1.0 ± 0.3 MU (p = 0.229). In four patients, we attempted to treat PPFH by 30° head-down tilt. This intervention increased SYS only slightly (to 89 ± 12 mmHg). PPFH seems to be mediated by severe cardiac depressio

Influence of Chemoreflexes on Respiratory Variability in Healthy Subjects

The background of this study was the hypothesis that respiratory variability is influenced by chemoreflex regulation. In search for periodicities in the variability due to instability of the respiratory control system, spectral analysis was applied to breath-to-breath variables in 19 healthy subjects at rest. During room-air breathing, coherent oscillations in end-tidal CO 2 (P ET CO 2 ) and mean inspiratory flow (V I /T I ) were found in 15 subjects with frequencies mostly below 0.15 cycles per breath. Coherent oscillations in P ET CO 2 and V I /T I were expressed by gain (0.13 to 0.34 L/second · kPa) and phase ( ؊ 170 ؇ to ؉ 8 ؇ ). The oscillations in V I /T I were in phase with inspiratory volume (V I ). A model that describes the effects of chemoreflex feedback to noise in the system could explain these gains and phases, whereas a model without chemoreflex could not. During 100% O 2 breathing, only eight subjects had coherent oscillations in P ET CO 2 and V I /T I . The coherent oscillations in P ET CO 2 and V I /T I were interpreted as a manifestation of chemoreflex activity. We conclude that respiratory variability is not a random process but contains information on chemoreflex properties, such as the chemoreflex gain. The analysis of respiratory variability therefore provides a new tool to study the action of the chemoreflexes without application of external stimuli. Keywords: chemoreceptors; respiratory variability; spectral analysis Is the normal variability of respiratory parameters from breathto-breath a random process? This would imply that, for example, inspiratory volume (V I ) or inspiratory and expiratory time (T I and T E , respectively) are independent of previous breaths. However, due to the circulatory delay from the lungs to the systemic arteries, an &quot;accidental&quot; change in V I causes a change in arterial P O 2 and P CO 2 that only becomes manifest during the following breaths at a normal breathing frequency (1, 2). An adaptation of V I to such a change therefore inevitably leads to a dependency between successive breaths. Conversely, purely random variability of V I implies that V I does not take part in the feedback control of Pa O2 and Pa CO 2 through the chemoreflexes. Several authors have found evidence for a nonrandom breath-to-breath variability of respiratory parameters in the normal steady state (3-5). Significant (auto)correlations have been found between successive values of V I , T I , and T E (4, 6). Specific variability patterns have also been found, mainly in the form of subtle oscillations with a cycle time of approximately 25 seconds to more than 3 minutes (6-10). Clear periodic breathing is seldom observed in healthy subjects during wakefulness The aim of the present study was to derive information on respiratory regulation from the normal breathing pattern in the steady state. The hypothesis was that because of the delays and time constants of the chemoreflexes, continuous regulation tends to induce oscillations in ventilatory drive (represented by mean inspiratory flow, V I /T I ) with a certain coherency with oscillations in end-tidal P CO 2 (P ET CO2 ). To identify such oscillatory components and their mutual relationships, power and cross-spectral analysis was applied to breath-tobreath respiratory variables in 19 healthy subjects at rest. To test the hypothesis that the features of coherent oscillations in P ET CO2 and V I /T I are compatible with the characteristics of chemoreflex-feedback regulation, experimental spectra were compared with theoretical spectra derived from a chemoreflex model. The breathing pattern was also analyzed during 100% O 2 breathing to estimate the contribution of the peripheral chemoreflex (20). METHODS Subjects and Measurements Nineteen healthy nonsmoking medical students were studied with a history free of cardiopulmonary disease and normal physical examination (9 male and 10 female, aged 23 Ϯ 3 years, body mass index 22.2 Ϯ 3.1 kg/m 2 , mean Ϯ SD). The hospital ethical committee approved the protocol. Informed consent was obtained. The subjects knew which measurements were performed. To prevent &quot;conscious&quot; breathing, they were told that the study involved blood pressure regulation. They sat in a comfortable chair in a quiet room and breathed through a cushion-sealed face mask fitted with elastic bands around the head (dead space ‫ف‬ 70 ml). A Lilly type pneumotachograph (Siemens pressure transducer, Munich, Germany) was connected to the mask and hung with an elastic cord to the ceiling. A two-way nonrebreathing valve (S and W, Copenhagen, Denmark) was connected to the pneumotachograph. The inspiratory limb was connected to a stopcock (through a 1-m spirometer tube) which could be switched from room air to 100% O 2 from a 100 L bag. The stopcock was hidden behind a curtain so that the subject did not know which gas was inspired. The experiments began between 9:00 and 10:00 A . M . Recordings started after a 5-minute acclimatizion period. There were two episodes of 30 minutes with more than 5 minutes in between, performed in a random order, during which the subjects breathed either air or 100% O 2 (starting when endtidal P O 2 exceeded 85 kPa). Also measured were P O 2 and P CO 2 in the facemask (partial pressures in dry air, Centronic 200 MGA mass spectrometer, Croydon, United Kingdom), arterial O 2 saturation (Sa O 2 , Ohmeda Biox ear pulse oximeter, Madison, WI), finger arterial pressure (Finapres BMI-TNO, Amsterdam, Netherlands) and a single-channel chest-lead ECG. All signals were recorded on a Bell and Howell T4 recorder (Durham, NC) with airflow, ECG and blood pressure on FM channels and the other signals on a direct record channel using a Kayser Threde K 1180 pulse code modulator (Munich, Germany). The frequency response was 0-625 Hz for FM channels and 0-105 Hz for pulse code modulated channels

Baroreflex sensitivity is higher during acute psychological stress in healthy subjects under β-adrenergic blockade

Acute psychological stress challenges the cardiovascular system with an increase in BP (blood pressure), HR (heart rate) and reduced BRS (baroreflex sensitivity). β-adrenergic blockade enhances BRS during rest, but its effect on BRS during acute psychological stress is unknown. This study tested the hypothesis that BRS is higher during acute psychological stress in healthy subjects under β-adrenergic blockade. Twenty healthy novice male bungee jumpers were randomized and studied with (PROP, n=10) or without (CTRL, n=10) propranolol. BP and HR responses and BRS [cross-correlation time-domain (BRSTD) and cross-spectral frequency-domain (BRSFD) analysis] were evaluated from 30 min prior up to 2 h after the jump. HR, cardiac output and pulse pressure were lower in the PROP group throughout the study. Prior to the bungee jump, BRS was higher in the PROP group compared with the CTRL group [BRSTD: 28 (24–42) compared with 17 (16–28) ms·mmHg−1, P<0.05; BRSFD: 27 (20–34) compared with 14 (9–19) ms·mmHg−1, P<0.05; values are medians (interquartile range)]. BP declined after the jump in both groups, and post-jump BRS did not differ between the groups. In conclusion, during acute psychological stress, BRS is higher in healthy subjects treated with non-selective β-adrenergic blockade with significantly lower HR but comparable BP

Multi-site and multi-depth near-infrared spectroscopy in a model of simulated (central) hypovolemia: lower body negative pressure

Purpose: To test the hypothesis that the sensitivity of near-infrared spectroscopy (NIRS) in reflecting the degree of (compensated) hypovolemia would be affected by the application site and probing depth. We simultaneously applied multi-site (thenar and forearm) and multi-depth (15-2.5 and 25-2.5 mm probe distance) NIRS in a model of simulated hypovolemia: lower body negative pressure (LBNP). Methods: The study group comprised 24 healthy male volunteers who were subjected to an LBNP protocol in which a baseline period of 30 min was followed by a step-wise manipulation of negative pressure in the following steps: 0, -20, -40, -60, -80 and -100 mmHg. Stroke volume and heart rate were measured using volume-clamp finger plethysmography. Two multi-depth NIRS devices were used to measure tissue oxygen saturation (StO2) and tissue hemoglobin index (THI) continuously in the thenar and the forearm. To monitor the shift of blood volume towards the lower extremities, calf THI was measured by single-depth NIRS. Results: The main findings were that the application of LBNP resulted in a significant reduction in stroke volume which was accompanied by a reduction in forearm StO2 and THI. Conclusions: NIRS can be used to detect changes in StO2 and THI consequent upon central hypovolemia. Forearm NIRS measurements reflect hypovolemia more sensitively than thenar NIRS measurements. The sensitivity of these NIRS measurements does not depend on NIRS probing depth. The LBNP-induced shift in blood volume is reflected by a decreased THI in the forearm and an increased THI in the calf

Cardiac oxygen supply is compromised during the night in hypertensive patients

The enhanced heart rate and blood pressure soon after awaking increases cardiac oxygen demand, and has been associated with the high incidence of acute myocardial infarction in the morning. The behavior of cardiac oxygen supply is unknown. We hypothesized that oxygen supply decreases in the morning and to that purpose investigated cardiac oxygen demand and oxygen supply at night and after awaking. We compared hypertensive to normotensive subjects and furthermore assessed whether pressures measured non-invasively and intra-arterially give similar results. Aortic pressure was reconstructed from 24-h intra-brachial and simultaneously obtained non-invasive finger pressure in 14 hypertensives and 8 normotensives. Supply was assessed by Diastolic Time Fraction (DTF, ratio of diastolic and heart period), demand by Rate-Pressure Product (RPP, systolic pressure times heart rate, HR) and supply/demand ratio by Adia/Asys, with Adia and Asys diastolic and systolic areas under the aortic pressure curve. Hypertensives had lower supply by DTF and higher demand by RPP than normotensives during the night. DTF decreased and RPP increased in both groups after awaking. The DTF of hypertensives decreased less becoming similar to the DTF of normotensives in the morning; the RPP remained higher. Adia/Asys followed the pattern of DTF. Findings from invasively and non-invasively determined pressure were similar. The cardiac oxygen supply/demand ratio in hypertensive patients is lower than in normotensives at night. With a smaller night-day differences, the hypertensives’ risk for cardiovascular events may be more evenly spread over the 24 h. This information can be obtained noninvasively