A beat-to-beat model of the cardiovascular system is developed to study the spontaneous short-term variability in arterial blood pressure (BP) and heart rate (HR) data from humans at rest. The model consists of a set of difference equations representing the following mechanisms: 1) control of HR and peripheral resistance by the baroreflex, 2) Windkessel properties of the systemic arterial tree, 3) contractile properties of the myocardium (Starling's law and restitution), and 4) mechanical effects of respiration on BP. The model is tested by comparing power spectra and cross spectra of simulated data from the model with spectra of actual data from resting subjects. To make spectra from simulated data and from actual data tally, it must be assumed that respiratory sinus arrhythmia at rest is caused by the conversion of respiratory BP variability into HR variability by the fast, vagally mediated baroreflex. The so-called 10-s rhythm in HR and BP appears as a resonance phenomenon due to the delay in the sympathetic control loop of the baroreflex. The simulated response of the model to an imposed increase of BP is shown to correspond with the BP and HR response in patients after administration of a BP-increasing drug, such as phenylephrine. It is concluded that the model correctly describes a number of important features of the cardiovascular system. Mathematical properties of the difference-equation model are discussed.

This study compared spontaneous baroreflex sensitivity (BRS) estimates obtained from an identical set of data by 11 European centers using different methods and procedures. Noninvasive blood pressure (BP) and ECG recordings were obtained in 21 subjects, including 2 subjects with established baroreflex failure. Twenty-one estimates of BRS were obtained by methods including the two main techniques of BRS estimates, i.e., the spectral analysis (11 procedures) and the sequence method (7 procedures) but also one trigonometric regressive spectral analysis method (TRS), one exogenous model with autoregressive input method (X-AR), and one Z method. With subjects in a supine position, BRS estimates obtained with calculations of alpha-coefficient or gain of the transfer function in both the low-frequency band or high-frequency band, TRS, and sequence methods gave strongly related results. Conversely, weighted gain, X-AR, and Z exhibited lower agreement with all the other techniques. In addition, the use of mean BP instead of systolic BP in the sequence method decreased the relationships with the other estimates. Some procedures were unable to provide results when BRS estimates were expected to be very low in data sets (in patients with established baroreflex failure). The failure to provide BRS values was due to setting of algorithmic parameters too strictly. The discrepancies between procedures show that the choice of parameters and data handling should be considered before BRS estimation. These data are available on the web site (http://www.cbi.polimi.it/glossary/eurobavar.html) to allow the comparison of new techniques with this set of results.

Respiratory sinus arrhythmia (RSA) has received much attention in recent years due to the large body of evidence indicating that variations in this phenomenon represent alterations in parasympathetic cardiac control. Although it appears that respiratory sinus arrhythmia is mediated by vagal mechanisms, the extent to which the well-known respiratory influences (i.e., rate and tidal volume) on respiratory sinus arrhythmia (in altering its magnitude) may moderate the relationship between RSA and cardiac vagal tone has never been systematically studied. We addressed this issue by examining intraindividual relationships among RSA magnitude, respiration (rate and tidal volume), and heart period among six healthy male adults after intravenous administration of 10 mg propranolol, a beta-adrenergic blocker. Subjects were exposed to various behavioral tasks which altered all physiological variables measured. Variations in heart period after beta blockade were assumed to be predominantly vagally mediated. Within-subject regression analyses consistently showed that respiratory parameters influenced RSA magnitude, but not tonic variations in beta-blocked heart period, suggesting that respiratory-mediated RSA alterations are not associated with changes in cardiac vagal tone. Only when respiratory variables were statistically controlled was there evidence of a reasonable correspondence between beta-blocked heart period and RSA amplitude, providing support for the idea that respiratory parameters need to be controlled when using RSA amplitude as an index of cardiac vagal tone. Repeated-measures analyses of variance of mean levels of heart period and respiratory sinus arrhythmia across subjects supplemented and supported the intraindividual results. These findings point to the importance of controlling for respiratory parameters when using respiratory sinus arrhythmia as a cardiac vagal index.

During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO(2)Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity ("the muscle pump"), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity (V(mean)) and near-infrared spectroscopy-determined cO(2)Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to V(mean) at low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in V(mean) on standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.

Abstract-Wave reflections affect the proximal aortic pressure and flow waves and play a role in systolic hypertension. A measure of wave reflection, receiving much attention, is the augmentation index (AI), the ratio of the secondary rise in pressure and pulse pressure. AI can be limiting, because it depends not only on the magnitude of wave reflection but also on wave shapes and timing of incident and reflected waves. More accurate measures are obtainable after separation of pressure in its forward (P f ) and reflected (P b ) components. However, this calculation requires measurement of aortic flow. We explore the possibility of replacing the unknown flow by a triangular wave, with duration equal to ejection time, and peak flow at the inflection point of pressure (F tIP ) and, for a second analysis, at 30% of ejection time (F t30 ). Wave form analysis gave forward and backward pressure waves. Reflection magnitude (RM) and reflection index (RI) were defined as RMϭP b /P f and RIϭP b /(P f ϩP b ), respectively. Healthy subjects, including interventions such as exercise and Valsalva maneuvers, and patients with ischemic heart disease and failure were analyzed. RMs and RIs using F tIP and F t30 were compared with those using measured flow (F m Key Words: aorta Ⅲ blood flow Ⅲ blood flow velocity Ⅲ blood pressure Ⅲ pulse A ortic pressure, and especially pulse pressure (PP), is now recognized as an important indicator of cardiovascular risk 1-4 and can guide pharmaceutical treatment. 5,6 Wave reflections affect the pressure and flow wave in the proximal aorta, 7 and their contribution depends on their magnitude (determined by the periphery and the large arteries) and time of return (mainly determined by the large, conduit arteries). When the reflected wave arrives in systole, it augments pressure, leading to increased systolic and PP. This augmentation is greater when the heart is hypertrophied. 8 In heart failure, wave reflections affect the flow wave negatively, thereby reducing stroke volume and cardiac output. 8 -10 One way to estimate the amount of reflection is by waveform analysis in which aortic pressure is separated into its forward and backward components. 7,11,12 The ratio of the magnitudes of the backward (reflected) wave and the forward (incident) wave, the reflection magnitude (RM), allows for the estimation of the amount of reflection, but this waveform analysis requires measurement of both pressure and flow waves. A method that requires the measurement of pressure only is computation of the augmentation index (AI). 13,14 AI gives reproducible results 15,16 and is in use in clinical settings. [17][18][19][20] However, AI is determined by both the magnitude and timing of the reflected wave. This is evident from Figure 1A. In this figure, the original pressure wave is separated into its forward and backward components and then reassembled for different delays of the same backward wave. AI is clearly influenced by the time of return of the reflected wave. Figure 1B gives 2 examples in w...

Internal jugular veins are the major cerebral venous outflow pathway in supine humans. In upright humans the positioning of these veins above heart level causes them to collapse. An alternative cerebral outflow pathway is the vertebral venous plexus. We set out to determine the effect of posture and central venous pressure (

Background and Purpose-We addressed whether dynamic cerebral autoregulation (dCA) is affected in middle cerebral artery (MCA) territory (MCAS) and lacunar ischemic stroke (LS). Methods-Blood pressure (MAP) and MCA velocity (V) were measured in 10 patients with large MCAS (National Institutes of Health Stroke score, 17Ϯ2; meanϮSEM), in 10 with LS (score, 9Ϯ1), and in 10 reference subjects. dCA was evaluated in time (delay of the MCA V mean counter-regulation during changes in MAP) and frequency domains (cross-spectral MCA V mean -to-MAP phase lead). Results-In reference subjects, latencies for MAP increments (5.3Ϯ0.5 seconds) and decrements (5.6Ϯ0.5 seconds) were comparable, and low frequency MCA V mean -to-MAP phase lead was 56Ϯ5 and 59Ϯ5°(left and right hemisphere). In MCAS, these latencies were 4.6Ϯ0.7 and 5.6Ϯ0.5 seconds in the nonischemic hemisphere and not detectable in the ischemic hemisphere. In the unaffected hemisphere, phase lead was 61Ϯ6°versus 26Ϯ6°on the ischemic side (PϽ0.05). In LS, no latency and smaller phase lead bilaterally (32Ϯ6 and 33Ϯ5°) conformed to globally impaired dCA. Conclusions-In large MCAS infarcts, dynamic cerebral autoregulation was impaired in the affected hemisphere. In LS, dynamic cerebral autoregulation was impaired bilaterally, a finding consistent with the hypothesis of bilateral small vessel disease in patients with lacunar infarcts. (Stroke. 2005;36:2595-2600.)

The xBRS method should be considered for experimental and clinical use, because it yielded values that correlated strongly with and were close to the EUROBAVAR averages, yielded more values per minute, had lower within-patient variance and measured baroreflex delay.