Interrelation between arterial pressure and speed of the pulse wave spreading

To describe the dependence of arterial pressure on the speed of spreading of pulse wave, an curvilinear regression equation with two constants was proposed. The causes of the discrepancy in the dependences reported in literature are discussed.     

Computation of aortic pulse wave velocity and aortic pulse wave velocity and aortic extensibility from pressure gradient measurements.

This study is concerned with the computation of aortic pulse wave velocity based on simultaneous recordings of the aortic pressure gradient and first-time derivative of aortic pressure. These variables were recorded by means of a double-lumen catheter introduced in the aorta of four anesthetized closed chest dogs, and connected to critically damped manometer systems. Results of aortic pulse wave velocity were then compared: (i) to the true phase velocity obtained from spectra of apparent phase velocity, and (ii) to the pulse wave velocity computed from the time shift between maximum slopes of the pressure wave. From the aortic valves to 37 cm down the aortic trunk, pulse wave velocity increased from 410-460 cm/s to approximately 600-800 cm/s. Based on the wave propagation equation presented of Bramwell and Hill (Bramwell, J.C., and Hill, A. V. 1922. Proc. R. Soc. 93, 298-306), volumetric extensibility coefficients were computed from pulse wave velocity data. Results indicated that, from the aortic valves to 37 cm down to the aorta, the mean volumetric extensibility decreased from 0.43-0.56% deltaV/cm H2O to 0.16-0.25% deltaV/cm H2O (1 cm H2O = 94.1 N/m2).     

Determination of wave speed and wave separation in the arteries using diameter and velocity

The determination of arterial wave speed and the separation of the forward and backward waves have been established using simultaneous measurements of pressure (P) and velocity (U). In this work, we present a novel algorithm for the determination of local wave speed and the separation of waves using the simultaneous measurements of diameter (D) and U. The theoretical basis of this work is the solution of the 1D equations of flow in elastic tubes. A relationship between D and U is derived, from which, local wave speed can be determined; C=±0.5(dU_±/d ln D_±). When only unidirectional waves are present, this relationship describes a linear relationship between ln D and U. Therefore, constructing a ln DU-loop should result in a straight line in the early part of the cycle when it is most probable that waves are running in the forward direction. Using this knowledge of wave speed, it is also possible to derive a set of equations to separate the forward and backward waves from the measured D and U waveforms. Once the forward and backward waveforms of D and U are established, we can calculate the energy carried by the forward and backward waves, in a similar way to that of wave intensity analysis. In this paper, we test the new algorithm in vitro and present results from data measured in the carotid artery of human and the ascending aorta of canine. We conclude that the new technique can be reproduced in vitro, and in different vessels of different species, in vivo. The new algorithm is easy to use to determine wave speed and separate D and U waveforms into their forward and backward directions. Using this technique has the merits of utilising noninvasive measurements, which would be useful in the clinical setting.     

The velocity of the arterial pulse wave: a viscous-fluid shock wave in an elastic tube

Background

The arterial pulse is a viscous-fluid shock wave that is initiated by blood ejected from the heart. This wave travels away from the heart at a speed termed the pulse wave velocity (PWV). The PWV increases during the course of a number of diseases, and this increase is often attributed to arterial stiffness. As the pulse wave approaches a point in an artery, the pressure rises as does the pressure gradient. This pressure gradient increases the rate of blood flow ahead of the wave. The rate of blood flow ahead of the wave decreases with distance because the pressure gradient also decreases with distance ahead of the wave. Consequently, the amount of blood per unit length in a segment of an artery increases ahead of the wave, and this increase stretches the wall of the artery. As a result, the tension in the wall increases, and this results in an increase in the pressure of blood in the artery.

Methods

An expression for the PWV is derived from an equation describing the flow-pressure coupling (FPC) for a pulse wave in an incompressible, viscous fluid in an elastic tube. The initial increase in force of the fluid in the tube is described by an increasing exponential function of time. The relationship between force gradient and fluid flow is approximated by an expression known to hold for a rigid tube.

Results

For large arteries, the PWV derived by this method agrees with the Korteweg-Moens equation for the PWV in a non-viscous fluid. For small arteries, the PWV is approximately proportional to the Korteweg-Moens velocity divided by the radius of the artery. The PWV in small arteries is also predicted to increase when the specific rate of increase in pressure as a function of time decreases. This rate decreases with increasing myocardial ischemia, suggesting an explanation for the observation that an increase in the PWV is a predictor of future myocardial infarction. The derivation of the equation for the PWV that has been used for more than fifty years is analyzed and shown to yield predictions that do not appear to be correct.

Conclusion

Contrary to the theory used for more than fifty years to predict the PWV, it speeds up as arteries become smaller and smaller. Furthermore, an increase in the PWV in some cases may be due to decreasing force of myocardial contraction rather than arterial stiffness.     

Use of impedance measurements to estimate numbers of antibiotic resistant Salmonella strains

Impedance detection times were compared with traditional plating methods for enumerating antibiotic-resistant strains of Salmonella stanley, Salm. thompson and Salm. infantis grown in laboratory medium and pork slurry. The correleation of log₁₀ counts of salmonellas with detection times was highly significant ( r = -0·96 for broth and r = -0·94 for slurries. The confidence limits (± og₁₀ 1·0 for broth and ± log₁₀ 1·65 for slurry) indicated that detection times could reliably be used as a rapid means of enumerating salmonellas when large numbers of counts of known strains are required for growth studies. Use of antibiotic-resistant strains also permitted their selective detection by impedance from the natural spoilage flora of pork slurry when the same antibiotics were incorporated in the detection medium.     

Use of an operant task to estimate food reinforcement in adult humans with and without BED

Objective: The purpose of this study was to demonstrate the utility of food‐reinforced operant task performance in modeling binge‐eating disorder (BED). We hypothesized that food reinforcement after a caloric preload would be related to BED status, but not hunger. Methods and Procedures: We investigated the association between reports of hunger, binge tendency, and food reinforcement in a sample of 18 women (12 non‐BED, 7 lean, 5 obese, and 6 obese BED). Participants completed two sessions of operant task performance after consuming 600 ml of flavored water or 600 ml of a 1 kcal/ml liquid meal. Results: Under the water condition, food reinforcement did not differ between the non‐BED and BED groups, and was positively correlated with hunger ratings across all participants (r = 0.55, P = 0.023). Under the liquid meal condition, food reinforcement was significantly decreased compared with the water condition in the non‐BED group (t = ?2.6, P = 0.026). There was also a significant difference between the non‐BED and BED groups in the fed condition (41 ± 40, 117 ± 60, F = 10.3, P = 0.005, non‐BED vs. BED, respectively, mean ± s.d.). The correlation between food reinforcement and hunger remained significant only in the non‐BED group (r = 0.69, P = 0.011). Discussion: Our results support the hypothesis that food reinforcement measured after a caloric preload is related to BED status but not hunger in those subjects with BED. The data also suggest that operant task performance can be useful in modeling BED criteria such as “eating when not physically hungry.”     

Intra- and extracranial artery blood velocity during a sudden blood pressure decrease in humans

The intra- and extracerebral Doppler artery blood velocity responses to a 10-mmHg abrupt blood pressure (BP) decrease in ten healthy men were studied. This decrease was obtained using two cuffs placed over both thighs. First, cuffs were inflated to pressures greater than the arterial BP for 5 min. Next, they were deflated to 60 mmHg in order to prevent venous return from the legs. We obtained a decrease in mean arterial BP of from 101 (10) to 90 (10) mmHg [mean (SD), P < 0.01] without modifications in the heart rate [HR, 88 (14) beats min⁻¹]. Middle cerebral artery mean blood velocity (MCAmv) decreased immediately from 50 (10) to 42 (12) cm s⁻¹ (P < 0.05). Simultaneously, temporal superficial artery mean blood velocity (TSAmv) decreased from 11 (3) to 7 (2) cm s⁻¹ (P < 0.05) and common carotid artery blood flow (CCAbf ) decreased from 305 (23) to 233 (33) ml min⁻¹ (P < 0.05). After 5 s, MCAmv and CCAbf returned to baseline values, whereas TSAmv [8 (2) cm s⁻¹], mean arterial BP [86 (10) mmHg] remained low and HR increased [92 (12) beats min⁻¹]. TSAmv, BP and HR returned to baseline values in 1 min. These data confirm that cerebral blood flow (CBF) is very rapidly regulated but that blood flow in extracranial territories is not and that it follows the arterial BP changes. Accepted: 8 April 1997     

Cerebral blood flow velocity response to induced and spontaneous sudden changes in arterial blood pressure

The influence of different types of maneuvers that can induce sudden changes of arterial blood pressure (ABP) on the cerebral blood flow velocity (CBFV) response was studied in 56 normal subjects (mean age 62 yr, range 23-80). ABP was recorded in the finger with a Finapres device, and bilateral recordings of CBFV were performed with Doppler ultrasound of the middle cerebral arteries. Recordings were performed at rest (baseline) and during the thigh cuff test, lower body negative pressure, cold pressor test, hand grip, and Valsalva maneuver. From baseline recordings, positive and negative spontaneous transients were also selected. Stability of PCO2 was monitored with transcutaneous measurements. Dynamic autoregulatory index (ARI), impulse, and step responses were obtained for 1-min segments of data for the eight conditions by fitting a mathematical model to the ABP-CBFV baseline and transient data (Aaslid's model) and by the Wiener-Laguerre moving-average method. Impulse responses were similar for the right- and left-side recordings, and their temporal pattern was not influenced by type of maneuver. Step responses showed a sudden rise at time 0 and then started to fall back to their original level, indicating an active autoregulation. ARI was also independent of the type of maneuver, giving an overall mean of 4.7 +/- 2.9 (n = 602 recordings). Amplitudes of the impulse and step responses, however, were significantly influenced by type of maneuver and were highly correlated with the resistance-area product before the sudden change in ABP (r = -0.93, P < 0.0004). These results suggest that amplitude of the CBFV step response is sensitive to the point of operation of the instantaneous ABP-CBFV relationship, which can be shifted by different maneuvers. Various degrees of sympathetic nervous system activation resulting from different ABP-stimulating maneuvers were not reflected by CBFV dynamic autoregulatory responses within the physiological range of ABP.     

The consistency of maximum running speed measurements in humans using a feedback-controlled treadmill,and a comparison with maximum attainable speed during overground locomotion

Consistent measurement of maximum running speed overground is problematic due to the difficulty in precise, continual measurement of speed, and the substantial workload in accelerating the body promoting the onset of fatigue. Treadmills remove the requirement for acceleration which enables more repeats. They also allow experiments to be carried out in controlled environments and where space is limited, but they usually depend on manual and subjective speed control. Here we used a draw-wire position sensor and a proportional–derivative (PD) controller to automatically adjust treadmill belt speed of a large equine treadmill. The feedback loop took the real-time position and velocity of the runner relative to the front of the treadmill as input. This control system allowed runners to accelerate from walking speed to a peak running speed within a few strides and then decelerate as quickly as they wished. We used the system to evaluate the variation in maximum speed determination that results from one trial to 10 trials, in eleven individuals. Three trials gave a maximum speed 97.8% of that achieved after ten. The approach used is appropriate for any treadmill where the running zone length is greater than three metres and the speed controller can be externally controlled. Subjects ran 11.5% faster on the treadmill than overground, part of which can be explained by the removal of aerodynamic drag and the fatigue of overground running. Additional factors may, however, contribute to athletes running faster on a treadmill, for instance some aspect of stability or control.     

Tolerance to central hypovolemia: the influence of oscillations in arterial pressure and cerebral blood velocity

Higher oscillations of cerebral blood velocity and arterial pressure (AP) induced by breathing with inspiratory resistance are associated with delayed onset of symptoms and increased tolerance to central hypovolemia. We tested the hypothesis that subjects with high tolerance (HT) to central hypovolemia would display higher endogenous oscillations of cerebral blood velocity and AP at presyncope compared with subjects with low tolerance (LT). One-hundred thirty-five subjects were exposed to progressive lower body negative pressure (LBNP) until the presence of presyncopal symptoms. Subjects were classified as HT if they completed at least the -60-mmHg level of LBNP (93 subjects; LBNP time, 1,880 ± 259 s) and LT if they did not complete this level (42 subjects; LBNP time, 1,277 ± 199 s). Middle cerebral artery velocity (MCAv) was measured by transcranial Doppler, and AP was measured at the finger by photoplethysmography. Mean MCAv and mean arterial pressure (MAP) decreased progressively from baseline to presyncope for both LT and HT subjects (P < 0.001). However, low frequency (0.04-0.15 Hz) oscillations of mean MCAv and MAP were higher at presyncope in HT subjects compared with LT subjects (MCAv: HT, 7.2 ± 0.7 vs. LT, 5.3 ± 0.6 (cm/s)(2), P = 0.075; MAP: HT, 15.3 ± 1.4 vs. 7.9 ± 1.2 mmHg(2), P < 0.001). Consistent with our previous findings using inspiratory resistance, high oscillations of mean MCAv and MAP are associated with HT to central hypovolemia.     

Middle cerebral artery flow velocity and pulse pressure during dynamic exercise in humans

Exercise challenges cerebral autoregulation (CA) by a large increase in pulse pressure (PP) that may make systolic pressure exceed what is normally considered the upper range of CA. This study examined the relationship between systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) and systolic (V(s)), diastolic (V(d)). and mean (V(m)) middle cerebral artery (MCA) blood flow velocity during mild, moderate, and heavy cycling exercise. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated using transfer function analysis. PP increased by 37% and 57% during moderate and heavy exercise, respectively (P < 0.05), and the pulsatility of MCA V increased markedly. Thus exercise increased MCA V(m) and V(s) (P < 0.05) but tended to decrease MCA V(d) (P = 0.06). However, the normalized low-frequency transfer function gain between MAP and MCA V(m) and between SBP and MCA V(s) remained unchanged from rest to exercise, whereas that between DBP and MCA V(d) increased from rest to heavy exercise (P < 0.05). These findings suggest that during exercise, CA is challenged by a rapid decrease rather than by a rapid increase in blood pressure. However, dynamic CA remains able to modulate blood flow around the exercise-induced increase in MCA V(m), even during high-intensity exercise.     

Temporal pattern of arterial CO2 partial pressure during exercise in humans

The major objective of this study was to test the hypothesis that arterial CO2 partial pressure (PaCO2) does not change in transitions from rest to steady-state exercise and between two levels of exercise. Nine young adults exercised on a treadmill or a bicycle (sit or supine) for 5 min at a mild work load (heart rate = 90 beats X min-1) and then 3 min at a moderate work load (heart rate = 150 beats X min-1). In some studies the moderate work load preceded the mild work load. Arterial blood was sampled from a catheterized artery. During all exercise tasks isocapnia was not strictly maintained (F greater than 4.0, P less than 0.001). For example, a 1-to 2-Torr hypocapnia was the dominant trend during the first 15-45 s after increasing treadmill speed, and a transient hypercapnia was most prevalent when treadmill speed was decreased. During steady-state exercise PaCO2 did not deviate by more than 1-3 Torr from PaCO2 during any resting posture, and PaCO2 differences between exercise intensities and conditions did not exceed 1-2 Torr. A mouthpiece-breathing valve system was not used in most studies, but when this system was used, it did not consistently affect exercise PaCO2. Increasing inspired O2 to 40% likewise did not consistently alter exercise PaCO2. Failure to maintain isocapnia throughout exercise indicates that the matching of alveolar ventilation (VA) to lung CO2 delivery is not exquisitely precise. Accordingly it is inappropriate to base theories of the exercise hyperpnea on the heretofore contention of precise matching.(ABSTRACT TRUNCATED AT 250 WORDS)