Arterial haemodynamics of hypertension.
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Biomedical subjects
Publications and source records attributed to N Westerhof.
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The objective of this study was to investigate if local myocardial metabolism can be determined from the transmural temperature distribution. Heat produced metabolically in the myocardium is carried away by the coronary blood and by diffusion. Transport by coronary flow (convectional heat loss) was determined from the coronary blood flow and the transcoronary temperature difference. This measured value was compared with one predicted from measured oxygen consumption, assuming a slab of tissue for the left ventricular free wall with homogeneous flow distribution and homogeneous metabolism. Measured and predicted convectional heat loss could not be shown to differ. Endocardial and epicardial heat production were estimated in two ways: 1) from the transmural temperature distribution (AT) and 2) from local flow (radioactive microspheres) and oxygen consumption (AO2). Ideally the ratio AT/AO2 should be unity. For flows in the resting physiological state (up to 100 ml X min-1 X 100 g-1) this ratio was not statistically different from one for both endocardium and epicardium: 0.86 +/- 0.11 and 1.09 +/- 0.07 (SE), respectively. For larger flows the ratio reduced to 0.66 +/- 0.08 endocardially. It is concluded that overall left ventricular metabolism can be predicted from conventional heat loss and that for physiological, but not for increased flow, the transmural temperature distribution predicts local metabolism.
We have used a computer-based parameter estimation method to obtain peripheral resistance, total arterial compliance, and characteristic resistance from the measurement of aortic pressure and flow in the open-thorax cat, assuming the three-element windkessel as a model of the systemic arterial tree. The method can be applied on a beat-to-beat basis in the steady state and in transients. We have validated this method by analyzing nonsteady-state data obtained from an electrical analog with fixed values of the resistances and compliance and by showing that the values obtained by this procedure were within 5% of the fixed values of the circuit. Changes in total peripheral resistance and arterial compliance were studied before, during, and after acute heart rate changes in five open-thorax cats with blocked autonomous nervous system. As expected, the peripheral resistance, estimated during the heart rate transient [3.93 +/- 0.94 (SE) kPa X ml-1 X s] was the same as before the transient (3.53 +/- 0.83 kPa X ml-1 X s); total arterial compliances were also identical (0.28 +/- 0.04 vs. 0.27 +/- 0.03 ml/kPa). In six cats without nervous blockade we obtained similar results. Calculation of peripheral resistance during transients from the mean pressure-to-mean flow ratio, i.e., without correction for arterial compliance, suggested changes in resistance values of less than or equal to 57%, which shows that correction is necessary. The findings indicate that peripheral resistance and total arterial compliance can be estimated in vivo on a beat-to-beat basis, even during hemodynamic transients.
Arterial pulse transmission and wave reflections were studied in five mature anesthetized baboons (Papio anubis) using multisensor micromanometry. Simultaneous pressures were recorded from the left ventricle and every 10 cm along the aorta and its terminal branches, and flow velocity was measured in the aortic root. Aortic input impedance and regional foot-to-foot and apparent phase velocities were calculated. Aortography provided dimensional data for local reflection coefficients. Regional foot-to-foot wave speeds were somewhat lower than corresponding segments in humans. Proximal aortic pressure waveforms and characteristic impedance (110 +/- 29 dyn X s X cm-5) were not characteristic of middle-aged humans. Reflection coefficients at the terminal aortic bifurcation (0.06) at the level of the renal artery branches (0.09) were less than those found in humans. We conclude that the junction of the renal artery branches and the aorta in the baboon is closely matched and represents much less of a discrete reflection site than in humans. Although the baboon may be used to study pulse transmission characteristics in the baboon, this species is not a good model for the proximal systemic reflective characteristics of normal middle-aged humans.
The coronary arterial system was characterized by its input impedance determined in systole and diastole from impulse response functions in five dogs. The impulse response technique was verified on a known hydraulic system. A second confirmation was obtained on the circumflex artery: reflected pulses were correlated with site of reflections generated by occlusions. The impulse response indicates discrete reflections, superimposed on the tail of the response, resulting from diffuse reflections. Input impedance was calculated from Fourier analysis of the impulse response. Characteristic impedance was 1.0 +/- 0.2 X 10(9) Pa X s X m-3 (0.13 +/- 0.02 mmHg X ml-1 X min) and impedance at 0 Hz was 2.6 +/- 0.8 X 10(9) Pa X s X m-3. No significant differences between systole and diastole were found in both characteristic impedance and impedance at 0 Hz. It is concluded that the coronary system consists of a proximal part that can be described with the three-element windkessel and a distal part not seen by oscillatory pressure or flow perturbations, which depends on the phase of cardiac contraction.
It has been reported that sodiumnitroprusside (SNP) decreases mean systemic pressure and simultaneously increases pressure pulse amplification towards the iliac periphery (Kenner and van Zwieten 1982). This unexpected finding was suggested to be due to a decrease in iliac peripheral resistance but an increase in iliac differential resistance. In order to investigate this apparent contradiction, the iliac periphery was hemodynamically isolated from the rest of the circulation and perfused with the dog's own blood by means of a pump. Perfusion pressure (P) and flow (F), femoral venous pressure (Pv), systemic pressure (Ps) and cardiac output (CO) were measured. Steady state pressure-flow relations of the isolated bed were obtained during control and during various i.v. infusion rates of SNP and adenosine (ADS) and were found to be straight (mean r = 0.99). Their slope (delta P/delta F) was defined as differential resistance (Rd). Peripheral resistance (Rp) of the iliac bed was defined as Rp = (P-Pv)/F, calculated at the flow value where perfusion pressure equalled the prevailing systemic pressure. Total peripheral resistance (TPR) was defined as TPR = Ps/CO. The changes of Rd, Rp, Ps, CO and TPR with respect to control show that during low SNP infusion rates Rd and Rp were both increased while TPR was decreased. During all infusion rates of SNP CO did not change while Ps decreased. During low infusion rates of adenosine CO increased while Ps, Rd and Rp did not change and TPR decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
Pressure, flow and diameter were measured in the abdominal aorta of five anesthetized dogs during normal heart beats and heart beats with a superimposed impulse (generated by rapidly injecting a small volume of saline into the system). From Fourier analysis it was found that the impulse enhanced the amplitudes of the higher harmonics so that frequencies up to 80 Hz could be studied. Both the input impedance and apparent phase velocity above 20 Hz were independent of frequency and their average values were designated as characteristic impedance and true phase velocity. Average characteristic impedance for all five animals was 2.0 +/- 0.1 X 10(8) Nsm-5 and average phase velocity was 8.3 +/- 0.6 ms-1. Phase velocities calculated from characteristic impedance (1.76-2.39 X 10(8) Nsm-5) and from the slope of the pressure-diameter relation (0.102-0.25 X 10(-8) Nm-3) were similar to the true phase velocity as defined above (6.79-9.85 ms-1). It may be concluded that the input impedance converges to characteristic impedance and apparent phase velocity converges to phase velocity for high frequencies.
The blood supply to the femoral bed was studied in anaesthetised dogs before and after producing arterial stenoses. The blood supply system consisted of the vessels proximal to the site of measurement in the femoral artery and was characterised by a supply graph, which related mean perfusion pressure to mean flow. The different pressures and flows were obtained using an artificial periphery, the impedance of which was changed from beat to beat. The supply graph was approximated by a parabola with two parameters: the intercepts with the pressure and flow axes, the latter indicating the maximum mean flow. For constant aortic pressure the maximum mean flow appeared to be linearly related to the cross sectional area of the stenosed section (r = 0.98). Maximum mean flow was already considerably reduced before the stenosis became critical--that is, before physiological flow was measurably diminished. The change in maximum mean flow was therefore used to quantify the haemodynamic effects of stenoses that were less than critical. Blood supply graphs of the superficial femoral arteries were determined also in seven patients undergoing a femoropopliteal bypass operation. The maximum mean flow correlated well with the degree of obstruction determined from the preoperative angiograms (r = 0.90).
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In a previous study we showed that under a variety of conditions the feline left ventricle operates at optimum external power. This condition was defined as matching. In the present study matching of left ventricle and systemic arterial tree has been further investigated in the open-thorax cat during control, after volume loading (n = 8), and during norepinephrine infusion (n = 8). The pump-function graph relating mean left ventricular pressure and mean flow was fitted with a parabola characterized by two parameters, the pressure axis and the flow axis intercepts (Pmax and Fmax, respectively). After volume loading, as well as during norepinephrine infusion, the pump-function graph showed an outward shift plus a clockwise rotation. Pmax and Fmax increased 27 and 8% during volume loading and 37 and 8% during norepinephrine. In the steady states the mean flows at the working point and at the point of optimum external power were determined. During control and volume loading these flow values could not be shown to differ. However, during norepinephrine infusion, flow at the working point was found to be smaller than at optimal external power. This finding implies that during norepinephrine, the left heart does not operate at optimum external power; so a mismatch of heart and periphery is obtained.
Total arterial compliance is an important haemodynamic variable which is difficult to measure in vivo. Using a Windkessel model, it can be determined from the ratio of the diastolic-decay time constant (tau) of the arterial system and the peripheral resistance. Using this technique, paired estimates of arterial compliance were determined in control and in mechanically produced low-compliance steady states. Since determination of compliance based on the three-element Windkessel model is tedious the same data were retrospectively analysed to evaluate the reliability of the stroke volume to pulse pressure ratio (SV:PP) for estimating and predicting changes in compliance. The linear correlation coefficient for 148 paired values of compliance determined by the two methods was r = 0.85, P less than 0.001. Both methods indicated similar values (mean +/- s.e.m.) for compliance in the control steady state: 0.35 +/- 0.01 ml/mmHg (using tau/R) versus 0.36 +/- 0.01 ml/mmHg (using SV:PP), P was NS, and both methods detected a significant decrease in compliance, P less than 0.001, in the low-compliance steady state: 0.18 +/- 0.01 ml/mmHg (using tau/R) and 0.21 +/- 0.01 ml/mmHg (using SV:PP). Thus, SV:PP compared with (tau/R) was a good index of compliance and changes in compliance and may prove to be a useful index for estimating compliance clinically.
This study was performed to elucidate the effects of cardiac contraction on coronary pressure-flow relations. On the basis of the waterfall mechanism, a lumped model of the coronary arterial system is presented consisting of a proximal (epicardial) compliance, a coronary resistance, and an intramyocardial compliance. A "back"-pressure, assumed to be proportional (constant k) to left ventricular pressure, impedes flow. From steady-state measurements of circumflex coronary artery flow and inflow pressure, together with left ventricular pressure, the values of the three model parameters and the constant k have been estimated. In the control condition proximal compliance is found to be 1.7 X 10(-12) m4s2kg-1, intramyocardial compliance 110 X 10(-12)m4s2kg-1, and resistance 7.5 X 10(9) kgm-4s-1. The proportionality constant k is close to unity. Effects of changes in left ventricular pressure and inflow pressure and the effect of vasoactive drugs on the parameters are also investigated. Changes in coronary resistance are always opposite to changes in intramyocardial compliance. Sensitivity analysis showed that epicardial compliance plays its major role during isovolumic contraction and relaxation; resistance plays a role throughout the cardiac cycle but is more important in diastole than in systole, whereas intramyocardial compliance plays a role in systole and in early diastole.
Steady-state and instantaneous pressure-flow relations were both obtained from the pump-perfused left coronary bed of the beating heart in seven mongrel dogs. The steady-state pressure-flow relation was obtained by changing flow, and measuring pressure after it reached a steady level; it showed a sigmoid shape, with flow-regulation around 70 ml . min-1 . 100 g-1, and it had an average zero-flow pressure intercept of 1.9 kPa (14 mmHg). This curve was represented by an equation, using four parameters. The quality of regulation of the coronary bed could be quantified with this equation by determining the pressure range, when flow was changed from 25% below to 25% above control level. We found this pressure range to be 8.7 +/- 2.4 kPa (65 +/- 18 mmHg) on the average. The tangent at each point of steady-state pressure-flow relation was called differential resistance. Instantaneous pressure-flow relations were obtained by superimposing stepwise changes of flow of different amplitude, at several steady-state levels of flow. Pressure followed these steps with a time-constant of 0.3 +/- 0.1 s, due to capacitive effects, then remained constant during 3 to 4 s, and thereafter changed due to regulation. Pressure was measured during the plateau, assuming it to be a regulation-free period. The instantaneous pressure-flow relations were found to be linear, and the slope was called instantaneous resistance. In the physiological range of flows, instantaneous resistance increased with flow. The ratio between instantaneous and differential resistance, the regulatory index, is suggested to quantify regulation at each point of the steady-state curve. This index was between one and zero up to the upper limit of the regulatory range; at higher flows it was negative. In the maximally vasodilated bed the instantaneous pressure-flow relations fell along the steady-state relation, and the regulatory index was thus equal to zero at all flow-levels.
The human aorta and its terminal branches were investigated in normal subjects during elective cardiac catheterization to evaluate regional wave travel and arterial wave reflections. A specially designed catheter with six micromanometers equally spaced at 10 cm intervals was positioned with the tip sensor in the distal external iliac artery and the proximal sensor in the aortic arch. Simultaneous pressures were obtained and analyzed for foot-to-foot wave velocity, and Fourier analysis was used to derive apparent phase velocity. These quantities were assessed during control (n = 9), during Valsalva (n = 8) and Müller (n = 4) maneuvers, and during femoral artery occlusion by bilateral manual compression (n = 8). During control, regional cross-sectional areas, determined from aortography, and regional foot-to-foot pulse wave velocities were used to calculate the local reflection coefficient in the proximal descending aorta (gamma = 0.05), at the junction of the renal arteries (gamma = 0.43), and at the terminal aortic bifurcation (gamma = 0.13). To test the hypothesis that significant reflections originate in the aorta, at the level of the renal arteries, aortograms were used to design a latex tube model with geometric properties similar to the descending aorta. Velocities and reflection characteristics in the model and in vivo were compared. Inspection of thoracic aortic pressures under control conditions revealed a reflected wave originating from the region of the aorta at the level of the renal arterial branches while abdominal pressures exhibited reflection from a site peripheral to the terminal aortic bifurcation. In the low frequency range, apparent phase velocity was found to be higher proximal to the renal arteries as compared with at the distal sites. In addition, the minimum value occurred at a higher frequency in the lower thoracic aorta than at more distal sites. The effects of reflection on apparent wave velocity in the tube model were consistent with data obtained in vivo. The Valsalva maneuver diminished the reflection from the aortic region of the renal arteries, thus allowing the distal reflected wave to become more evident on the thoracic pressure waveforms. Bilateral femoral artery occlusion usually enhanced the distal reflection and the Müller maneuver usually resulted in small increases in reflections. In conclusion, the geometric and elastic nonuniformity of the aorta results in two major sites of arterial wave reflection that influence the aortic pressure waveforms in man.(ABSTRACT TRUNCATED AT 400 WORDS)
We studied the interaction of the left ventricle and the systemic arterial bed in the open thorax cat. In the steady state, the ventricle can be characterized by the pump function graph (i.e., the relationship between mean left ventricular pressure and mean outflow). From this pump function graph, the apparent source resistance of the heart is found. Apparent source resistance is defined as the ratio of the difference between maximal and actual mean left ventricular pressure, and mean outflow. The arterial system can be characterized by the ratio of mean aortic pressure and mean flow (peripheral resistance). The pressure and flow at which the heart operates is defined as the working point. We have investigated whether the ventricle in the intact cat is working optimally, i.e., that it cannot increase work output further at the end-diastolic volume, contractile state, and prevailing heart rate. This condition is considered as "matching" of ventricle and load. It could be shown that optimal power is transferred when the ratio of peripheral and apparent source resistance equals twice the ratio of mean aortic and mean left ventricular pressure (the matching principle). In four cats, we observed that mean aortic and mean left ventricular pressures are proportionally related. Mean external power (the time integral of the product of pressure and flow divided by cycle length) and steady power (the product of mean pressure and mean flow) were found to be proportional as well. These proportionalities allow for the calculation of peripheral resistance and mean external power from the pump function graph. Pump function graphs were determined in three groups: control (n = 9), atrial pacing (n = 8), and halothane (n = 5). We compared the ratio of peripheral and source resistance at the working point and at the point of optimal work output (expressed in steady ventricular power). It could be shown that, in all investigated groups, the power optimum and the working point coincide. It was concluded that circulatory control in the intact anesthetized cat keeps the ventricle at optimal work output under the conditions studied.
We have studied the interrelation of left ventricle and arterial system in the anesthetized open-thorax cat. The ventricle was characterized by its pump function graph, relating mean ventricular pressure (Plv) and mean aortic flow (F). The pump function graph was determined by means of an artificial periphery and on a beat-to-beat basis. The periphery was characterized by relating mean aortic pressure (Pao) and mean flow. Mean aortic and mean left ventricular pressure could be related over a wide range of values by a proportionality factor Pao = a . Plv. In a series of five separate experiments a value of a = 1.72 +/- 0.14 (mean +/- SD) was found. This simplified relation allows direct comparison of apparent source resistance (i.e., slope of pump function graph), (Rs), and peripheral resistance (Rp). It was also found experimentally that total external power (w) could be calculated from mean aortic pressure and mean flow as well as from mean left ventricular pressure and mean flow (thus from the pump function graph) by w = c . Pao . F = c . a . Plv . F. The value of c = 1.16 +/- 0.12 (mean +/- SD, n = 4). Maximum external power was predicted for Rp/Rs = Pao/Plv = a. In six different cats Rp/Rs ratio in the working point (i.e., mean left ventricular pressure and mean flow when the normal periphery loaded the heart) was found to be Rp/Rs = 2.63 +/- 0.92. This value could not be shown to differ from that in the point where maximal external power was found, i.e., Rp/Rs = 1.81 +/- 0.08 (n = 6).
Arterial compliance is part of the load faced by the heart. Decreased compliance increases this load. We have studied the cardiovascular consequences of decreased systemic compliance in six closed chest anaesthetised dogs where ascending aortic flow transducers and left ventricular crystals had previously been implanted. A stiff tube was put into the abdominal aorta from the left flank and moved to the ascending aorta. Inflation of a cuff on the proximal end of the tube forced the heart to eject into a non-compliant outflow conduit. The distal end of the tube was connected to the distal aorta and, via a pump, to a carotid artery where mean pressure was kept above 80 mmHg. We measured systemic pressures (catheter-tip manometer), cardiac output (electromagnetic flowmeter) and either left ventricular end-diastolic pressure (fluid filled catheter, Statham P23Db) or left ventricular diameter (ultrasound transit time method). From these variables we calculated systemic compliance and input impedance. A 35% decrease in compliance caused a 12% increase in systolic, and a 12% decrease in diastolic pressure while mean pressure and cardiac output did not change significantly. With a decrease in compliance of 63% systolic pressure increased by 18%, while diastolic pressure decreased by 24%. Mean pressure did not change significantly but cardiac output fell by 21%. In both groups of altered compliance peripheral resistance rose slightly but this was not significant. Decreased compliance mainly caused changes in the low frequency range of the input impedance: moduli increased and phase angles became more negative.(ABSTRACT TRUNCATED AT 250 WORDS)
Oxygen consumption following isometric tetanic contractions of single fibres and multifibre preparations of the tibialis anterior muscle of Rana temporaria was determined by continuous polarographic measurement of the PO2 in a 280 microliter glass chamber. Mixing of the fluid surrounding the muscle was achieved by an Archimedian screw. Force was measured via a stainless-steel wire leaving the chamber via a glass capillary. The characteristics of the oxygen-measuring system were assessed by injection of 1.6 microliter dye into the chamber and filming its subsequent distribution, and by injection of 1.6 microliter Ringer solution with a high (or low) oxygen content into the chamber and measuring the subsequent change of oxygen. It was found that a change in oxygen was measured after a true delay of 3 s and with an over-all time constant of 3.25 s following that delay. For seven single fibres the oxygen consumption following a 3 s tetanus was on average 2.46 mumol g-1; the average integrated value of the developed stress was 0.98 N mm-2 s. These two values were on average about 45% lower for the same tetani of multifibre preparations, but the average ratio of oxygen consumption to integrated stress was the same. Oxygen consumption was varied by changing tetanus duration. When the amount of oxygen consumed was plotted against stress integral a non-linear relationship was found because oxygen consumption increased less than the integrated stress value with longer tetani. Oxygen consumption did not start at the onset of contraction but about 10 s later. It then followed an exponential time course with an average time constant of 120 s. Delay and time constant were independent of the amount of oxygen consumed. The finding that oxygen consumption follows contraction after a delay of a few seconds confirms a similar conclusion drawn indirectly from studies on recovery heat by other investigators. A dependency of the time course of oxygen consumption on tetanus duration, as reported in the literature for frog muscle at 0 degree C, was not found.