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Biomedical subjects

W L Maughan

Publications and source records attributed to W L Maughan.

At least 55 records · Page 3Linked to original sources
PubMed1984

Ventricular interaction with the loading system.

The purpose of this investigation was to develop a theoretical framework to predict stroke volume (and therefore cardiac output) when the ventricle is coupled with the arterial impedance. The ultimate objective is to arrive at an analytical description of cardiac output in the closed hydraulic loop of the entire circulatory system on the basis of the properties of the major system components. We developed the framework of analysis of ventriculo-arterial coupling by characterizing both the ventricle and arterial system in terms of the end-systolic pressure vs. stroke volume (Pes-SV) relationships. This approach, motivated by the load-insensitivity of ventricular end-systolic pressure-volume relationship (ESPVR), yielded stroke volume as the intersection between the ventricular Pes-SV relationship and arterial Pes-SV relationship. The theoretical outcome was validated by comparing the stroke volume predicted as a result of interaction between a given ventricular ESPVR and a set of arterial impedances against those SVs actually measured by imposing the same arterial impedance on the isolated canine ventricles. Furthermore, because of the mathematical simplicity of this approach, it enabled us to describe cardiac output in the closed circulatory loop with a small set of analytical equations. We conclude that the proposed framework is useful in analyzing the ventriculo-arterial coupling and various mechanisms which affect cardiac output in the closed circulatory loop.

Arteries↗
PubMed1984

Effects of arterial input impedance on mean ventricular pressure-flow relation.

The mean left ventricular pressure-flow relationship (Pv-Fv), determined under a constant preload and variable peripheral resistance, has been proposed as a quantitative representation of ventricular pump function (9). We determined the Pv-Fv relation in seven isolated cross-perfused canine hearts by varying resistance of a simulated arterial load in five steps from 6.0 to 0.375 mmHg X s X ml-1 while keeping end-diastolic volume, inotropic state, compliance, and characteristic impedance at various constant values. All of the 27 Pv-Fv relations thus determined were moderately nonlinear. Varying end-diastolic volume at three levels shifted the relation curve in an approximately parallel fashion (P less than 0.0001). At three levels of inotropic state (mean LVP of isovolumic contractions 34.3 +/- 8.2, 48.0 +/- 6.3, and 59.2 +/- 9.6 mmHg), the Pv-Fv relation shifted with predominantly a slope change (P less than 0.0001). Changing compliance at three levels (0.2, 0.4, and 0.8 ml/mmHg) caused a statistically significant but quantitatively small crossover of the Pv-Fv curves (P less than 0.0001). Changing characteristic impedance to 0.1, 0.2, and 0.4 mmHg X s X ml-1 caused a highly significant (P less than 0.0001) divergence of Pv-Fv relation over the high Fv range. We conclude that this sensitivity of the Pv-Fv relation to characteristic impedance limits its use as a contractility index.

Animals↗
PubMed1984

The use of left ventricular end-ejection pressure and peak pressure in the estimation of the end-systolic pressure-volume relationship.

The end-systolic pressure-volume relationship (ESPVR) as derived from left ventricular pressure-volume loops has gained increasing acceptance as an index of ventricular contractile function. In animal experiments the ESPVR has been defined as a line connecting the upper left corners of several differently loaded pressure-volume (P-V) loops with a slope parameter Ees and a volume axis intercept parameter Vo. In the clinical setting, several variants of the ESPVR have been determined with use of peak left ventricular pressure, end-ejection pressure, and end-ejection volume. The maximum P-V ratio has also frequently been measured. We attempted to determine which of these alternatives resulted in good approximations of the reference ESPVR in eight isolated canine ventricles that ejected into a simulated arterial impedance system with resistance, compliance, and characteristic impedance. We determined various versions of the ESPVR from the same set of beats quickly obtained with little change in inotropic background. To vary ventricular pressure wave forms, each of the arterial impedance parameters was independently controlled at 50%, 100%, and 200% of normal. Against each of the nine combinations of the impedance parameters four P-V loops were obtained under four preloads and from each of the sets of four P-V loops, the reference ESPVR, linear regression of the peak pressure on end-ejection volume (ESPVRPP-EEV), and linear regression of end-ejection pressure on end-ejection volume (ESPVREEPV) were determined. In addition, the maximum P-V ratio (MPVR) was calculated for each P-V loop.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Quantitative comparison of the force-interval relationships of the canine right and left ventricles.

We quantitatively compared the extrasystolic and postextrasystolic responses of the right ventricle and left ventricle of the same heart, which have vastly different geometries, architectures, and muscle masses. We studied nine isolated, supported canine hearts whose right and left ventricles were made to contract isovolumically with balloons placed in both chambers. The ventricles were paced with the following pattern: 20 regularly timed priming stimulations, followed by a test stimulation at a variable test pulse interval, and, finally, by a second test stimulation which was always delivered 1200 msec after the first test pulse. In each heart, approximately 15 different test pulse intervals between 300 and 1200 msec were investigated. Both the maximum developed pressure and maximum rate of pressure development, expressed as a percentage of their steady state values during the priming period were used to quantify the extra- and postextrasystolic responses. For each extrasystolic and postextrasystolic test beat, the normalized response of the right ventricle was plotted vs. that of the left ventricle. The regression line and correlation coefficient between the two were determined. The average result from nine hearts gave a slope of 0.96 +/- 0.05, an intercept of 4.52 +/- 4.05% and a correlation coefficient of 0.995 +/- 0.004. This analysis indicated that, despite the differences in right and left ventricular geometry, architecture, and mass, their force-interval behaviors were nearly identical.

Animals↗
PubMed1984

Effect of arterial impedance changes on the end-systolic pressure-volume relation.

To study the end-systolic pressure-volume relationship of left ventricle ejection against physiological afterload, we imposed seven simulated arterial impedances on excised canine left ventricles connected to a newly developed servo-pump system. We set each of the impedance parameters (resistance, capacitance, and characteristic impedance) to 50, 100, and 200% of normal value (resistance: 3 mm Hg sec/ml; capacitance: 0.4 ml/mm Hg; characteristic impedance: 0.2 mm Hg sec/ml), while leaving the other parameters normal. Under a given impedance, the end-systolic pressure-volume relationship was determined by preloading the ventricle at four different end-diastolic volumes. There was no significant change in the slope of the end-systolic pressure-volume relationship with changes in any of the afterloading impedance parameters. However, the volume intercept of the end-systolic pressure-volume relationship decreased significantly with resistance from 5.5 +/- 1.0 (SE) ml at resistance equal to 1.5 mm Hg sec/ml to 0.6 +/- 1.8 ml at resistance equal to 6 mm Hg sec/ml (P less than 0.01). The volume axis intercept also decreased with characteristic impedance, from 5.9 +/- 2.0 ml at a characteristic impedance of 0.1 mm Hg sec/ml to 5.4 +/- 2.1 ml at a characteristic impedance of 0.4 mm Hg sec/ml, (P less than 0.05). We conclude that the slope of the end-systolic pressure-volume relationship is insensitive to a wide range of changes in afterload impedance, but its volume intercept is dependent on resistance and characteristic impedance.

Animals↗
PubMed1984

Factors affecting the end-systolic pressure-volume relationship.

The end-systolic pressure-volume relationship (ESPVR) defines the systolic limits of cardiac performance. Using an isolated cross-circulated canine heart preparation, we examined the influence of afterload impedance changes, changes in coronary artery pressure (CAP), and regional ischemia on the ESPVR. We found that afterload impedance did not change the slope of the ESPVR but that increases in resistance and characteristic impedance did shift the relation slightly to the left. There was no change in the ESPVR with changes in CAP above a certain critical value. A decrease in CAP below this value caused a progressive decline in the slope of the ESPVR. With regional ischemia the ESPVR became nonlinear, and there was a near parallel downward shift of the ESPVR in the high-volume range. This shift was directly proportional to the extent of ischemic area. We conclude that an adequate measurement of the ESPVR demands at least three pressure-volume points to check for linearity and characterization of both the slope and volume intercept.

Animals↗
PubMed1983

Left ventricular interaction with arterial load studied in isolated canine ventricle.

We developed a framework of analysis to predict the stroke volume (SV) resulting from the complex mechanical interaction between the ventricle and its arterial system. In this analysis, we characterized both the left ventricle and the arterial system by their end systolic pressure (Ps)-SV relationships and predicted SV from the intersection of the two relationship lines. The final output of the analysis was a formula that gives the SV for a given preload as a function of the ventricular properties (Ees, V0, and ejection time) and the arterial impedance properties (modeled in terms of a 3-element Windkessel). To test the validity of this framework for analyzing the ventriculoarterial interaction, we first determined the ventricular properties under a specific set of control arterial impedance conditions. With the ventricular properties thus obtained, we used the analytical formula to predict SVs under various combinations of noncontrol arterial impedance conditions and four preloads. The predicted SVs were compared with those measured while actually imposing the identical set of arterial impedance conditions and preload in eight isolated canine ventricles. The predicted SV was highly correlated (P less than 0.0001) with the measured one in all ventricles. The average correlation coefficient was 0.985 +/- 0.004 (SE), the slope 1.00 +/- 0.04, and the gamma-axis intercept 1.0 +/- 0.2 ml, indicating the accuracy of the prediction. We conclude that the representations of ventricle and arterial system by their Ps-SV relationships are useful in understanding how these two systems determine SV when they are coupled and interact.

Animals↗
PubMed1983

Accuracy of volume determination by two-dimensional echocardiography: defining requirements under controlled conditions in the ejecting canine left ventricle.

The accuracy of two-dimensional echocardiographic left ventricular volume measurement in an isolated heart preparation was tested using Simpson's reconstruction of progressively fewer short-axis cross sections of known location. Echocardiographic images from five ejecting hearts submerged in a special tank were obtained under conditions designed for maximal accuracy of echocardiographic volume assessment. Echocardiographic determinations of 52 volumes at various times throughout the cardiac cycle were compared, by least-squares linear regression, with simultaneous direct-volume measurements by volumetric chamber (range 9.4-44.8 ml). Echocardiographic and direct measurements correlated well for all numbers of cross sections from 1-19 (r = 0.84-0.97); however, variability of direct volume predicted from a given echocardiographic measurement increased nonlinearly as the number of cross sections per heart decreased, and was especially large when three or fewer cross sections were used (SEE = 4.6-7 ml). The accuracy of echocardiographic measures was compared for each number of cross sections per heart, varying from one to 19; accuracy was defined as the mean absolute difference between echocardiographic and direct measurements of volume, ejection fraction, and maximal rate of ejection. The accuracy of echocardiographic measurements was significantly reduced with fewer than four cross sections per heart for ventricular volume, three cross sections for ejection fraction, and five cross sections for maximal rate of ejection. In light of what appears to be required for accurate echocardiographic volume measurement in this controlled, ejecting, noninfarcted, in vitro preparation, additional cross sections may be required in intact animals and human subjects, especially in those with diseases that cause ventricular asymmetry or regional dysfunction.

Animals↗
PubMed1983

Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure.

We studied the effect of nitroprusside on the hydraulic vascular load of the right and left ventricle in seven patients with severe left ventricular failure. At doses of 0.25-0.75 micrograms/kg/min, stroke volume increased progressively from 40.1 to 48.6 ml and left ventricular end-diastolic pressure decreased from 24.5 to 11.2 mm Hg. Accompanying this improvement in left ventricular performance were dose-related decreases in mean ventricular pressures, pulmonic and systemic resistances and the lower-frequency components of input impedance moduli. Characteristic impedance and both total and oscillatory external power were decreased in the pulmonic, but not the aortic, vasculature. In this class of patients, right ventricular unloading is a striking and direct effect of nitroprusside and may account, in part, for improved left ventricular performance through ventricular interdependence.

Adult↗
PubMed1983

Effect of regional ischemia on the left ventricular end-systolic pressure-volume relationship of isolated canine hearts.

We studied the effects of regional ischemia on the left ventricular isovolumic end-systolic pressure-volume relationship (ESPVR) in six excised, blood-perfused canine ventricles. We created different extents of regional ischemia by ligating various branches of the coronary arteries while keeping the coronary arterial pressure constant (80 mm Hg). The extent of regional ischemia (Rm) relative to the total mass of the left ventricular myocardium was determined by regional myocardial blood flow measured by the radioactive microsphere technique. With regional ischemia, the ESPVR shifted rightward without significant change in slope in the physiologic end-systolic pressure range. In the subphysiological end-systolic pressure range, however, its slope became lower than control. In order to quantify the degree of the rightward shift, we measured the extrapolated volume axis intercept (Vo) by fitting a straight line to the ESPVR in the physiological range under control and ischemic conditions. The shift in Vo (delta Vo) associated with ischemia was linearly correlated with Rm (delta Vo = 50.7Rm-0.6, n = 28, r = 0.944, P less than 0.001). We conclude that the major effect of acute regional ischemia on the ESPVR in the physiological pressure range is a parallel rightward shift. This forms a striking contrast to the effect of global ischemia (under which only the slope is affected without a substantial change in Vo).

Animals↗
PubMed1982

Effects of coronary arterial pressure on left ventricular end-systolic pressure-volume relation of isolated canine heart.

In the excised canine left ventricle, the end-systolic pressure-volume relationship (ESPVR) has been shown to be approximately linear over the working range of loading conditions when coronary arterial pressure (CAP) is maintained constant, independent of loading conditions. To investigate the ESPVR under the more intact physiological condition in which the CAP varies with loading on the left ventricle, we studied the effect of changes in CAP on the ESPVR in 10 excised cross-circulated canine ventricles which were contracting isovolumically. The ESPVR, determined from isovolumic contractions at four different volumes, was reasonably independent of CAP as long as CAP remained above a critical pressure (67.0 +/- 22.1 mm Hg). Below this pressure, the slope of ESPVR decreased although the volume axis intercept (V0) remained unaltered. These findings indicate that under physiological conditions, where there is a close coupling of CAP to systolic left ventricular pressure, the ESPVR should become nonlinear in the low preload or afterload regions. When CAP was varied with the left ventricular pressure in five ventricles, the ESPVR indeed became nonlinear in the low-load region. We conclude that the ESPVR in intact conditions is reasonably linear in the physiological load range, but it can be nonlinear in the low-load range.

Animals↗
PubMed1981

Ventricular size and shape by two-dimensional echocardiography.

The evaluation of cardiac size and shape has been aided by the recent development of high resolution real-time two-dimensional echocardiography, which permits dynamic cross-sectional evaluation of all or a large portion of the left ventricle throughout the cardiac cycle. This review addresses itself to the determination of left ventricular size and shape by two-dimensional echocardiography. A method is described for accurate volume determination in the intact, isolated, ejecting canine heart. By combining the two-dimensional echocardiogram with knowledge of transducer position and orientation with respect to the heart, it is possible to reconstruct a three-dimensional representation of a chamber and thereby measure volume without reliance on major geometric assumptions. Because of the unique ability of two-dimensional echocardiography to produce a cross-sectional image of the beating heart in a large number of planes, it is suitable for the determination of cardiac shape and architecture. The recognition of early regional cardiac dilatation in acute myocardial infarction is described. Changes in ventricular shape brought about by the dynamic alterations lend themselves well to two-dimensional echocardiographic study. The pivotal nature of the interventricular septum renders it susceptible to changes in the functional state of both ventricles. That the interventricular septum may mediate ventricular interaction acutely is suggested by the acute effects of right ventricular loading in man using the Mueller maneuver. Leftward septal displacement and flattening of the septum during the early maximal Mueller maneuver is evidenced by a substantial increase in the radius of curvature of the septal segment, without a change in the left ventricular free wall. This septal flattening occurs in diastole and persists during systole. Diastolic events thus appear to influence systolic shape. Changed septal shape may be an important mechanism of, and evidence for, ventricular interdependence in normal man.

Animals↗
PubMed1981

Transseptal pressure gradient with leftward septal displacement during the Mueller manoeuvre in man.

Septal displacement is postulated as an important mediator of ventricular interdependence. During acute right ventricular loading with the Mueller manoeuvre the septum flattens and shifts leftward. To investigate the mechanism of this septal deformation, we measured transseptal pressures in nine patients during Mueller manoeuvres with simultaneous right and left ventricular micromanometers, and left ventricular configuration with two-dimensional echocardiograms. Data were analysed throughout diastole and at end-systole during control and maximum Mueller manoeuvre (-40 to -80 mmHg airway pressure). Leftward septal displacement during the Mueller manoeuvre was evidenced by an increase in septal radius of curvature at end-diastole persisting through end-systole. The left ventricular free wall radius of curvature was unchanged. During the Mueller manoeuvre, the left ventricular cavity area decreased significantly in the cross-sectional view. All Mueller manoeuvres were associated with a decrease in left-to-right ventricular transseptal pressure gradient throughout diastole. There was no significant change in the gradient at end-systole; septal flattening persisted, however, despite a pronounced left to right pressure gradient. Thus, diastolic septal flattening during right ventricular loading is associated with a decreased transseptal pressure gradient but does not require right ventricular diastolic pressure to exceed left ventricular diastolic pressure. The persistence of flattening in systole suggests that once septal shift occurs during diastole, other forces during systole maintain the deformity despite a large intracavitary transseptal gradient.

Blood Pressure↗
PubMed1981

The effect of right ventricular filling on the pressure-volume relationship of ejecting canine left ventricle.

Acute shifts in the pressure-volume relationship of the left ventricle occur under several conditions. One potential mechanism for this phenomenon is ventricular interdependence, that is, the influence of right ventricular filling on the left ventricle. This mechanism was studied in an isolated cross-circulated ejecting canine heart preparation with balloons sewn into both right and left ventricles and connected to volumetric chambers allowing continuous and accurate simultaneous measurement of right and left ventricular pressures and volume. Sets of left ventricular pressure-volume loops were obtained under a variety of right ventricular volumes. Experiments were repeated with and without the pericardium. Both diastole and systole were studied. We show that in the pericardium-free heart working over a normal range of volumes, the right ventricle exerts little influence on left ventricular pressure. With the pericardium present, there is a small but significant effect of right ventricular volume on left ventricular pressure during systole and diastole. Over a wider range of volumes imposed in the arrested heart, the right ventricle does influence left ventricular pressure even without the pericardium. Thus we have demonstrated that ventricular interdependence is not likely to lead to large acute pressure-volume shifts, either during diastole or systole, except in the presence of considerably above normal right ventricular volumes.

Animals↗