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Biomedical subjects

D Burkhoff

Publications and source records attributed to D Burkhoff.

125 records · Page 7Linked to original sources
PubMed1986

Influence of pacing site on canine left ventricular contraction.

We investigated the influence of pacing site on several aspects of left ventricular (LV) performance to test the hypothesis that "effective ventricular muscle mass" is reduced with direct ventricular pacing. All studies were performed on isolated supported canine hearts that were constrained to contract isovolumically. To determine the influence of pacing site on magnitude and time course of isovolumic LV pressure (P) generation, LVP waves were recorded in eight isolated hearts paced at 130 beats/min. Pacing was epicardially from atrium, LV apex, LV free wall, right ventricular free wall (RVF), and endocardially from right ventricular endocardium. In a given heart, peak LVP was greatest with atrial pacing and smallest with RVF pacing, the difference being on average 26 +/- 10% (mean +/- SD) of the former pressure. The other pacing sites produced intermediate peak LVPs. When instantaneous LVP waves, obtained while pacing from each of the five sites, were normalized by their respective amplitudes, they were virtually superimposable up to the time of peak pressure and only slightly different during the remainder of the cardiac cycle. With changes in pacing site there was a linear negative correlation (r = 0.971) between changes in peak pressure and changes in duration of the QRS complex of a bipolar epicardial electrogram with an average slope of -0.51 mmHg/ms. Compared with atrial pacing, the slope of the end-systolic pressure-volume relation, Ees, was decreased with ventricular pacing, but Vo, the volume axis intercept, was relatively constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Time sequential prediction of ventricular-vascular interactions.

A new analytical method (sequential convolution) for describing ventricular-vascular interactions was used to predict instantaneous pressure and flow in four isolated canine left ventricles ejecting into a computer-simulated arterial system. Ventricular pumping ability was described by a load-independent elastance, [E*(t)] combined with a ventricular internal resistance. "Arterial" properties were characterized using a time-based impulse response function that is derived from impedance measurements. Sequential convolution was then used to couple these independent descriptions of ventricular and vascular properties. Predicted pressure-volume trajectories, as well as instantaneous pressures and flows, closely matched the experimental data. Stroke volume, peak pressure, and peak flow were typically within 5% of measured values. This method provides a powerful analytical technique for examining ventricular-vascular interactions and has potential application in evaluating the ventricular-loading effects of more complex in vivo vascular properties.

Animals↗
PubMed1986

Ventricular efficiency predicted by an analytical model.

Based on the recent data from the literature, we derived analytic expressions for ventricular stroke work (SW), ventricular O2 consumption, and the ratio of the former to the latter, defined as ventricular efficiency, in terms of ventricular contractile properties and arterial afterloading properties. The ventricular properties were quantified by Ees and V0, the slope and volume axis intercept, respectively, of the linear end-systolic pressure-volume relationship. Ventricular afterload was represented by the effective arterial elastance (Ea), a parameter that is dependent on aortic input impedance parameters. O2 consumption was assessed by estimating ventricular pressure-volume area, which has been shown to be linearly related to O2 consumption. Model analysis indicated that SW is maximum when Ea = Ees, the afterload that results in the greatest efficiency is always less than that which provides the maximum SW, the SW and efficiency of a weak heart are more sensitive to changes in afterload than in a strong heart, and there is a sigmoidal relation between ventricular efficiency and end-diastolic volume that reaches its maximum at volumes outside the upper limit of the physiological range. Further analysis of the model indicated that under physiological conditions ventricular and arterial properties may be adjusted more toward optimization of efficiency than SW.

Forecasting↗
PubMed1986

Determination of left ventricular end-systolic pressure-volume relationships by the conductance (volume) catheter technique.

Using a multielectrode conductance catheter to estimate continuous left ventricular volume we determined the end-systolic pressure-volume relationship (ESPVR) in situ in open-chest anesthetized dogs. Dogs (n = 8) were studied in the control state and after pharmacologic sympathectomy (hexamethonium) and surgical vagotomy both before and after the administration of dobutamine. ESPVR was measured during brief (5 to 6 sec) preload reduction by balloon occlusion of the inferior vena cava (IVCBO). The relationship was highly reproducible. The slope (Ecs) and volume intercept (Vo) (mean +/- SD) in the control series were 5.8 +/- 3.6 mm Hg/ml and 6.5 +/- 12.5 ml, respectively. Upon release of the IVCBO (preload recovery), Ecs was 7.7 +/- 3.6 mm Hg/ml and Vo was 12.4 +/- 9.6 ml (p less than .01). Autonomic blockade produced a 50% reduction in Ecs and a concomitant decrease in Vo (p less than .01), and eliminated the difference between ESPVR generated by preload reduction (IVCBO) and preload recovery (IVCBO release). Subsequent dobutamine infusion increased Ecs to 6.1 +/- 3.5 mm Hg/ml and Vo to 4.1 +/- 6.9 ml, consistent with reported changes of the ESPVR with positive inotropic intervention. A small artifact of right ventricular filling was observed in the left ventricular volume catheter signal, but this did not appreciably alter the ESPVR. These results demonstrate the feasibility of the determination of ESPVR in situ by the conductance catheter and brief IVCBO and underline the importance of the use of rapid load changes to minimize reflex activation during the measurements.

Animals↗
PubMed1985

Accuracy of volume measurement by conductance catheter in isolated, ejecting canine hearts.

We evaluated the accuracy of the recently reported technique of estimating intraventricular volume by measurement of intracavitary electrical conductance in six isolated, ejecting, canine left ventricles. Left ventricular volumes were measured directly by a previously validated servosystem that employed an electroconductive balloon placed in the left ventricular cavity. The volume measured continuously by the balloon method (Vbal) was compared with that estimated by the conductance method (Vcath). For this test, the hearts were made to eject and fill physiologically by the use of a previously described computer-simulated arterial loading system. Complex ejection and filling patterns were created by stimulating the atrium mechanically, which resulted in irregular arrhythmatic contractions spanning a wide range of volumes. We found that there was a highly linear relationship (r2 = .982 +/- .014) between Vbal and Vcath: Vcath = 0.82 (+/- .05) Vbal + 26.7 (+/- 11.8) ml. Despite the wide variation in the offset term of this relationship among the different hearts, the offset within a given heart was predicted within 3.5 ml by a previously detailed "dilution" method that is applicable to the heart in situ within a closed thorax. Thus, since the offset term is obtainable in situ, the conductance method provides a signal that is proportional to the actual volume. To determine whether right ventricular volume influenced the accuracy of left ventricular measurement, we compared the relationship between Vcath and Vbal obtained with right ventricular volumes of 0 and 30 ml. Increasing the right ventricular volume shifted the relationship upward by less than 3 ml in the working range.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of heart rate on the canine end-systolic pressure-volume relationship.

Although the rate dependence of isolated muscle contractility is well known, the ventricular end-systolic pressure-volume relationship (ESPVR) has been reported to be insensitive to heart rate. To resolve this contradiction, we used an isolated, ejecting canine heart preparation perfused at a constant coronary arterial pressure. Heart rate was changed from 60 to 200 beats/min in steps of 20 beats/min. At least 10 pressure-volume loops under different filling pressures were obtained at each heart rate in each of six hearts. Over a heart rate range from 60 to 120 beats/min, the slope of the ESPVR (Ees) increased significantly from 3.5 +/- 0.4 (SE) to 5.3 +/- 0.6 mm Hg/ml. In the range between 120 and 180 beats/min there was little change in Ees (5.3 +/- 0.6 to 5.4 +/- 0.6 mm Hg/ml), but at 200 beats/min Ees increased slightly to 5.7 +/- 0.5 mm Hg/ml. The volume axis intercept (V0) of the ESPVR changed little over the range of heart rate from 60 to 160 beats/min (10.2 +/- 2 ml to 9.4 +/- 1.3 ml) but increased to 15.2 +/- 1.2 ml at a rate of 200 beats/min. The change in ESPVR with increase in heart rate from 60 to 120 beats/min (i.e., increase in Ees without change in V0) is the same as those seen with a positive inotropic intervention with calcium or cathecholamines, whereas the V0 changes over the range from 160 to 200 beats/min is similar to those seen with regional ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Postextrasystolic potentiation of the isolated canine left ventricle. Relationship to mechanical restitution.

We established, for the isolated, isovolumically beating canine left ventricle, a comprehensive description of postextrasystolic contractile strength (dP/dtmax) as a function of extrasystolic and postextrasystolic stimulus intervals. In contrast to previous studies of postextrasystolic beats in in situ hearts, these isolated ventricles contracted isovolumically so that dP/dtmax was not affected by fluctuations in preload and afterload and was therefore considered to be a reliable index of intrinsic contractility. With the interval preceding extrasystoles constant, postextrasystolic contractile strength increased monoexponentially to a plateau as the interval preceding postextrasystoles lengthened, with a mean time constant (+/- SD) of 182 +/- 44 msec (n = 53). The onset of this increase in postextrasystolic contractile strength coincided with repolarization of the extrasystolic action potential. With the interval preceding postextrasystoles held constant and long (1200 msec), postextrasystolic contractile strength decreased according to a monoexponential function as the interval preceding extrasystoles lengthened [mean time constant (+/- SD) of 176 +/- 18 msec (n = 10)]. These phenomena could be quantitatively summarized by a single equation description of postextrasystolic contractile strength which involved monoexponential functions with one time constant. The mathematical form of this description led us to a simple interpretation of these phenomena in terms of currently proposed excitation-contraction coupling models of the heart.

Animals↗
PubMed1985

Mechanoelectrical feedback: independent role of preload and contractility in modulation of canine ventricular excitability.

Mechanoelectrical feedback, defined as changes in mechanical state that precede and alter transmembrane potential, may have potential importance in understanding the role of altered load and contractility in the initiation and modulation of ventricular arrhythmias. To assess the independent effects of preload and contractility on myocardial excitability and action potential duration, we determined the stimulus strength-interval relationship and recorded monophasic action potentials in isolated canine left ventricles contracting isovolumically. The strength-interval relationship was characterized by three parameters: threshold excitability, relative refractory period, and absolute refractory period. The effects of a threefold increase in left ventricular volume or twofold increase in contractility on these parameters were independently assessed. An increase in preload did not change threshold excitability in 11 ventricles but significantly shortened the absolute refractory period from 205 +/- 15 to 191 +/- 14 ms (P less than 0.001) (mean +/- SD). Similarly, the relative refractory period decreased from 220 +/- 18 to 208 +/- 19 ms (P less than 0.002). Comparable results were observed when contractility was increased as a result of dobutamine infusion in 10 ventricles. That is, threshold excitability was unchanged but the absolute refractory period decreased from 206 +/- 14 to 181 +/- 9 ms (P less than 0.003), and the relative refractory period decreased from 225 +/- 17 to 205 +/- 18 ms (P less than 0.003). Similar results were obtained when contractility was increased with CaCl2, indicating that contractility associated changes were independent of beta-adrenergic receptor stimulation. An increase in preload or contractility was associated with shortening of the action potential. A threefold increase in preload and twofold increase in contractility were associated with a decrease in action potential duration of 22 and 24 ms, respectively. There was a significant linear correlation between action potential duration and excitability (absolute refractory period). The similar effects of increased preload and contractility on threshold excitability and refractoriness can be explained by the action these perturbations have on the time course of repolarization. Therefore, excitability of the ventricle is sensitive to and is modulated by alteration of load or inotropic state. The similar effects of either increased preload or contractility on excitability may be mediated by a common cellular mechanism which results in a rise in intracellular free Ca2+ and secondary abbreviation of the action potential.

Action Potentials↗
PubMed1984

Mechanical restitution of isolated perfused canine left ventricles.

We measured cardiac mechanical restitution curves, which describe the time course of recovery of ventricular contractile strength following a steady-state beat. In the first series of experiments, we studied left ventricles that beat isovolumically throughout the experiment, allowing use of dP/dtmax as a reliable index of contractile strength independent of the influence of changing ventricular pre- and afterload. The commencement of mechanical restitution was found to be associated with the onset of electrical diastole; thereafter, contractile strength rose monoexponentially to a plateau that was maintained for test pulse intervals as long as 15 s. The time constant of restitution (typically 245 ms) was independent of priming frequency and ventricular volume. These findings were interpreted in terms of a model of intracellular calcium fluxes within the myocardial cells. In a second series of experiments, we measured mechanical restitution curves from isolated ventricles that ejected against a simulated arterial impedance system. Under this condition, we did not observe the monoexponential time course of mechanical restitution as was measured under isovolumic conditions. The differences between the mechanical restitution curves measured under isovolumic and ejecting conditions were attributed to the influences of changing hemodynamic conditions on dP/dtmax that caused it to be an unreliable index of contractile strength.

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↗
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↗
PubMed1982

Microprocessor control of a ventricular volume servo-pump.

Measurement of the instantaneous pressure-volume relationship of the left ventricle is fundamental to the study of ventricular mechanics. In order to effectively investigate this relationship, it is necessary to vary and control the time course of ventricular volume change in a variety of prescribed manners. In the past, we used an analog circuit to generate command signals for a servo-pump system which controlled ventricular volume. The use of analog control limited the variety of volume waveforms which could be generated. To overcome this limitation, we developed a new system in which the servo-pump is controlled by an inexpensive microprocessor based computer, capable of generating an unlimited repertoire of volume waveforms. The computer system also made possible the use of adaptive control to increase the system fidelity. Finally, such a system provides for ease of adjustment to new hardware, should future research require it.

Animals↗
PubMed1982

Impedance loading servo pump system for excised canine ventricle.

To investigate ventricular-arterial system interaction, we have developed a hybrid-computer-controlled impedance loading servo pump system that enables us to impose a simulated arterial hydraulic impedance on an excised canine ventricle. An analog computer programmed to simulate a three-element Windkessel model of the arterial system computes instantaneous aortic flow from the instantaneous ventricular pressure. The time integral of this flow is used to command a volume servo pump system that controls the instantaneous ventricular volume. All parameter values in the loading system are controlled by a digital computer. The actual impedance spectrum generated by the system was reasonably close to that expected from the arterial model. The unique features of this system are the following. 1) The instantaneous volume of the ventricle, which is crucial information, can be measured. 2) If needed, the arterial impedance model can easily be reprogrammed to generate more complex impedance spectra. 3) The vascular parameters can be made nonlinear or time varying through the digital computer control.

Animals↗
PubMedDate not supplied

Left ventricular assist device-induced reverse ventricular remodeling.

Left ventricular assist devices provide chronic pressure and volume unloading of the dilated left ventricle in patients with end-stage heart failure. This is associated with reverse structural remodeling (normalization of the passive pressure-volume relationship), reverse molecular remodeling (increased expression of several genes involved in calcium metabolism that are down-regulated in heart failure), improved baseline contractility, and improved contractile response to increased heart rate and to beta-agonist stimulation. These findings indicate the profound degree of recovery of myocardial properties in hearts previously considered to have invincible end-stage heart failure.

Calcium↗
PubMedDate not supplied

Computer model of ventricular interaction during left ventricular circulatory support.

The authors used a computer model of the heart and circulation to test the hypothesis that anatomic ventricular interactions are responsible for the observed instances of right ventricular failure during use of a left ventricular assist device. The model predicts that left ventricular pressure-unloading with a LVAD, in the presence of isolated systolic interaction, results in impairment of RV function, whereas with isolated diastolic interaction, RV function is improved. Due to competition between these two interactions, there is a negligible overall effect of ventricular anatomic interactions in determining right ventricular function in the normal heart.

Computer Simulation↗