Left ventricular end-systolic pressure-volume relationships as a measure of ventricular performance

1985 ◽  
Vol 80 (6) ◽  
pp. 594-607 ◽  
Author(s):  
G. Kissling ◽  
N. Takeda ◽  
M. Vogt
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Performance

Metabolism of the perfused rabbit heart. V. Verapamil-induced release of creatine kinase

1982 ◽  
Vol 60 (7) ◽  
pp. 952-959 ◽  
Author(s):  
Miguel A. Chiong
Keyword(s):  
Creatine Kinase ◽  
Adenine Nucleotides ◽  
Systolic Pressure ◽  
Creatine Phosphate ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Calcium Stores ◽  
Ventricular Performance ◽  
Permeability Characteristics ◽  
Energy Stores

The effects of verapamil (VER), at concentrations of 0, 10−9, 10−8, 10−7, and 5 × 10−7 M (or 0, 0.5, 5, 50, and 250 ng/mL) were studied in the isolated rabbit heart during 70 min of aerobic perfusion with a standard Krebs–bicarbonate medium at 37 °C. The studied variables were left ventricular performance (RPP, heart rate times left ventricular (LV) systolic pressure), coronary sinus flow (CSF), oxygen uptake [Formula: see text], rate of creatine kinase (CK) release, and energy stores (glycogen, creatine phosphate (CP), ATP, and total adenine nucleotides (TAN)).The results show that (i) VER depressed RPP in a dose-related manner; (ii) [Formula: see text] declined as VER concentration increased except in the 5 × 10−7 M group which showed a paradoxical increase in O2 uptake; (iii) CSF was only slightly decreased by VER with the exception of the 5 × 10−7 M group, which showed an increase in flow; (iv) VER was associated with increments in the rates of CK release in a dose-related fashion (2, 4, 15, and 29 times the rate observed in the untreated group), and (v) VER was associated with slight decrease in glycogen levels, but no changes in CP or adenine nucleotides.It is concluded that, in our preparation, VER caused marked increases in the rate of CK loss in the absence of depletion of total energy stores. The data suggest that the drug affects the permeability characteristics of the sarcolemma, perhaps via localized depletion of calcium stores.

Ventricular performance, pressure-volume relationships, and O2 consumption during hypothermia

1964 ◽  
Vol 206 (1) ◽  
pp. 67-73 ◽  
Author(s):  
R. G. Monroe ◽  
R. H. Strang ◽  
C. G. LaFarge ◽  
J. Levy
Keyword(s):  
Peak Pressure ◽  
Diastolic Pressure ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Heart Rates ◽  
Performance Pressure ◽  
Air Chamber ◽  
Lower Temperature

Left ventricular performance in the isolated heart of a dog was observed at normal temperatures (37.7 C) and under hypothermia (32.2 C) at comparable heart rates. The peak pressure of isovolumic contractions at the same ventricular end-diastolic pressures averaged 40% higher at the lower temperature. Diastolic pressure-volume relationships were similar at both temperatures. In studies in which the ventricle ejected fluid and performed work the hypothermic ventricle was capable of performing greater work at comparable heart rates, left ventricular end-diastolic pressures, and loading. When the ventricle was allowed to perform work by compressing air into a chamber of constant volume left ventricular oxygen consumption (Vo2) increased with the peak systolic pressure as the temperature was lowered. If the peak systolic pressure was maintained constant by increasing the volume of the air chamber as the temperature was lowered no consistent relationship could be shown between left ventricular Vo2 and the integral of systolic pressure in time which invariably increased with hypothermia.

Effect of vasopressin on left ventricular performance

1993 ◽  
Vol 264 (1) ◽  
pp. H53-H60
Author(s):  
C. P. Cheng ◽  
Y. Igarashi ◽  
H. S. Klopfenstein ◽  
R. J. Applegate ◽  
Z. Shihabi ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
The Right

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Nonlinearity of indexes of left ventricular performance: effects on estimation of slope and diameter axis intercepts

1991 ◽  
Vol 260 (6) ◽  
pp. H1802-H1809
Author(s):  
C. F. Toombs ◽  
J. Vinten-Johansen ◽  
H. Yokoyama ◽  
W. E. Johnston ◽  
J. S. Julian ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Accurate Estimation ◽  
Stroke Work ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Wide Range ◽  
Performance Effects ◽  
Linear Fit

The slope and diameter axis intercept (D0) of the linear indexes end-systolic pressure-diameter relation (ESPDR), maximum of the first derivative of left ventricular pressure (dP/dtmax)-end-diastolic diameter relation (dP/dtmax-Ded), and dimensional preload-recruitable stroke work relation (PRDSW) are used to describe left ventricular performance. We tested the hypothesis that nonlinearity in these indexes would preclude accurate estimation of slope and D0. In nine pentobarbital-anesthetized dogs, right heart bypass was used to obtain a wide range of pressure-minor axis diameter (sonomicrometry) points from which the three indexes were derived. For ESPDR and dP/dtmax-Ded, a nonlinear fit (y = ax2 + bx + c) approximated the data better than a linear fit, with significant nonlinearity toward the diameter axis (a = -10.28 +/- 3.42 and -111.2 +/- 26.2, respectively, P less than 0.05). Although linear D0 was significantly less than nonlinear D0, this difference was overcome by the diameter intercept at a midrange value of end-systolic pressure or dP/dtmax. PRDSW demonstrated no significant nonlinearity (a = -4.40 +/- 3.53, P = 0.86) but extrapolation to D0 demonstrated linear and nonlinear differences. We conclude that 1) ESPDR and dP/dtmax-Ded demonstrate significant nonlinearity, while PRDSW is well-approximated by a linear fit over a large range of data points; and 2) extrapolation of D0 is inaccurate in all three indexes, while a midrange intercept is independent of the model used to fit the data. Left ventricular performance may be more accurately described by linear slope and midrange diameter intercept over comparable ranges of data.

Effects of ventricular pacing on regional left ventricular performance in the dog

1980 ◽  
Vol 238 (6) ◽  
pp. H858-H867 ◽  
Author(s):  
F. R. Badke ◽  
P. Boinay ◽  
J. W. Covell
Keyword(s):  
Myocardial Function ◽  
Systolic Pressure ◽  
Lateral Wall ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Ventricular Pacing ◽  
Regional Myocardial Function ◽  
Ventricular Performance ◽  
Reciprocal Interaction ◽  
Anesthetized Dogs

Changes in regional left ventricular (LV) performance induced by ventricular pacing were studied in two groups of open-chest anesthetized dogs. In the first group of five dogs, local function at the LV anterior base, anterior apex, and posterior apex was assessed by ultrasonic crystal pairs with atrial, right ventricular, LV apical, and LV base pacing. Ventricular pacing produced asynchrony of contraction and marked changes in the shortening pattern at each site, as well as an average 27% reduction in peak systolic pressure and peak dP/dt compared to atrial pacing. Moreover, the extent of shortening during LV ejection was reduced or unchanged at all sites measured during ventricular pacing. In the second group of five dogs, function of the septum and opposing LV lateral wall was studied with atrial and LV lateral wall pacing. Lateral function was assessed with a crystal pair and septal function by cineradiography of a lead bead implanted in the septum. Ventricular pacing produced reciprocal interaction between the two walls, with early lateral shortening inducing septal bulging and late septal shortening inducing lateral wall systolic lengthening. We conclude that ventricular pacing produces significant changes in regional myocardial function, likely induced by reciprocal interaction of opposing myocardial regions. Furthermore, such interaction appears deleterious to global ventricular function, presumably because volume is sequestered and pressure is dissipated into relatively inactive segments that are out of phase with the bulk of contracting myocardium.

Evaluation of long-term variance of left ventricular performance indexes in closed-chest dogs

1989 ◽  
Vol 257 (1) ◽  
pp. H70-H78
Author(s):  
G. L. Freeman ◽  
J. T. Colston
Keyword(s):  
Ejection Fraction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Left Ventricular Performance ◽  
Mean Velocity ◽  
Ventricular Performance ◽  
End Diastolic Volume ◽  
Pressure Development

To assess the long-term variance of several parameters of left ventricular performance, we evaluated maximum rate of pressure development (dP/dtmax), ejection fraction, mean velocity of circumferential fiber shortening (VCF), the slope and volume-axis intercept of the end-systolic pressure-volume (PES-VES) relation, the stroke-work end-diastolic volume (SW-EDV) relation, and the dP/dtmax-EDV relation in six chronically instrumented dogs. Each dog was studied five times over a period of 3 wk in the conscious autonomically intact state, after autonomic blockade, and after administration of anesthesia. For each index under each set of testing conditions, a coefficient of variation was determined, defined as (SD/mean) x 100, and expressed as a percent. In conscious autonomically intact dogs, a low day-to-day variance was present in dP/dtmax (6.4%), ejection fraction (6.8%), mean VCF (6.5%), and the slope and volume intercept of the SW-EDV relation (7.2 and 6.2%), whereas higher variance was seen in the slope and intercept of the PES-VES relation (18.1 and 36.1%). The highest variance was present in parameters of the dP/dtmax-EDV relation. Thus dP/dtmax, ejection fraction, and the slope and volume intercept of the SW-EDV relation may be the most reliable indexes for long-term evaluation of left ventricular performance.

Intracavitary ultrasound impairs left ventricular performance: presumed role of endocardial endothelium

1992 ◽  
Vol 263 (3) ◽  
pp. H857-H865 ◽  
Author(s):  
Thierry C. Gillebert ◽  
Stefan G. De Hert ◽  
Luc J. Andries ◽  
Anton H. Jageneau ◽  
Dirk L. Brutsaert
Keyword(s):  
High Power ◽  
High Frequency ◽  
Continuous Wave ◽  
Recovery Period ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Limited Area ◽  
Time Interval ◽  
Ventricular Performance ◽  
Endocardial Endothelium

Irradiation of isolated cardiac muscle by high-power, high-frequency, continuous wave ultrasound selectively damages endocardial endothelium (EE). We evaluated this ultrasound effect in vivo on the performance of the intact ejecting canine left ventricle (LV). A cylindrical ultrasound probe (0.9 MHz, 25 W), mounted on a catheter, was inserted in the LV cavity through an apical stab wound and was activated for 60, 120, and 240 s, followed each time by a recovery period of 10–15 min. Ultrasound transiently and repeatedly abbreviated the time interval from end diastole to peak (-)dP/dt (from 241 ± 30 to 229 ± 32 ms after 240 s; P < 0.001), accelerated LV pressure fall, did not alter peak (+)-dP/dt or peak systolic pressure, increased diastolic and systolic segment lengths, and decreased fractional shortening. Microscopic analysis revealed dispersed granulocytes attached to the EE. EE cells were visibly damaged only in a limited area surrounding the probe. Accordingly, high-power, high-frequency, continuous wave ultrasound reversibly modulated LV performance, presumably by transient alteration of EE function. cardiac function; contractility; diastole; relaxation Submitted on May 7, 1991 Accepted on April 28, 1992

Effect of timing of transient diastolic changes in ventricular filling on LV performance in dogs

1989 ◽  
Vol 257 (1) ◽  
pp. H305-H313 ◽  
Author(s):  
M. W. Van Hessen ◽  
P. Schiereck ◽  
A. A. Stokhof ◽  
E. L. De Beer ◽  
J. B. Hak ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Cavity ◽  
Volume Changes ◽  
Ventricular Performance ◽  
Pump System ◽  
Contraction Phase ◽  
Atrial Contraction ◽  
Ventricular Filling

The influence of acute volume changes during diastole on the contractile state of the left ventricle has been studied in the closed-chest dog. Volume changes were introduced by means of a servo-controlled pump system connected to the left ventricular cavity by an apical cannula. Pressure measurements were made in the left ventricle and aorta. Flow sensors in the mitral valve and around the ascending aorta monitored ventricular inflow and outflow patterns. The ventricular performance was evaluated in terms of the ratio between end-systolic pressure and end-systolic volume (P/Ves). By changing the time of occurrence of the volume interventions from the rapid filling phase of diastole to the atrial contraction phase, the relative contributions of rapid filling and atrial contraction to the mitral flow were changed. When the rapid filling was changed by the volume intervention, the effect on the contractile status of the heart, expressed as the P/Ves value, was small. In contrast, when the volume intervention took place during the atrial contraction phase, the effect on the P/Ves value was much larger. Comparison with muscle fiber experiments suggests that length-dependent calcium sensitivity of troponin and length-dependent conductivity of the sarcolemma are the underlying fundamental mechanisms. Therefore, we conclude that the influence of an intervention in ventricular filling on the inotropic state of the left ventricle is dependent on the timing of the intervention.

Evidence and quantitation of left ventricular systolic resistance

1985 ◽  
Vol 249 (2) ◽  
pp. H358-H370 ◽  
Author(s):  
S. G. Shroff ◽  
J. S. Janicki ◽  
K. T. Weber
Keyword(s):  
Quantitative Description ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Ventricular Pressure ◽  
Elastic Behavior ◽  
Volume Data ◽  
Ventricular Performance ◽  
Pressure Flow

Instantaneous left ventricular pressure is a function of both volume (elastic behavior) and flow (resistive behavior). However, a quantitative description of ventricular resistance and its effects on ventricular performance remains to be elucidated. Accordingly, ventricular resistive behavior was studied in six isolated canine hearts. Our experimental findings indicate 1) for a specified time (ts), volume (Vs), and contractile state (CS), the ventricular pressure-flow relation was linear (r = 0.96-0.99) within the range of flows examined (0-250 ml/s); 2) ventricular resistance increased with increments in ts, Vs, and CS, whereas the zero-pressure flow intercept was invariant; 3) resistance could be uniquely quantified as a linear function of isovolumetric pressure. In six experiments, the slope of this relationship ranged from 1.1 to 2.1 X 10(-3) s/ml while the intercept did not differ from zero; and 4) end-systolic elastance, estimated from end-systolic pressure-volume data, was in substantial error under the conditions of finite (greater than 35 ml/s) end-systolic flows. Finally, the results from a computer simulation of the coupled ventricular-arterial system indicated that ventricular resistance primarily affects the pulsatile nature of aortic flow. The unique isovolumetric pressure-resistance relation suggests that the rate-limiting properties of the contractile process may be causally related to the observed ventricular resistive behavior.

Left ventricular performance in endotoxin shock in dogs

1982 ◽  
Vol 242 (2) ◽  
pp. H172-H176 ◽  
Author(s):  
W. G. Guntheroth ◽  
J. P. Jacky ◽  
I. Kawabori ◽  
J. G. Stevenson ◽  
A. H. Moreno
Keyword(s):  
Heart Rate ◽  
Average Rate ◽  
Systolic Pressure ◽  
Work Load ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Maximal Velocity ◽  
Ventricular Performance ◽  
Untreated Subject ◽  
Mean Pressure

Endotoxin shock, with maximal velocity of contraction (Vmax) as our index of contractility, showed no myocardial depression in an earlier 4-h study (Guntheroth, Proc. Soc. Exp. Biol. Med. 157: 610--614, 1978). Because of reports of late deterioration, we studied six dogs until spontaneous death (9--18 h). Heart rate nearly doubled and left ventricular filling pressure and aortic mean pressure fell, but Vmax did not change significantly. Because of concern that the marked increase in heart rate may have contributed to an artifactual maintenance of Vmax (due to its frequency dependence, inherent in dp/dt), we studied a final group of five dogs with three additional indicators of contractility. End-systolic pressure-diameter ratio (Emax), ejection fraction (sonar-determined from the minor axis of the left ventricle), and frequency-normalized average rate of generation of power density (FARPD) all fell early and remained low until death. We conclude that myocardial contractility is significantly reduced in endotoxin shock, early and sustained. Its presence is masked somewhat in the untreated subject by the reduced work load, secondary to hypovolemia.

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