Afterload Sensitivity of Nonlinear End-Systolic Pressure–Volume Relation vs Preload Recruitable Stroke Work in Conscious Dogs

1998 ◽  
Vol 75 (1) ◽  
pp. 6-17 ◽  
Author(s):  
L.Carr McClain ◽  
Leon D. Wright ◽  
Raj K. Bose ◽  
John A. Spratt ◽  
George W. Maier
Keyword(s):  
Systolic Pressure ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Volume Relation

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

scholarly journals Altered LV inotropic reserve and mechanoenergetics early in the development of heart failure

2000 ◽  
Vol 278 (3) ◽  
pp. H698-H705 ◽  
Author(s):  
Sumanth D. Prabhu ◽  
Gregory L. Freeman
Keyword(s):  
Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Short Term ◽  
Before And After ◽  
Autonomic Blockade ◽  
Anesthetized Dogs ◽  
Rapid Ventricular Pacing ◽  
Volume Relation

To test the hypothesis that alterations in left ventricular (LV) mechanoenergetics and the LV inotropic response to afterload manifest early in the evolution of heart failure, we examined six anesthetized dogs instrumented with LV micromanometers, piezoelectric crystals, and coronary sinus catheters before and after 24 h of rapid ventricular pacing (RVP). After autonomic blockade, the end-systolic pressure-volume relation (ESPVR), myocardial O2 consumption (MV˙o 2), and LV pressure-volume area (PVA) were defined at several different afterloads produced by graded infusions of phenylephrine. Short-term RVP resulted in reduced preload with proportionate reductions in stroke work and the maximum first derivative of LV pressure but with no significant reduction in baseline LV contractile state. In response to increased afterload, the baseline ESPVR shifted to the left with maintained end-systolic elastance ( E es). In contrast, after short-term RVP, in response to comparable increases in afterload, the ESPVR displayed reduced E es ( P < 0.05) and significantly less leftward shift compared with control ( P< 0.05). Compared with the control MV˙o 2-PVA relation, short-term RVP significantly increased the MV˙o 2 intercept ( P< 0.05) with no change in slope. These results indicate that short-term RVP produces attenuation of afterload-induced enhancement of LV performance and increases energy consumption for nonmechanical processes with maintenance of contractile efficiency, suggesting that early in the development of tachycardia heart failure, there is blunting of length-dependent activation and increased O2requirements for excitation-contraction coupling, basal metabolism, or both. Rather than being adaptive mechanisms, these abnormalities may be primary defects involved in the progression of the heart failure phenotype.

Left ventricular spherical dilation and regional contractile dysfunction in dogs with heart failure

1997 ◽  
Vol 273 (3) ◽  
pp. H1058-H1067 ◽  
Author(s):  
M. Suzuki ◽  
C. P. Cheng ◽  
N. Ohte ◽  
W. C. Little
Keyword(s):  
Heart Failure ◽  
Structural Changes ◽  
Contractile Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Work Area ◽  
Rv Pacing ◽  
Volume Relation

Left ventricular (LV) short- and long-axis contractile function and LV structural changes were serially measured in eight instrumented dogs during the development of congestive heart failure (CHF) induced by rapid right ventricular (RV) pacing. After 10 days of pacing, LV end-diastolic volume (VED) had not increased; however, the slope of LV end-systolic pressure-volume relation had decreased from 7.4 +/- 2.6 to 4.9 +/- 1.1 mmHg/ml (P < 0.05), and the slope of LV stroke work-VED relation had fallen from 78.4 +/- 9.1 to 64.2 +/- 7.2 mmHg (P < 0.05). The slopes of end-systolic pressure-dimension relation and the stroke work area-end-diastolic dimension relation in the short axes (i.e., anteroposterior and septal-lateral) had decreased by 30% (P < 0.05), whereas the slopes of the long-axis (i.e., apical-basal) relations were unchanged (not significant). After 20 days of pacing, VED had significantly increased by 14% due to selective dilation of the short axes by 7%, and LV global contractility had further declined with a 40% contractile depression in the short axes and a 25% contractile depression in the long axis. After 30 days, the long-axis dimension at end diastole was also significantly increased with a further increase in the short-axis dimensions. In contrast to the spherical dilation occurring during CHF, acute volume loading of normal animals produced symmetrical LV dilation. These observations suggest that heterogeneous contractile depression initiates the spherical end-diastolic chamber dilation in pacing-induced CHF.

Physiology of cardiac tamponade and paradoxical pulse in conscious dogs

1993 ◽  
Vol 265 (6) ◽  
pp. H1996-H2008 ◽  
Author(s):  
M. A. Savitt ◽  
G. S. Tyson ◽  
J. R. Elbeery ◽  
C. H. Owen ◽  
J. W. Davis ◽  
...  
Keyword(s):  
Cardiac Tamponade ◽  
Interventricular Septum ◽  
Systolic Pressure ◽  
Physiological Mechanism ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Lv Dysfunction ◽  
Volume Curve

The physiological mechanism of paradoxical pulse in cardiac tamponade remains controversial. In eight conscious dogs with intact pericardia, ultrasonic dimension transducers assessed biventricular geometry and volumes, while micromanometers measured right ventricular (RV), left ventricular (LV), pleural, and pericardial pressures. With normal inspiration, peak LV pressure fell by 7.7 +/- 1.3 mmHg at control and by 20.3 +/- 3.7 mmHg during tamponade (P < 0.001), consistent with the development of paradoxical pulse. At peak inspiration during tamponade, RV filling increased, the interventricular septum shifted leftward, transeptal pressure became negative, and LV septal arc length (l theta) became smaller than its respective unpreloaded value at maximal vena caval occlusion (l(o)). Analysis of stroke work (SW)-end-diastolic volume (EDV) and end-systolic pressure-volume coordinates at peak inspiration during tamponade revealed that end-systolic pressure was 19.1 +/- 10.2 mmHg below the baseline end-systolic pressure-volume curve (P < 0.01), and SW was 24.2 +/- 8.8% below the baseline SW-EDV curve (P < 0.01), indicating transient inspiratory LV dysfunction. It is proposed that inspiratory leftward interventricular septal shifting at low LV EDV during tamponade completely unloads the septum (l theta < l o), eliminates the septal contribution to global LV SW, results in transient inspiratory LV dysfunction, and contributes to the phenomenon of paradoxical pulse.

Mechanical determinants of myocardial oxygen consumption in conscious dogs

1995 ◽  
Vol 269 (2) ◽  
pp. H609-H620 ◽  
Author(s):  
J. R. Elbeery ◽  
J. C. Lucke ◽  
M. P. Feneley ◽  
G. W. Maier ◽  
C. H. Owen ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Virtual Work ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
External Energy ◽  
Work Model

A new practical descriptor of metabolic to mechanical myocardial energy transfer (MET), termed the virtual work model, was evaluated in 32 conscious dogs and in 8 isolated canine hearts. An index of total mechanical energy expenditure (TME) was calculated as the sum of external energy (stroke work) and an internal energy index of heat (left ventricular end-diastolic volume times left ventricular mean ejection pressure). Physiological comparison of TME (x-axis) and myocardial oxygen consumption (MVO2; y-axis) yielded highly linear MET relationships (mean r = 0.93 +/- 0.07), with an average slope of 0.86 +/- 0.39 (SD) and a y-intercept of 9.1 +/- 6.4 mW/ml myocardium. The linear MVO2-TME relationship did not vary under steady-state vs. dynamic vena caval occlusion, increased heart rate, increased afterload, or increased inotropic state with calcium infusion. Compared with five other indexes of myocardial energetics, the virtual work model of MET was the most linear, the most practical in not requiring determination of the end-systolic pressure-volume relationship, and the most accurate predictor of MVO2 under normal and altered hemodynamic conditions.

Linear O2 Use-Pressure-Volume Area Relation from Curved End-Systolic Pressure-Volume Relation of the Blood-Perfused Rat Left Ventricle.

1998 ◽  
Vol 48 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Yoshiki HATA ◽  
Taisuke SAKAMOTO ◽  
Shingo HOSOGI ◽  
Tohru OHE ◽  
Hiroyuki SUGA ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Volume Relation

Effect of alkali therapy with NaHCO3 or THAM on cardiac contractility

1996 ◽  
Vol 270 (5) ◽  
pp. R955-R962
Author(s):  
C. D. Mazer ◽  
B. Naser ◽  
K. S. Kamel
Keyword(s):  
Myocardial Ischemia ◽  
Contractile Function ◽  
Venous Blood ◽  
Systolic Pressure ◽  
Ischemic Myocardium ◽  
Stroke Work ◽  
Length Relationship ◽  
Alkali Therapy ◽  
Myocardial Contractile ◽  
The Impact

We examined the impact of alkali therapy on myocardial contractility in a model of myocardial ischemia in dogs using direct measurements of myocardial contractile function. Myocardial ischemia in the left anterior descending (LAD) artery territory was induced using a perfusion circuit from the internal carotid artery to the LAD artery. Myocardial contractile function was assessed using sonomicrometry for measurement of percent systolic shortening (%SS), preload recruitable stroke work (PRSW) slope, and end-systolic pressure-length relationship (ESPLR) area. Because the blood flow in LAD artery was diminished by approximately 70%, there was a significant decrease in O2 delivery and uptake by the ischemic myocardium. Ischemia led to a significant fall in LAD regional contractile function with %SS decreasing from 15 +/- 2 to 7 +/- 2%, PRSW slope from 82 +/- 10 to 37 +/- 5 mmHg, and ESPLR area from 121 +/- 2 to 48 +/- 14 mmHg.mm (P < 0.05). In six dogs, the intracoronary administration of NaHCO(3) resulted in a significant increase in pH in LAD arterial and venous blood. There was, however, no significant increase in %SS (6 +/- 2), PRSW slope (43 +/- 10 mmHg), or ESPLR area (60 +/- 13 mmHg.mm). Since administration of NaHCO(3) resulted in a significant increase in PCO2 in LAD arterial and venous blood, similar experiments were carried out in five dogs, but with the intracoronary infusion of the amine buffer THAM [tris(hydroxymethyl)aminomethane (Tris) buffer; 2-amino-2-hydroxyl-1,3-propandiol] instead of NaHCO3. Although administration of THAM resulted in a significant increase in pH and a significant decrease in PCO2, in both LAD arterial and venous blood, there was no significant improvement in any of the parameters used to assess myocardial contractile function. In conclusion, administration of alkali (NaHCO3 or THAM) does not enhance the contractile function of the ischemic myocardium.

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