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Systolic and Diastolic Function (Mechanics) of the Intact Heart

James W. Covell, John Ross

10.1002/cphy.cp020120

Source: Supplement 6: Handbook of Physiology, The Cardiovascular System, The Heart

Originally published: 2002

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Determinants of Systolic Function
1.1 Changes in Cardiac Shape and Dimensions
1.2 Performance of the Intact Ventricle Viewed from the Perspective of Isolated Muscle Function
1.3 The End‐Systolic Pressure—Volume Relationship
1.4 Preload
1.5 Afterload
1.6 Contractility (Inotropic State)
1.7 Length‐Dependent Activation
1.8 Strength‐Interval Relations
1.9 Interaction Between Heart Rate and β‐Adrenergic Stimulation
1.10 Mechanical Restitution and Postextrasystolic Potentiation
2 Assessing Contractility (Inotropic State) of the Heart
2.1 Acute Changes In Contractility
2.2 Methods Based on Changes in Ventricular Volumes and Dimensions in a Steady State
2.3 Methods Derived from Left Ventricular Pressure and the Rate of Change of Pressure
2.4 Comparison of Indices
2.5 Methods Based on Examination of Ventricular Function over a Range of Loading Conditions
2.6 The Absolute Level of Inotropic State
2.7 Evaluation of Ventricular Function in Mice and Rats
3 Regional Function
3.1 Regional Right Ventricular Systolic Function
3.2 Regional Left Ventricular Structure‐Function Relationships
3.3 Left Ventricular Structure‐Function Relationships
3.4 Mechanical Correlates of Cardiac Energy Consumption
4 Determinants of Diastolic Function
4.1 Cardiac Structural Components
4.2 Passive Pressure‐Volume Relationships
4.3 Time‐Dependent Properties
4.4 Passive Ventricular Diastolic Structure‐Function Relationships
4.5 Regulation of Ventricular Filling
4.6 Role of the Pericardium
Figure 1. Figure 1.

Plot of the simultaneous changes in left ventricular circumference, base‐to‐apex length, circumflex‐to‐apex length (L1), aorta‐to‐apex length during a single cardiac contraction in an awake dog. Dimensions are determined with biplane cineradiography of radiopaque markers.

Reproduced from Hinds et al. 126, with permission
Figure 2. Figure 2.

Data obtained from surgically implanted intramyocardial markers in transplanted human hearts by Hansen et al. 117. Data shown indicate the relationship between left ventricular volume [V(t)] during four successive contractions and torsional rotation [θ(t)] of the apex with respect to the base shown as a clockwise angular rotation during systole.
Figure 3. Figure 3.

Data from an isolated servocontrolled canine left ventricular preparation 45. Solid symbols show peak calculated stress in isovolumic beats. Open symbols depict three isotonic contractions obtained at different afterloads.
Figure 4. Figure 4.

Data from an isolated canine left ventricular preparation in which left ventricular pressure and volume are determined throughout contraction 323. Note that the ratio of pressure to volume reaches a stable maximum at end‐systole.
Figure 5. Figure 5.

Data from the same preparation shown in Figure 4, demonstrating four contractions at variable systolic pressures before and after the administration of norepinephrine. The solid points indicate the maximum pressure‐volume ratio in each contraction. The linear relationship formed by these points has been termed “the end‐systolic pressure‐volume relationship.” The slope of this relationship, designated Emax by Suga and Sagawa 322, changes with changes in inotropic state induced by norepinephrine.
Figure 6. Figure 6.

Schematic diagram of the effects of alterations in preload and afterload on ventricular stroke volume.
Figure 7. Figure 7.

Data from conscious animals before (open symbols) and after tachycardia‐induced heart failure (closed symbols). Stroke volume is plotted on the ordinate. Note that baseline stroke volume is maintained by an increase in end‐diastolic volume 158.
Figure 8. Figure 8.

Data from the isolated heart preparation 45. Note that in isotonic contractions there is a linear relationship between stroke volume or change in circumference (ΔL) and ventricular stress or pressure.
Figure 9. Figure 9.

Effects of varying the left ventricular pressure at the onset of contraction in an isolated supported canine heart preparation (A) and, in the same preparation, the pressure during ejection is varied (B). In both panels the end‐systolic pressure is maintained constant and the stroke volume is largely unchanged

Reproduced by permission from Suga et al. 321, with permission
Figure 10. Figure 10.

Relationship between global and regional indices of stroke work and ventricular end‐diastolic pressure or ventricular volume in conscious instrumented dogs. Changes in diastolic pressures and volumes were induced by caval occlusion. The relationships between ventricular end‐diastolic pressure and segment work and stroke work are non‐linear, but sensitive to the inotropic effect of calcium. The relationship ventricular between end‐diastolic volume or segment work and stroke work are linear and sensitive to changes in inotropic state.

After Glower et al. 104
Figure 11. Figure 11.

Left ventricular pressure segment length (SL) relationships determined in the dog by caval occlusion before (solid lines) and after (dotted lines) a sustained increase in end‐diastolic pressure. Following the increases in end‐diastolic pressure the end‐systolic pressure length points are all shifted to the left, indicating a shift in the end‐systolic pressure‐length relationship 170.

Reproduced with permission from Lew 170
Figure 12. Figure 12.

Data from studies on the interaction of the adrenergic system and the force–frequency relationship obtained in intact dogs. The plot shows the relation between heart rate and max dP/dt (left ventricular maximum dP/dt) in conscious dogs standing at rest and during sustained exercise at several heart rates. The lowest heart rate represents the resting condition (C) and the highest heart rate, that during exercise with atrial pacing at 240 beats per minute. The intermediate heart rates show the effects of reducing the pacing rate progressively during continued exercise, with the sinus node rate controlled at a low level by zatebradine. ** = p <0.001 vs. 240 beats/min. Values are mean ± SD.

Reproduced with permission from Miura et al 217
Figure 13. Figure 13.

Schematic diagram of the four major factors influencing myocardial inotropic state 279.
Figure 14. Figure 14.

Relative sensitivity of several indices to inotropic stimulation in an isolated canine heart preparation Ees = slope of the end‐systolic pressure–volume relationship. Ef = ejection fraction, V = volume SW = stroke work; SW/Ved = stroke; MSER = stoke volume/systolic ejection period; VCFmax = maximal value of (−dV/dT)/Ved; dp/dt/IP = maximum +dP/dT/ developed pressure at the time of dp/dtmax.

Reproduced from Kass et al 150, with permission
Figure 15. Figure 15.

Relative load sensitivity of several indices determined in an isolated canine heart preparation. The maximum percent change (comparing the highest and lowest load) was calculated for each index See Fig. 20–140 150.
Figure 16. Figure 16.

Coefficient of variation defined as (SD/mean) × 100 for several inotropic indices determined five times over 3 weeks. C = control; AB = autonomic blockade; AN = anesthesia 85.

Reproduced by permission from Freeman et al 85
Figure 17. Figure 17.

Dimension gauge signals from an open‐chest canine preparation. All three gauges are orientated in the circumferential direction. Gauges are located at three apex base levels (apex, mid, base) 173.

Reproduced by permission from Le Winter et al 173
Figure 18. Figure 18.

Finite strains determined in the left ventricular free wall in an open‐chest canine preparation. Data shown are from the inner half of the ventricular wall. E11 = circumferential strain; E22 = longitudinal strain; E33 = radial (wall thickening strain); E12 = circumferential longitudinal shear; E13 = circumferential radial shear; E23 = longitudinal radial shear.

Unpublished data from Villareal et al. 340
Figure 19. Figure 19.

Reconstructed sarcomere lengths (C and D) during a single cardiac cycle. Note that there are marked differences between cavity volume and sarcomere length during filling and ejection and that during isovolumic contraction there are large transitions in sarcomere length without a corresponding change in ventricular volume (B).

Reproduced from Rodriguez et al 269
Figure 20. Figure 20.

Average end‐systolic wall thickening strain (E33) and longitudinal radial shear (E23) in the subendocardium of the left ventricular free wall (solid bars) and septum (hatched bars). B shows the cleavage plane orientation at the two sites.

Reproduced from LeGrice et al. 165, with permission
Figure 21. Figure 21.

Proposed mechanism of ventricular wall thickening.

Reproduced from LeGrice et al. 165, with permission
Figure 22. Figure 22.

Schematic representation of pressure‐volume area (PVA). Solid line indicates the pressure volume trajectory of a single contraction (P‐V loop) plotted in the end‐systolic and end‐diastolic pressure‐volume framework. The area shown by the diagonal lines is the pressure volume area.
Figure 23. Figure 23.

Correlations between cardiac oxygen consumption per beat (VO2) and PVA in control panels (A, C) and following epinephrine (B) and calcium (D). Inset shows the contractions from which the ESPVR is determined for each panel (closed symbols represent isovolumic beats, opening ejecting contractions).

From Suga et al. 320, with permission
Figure 24. Figure 24.

Left ventricular pressure‐volume relationship adapted from the work of Taylor et al. 329. Dashed line indicates the pressure‐volume relationship corrected for the contribution of the right ventricle in a single animal, and the error bars indicate the SD over 8 animals. Solid line schematically estimates the pressure‐volume relationship on deflation.
Figure 25. Figure 25.

Left ventricular pressure diameter relationships from three contractions in a conscious dog. The dashed line indicates the passive pressure diameter relationship determined in the same animal from the end‐diastolic pressure diameter point in several contractions 254.
Figure 26. Figure 26.

Length‐tension relationship in single cardiac myofibrils determined in relaxing solution with and without BDM (solid lines, open and closed symbols). The dashed lines indicate the sarcomere length‐tension relationship in intact rabbit and rat papillary muscles and trabeculae

From Linke et al 180, with permission
Figure 27. Figure 27.

Pressure‐volume curves in an isolated buffer perfused rat heart showing the effects of progressive infusion with collagenase. There is a shift toward greater volumes at all pressures that increases with progressive disruption of the extracellular matrix.

Reproduced with permission from MacKenna et al 190
Figure 28. Figure 28.

Tracings from a conscious dog, illustrating the temporal relationships between mitral valve flow and atrial and left ventricular pressures.

Modified from Yellin et al. 361, with permission


Figure 1.

Plot of the simultaneous changes in left ventricular circumference, base‐to‐apex length, circumflex‐to‐apex length (L1), aorta‐to‐apex length during a single cardiac contraction in an awake dog. Dimensions are determined with biplane cineradiography of radiopaque markers.

Reproduced from Hinds et al. 126, with permission


Figure 2.

Data obtained from surgically implanted intramyocardial markers in transplanted human hearts by Hansen et al. 117. Data shown indicate the relationship between left ventricular volume [V(t)] during four successive contractions and torsional rotation [θ(t)] of the apex with respect to the base shown as a clockwise angular rotation during systole.



Figure 3.

Data from an isolated servocontrolled canine left ventricular preparation 45. Solid symbols show peak calculated stress in isovolumic beats. Open symbols depict three isotonic contractions obtained at different afterloads.



Figure 4.

Data from an isolated canine left ventricular preparation in which left ventricular pressure and volume are determined throughout contraction 323. Note that the ratio of pressure to volume reaches a stable maximum at end‐systole.



Figure 5.

Data from the same preparation shown in Figure 4, demonstrating four contractions at variable systolic pressures before and after the administration of norepinephrine. The solid points indicate the maximum pressure‐volume ratio in each contraction. The linear relationship formed by these points has been termed “the end‐systolic pressure‐volume relationship.” The slope of this relationship, designated Emax by Suga and Sagawa 322, changes with changes in inotropic state induced by norepinephrine.



Figure 6.

Schematic diagram of the effects of alterations in preload and afterload on ventricular stroke volume.



Figure 7.

Data from conscious animals before (open symbols) and after tachycardia‐induced heart failure (closed symbols). Stroke volume is plotted on the ordinate. Note that baseline stroke volume is maintained by an increase in end‐diastolic volume 158.



Figure 8.

Data from the isolated heart preparation 45. Note that in isotonic contractions there is a linear relationship between stroke volume or change in circumference (ΔL) and ventricular stress or pressure.



Figure 9.

Effects of varying the left ventricular pressure at the onset of contraction in an isolated supported canine heart preparation (A) and, in the same preparation, the pressure during ejection is varied (B). In both panels the end‐systolic pressure is maintained constant and the stroke volume is largely unchanged

Reproduced by permission from Suga et al. 321, with permission


Figure 10.

Relationship between global and regional indices of stroke work and ventricular end‐diastolic pressure or ventricular volume in conscious instrumented dogs. Changes in diastolic pressures and volumes were induced by caval occlusion. The relationships between ventricular end‐diastolic pressure and segment work and stroke work are non‐linear, but sensitive to the inotropic effect of calcium. The relationship ventricular between end‐diastolic volume or segment work and stroke work are linear and sensitive to changes in inotropic state.

After Glower et al. 104


Figure 11.

Left ventricular pressure segment length (SL) relationships determined in the dog by caval occlusion before (solid lines) and after (dotted lines) a sustained increase in end‐diastolic pressure. Following the increases in end‐diastolic pressure the end‐systolic pressure length points are all shifted to the left, indicating a shift in the end‐systolic pressure‐length relationship 170.

Reproduced with permission from Lew 170


Figure 12.

Data from studies on the interaction of the adrenergic system and the force–frequency relationship obtained in intact dogs. The plot shows the relation between heart rate and max dP/dt (left ventricular maximum dP/dt) in conscious dogs standing at rest and during sustained exercise at several heart rates. The lowest heart rate represents the resting condition (C) and the highest heart rate, that during exercise with atrial pacing at 240 beats per minute. The intermediate heart rates show the effects of reducing the pacing rate progressively during continued exercise, with the sinus node rate controlled at a low level by zatebradine. ** = p <0.001 vs. 240 beats/min. Values are mean ± SD.

Reproduced with permission from Miura et al 217


Figure 13.

Schematic diagram of the four major factors influencing myocardial inotropic state 279.



Figure 14.

Relative sensitivity of several indices to inotropic stimulation in an isolated canine heart preparation Ees = slope of the end‐systolic pressure–volume relationship. Ef = ejection fraction, V = volume SW = stroke work; SW/Ved = stroke; MSER = stoke volume/systolic ejection period; VCFmax = maximal value of (−dV/dT)/Ved; dp/dt/IP = maximum +dP/dT/ developed pressure at the time of dp/dtmax.

Reproduced from Kass et al 150, with permission


Figure 15.

Relative load sensitivity of several indices determined in an isolated canine heart preparation. The maximum percent change (comparing the highest and lowest load) was calculated for each index See Fig. 20–140 150.



Figure 16.

Coefficient of variation defined as (SD/mean) × 100 for several inotropic indices determined five times over 3 weeks. C = control; AB = autonomic blockade; AN = anesthesia 85.

Reproduced by permission from Freeman et al 85


Figure 17.

Dimension gauge signals from an open‐chest canine preparation. All three gauges are orientated in the circumferential direction. Gauges are located at three apex base levels (apex, mid, base) 173.

Reproduced by permission from Le Winter et al 173


Figure 18.

Finite strains determined in the left ventricular free wall in an open‐chest canine preparation. Data shown are from the inner half of the ventricular wall. E11 = circumferential strain; E22 = longitudinal strain; E33 = radial (wall thickening strain); E12 = circumferential longitudinal shear; E13 = circumferential radial shear; E23 = longitudinal radial shear.

Unpublished data from Villareal et al. 340


Figure 19.

Reconstructed sarcomere lengths (C and D) during a single cardiac cycle. Note that there are marked differences between cavity volume and sarcomere length during filling and ejection and that during isovolumic contraction there are large transitions in sarcomere length without a corresponding change in ventricular volume (B).

Reproduced from Rodriguez et al 269


Figure 20.

Average end‐systolic wall thickening strain (E33) and longitudinal radial shear (E23) in the subendocardium of the left ventricular free wall (solid bars) and septum (hatched bars). B shows the cleavage plane orientation at the two sites.

Reproduced from LeGrice et al. 165, with permission


Figure 21.

Proposed mechanism of ventricular wall thickening.

Reproduced from LeGrice et al. 165, with permission


Figure 22.

Schematic representation of pressure‐volume area (PVA). Solid line indicates the pressure volume trajectory of a single contraction (P‐V loop) plotted in the end‐systolic and end‐diastolic pressure‐volume framework. The area shown by the diagonal lines is the pressure volume area.



Figure 23.

Correlations between cardiac oxygen consumption per beat (VO2) and PVA in control panels (A, C) and following epinephrine (B) and calcium (D). Inset shows the contractions from which the ESPVR is determined for each panel (closed symbols represent isovolumic beats, opening ejecting contractions).

From Suga et al. 320, with permission


Figure 24.

Left ventricular pressure‐volume relationship adapted from the work of Taylor et al. 329. Dashed line indicates the pressure‐volume relationship corrected for the contribution of the right ventricle in a single animal, and the error bars indicate the SD over 8 animals. Solid line schematically estimates the pressure‐volume relationship on deflation.



Figure 25.

Left ventricular pressure diameter relationships from three contractions in a conscious dog. The dashed line indicates the passive pressure diameter relationship determined in the same animal from the end‐diastolic pressure diameter point in several contractions 254.



Figure 26.

Length‐tension relationship in single cardiac myofibrils determined in relaxing solution with and without BDM (solid lines, open and closed symbols). The dashed lines indicate the sarcomere length‐tension relationship in intact rabbit and rat papillary muscles and trabeculae

From Linke et al 180, with permission


Figure 27.

Pressure‐volume curves in an isolated buffer perfused rat heart showing the effects of progressive infusion with collagenase. There is a shift toward greater volumes at all pressures that increases with progressive disruption of the extracellular matrix.

Reproduced with permission from MacKenna et al 190


Figure 28.

Tracings from a conscious dog, illustrating the temporal relationships between mitral valve flow and atrial and left ventricular pressures.

Modified from Yellin et al. 361, with permission
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Article Title: Systolic and Diastolic Function (Mechanics) of the Intact Heart
 

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James W. Covell, John Ross. Systolic and Diastolic Function (Mechanics) of the Intact Heart. Compr Physiol 2011, Supplement 6: Handbook of Physiology, The Cardiovascular System, The Heart: 741-785. First published in print 2002. doi: 10.1002/cphy.cp020120