1. Ventricular Pressure-Volume Loops
Steve Wood, PhD

5. + + - + - + + + II. The Ventricle as a Pump: Cardiac Output = HR x SV
Heart
Rate
Stroke
Volume + + - + -
Preload
Afterload
Inotropy + + +
Sympathetic/ Parasympathetic Heart   Chronotropy (rate) + + +/ − − −   Inotropy (contractility) /− 1   Lusitropy (relaxation) + + +/ − 1   Dromotropy (conduction velocity) + +/ − − − Vessels   Arterial constriction /0 2   Venous constriction + + +/ 0
PNS
SNS

6. III. The Ventricle as a Pump: Frank-Starling Curves
Single Starling Curve
Normal values are LVEDP  8 mmHg and SV of  70 ml/beat.
Cytosolic Ca++ constant. Inotropy (contractility) is constant.
The increased force of contraction at greater preload is due to: (1) favorable overlap of thin and thick filaments; and (2) increased affinity of Ca++ for Troponin C.
Pulmonary edema occurs when LVEDP = 25 mm Hg.
Preload

7. Frank-Starling Curves
Changes in afterload and contractility (inotropy ) shift the Frank-Starling curve up or down (at any given preload)
PV loops explain this – slide 18
Inotropy
afterload
inotropy
afterload
Preload

8. A drug which caused vasoconstriction of systemic veins (alpha agonist) would shift point 1 to point ___. A B C D

9. (or end-diastolic volume)
(or cardiac output)
Stroke Volume
Left Ventricular end-diastolic pressure
(or end-diastolic volume)
Normal
Heart failure
Increased
contractility a b c
Starling Curves in Heart Failure
Hypotension
Pulmonary congestion
From Lilly, p reduced EF causes increased ESV with nl venous return = increased EDV. Increase in SV is minimal due to flatness or curve

10. IV. Pressure-Volume Relationships in the Ventricles
This isovolumic curve is also called Po (pressure at zero ejection), or the end-systolic pressure volume relationship (ESPVR).
This "resting" curve represents pressures during diastolic filling of the ventricle, and reflects passive properties of the ventricular wall that resist stretch; i.e., the compliance of the ventricle and factors that impair Ca++ reuptake into SR (e.g., hypoxia) (Lusitropy)

11. c d b a V. PRESSURE-VOLUME LOOPS ESPVR Afterload SV EDPVR Preload
LV Volume, ml
200 50
120
LV Pressure, mm Hg
100 3 c
LV Pressure, mm Hg
Afterload 2 3 4 2 d SV 1 b
EDPVR
EDV
LV Volume, ml 1 4
ESV a
Preload

14. Cardiac Work = Stroke work x HR
Work of the Heart
Cardiac Work = Stroke work x HR
Work = force x distance = force x cm
P = force/unit area = force/cm2
Volume = cm3
P x V = force/cm2 x cm3 = force x cm

15. Oxygen Demand of the Heart
HR x SBP  VO2
Myocyte contraction is the primary factor determining myocardial oxygen consumption (MVO2) above basal levels. Therefore, factors that enhance tension development by the cardiac muscle cells, the rate of tension development, or the number of tension generating cycles per unit time will increase MVO2. For example, doubling heart rate approximately doubles MVO2 because ventricular myocytes are generating twice the number of tension cycles per minute. Increasing inotropy also increases MVO2 because the rate of tension development is increased as well as the magnitude of tension, both of which result in increased ATP hydrolysis and oxygen consumption. Increasing afterload, because it increases tension development, also increases MVO2. Increasing preload (e.g., ventricular end-diastolic volume) also increases MVO2; however, the increase is much less than what might be expected because of the LaPlace relationship.
The LaPlace relationship says that wall tension (T) is proportional to the product of intraventricular pressure (P) and ventricular radius (r).
(Law of  LaPlace)
Wall tension can be thought of as the tension generated by myocytes that results in a given intraventricular pressure at a particular ventricular radius. Therefore, when the ventricle needs to generate greater pressure, for example with increased afterload or inotropic stimulation, the wall tension is increased (i.e., increased myocyte tension development). This relationship also shows us that a dilated ventricle (as occurs in dilated cardiomyopathy) has to generate increased wall tension to produce the same intraventricular pressure.
We observe empirically that wall tension and MVO2 are closely related. For this reason, changes in intraventricular pressure and ventricular radius affect MVO2. As stated above, changes in ventricular preload volume do not affect MVO2 to the same extent quantitatively as changes in afterload. This is because preload is usually expressed as the ventricular end-diastolic volume, not radius. If the ventricle is assumed to be a sphere, then the ventricular volume (V) is related to radius (r) by:
Wall tension determines O2 uptake. And radius is proportional to the cube root of volume. This is why volume has a smaller effect on VO2 than the other factors.

16. Inotropy
Stroke Work Curve
inotropy
When stroke work is plotted against preload ONLY changes in inotropy will shift curve.
Stroke Work
(P x V)

17. A. Effect of Preload on Stroke Volume
VI. Effects of Preload, Afterload, Inotropy and
Lusitropy on Ventricular Pressure-Volume Loops
A. Effect of Preload on Stroke Volume
Effect of Increased Preload
At constant afterload and inotropy
SV increases and ESV remains constant
EF increases
Dashed lines are systolic and diastolic pressures

18. Effect of Decreased Preload
At constant afterload and inotropy
SV decreases and ESV remains constant
EF decreases slightly
Effects of changing preload = Starling’s Law

19. B. Effect of Afterload on Stroke Volume
Effect of Increased Afterload
At constant preload and inotropy
SV decreases and ESV increases
EF decreases
No change in contractility (aortic closure occurs on the same line)
This is an acute effect of sudden increase in afterload; in subsequent beat increased EDV will increase SV

20. Effect of Decreased Afterload
At constant preload and inotropy
SV increases and ESV decreases
EF increases
No change in contractility (aortic closure occurs on the same line)

21. Effect of Increased Contractility (+ Inotropy)
C. Effect of Contractility on Stroke Volume
Effect of Increased Contractility (+ Inotropy)
 At constant preload and afterload
SV increases and ESV decreases
EF increases

22. Effect of Decreased Contractility (- Inotropy)
At constant preload and afterload
SV decreases and ESV increases
EF decreases
Over time, EDV increases causing increased LV and LA pressure – next slide

23. D. Systolic and Diastolic Heart Failure
Systolic Failure
EDV increases with loss of inotropy because increased ESV is added to normal venous return.
Increased EDV causes increased LV and LA pressure.
EF decreased
Shown at constant heart rate. The reason for preload rising as inotropy declines is that the increased end-systolic volume is added to the normal venous return filling the ventricle. For example, if end-systolic volume is normally 50 ml of blood and it is increased to 80 ml in failure, this extra residual volume is added to the incoming venous return leading to an increase in end-diastolic volume and pressure

24. Compliance = V/P Diastolic Failure
Reduction in ventricular compliance
Mechanisms: Hypertrophy; Reduced Lusitropy
LV  Increased LA and pulmonary venous pressure  pulmonary congestion
RV  Increased RA pressure and systemic venous pressure  peripheral edema
EF may not change

25. Combined Systolic & Diastolic Failure
Decreased SV and EF
Increased end diastolic pressure
Compensatory volume expansion further increases end diastolic pressure

26. VII. Practice Questions

27. Summary

28. Huh?