Ventricular Pressure-Volume Loops
Steve Wood, [email protected]
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Cardiac Output
HeartRate
StrokeVolume
Preload Afterload Inotropy
SNSPNS
+- + +-
+ + +
II. The Ventricle as a Pump: Cardiac Output = HR x SV
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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.
III. The Ventricle as a Pump: Frank-Starling Curves
Preload
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Inotropyafterload
Frank-Starling Curves
inotropy
afterload
Changes in afterload and contractility (inotropy ) shift the Frank-Starling curve up or down (at any given preload)
PV loops explain this – slide 18
Preload
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A drug which caused vasoconstriction of systemic veins (alpha agonist) would shift point 1 to point ___.
ABCD
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Stro
ke V
olum
e(o
r car
diac
out
put)
Left Ventricular end-diastolic pressure(or end-diastolic volume)
Normal
Heart failure
Increased contractility
a
bc
Starling Curves in Heart Failure
Hyp
oten
sion
Pulmonary congestion
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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)
IV. Pressure-Volume Relationships in the Ventricles
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1
2
3
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V. PRESSURE-VOLUME LOOPSLV
Vol
ume,
ml
LV P
ress
ure,
mm
Hg
aLV Volume, ml
0 20050 120
LV P
ress
ure,
mm
Hg
0
100
ESV
EDVb
c
d
ESPVR
EDPVR1
2
3
4
SV
Preload
Afterload
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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
Work of the Heart
Cardiac Work = Stroke work x HR
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Oxygen Demand of the Heart
HR x SBP VO2
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Inotropy
Stroke Work Curve
inotropyStro
ke W
ork
(P x
V)
When stroke work is plotted against preload ONLY changes in inotropy will shift curve.
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• At constant afterload and inotropy• SV increases and ESV remains constant• EF increases• Dashed lines are systolic and diastolic
pressures
Effect of Increased Preload
A. Effect of Preload on Stroke Volume
VI. Effects of Preload, Afterload, Inotropy and Lusitropy on Ventricular Pressure-Volume Loops
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• At constant afterload and inotropy• SV decreases and ESV remains
constant• EF decreases slightly
Effect of Decreased Preload
Effects of changing preload = Starling’s Law
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• 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
Effect of Increased Afterload
B. Effect of Afterload on Stroke Volume
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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)
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C. Effect of Contractility on Stroke Volume
• At constant preload and afterload• SV increases and ESV decreases• EF increases
Effect of Increased Contractility (+ Inotropy)
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• At constant preload and afterload• SV decreases and ESV increases• EF decreases • Over time, EDV increases causing
increased LV and LA pressure – next slide
Effect of Decreased Contractility (- Inotropy)
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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
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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
Compliance = V/P
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Combined Systolic & Diastolic Failure• Decreased SV and EF• Increased end diastolic pressure • Compensatory volume expansion
further increases end diastolic pressure
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VII. Practice Questions
http://www.unmphysiology.org/boardreview/cardioquestions.html
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Summary
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Huh?
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