Ventricular Pressure-Volume Loops

Steve Wood, PhDscwood@salud.unm.edu

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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?