Cardiac Mechanics: With Thad Wilson

Cardiac Mechanics
With Thad Wilson
DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

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What Determines Cardiac Output and How Is it Regulated?
Cardiac output Stroke volume Heart rate
CO = SV x HR
(ml/min) (ml/beat) (beats/min)
Autonomic nerves Autonomic nerves

Hormones Hormones
Intrinsic factors

Flow, Pressure and Resistance Theory
Stroke volume End-diastolic volume End-systolic volume
SV = EDV - ESV
Afterload
Preload
Inotropy

What Is Preload?
• Preload is related to
ventricular filling just
prior to contraction left-
ventricular end-diastole
volume (LVEDV)
• At the cellular level,
preload is related to the
cardiac fiber length that
occurs at LVEDV
Peggy_Marco, CC0
The Relationship between LV Pressure and Volume
Small preload Large preload

Maximal pressure that LV pressure (mm Hg) Maximal pressure that
develops upon LVPmax develops upon contraction
200
contraction is modest. is much greater.
LVPmax
100
Contract
Fill Fill
0
Ventricle Ventricle
0 50 100
LV volume (ml)
© Lecturio GmbH
Factors Determining Preload
Atrial Afterload
inotropy
Ventricular compliance Heart rate

Venous pressure preload Ventricular inotropy
Venous Venous blood volume

compliance • Total blood volume
• Venous return

Frank-Starling Law
100
• Increased ventricular filling increases B
stroke volume Increased
A venous return
• The relationship between SV and preload
SV
(measured as LVEDP or LVEDV) is called 50
(ml)
• Frank-Starling relation
• Frank-Starling mechanisms
0
• Starling's law of the heart 0 10 20
• Length-dependent activation LVEDP
(mm Hg)
Cf. Richard E.DARRYL

Klabunde,JOHN
www.CVphysiology.com, 2009
PASAMBA, pasambad1306@uerm.edu.ph
Effects of Preload on PV Loops
200
ESPVR Increased ESPVR Decreased
venous venous
LV pressure (mm Hg)
return return
100
Control Control
loop loop
SV EDV SV EDV
0
0 100 200 0 100 200
LV volume (ml) LV volume (ml)
ESPVR = end-systolic pressure-volume relationship; EDV = end-diastolic volume; SV = stroke volume
Klabunde,JOHN
What Is Ventricular Afterload?
• Ventricular afterload is related to

the pressure the ventricle must
generate in order to eject blood
into the aorta.
• Theoretically, afterload is the
ventricular wall stress at this point.

Effects of Afterload on Ventricular Function
Cardiac Contraction
myocyte
Afterload
Minimal afterloads
allow for maximal
Contraction
contraction
velocity
velocity
High afterloads decrease

contraction velocity
Afterload
© by LecturioDARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph
Effects of Afterload on Ventricular Function
Increasing afterload (A  B) 100

• Decreases SV
C
• Increases preload A
(compensatory response) SV
50 B
(ml)
Decreasing afterload (A  C)
• Increases SV 0
0 10 20
• Decreases preload
(compensatory response) LVEDP
(mm Hg)

Klabunde,JOHN
www.CVphysiology.com, 2009 and Bitzblitz, https://commons.wikimedia.org/wiki/File:Frank-Starling_Curve.jpg
Other Effects of Afterload
Arterial (aortic) pressure impedes ventricular ejection

• Lowering arterial (aortic) pressure enhances ventricular stroke volume
'Afterload' and 'Velocity of muscle fiber shortening' are inversely related

Reducing afterload increases:
• Muscle shortening velocity and ejection velocity
• Muscle shortening and therefore decreases the end-systolic volume
• Stroke volume

Effects of Afterload on PV Loops
160
LV pressure (mm Hg)
Aortic
pressure
80 Control Control
SV
SV
Aortic
pressure
0
0 100 200 0 100 200
ESV EDV ESV EDV
ESV = end-systolic volume; EDV = end-diastolic volume; SV = stroke volume

Klabunde,JOHN
What Is Inotropy?
• Ability of the heart to regulate the force

of contraction independent of changes
in preload (length-independent
activation)
• At a given preload, increased inotropy
increases SV by increasing the force of
contraction
Pezibear, CC0DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

Regulation of Inotropy
Sympathetic
activation
Circulating
catecholamines
Afterload (norepinephrine (NE),
(Anrep effect) inotropy epinephrine (epi), and
dopamine)
Heart rate
(Bowditch effect)
Effects of Increased Inotropy on Ventricular Function
Increasing inotropy (A
• Increases SV
100
• Increases rate of ventricular pressure
development (dP/dt) and
C
ejection fraction (EF) A
• Decreases preload SV
50 B
(compensatory response) (ml)
Decreasing inotropy (A
• Decreases SV 0
• Decreases dP/dt and EF 0 10 20
LVEDP
• Increases preload
(mm Hg)
(compensatory response)
• Decreased inotropy (A effects
Klabunde,JOHN
www.CVphysiology.com, 2009 and Bitzblitz, https://commons.wikimedia.org/wiki/File:Frank-Starling_Curve.jpg
Arterial Phase 4
200
pressure
180
(mm Hg) Phase 1
160 Late phase 2
140 Early
phase 2
120
100
80
60 Phase 3
Valsalva maneuver
Baseline consisting of 20 mm Hg Recovery
expiratory pressure

L-type Ca2+ Sarcoplasmic reticulum Phospho-

channel Ca2+ 2+ lamban
Ca
Ca2+Ca2+
P
Ca2+
Ca2+ 2+ P
Ca2+Ca
Ca2+
ATP P Phosphorylation of
Ca2+
Ca2+ Ca2+ phospholamban allows
P Ca2+ Ca2+ pump the Ca2+ pump to add
Ca2+
Ca2+ to the stores
cAMP-dependent phosphorylation between heartbeats.
β-adrenergic receptor
+
norepinephrine

L-type Ca2+ Sarcoplasmic reticulum Phospho-

channel Ca2+ 2+ lamban
Ca
Ca2+Ca2+
P
Ca2+
Ca2+ 2+ Ca2+ 2+ P
Ca2+
Ca Ca2+Ca
Ca2+
ATP P
Ca2+ Ca2+ influx +
Ca2+ Ca2+
P Ca2+ release
Ca2+ Ca2+ pump
Ca2+ = increases force of
contraction
cAMP-dependent phosphorylation
β-adrenergic receptor
+
norepinephrine

Effects of Inotropy on PV Loops
160
Inotropy Control loop
Inotropy
80
SV SV
0
0 100 200 0 100 200
ESV EDV ESV EDV
ESV = end-systolic volume; EDV = end-diastolic volume

Klabunde,JOHN
Frank-Starling Curve Summary
100
Increased Control
preload
SV 50
(ml)
0
0 10 20
Klabunde,JOHN
www.CVphysiology.com, 2009, BitzBlitz, https://commons.wikimedia.org/wiki/File:Frank-Starling_Curve.jpg
100
Decreased Control
preload
SV 50
(ml)
0
0 10 20
Klabunde,JOHN
100
Afterload
Inotropy
Control
Afterload
SV 50 Inotropy
(ml)
0
0 10 20
Klabunde,JOHN
Combined Increase in Inotropy and Preload
Peripheral veins constrict during SNS

activation, and their contents are ESPVR
forced forward to the heart. EDV 100 D
increases (A to B).
LV pressure (mm Hg)

C
SNS stimulation of the myocardium
increases inotropy. The ESPVR shifts Before SNS
to the left. activation
EDV
Combination of increased preload After SNS activation
and inotropy causes increased stroke B
volume (C to D). Cardiac output is A
increased. 0
0 100 200
LVEDP
Klabunde,JOHN
Atrial Dynamics
Atria respond to preload, afterload, and inotropic interventions similar to the way ventricles do
• Force of atrial contraction increases with increased atrial volume (preload) caused by:
• Increased venous return
• AV valve regurgitation and stenosis
• Sympathetic nerve stimulation (and increased circulating catecholamines) increases atrial
inotropy and therefore atrial force of contraction and ejection
• Vagal stimulation decreases atrial inotropy, unlike ventricles

This document is a property of: DARRYL JOHN PASAMBA
Note: This document is copyright protected. It may not be copied, reproduced, used, or
distributed in any way without the written authorization of Lecturio GmbH.


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Cardiac Mechanics

With Thad Wilson

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

Cardiac output Stroke volume Heart rate

Autonomic nerves Autonomic nerves

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

Stroke volume End-diastolic volume End-systolic volume

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

Small preload Large preload

Ventricular compliance Heart rate

Venous Venous blood volume

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

Cf. Richard E.DARRYL

• Ventricular afterload is related to

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

High afterloads decrease

Increasing afterload (A  B) 100

Cf. Richard E.DARRYL

Arterial (aortic) pressure impedes ventricular ejection

'Afterload' and 'Velocity of muscle fiber shortening' are inversely related

• Muscle shortening and therefore decreases the end-systolic volume

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

ESV = end-systolic volume; EDV = end-diastolic volume; SV = stroke volume

• Ability of the heart to regulate the force

Pezibear, CC0DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

L-type Ca2+ Sarcoplasmic reticulum Phospho-

© by LecturioDARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

L-type Ca2+ Sarcoplasmic reticulum Phospho-

© by LecturioDARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

ESV = end-systolic volume; EDV = end-diastolic volume

Peripheral veins constrict during SNS

LV pressure (mm Hg)

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

DARRYL JOHN PASAMBA, pasambad1306@uerm.edu.ph

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