Frank Starling

CO = HR*SV

1. Scientist of Physiology

Ernest Henry Starling
(1866-1927)

Contribution:-

1.Starling Equation — describe fluid shiftin the body

2.The discovery of Peristalsis

3.Secretin- the first Hormone, Introduction ofconceptof
hormone

4.Discovers - Distal convoluted tubules of Kidney reabsorbs
water and various Electrolyte.

5.Develop “Frank-starling law of Heart” in 1915.

2. Regulation of Heart Pumping

(1) INTRINSIC cardiac regulation of
pumping in response to changes in
volume of blood flowing into the heart
(Frank-Starling Law)

(2) Control of heart rate and strength of
heart pumping by ANS

3. Poiseille Law and vasomotor tone

affected by
e rs
Cardiac Output and —»| 4— increases
—— decreases

Caiculate

HR x sv )— SV = stoke volume
7
ae SV affected by
HR regulatéd by A

va Preload, contractility, capacitance, afterload, HR
Action Potential

_modifies 7

7 IE Prelosá
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modifies
7
Frank Starling curve
ER

IN A

H >
ES ———+ (ue

Upstroke (cardiac myocytes) Repolarization

4. | Factors Affecting Hoart Fate (HR) Factors Affecting Stroko Volume (54) ;

Hüart Rate (HA)

Cardiac Output (co) =

5. A Summary of the Factors Affecting
Cardiac Output

Skeletal Blood Changes in
muscle volume peripheral
activity | circulation
Atrial Venous
reflex return Hormones
Autonomic
innervation Hormones Preload Contractility | Afterload
Filling End- | End-systolic
ra time volume

zu

| En
ES (6) Factors affecting
{a) Factors affecting heart rate stroke volume
N SARDIAC

6. To increase cardiac output

Increase stroke volume
or

Increase heart rate
or
increase both

7. Introduction

1. Cardiac output — the volume of blood pumped
from each ventricle per minute:

co = SV x HR

cardiac output stroke volume X heart rate
(ml/minute) (ml/beat) (beats/min)

a. Average heart rate = 70 bpm
b. Average stroke volume = 70-80 ml/beat
c. Average cardiac output = 5,500 ml/minute

8. *Regulation of Cardiac Output

Total peripheral resistance
and mean arterial pressure

1
x

t

I Contraction

I strength

1 Sympathetic End-

1 Bowes diastolic

! volume
Parasympathetic Stretch (EDV)

nerves | |
Frank-

Starling

9. Lo CE CLS LITE LIL TES Mean arterial
MATES

1

i

x
__ Kuntraction
[—— sbrengeh >
Eynmparbetio es
oe volume

Strebeha (EDV)

Frank-
Starling

10. TABLE 9-3

Area Affected Effect of Parasympathetic Stimulation Effect of Sympathetic Stimulation

SA node Decreases the rate of depolarization to Increases the rate of depolarization to threshold;
threshold; decreases the heart rate increases the heart rate

AV node Decreases excitability; increases the AV nodal delay _ Increases excitability; decreases the AV nodal delay

Ventricular conduction
pathway

Atrial muscle
Ventricular muscle

Adrenal medulla
(an endocrine gland)

Veins

No effect

Decreases contractility, weakens contraction
No effect
No effect

No effect

Increases excitability; hastens conduction through
the bundle of His and Purkinje cells

Increases contractility; strengthens contraction
Increases contractility; strengthens contraction

Promotes adrenomedullary secretion of epinephrine,
a hormone that augments the sympathetic nervous
system’s actions on the heart

Increases venous return, which increases the strength
of cardiac contraction through the Frank-Starling
mechanism

11. determined by

determined by
Fluid Fluid | Heart Stroke | | Diameter of |
intake loss rate volume ¡the arterioles|
bem
may be
Y y
Regulated
Passive! | at kidneys|

Copyright © 2009 Pearson Education, Inc.

determined by

Diameter
of the veins

12. Question: Why is the pressure same in Arteries and aorta?

Because they do not coil (only arch of aorta), so the Frank-Starling equation
does not hold but Laplace law instead. Laplace law is the reason why you
can have the same pressure in aorta (big) and arteries (small), because the
pressure depends inversely on the pressure.

Question: Why is the pressure same in Arteries and aorta?

Because they do not coil (only arch of aorta), so the Frank-Starling equation
does not hold but Laplace law instead. Laplace law is the reason why you
can have the same pressure in aorta (big) and arteries (small), because the
pressure depends inversely on the pressure.

13. Cardiac Muscle Function

Preload

3
=
£
8
5
É

a
Muscle Length (mm)

+The length of a cardiac
muscle fiber prior to the
onset of contraction.
«Frank Starling

Tension (g)

Afterload

Muscle Length (mm)

-The against which a
cardiac muscle fiber
must shorten.
-Isotonic Contraction

Contractili

+norepinephrine

Tension (g)

Muscle Length (mm)

«The force of contraction
independent of preload
and afterload.

-Inotropic State

14. Preload and Afterload

Preload: :

volume 7

entering Afterload: q

ventricles resistance eft
ventricle must

overcome to
circulate blood

15. Starling’s Law of the Heart

- The greater the stretch of the myocardial
fibers, the stronger the force of the
contraction.

Aortic

== T7 Valve
ao

Left Coronary
Artery

Right Coronary
Artery ™

16. Preload

« Frank Starling’s Law of
the Heart

Ability of the muscle fibers to stretch
according to incoming volume.

+ Degree of fiber stretch as a result
of a quantity of blood placed on
the muscle prior to contraction.

+ The more diastolic volume or
fibre stretch at end diastole, the
greater the force of the next
contraction during systole

+ Measured by LVEDP - left
ventricular end diastolic pressure
- prior to systole (max. full)

+ Normal value 6-12 mmHg

The > stretch = > contractility
If preload increases so does C.O.

++

17. _ Negative
intrathoracic
pressure
Blood volume Venous pressure
AN

he Breathing
we EN
Y EN
Urine Tissue-fluid Venoconstriction Skeletal
volume volume muscle

pump

Sympathetic
nerve stimulation

18. Frank-Starling Law of the Heart

+ Preload : degree of myocardial
stretch is related to the volume of
blood in the ventricles .The
greater the stretch on the
ventricular walls, the greater the
force the myocardium will
contract thus increasing stroke
volume.

— Slower heart rate increase
ventricular filling time
(venous return) increasing SV

« How will blood loss effect heart

rate and stroke volume?

(a) Preload

19. Frank-Starling Law

“Volume of blood ejected by the

ventricle depends on the volume

present in the ventricle at the end

of diastole”

Underlying principle

— Length-tension relationship in cardiac
muscle fibers

SV & CO correlate directly with

EDV

EDV correlates with VR

CO = VR (FS Law ensures this)

Cardiac muscle nomaly operates

only on the ascending fimb of the

systolic curve

Developed force or ventricular pressure —>

Initial myocardial fiber length

20. Frank-Starling Law of the Heart

Relationship

between EDV Frank-Starling Mechanism
contraction (Law of the Heart)
Resting sarcomere lengths
strength and
SV.
Intrinsic <a) 24 um
mechanism: 2 La
: 3 te) et Myosin
— Varying degree g PA oe
of stretching of 2 (6) = F22um{
myocardium by À &
EDV. | ae
— AsEDV = abs 350 2.0 um
increases, ee
myocardium is er a a?
increasingly Time H:5 amd
stretched, and

contracts more

A a

21. ARDIOVASCULAR SYSTEM, and CORONARY CIRCULATION

Frank Starling Curves

+ Ability of the heart to change
force of contraction in response
to changes in venous return.

» If EDV increases, there is a
corresponding increase in
stroke volume, suggesting heart
failure and inotropy.

» Reduced stroke volume
suggests increased preload
and decreased ejection fraction.

LVEDP (mmHg)

22. Changes in contractility shift the Frank-Starling
curve upward (increased contractility) or
downward (decreased contractility).

a. Increases in contractility cause an increase in cardiac

output for any level of venous pressure, right atrial
pressure, or end-diastolic volume.

b. Decreases in contractility cause a decrease in cardiac
output for any level of venous pressure, right atrial
pressure, or end-diastolic volume.

23. Cardiac output

> Cardia output

(Umi)

Right ventricle

Increased contractility
— 7 (sympathetic stimulation)

20 f
E
== 15 i
3 Normal
er 10
5 D si
set — Failing heart
a
—A © 4 a 12 16 20
Central venous pressure
(rm Hag)
Left ventricle Increased contract
2o — TT Oo sympathetic
- Stimulation)
a= f Normal
10
si _ BR — Failing heart
o =
—4 o a =] 12 16 20

Pulmonary capillary wedge pressure
(mm Hg)

24. Starling curves and the effects of haemorrhage
and exercise

Stroke volume

Position in

ee
a normal Positive
individual inotropic
at rest Exercise: ___—_——.
><] Negative

ri inotropic
ft PASS e
L —

effect

Starling curve

effect

End-diastolic volume

25. 15. Frank Starling Law of the Heart
= The heart will pump and stretch at a rate that will allow it to increase the
strength of the contraction

Normal during

Maximal _ exercise
activity
A B Normal
Stroke at rest
Vol Contractile
Walking State
Heart
e] _failure

Cardiogenic
shock

Ventricular End-Diastolic
Volume

26. Cardiac output (L/min)

+ Contractility or t afterload

Normal contractility and afterload

+ Contractility or t afterload

Cardiogenic shock

10 20 30
Pulmonary capillary wedge pressure (mm Hg)

Pulmonary
edema

40

27. Compensated

28. Causes of Decreased
Cardiac Output

» Hypertension
» Cardiomyopathy
> Myocardial infarction

29. Myocardial

al Infarction "ih.

Cardiac Ischemia Arrhythmias and Sudden

Mechanical Ventricular Dysfunction Death

& Neurohumoral
Mechanisms *
tAtherosclerosis

Remodeling —+ Stage B
mes but

Remodeling ce N ”

\

Left Ventricle Hypertrophy
Diastolic Dysfunction -
RISK FACTORS
= Hypertension
» Coronary Artery Disease
* Valvular disease
Stage A -— - Obesity
= Diabetes
* Kidney disease

/

Heart Failure — Stage C & D

A

Pump Failure
Death

Sudden
Death

30. Compensatory mechanisms in heart failure

(1) Cardiac compensation
— increased HR and cardiac contractility
— Cardiac dilatation (The Frank-Starling mechanism)
— Myocardial hypertrophy
(2) Systemic compensation
— Increase the blood volume
— Redistribution of blood flow
— Increase of erythrocytes
— Increased ability of tissues to utilize oxygen
(3) neurohormonal compensation
— Sympathetic nervous system
— Renin-angiotensin system
— Atrial natriuretic peptide; endothelin

31. Decreased Cardiac Output

| |

T Sympathetic T Renin-angiotensin T Antidiuretic
nervous system system hormone
{ | 1 fd |
T Contractility T Heart Vasoconstriction T Circulating volume

rate | |

Arteriolar Wenous

Maintain
Blood
Pressure

T Venous return to
heart cotées -
(T preload)

Peripheral edema

& and pulmonary
congestion
T Stroke
volume

32. NORMAL

Heart energy excess

Low ventricular inlet pressure
Incompletely fled vertrices
Increase in tale — no increase in
cardiac cuiput

Increase contraction — no increase
in cardiac oulpul

Cardiac output = f mevpiiniet
impedarses

Body water equilibrium

Normal cardiac output

HEART FAILURE

Heart energy deficit

High inlet pressure

Completely filled venbicks
Increase in fale — increase in
cardiac oulput

Increase contraction — increase in
cardiac culput

Heart delermines cardiac output

Progressive water retention
Low cardiac output

33. Aca rdiac output

Tstroke volume (1 Heart rate ) (1 Heart rate ) rate

Z IL

t End-diastolic Plasma t Sympathetic
volume De stimulation

Venous vasoconstriction

34. y CARDIAC OUTPUT QY

ST
=>
=HRX eee
Cardiac Output Heart Rate Volume

BES 22007 Nursira Educstion Cs

35. Frank-Starling

Family of Starling curves

Normal—exercise

Running Normal—rest

Contractile state
of myocardum

Walking ------
/ Heart failure

2
3
FS
E
Ss

2
5
El

=
Ss

2

=
E
=

Rest

Fatal myocardum
depression

Ventricular end-diastolic volume >
(Myocardial stretch)