Control of Cardiac Output

8/3/2019 Control of Cardiac Output

1/49

Control

of

Cardiac Output


2/49

Reading

Klabunde, Cardiovascular Physiology

Concepts

Chapter 4 (Cardiac Function)


3/49

Basic Theory of

Circulatory Function The blood flow to each tissue of the body is almost always

precisely controlled in relation to the tissue needs

The cardiac output is controlled mainly by the sum of allthe local tissue flows

Frank-Starling Relationship is the predominant factor inmatching venous return and cardiac output

In general, the arterial pressure is controlled independentlyof either local blood flow or cardiac output control


4/49

Definitions

Cardiac Output

The quantity of blood pumped into the aorta

each minute

Venous Return

The quantity of blood flowing from the veinsinto the right atrium each minute


5/49

Cardiac Output

CO = HR x SV

SV = EDV ESV

EDV

ESVEDV

EDV

SVEF


6/49

End-DiastolicVolume

End-SystolicVolume

End-Diastolic Volume End-Systolic Volume = Stroke Volume


7/49

Cardiac

Output

Determinants of Cardiac Output

Heart Rate Preload

AfterloadContractility


8/49

CONTRACTILITY PRELOAD AFTERLOAD

STROKE

VOLUME

HEART

RATE

CARDIAC

OUTPUT

(+)(+)

(+) (+)

(-)

IMPORTANT RELATIONSHIPSIMPORTANT RELATIONSHIPS


9/49

Heart Rate


10/49

Heart Rate

Changes in heart rate are generally more

important quantitatively in producing

changes in cardiac output than are changesin stroke volume

Changes in heart rate alone inversely affectstroke volume


11/49

Heart Rate

At low HR

Increase in HR is greater than decrement in SV

At high HR

The decrease in SV is greater than the increase

in HR (decreased filling time)


12/49

Effects of Heart Rate

on Cardiac Output

Heart Rate

(Increased by Pacing)

CardiacOutp

ut


13/49

Bowditch (Treppe) Effect

An increase in heart rate will also cause positive

inotropy (Bowditch effect, Treppe or staircase

phenomenon).

This is due to an increase in intracellular Ca++

with a higher heart rate:

More depolarizations per minute

Inability of Na+/K+-ATPase to keep up with influx of

Na+, thus, the Na+-Ca++ exchange pump doesnt

function as well


14/49

Factors Affecting

Stroke Volume


15/49

Stroke Volume= EDV-ESV

EndDiastolicVolume

Preload

EndSystolicVolume

Afterload

Contractility


16/49

Preload


17/49

Preload

Preload can be defined as the initial stretching ofthe cardiac myocytes prior to contraction. It isrelated to the sarcomere length at the end of

diastole.

Because we cannot measure sarcomere lengthdirectly, we must use indirect indices of preload.

LVEDV (left ventricular end-diastolic volume) LVEDP (left ventricular end-diastolic pressure)

PCWP (pulmonary capillary wedge pressure)

CVP (central venous pressure)


18/49

Determinants of Preload

Venous Blood Pressure Venomotor tone (Venous compliance)

Venous volume Venous Return

Total Blood Volume Respiration

Exercise/Muscle contraction

Gravity

Filling time (Heart rate)

Ventricular compliance Atrial contraction

Inflow or outflow resistance

Ventricular systolic failure


19/49

Frank-Starling Mechanism


20/49


When venous return to the heart is increased,

ventricular filling increases, as does preload. This

stretching of the myocytes causes an increase inforce generation, which enables the heart to eject

the additional venous return and thereby increase

stroke volume.

Simply stated: The heart pumps the blood that is

returned to it


21/49


Allows the heart to readily adapt to changes invenous return.

The Frank-Starling Mechanism plays an importantrole in balancing the output of the 2 ventricles.

In summary: Increasing venous return andventricular preload leads to an increase in strokevolume.


22/49



23/49

Frank-Starling Relationship


24/49


There is no single Frank-Starling Curve for

the ventricle. Instead, there is a family of

curves with each curve defined by theexisting conditions of afterload and

inotropy.


25/49

Frank-Starling Curves


26/49

Afterload


27/49

Afterload

Afterload can be viewed as the "load" that

the heart must eject blood against.

In simple terms, the afterload is closely

related to the aortic pressure.


28/49

Afterload

More precisely defined in terms of

ventricular wall stress:

LaPlaces Law: Wall stress = Pr/h

P = ventricular pressure R = ventricular radius

h = wall thickness


29/49

Afterload is better defined

in relation to ventricular wall stress LaPlaces Law

h

Pr

Wall Stress

P

r

Wall Stress

h


30/49

Afterload

Afterload is increased by:

Increased aortic pressure

Increased systemic vascular resistance

Aortic valve stenosis

Ventricular dilation


31/49

Effects of Afterload


32/49

Anrep Effect

An abrupt increase in afterload can cause a

modest increase in inotropy.

The mechanism of the Anrep Effect is not

fully understood.


33/49

Contractility


34/49

Contractility

The inherent capacity of the myocardium tocontract independently of changes in afterload orpreload.

Changes in contractility are caused by intrinsiccellular mechanisms that regulate the interactionbetween actin and myosin independent of

sarcomere length.

Alternate name is inotropy.


35/49

Contractility

Force of contraction

Increased rate and/or quantity of Calciumdelivered to myofilaments duringcontraction

Heart functions at lower end-systolicvolume and lower end-diastolic volume


36/49


37/49

Factors Regulating Inotropy

(-)

Para-sympatheticActivation

(+)

Afterload(Anrep)(-)

SystolicFailure

(+)Heart

Rate(Treppe)

(+)Catechol-amines

(+)Sympathetic

Activation

InotropicState

(Contractility)


38/49

Ancillary Factors


39/49

Ancillary Factors Affect the Venous

System and Cardiac Output Gravity

Venous pooling may significantly reduce CO

Muscular Activity and Venous Valves

Respiratory Activity


40/49

Effects of Gravity on theVenous System and Cardiac Output

Gravity

Venous pooling may significantly reduce CO


41/49

Muscular Activity and Venous Valves


42/49

Effects of Respiration

Spontaneous respiration Decreased intra-thoracic pressure results in a decreased right atrial

pressure which enhances venous return

Mechanical ventilation

Increased intra-thoracic pressure during positive-pressure lunginflation causes increased right atrial pressure which decreasesvenous return

Valsalva Maneuver Causes a large increase in intra-thoracic pressure which impedes

venous return to the right atrium


43/49

Summary of Factors

That Influence

Cardiac Outputand

Mean Arterial Pressure


44/49


45/49

Myocardial Oxygen

Consumption


46/49

Myocardial Oxygen Consumption

Oxygen consumption is defined as the

volume of oxygen consumed per minute

(usually expressed per 100 grams of tissueweight)


47/49

Myocardial Oxygen Demand

is Related to Wall Stress LaPlaces Law

h

Pr

Wall Stress

P

r

Wall Stress

h


48/49

Factors Increasing

Myocardial Oxygen Consumption

Increased Heart Rate

Increased Inotropy (Contractility)

Increased Afterload

Increased Preload Changes in preload affect myocardial oxygen consumption less

than do changes in the other factors


49/49

The End

Documents

Control of Cardiac Output