3. cardiac output · 2013-12-29 · 1 cardiac output and venous return dr badri paudel gmc...

1

Cardiac Output and venous return

Dr Badri Paudel GMC

Definitions Cardiac Output

– The quantity of blood pumped into the aorta each minute

– measured in milliliters (mL) per minute (min) or liters (L) per minute

–  normally around 5,000 mL (5 L) per minute (5,000 mL/min or 5 L/min)

Venous Return – The quantity of blood flowing from the veins

into the right atrium each minute

11/13/13 badri@GMC 2


End-Diastolic Volume

End-Systolic Volume

End-Diastolic Volume – End-Systolic Volume = Stroke Volume


Cardiac Output (CO)

Volume of blood ejected from one ventricle

Beat = stroke volume (SV) = EDV – ESV = 70 ml

Minute = Cardiac output (CO) = SV x HR = 5 liters / min

Minute / square meter of body surface area = Cardiac index = 3.2 liter / min / m2


2

Cardiac'output'(CO)%is%directly%affected%by…%

 heart'rate'(HR),%the%number%of%<mes%the%heart%beats%each%

minute;%and%

 stroke'volume'(SV),%the%amount%of%blood%

ejected%during%each%beat%

CO%=%HR%x%SV%%

  If#HR#increases,#what#will#happen#to#cardiac#output?#

  If#SV#decreases,#what#will#happen#to#cardiac#output?#

11/13/13' badri@GMC' 7'

Ejection Fraction: ! Definition: It is the ratio of SV compared to EDV.

SV 70

= EDV 135

! Importance: It is used as indicator for myocardial contractility.

! Value: Normally it is about 50 – 60 %.

X 100

X 100 =


  During exercise CO (Cardiac Output) may

increase up to 20-25 liters/minute and up to 40 liters/minute during heavy exercise in athletes

  Cardiac reserve is the difference between the

cardiac output at rest and maximal cardiac output during heavy exercise.


Cardiac Reserve

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CONTRACTILITY PRELOAD AFTERLOAD

STROKEVOLUME

HEARTRATE

CARDIACOUTPUT

(+) (+)

(+) (+)

(-)

IMPORTANT RELATIONSHIPSIMPORTANT RELATIONSHIPSDeterminants of Cardiac Output

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Some definitions "  Preload: the initial stretching of the cardiac

myocytes prior to contraction. "  End diastolic volume: the volume of blood in

a ventricle at the end of filling

"  Determining factor: #  Venous return

Preload Pumps up the heart. 11/13/13 badri@GMC 12

3

Some definitions

"  Afterload: the force the sarcomere must overcome in order to shorten during systole

"  Determining factor: #  Aortic pressure

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"  Electromagnetic flowmeter "  Indicator dilution (dye such as cardiogreen) "  Thermal dilution "  Oxygen Fick Method "  CO = (O2 consumption / (A-V O2 difference)

Measurement of Cardiac Output

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Fick Principle

"  Cardiac output = "  A man has a resting O2 consumption of 250 ml O2/min, a

femoral arterial O2 content of 0.20 ml O2/ml blood, and a pulmonary arterial O2 content of 0.15 ml O2/ml blood.

"  CO = 250 ml O2/min = 5000 ml/min

O2 Consumption

[O2] pulmonary vein – [O2] pulmonary artery

0.20 ml O2/ml – 0.15 ml O2/ml 11/13/13 badri@GMC 15

O2 Fick Problem "  If pulmonary vein O2 content = 200 ml O2/

L blood "  Pulmonary artery O2 content =

160 ml O2 /L blood "  Lungs add 400 ml O2 /min "  What is cardiac output? "  Answer: 400/(200-160) =10 L/min

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Intrinsic regulation (Auto regulation) Extrinsic regulation

Homeometic autoregulation

Heterometric autoregulation

Regulation of Cardiac output

*It is the ability of the heart to change its stroke volume independent of nervous chemical or hormonal factors. * It include

* It depends on - Nervous supply of the heart. - Hormones or chemical * It adjust both stroke volume and heart rate.

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Intrinsic autoregulation 1-Heterometric autoregulation: Initial Length (Preload):   The major determinant of the force of contraction is the

initial length of the muscle fiber.

  The end diastolic volume (EDV) is used instead of

length of muscle fiber.

  The EDV is determined by the preload.

  The term preload refers to the degree of passive stress

exerted by the volume of blood in the ventricle just

before its contraction.

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4

Characters of heterometric auto-regulation

" It is preload phenomena . " It is of a short duration . " There is an increase in the length of muscle fiber . " End diastolic volume ( E.D.V ) increases . " Stroke volume ( S.V ) increases . " End systolic volume slightly increases . " It is usually followed by Homeometric regulation . Examples of heterometric regulation : " a - In case of changing position from standing into

supine position e.g. lying in bed. " b - In the ( early stage ) beginning of muscular

exercise . 11/13/13 badri@GMC 19

Preload

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

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Frank-Starling Relationship

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Preload%…% stretches%the%myocardium%so%that%the%myofibers%are%lengthened%before%contrac<on%resul<ng%in%a%

stronger%contrac<on,%up%to%a%point%(above%which%strength%decreases),%according%to%the%Frank>Starling'law'of'the'heart.%

11/13/13 badri@GMC 22

  Because we cannot measure sarcomere length directly, 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)

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Preload'is%directly%affected%by…%

 filling%<me%and%

 venous%return%

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5

Frank-Starling Mechanism

  When venous return to the heart is increased, ventricular filling increases, as does preload. This stretching of the myocytes causes an increase in force 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

11/13/13 badri@GMC 25


  Allows the heart to readily adapt to changes in venous return.

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

  In summary: Increasing venous return and ventricular preload leads to an increase in stroke volume.

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Length-tension curve (Frank-Starling )

Optimal length

(Cardiac muscle does not normally operate within the descending limb of the length– tension curve.)

End-diastolic volume (EDV) (ml) (related to cardiac-muscle fiber length)

Normal resting length

Increase in SV

Stro

ke v

olum

e (S

V) (m

l) (r

elat

ed to

mus

cle

tens

ion)

B1 A1

Increase in EDV

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The muscle developed tension is increased upon increasing the initial length ( preload ) up to certain limit .Further increase in muscle length beyond this limit depresses the muscle developed tension and this is not seen in the normal heart but only in heart failure

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  There is no single Frank-Starling Curve for the ventricle. Instead, there is a family of curves with each curve defined by the existing conditions of afterload and inotropy.

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6

Frank-Starling Curves

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Frank Starling "  Intrinsic regulation of

heart pumping "  Increased venous

return leads to increased stroke volume

"  CO=SV x HR

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2-Homeometic autoregulation

$ It follows the heterometric regulation. $ It can occur for long time. $ It is an after load phenomenon. $ It is initiated by the increase in aortic

pressure. $ The increase in myocardial contraction

increase SV by the decrease in ESV. $  EDV returns to the normal value (not

changed).

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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.

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Afterload

  More precisely defined in terms of ventricular wall stress:

– LaPlace s Law: Wall stress = Pr/h

  P = ventricular pressure   R = ventricular radius   h = wall thickness

11/13/13 badri@GMC 35

Afterload is better defined in relation to ventricular wall stress   LaPlace s Law

hPr

∝σ

Wall Stress

P

r

Wall Stress

h

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7

Afterload

  Afterload is increased by: –  Increased aortic pressure –  Increased systemic vascular resistance – Aortic valve stenosis – Ventricular dilation

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Effects of Afterload

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  What#effect#will#hypertension#have#on#a=erload?#

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ADerload…%% inversely%affects%stroke%volume;%and% directly%affects%end'systolic'volume;'ESV%

  What#effect#will#hypertension#have#on#stroke#volume?#

11/13/13 badri@GMC 40

Heterometric Homeometeric $ Sequence $ Onset

$ Duration $ EDV

Occurs at first (followed by homeometic regulation).

Rapid (Immediate after increase

in VR)

Short (few minutes)

Increase

Following the heterometric regulation.

Slow

(after few min)

Long (Maintain the elevated stroke volume for long

time). No change

Heterometric Homeometeric $ ESV $ SV $ Stretch of ventricular muscle fibers. $ Mechanism $ Phenomenon

Constant (or slightly increased)

Increase

Present

Starling law

Pre load

Decrease

Increase

Absent

Increase of the aortic pressure

After load.

8

Anrep Effect

  An abrupt increase in afterload can cause a modest increase in inotropy.

  The mechanism of the Anrep Effect is not fully understood.

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! It is the adjustment of CO via change of heart rate (HR) and/or stroke volume (SV). ! It acts through either autonomic nerve supply of the heart and/or hormones (chemicals) in the blood.

Extrinsic regulation

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Nervous regulation Hormonal (chemical)

regulation

Sympathetic NS Parasympathetic NS

Extrinsic regulation

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Heart Rate is directly affected by factors called chronotropic agents (or factors). These factors may be positive or negative.

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PosiIve'chronotropic'agents…' increase%heart%rate%and%%

 include%epinephrine,%norepinephrine%

and%beta%agonists%(e.g.,%isoproterenol).%%

  What#effect#will#sympathe@c#nerve#impulses#have#on#heart#rate?#

11/13/13 badri@GMC 47

NegaIve'chronotropic'agents…' decrease%heart%rate%and%

 include%acetylcholine%(ACh)%and%beta%

antagonists%(e.g.,%propranolol).%

  What#effect#will#parasympathe@c#nerve#impulses#have#on#heart#rate?#

11/13/13 badri@GMC 48

9

Heart Rate

  Changes in heart rate are generally more important quantitatively in producing changes in cardiac output than are changes in stroke volume

  Changes in heart rate alone inversely affect stroke volume

11/13/13 badri@GMC 49

Effects of Heart Rate on Cardiac Output

Heart Rate (Increased by Pacing)

Car

diac

Out

put

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Heart Rate

  At high HR – The decrease in SV is greater than the increase

in HR (decreased filling time)   At low HR

–  decrease in HR is greater than decrement in SV

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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 doesn t function as well

11/13/13 badri@GMC 52

Heart rate regulation:

The SA node is the normal pace maker of the heart that set the heart

rate during rest at average rate=70 beats/minute The autonomic nervous system supply of the heart:   The atria (SA node and AV node) are supplied by the

parasympathetic nervous system (The vagus nerve) and the sympathetic nervous system (Dual supply from both divisions of A.N.S)

  The ventricles are mainly supplied by the sympathetic nervous

system. There is very little Parasympathetic supply of the ventricles

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Area affected: Parasympathetic stimulation Sympathetic stimulation

1-SA Node Decrease heart rate Increase heart rate 2-Atrial muscle Decrease contractility Increase contractility 3-AV Node

Decrease excitability (increase AV node delay)

Increase excitability (decrease AV node delay)

4-Ventricles conductive system

No effect Increase conduction through His bundle and purkinje cells

5-Ventricle muscle No effect Increase contractility 6-Adrenal medulla No effect Increase epinephrine

secretion which enhance sympathetic stimulation on heart

7-Veins No effect Increase venous return (by vasoconstriction of veins) which increase cardiac contraction (Frank-Starling mechanism) 11/13/13 badri@GMC 54

10

Effect Of ANS on HR: Heart rate

Parasympathetic activity

Sympathetic activity (and epinephrine)

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Threshold potential

Threshold potential

= Inherent SA node pacemaker activity = SA node pacemaker activity on parasympathetic stimulation = SA node pacemaker activity on sympathetic stimulation

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The parasympathetic and sympathetic nervous systems act together on

heart rate in antagonistic (opposing) way, during rest the parasympathetic nervous system dominate more than the sympathetic nervous system

What happen if all autonomic nerves to the heart are cut? The heart rate will be 100/minute,which is he inherent rhythm of the

SA (which is the SA Node discharge when it is free from the normal inhibitory dominant parasympathetic effect at rest)

A Cardiovascular control center in the brain stem coordinates the

autonomic activity to the heart, if heart rate is to be increased this center control the increase in sympathetic activity and at same time decrease the parasympathetic activity and vice versa

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Stroke volume

Strength of cardiac contraction

Extrinsic control

Intrinsic control

End-diastolic volume

Intrinsic control

Venous return


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Sympathetic stimulation can increase stroke volume and cardiac output by:

A-Increase force of contraction: -Under sympathetic stimulation with the EDV=135 ml___The Stroke volume

will be 100 ml and End Systolic Volume(ESV)=35 ml only -Sympathetic stimulation shift the Frank-Starling curve up and to the left and

according to the degree of sympathetic stimulation is the degree of the shift up to a maximal increase in strength of contraction 100% greater than resting strength

B-Increase venous return: Sympathetic stimulation also cause vasoconstriction of the veins which

squeezes more blood from the veins to the heart (=more filling) which in turn increase EDV and stroke volume

11/13/13 badri@GMC 59

End-diastolic volume 135 ml

Stroke volume 70 ml

End-systolic volume 65 ml

Resting heart without sympathetic:

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11

Sympathetic stimulation: End-diastolic volume 135 ml

Stroke volume 100 ml

End-systolic volume 35 ml

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Shift of Frank-Starling curve up and to the left by sympathetic stimulation:

Frank-Starling curve on sympathetic stimulation

Normal Frank-Starling curve

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Increased slope of Pace maker potential

Increased force of ventricular contraction

Increased heart rate Increased stroke volume

Increased

cardiac output

Increased preload

Increased venous return

Increased venoconstriction Effects of increased sympathetic stimulation on Cardiac output

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decreased slope of Pace maker potential

decreased force of atrial contraction

decreased heart rate Decreased ventricular filling

decreased

cardiac output

Effects of increased parasympathetic stimulation on Cardiac output

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Cardiac output

Heart rate Stroke volume

Parasympathetic activity


End-diastolic volume

Venous return

Extrinsic control

Intrinsic control

Intrinsic control

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  Filling'Ime'is%inversely%related%to%heart%rate;%as%heart%rate%increases,%filling%<me%decreases.%

  Chronotropic%agents%affect%filling%<me,%thus%they%affect%EDV.%However,%these%agents%may%also%affect%contrac<lity%such%that%the%effects%on%stroke%volume%are%less%straighMorward.%

  What#effect#will#increased#heart#rate#have#on#stroke#volume##(if#other#factors#stay#the#same)?#11/13/13' badri@GMC' 66'

12

2- Hormonal (chemical) regulation

$ Catecholamine: Causes increase CO (Its actions

similar to sympathetic stimulation).

$ Thyroxin hormone: Causes increase CO by

increasing the number and sensitivity of B1 receptors

to catecholamine.

$ Insulin hormone: Causes increase of CO. It has +ve

inotropic action (increases SV and CO).

11/13/13 badri@GMC 67

$ Glucagon hormone: Causes increase of CO. It

has +ve inotropic action (increases SV and CO).

$ Digitalis drug: Causes increase of CO (It has

+ve inotropic action).

$ Acetyl choline: Causes decrease CO (Action

similar to parasympathetic stimulation).

11/13/13 badri@GMC 68

Extrinsic factors Affecting Myocardial Contraction

Force ( Inotropic Factors )

Contractility

Contractility   The inherent capacity of the myocardium to contract independently of changes in afterload or preload.   Changes in contractility are caused by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length.   Increased rate and/or quantity of Calcium delivered to myofilaments during contraction   Alternate name is inotropy.

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11/13/13 badri@GMC 71

PosiIve'inotropic'agents…'  increase%contrac<lity%and%  epinephrine,%norepinephrine%and%cardiac%glycosides%(e.g.,%digitalis)%

  What#effect#will#epinephrine#have#on#stroke#volume?#

11/13/13 badri@GMC 72

13

NegaIve'inotropic'agents…'  decrease%contrac<lity%and%  include%calcium%channel%blockers%(e.g.,%

verapamil).%  What#effect#will#blocking#calcium#channels#have#on#stroke#volume?#

11/13/13 badri@GMC 73 11/13/13 badri@GMC 74

Extrinsic factors Affecting Myocardial Contraction Force ( Inotropic Factors )

1) Nervous Factors: Sympathetic stimulation increases strength of

contraction (positive inotropic factor ) through its Ca ++ raising effect .

b) Parasympathetic stimulation has a negative inotropic effect due to its intracellular Ca++ lowering action (opposite to sympathetic).

2) Neurohormones: a. Epinepherine & norepinepherine : are povitive

inotropic factors (similar to sympathetic) . b. Acetyl choline : is negative inotropic factor

(similar to parasympathetic).

11/13/13 badri@GMC 75

3) ECF ions: Effects of variations in Ca++ and K + ions: a. Ca++ infusion (intravenous) may stop the heart

during systole (Ca++ rigor). b. Effects of hyperkalaemia: Depresses cardiac contractility and may stop the heart during diastole so increased K + ions have a negative inotropic effect 4) Drugs : Digitalis used in the treatment of heart failure is the most important of all; it acts through inhibition of Na+ K+ ATP ase & thus Na+ ions accumulate inside the cells & stimulate Na+ Ca++ exchanger (between intracellular Na+ & extracellular Ca++) which increases the intracellular Ca++ concentration

11/13/13 badri@GMC 76

Factors Regulating Inotropy

(-) Para-

sympathetic Activation

(+) Afterload (Anrep)

(-) Systolic Failure

(+) Heart Rate

(Treppe)

(+) Catechol- amines

(+) Sympathetic

Activation

Inotropic State

(Contractility)

11/13/13 badri@GMC 77

Ancillary Factors

14

Ancillary Factors Affect the Venous System and Cardiac Output

  Gravity – Venous pooling may significantly reduce CO

  Muscular Activity and Venous Valves

  Respiratory Activity


Venous'return'depends%on%how%much%blood%

returns%to%the%heart,%which%is…%

affected%by:%

 blood%volume,%

 venous%pressure%and%%

 intrathoracic%pressure%

  What#effect#will#increased#venous#return#have#on#EDV?#

11/13/13' badri@GMC' 81'

Gravity "  Gravity acts on vascular volume

#  Mostly venous due to high compliance #  Preload decreases #  CO and arterial pressure fall #  Baroreceptor reflex

"  HR increases "  Vasoconstriction

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Effects of Gravity on the Venous System and Cardiac Output   Gravity

– Venous pooling may significantly reduce CO

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Effect Of Gravity on Venous Pressure

11/13/13 badri@GMC 8844

15


Skeletal Muscle Pump (Increase Venous Return)

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Muscular Activity and Venous Valves

11/13/13 badri@GMC 88

Effect of Venous Valves

11/13/13 badri@GMC 8899

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 lung

inflation causes increased right atrial pressure which decreases venous return

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

venous return to the right atrium

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16

Increase Pleural Negative Pressure (Increase Venous Return)

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10

5

0

CA

RD

IAC

OU

TPU

T (L

/min

)

RIGHT ATRIAL PRESSURE (mmHg)

-4 0 4 8 12

15

IPP=

-4m

mH

g

IPP=

-2m

mH

g

IPP = INTRAPLEURAL PRESSURE

IPP=

-5.5

mm

Hg

IPP=

2m

mH

g

CARDIAC TAMPONADE

11/13/13 badri@GMC 9922

  Intrathoracic'pressure'(which%decreases%

during%inspira<on%and%

increases%during%expira<on)%inversely%affects%

venous%return.%

  What#effect#will#inhaling#more#deeply#have#on#venous#return?#

11/13/13' badri@GMC' 93'

  Blood'volume'and%venous''pressure'(which%increases%during%venoconstric<on%

[constric<on%of%the%veins])%directly%affect%

venous%return.%

  What#effect#will#blood#loss#have#on#EDV?#

11/13/13' badri@GMC' 94'

11/13/13 badri@GMC 9955

Factors that Facilitate Venous Return

11/13/13 badri@GMC 9966

17




18

Plateau of CO curve determined by heart strength (contractility + ↑HR)" ↑ Sympathetics ⇒ ↑ plateau

↓ Parasympathetics (HR↑) ⇒ (? plateau)" ↑ Plateau Heart hypertrophy ⇒↑ s plateau Myocardial infarction ⇒ (? plateau) ↓ Plateau

The Cardiac Output Curve

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NORMAL

HYPEREFFECTIVE

-4 0 +4 +8

25

20

15

10

5

0

CA

RD

IAC

OU

TPU

T (L

/min

)


HYPOEFFECTIVE

CARDIAC OUTPUT CURVES

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  Valvular disease ⇒ ↓ plateau (stenosis or regurgitation)

  Myocarditis ⇒ ↓ plateau   Cardiac tamponade ⇒ (? plateau)

↓ Plateau   Metabolic damage ⇒ ↓ plateau

The Cardiac Output Curve (cont d)


Cardiac and Vascular function curves "  Point of equilibrium % predicts cardiac

output and central venous pressure "  Steady state of this particular system


19

25

20

15

10

5

0

CA

RD

IAC

OU

TPU

T A

ND

VE

NO

US

RE

TU

RN

(L/m

in/m

)


-4 0 4 8 12 16

NORMAL CARDIAC

VR CURVE NORMAL

SPINAL ANESTHESIA

SPINAL ANESTHESIA

MAXIMAL SYMPATHETIC STIMULATION

SYMPATHETIC STIMULATION

MAX

Copyright © 2006 by Elsevier, Inc.!11/13/13 badri@GMC 110099

Changes in contractility "  Digoxin:

#  inhibits Na-K ATPase #  Ca++ builds up

Ejection fraction is an indicator of contractility

EF= SV/EDV

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Changes in volume: mean systemic pressure

"  Decreased blood volume "  Decreased venous compliance


20

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Changes in Total Peripheral Resistance "  Constrict arterioles

#  Increased afterload #  Decreased venous return

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Pressure-Volume Loop "  ↑Preload "  ↑Afterload "  ↑Contractility

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21


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Sympathetic and parasympathetic control "  Sympathetic

#  Stimulate: increase HR and increase vasoconstriction

#  Inhibit: decrease HR and decrease vasoconstriction

"  Parasympathetic (vagus) #  Stimulate: decreases HR

and causes vasodilation

11/13/13 badri@GMC 123

Stroke Volume = EDV-ESV

End Diastolic Volume

Preload

End Systolic Volume

Afterload

Contractility

11/13/13 badri@GMC 124

Summary of Factors That Influence Cardiac Output

and Mean Arterial Pressure

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22

Control of Cardiac Output

11/13/13 badri@GMC 112277

Factors that affect the Cardiac Output

11/13/13 badri@GMC 112288

Cardiac%Output%Concept%Map%

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Myocardial Oxygen Consumption

Myocardial Oxygen Consumption

  Oxygen consumption is defined as the volume of oxygen consumed per minute (usually expressed per 100 grams of tissue weight)

11/13/13 badri@GMC 132

23

Myocardial Oxygen Demand is Related to Wall Stress

  LaPlace s Law

hPr

∝σ

Wall Stress

P

r

Wall Stress

h

11/13/13 badri@GMC 133

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

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Magnitude & Distribution of CO at Rest & During Moderate Exercise

11/13/13 badri@GMC 113355

In%Summary…%

  Heart%rate%and%stroke%volume%are%the%two%factors%that%determine%cardiac%output.%

  Each%of%these%is%affected%by%many%factors.%

  Chronotropic%agents%affect%heart%rate%while%inotropic%agents%affect%contrac<lity,%which%

affects%stroke%volume.%

  Some%factors%(e.g.,%epinephrine%and%

norepinephrine)%affect%both.%

11/13/13' badri@GMC' 136'

Shift to the right and downwards of the (Frank-Starling )curve

by heart failure

Normal stroke volume

Decrease in stroke volume

Stroke volume with uncompensated heart failure Normal end-diastolic volume

Normal heart

Failing heart

11/13/13' badri@GMC' 137'

Answers%to%Ques<ons%

  If#HR#increases,#what#will#happen#to#cardiac#output#TCardiac%output%increases.%

  If#SV#decreases,#what#will#happen#to#cardiac#output?#

9Cardiac%output%is%expected%to%decrease%(note%that%heart%rate%can%be%increased%to%compensate).%  What#effect#will#sympathe>c#nerve#impulses#have#on#heart#rate?#

TThe%norepinephrine%released%will%increase%heart%rate.%

  What#effect#will#parasympathe>c#nerve#impulses#have#on#heart#rate?##

GThe%ACh%released%will%decrease%heart%rate.%11/13/13' badri@GMC' 138'

24


  What#effect#will#increased#heart#rate#have#on#stroke#volume#(if#other#factors#stay#the#same)?#

#Stroke%volume%will%increase%to%some%extend%and%if%further%increases%will%lead%to%reduced%filling%<me%and%SV%will%decrease%

(note%that%SV%may%be%maintained%if%the%cause%of%the%increased%

heart%rate%also%increases%contrac<lity).##  What#effect#will#increased#venous#return#have#on#EDV?#EDV%will%increase.#  What#effect#will#blood#loss#have#on#EDV?##EDV%%will%decrease%(note%that%the%body%has%compensatory%

mechanisms%to%ini<ally%maintain%SV%when%blood%is%lost).%

11/13/13' badri@GMC' 139'


  What#effect#will#inhaling#more#deeply#have#on#venous#return?#

%Venous%return%will%increase%because%deeper%inhala<on%lowers%thoracic%pressure%more%than%normal.%

  What#effect#will#epinephrine#have#on#stroke#volume?#

Stroke%volume%will%increase%due%to%the%increased%

contrac<lity.%

11/13/13' badri@GMC' 140'


  What#effect#will#blocking#calcium#channels#have#on#stroke#volume?#

##Stroke%volume%will%decrease.%

  What#effect#will#hypertension#have#on#aGerload?###AVerload%will%increase.##  What#effect#will#hypertension#have#on#stroke#volume?##

Stroke#volume#will#decrease#(and#the#heart#will#have#to#work#harder#to#eject#blood).#

11/13/13' badri@GMC' 141'

The End

3. cardiac output · 2013-12-29 · 1 cardiac output and venous return dr badri paudel gmc...

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