Download Cardiac Out Put

Cardiac Out Put
LECTURE BY
DR.MOHAMMED SHARIQUE AHMED QUADRI
ASSISTANT PROFESSOR ,PHYSIOLOGY
CARDIAC OUTPUT
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What is Cardiac Output?
 It is volume of the blood pumped out by each
ventricle per minute .It is about 5 – 5.5 Lit/min
 Cardiac Output [COP ]
= Heart rate × Stroke volume
= 70 beats/min × 70ml/beat
= 4900 ml/min ≈ 5liters/min
 COP of each ventricle is same.
CARDIAC OUTPUT [COP]
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 COP increases during exercise, and depending on
exercise, it can increase to 20–25 liters/min [up to
35 liters/min is recorded in trained athlete during
heavy exercise].
 How ?
- By increasing stroke volume and heart rate.
CARDIAC INDEX
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What is Cardiac Index ?
 It is cardiac output per minute per square meter of
body surface area.
 Normal Cardiac Index = 3.2 Liter /min/ sq meter
body surface area.
What is Cardiac Reserve ?
 It is the difference between cardiac output at rest and
maximum volume of blood that heart can pump per
minute.
DEFINITIONS WHICH WE WILL
USE DURING DISCUSSION OF COP
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Stroke Volume: It is a volume of blood pumped out
by each ventricle per beat. It is about 70 - 80 ml.
Stroke volume (SV) = EDV – ESV
 End Diastolic Volume: Volume of blood in each
ventricle at the end of diastole.
It is about 120 – 130 ml.
 End Systolic Volume: Volume of blood in each
ventricle at the end of Systole. It is about 50 to 60 ml
• Ejection fraction (EF) is the percentage of
ventricular end diastolic volume (EDV) which
is ejected with each stroke.
SV (EDV – ESV)
EF =
X 100
EDV
75
X 100 = 62.5%
120
Normal ejection fraction is about 60 – 65 %.
Ejection fraction is good index of ventricular function.
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Factors controlling cardiac out put
Factors controlling cardiac out put
 Heart rate : is determined primarily by autonomic
influences on SA node
 The heart is innervated by both division of autonomic nervous
system which can modify the rate as well as strength of
contraction.
 Parasympathetic innervation through vagus primarily
supplies atrium (SA node & AV node) ,parasympathetic
innervation of ventricle is sparse.
 Cardiac sympathetic innervation supplies both SA node &
AV node & also to ventricles.
Area affected Effect of parasympathetic
stimulation
Effect of sympathetic
stimulation
SA node
Decrease rate of
depolarization to threshold,
decrease heart rate
Increase rate of depolarization
to threshold &, increase heart
rate
AV node
Decrease excitability, increase
AV nodal delay
Increase excitability ,decrease
AV nodal delay
Ventricular
conduction
pathway
No effect
Increase excitability, hasten the
conduction through bundle of
hiss & purkinje fibers
Atrial muscle
Decrease contractility,
Increase contractility
Ventricular
muscle
No effect
Increase contractility
No effect
Promotes secretion of
epinephrine ,that augments the
sympathetic nervuos system
actions on heart
No effect
Increaser venous return which
increases the strength of
cardiac contraction through
Frank-starling mechanism
Adrenal
medulla
Veins
Factors controlling cardiac out put
 Autonomic control of heart rate
Heart rate
Increase
Parasympathetic
activity
+
Increase
sympathetic
activity
Factors controlling cardiac out put
 Control of heart rate:
 Heart rate is determined by balance between Inhibition of SA
node by vagus(parasympathetic) & stimulation by
sympathetic

Under resting condition parasympathetic discharge dominates

Although heart rate is primarily regulated by autonomic
innervation the other factor affect it as well ,the most imp is
EPINEPHRINE ,a hormone secreted by adrenal medulla
and that act on heart & increases heart rate
Factors controlling cardiac out put
 Stroke volume : two types of control influence
stroke volume

INTRINSIC CONTROL related to venous return &
peripheral resistance

EXTRINSIC CONTROL related to extent of
sympathetic stimulation of heart .

Both factors( Intrinsic and Extrinsic ) increase stroke
volume by increasing the strength of heart
contraction.
Intrinsic & extrinsic control of stroke volume
Factors controlling cardiac out put
 Intrinsic control of stroke volume:
 Direct correlation between end diastolic volume & stroke
volume

This depends on length tension relationship of cardiac
muscle

For cardiac muscle resting cardiac length is less than optimum
length at which maximum tension develops

Therefore increasing the increasing the cardiac muscle fiber
length closer to optimum length, increases the contractile
tension of the heart on the following systole .
Factors controlling cardiac out put
 Frank -Starling law of heart: force of contraction
is proportional to initial length of cardiac muscle
fiber .( intrinsic relation between end diastolic
volume and stroke volume)
 Greater the diastolic filling larger the end
diastolic volume & more the heart is stretched
.the more the heart stretched , longer the initial
cardiac fiber length before contraction , more will be
the force of contraction
 EXTENT OF FILLING IS REFFERED TO AS
PRELOAD
Factors controlling cardiac out put
Factors Controlling Venous Return
VENOUS RETURN TO THE HEART
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i). Increased Blood Volume
 Veins are capacitance vessels and hold about 60 to
70% of blood, when veins store less blood, more
blood is returned to the heart.
ii). Skeletal Muscle Pump
 Muscle contraction compresses the veins.
 This external venous compression decreases venous
capacity and increases venous pressure and moves
blood towards the heart.
VENOUS RETURN TO THE HEART
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iii). Respiratory Pump
 During respiration, intra-thoracic pressure decreases
and is less than atmospheric pressure [-5 mmHg].
 This negative chest cavity pressure squeezes blood
from the lower veins to the chest, increasing venous
returns.
VENOUS RETURN TO THE HEART
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iv). Increased Sympathetic Vasoconstriction
 Sympathetic Stimulation causes vasoconstriction,
which increases venous pressure and drives more
blood to right atrium, therefore, more venous returns
and increase EDV.
v). Cardiac suction effect
 Heart plays role in its own filling. During ventricular
contraction, AV valves are pulled downward enlarging
atrial cavities.
 Atrial pressure drops below 0 mmHg and increases
venous returns.
VENOUS RETURN TO THE HEART
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vi). Venous Valves
 In the veins, blood can be driven forward only as
large veins have one way valve placed at 2 to 4 cm
intervals.
 These valves prevent back flow of blood that tends to
occur when a person stands up.
CARDIAC OUTPUT [COP]
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 EXTRINSIC CONTROL [factors outside the heart]
 Extrinsic control is through sympathetic stimulation.
 Sympathetic stimulation and epinephrine increases
heart contractility, at any given end – diastolic
volume.
 Increased contractility results from increased Ca2+
influx triggered by nor- epinephrine and
epinephrine.
Effect of Sympathetic stimulation on stroke
volume
Factors controlling cardiac out put
 Sympathetic stimulation
increases the
contractility of the heart
 Sympathetic stimulation
shift the frank starling’s
curve to left
EJECTION FRACTION
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 Ejection Fraction is ratio of Stroke Volume to End –
Diastolic Volume.
EF = [SV ÷ EDV] × 100
 Normal healthy heart has Ejection Fraction of 50 –
75% [55 – 65%] under resting conditions and may go
up to 90% during strenuous exercise.
 A failing heart (cardiac failure)  EF maybe 30% or
less.
MEASUREMENT OF CARDIAC OUTPUT
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 Cardiac Output can be measured
1. Fick Principle
2. Dye Dilution Method
3. Doppler Combined with Echocardiography
FICK PRINCIPLE
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Output of Left Ventricle
Oxygen Uptake by lungs
=
ml/min
AO2 - VO2
=
200 ml / min
200 ml / L – 160 ml / L
Art blood – Venous blood
[Pul artery]
= 200 ml/min
40ml / liter
= 5 L/min
Conditions which alters the cardiac out put
 Physiological
 Muscular exercise
 Emotional states
 Posture
 Pregnancy
 Pathological
 Increase in cardiac out put





Hyperthyroidism
Beriberi
Anemia
Fever
Hypoxia
 Decrease in cardiac out put





Hypothyroidism
Myocardial damage & cardiac failure
Valvular heart diseases
Arrhythmias
Hemorrhage & shock
APPLIED
HEART FAILURE
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What is Heart Failure ?
 It is inability of heart to give cardiac output,
sufficient to keep pace with body’s demand.
 There may be left ventricular failure or right
ventricular failure or bi – ventricular failure.
 Most common cause heart failure is
1. Heart Attack or Myocardial Infarction
2. Working against Increased after load e.g. hyper
tension or aortic valve stenosis
PRE LOAD & AFTER LOAD
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 PRE LOAD – load on the heart before contraction
i.e. end – diastolic volume.
 AFTER LOAD – load against which ventricle has to
pump i.e. pressure in the artery or arterial blood
pressure.
Frank Starling Curve In Heart Failure
Cardiac failure
SIGNS OF HEART FAILURE
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 In Left Ventricular Failure – pulmonary congestion
or pulmonary edema occurs which causes decrease
exchange of O2 and CO2 in the lungs.
 In Right Ventricular Failure – due to back
pressure, there is engorgement of neck veins, peripheral
edema, liver enlargement.
Treatment of Heart failure
-- positive Inotropic drugs e.g. digitalis
-- diuretics - to get rid of salt and water
-- ACE Inhibitors [Angiotensin Converting Enzyme]
inhibitors which decrease preload and after load.
References
 Human physiology by Lauralee Sherwood, seventh edition
 Text book physiology by Guyton &Hall,11th edition
 Text book of physiology by Linda .s contanzo,third edition