Cardiac Out Put

LECTURE BY DR.MOHAMMED SHARIQUE AHMED QUADRI

ASSISTANT PROFESSOR ,PHYSIOLOGY

Cardiac Out Put

CARDIAC OUTPUT

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.

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CARDIAC OUTPUT [COP]

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.

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CARDIAC INDEX

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.

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DEFINITIONS WHICH WE WILL USE DURING DISCUSSION OF

COP

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

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• Ejection fraction (EF) is the percentage of ventricular end diastolic volume (EDV) which is ejected with each stroke.

EF =

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SV (EDV – ESV)

EDVX 100

75

120X 100 = 62.5%

Normal ejection fraction is about 60 – 65 %.

Ejection fraction is good index of ventricular function.

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

Adrenal medulla

No effect

Promotes secretion of epinephrine ,that augments the sympathetic nervuos system actions on heart

Veins No effect

Increaser venous return which increases the strength of cardiac contraction through Frank-starling mechanism


Autonomic control of heart rate

- +

Heart rate Heart rate

Increase Parasympathetic

activity

Increase Parasympathetic

activity

Increase sympathetic

activity

Increase sympathetic

activity


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


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


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 .


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 Venous Return

VENOUS RETURN TO THE HEART

i). Increased Blood VolumeVeins 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 PumpMuscle contraction compresses the veins.This external venous compression decreases

venous capacity and increases venous pressure and moves blood towards the heart.

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iii). Respiratory PumpDuring 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.

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iv). Increased Sympathetic VasoconstrictionSympathetic Stimulation causes

vasoconstriction, which increases venous pressure and drives more blood to right atrium, therefore, more venous returns and increase EDV.

v). Cardiac suction effectHeart 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.

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vi). Venous ValvesIn 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.

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CARDIAC OUTPUT [COP]

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.

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Effect of Sympathetic stimulation on stroke volume


Sympathetic stimulation increases the contractility of the heart

Sympathetic stimulation shift the frank starling’s curve to left

EJECTION FRACTION

Ejection Fraction is ratio of Stroke Volume to End – Diastolic Volume.

EF = [SV ÷ EDV] × 100Normal 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.

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MEASUREMENT OF CARDIAC OUTPUT

Cardiac Output can be measured 1. Fick Principle 2. Dye Dilution Method 3. Doppler Combined with Echocardiography

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FICK PRINCIPLE27

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

PathologicalIncrease 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

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

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PRE LOAD & AFTER LOAD

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.

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Cardiac failure Frank Starling Curve In Heart Failure

SIGNS OF HEART FAILURE

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.

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References

Human physiology by Lauralee Sherwood, seventh edition

Text book physiology by Guyton &Hall,11th editionText book of physiology by Linda .s contanzo,third edition

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Cardiac Out Put