Cardiac Out Put

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# Cardiac Out Put - PowerPoint PPT Presentation

Cardiac Out Put. Lecture by Dr.Mohammed Sharique Ahmed Quadri Assistant professor ,Physiology. 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 ]

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### Cardiac Out Put

Lecture by

Assistant professor ,Physiology

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.
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.

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.
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

SV (EDV – ESV)

X 100

EDV

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

EF =

75

X 100 = 62.5%

120

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.
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.
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

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.

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.

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.

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]
• 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.
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
• 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
• Cardiac Output can be measured

1. Fick Principle

2. Dye Dilution Method

3. Doppler Combined with Echocardiography

FICK PRINCIPLE

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

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 – 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.
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.

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