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

2. Objectives
Define and describe the terms COP, stroke volume, EDV, ESV the ejection fraction.
Describe factors affecting cardiac output and venous return.
Recognize the effect of sympathetic and parasympathetic ANS on heart rate and COP.
Identify Frank starling law.
Understand the principle of measuring the COP (Fick principle, dye dilution method).
Apply the physiological knowledge of factors affecting COP on conditions causing low COP and high COP .

3. 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.

4. 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.

5. CARDIAC INDEX What is Cardiac Reserve ?
It is the difference between cardiac output at rest and maximum volume of blood that heart can pump per minute.
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.

6. 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 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

7. Ejection fraction (EF) is the percentage of ventricular end diastolic volume (EDV) which is ejected with each stroke.
EF =
SV (EDV – ESV)
EDV
X 100 75
X 100 = 62.5%
120
Normal ejection fraction is about 50 – 75 %.
Ejection fraction is good index of ventricular function.

8. Factors controlling cardiac out put

9. 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.

10. 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
Adrenal medulla
Promotes secretion of epinephrine ,that augments the sympathetic nervuos system actions on heart
Veins
Increaser venous return which increases the strength of cardiac contraction through Frank-starling mechanism

11. Factors controlling cardiac out put
Autonomic control of heart rate
- +
Heart rate
Increase Parasympathetic activity
Increase sympathetic activity

12. 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

13. 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.

14. 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 .

15. 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

16. Factors controlling cardiac out put

17. Factors Controlling Venous Return

18. VENOUS RETURN TO THE HEART
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.

19. VENOUS RETURN TO THE HEART
iii). Respiratory Pump
During respiration(inspiration), 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.

20. VENOUS RETURN TO THE HEART
iv). Increased Sympathetic activity(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.

21. VENOUS RETURN TO THE HEART
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.

22. 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.

23. Effect of Sympathetic stimulation on stroke volume

24. Factors controlling cardiac out put
Sympathetic stimulation increases the contractility of the heart
Sympathetic stimulation shift the frank starling’s curve to left

25. Intrinsic & extrinsic control of stroke volume

26. 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% under resting conditions and may go up to 90% during strenuous exercise.
A failing heart (cardiac failure)  EF maybe 30% or less.

27. MEASUREMENT OF CARDIAC OUTPUT
Cardiac Output can be measured
1. Fick Principle
2. Dye Dilution Method
3. Doppler Combined with Echocardiography

28. 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 = =

29. Conditions which alters the cardiac out put
Physiological
Muscular exercise
Emotional states
Posture
Pregnancy

30. Increase in cardiac out put
Pathological
Increase in cardiac out put
Hyperthyroidism
Anemia
Fever
Decrease in cardiac out put
Hypothyroidism
Myocardial damage & cardiac failure
Valvular heart diseases
Arrhythmias
Hemorrhage & shock

31. 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

32. 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.

33. Frank Starling Curve In Heart Failure
Cardiac failure

34. 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