Cardiac output

Dr Gauhar Hussain, MD

Assistant Professor of Physiology

College of Medicine, Duwadimi 1

 Objectives

• Define various related terms like stroke volume, minute volume,

cardiac index, ejection fraction, cardiac reserve, ESV and EDV.

• Describe the principles for various methods used to determine

cardiac output.

• Enumerate various physiological factors that change cardiac output.

• Explain how cardiac output is regulated.

2
 Cardiac output
• Amount of blood pumped by each ventricle per minute into
circulation  

• CO = stroke volume (SV) x heart rate (HR) 

• Normal range: 5 to 6 L/min (10-20 % < females)

• CO is controlled, why?

1.To maintain proper Blood Flow to tissues

2.Prevent undue stress on heart

3
 Cardiac Index (CI)
• CO per square meter surface area.      

• Average surface area of adult male of 70 Kg = 1.73 m2. 

•  CI = CO/m2 =  5L/1.73m =  3.2 L/min/m2.

• CI - marker of heart as a pump

• CI < 1.8 L/min/m2 indicates cardiogenic shock

4
• End diastolic volume (EDV)-135 -140 ml = blood in ventricle at end of diastole

• End systolic volume (ESV): 70 ml = blood in ventricle at end of systole.

• Stroke volume (SV):

• Amount of blood pumped by each ventricle per beat

• SV = EDV – ESV = 140 -70 = 70 ml/beat

• Ejection fraction: 50-65%

= % of blood ejected out of ventricles during each contraction

= SV/End Diastolic Vol %.

5
• Heart rate(HR): Number of
heart beats per minute. 

• About 70 beat/minute

• CO= SV X HR

= 70 x 70
= 4900 ml
≈5000 ml/minute
(5 L/minutes)

 
6
 Cardiac reserve
• Difference between cardiac work during maximum exercise &
cardiac work during rest.

• Expressed as percent of normal

• Normal young adult cardiac reserve = 300 – 400%

• Athletes trained person it reaches = 500 - 700%

• In heart failure there is no reserve = zero

7
 Methods of Measurement
• In experimental animals: Electromagnetic flow meter

• In human:

I. Direct & Indirect Fick's method

II. Indicator dilution techniques: (l) Dye Method,

(2) Thermo dilution technique

III. Pulsed Doppler method, echocardiography

IV. Radionuclide angiography.

8
 I- Direct Fick’s Method: Principle
• Rate of blood flow through lungs = change in O2 conc. in blood (A - V
difference across lung) x pulmonary blood flow

• COP (L/min) = Oxygen uptake (ml/min)

• Indirect Fick: Respired air is used to calculate COP

• Used in Cardiopulmonary exercise testing, not accurate

9
10
 II. Indicator dilution techniques:
1. Dye Method:  Known amount of a dye (Indocyanine green or
radioactive isotope) given IV. Conc. of dye determined each 2 sec and
is plotted against time 

• Time from first appearance of dye in arterial sample till its

disappearances is determined (T) from  curve. 

• COP = mg of dye injected x 60 / average conc. of dye in dL of blood x

Duration of curve in seconds (T)

11
 II. Indicator dilution techniques:
2. Thermo dilution technique

• Cold saline injected into RA - change in blood temperature in PA is

noted.  

• Advantages: Cold is lost in tissue - Saline is not harmful. 

12
 Other methods
• III-Pulsed Doppler method, echo : pulse of ultrasound (US) is
directed down ascending aorta from transducer

• COP = Average velocity X Cross sectional area of aorta 

• Echo machine - Non-invasive, beat-by-beat analysis

• IV-Radionuclide angiography: technetium - binds to RBC

13
 Regulation of CO (Cardiac output)
A. Control of stroke volume(intrinsic):

• Two mechanism:

• Heterometric regulation: change in

myocardial contractility VARIES with the

resting length of cardiac muscle fibers.

• Length-tension relationship: Frank-Starling Law

• Homometric regulation: change in myocardial contractility is INDEPENDENT of the resting length of

cardiac muscle fibers.

B. Control of heart rate (extrinsic)

ANS , Hormones & chemicals

14
 Heterometric regulation
• Force of contraction of myocardium is dependent upon its pre-load and
afterload.

Control of stroke volume(intrinsic):

• End diastolic volume (preload)

• Peripheral resistance(afterload)

• Myocardial contractility

15
 Control of stroke volume(intrinsic)
• Preload: EDV that stretches Rt or Lt ventricle.

• Force imposed on a resting muscle i.e. prior to

the onset of muscle contraction which stretches
the muscle to a new length

• Determined by : ventricular EDV

• Factors affecting preload

• Venous return

• Ventricular compliance

• Atrial pump

16
 Frank-Starling Law
• Within physiological limit, Force of ventricular
muscle contraction is directly proportional to its
initial length.

• Greater the EDV greater the force of cont of heart & SV

• ↑ Stretch of ventricle → ↑ Force of contraction→ ↑ CO

• Over stretch of myocardial fibers → weakening of

contraction, ↓ in SV & CO

• Starling's law of the heart explains that increase in

cardiac output due to increased venous return 

17
• Venous return (VR) (preload):

• CO is controlled by VR –

• ↑ VR → ↑ EDV → ↑ SV (Heterometric autoregulation)

• ↑ VR→ ↑ HR (Bainbridge reflex). ↑ in SV & HR → ↑ CO

18
 Control of stroke volume(intrinsic)
• Afterload (TPR) : Load which acts on
muscle after it begins to contract

• Opposes muscle contraction

• Systolic ventricular wall stress

• In vivo, the afterload is the resistance

against which blood is expelled

• Depends upon

―Vessel diameter

―Viscosity of blood
19
• Mean Arterial BP (MAP) (Afterload):

• Force against which heart is contracting (aortic pressure).

• ↑ MAP → heart pumps ↓ blood than it receives → blood accumulates

in ventricles & size of heart ↑

• ↑ vascular resistance → ↑ myocardial workload & ↑ myocardial

oxygen usage

20
Homometric regulation

21
Factors affecting venous return

22
Control of stroke volume(intrinsic)

23
 Extrinsic regulation
• Regulation of HR - Mild, moderate change in HR does not affect COP but affect SV
inversely. 

• ↑ HR→ ↓ diastolic period → ↓ filling of ventricle → ↓ SV

• ↑ HR → ↓ COP due to short diastolic period leading to: 

• ↓ ventricular  filling → ↓ EDV → ↓ SV & COP 

• ↓ Time for coronary flow → ↓  FOC → ↓ SV & COP

• Marked ↓ HR (< 60 beat/min)

• ↑ time of diastole , ↑ filling of ventricle, ↑ SV

• But still, ↑ SV cannot compensate for marked ↓ in HR

24
 Extrinsic regulation
• Athletes have slow HR at rest however COP is kept constant by ↑ in SV

• Venoconstriction → ↑ VR & heart filling

• SNS stimulation → ↑ COP due to:- ↑ HR and ↑ contractility

• PNS → ↓ COP: ↓ HR

• Catecholamines, Thyroxine, Glucagon, Xanthines have impact

• Digoxin → ↑ calcium influx → ↑ contractility

25
 Cardiac output in some conditions
• CO is ↑ in:

1-Excitement: ↑ CO by 50 -100% due to sympathetic stimulation.

2-Extremes of temperature,

3-Eating: ↑GIT blood flow.

4-Exercise: can ↑ CO up to 700% in trained athletes.

5-Pregnancy

26
 Cardiac output in some conditions
• Constriction of veins → ↑ VR → ↑ COP 

• Beriberi: ↓ vitaminB1(thiamine)→ peripheral vasodilatation

• Hyperthyroidism:↑ metabolism → vasodilatation

• Anemia: ↓ viscosity & ↓ oxygen delivery → ↑ COP 

27
 Cardiac output in some conditions
• COP is ↓ in - Sitting or standing from lying down

• Pathological ↓ COP: Myocardial infarction: ↓ pumping ability,

Hemorrhage: ↓ blood volume, Fainting

• Marked arrhythmia: Tachycardia (Shortening of diastolic filling) &

Bradycardia: ↓ HR → ↓ COP

28
 References:

• Guyton and Hall Textbook of Medical Physiology: 14th edition

• Ganong’s review of medical physiology:25 th edition

Thank You
29