CARDIAC OUTPUT

Cardiac output is defined as: The volume of the blood pumped out by each ventricle per minute.
Cardiac output = CO = = = Stroke volume x Heart rate SV x HR 70 x 70 4900ml/min (5000ml/min)

STROKE VOLUME (SV)

Volume of blood pumped out by each ventricle per beat. 70ml / beat (70 to 80ml / beat) SV = EDV ESV

END-DIASTOLIC VOLUME (EDV)

Volume of blood present in the ventricular cavity at the end of ventricular diastole. EDV = 120 to 130ml

END-SYSTOLIC VOLUME (ESV)

Volume of blood present in the ventricular cavity at the end of ventricular systole. ESV = SV = 40 to 50ml EDV ESV

More EDV, more SV More ESV, less SV

EJECTION FRACTION
Percentage (fraction) of EDV ejected out by each ventricle per beat. It is 60 to 65% of EDV Ejection Fraction is a valuable index of ventricular function

FRACTIONAL SHORTENING
Percentage number of cardiac muscle fibers shortened per beat. It is 35-45%.

Fractional Shortening decreases in: Hypertension Congestive Cardiac Failure

CARDIAC INDEX
It is the cardiac output with respect to bodysurface area, i.e; cardiac output per square meter of body surface area.
70 kg adult male = 1.7 sq m of body surface area. CI CO = -----------------------Body Surface area 5 = -----------1.7

= 3 lit /min/ m2 80 years man :- CI = 2.4 lit/min/m2 10 years child :- CI = 4 lit/min/m2

CARDIAC RESERVE
Maximum percentage to which cardiac output can increase above normal. It is 300-400 % in young healthy adults. In athletes, it may reach upto 500 600 %.

CARDIAC OUTPUT MEASUREMENT

DIRECT METHOD
Animal anesthetized Direct cannulation of great vessels Electromagnetic / Doppler flowmeter

INDIRECT METHODS
Oxygen Fick Method Dye Dilution Method Thermal Dilution Method Dopplers Method Ballistocardiography Echocardiography Radionucleotide angiography

OXYGEN FICK METHOD: Ficks Principle

The amount of a substance taken up by an organ or the whole body in a unit time is equal to arteriovenous difference times the blood flow.

Q CA CV FA FV

= Amount of substance = Concentration of substance in arterial blood = Concentration of substance in venous

blood = Arterial flow = Venous flow

Q = CA x FA CV x FV [But FA = FV per unit time, so, FA= FV = F] Hence Q = CA x F CV x F Q = F (CA CV) Q ---------CA CV 250 ---------- = 195-145 250 -----------50

F = =

5 L/min (cardiac output)

PROCEDURE
100% O2 is breathed in from a spirometer for 5-10 minutes. O2 concentration from arterial blood can be measured from any peripheral artery. O2 concentration from mixed venous blood is measured by passing a catheter via subclavian or medial cubital vein to right atrium & then venous blood is obtained either from right ventricle or pulmonary trunk.

LIMITATIONS
Requires a trained person Slow method Chances of ventricular fibrillation Cant be used during exercise

DYE DILUTION (HAMILTONS DILUTION) METHOD (Indicator Dilution Method)

Evans blue (T-1824) Albumin labeled with I131 Cardiogreen Brilliant violet red

Dye must be :
Easily available, non-toxic, easy to measure, should not bring any change in the circulation. Known quantity (I=5mg) of dye injected into arm vein, SVC or right atrium Concentration of the dye (C) in the arterial blood is monitored continuously by drawing blood from any peripheral artery (mg/L).

 Time between 1st appearance and then disappearance (t) is noted (seconds). Flow Volume = = Volume per unit time (F=V/t) Mass of indicator (I) -----------------------Concentration (C) I/C ------t I x 60 ------Cxt

Flow

 A plot of dye concentration (C) on y-axis against time (t) along x-axis is made. It should be plotted on a semi-logarithmic paper. A straight line is obtained which can easily be extrapolated to baseline. Average concentration of dye (C) is obtained from area under the curve.

I = 5mg C = 2.5mg/L t = 25 sec Flow (L/min) is cardiac output = I x 60 ----------C x t 5 x 60 -----------2.5 x 25 4.8 L/min

= =

ADVANTAGES:
Quick method Can be used during exercise Non-invasive (in comparison with Oxygen Fick Method)

THERMAL DILUTION METHOD

Change in temperature is an indicator Cold saline into right atrium Swan-Ganz catheter (Double lumen catheter) Thermistor- To record change in temperature

Advantages: Problem of re-circulation solved Unlike dye, saline is harmless

DETERMINANTS OF CARDIAC OUTPUT

Stroke Volume Heart Rate

Stroke Volume
Reflects the state of myocardial performance

Heart Rate
Reflects the activity of cardiac pacemaker

FACTORS REGULATING HEART RATE

Physiological Variations
Sleep
Vagal tone increases during sleep

Age
HR decreases with age

Physical activity
Athletes have more vagal tone than non-athletes

Posture
Lying to standing BP falls Baroreceptor stimulation leads to TACHYCARDIA

Other Factors
Impulses from higher centres
Emotional excitement leads to TACHYCARDIA Emotional shock/grief/fear lead to BRADYCARDIA (Vasovagal syncope) Parasympathetic stimulation leads to BRADYCARDIA Sympathetic stimulation leads to TACHYCARDIA

Role of Autonomic Nervous System

Baroreceptor Reflex
Rise in blood pressure leads to stimulation of baroreceptors and hence BRADYCARDIA

Bainbridge Reflex
Rise in venous return leads to TACHYCARDIA

Cardiac Stretch Receptors

Atrial stretch receptor stimulation leads to TACHYCARDIA Ventricular stretch receptor stimulation leads to BRADYCARDIA

Respiration
Inspiration TACHYCARDIA Expiration BRADYCARDIA Sinus arrhythmia

Blood gases & pH

Hypoxia, Hypercapnia & Acidosis increase the HEART RATE

Hormones
Epinephrine & Thyroxine will cause TACHYCARDIA Norepinephrine Reflex BRADYCARDIA

Rise in Body Temperature

Enhanced ionic flow due to rise in body temperature 1F rise in body temperature increases the heart rate by 10 beats/min

Drugs
Atropine, Caffeine & Nicotine increase heart rate. Digitalis & Beta-blockers decrease the heart rate

Intracranial Pressure Rise in intracranial pressure leads to BRADYCARDIA Bacterial toxins Diphtheria toxin produces TACHYCARDIA Pressure on Eyeballs (Oculocardiac reflex) There is vagal-mediated BRADYCARDIA

FACTORS REGULATING STROKE VOLUME

Intrinsic Myocardial Activity Extrinsic Neural Activity (Autonomic Nerves) Preload Afterload Hormonal Factors Chemical Factors Drugs Plasma Ions BMR

Intrinsic Myocardial Activity Frank-Starlings Law Myocardial hypertrophy Physiological hypertrophy (Exercise). Hence rise in SV Pathological hypertrophy (Systemic hypertension, Aortic valve disease, Cardiomyopathies) Hence fall in SV Frank-Starling Curve (Cardiac Function Curve)

SV

Frank-Starling Curve (Cardiac Function Curve)

EDV

Extrinsic Neural Activity

Sympathetic Stimulation Positive inotropic effect (SV increases) Positive Chronotropic effect Upto 180 beats / min (SV increases) Beyond 180 beats /min (SV decreases) Exercise-induced TACHYCARDIA Bainbridge reflex Shift of Frank-Starlings curve

Parasympathetic Stimulation Primarily negative chronotropic effect Negative inotropic effect Baroreceptor reflex-mediated effect

Preload
It is the force that stretches the relaxed cardiac muscle fibres. It is actually the incoming blood which stretches the myocardial wall during diastole (EDV) Adequate diastolic filling time sufficient EDV Greater the EDV-Greater the SV Atrial systole 25% ventricular filling

 More venous return more EDV More MSFP & MCFP more venous return More blood volume rise in MSFP & MCFP Rise in right atrial pressure VR, EDV, SV

End-diastolic volume 120 ml

End-diastolic volume 120 ml

End-diastolic volume 175 ml

Stroke volume 70 ml

Stroke volume 90 ml

Stroke volume 145 ml

End-systolic volume 50 ml

End-systolic volume 30 ml

End-systolic volume 30 ml

(a)

(b)

(c)

Mean Systemic Filling Pressure

It is the pressure which forces the systemic blood towards heart & is measured everywhere in the systemic circulation when all the blood flow is stopped.

Its value is 7 mm of Hg

Mean Circulatory Filling Pressure

When heart pumping is stopped due to ventricular fibrillation or any other reason, the flow of blood everywhere in the circulation ceases. By this time, pressure everywhere in the circulation is equilibrated & is known as mean circulatory filling pressure .

Its value is 7 mm of Hg

 Both these pressures (MSFP & MCFP) increase if there is more blood volume. Sympathetic stimulation causes increase in these pressures If these pressures increase, VR is increased

 Greater the difference between any of these pressures & the right atrial pressure, a pressure gradient for VR will be established & hence VR will increase. MSFP VR SV Right atrial pressure VR SV

Afterload
It is the resistance against which blood is to be pumped by the myocardium.

For proper ventricular ejection, pressure generated in the ventricle must be greater than the pressure in systemic arteries. More the TPR, more systemic arterial pressure & more will be afterload.

Law of Laplace Distending pressure in a distensible hollow viscera (viscus) is equal to tension developed in its wall at equilibrium 2Th P= --------- (Myocardium) r 2T P= --------- (Small thin-walled vessels) r

 When radius increases (as in dilated heart), greater tension is developed in the myocardial wall to overcome the distending pressure. More energy is required for a dilated heart to perform work than a normal heart A dilated heart is unable to effectively eject the stroke volume than a normal heart. Hence cardiac failure is likely to occur.

 Rise in afterload is responsible for impedence to ventricular ejection Afterload increases in systemic hypertension (due to rise in TPR), aortic stenosis & aortic regurgitation Rise in afterload fall in SV

Hormonal Factors
Catecholamines (Dopamine, Epinephrine & Norepinephrine) & Glucagon increase the intracellular cAMP

Chemical Factors
Hypoxia, Hypercapnia & Acidosis exert negative inotropic effect by depressing the myocardial functioning

Drugs
Positive inotropic effect Digitalis & ouabain (Block Na+ K+ ATPase) Caffeine & theophylline (decrease breakdown of cAMP) Negative inotropic effect Quinidine & Procainamide

Plasma ions
Hypercalcemia Calcium rigor & Systolic cardiac arrest Hyperkalemia Diastolic cardiac arrest

Basal Metabolic Rate (BMR)

Rise in BMR increased demand for oxygen & nutrients, so rise in SV Rise in BMR Rise in body temperature stimulation of SA node.

Cardiac output

INSPIRATORY PHASE OF THE RESPIRATORY CYCLE

Heart rate increases due to increased vasomotor discharge. Venous return to the right heart increases. Cardiac output of right heart increases. Venous return to the left heart decreases.

 Cardiac output of left heart decreases. Systemic arterial blood pressure decreases. Right atrium starts contracting before the left atrium. Left ventricle starts contracting before the right ventricle.

 Right ventricular ejection starts before the left ventricular ejection. Right ventricular ejection ends after the left ventricular ejection. Cardiac output of left ventricle is more than the cardiac output of right ventricle. During inspiration, cardiac output of left ventricle is less than the cardiac output of right ventricle.