CARDIAC OUTPUT

CARDIAC OUTPUT (CO)

• Quantity of blood pumped by left ventricle into aorta per minute.

• Cardiac output – Product of stroke volume & heart rate.

– Ie., Amount pumped in unit time (per minute) depends on both stroke volume & heart rate.

• Average CO in adults – 5 liters/min.

• Cardiac output of right ventricle is equal to left ventricle.

– Due to equal ventircular stroke volume.

CARDIAC INDEX:

• Cardiac output per minute per square meter of body surface area.

– Ie.,Cardiac index – Cardiac output / Body surface area.

• Cardiac output varies with body size.

– Hence, measured per unit body surface area (relatively constant).

• Average cardiac index is about 3.2 /min/m³.

STROKE VOLUME:

• Amount of blood pumped out by left ventricle in each stroke/every heart rate.

• Given by difference between end-diastolic ventricular volume & end-systolic ventricular volume.

• End-diastolic ventricular volume – 

– Blood volume in left ventricle at end of diastole.

– Normally 120 ml.

• End-systolic ventricular volume –

– Blood volume at end of systole.

– Normally 50 ml.

• Also calculated by, 

– Stroke volume – Cardiac output / Heart rate.

EJECTION FRACTION:

• Percentage of end-diastolic ventricular volume, ejected by each stroke.

– Ejection fraction – Stroke volume / End-diastolic ventricular volume.

• Normally around 60%.

– Ie., Out of 120 ml blood of left ventricle.

– 70 ml is ejected by each stroke.

• Valuable index for ventricular pump function.

• Decreases with heart failure.

MEASUREMENT OF CARDIAC OUTPUT:

• Done using indirect methods in humans.

1. Fick principle method:

• Amount of substance taken up by an organ/whole body per unit of time is equal to arterial level of substance minus venous level (A-V difference).

Eg., For lung – 

• Substance is oxygen.

• Ie., Oxygen consumption per minute & blood flow is equal to cardiac output.

• Hence, amount of oxygen taken up by lung = Cardiac output x Arteriovenous oxygen difference.

Formula:

• Cardiac output – Oxygen consumption/uptake per minute/Arteriovenous oxygen difference.

2. Dye (Indicator) Dilution method:

• Based on “Stewart-hamilton” principle.

• Cardiac output – Amount of dye injected /(Average concentration of dye * circulation time).

3. Thermodilution method:

• Modification of dye dilution technique.

• Cold saline is used instead of dye.

• Dilution of its temperature by blood is used.

• Same principle followed. (Stewart – Hamilton principle).

4. Combining doppler techniques with echocardiography.

5. Cineradiography technique.

6. Most recent advance noninvasive method –

• Electrical impedance cardiograph technology.

FACTORS AFFECTING CARDIAC OUTPUT:

• CO – Product of stroke volume & heart rate.

• Hence factors affecting stroke volume or heart rate or both, in turn, affects CO.

1. FACTORS AFFECTING STROKE VOLUME:

• Preload, ventricular contractility, & Afterload. 

1A. PRELOAD:

• Degree of ventricular filling during diastole.

Cardiac preload – 

• Represented by venous blood volume distending ventricle.

• I.e., Venous return determines preload.

• Increased preload

– (I.e., Increased venous return)

– Results in higher end-diastolic volume.

– Causes myocardial fiber stretching —-> Increasing myofibril length —> Increasing cardiac contraction strength.

– Accordance with “Frank-Sterling Law/ Starling’s law of Heart”.

• Opposite for decreased preload.

• I.e., Factors increasing end-diastolic ventricular muscle fiber length.

– In turn, increasing venous return/preload.

1. Increased total blood volume.

2. increased venous tone.

3. Increased skeletal muscle pumping action.

4. Increased negative intrathoracic pressure.

• (e.g. inspiration)

5. Lying down from sitting or standing position

6. Sympathetic discharge → Causing decreased venous compliance → resulting in decreased venous capacitance.

II. Conditions associated with ↓^ed Stroke volume:

• I.e., Factors decreasing end-diastolic ventricular muscle fiber length

– In turn, decreasing venous return/preload.

1. Decreased total blood volume.

2. Decreased venous tone

3. Decreased skeletal muscle pumping action.

4. Less negative or positive intrathoracic pressure

• (Eg: In expiration)

5. Sitting or standing (Venous blood pooling)

1B. VENTRICULAR CONTRACTILITY:

• Increased ventricular contractile strength → Increased stroke volume 

– By increasing sympathetic discharge

– Ie., Circulating catecholamines (epinephrine).

• Eg: During exercise.

1C. AFTERLOAD:

• Blood pumped out of left ventricle against aortic resistance.

– Ie., Resistance offered to ventricular pumping action.

• Afterload is defined by mean arterial pressure.

– Further depends on total peripheral resistance.

• Increased aortic resistance → Decreases stroke volume.

– E.g., high BP

• Decreased peripheral resistance → Increases cardiac output.

– Eg. as in, 

– Exercise

– AV fistula or shunt.

– Severe anemia (due to vasodilatation by anemic hypoxia).

– Thyrotoxicosis (due to vasodilation caused by increased O₂ consumption).

– Wet Beri-Beri.

II. FACTORS AFFECTING HEART RATE:

• Heart rate is predominantly under neuro-humoral influence.

• Sympathetic stimulation increases heart rate & hence, cardiac output.

– Mainly by, Increasing stroke volume by increasing contractility.

– Also by increasing heart rate but without increasing end-diastolic volume.

EFFECTS OF VARIOUS CONDITIONS ON CARDIAC OUTPUT:

1. UNAFFECTED CO:

• Sleep.

• Moderate changes in environmental temperature.

2. INCREASED CO:

• Anxiety & excitement (50-100%).

• Eating (30%).

• Exercise (up to 700%)

• High environmental temperature.

• Pregnancy (40%).

• Epinephrine.

3. DECREASED CO:

• Sitting or standing from lying position (20% -30%).

• Rapid arrhythmias.

• Heart disease.

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