CVS - Cardiac Output

Dr. M. N. Afzal

Arterial Venous

Nerve supply of heart

Cardiac Output Amount of blood pumped by each ventricle per minute

Determinants of CO
Two determinants of CO are:

Heart rate Stroke volume

CO = heart rate
= 4900

x stroke volume
(70 ml / beat)

(70 beats / min) x

ml / min

Cardiac Output
Cardiac Index
CO per square meter area of the body

Cardiac Reserve
Difference between CO at rest and maximum volume of blood

the heart is capable of pumping per minute

Control of CO
CO =
1.

Heart rate:
-Parasympathetic NS -Sympathetic NS -Epinephrine

2.

Stroke volume:
-Intrinsic control -Extrinsic control -Sympathetic NS -NE & Epinephrine

1. Autonomic Innervation 2. Hormones

(Epinephrine) 3. Atrial reflex

Contractility
(Frank-Starling law)
1. Intrinsic control Preload (EDV) Afterload (R) 2. Extrinsic control Sympathetic NS Epinephrine

Stroke Volume

Amount of blood ejected by each ventricle per beat

Stroke Volume
Two control systems influence SV

Intrinsic control Extrinsic control

Both systems increase SV by increasing strength of contraction of heart

Intrinsic control
Influenced by:
End-diastolic volume (preload)
Total peripheral resistance (afterload)

Intrinsic control
Frank-Starling Law Intrinsic relationship between EDV & SV (Heart pumps all the blood returned to it) A built-in / intrinsic property of heart muscle Increased EDV results in increased SV Length-tension relationship

Intrinsic control of SV
(FrankStarling Curve)

(FrankStarling Curve)
Advantages Equalization of output between right and left side of the heart When larger output is needed, increase in venous return automatically increases stroke volume correspondingly

Extrinsic control of CO
Sympathetic NS Epinephrine

Strengthens cardiac contractility (Shifts Frank-Starling curve to left) Enhances venous return

Effect of SNS & catecholamines on contractility

Positive inotropic effect:
Increased peak tension Increased rate of tension Faster rate of relaxation

Mediated via activation of Beta-1 receptors

Phosphorylation of Ca2+ channels Phosphorylation of phospholamban

Effect of Sympathetic stimulation on Frank-Starling curve

ANS control of SV

Control of CO summary

High Cardiac Output

Hyperthyroidism Anemia Arteriovenous Fistula Beriberi

Low Cardiac Output

Caused by Cardiac factors:
Myocardial infarction, myocarditis, tamponade Valvular heart disease Arrhythmias

Caused by peripheral factors: decreased VR

Hemorrhage (decreased blood volume) Acute venous dilatation (fainting) Obstruction of large veins

Afterload
Workload imposed on heart Heart compensates by enlarging (hypertrophy) Sustained extra workload eventually leads to

Heart Failure

Heart Failure
Inability to keep pace with demands of body Most common causes:
Myocardial infarction Hypertension (sustained elevated BP) Stenotic semilunar valves

Heart operates on lower length-tension curve (Frank-Starling curve is shifted downward)

Frank-Starling curve in heart failure

Normal heart

Normal stroke volume Decrease in stroke volume Stroke volume with uncompensated heart failure

Failing heart

Normal end-diastolic volume

Acute compensation

Heart Failure consequences

Forward failure:
Stroke volume becomes smaller progressively Adequate amount of blood cannot be delivered to tissues

Backward failure:
Blood cannot be pumped out Blood start accumulating in the venous system

Sudden death due to arrhythmias

Ventricular Pressure-Volume loops

Question
A volume-pressure diagram of the left ventricle during one cardiac cycle of a normal heart is shown above. Which point on the diagram marks the beginning of ventricular diastole? A. A B. B C. C D. D E. E

Question
A volume-pressure diagram of the left ventricle during one cardiac cycle of a normal heart is shown above. Which points on the diagram marks the systolic phase? A. ABC B. BCD C. CDA D. DAB