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 THE
CARDIOVASCULAR
SYSTEM

THE HEART AS A PUMP

END- DIASTOLIC VOLUME - volume of blood filling the ventricle
During rapid filling = 110ml to 120ml - 130 ml

STROKE VOLUME - volume of blood ejected as he ventricles

contract
During systole = 70ml to 90 ml
END -SYSTOLIC VOLUME - remaining volume in each ventricle
= 40 - 50 ml
PRELOAD - degree of tension on the muscle when it
begins to contract
End Diastolic Volume = 110 to 120 - 130ml
EJECTION FRACTION - fraction of the end -diastolic
volume that is ejected = 60% to 65% volume
 AFTERLOAD - load against which the muscle exerts its contractile
force - pressure in the artery leading from the
ventricle
CARDIAC OUTPUT - the quantity of blood pumped
into the aorta each minute by the heart
VENOUS RETURN- quantity of blood flowing from the
veins into the right atrium each minute
ABSOLUTE REFRACTORY PERIOD
Ventricle - 0.25 to 0.3 second
Atrium - 0.15 second
RELATIVE REFRACTORY PERIOD - 0.05 second
Causes of Plateau in Cardiac Action Potential
1. Opening of slow calcium - sodium channels
2. Decreased potassium permeability
 CARDIAC CYCLE
EVENTS
I. LATE DIASTOLE
A. Rapid Filling - 70 to 80% from atria to ventricle
B. Slow Filling - Diastasis
C. Atrial Systole - 30 to 20% from atria to ventricle
II. SYSTOLE (Ventricular)
A. Isometric Ventricular Contraction
Right ventricle pressure above 10 mmHg
Left ventricular pressure above 80 mmHg
B. Rapid Ejection - 70% of blood from ventricle to aorta
and pulmonary artery

C. Slow Ejection - 30% of blood from ventricle to aorta and

pulmonary artery
III. EARLY DIASTOLE
A. Protodiastole
B. Isometric Ventricular Relaxation

ATRIAL PRESSURE WAVES

a wave - caused by atrial contraction
Right atrial pressure increases 4 to 6 mmHg
Left atrial pressure increases 7 to 8 mmHg
c wave - back bulging of A - V valves when ventricles contract
v wave - slow flow of blood into the atria from the veins while A-V
valves are closed during ventricular contraction

Efficiency of the Heart or Efficiency of cardiac

Contraction - ratio of work output to total chemical
energy expenditure
Normal Heart - 20 to 25 %
 VARIATION IN LENGTH OF ACTION
POTENTIAL AND ASSOCIATED PHENOMENA
WITH CARDIAC RATE
Heart Rate Heart rate Skeletal
75.min 200/min Muscle

Duration its cardiac cycle 0.80 0.30 …

Duration of systole 0.27 0.16 …

Duration of action potential 0.25 0.15 0.005

Duration of absolute refractory period 0.20 0.13 0.004

Duration of relative refractory period 0.05 0.02 0.003

Duration of diastole 0.53 0.14 …

EFFECT OF VARIOUS CONDITIONS ON CARDIAC OUTPUT.
APPROXIMATE PERCENTAGE CHANGES ARE SHOWN IN
PARENTHESIS

Condition or Factor
Sleep
No ChangeModerate changes in environmental temperature
Anxiety and excitement 50 - 100%
Eating 30%
Exercise up to 700%
High environmental temperature
Pregnancy
Epinephrine
Increase Histamine
Sitting or standing from lying position 20 - 30%
Rapid arrhythmia
Decrease Heart Disease
 REGULATION OF CARDIAC PUMPING
A. BASIC MEANS of regulating volume pumped by the heart.

1. Intrinsic Cardiac Regulation of pumping in response to

changes of volume of blood flowing to the hear.

FRANK - STARLING MECHANISM

- the greater the heart is stretched during filling, the
greater the force of contraction and the greater the
quantity of blood pumped into the aorta
HETEROMETRIC REGULATION
- regulation of cardiac output as a result of changes
in cardiac muscle fiber length.

2. Control of the Heart by the Sympathetic and Parasympathetic

nerves
 Changes in Cardiac output caused by nerve stimulation
result from changes in heart rate and from changes in
contractile strength of the heart

Chronotropic Action - cardiac accelerator action of catecholamines

Inotropic Action - effect on strength of cardiac contraction

Homometric Regulation - regulation due to changes in contractility

independent of length.
B. Other Factors:
1. Effect of Potassium and Calcium Ions

Excess potassium in the ECF causes the heart to become dilated

and flacid and slows the heart rate

Excess calcium ions causes the heart to go into Spastic

contraction

2. Effect of temperature on Heart Function

Increased temperature caused greatly increased heart rate

Catecholamines exert their inotropic effect by activation of
adenylyl cyclase and increase
intracellular cAMP

Xanthines such as caffeine and theophylline - inhibit the breakdown

of cAMP
- are positively inotropic.
Glucagon - increases the formation of cAMP
- is positively inotropic

Digitalis - inhibitory effect on Na+ - K + ATPase in the myocardium

- is positively inotropic

Hypercapnia,hypoxia, acidosis, barbiturates - decrease myocardial

contractility
HEART SOUNDS
AND
MURMURS
 RHYTHMIC
EXCITATION
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