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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 mlPRELOAD - 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

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 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

CARDIAC CYCLE EVENTS

I. LATE DIASTOLEA. 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 Skeletal75.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 FactorSleepModerate changes in environmental temperatureAnxiety and excitement 50 - 100%Eating 30%Exercise up to 700%High environmental temperaturePregnancyEpinephrineHistamineSitting or standing from lying position 20 - 30%Rapid arrhythmiaHeart Disease

No Change

Increase

Decrease

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

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

- are positively inotropic.

HEART SOUNDS

AND

MURMURS

RHYTHMIC EXCITATION

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