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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
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 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
Moderate changes in environmental temperature
Anxiety and excitement 50 - 100%
Eating 30%
Exercise up to 700%
High environmental temperature
Pregnancy
Epinephrine
Histamine
Sitting or standing from lying position 20 - 30%
Rapid arrhythmia
Heart 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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Cardiac

  • 1. www.Examville.com Online practice tests, live classes, tutoring, study guides Q&A, premium content and more.
  • 3.
  • 4.
  • 5.
  • 6.
  • 7.
  • 8. 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
  • 9. 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
  • 10. 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
  • 11. 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 %
  • 12. 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 …
  • 13. EFFECT OF VARIOUS CONDITIONS ON CARDIAC OUTPUT. APPROXIMATE PERCENTAGE CHANGES ARE SHOWN IN PARENTHESIS Condition or Factor Sleep Moderate changes in environmental temperature Anxiety and excitement 50 - 100% Eating 30% Exercise up to 700% High environmental temperature Pregnancy Epinephrine Histamine Sitting or standing from lying position 20 - 30% Rapid arrhythmia Heart Disease No Change Increase Decrease
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  • 15. 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
  • 16. 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.
  • 17. 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
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  • 21. 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.
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