APPLIED PHYSIOLOGY OF

CARDIO VASCULAR SYSTEM

CONTENTS

1. INTRODUCTION

2. DEVELOPMENTAL ASPECTS OF THE HEART

3. THE CARDIO VASCULAR SYSTEM ANATOMY

4. CIRCULATION THROUGH HEART

5. HEART SOUNDS

6. CARDIAC CYCLE

7. MICROSCOPIC ANATOMY OF HEART MUSCLE

8. ECG

9. CARDIAC ACTION POTENTIALS

10. STROKE VOLUME

11. CARDIAC OUTPUT

12. BLOOD PRESSURE

13. APPLIED ASPECTS

14. CARDIAC TOOTH PAIN

15. ARTIFICIAL HEARTS

16. SUMMARY

17. REFERENCES
 Did you know???
•Your heart is about the size of your clenched fist.

•It beats about 4000 times an hour and about 100,000 times a day.

•It will beat over 2 billion times in a lifetime.

•Each heartbeat pumps half a cup of blood.

•The force of your heartbeat is sufficient to shoot blood 30 feet into the air.

I. INTRODUCTION
 According to “ Indian Heart Association “ 2015 there are 30 million heart
patients in India – 14 million reside in urban areas and 16 million in rural
areas.
 Cardiac hospitals in India perform over 2,00,000 open heart surgeries/year.
And a steady annual rise to the tune of 20-30 % / year.
 If the current trend continues by 2020 the burden of atherothrombotic CVD In
India will surpass that of any other country in the World.

Ref : http://indianheartjournal.com/Jan-Feb2015/Jan-Feb2015.htm

II. DEVELOPMENTAL ASPECTS OF THE HEART

Development of heart:

 Human heart starts to develop during the 3rd week of embryonic life. Till then
the needs of the embryo are met through simple diffusion of blood between
the germ layers.
 Cardiogenesis in humans is associated with complex morphogenetic events
 In human embryos the heart begins to beat at about 22-23 days, with blood
flow beginning in the 4th week. The heart is therefore one of the earliest
differentiating and functioning organs.
III. THE CARDIO VASCULAR SYSTEM ANATOMY

 Heart size varies with body size. The average adult’s heart is about 5.5 inches
(14 centimeters) long and 3.5 inches (9 centimeters) wide, or approximately
the size of one’s fist.
 The heart is located just above the diaphragm, between the right and left lungs.
One-third of the heart is located on the right size of the chest, while two third
is located on the left side of the chest.

Coverings of the Heart: Anatomy

 Pericardium – a double-walled sac around the heart composed of:

1.A superficial fibrous pericardium

2.A deep two-layer serous pericardium

The Function of the Pericardium:

 Protects and anchors the heart

 Prevents overfilling of the heart with blood
 Allows for the heart to work in a relatively friction-free environment

 Heart Wall
 Epicardium – visceral layer of the serous pericardium.
 Myocardium – cardiac muscle layer forming the bulk of the heart.
 Endocardium – endothelial layer of the inner myocardial surface,

Four chambers:

 2 atria: anterior part of heart – receive blood from veins

 2 ventricles: inferior part of heart – pump blood through arteries
  Heart Chambers
 Septum: divides left from right heart
 Valves: keep blood flowing in one direction

Four valves:

 2 AV valves,
 2 semilunar valves

Atrioventricular Valves

 AV valves: between atria and ventricles

 Bicuspid (mitral) valve: on the left
 Tricuspid valve: on the right
 When valves are open blood drains from atria into ventricle
 When ventricle contract, valve flaps are forced shut, blocking blood from
reentering atria.
IV. CIRCULATION THROUGH HEART

PULMONARY

 Right side of the heart

1.Blood from the body, low O2 high CO2, right atriumright ventriclelungs
via pulmonary trunk.

2.Unloading of CO2 pick up O2 to left side of the heart.

SYSTEMIC

 Left side of heart

1.Oxygen rich blood - lungs- left atrium- left vent. – aorta

2.Blood transported via systemic arteries to body tissues, gas and nutrient exchange
across capillary walls

3.Blood is then returned to the right side of the heart through superior and inferior
venae cavae.
V. THE CAUSES OF THE 1ST HEART SOUND:

 During systole the AV valves are closed & blood tries to flow back to the
atrium back bulging the AV valves. But the taut chordaetendinae stop the back
bulging and causes the blood to flow forward.
 This will cause vibration of the valves, blood & the walls of the ventricles
which is presented as the 1st heart sound.

THE CAUSES OF THE 2ND HEART SOUND:

 During diastole, blood in the blood vessels tries to flow back to the ventricles
cause the semilunar valves to bulge. But the elastic recoil of the arteries cause
the blood to bounce forward which will vibrate the blood the valves and the
ventricle walls.
 Physiological splitting of the second heart sound occurs because left
ventricular contraction slightly precedes that of the right ventricle so that the
aortic valve closes before the pulmonary valve.

DIFFERENCE BETWEEN THE 1ST AND2ND HEART SOUNDS

 The 1st sound lasts longer because the AV valves are less taut than the
semilunar valves which will enable them to vibrate for longer time.
 The 2nd heart sound has higher frequency as the semilunar valves are more
taut.
 It is louder and higher-pitched than the first sound, and the aortic component
is normally louder than the pulmonary one.

THIRD HEART SOUND

 A third heart sound (S3) is a low-pitched early diastolic sound best heard with
the bell at the apex.
 It coincides with rapid ventricular filling immediately after opening of the
atrioventricular valves and is therefore heard after the second as 'lub-dub-
dum'.
  A third heart sound is a normal finding in children, in young adults and during
pregnancy.
 A third heart sound is usually pathological after the age of 40 years.

CAUSES OF A THIRD HEART SOUND

Physiological

o Healthy young adults

o Athletes
o Pregnancy
o Fever

Pathological

Large, poorly contracting left ventricle

Mitral regurgitation

FOURTH HEART SOUND

 A fourth heart sound (S4) is less common. It is soft and low-pitched, best
heard with the bell of the stethoscope at the apex. It occurs just before the first
sound (da-lub-dub). 0.11'' prior to S1
 It is always pathological and is caused by forceful atrial contraction against a
non-compliant or stiff ventricle.
VI. CARDIAC CYCLE

Cardiac Cycle Coordinating the activity

 Cardiac cycle is the sequence of events as blood enters the atria, leaves the
ventricles and then starts over
 Synchronizing this is the Intrinsic Electrical Conduction System
 Influencing the rate is done by the sympathetic and parasympathetic divisions
of the ANS
Cardiac Cycle Coordinating the activity - Electrical Conduction Pathway

 Initiated by the Sino-Atrial node (SA node) which is myogenic at 70-80

action potentials/minute
 Depolarization is spread through the atria via gap junctions and internodal
pathways to the Atrio-Ventricular node (AV node)
 The fibrous connective tissue matrix of the heart prevents further spread of
APs to the ventricles
 Action potentials travel down the Atrioventricular bundle (Bundle of His)
which splits into left and right atrioventricular bundles (bundle branches) and
then into the conduction myofibers (Purkinje cells)

Cardiac Cycle Coordinating the activity

AV node

· Bottom wall of the RA – inter atrial septum

· Firing frequency: 40-60bpm

1) Delays heart impulse: 0.1 sec complete ventricular filling

2) Delays frequency of impulse propagation

Purkinje fibers

 branches of the left and right bundle branch

 impulse propagation to contractile cells in ventricle
 Purkinje cells are larger in diameter & conduct impulse very rapidly
 Causes the cells at the apex to contract nearly simultaneously
 Good for ventricular ejection
 Cardiac Cycle Coordinating the activity

 The electrical system gives rise to electrical changes

(depolarization/repolarization) that is transmitted through isotonic body fluids
and is recordable
 The ECG!
 A recording of electrical activity
 Can be mapped to the cardiac cycle
VII. ECG

HISTORY

 1842- Italian scientist Carlo Matteucci realizes that electricity is associated

with the heart beat
 1876- Irish scientist Marey analyzes the electric pattern of frog’s heart
 1895 - William Einthoven , credited for the invention of EKG
 1906 - using the string electrometer EKG, William Einthoven diagnoses some
heart problems
 1924 - the noble prize for physiology / medicine is given to William
Einthoven for his work on EKG
 1938 -AHA and Cardiac society of great Britan defined and position of chest
leads
 2005- successful reduction in time of onset of chest pain and PTCA by
wireless transmission of ECG on PDA.

RECORDING ECG

Clinical application of the ECG

Determination of:

• HR, heart rhythm

• Presence of hypertrophy or atrophy

• Abnormal conduction patterns

• The cardiac axis (electrical axis)

Normal heart rhythm

Sinus rhythm – bradycardia or tachycardia

Useful in diagnosis of :

 Cardiac Arrhythmias
 Myocardial ischemia and infarction
 Pericarditis
 Chamber hypertrophy
 Electrolyte disturbances
 Drug effects and toxicity

ATRIAL SYSTOLE

 Lasts for 0.1 sec

 Atrial depolarization causes atrial systole
 It contributes a final 25ml of blood to each ventricle.
 End of atrial systole is also end of ventricular diastole
 End diastolic value is 130 ml

VENTRICULAR SYSTOLE

 Lasts for 0.3 sec

 It is caused by ventricular depolarization
 Isovolumetric contraction lasts for 0.05 seconds when both the semilunar and
atrioventricular valves are closed.
 The SL valves open when
 -The left ventricular pressures surpasses aortic pressure(80 mm of mercury)
 -The right ventricular pressure rises above pulmonary pressure (20 mm/hg)
 SL valves open for 0.25 sec.
 The left ventricle ejects about 70 ml into the aorta
 The right ventricle ejects the same volume into the pulmonary trunk.
 End systolic volume is 60ml in each ventricle .
RELAXATION PERIOD

 Both atria and ventricles are relaxed .It lasts for 0.4 sec.
 When heart beats faster the relaxation time shortens.
 Ventricular repolarization causes ventricular diastole.

Cardiac Cycle -Phases

 How Does the Heart Move Blood?

 Blood can flow in the cardio vascular system if one region develops higher
pressure than other regions
 The ventricles are responsible for creating a region of high pressure
 When the blood filled ventricles undergo systole, the pressure exerted on the
blood increases and blood flows out of (empties) the ventricles into the
arteries displacing the lower pressure blood in the vessels
 As blood moves through the vasculature, pressure is lost due to friction
between the blood and the walls of the vessels
 When the blood filled ventricles undergo diastole, the pressure exerted on the
blood decreases and blood flows into (fills) the ventricles
 The filled ventricle undergoes systole again and repressurizes the blood .

Microscopic Anatomy of Heart Muscle

 Cardiac muscle is striated, short, fat, branched, and interconnected.

 The connective tissue endomysium acts as both tendon and insertion.
 Intercalated discs anchor cardiac cells together and allow free passage of ions.
 Heart muscle behaves as a functional syncytium.
 PHYSIOLOGIC CHARACTERISTICS OF THE CONDUCTION CELLS

Cardiac Muscle Cells

General cardiac cell stuff:

 Intercalated discs
 Allow branching of the myocardium
 Gap Junctions (instead of synapses)
 Fast Cell to cell signals
 Many mitochondria
 Large T tubes
VIII. CARDIAC ACTION POTENTIALS
 Determination of Stroke Volume
 Preload
 Amount of blood delivered to the chamber.
 Depends upon venous return to the heart.

 Contractility
 The efficiency and strength of contraction
 Frank Starling’s Law
 Afterload

Resistance to forward blood flow by the vessel walls

Frank-Starling Law of the Heart

 States that strength of ventricular contraction varies directly with EDV

 Is an intrinsic property of myocardium
 As EDV increases, myocardium is stretched more, causing greater contraction
& SV

Anrep's effect

 Increase of blood flow in aorta and so coronary arteries leads to excessive

stretching surrounding myocardial cells.
  According to Frank Starling low cardiac contraction is directly proportional to
initial length of its fibers. So increase of coronary blood flow leads to
stimulation heartbeat.

IX. CARDIAC OUTPUT

BLOOD PRESSURE

 Blood pressure: the force that is exerted by blood against blood vessel walls
 In arterioles and arteries – 35 mm Hg
 In venous end of capillaries– 16mm Hg
 When blood flow in Rt. ventricle -0 mm Hg

CO – determined by two variables 1) Heart rate (HR) and,

2) Stroke volume (SV)

SV and HR - regulated by two mechanisms:

1.Intrinsic (auto-regulation), Eg: Stretch of muscle fibers, frequency of

contraction, tension and temperature.

2. Extrinsic, Eg. by nerves, hormones and electrolytes.

EFFECT OF THYROID HORMONES IN HEART

 Thyroid hormones increase protein synthesis. Also increases glucose

absorption and uptake of glucose by cells
 Increase activity of mitochondria in heart cells and ATP formation in it. So,
both activity of heart muscle and conduction of impulses are stimulated.
HEART AND GRAVITY

Cardiac Toothache

 When cardiac pain presents in the orofacial region commonly affected areas
include pain(s) in the neck, throat, ear, teeth, mandible and headache .
 In one study, 6% of patients presenting with coronary symptoms had pain
solely in the orofacial region while 32% had pain referred elsewhere.
Interestingly, bilateral referred craniofacial pain was noted more commonly
than unilateral pain at a ratio of 6:1 .

REFERRED PAIN

 The pain of Angina pectoris is referred to jaws and teeth.

 Because of the overlapping of the 5th cranial nerve , third cervical nerve and
first thoracic nerve.
 Anginal pain is characterized by its severity, onset association with exertion
and its disappearance with rest.

ARTIFICIAL HEART

 An artificial heart is a prosthetic device that is implanted into the body to

replace the biological heart.
 It is different from a heart bypass machine, which is an external device (a
Cardio-Pulmanory Bypass - CPB).
 A CPB is only suitable for a few hours use, while artificial hearts have so far
been used for periods of well over a year.

Ref : http://www.abiomed.com/assets/2010/11/abiocor-faq-final.pdf
X. SUMMARY

 Blood pressure = total peripheral resistance X cardiac output

(BP = TPR x CO)

 Cardiac output = heart rate X stroke volume

(CO = HR x SV)

—Heart Rate (HR) = 70 beats/min

—Stroke volume (SV) = blood pumped/beat by each ventricle

◦Average is 70-80 ml/beat

Pulse pressure = (systolic pressure) – (diastolic pressure)

XI. REFERENCES

WEB REFERENCES

1.http://indianheartjournal.com/Jan-Feb2015/Jan-Feb2015.htm.

2.http://www.abiomed.com/assets/2010/11/abiocor-faq-final.pdf

3.http://dx.doi.org/10.7243/2052-4358-2-5 .

BOOK REFERENCES

3.Guyton A.C, Hall J.E. Textbook of Medical Physiology. Elsevier Saunders,

Philadelphia, 11th edition, 2006.

4.Opie, LH. Heart Physiology. From Cell to Circulation. 4th Edition, 2004.

5.Edwards C.R.W, Bouchier I.A.D , Haslett C, Chilvers E. R, Davidson’s Principles

and Practices of Medicine . 17th Edition , Edinburgh New York : Churchill
Livingstone, 1995.
6.Katz, AM. Physiology of the Heart. Lippincott, Williams, and Wilkins, 12th edition,
Philadelphia, 2010.

7.Bers DM. Excitation-Contraction Coupling and Cardiac Contractile Force. 2nd

edition. Kluwer Academic Publishers, Dordrecht/Boston/London, 2001.

JOURNAL REFERENCES

8.Kobayashi T, Solaro RJ. Calcium, thin filaments, and the integrative biology of
cardiac contractility. Annu Rev Physiol. 2005;67:39–67.

9.MacLennan DH, Kranias EG. Phospholamban: a crucial regulator of cardiac

contractility. Nat Rev Mol Cell Biol. Jul 2003;4(7):566–577.

10.Kruger M, Linke WA. The giant protein : a regulatory node that integrates
myocytes signaling pathways. J Biol Chem. 2011 Jan 21.

14.Langewouters GJ, Settels JJ, Roelandt R and Wesseling KH. Why use Finapres or
Portapres rather than intra-arterial or intermittent non- invasive techniques of blood
pressure measurement? J Med Eng Technol. 1998; 22:37-43 .

15.Heart rate variability: standards of measurement, physiological interpretation and

clinical use. Task Force of the European Society of Cardiology and the North
American Society of Pacing and Electrophysiology. Circulation. 1996; 93:1043-65.

18.Goernig M, Schroeder R, Kleindienst R, Figulla HR, Voss A and Leder U. Blood

pressure variability analysis enhances risk stratification in chronic heart failure.
Cardio Vascular Syst. 2014; 2:5.

19.Hinken AC, Solaro RJ. A dominant role of cardiac molecular motors in the
intrinsic regulation of ventricular ejection and relaxation. Physiology (Bethesda). Apr
2007;22:73–80.