Professional Documents
Culture Documents
CONTENTS
1. INTRODUCTION
5. HEART SOUNDS
6. CARDIAC CYCLE
8. ECG
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.
•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
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.
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:
Four valves:
2 AV valves,
2 semilunar valves
Atrioventricular Valves
PULMONARY
1.Blood from the body, low O2 high CO2, right atriumright ventriclelungs
via pulmonary trunk.
SYSTEMIC
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.
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.
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.
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.
Physiological
Pathological
Mitral regurgitation
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 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
AV node
Purkinje fibers
HISTORY
RECORDING ECG
Determination of:
Useful in diagnosis of :
Cardiac Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances
Drug effects and toxicity
ATRIAL SYSTOLE
VENTRICULAR SYSTOLE
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.
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
Anrep's effect
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
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
ARTIFICIAL HEART
Ref : http://www.abiomed.com/assets/2010/11/abiocor-faq-final.pdf
X. SUMMARY
(CO = HR x SV)
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
4.Opie, LH. Heart Physiology. From Cell to Circulation. 4th Edition, 2004.
JOURNAL REFERENCES
8.Kobayashi T, Solaro RJ. Calcium, thin filaments, and the integrative biology of
cardiac contractility. Annu Rev Physiol. 2005;67:39–67.
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 .
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.