Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
S. J. JOSHI
FIRST YEAR B. PHARM (SEM – I)
SUBJECT: HUMAN ANATOMY & PHYSIOLOGY – I
UNIT – V
CHAPTER – I
CARDIOVASCULAR SYSTEM
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OBJECTIVES:
Composed of tough, inelastic, dense irregular connective tissue
Functions:
 Prevents overstretching of heart
 Provides protection to heart
 Fixes heart in the Mediastinum
Serous Pericardium:
 Thin and delicate inner layer of pericardium with 2 sub-layers – Parietal and
Visceral layers
 Parietal layer is fixed to fibrous pericardium
 Visceral layer is fixed to heart wall
 Space between Parietal and Visceral layers of Serous Pericardium is called
Pericardial Cavity containing thin, slippery fluid called ‘Pericardial Fluid’
 Functions:
 Pericardial fluid reduces friction when the heart contracts
 Allows contractile movement of heart within tough fibrous pericardium
At the end of this chapter the student should be able to –
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Explain external and internal structure of heart
Describe conduction system of heart
Explain Cardiac Action Potentials, ECG
Elaborate concept of Cardiac Cycle and Cardiac output
Describe regulation of blood pressure
Summarize systemic, pulmonary and coronary circulation
Brief out structure & functions of arteries, veins and capillaries
Brief out disorders of heart
ANATOMY OF HEART:
Size Shape and Location of Heart:
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Heart is about the size of a person’s closed fist
It is 11 cm in length, 9 cm in width and 6 cm in thickness
Average mass – 250 gm (females) and 300 gm (males)
Its shape is like a tilted cone resting on diaphragm
It is located within the thoracic cavity between sternum and vertebral column
(Mediastinum) with right and left lungs on its sides
The pointed lower (inferior) end of heart is called ‘Apex’ and broad upper
(anterior) surface of heart is called ‘Base’ of the heart.
It is slightly tilted towards left with its apex pointing towards left hip.
COVERINGS OF HEART:
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Heart is a muscular pump with four chambers
Heart wall is surrounded by a covering called ‘Pericardium’
Pericardium has two layers – Fibrous Pericardium and Serous Pericardium
Fibrous Pericardium:
 Outermost layer of pericardium resting on diaphragm
 Provides attachment of blood vessels supplying heart wall (Coronary Blood
Vessels)
HEART WALL
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Heart wall has 3 layers – Epicardium, Myocardium and Endocardium
Epicardium –
 Outermost, thin layer
 Also known as Visceral Layer of Serous Pericardium
 Composed of mesothelial cells and delicate connective tissue
 Provides smooth frictionless outer surface to heart wall
Myocardium –
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Middle layer composed of cardiac muscles arranged in bundles
95% of total heart wall tissue
Provides pumping action due to contraction of cardiac muscles
Endocardium –
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Innermost, thin layer of endothelial cells supported by connective tissue
Provides smooth surface for heart chambers and valves
Continuous with endothelium of blood vessels which enter or leave heart
1
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
S. J. JOSHI
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The opening between left atrium and left ventricle is guarded by ‘Bicuspid
Valve’ or ‘Left Atrioventricular Valve’ or ‘Mitral valve’
Left and right atria are separated by a partition of cardiac muscles called
‘Interatrial Septum’
Right Ventricle:
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Wall of right ventricle is thicker than atria but less thick than left ventricle
because it pumps blood to lungs over a short distance
Inner surfaces of ventricles (both right and left) have many folds of cardiac
muscles called ‘Trabeculae Carnae’
Some of these trabeculae are cone shaped and called ‘Papillary Muscles’
Papillary muscles are connected to Atrioventricular valves by tendon
threads called ‘Chordae Tendineae’
Opening between right ventricle and pulmonary trunk is guarded by a
semilunar valve called ‘Pulmonary Valve’
Left Ventricle:
Fig. Coverings of Heart and Heart Wall
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INTERNAL ANATOMY / STRUCTURE OF HEART:
CHAMBERS OF HEART:
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Heart has four chambers
Upper, right and left blood receiving chambers are called ‘Atria’
Lower, right and left blood pumping / ejecting chambers are called ‘Ventricles’
Each atrium has a wrinkled pouch like extensions called ‘Auricles’
Auricles increase blood holding capacity of atria slightly
Right Atrium:
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Walls of atria are thinner than ventricles
Posterior wall of right atrium is smooth and anterior wall is rough
Right atrium receives deoxygenated blood through 3 large veins called –
Superior Vena Cava (from head, neck and arms); Inferior Vena Cava (from
trunk and legs) and Coronary Sinus (from heart wall)
The opening between right atrium and right ventricle is guarded by ‘Tricuspid
Valve’ or ‘Right Atrioventricular Valve’
Left Atrium:
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Both anterior and posterior walls of left atrium are smooth
Left atrium receives oxygenated blood from via pulmonary veins
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Wall of left ventricle is thickest of all heart chambers because it pumps blood
through aorta and its branches to entire body over a large distance
The inner surface of left ventricle shows presence of Trabeculae Carnae
Papillary Muscles and Chordae Tendineae similar to right ventricle
The right and left ventricle is separated by a thick partition called
‘Interventricular Septum’
Opening between left ventricle and aorta is guarded by a semilunar valve called
‘Aortic Valve’
VALVES OF HEART:
Atrioventricular Valves:
 These valves are made up of leaflet like flaps of dense connective tissue covered
with endothelium
 The flaps of these valves are called ‘Cusps’
 The Right Atrioventricular valve has 3 cusps hence called ‘Tricuspid Valve
 The Left Atrioventricular valve has 2 cusps hence called ‘Bicuspid Valve’
 Bicuspid valve appears like a bishop’s hat (miter) hence it is called ‘Mitral valve
 When the pressure in the ventricles is lower than that in atria, Atrioventricular
valves open
 These valves open when the ventricles and papillary muscles are relaxed
Chordae Tendineae are slack
 Blood flows from atria at higher pressure to ventricles at lower pressure
through these valves
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
S. J. JOSHI
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Semilunar valves prevent backflow of blood from arteries into ventricles
Fig. Superior (top) View - Atrioventricular Valves open, Semilunar Valves Closed
Fig. Superior (top) View - Semilunar Valves open, Atrioventricular Valves Closed
Fig. Internal Structure of Heart
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These valves close off when the ventricles and papillary muscles contract →
Chordae Tendineae become stiff and push the cusps of valves upwards and
close them tightly
Atrioventricular Valves prevent back flow of blood from ventricles to atria during
ventricular contraction
Semilunar Valves:
 The valves guarding opening between ventricles and blood vessels carrying
blood out of heart (pulmonary trunk and aorta) are called semilunar valves
(Pulmonary and Aortic Valves)
 The name indicates that the flaps of these valves are ‘Half Moon’ or ‘Crescent’
(Semilunar) shaped.
 Semilunar valves open when pressure in the ventricles exceeds the pressure in the
arteries
 When the ventricles relax, back-flowing blood fills the valve cusps, this causes the
semilunar valves to close tightly
CARDIAC MUSCLES:
 Striated but involuntary, contraction- relaxation regulated by autonomic
nervous system and circulating hormones like adrenaline
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
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Possess single large nucleus, many mitochondria, lesser T-tubules as compared
to skeletal muscles
Attachments between adjacent cardiac muscles are called ‘Intercalated Discs’
which hold them together during contractions
Intercalated discs contain many ‘Gap Junctions’ which allow free movement of
ions from one cardiac muscle to another
Cardiac muscles are branched at the ends and connect with neighbouring cardiac
muscles (Syncytium)
Gap junctions and branching allow rapid conduction of electrical impulses
(signals) throughout heart wall
CHARACTERISTICS / PHYSIOLOGICAL PROPERTIES OF
CARDIAC MUSCLES:
Unique, automatic, rhythmic and tireless working of cardiac muscles is possible
because of following special properties
1. Automaticity:
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S. J. JOSHI
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These contractions occur in similar way to that of skeletal muscles (Calcium
mediated Sliding of Thick and Thin filaments i.e. Actin – Myosin in
sarcomeres)
This property is called ‘Contractility’
5. Refractoriness: (toughness even in repeated/ continuous working/ effort)
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When a cardiac muscle is contracting, a second contraction cannot
triggered by any strong electrical signal.
Because of this, contractions of cardiac muscles are rhythmic and not
sustained/ long or short/brief
Thus, cardiac muscles always relax sufficiently between two contractions
This is also the reason why tetany or fatigue does not occur in cardiac
muscles (fatigue or tetany occurs in skeletal muscles)
This property is called ‘Refractoriness’
This property is also essential for pumping action of heart (if contractions
are prolonged, pumping action would stop)
Some cardiac muscle fibers (Automatic or Autorhythmic Fibers) are
specialized to produce their own electrical impulses (signals)
spontaneously.
This property is called ‘Automaticity’
2. Rhythmicity:
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Automatic Cardiac Muscle Fibers generate their spontaneous electrical
impulses (signals) rhythmically (e.g. 75 signals or beats per min)
This property is called ‘Rhythmicity’
3. Conductivity:
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All cardiac muscle fibers (both automatic and non-automatic) can
conduct an electrical impulse (signal) through them
This property is called ‘Conductivity’
4. Contractility:
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Non-automatic cardiac muscle fibers (Contractile Fibers) contract
forcefully when an electrical impulse (signal or current) passes through
them.
Fig. Cardiac Muscle Fibers with branching and gap junctions
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
S. J. JOSHI
CONDUCTION SYSTEM OF HEART:
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Special properties of cardiac muscle fibers allow them –
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to generate own electrical impulses continuously
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to conduct electrical impulses through entire heart wall
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to contract at the same time (atria first and then ventricles) and rhythmically
Purkinje fibers receive impulses from right and left bundle branches
and conduct them rapidly through entire ventricular wall
A specialized network of cardiac muscles called ‘Conduction System’ of heart
possesses two types of muscle fibers –
a. Autorhythmic Fibers/ Automatic Fibers: these are capable of generation
and conduction of own electrical impulses
b. Conducting or Contractile (Non-automatic fibers): These do not generate
their electrical impulses but conduct them and contract in response
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The conduction system of heart consists of following components –
1. Sinoatrial Node (SA Node):
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Present in right atrium lateral & inferior to opening of superior vena cava
SA Node fibers do not have stable resting membrane potential
These fibers depolarize spontaneously, rhythmically and continuously –
thus SA node sets pace of the heart – hence called ‘Pacemaker’
SA node action potentials travel through Gap Junctions and branching
rapidly through walls of both atria to Atrioventricular node (AV Node)
Other automatic fibers can also show pacemaker activity only when SA
Node function is disturbed or its signals do not reach them properly
2. Atrioventricular Node (AV Node):
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Located in the interatrial septum just above opening of coronary sinus
Electrical impulse slows down a little in AV node and travels to a bundle
of Autorhythmic fibers in interventricular septum after a slight delay
3. Bundle of His:
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It is a bundle of automatic fibers present in the upper segment of
interventricular septum
It is the only site at which atrial signals travel to ventricles
The signal enters right and left branches of Bundle of His
Bundle branches reach the apex of heart through interventricular septum
4. Purkinje Fibers:
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These are large diameter automatic fibers present throughout the
ventricular walls (right and left)
Fig. Conducting System of Heart
CARDIAC ACTION POTENTIALS:
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Action potentials are the changes in membrane potentials occuring rhythmically
in cardiac muscle fibers
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These occur due to movement of ions through ion channels present in the
membranes of cardiac muscles
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There are two basic types of action potentials generated –
a. Slow Channel Potentials: Initiated by slow conducting Ca2+ Channels in SA
Node fibers
b. Fast Channel Potentials: Initiated by fast conducting Na+ Channels in
Conducting Fibers
SLOW CHANNEL POTENTIALS:
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Occur in SA Node fibers
SA Node fibers possess leak Na+ Channels in their membranes → Na+ enters
inside SA Node cells at potentials of less than – 40 to – 45 mV
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
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Thus, the resting membrane potential of SA node fibers is not stable →
reaches the threshold potential spontaneously (Due to entry of Na+ ions through
leak channels) (Pacemaker Potential)
Once membrane potential reaches threshold (– 40 to – 45 mV), → Ca2+
channels in the membrane open and depolarization occurs due to entry of Ca2+
ions (Phase of Depolarization)
When the membrane potential crosses 0 mV and reaches +10 mV, → Ca2+
channels close and K+ Channels open
K+ ions move out and membrane repolarizes back to resting membrane potential
(Phase of Repolarization)
S. J. JOSHI
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At this potential of ~ 0 mV, voltage dependent L-type Ca2+ channels in the
membranes of cardiac muscle fibers open and Ca2+ enters cell. This Calcium is
called ‘Trigger Calcium’
Ca2+ entry leads to release of Ca2+ ions stored in the sarcoplasmic reticuli
cardiac muscle cell.
But, Ca2+ entry is matched by K+ exit from K+ channels → potential remains
stable for ~ 0.25 seconds. This phase is called ‘Plateau Phase’ or ‘Phase 2’
During this phase, excess Ca2+ ions bind with Troponin → Actin and Myosin
filaments interact → muscle fiber contracts forcefully (Systole)
At the end of this phase, Ca2+ channels close and Ca2+ from Sarcoplasmic
reticulum moves back inside and K+ channels open further
This leads to reduction in membrane potential to resting membrane potential
and the cell repolarizes.
This phase is called ‘Repolarization Phase’ or ‘Phase 3’
The membrane potential remains stable at resting potential till the next signal
from SA node arrives and resting membrane potential again reaches threshold
potential. This phase is called Phase 4.
Cardiac muscles relax completely during this phase (Diastole)
Fig. Pacemaker Potentials and Action Potentials (slow channel) in SA Node Fibers
FAST CHANNEL POTENTIALS:
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Occur in conducting fibers in response to action potentials from SA Node
Resting membrane potential of the conducting fibers is stable ~ – 90 mV
When SA node signal current enters conducting fibers, resting membrane
potential reaches threshold potential (– 70 mV) due to entry of positive ions
from neighbouring cells via gap junctions
At threshold potential (– 70 mV), voltage dependent Na+ channels in the
membrane of conducting fibers open and membrane potential quickly reaches
+20 to +30 mV. This phase is called Rapid Depolarization / Phase 0
At +20 to +30 mV, Na+ channels close rapidly and some K+ channels open →
Na+ entry stops and K+ exit starts → membrane potential drops to ~ 0 mV.
This phase is called Early Repolarization or Phase 1
Fig. Fast Channel Potentials in Conducting / Contractile Fibers
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
S. J. JOSHI
CARDIAC CYCLE: (*********)
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Events taking place during one heart beat are called a ‘Cardiac Cycle’
Cardiac Cycle includes –
o Atrial Systole and Diastole
o Ventricular Systole and Diastole
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PRESSURE AND VOLUME CHANGES DURING CARDIAC CYCLE:
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Atria and ventricles contract and relax alternately
Blood is pumped from areas of higher pressure to lower pressure
When a heart chamber contracts, pressure inside it increases
When a heart chamber relaxes, pressure inside it reduces
Each ventricle (right and left) pumps equal volume (amount) of blood during
each stroke or beat
Cardiac Cycle duration is 0.8 seconds when Heart Rate is 75 beats/ min
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ATRIAL SYSTOLE AND VENTRICULAR DIASTOLE:
Atrioventricular valves close causing First Heart Sound (S1) → both ventricles
contain same amount of blood while they are contracting but Atrioventricular
and semilunar valves are still closed (for about 0.05 Sec). This is called
Isovolumetric Contraction
When pressure in ventricles increases above aortic pressure (~80 mm Hg) or
pressure in pulmonary trunk (~20 mm Hg) both the semilunar valves (Aortic
and Pulmonary) open → ~ 70 ml blood is pumped into Aorta and Pulmonary
Trunk at the same time
Duration of Ventricular Contraction (Systole) = 0.25 seconds
Volume of blood remaining inside each ventricle at the end of ventricular
systole = 60 ml. This is called End Systolic Ventricular Volume (ESV)
Amount of blood pumped into aorta or pulmonary trunk after each ventricular
systole is called Stroke Volume (SV). SV = EDV – ESV = 130 – 60 = 70 ml
Ventricles start relaxing (Ventricular Diastole) after systole. It is represented by
T wave in ECG
RELAXATION PERIOD:
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Atria contract (Systole) and Ventricles relax (Diastole) at the same time
SA node signal spreads in both atria → both atria depolarize (P wave in ECG)
Atrial Depolarization → both atria contract (Systole) simultaneously →
Pressure in atria increases → Atrioventricular (Tricuspid & Mitral) Valves open
→ ~ 25 ml blood is pumped into each relaxing ventricle (Ventricular
Relaxation = Ventricular Diastole)
Duration of atrial systole = 0.1 Seconds
Relaxing Ventricles already contain ~ 105 ml blood
The volume of blood in each ventricle at the end of Ventricular Diastole or
Atrial Systole = 105 + 25 = 130 ml. This is called End Diastolic Ventricular
Volume (EDV)
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VENTRICULAR SYSTOLE AND ATRIAL DIASTOLE:
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Ventricles contract (Systole) and Atria relax (Diastole) at the same time
Signal from AV node spreads through ventricular wall through right and left
bundle branches and Purkinje fibers
Both ventricles depolarize (QRS wave in ECG) → Ventricles contract as the
depolarization wave spreads → pressure inside ventricles increases →
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Duration of Relaxation = 0.4 Seconds
Atria and Ventricles are both relaxed
Relaxation period decreases if heart rate increases
Ventricular repolarization → Pressure in ventricles reduces → blood in aorta
and pulmonary trunk flows back and fills the cusps of semilunar valves →
semilunar valves close → gushing of blood during back flow and closure of
semilunar valves causes Second Heart Sound (S2)
All four valves are closed and ventricular volume does not change →
Isovolumetric Relaxation
Ventricles continue to relax → ventricular pressure falls below atrial pressure →
Atrioventricular Valves open → major part of ventricular filling begins (60 ml
remaining after ventricular systole (ESV) + 45 ml filled from atria before atrial
systole = 105 ml = Residual Volume)
SA node fires next signal → Atrial Depolarization → P wave in the ECG → Next
Cycle begins
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Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
S. J. JOSHI
CARDIAC CYCLE
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
CARDIAC OUTPUT:
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Cardiac Output is amount of blood pumped by heart in one minute
Cardiac Output = Stroke Volume (SV) X Heart Rate (HR)
Stroke Volume is amount of blood pumped by ventricles during every beat = ~ 70 ml
Thus Cardiac Output at normal heart rate of 75 beats per minute = 75 x 70 = 5250 ml i.e.
5.25 Liters (roughly equal to total blood volume)
Stroke volume is governed by Frank – Sterling Law of Heart or Laplace’s Relation
It states that: Force of contraction of ventricles is proportional to ventricular filling i.e.
End Diastolic Volume (EDV)
EDV depends on  Duration of Ventricular Diastole
 Venous Return i.e. amount of blood returned to heart by veins
S. J. JOSHI
7. Q-T interval Prolongation – Myocardial Ischemia (reduced blood flow to heart
wall), Damage to heart wall or Conduction defects
8. S-T segment Elevation – Myocardial Infarction (Heart Attack)
9. S-T segment Depression – Reduced blood flow to heart wall (Angina Pectoris)
ELECTROCARDIOGRAM:
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ECG is the record of action potentials produced by all the heart muscles during
each heart beat
It is measured by an instrument called ‘Electrocardiograph’
Electrodes are placed on arms, legs (limb leads) and chest (6 chest leads). These
electrodes amplify and record electrical currents produced in the heart wall and
display it on a paper tracing
ECG tracing shows characteristic P, Q, R, S, and T waves
 P wave represents Atrial Depolarization
 QRS complex represents Ventricular Depolarization
 T wave represents Ventricular Repolarization
 P-Q interval represents time interval between atrial and ventricular
depolarization
 S-T Segment represents plateau phase of ventricular fibers during contraction
 Q-T interval represents time interval between ventricular depolarization and
ventricular repolarization
SIGNIFICANCE OF ECG:
Comparison of patients ECG with normal ECG helps in determining 1. If the conducting pathway is abnormal,
2. If the heart is enlarged,
3. If certain regions of the heart are damaged,
4. Cause of chest pain
5. Abnormal P wave – SA node or Atrial disturbances
6. P-Q interval Prolongation – Atrial Conduction Disturbance (Arrhythmia)
Fig. Electrocardiogram Tracing
BLOOD PRESSURE:
 Blood Pressure is the pressure exerted by blood on the walls of blood vessels.
 It is measured as Systolic and Diastolic Blood Pressure.
 Systolic blood pressure is the blood pressure produced in arterial system when
left ventricle of heart contracts and pushes the blood into aorta
 Diastolic blood pressure is the blood pressure produced in arterial system when
the heart is relaxing in a diastole after ejection of the blood.
 Systolic BP ranges from 110-130mm Hg and Diastolic BP ranges from 70mm Hg.
 Blood Pressure above normal range us called Hypertension and Blood Pressure
below normal range is called Hypotension.
Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
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S. J. JOSHI
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Classification of Blood Pressure in Adults:
Category/ Stage
Optimal
Normal
High Normal
Hypertension Grade – I (Mild)
Hypertension Grade – II
(Moderate)
Hypertension Grade – III (Severe)
Isolated Systolic Hypertension
Systolic BP
<120
120 – 129
130 – 139
140 – 159
Diastolic BP
<80
80 – 84
85 – 89
90 – 99
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160 – 179
110 -109
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> 180
>140
> 110
< 90
When plasma volume is reduced → Blood Flow and Blood Pressure to
Kidneys is reduced → Kidneys release a hormone called ‘Renin’ → Renin
causes increased formation of Angiotensin – II → Angiotensin – II causes
vasoconstriction which increases blood pressure
Angiotensin – II also increases release of Aldosterone from Adrenal
Glands → Aldosterone reduces Sodium and Water excretion from kidneys
→ Plasma Volume increases → Blood Pressure increases
ADH and ANP also adjust blood pressure by adjusting kidney function
and plasma volume
HYPERTENSION:
REGULATION OF BLOOD PRESSURE:
Definition: Elevated / Increased Arterial Blood Pressure above normal values as seen
after repeated measurements is called Hypertension
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CAUSES AND TYPES OF HYPERTENSION:
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Mean Arterial Blood Pressure = Cardiac Output (CO) X Total Peripheral
Resistance (TPR)
Cardiac output is amount of blood pumped by heart per minute (CO = SV x HR)
Total Peripheral Resistance is the pressure against which heart must pump blood
Peripheral resistance depends on diameter of blood vessels and plasma volume
Blood pressure is regulated by Neural and Hormonal Mechanisms
Neural mechanisms regulate blood pressure from moment to moment (short term)
Hormonal Mechanisms maintain blood pressure on long term basis
1. Neural Mechanisms –
 Autonomic Nervous System senses changes in blood pressure and blood
composition through Baroreceptors and Chemoreceptors
 Sympathetic Nervous system increases blood pressure by increasing heart
rate (HR), Force of Contraction of Heart and Cardiac Output (CO)
 Parasympathetic Nervous System reduces blood pressure by decreasing
Heart Rate (HR), Force of contraction of heart and Cardiac Output (CO)
2. Hormonal Mechanisms:
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Blood Pressure is also regulated by hormones like Angiotensin – II,
Atrial Natriuretic Peptide (ANP), Antidiuretic Hormone (ADH) and
Circulating Adrenaline
A. Primary Hypertension: A single cause cannot be identified. It is also called
Idiopathic Hypertension
B. Secondary Hypertension: It can be due to various causes –
a. Renal Hypertension: Renin producing tumors, Sodium excess in plasma,
thickening of renal artery etc.
b. Endocrine Hypertension: Thyroid Disorders, Excess plasma Ca2+, Adrenal
Cancer, Excess Aldosterone Release (Aldosteronism), Cushing’s Syndrome,
Excess ADH activity, Excess Adrenaline, Noradrenaline Activity (Sympathetic
Nervous System Overactivity) etc.
c. Increased Cardiac Output
d. Rigidity and Thickening of Aorta
e. Heart Beat Defects (Cardiac Arrhythmias)
f. Atherosclerosis (Thickening of Blood Vessel walls due to deposition of
cholesterol and lipids)
Risk Factors for Development of Hypertension:
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Age (> 55 years in men and > 65 years in women)
Cigarette Smoking
Abnormal Plasma Lipid Concentrations (Dyslipidemia)
Family History of premature heart disease
Abdominal Obesity
Lack of Exercise
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Dr. SHIVAJIRAO KADAM COLLEGE OF PHARMACY, KASABE DIGRAJ
Other Clinical Conditions Associated with Hypertension:
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Cardiovascular Disease: Ischemic heart Disease, Stroke, Peripheral Vascular
Disease,
 Angina Pectoris, Heart Attack (Myocardial Infarction, Heart Failure etc.
 Kidney Disease: Diabetic Kidney Damage (Nephropathy)
SYSTEMIC AND PULMONARY CIRCULATION:
 Heart is a dual pump i.e. it pumps blood in two directions
o From Heart to body organs and back to heart i.e. Systemic Circulation
o From Heart to lungs and back to heart i.e. Pulmonary Circulation
S. J. JOSHI
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This circulation of blood from heart to body organs and back to heart is called
Systemic Circulation.
PULMONARY CIRCULATION:
 Blood is returned to right atrium heart from veins via superior and inferior
vena cava
 Right Atrium drain and pump blood into Right Ventricle
 Right Ventricle pumps deoxygenated blood to lungs via Pulmonary Trunk
which divides into right and left Pulmonary Arteries
 Pulmonary Arteries divide in lungs forming pulmonary alveolar capillaries
 Pulmonary alveolar capillaries exchange CO2 with O2 and form Pulmonary
veins by joining together
 Pulmonary Veins empty Oxygenated blood to Left Atrium
 This Circulation of blood from heart to lungs and back to heart is called
Pulmonary Circulation
SYSTEMIC CIRCULATION:
 Oxygenated blood in Left Atrium is pumped into left ventricle
 Left ventricle pumps this blood into Aorta
 Aorta divides at the beginning to give out coronary arteries and then arches
forming ‘Aortic Arch’
 Three braches come out of Arch of aorta which supply oxygenated blood to
Head, Neck and Arms i.e. Left Common Carotid Artery Left Subclavian
Artery and Brachiocephalic Trunk
 Aorta then moves down (Descending Aorta) through thoracic cavity (Thoracic
Aorta) through diaphragm into abdomen (Abdominal Aorta)
 Thoracic and Abdominal Aorta divide into many branches which supply
organs and tissues in Chest, Abdomen (GIT), Pelvis and Legs.
 Capillaries unite to form Veins and veins for Superior and Inferior Vena Cava
which carry deoxygenated blood to heart
Fig. Systemic and Pulmonary Circulation