Circulatory system

Chapter # 2

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 Properties of cardiac muscle
Cardiac muscle - involuntary & striated
3 types – atrial muscle, ventricular muscle, specialized
conductive muscle fibers.
Properties
1. Functional syncytium
Cardiac muscle – made of many cells connected by means of
dark intercalated discs;
 cell membranes that separate individual cardiac muscle from
each other.
Electrical resistance through intercalated disc – less than
resistance through outside membrane of cardiac muscle fibers

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 Thus action potential travels from one muscle cell to
another without hindrance.
Heart compose of 2 separate functional syncytium;
Atrial & ventricular syncytiums

2. All or none law

“if a stimulus is applied to heart muscle, it will respond
to the best of its ability whether the current is of
threshold or sub-threshold level”.

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 3. Excitability
Excitable by adequate stimulus – responds by contraction

4. Peculiar action potential

Resting membrane potential = -80 to -95 mv
Excitation membrane potential = +20 mv
Maintains steady state for while – then gets down to
resting state
Causes formation of plateau – may be due to;
 Delay Na channels to close
 Increase Ca influx

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 5. Refractory period
During which cardiac muscle – will not respond to any
stimulus of whatever strength
Cardiac muscle – refractory to re-stimulation during
action potential
Refractory period of heart – divided into;
Absolute refractory period – extends throughout whole
period of contraction
Relative refractory period – heart can be stimulated by
very strong stimulus

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 6. Contractility
Contractile unit – myofibril (contains actin & myosin)
During contraction – these 2 units associate (ATP –
utilized)
During rest – dissociated (ATP re-synthesize)
Contraction duration;
Atrial muscle – 0.2 sec
Ventricular muscle – 0.3 sec

7. Conductivity
Occurs in mycocardium
Velocity of conduction of action potential – 0.3-0.5
m/s
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 8. Staircase effect
If cardiac muscle stimulated after period of rest;
First few contractions are weak
Gradually increase in strength – then become steady
Known as staircase phenomenon

9. Tone
Partial contraction of muscle
Independent of nerves & can be adjusted

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 10. Fatigue
Cannot be fatigued – b/c of absolute refractory period

11. Frank-Starling Law

“heart has intrinsic ability to changing loads of
inflowing blood”

12. Rhythmicity
Rate of rhythmicity is 70-80 beats/min

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 Origin and conduction of heart beat
Heart beat is MYOGENIC;
i.e. electrical signals needed to make muscles contract
originate in muscle itself (rather than via nerves)

Sino-atrial node, part of muscle in right atrium - origin

of electrical signals (impulses)
called the ‘pacemaker’

Wave of impulses from SAN spread along muscle cells

across wall of both atria
causes muscles to contract  atrial systole

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 Impulses do not travel directly to ventricles;
 because of ring of non-conducting tissue b/w atria & ventricles
Impulses reach atrioventricular node (AVN) at beginning of
septum - slight delay

Impulses conducted down specialised muscle cells in wall

of septum called Bundle of His.
 only direct muscular communication b/w atria & ventricles

 divides into right and left bundle branches

 distributed respectively to right & left ventricle

 bundle branches terminate in thin fibers called Purkinje fibers

 through which impulses reach ventricular muscles

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 While ventricles contract – atria relax
This sequence is repeated again and again

 Contraction passes from base of heart upwards

so blood is pumped upwards and through semi lunar valves

 Impulses travel from SAN  AVN  base of ventricles 

time delay so atria contract to fill ventricles before
ventricles contract.

Thus conducting system of heart consist of;

SA node, AV node, bundle of HIS & purkinje fibres

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 Cardiac cycle
Period from beginning of one heart beat to beginning of next
Stages
 Consist of 2 phases

1. Systole
Period of contraction of heart
divided into following stages;

Period of isovolumic or isometric contraction

 Ventricular contraction – ventricular pressure rises
 AV & semilunar (aortic & pulmonary) valves closed
 So contraction is occurring, but no emptying
 This period – period of isovolumic contraction

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 Period of ejection
When left ventricular pressure rises above 80 mmHg,
Right ventricular pressure – above 8 mmHg,
Ventricular pressure pushes semilunar valves open &
blood begins to flow out

Ejection of blood – divided into 3 thirds;

Period of rapid ejection – first 1/3rd of period;
 70% of blood ejected
Period of slow ejection – last 2/3rd of period;
 30% of blood pumped

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 2. Diastole
Period of relaxation – during which heart fills with blood
divided into following stages;

Period of isovolumic or isometric relaxation

 Ventricular muscles – continue to relax
 But ventricular volume does not change

Period of rapid filling of ventricles

 Occurs during 1st 1/3rd of diastole
 Atrial pressure becomes greater than intraventricular pressure
 AV valves open & blood flows rapidly into respective ventricle

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 Diastasis
Middle 1/3rd of diastole
Blood passes directly into ventricle without contraction

Atrial systole
In last 1/3rd of diastole – atria contracts & pushes
remaining 20-30% of blood into ventricles

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 Heart sounds
Sounds produced by heart during cardiac cycle
detected by direct or immediate auscultation &
by means of phonocardiogram

Mechanism of heart sounds

Produced due to closure of valves
So vibration starts in valves, walls of heart & in adjacent
blood

This vibration is heard in form of sounds from chest

wall
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 Types of heart sounds
4 types of heart sounds;

First heart sound

Nature – dull & prolonged
 described as LUB
Occurrence – at beginning of ventricular systole
Duration – 0.09-0.16 sec
Cause – due to closure of AV valves
Area of auscultation; for mitral valve – apex of heart at 5th
intercostal space
 for tricuspid valve – left sternal border in 4th intercostal space

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 Mechanism of production – sudden changes in ventricular
pressure causes vibration of walls & vessels
 this causes vibration in wall of aorta & in blood itself
Significance – indicates ventricular systole
 duration & loudness indicates condition of myocardium
 indicates compliance of AV valves

Second heart sound

Nature – sharp & short
 described as DUB
Occurrence – at end of ventricular systole
Duration – 0.11 sec
Cause – due to closure of semilunar valves

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 Area of auscultation; for pulmonary valve is 2nd left
intercostal space
for aortic valve - 2nd right intercostal space
Mechanism of production – closure of semilunar
valves & vibration of valves
Vibration of blood & walls of pulmonary artery
Significance – indicates end of systole & beginning of
diastole
Indicates compliance of semilunar valves

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 Third heart sound
Nature – occasionally heard, weak & rumbling
Occurrence – at beginning of middle 3rd of diastole
Duration – 0.04 sec

Cause & Mechanism – due to oscillation of blood back

& forth b/w walls of ventricles
initiated by inrushing blood from atria
Significance;
indicates beginning of ventricular filling

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 Fourth heart sound
Nature – weak & rumbling
never heard with stethoscope
recorded on phonocardiogram
Occurrence – occurs when atria contract
Cause & Mechanism;
Caused by inrushing of blood into ventricles
initiates vibrations similar to those of 3rd heart sound
Significance;
indicates end of ventricular filling & occurs just before
1st heart sound

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 Cardiac output
Quantity of blood pumped into aorta each minute by heart
Normal values
 For men – 5.6 lit/min
 For women – 10-20% less than men
 Avg. 5 lit/min
Formula
Cardiac output = stroke vol. output x heart rate
Cardiac index
Cardiac output/m2 of body surface area
 Avg. cardiac index for adults – 3 lit/min per m 2 of body
surface area

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 Variations in cardiac output
Following physiological factors causing variations in
cardiac output
Sex – 10-20% lower in females
Age – decreases with increase in age
2.4 lit/min at 80 years

Surface area – directly proportional to body surface

area
Weight – directly proportional to body weight
Effect of metabolism – greater metabolic rate, greater
will be cardiac output

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 Effect of exercise – directly proportional, due to increased
metabolism in muscles
Blood volume – varies directly with blood volume

Control of cardiac output

 Following factors involved in regulation of cardiac output

 Venous return (Role of Frank Starling Law)

According to this law – whatever amount of blood reaches
heart, all of it is pumped by ventricles
When increased quantities of blood flow into heart - this
stretches walls of heart
 So cardiac muscle contract with increased force & empties
ventricle

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  Force of cardiac contraction
Directly proportional to force of contraction
Strength of cardiac contraction depends on;
Initial length of cardiac muscle fibers
Nutrition & oxygen supply
Diastolic pause which is filling time of heart

 Blood pressure
Directly proportional to cardiac output – provided
peripheral resistance remains same

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  Peripheral resistance
Impedance to blood flow in systemic vascular bed
Inverse relationship with cardiac output
If peripheral blood vessel dilates – venous return & cardiac
output increase
 Cardiac output depends upon dilation & constriction of number of
vessels
 Cardiac output = arterial pressure / total peripheral
resistance

 Blood volume
If amount of blood is less in circulatory system, blood will
flow poorly from peripheral vessels to heart
Venous return will be low – low cardiac output

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  Local tissue metabolism
Increased local tissue metabolism – increased venous
return
So increase in cardiac output

High cardiac output

Due to chronically reduced total peripheral resistance
Causes
Beriberi
Atriovenous fistula (shunt)
Anemia

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 Low cardiac output
Due to those abnormalities that causes pumping
effectiveness of heart to fall too low
Due those conditions that cause venous return to fall
too low
Causes
Cardiac diseases
 Myocardial infarction
 Valvular heart disease
 Cardiac tamponade
Peripheral causes
 Decreased blood volume
 Acute venous dilatation
 Obstruction of large veins

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 Stroke volume (SV)
Volume of blood pumped from one ventricle of
heart with each beat
Calculated using measurements of ventricle volumes from
an echocardiogram
Formula
SV = end diastolic volume (EDV) – end systolic volume
(ESV)

End-diastolic volume - amount of blood in ventricle

immediately after ventricular diastole and right before
ventricle contracts again
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 End-systolic volume - blood volume left in ventricles
immediately after contraction

In healthy 70-kg man,

EDV - approximately 120 ml
ESV - approximately 50 ml
giving a difference of 70 ml for stroke volume

Stroke volume can apply to each of two ventricles

although it usually refers to left ventricle

Important determinant of cardiac output

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 Stroke volume depends on several factors;
gender
heart size
contractility
duration of contraction
exercise

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 Heart rate
Speed of heartbeat, specifically number of heartbeats per
minute
 expressed as beats per minute (bpm)

Normal human heart rate - 60–100 bpm (avg. 70 bpm)

Bradycardia - slow heart rate, as below 60 bpm

Tachycardia - fast heart rate, as above 100 bpm
Arrhythmia – when heart is not beating in a regular pattern
 May indicate disease

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 Measurement of heart rate
Measured by finding pulse of heart

Pulse rate can be found at any point on the body

where artery pulsation is transmitted to surface by
pressuring it with index and middle fingers

A good area is on neck, under corner of jaw

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 Regulation of heart rate
By two mechanisms:
Local mechanism
Neural mechanism

Local mechanism
SA nodal rhythmicity can be increased upto 10-20% as
follows;
Increase venous return  stretch of atrial wall 
increase permeability of SA node  increase heart rate

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 Neural mechanism
Acts through sympathetic & parasympathetic system

Sympathetic control
Sympathetic nerves – distributed to SA node, AV node
& mycocardium
Sympathetic stimulation causes;
Positive ionotropic effect i.e. increase strength of
contraction
b/c it increase myocardial permeability of Ca ions

Positive chronotrpic effect i.e. increase heart rate

b/c it causes an increase in Na influx into SA node
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 Mechanism
Sympathetic stimulation of heart causes release of
norepinephrine at sympathetic nerve endings
Increases permeability of SA node to Na ions which
cause in heart rate
While it increase Na & Ca influx – which increases
force of contraction

Parasympathetic control
Parasympathetic nerves distributed mainly to SA node,
AV node, atria

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 Parasympathetic stimulation causes;
Negative chronotropic effect
Slightly negative ionotropic effect

Mechanism
Parasympathetic stimulation of heart causes release of
acetylcholine
Increases permeability of cardiac fibers to K ions
Causes increased negativity inside fiber
Which makes excitable tissues less excitable
Results in decreased rate & force of contraction of
cardiac muscle

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 Factors affecting heart rate
Anoxia – decrease in oxygen conc.
 Increases heart rate

Acidosis – CO2 & acid accumulation blood

 Decreases heart rate

Body temperature – increased body temp increases heart

rate
 e.g., fever, infection etc

Ions – hyperkalemia decreases heart rate

 hypercalcemia increases heart rate

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 Thyroxine – increase heart rate by increasing BMR of
SA node

Circulating catecholamines – adrenaline increase heart

rate by its positive chronotropic effect

Respiration – during inspiration heart rate increases

expiration – heart rate decreases

Marey’s law
Statement – heart rate is inversely proportional to BP

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 Mechanism
Stretch receptors are present in carotid and aortic bodies

When BP rises – these become stimulated due to stretching

& increase vagal tone

Due to parasympathetic or vagal stimulation – heart rate

decreases

When BP falls – no inhibition of impulses occur & heart rate

rises back to normal

Marey’s law – also called as “sinoaortic reflex”

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 Nerve supply of heart
Heart - innervated by sympathetic & parasympathetic
fibers of ANS
 via cardiac plexuses situated below arch of aorta

Sympathetic supply arises from cervical & upper thoracic

portions of sympathetic trunks &
Parasympathetic supply comes from vagus nerves

Activation of these nerves results in;

 cardiac acceleration, increased force of contraction &
dilatation of coronary arteries

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 Postganglionic parasympathetic fibers terminate on SA &
AV nodes

Activation of parasympathetic nerves results in;

 reduction in rate & force of contraction

Afferent fibers running with sympathetic nerves carry

nervous impulses that normally do not reach
consciousness

However, if blood supply to myocardium become

impaired;
 pain impulses reach consciousness via this pathway

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 Blood pressure
Perpendicular pressure exerted by blood on walls of blood vessels
as it passes through it
Systolic pressure – maximum pressure during systolic phase
 Normal value – 120 mmHg
Diastolic pressure – minimum pressure during diastolic phase
 Normal value – 80 mmHg

Mean arterial pressure

 Average pressure tending to push blood through systemic circulation
 Nearer to diastolic pressure i.e., usually 96 mmHg, but often taken as
100 mmHg
Mean arterial pressure = cardiac output x total peripheral resistance

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 Marey’s law
 In resting state – heart rate is inversely proportional to blood
pressure
 This law fails during muscular exercise

Regulation of arterial pressure

 3 main mechanisms – depending upon duration of effectiveness
1. Rapid acting mechanisms
2. Intermediately acting mechanisms
3. Long term mechanisms

1. Rapid acting mechanisms

 Includes
A. Nervous regulation
B. Humoral regulation

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 A. Nervous regulation
 Regulated by vasomotor system of brain
 Located bilaterally in reticular formation of medulla & lower
1/3rd of pons

 Composed of certain important areas as follows;

 Vasoconstrictor area C-1: Causes rise in BP
 Vasodilator area A-1: Tends to decrease BP
 Sensory area A-2: Acts as sensory center for both areas C-1 &
A-1

 Afferent connections of these areas include;

I. Baroreceptors
II. Chemoreceptors
III. CNS ischemic response

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 I. Baroreceptors
Non-capsulated nerve endings, that are stimulated when
stretched
Location; Carotid sinus, Aortic arch, Wall of atrium,
Wall of left ventricle, Pulmonary trunk & its divisions
Innervation
Carotid sinus is supplied by glossopharyngeal nerve
All other receptors are supplied by vagus nerves
Stimulation
Not stimulated at all by pressure b/w 0 & 60 mmHg
But above 60 mmHg – they respond more and more &
reach max stimulation at 180 mmHg

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  Baroreceptor reflex
 Increase in BP – stretches baroreceptors in carotid sinus &
aortic arch
 Impulses from;
 carotid sinus are transmitted through glassopharyngeal nerve &
 aortic arch through vagus nerve to vasomotor center

 If these receptors are stimulated by increase of BP, then

they cause;
 Vasodilatation
 Decreases heart rate

 If these receptors are stimulated due to fall in BP – then

opposite results are produced

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  Buffer function of baroreceptors
 b/c baroreceptor system opposes either increase or decrease in
BP
 It is often called as pressure buffer system
 Nerves from barorectors are called – buffer nerves

II. Chemoreceptors
 Specialized nerve endings
 Location; Aortic bodies, Carotid bodies
 Innervation; Innervated by same nerves as those of baroreceptors
 Stimulation;
 They are chemosensitive i.e., stimulated by decreased O 2,
increased CO2 & increased H+ conc. due to decrease in BP
 They do not respond strongly until arterial BP falls below 80
mmHg
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 Chemoreceptor reflex
Whenever blood flow to chemoreceptor falls too low;
 they become excited
 impulses are transmitted through glassopharyngeal & vagus nerve
to vasoconstrictor area
As a result vasonconstriction occurs which elevates
arterial pressure back to normal

III. CNS ischemic response

When blood flow to vasomotor center decrease – result in
cerebral ischemia
Neurons in vasomotor center are strongly excited due to
ischemia;
 causing systemic BP to rise to normal

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 B. Humoral regulation
3 hormones – provide rapid regulation of BP i.e.,
I. Adrenaline & noradrenaline
II. Renin angiotensin
III. Vasopressin

I. Adrenaline & noradrenaline

When SNS stimulated – adrenaline & noradrenaline
secreted
These hormones on entering circulation causes
vasoconstriction
Increase heart rate

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 II. Renin angiotensin
Angiotensin II – most potent vasoconstrictor
Its release & action is given;

Low BP

Ischemia of kidney

Renin secretion

Renin substrate  angiotensin I

Angiotensin I  angiotensin II

Vasoconstriction

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52 Rises BP (to normal)
 III. Vasopressin
When low blood volume is reason for fall in BP
Then hypothalamus secretes large amount of ADH
ADH – responsible for water retention, vasoconstriction
& elevating BP back to normal value

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 2. Intermediately acting mechanisms
These mechanisms become activated within 1 st two
minutes of fall in BP
Becomes fully activated within 1 hour
Include;
Capillary fluid shift mechanism
Stress relaxation

Capillary fluid shift mechanism

Increase in BP – loss of fluid into interstitial spaces
Blood volume falls – causes return of BP back to normal

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 Stress relaxation
Due to natural elasticity, blood vessels are capable of
adapting new sizes according to blood volume present in
them
Helps them to prevent rapid changes in BP

3. Long term mechanism

Include;

Renal body fluid mechanism

When body contains too much ECF – BP rises
Increased BP has direct effect on kidneys to excrete
excess ECF
Thus returning pressure back to normal
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 HYPERTENSION
When arterial pressure is greater than upper range of
accepted normal limit
Hypertension limits are;
Mean BP – greater then 110 mmHg
Systolic BP – greater than 135-140 mmHg
Diastolic BP – greater than 90 mmHg

Major effects of hypertension

Excessive work load on heart may lead to various
diseases;
such as heart failure, coronary heart disease etc
High BP may rupture major blood vessel in brain
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 Very high BP causes multiple hemorrhages in kidneys
High BP causes derangements in eyes

Types of hypertension

a. Volume loading hypertension

Results from increased accumulation of salt & water in
body
Causes
Increased aldosterone secretion by kidney
Decreased functional capacity of kidneys

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 b. Renal hypertension
Results from over-secretion of vasoconstrictor
substances from kidneys
 such as angiotensin II, epinephrine, norepinephrine
Causes
Phenochromocytoma (i.e., a tumor which secretes
epinephrine & norepinephrine)
Renin secreting tumors

c. Goldblatt hypertension
When one kidney is removed
Then immediate result (in form of hypertension) –
termed as One-kidney goldblatt hypertension

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 d. Hypertension in toxemia of pregnancy
Occurs during pregnancy – due to thickening of
glomerular membrane
This reduces rate of fluid filtration from glomeruli into
renal tubules
Leading to volume overload & hypertension

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 e. Neurogenic hypertension
 Results from strong stimulation of SNS
 e.g.,when a person becomes excited or anxious,
sympathetic system becomes excessively stimulated
 And acute hypertension occurs

f. Essential hypertension
 Hypertension of unknown origin

 Characterized by;
 Raised mean arterial pressure
 Reduced renal blood flow
 Increased resistance to blood flow in kidneys

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  Normal glomerular filtration rate
 Normal cardiac output
 Increased total peripheral resistance
 Reduced ability of kidneys to secrete salt & water

HYPOTENSION
Blood pressure below normal value
 Systolic BP – below 90 mmHg
 Diastolic BP – below 60 mmHg

Causes
 Hypovolumic shock
 Anaphylactic shock
 Nerogenic shock

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 Electrocardiography (ECG)
Graphic recording of changes in electrical potential
generated by transmission of depolarization wave (cardiac
impulse) through heart

Transthoracic interpretation of electrical activity of

heart over a period of time
 detected by electrodes attached to surface of skin and recorded
by a device external to body
 recording produced – electrocardiogram

ECG is used to measure heart’s electrical conduction system

 picks up electrical impulses generated by polarization and
depolarization of cardiac tissue and translates into a waveform
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 Uses of ECG
With the help of ECG we can detect
Heart rate
Heart rhythm
Site of pacemaker
Site & type of heart disease
Effects of electrolytes & drugs

Components of ECG
ECG waves
Intervals b/w ECG waves

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 ECG waves
P wave ------------------- Depolarization
QRS complex ----------- waves
T wave ------------------- Repolarization wave

P wave
Caused by electrical potentials generated by atrial
depolarization or contractions
Represents – passage of impulse from SA node over
atria
Impulse reaches AV node about middle of P wave

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 Significance – normal P wave indicates;
 SA node is acting as pacemaker
 Impulses travel in a normal direction
 No ectopic focus
 Voltage of P wave indicate mass of atrial muscle

QRS complex
Caused by potentials generated by ventricular repolarization
Represents – spread of impulse through ventricles
Consists of;
 Q wave – small downward reflection
 R wave – large upward deflection
 S wave – sharp downward deflection

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 Significance – indicates ventricular muscle mass,
strength of contraction, duration of contraction

T wave
Caused by electrical potential generated by ventricular
repolarization
Significance – helps in assessing ventricular
repolarization defects such as;
Ischemic heart disease causes inverted T wave
High & peaked T wave in hyperkalemia

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 Intervals of ECG
P-R or P-Q interval
Duration of time b/w beginning of P wave &
beginning of QRS wave
Represents – interval b/w beginning of contraction of
atrium & beginning of contraction of ventricle
Duration – approx – 0.35 sec

Total duration of one ECG

Time period from one heart beat to other
Duration – approx; 0.83 sec

68 Imran Rabbani
 Electrocardiographic leads
Electrode system that picks up electrical potential from
surface of body to ECG machine
Types of leads
 Bipolar limb leads
 Chest leads
 Augmented unipolar limb leads

 Bipolar limb leads

Uses specific electrodes connected to limbs
 Lead I
 Positive terminal is attached to left arm
 Negative terminal is attached to right arm

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 Lead II
Positive terminal is attached to left leg
Negative terminal is attached to right arm
Lead III
Positive terminal is attached to left leg
Negative terminal is attached to left arm

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 Chest leads
Electrode placed on anterior surface of chest over heart at
one of six specific separate points
While negative electrode is simultaneously attached to right
arm, left arm and left leg
Position of chest leads
 Lead V1 = in 4th intercostal space 2 cm to right of right sternal
border
 Lead V2 = in 4th intgercostal space 2 cm to left of left sternal
border
 Lead V3 = lies in b/w V2 & V4
 Lead V4 = in 5th intercostal space
 Lead V5 = intercostal space at left anterior axillary line
 Lead V6 = in 5th intercostal space at left mid axillary line

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 Augmented unipolar leads
2 of limbs are connected to negative terminals
while 3rd limb is connected to positive terminal of ECG
machine
Gives following combinations
VR lead
When positive terminal is connected to right arm
VL lead
When positive terminal is connected to left arm
VF lead
When positive terminal is connected to left leg

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 Eithonven’s triangle
Triangle drawn around area of heart
Upper base of triangle represent plane at which 2 arms
connect electrically with fluids around heart
Lower apex of triangle is point at which left leg
connects with fluids

Einthoven’s law
Sum of voltages in lead I & III equals to voltage in
lead II
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 ECG abnormalities
P wave abnormalities
Inverted P wave – when pacemaker shifts from SA
node to AV node
Absent P wave – seen in atrial fibrillation
P pulmonale – tall & peaked P wave seen in right atrial
hypertrophy

QRS complex abnormalities

Prolonged QRS complex – caused by hypertrophy or
dilatation of left or right ventricle

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 High voltage QRS – caused by right & left ventricular
hypertrophy
Bizarre QRS complex – caused by destruction of
cardiac tissue & its replacement by scar tissue

T wave abnormalities
Inverted T wave – seen in myocardial ischemia
Tall T wave – feature of hyperkalemia

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 Coronary circulation
Main coronary arteries arise from aorta & are;
Left coronary artery – supplies mainly anterior &
lateral portions of left ventricle
Right coronary artery – supplies most of right
ventricle & posterior part of left ventricles

Normal coronary blood flow

Resting coronary blood flow in human averages
approx. 225 ml/min
which is 4-5% of total cardiac output

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 Control of coronary blood flow
Controlled by;
Local control
Nervous control

Local control
Blood flow through coronary system is regulated by
vascular response to local needs of cardiac
musculature for nutrition & oxygen
Decrease in oxygen conc. in heart – causes vasodilator
substances to be released from muscle cell
which dilates arterioles to increase coronary blood flow

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 Nervous control
Stimulation of autonomic nerves of heart can effect coronary
blood flow in two ways
 Direct effects
 Indirect effects

Direct effects
Result from release of acetylcholine from vagus &
norepinephrine from sympathetic nerves, which act on
coronary vessels
Indirect effects
More important in normal control of blood flow
Result from secondary changes in coronary blood flow
caused by increased or decreased activity of heart
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 Pulmonary circulation
Pulmonary trunk – divided into;
 Right pulmonary artery
 Left pulmonary artery

These further subdivided into;

 Terminal branches
 Muscular arteries

Pulmonary arterioles
 Contain only thin rim of muscle
 Divided to form capillaries
 Pulmonary capillaries
 Network of pulmonary capillaries surround alveoli

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 Pulmonary venules & veins
 Receive oxygenated blood from capillaries
 Join to form 4 major veins which finally open in left atrium

At rest 1L of blood is contained in thorax, of which;

 400 ml is in heart
 600 ml is in pulmonary circuit

Pulmonary blood volume is higher in recumbent

position
 During standing, it decreases
 Pulmonary arterial pressure – much less than systemic
artery pressure, i.e., 10-15 mmHg

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 Distensible low pressure system
 Pulmonary artery is very distensible b/c of low pulse
pressure
 Therefore during mild to moderate exercise, cardiac output
increases without much increase in pulmonary artery
pressure
 Thus pulmonary vascular system is called as distensible low
pressure system

Pulsatile flow
 Pulmonary capillary flow through lungs is pulsatile at rest;
i.e.,
 During systole flow reaches above 10 L/min
 During diastole flow falls to 2-3 L/min

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 Pulmonary vascular reflexes
Stimulation of baroreceptor – causes reflex dilatation of
pulmonary vessels
Stimulation of chemoreceptor – via sympathetic nerves
causes reflex pulmonary vasoconstriction

Functions of pulmonary circulation

Reservoir for left ventricle – if LV output becomes
greater than systemic venous return
LV output can be maintained for few strokes by drawing
out blood stored in pulmonary circulation

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 Acts as filter – particles filtered include;
Small fibrin clots, fat cells, cancer cells, gas bubbles,
agglutinated RBC’s, masses of platelets or WBC’s
Fluid exchange & drug absorption – low pulmonary
pressure tends to pull fluid from alveoli into
pulmonary capillaries
So drugs administered by inhalation like anesthetics,
bronchodilators

83 Imran Rabbani
 Skin circulation
Skin weighs about 2 kg in adult
Skin blood flow depends upon;
Requirements of body temperature maintenance
Metabolic activity of skin

Average skin flow in comfortable environmental temp.

of approx. 27˚ C = 10-15ml/100gm per min
during cold, flow decreases to 1 ml/100gm per min
during heat, flow increases to 150 ml/100gm per min

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 Regional variations in skin blood flow
Skin vessels are normally under influence of low
sympathetic discharge;
which effectively limits flow through them
but it is not true for skin of hands & feet

Vascular circuit of skin in hands, feet & ear lobes

shows numerous AV anastomoses
which are much less frequent in rest of body skin

AV anastomoses – richly innervated by sympathetic

vasoconstrictor activity and are closed

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 During heat stress – hands & feet skin flow increases
(70-80 ml/100gm per min)
whereas skin which has less AV anastomoses, flow
increases to only 25-30 ml/100gm per min
under heat stress or sympathetic blockade

Nervous control of skin circulation

Skin vessels are not innervated by vasodilator nerves
Vasodilatation is due to;
Reduction of vasoconstrictor impulse activity
Local production of bradykinin in sweat glands
Local vasodilator metabolites

86 Imran Rabbani
 Control of vasoconstrictor activity to skin blood
vessels is modified from;
Hypothalamus in response to temperature changes
Stimulation of lateral spinothalamic tract by temperature
receptors in skin

As heat load rises gradually;

AV anatomoses of hands, ear & feet dilate due to
reduction of their regional sympathetic discharge
Remainder of skin vessels dilate due to progressive
withdrawal of sympathetic vasoconstrictor activity

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 Sweat glands are activated due to bradykinin released
from sympathetic discharge
 This helps to restore thermal equilibrium
 Also causes vasodilatation of skin

Cold blue skin – is one in which arterioles are

constricted & capillaries dilated
Warm red skin – is one in which both arterioles &
capillaries are dilated

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 Capillary circulation
At a time, only 5% of circulating blood is in capillaries
Allows continuous exchange of O2, CO2, nutrients &
waste products

Transcapillary exchange – essential for survival

It is three types;
1. Filtration-absorption
2. Diffusion
3. Micropinocytosis

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 1. Filtration-absorption
Maintains blood volume constant
Rate of filtration at any point depends upon balance b/w forces
– starling forces

Starling forces are;

Hydrostatic pressure – exerted across capillary wall
Called capillary pressure
Favors filtration through pores

Colloidal osmotic pressure – due to plasma proteins

Favors absorption of interstitial fluid through pores
Normally it is 25 mmHg

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 Hydrostatic pressure in interstitial fluid – does not
vary much in most tissues & 2-3 mmHg
Interstitial fluid contains some proteins
Exert osmotic pressure from outside

Diffusion
Responsible for supply of nutrients, waste removal,
gaseous exchange
Factors affecting diffusion across capillary wall
Lipid solubility
Lipid soluble substances (O2 & CO2) diffuse with
ease
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 Size of substance
Permeability of capillary wall to substance falls rapidly due
to increase in MW
Velocity of blood flow
If decreases – diffusion decreases
If increases – diffusion decreases

Micropinocytosis
Very slow process
Provides an active transport for macromolecules against
conc. gradient from blood to tissues through intercellular
pores
e.g., gamma-globulin, immunological proteins

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 Two types of pore system exist in capillary wall

Large pores – more than 4.5 nm, accounts for process

of micropinocytosis
Small pores – 3-4.5 nm, accounts for diffusion process

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 Circulatory changes during
exercise
Three major effects occur during exercise that are
necessary to meet excessive blood demand required by
muscles
1. Mass sympathetic discharge
2. Increase in arterial pressure
3. Increase in cardiac output

1. Mass sympathetic discharge

At onset of exercise signals are transmitted from brain
into vasomotor center to initiate mass sympathetic
discharge
94  SoRabbani
Imran major circulatory effects occur such as;
 Increased heart ability
Heart is stimulated to great increased heart rate &
pumping strength
due to sympathetic stimulation & parasympathetic
inhibition

Increased venous return

Most of arterioles of peripheral circulation are strongly
contracted
Except arterioles of active muscles – strongly
vasodilated by local vasodilator effects
This increases venous return

95 Imran Rabbani
 2. Increase in arterial pressure
Results from;
Vasoconstriction of arterioles & small arteries in most
of tissues except active muscles
Increased pumping activity of heart
Great increase in mean circulatory filling pressure
caused mainly by venous contraction

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 3. Increase in cardiac output
Essential to supply large amounts and other nutrients
needed by working muscle
May be up to 30 liters/min as in athletes
with oxygen intake of 4 lit/min
Increase in cardiac output is due to increase in stroke
volume output & heart rate
Cardiac output = stroke volume output x heart rate

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 Axon reflex
Normally afferent impulses in sensory nerve from skin
are conducted in orthodromic fashion to reach spinal
cord
called orthrodomic conduction

However, if firm stroke applied across skin;

afferent impulses are relayed down the branches of
sensory nerve to endings near cutaneous arterioles
called antidromic conduction
where it releases vasodilator substance – cause long
lasting cutaneous arteriolar dilatation

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 Local neural mechanism & does not involve CNS
connections
Therefore called as axon reflex
Responsible for redness spreading out from injury site

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 Triple response
Three part response of normal reaction to injury
e.g. a firm stroke across skin by blunt pointed object –
evokes series of reactions;

Red reaction or red line – reddening at site, that

appears in approx 10 sec
Dilatation of pre-capillary sphincters directly
It is due to;
Release of histamine and/or
Polypeptides e.g. bradykinin

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 Flare – redness spreading out from injury
Due to dilatation of;
 Arterioles
 Terminal arterioles
 Pre-capillary sphincters
Characterized by raised skin temp of the area

Wheal – local diffuse swelling

If stroke of stimulus has been strong enough – a blister
like appearance develops
This is due to;
 Increased capillary permeability produced by histamine
 Rise of capillary pressure due to dilatation of pre-capillary
resistance vessels
101 Imran Rabbani
 Lymph (Lymphatic system)
Lymphatics at periphery – closed system of tubes
Walls formed of single layer of cells
Lymph vessels contain valves & regularly transverse lymph
nodes along their course

All lymph from body is collected in 2 big channels

 Right lymphatic duct – which opens into right sub-clavian vein
 Thoracic duct – which opens into left sub-clavian vein

Lymphatic system exist in all organs except CNS & cornea

102 Imran Rabbani

 Composition of lymph
Modified tissue fluid, transparent, yellowish, faintly
alkaline, clots slowly
Protein – content varies with different tissue;
But slightly less than that of plasma
Lipids – more in intestinal region & less in thoracic
duct;
b/c intestinal villi absorb & transport lipids
Lipoprotein absorption from GIT – responsible for milky
color to lymph, called chyle
Carbohydrates – less than plasma conc.

103 Imran Rabbani

 Coagulation factors – more in liver lymph b/c they are
formed in liver
In vitro, lymph clots b/c of clotting factors

Cellular components
Contain large number of lymphocytes
No granulocytes (rarely monocytes & macrophages)
Few RBCs & platelets

Formation of lymph
Lymph formed from tissue fluids
Formation based on transcapillary exchange

104 Imran Rabbani

 Functions of lymph
1. Transport of proteins

2. Transport of absorbed long chain fatty acids & cholesterol

3. Transport of RBCs, WBCs & bacteria to regional lymph

nodes

4. Transport of antibiotics

5. Some substance like histamine & lipase reach circulation

by lymphatics mainly after their secretion from cells into
interstitial fluid

105 Imran Rabbani

 7. Enhances efficiency of immune system by theses
mechanisms;
it transports antigen to organ of immune system
continual movement of lymphocytes exposes antigen to
large number of lymphocytes which specifically react
with it
disperses memory lymphocytes for second encounter
with antigen

106 Imran Rabbani

 Circulatory shock
Generalized insufficiency of blood flow throughout
body to extent that tissues are damaged;
b/c of too little flow, oxygen & nutrients

Causes
Due to decreased cardiac output
Without decreased cardiac output

Shock due to decreased cardiac output

Two types of factors that reduce cardiac output are;

107 Imran Rabbani

 Cardiac abnormalities that decrease ability of heart to
pump blood;
e.g. myocardial infarction, valvular heart diseases,
arrhythmias
Factors that decrease venous return
e.g. diminished blood volume, decreased vasomotor
tone, obstruction of blood flow

Shock without decreased cardiac output

This can result from;
Excessive metabolism of body
Abnormal tissue perfusion pattern such that cardiac
output is normal but still not supplying local tissue with
nutrition
108 Imran Rabbani
 Stages of shock
Three major stages;
Non-progressive stage
In this stage normal circulatory compensatory
mechanism will eventually cause full recovery

Progressive stage
In this stage shock becomes worst until death

Irreversible stage
Shock has progressed to such an extent that all forms
of treatment are unable to save life of person
109 Imran Rabbani
 Types of shock
 4 types
Hypovolemic shock
Results from decreased blood volume
Causes
 Hemorrhage
 Dehydration
 Plasma loss due to burns
Mechanism
 Decreased blood volume decreases mean systemic filling
pressure
 As a result decreases venous return
 So cardiac output falls below normal & shock occurs

110 Imran Rabbani

 Neurogenic shock
Results from sudden loss of vasomotor tone
throughout body
Causing massive dilatation of veins
As a result normal volume of blood becomes incapable
of adequately filling circulatory system

Causes
Deep general anesthesia
Spinal anesthesia
Brain damage

111 Imran Rabbani

 Anaphylactic shock
Results from antigen antibody reaction & release of
histamine or histamine like substances, which cause;
 An increase in vascular capacity
 Dilatation of arteries & arterioles
 Greatly increased capillary permeability
Net result is greatly reduced venous return & serous
shock

Causes
 Penicillin sensitivity
 Mismatching blood transfusion
 Anaphylaxis

112 Imran Rabbani

 Septic shock
Due to widely spread infection of many areas of body
Infection is carried by blood from one tissue to another
causing extensive damage
Also known blood poisoning

Causes
Peritonitis
Streptococcal skin infection
Infection carried from kidneys

113 Imran Rabbani

 Effects of shock on body
Decreased metabolism & cellular deterioration
Muscular weakness
Decreased body temperature
Decreased mental functions
Reduced renal functions

Treatment of shock
Head down position
Oxygen therapy
Blood & plasma transfusion
Glucocorticoids

114 Imran Rabbani