CVS Physiology - 220505 - 061700

CVSPHYSI
OLOGY
Ac
ademi
cCirc
le
MFSURagama
OBJECTIVES
01) Electrical properties of the heart………………………………….02
02) Electrocardiography……………………………………………………..15
03) Cardiac cycle………………………………………………………………..34
04) Cardiac output……………………………………………………………..44
05) Hemodynamics…………………………………………………………….53
06) Structural features of circulation………………………………….58
07) Blood pressure……………………………………………………………..64
08) Heart sounds and murmurs………………………………………….67
09) CVS regulation………………………………………………………………75
10) Coronary circulation……………………………………………………..92
11) Cerebral circulation……………………………………………………….97
12) Splanchnic, Cutaneous and Skeletal muscle circulation.104
13) Cardiovascular changes in exercise……………………………..109
14) Shock…………………………………………………………………………..115
15) Heart failure…………………………………………………………………122
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REPEAT CAMPAIGN|2021 Batch 30 |1
01. ELECTRICAL ACTIVITY OF HEART
Structure - function relationship of cardiac muscle
Structure Function
1 Contractile proteins • Actin & myosin filaments • Engage in contractile response
• Arrange in sarcomeres
2 Arrangement of • Branching & interdigitating • Easy to spread depolarization
fibers nature (helps in mechanical syncytium)
• Lie in parallel and series with
each other
3 Intercalated discs • Multiple folds in cell • Maintain connection with
membrane adjacent cells & enable
transmission of pull along its axis
to the adjacent fiber (
Mechanical syncytium)
4 Desmosomes • Located in intercalated discs • maintain muscle physical
• formed by cadherin catenin connection during contraction
complex
5 Gap junctions • Located in intercalated discs • Enable ions to diffuse quickly
from one fiber to next by
providing low resistance bridges
for the spread of excitation
( functional / electrical
syncytium)
6 Arrange in 2 • Excitation of one cell in the • Allow ventricle to contract as a
syncytium syncytium rapidly moves to one unit & pump blood in
(Atria & ventricle) all other cells & depolarize ventricles
at the same time. • Allow ventricles to contract as a
one unit & pump blood out of
the heart
2+
7 sarcoplasmic • Internal Ca source
reticulum ( but not sufficient)
2+
8 T- tubules • Wide than in skeletal muscle • External Ca source
• At Z lines
9 Mitochondria • Numerous • Energy supplier for cardiac
muscle
10 Pacemaker cells • Cardiac muscles has the
ability to generate impulses • Generate impulses
without an external ( Heart continuous to beat even
stimulation after fully denervation
11 Conducting system • specialized conducting • Conduct impulses generated by
system SA node through out the heart
• Composed of specialized
cardiac myocytes modified
for conduction not for
contraction
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REPEAT CAMPAIGN |2021 Batch 30 |2
Electrical properties of heart
1) RMP of ventricular muscle
2) AP of ventricular muscle
3) Pacemaker cells
-SA node electrical changes
4) Conducting system
RMP of ventricular muscle

 Around -90mv
 Caused by K+ leak channels Hypokalaemia – inside the cell become more
+ +
Na - K ATPase pump negative ( difficult to depolarize)
 RMP is depend on ECF [K+] Hyperkalaemia- inside the cell become less
 Variations of [K ] in plasma affect RMP
+ negative (easy to excite)
RMP Depolarization AP Propagation of AP Contraction

via ventricular syncytium
AP of Ventricular muscle
 Cardiac muscle action potential has 5 phases.

I. Phase 0 (Rapid depolarization)
II. Phase 1 (Partial repolarization/ Initial rapid repolarization)
III. Phase 2 (Plateau phase)
IV. Phase 3 ( Final slow repolarization)
V. Phase 4 ( RMP)
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 Time duration (AP lasts about )
Cardiac muscle About 300ms

Depolarization 2ms
Repolarization 200ms or more
Skeletal muscle About 2-5 ms
Nerve cell About 1ms
 Magnitude is determined by ECF [Na+]
 Events occur in each phase
Phase Channels get opened Channels get Events

closed
Phase 0 Voltage gated Na+ Na+ influx
channels -Cause depolarization
-overshoot about 20ms
-Last about 2ms
Phase 1 Transient K+ channels Voltage gated Na+ influx decrease

Na+ channels K+ efflux
-Cause repolarization
Phase 2 Voltage gated Ca2+ Ca2+ influx

channels -cause depolarization
K+ efflux
Rectifier K+ channels -keep depolarization constant
Phase 3 Various K+ channels Voltage gated K+ efflux

Ca2+ channels -cause repolarization
Phase 4 K+ leak channels K+ diffuse out of the cell
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Mechanical properties of cardiac muscle
Excitation - contraction coupling

 AP of cardiac muscles is coupled with contraction.
AP of cardiac muscle - electrical response
Contraction of cardiac muscle - mechanical response
 Contraction begins just after start of depolarization.
 Lasts 1.5 times as long as the action potential.
Contraction Mechanism
 AP spreads inside the muscle cell via T- tubules
 Causes entry of Ca2+ from ECF to ICF. (Via DHP channels)
 Release Ca2+ from SR.
 Ca2+ binds with troponin c
 Take away tropo myosin filaments from myosin binding sites on actin.
 Myosin binds with actin.
 Initiate contraction.
• Releasing of Ca2+ from SR triggers by ECF Ca2+ entry.

Cardiac muscle needs influx of Ca2 from ECF because less stored Ca2+ in SR.
T- tubules wider in cardiac muscle than in skeletal muscle.
• When ECF [Ca2+] decrease reduce cardisac muscle contraction.
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Relaxation mechanism
 Ca2+ pump out from troponin C ( To SR / To ECF)
 This needs energy.
 Pump to SR - Use energy from Ca- ATPase pump.
 Pump to ECF - Use Na-Ca exchanger & Na- K ATPase pump.
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Why cardiac muscle doesn’t get tetanized
 Tetanization means sustained contraction without any relaxation
 But even at very high heart rates cardiac muscle doesn’t get tetanized.
 This can explain by using the refractory period concept.
Cardiac muscle action potential refractory periods
 Absolute refractory period

– The cardiac muscle cannot be excited again.
– Includes phases 0, 1, 2 & first half of phase 3
– Until the membrane potential reaches approximately 50mV
 Relative refractory period

– During the rest of phase 3 & phase 4,
– cardiac muscle remains relatively refractory.( A supra threshold
stimulus can generate an AP.
o Because of this long absolute refractory period tetanization of the

cardiac muscle does not occur.
o Because within ARP the cardiac muscle begins to relax.
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Origin of the heart beat
 Parts of the heart beat in orderly sequence
 Atrial systole (0.1 S)  Ventricular systole (0.3 S)  Diastole (0.4 S)
 During diastole all 4 chambers are relaxed (0.4 S)
 Heart beat originates in specialized cardiac conduction system, which spreads via this
system to all parts of myocardium.
The cardiac conduction system
 Capable of spontaneous discharge.

 Made up of:
1) Sino atrial node (SA node)
2) Inter nodal atrial pathways
3) Atrio ventricular node (AV node )
4) Bundle of his & its branches
5) Purkinje system
 Under abnormal conditions even the parts of myocardium is capable of spontaneous
discharge – LATENT PACEMAKERS.
 Cardiac conduction system composed of modified cardiac muscle fibers.
 One way transmission of impulses.
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1) SA node – the cardiac pacemaker
 Located in the right atrium at the opening of SVC.

 Contain pacemaker cells – P cells.
 Discharge most rapidly than other pacemakers.
 Depolarizes other areas before their spontaneous discharge.
 Its discharge rate determines the rate of heart beat.
 Develops from the structures on the right side of the embryo
 Innervation primarily through right vagus & sympathetic fibers on the right side.
2) Inter nodal atrial pathways
 Three bundles of atrial fibers. (anterior, middle, posterior)

 Connect the SA node to AV node.
 Impulses generated in the SA node passes through these pathways to AV node. ( fast)
(Conduction also occurs through the atrial myocytes, but it is slow.)
3) AV node
 Located at the right posterior portion of the inter-atrial septum, just above the opening
of coronary sinus.
 It is the only conduction pathway between atria & ventricles.
 Continuous with the bundle of his.
 Develops in the structures in the left side of the embryo.
 Therefore, innervation primarily through left vagus & the sympathetic fibers of the left
side.
4) His bundle
 Only connection between atria and ventricular musculature.

 Gives off left bundle branch at the top of the inter-ventricular septum.
 Then continuous as the right bundle branch.
 Left bundle branch divides into anterior & posterior fascicle.
 Branches of the fascicles runs sub endocardially on either side of the septum.
 Then continuous with the purkinje system.
5) Purkinje system
 Specialized conducting fibers.

 Found in sub-endocardium.
 Fibers spread to all parts of the ventricular myocardium.
 Connected together by desmosomes & gap junction.
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Spread of cardiac excitation
 Depolarization initiated in the SA
node.
 Spreads rapidly through the atria.
 Converges on the AV node via 3 inter
nodal atrial pathways.
 AV node conduction is slow.
 Therefore there is a delay of 0.1S
(AV nodal delay).
 Then, impulses reaches to the bundle
of his.
 Passes to the purkinje system
 Depolarizes the inter-ventricular

septum first, from left to right across
the mid portion of the septum.
 The wave of depolarization then

spread to apex down the septum
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 Depolarize the major portion of the
ventricular myocardium from
endocardium to epicardium
 Finally depolarizes the
– Posterobasal left ventricle
– Pulmonary conus
– Uppermost septum
Pacemaker potential
 Pacemaker cells discharge rhythmically & spontaneously.
 After each impulse their membrane potential declines to the firing level.
 This fires another action potential.
 This declining potential is known as Pacemaker potential or Pre potential.
 Prominent in SA & AV node.
 Can be seen in latent pacemakers also.
 However, “latent pacemakers” are present in other portions of the conduction system
that can take over when the SA and AV nodes are depressed or conduction from them is
blocked.
 Atrial and ventricular muscle fibers do not have pre-potentials, and they discharge
spontaneously only when injured or abnormal.
Electrical changes occurs in SA node
 Normal pacemaker of the heart – SA node

-Because of its highest rate of impulse generation (100/min)
-But under vagal control reduce the rate up to 70/min
 Electrical changes of SA node can describe in 3 phases.

1. Pre potential
2. Depolarization
3. Repolarization
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PRE POTENTIAL
 RMP varies -60mv to -55mv
 At -60mv funny channels (h channels) open
Influx of Na+ (& K+)
 Depolarize the membrane up to -50mv
 Complete first part of pre potential
 At -50mv T (transient) Ca2+ channels open
 Cause influx of Ca2+
 Depolarize the membrane up to -40mv ( Threshold level)
 Complete 2nd part of pre potential
DEPOLARIZATION
 At -40mv Long lasting Ca2+ channels open
 Influx of Ca2+
 Depolarize the membrane
 Triggers AP
REPOLARIZATION
 At the peak of the action potential
- Ca2+ channels close
- K+ channels open (K+ efflux )
 Results repolarization.
 K+ channels are slow to close cause hyperpolarization
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Regulation of impulse generation at SA node
 Parasympathetic nervous system regulation

• Prasympathetic innervation to SA node from R vagus.
• Ach released by vagal fibers act on muscarinic receptors (M2).
1) Increase K+ conductance.
-Hyperpolarize the membrane
-Reduce the slope of pre potential.
2) Slow Ca2+ channel opening
- frequency of the action potential is decreased.
- Results reduction heart rate.
- Negative chrono tropic action.
 DIGITALIS decreases the discharge frequency. (Treatment for heart failure & atrial
fibrillation to avoid ischemia)
 Effect of sympathetic stimulation
• Sympathetic innervation to SA node by R stellate ganglion.

• R stellate ganglion nerve fibers release noradrenaline
• Act on β1 adrenergic receptors
• Facilitate opening of L- Ca2+ channels
- Increase rate of depolarization
- Increase heart rate
- Positive chronotropic effect.
 RISE OF TEMPERATURE increases the discharge frequency. (EX: fever)
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Regulation of impulse conductance at AV node
 Effect of Parasympathetic nervous system

• By L vagus node
• Slow transmission of AP at SA node ( increase AV nodal delay)
 Effect of sympathetic nervous system

• By L stellate ganglion.
• Speed up transmission of AP at AV node. ( decrease AV nodal
delay/ shorten refractory time)
chronotropic action & inotropic action
 chronotropic – about action of heart rate

– Positive chronotropic – increase heart rate
(EX: rise of temperature, sympathetic stimulation via β1 receptors)
– Negative chronotropic – decrease heart rate

(EX: digitalis action, parasympathetic vagal stimulation via M2 receptors)
 Inotropic – about force of contraction of heart

– Positive inotropic action – the force of contraction is increased by
catecholamines (Adrenalin & noradrenalin), mediated via β1 receptors
– Negative inotropic action – reduction of force of contraction.
SEQ
1) Briefly describe the ventricular myocardial action potential and the electrical basis of the
each phase (35 marks) (25th R /23rd R )
2) Briefly describe the effect of atropine on the potential of the sinoatrial node(15 marks)
(23rd R/29th P)
3) Draw a diagram of the electrical activity of the sinoatrial node indicating the ions and
channels involved in its activity (10 marks) (29th P)
4) Describe the spread of cardiac excitation (15 marks) (29th P)
5) List the sequences of depolarization of the heart (10 marks) (29 th P)
6) Outline using a diagram, the reason why cardiac muscle does not tetanize (20 marks) (29th P)
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2.) ELECTROCARDIOGRAM (ECG)
 The electrical activity of heart can be recorded from the body surface.
– The body fluid contains ions
– Therefore it is a volume conductor
 The surface electrode

– Records algebraic sum of the electrical fluctuations of the heart muscle fibers.
 The record of these potential fluctuations during a cardiac cycle is the ECG.
 The surface electrodes are known as ECG leads.
1) Bipolar lead
– Both the electrodes are actively recording.
2) Unipolar lead
– Active electrode is connected to an indifferent electrode at zero point.
Einthoven’s triangle
– A triangle with a heart at its center.
– The sum of the potential at the points of this equilateral triangle is zero.
 Can be formed by
– Placing electrodes on the both arms & the left leg.
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 Depolarization moving towards an active electrode records a positive deflection.

--ᴖ--
Depolarization moving away from an active electrode records a negative deflection.

--ᴗ--
No potential difference between leads records a flat line.
 Repolarization moving towards an active electrode records a negative deflection.
 Repolarization moving away from an active electrode records a positive deflection.
ECG leads
1.) Bipolar leads – both leads are actively recording.
 Standard limb leads – records potential difference between 2 arms.

– Lead I – L I
– Lead II – L II
– Lead III – L III
2.) Unipolar leads (V leads) – one active lead recording the potential while it is
connected to an indifferent electrode at zero potential.
i. 3 unipolar limb leads.

ii. 6 unipolar chest leads.
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i. 3 unipolar limb leads.
 They are augmented (amplified) unipolar limb leads.

 Designated by ‘’a’’.
 Records between one limb & two other limbs.
 Increases the size of the potential by 50% without changing the configuration of the
non-augmented lead.
– aVR
– aVL
– aVF
ii. 6 unipolar chest leads – V1 to V6
Fixing of ECG leads - +

RA Lead I LA
 Standard limb leads :( Bipolar limb leads ) – I / II / III
– Lead I [left arm (+ve) – right arm (-ve)]
– Lead II [right arm (-ve) – left leg (+ve)]
– Lead III [left leg (+ve) – left arm (-ve)]
 Unipolar limb leads: ( Augmented leads )

– aVR [ right arm (+ve) ] LL
– aVL [ left arm (+ve) ]
– aVF [ left leg (+ve) ]
 Limb leads look at the

heart at a vertical
plane.
 Chest leads look at the

heart at a horizontal
plane.
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 Unipolar chest leads:
 V1 – 4th intercostal space just to the right of sternum

 V2 – 4th intercostal space just left to the sternum
 V3 – halfway between V2 & V4
 V4 – left 5th intercostal space in the mid-clavicular line
 V5 – on same horizontal line as V4 in anterior axillary line
 V6 – on same horizontal line as V4 in the mid axillary line
ECG paper
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 A paper with a grid.
 Has small & large squares.
 Small Square is of 1mm × 1mm size.
 Five small squares make a one large square.
 Horizontal axis records the time scale.
 Vertical axis records the voltage.
Paper speed of the machine

 Standard speed is 25mm/s (5 large squares)
 One large square = 1/5 = 0.2 s
 One small square = 1/25 = 0.04 s
Calculate the number of large & small squares for a minute?
Voltage
 Record on the vertical axis
 Standard ECG 1mv is shown by 10mm (2 large squares )
Normal ECG
 P wave : atrial depolarization

 QRS complex : ventricular depolarization ( & atrial repolarization)
Less than or equal 0.11s
 T wave : ventricular repolarization
 U wave : upward deflection after T wave
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ECG wave
 ECG wave forms named from letters P/Q/R/S/T/U.
1) P wave:
– Is the 1st wave in an ECG.
– Produced by atrial depolarization.
2) Q wave:
– First negative deflection after p.
– Produce by septal depolarization.
3) R wave:
– First positive wave after P.
– Produce by rest of the ventricular depolarization.
3) S wave:
– Negative wave after R.
4) T wave:
– Produced by part of the ventricular repolarization.
5) U wave:
– Inconstant finding.
– Due to slow repolarization of papillary muscles.
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Durations & intervals
0.12 – 0.22 s
0.08 – 0.10 s
 PR interval – (0.12 – 0.22 s) / (3 – 5 small squares in ECG paper)

– Beginning of the P to beginning of QRS.
– Atrial depolarization & AV node conduction occurs during this time.
– Includes AV nodal delay (0.1 s)
 QRS duration- (0.08 – 0.10 s)

– Ventricular depolarization
– Atrial repolarization is hidden in QRS complex
 ST segment & T wave

– Whole ventricular repolarization
 ST segment
– From end of QRS to beginning of T wave
 QT Interval (0.4- 0.43 s)
– Beginning of Q wave to end of T wave
Configuration of ECG wave pattern
 Depends on
– Sequential electrical activity of heart.
– Position of the electrodes relative to the heart
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1) aVR lead
R R’
 aVR lead looks at the cavities of the heart.

 All the electrical activities are moving away from the lead, except septal depolarization.
 Therefore all the wave forms are negative deflections except septum.
 Results small R wave.
2) Right sided V1 lead & V2 lead
 There is no Q wave.
 As septum depolarizes from left to right.
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3) Left sided V4, V5, V6 & aVL leads
 Small Q wave due to septal depolarization.
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Calculation of the heart rate from ECG
 In ECG paper
– 1 second = 5 large squares
– One minute = 5 × 60 = 300 large squares / 1500 small squares
(Heart rate = number of QRS complex for 1 minute)
Heart rate = 300 / number of large squares between consecutive R waves (large
squares in R-R interval)
Heart rate = 1500 / number of small squares between consecutive R waves

(small squares in R-R interval)
Cardiac arrhythmias
 Normal cardiac rhythm originates in SA node
– Known as normal sinus rhythm (NSR)
– Rate about = 70/min
– Normal range = 60-100/min
Sinus arrhythmia
– Variations of heart rate during phases of respiration

– Normal phenomenon – commonly seen in young, rarely seen in old age
– Heart rate increases in inspiration & heart rate decreases in expiration
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Mechanism of sinus arrhythmia
Normal phenomenon due to fluctuations of parasympathetic output to the heart
During inspiration  expands the lungs  stretch receptors in the lung parenchyma
 impulses from vagal afferent RVLM (Rostral ventral - lateral medulla) increase
sympathetic discharge to the heart  increase HR
Sinus bradycardia
– Heart rate less than 60/min.
EX: Hypothermia, Heart failure, Jaundice, Athlete, Myxedema (hypothyroidism),Increased ICP,

Sleep, β blockers, Organophosphate poisoning, Ca2+ blockers.
Sinus tachycardia
– Heart rate more then 100/min.
EX: Hyperthermia, Hyperthyroidism (thyrotoxicosis), Exercise, Fever, Fear, Pain, Anemia.
Clinical: sick sinus syndrome

– Usually know as bradycardia-tachycardia syndrome
– Uncommon
– Seen in people older than 50 years
– Scar like degeneration of heart’s conducting system
– In young children common cause is, heart surgeries in upper chambers
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Heart blocks (atrio-ventricular blocks)
type Cause Atrio-ventricular ECG findings
conduction
1st degree heart block Incomplete - Conduction - PR interval > 0.22s
damage to the between atria and but regular
inter-nodal atrial ventricles is slowed, - RR Interval regular
pathways but not completely - All P waves are
(incomplete heart interrupted. followed by QRS
block) - So all the atria complexes
impulses reach the
ventricles.
2nd degree heart block Incomplete - Some impulses are - Dropped beats
damage to the AV conducted, some - Progressively
node or bundle of are not. (Not all the prolonged PR
his atrial impulses interval
(Incomplete heart reach the ventricles) - PR intervals and
block) - Depending on RR intervals are
atrial rate, every irregular.
2:1/ 3:1 P waves
are conducted to
ventricles.
3rd degree heart block Damage to His - Conduction from - Only a few QRS
bundle/ block at atria to ventricle is complexes per lead
AV node or below completely - Regular RR
it. interrupted. intervals
Eg-: - Ventricles beat - Ever changing PR
- Septal independently from intervals
myocardial atria (idioventricular
infarction. rate) at a low rate
- Damage to His on their own
bundle during generated by latent
surgical correction pacemakers.
of congenital IV - Latent pacemakers
septal defect have their average
rate of 35/ min.
Resulting cerebral
ischemia, cause
fainting attacks/
syncope (stroke,
Adams syndrome)
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Atrial arrhythmias
 Atrial flutter
– Most common form of arrhythmia

– The atrial discharge rapidly
– The atrial rate is 200-350/min
– AV node cannot conduct more than 300/min (Ganong -230/min )
– Therefore associated with 2:1 or greater AV block
 ECG findings:
– Rapid atrial rate
– P Waves produces a characteristics saw-tooth pattern of flutter waves
– R waves occur at regular intervals
– So, pulse is regular
Fibrillation = rapid, irregular, unsynchronized, contraction of the muscle fibers of the

heart.
 Atrial fibrillation
– Atria depolarization occurs at very rapid rate
– In complete irregular & disorganized fashion
– Rate 300-500/min.
– AV node discharges at irregular intervals
– Ventricles depolarize at completely irregular rate (no electrical syncytium)
– Ventricular contractions become irregular
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 ECG findings:
– P waves are not seen – replaced by fine irregular fibrilatory waves
– R waves occur completely irregular
– QRS complexes become irregular
– Pulse become irregularly irregular
 Atrial ectopic beats
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Ventricular arrhythmias
 Ventricular tachycardia
– Series of rapid ventricular depolarization

– Ventricular rate is regular
– So, pulse is regular
– Results, reduction of cardiac output (because no adequate time to fill the blood to the
ventricles)
– If sustained causes abnormalities in circulation
 ECG findings
– Wide QRS complex
 Ventricular fibrillation
– A life threatening condition

– An occasional complication of ventricular tachycardia
– Most frequent cause of sudden death of patients with myocardial infarction
– Need immediate correction with defibrillation
– Ventricles depolarize & contract in a totally irregular, disorganized & ineffective way.
– Contracts like a “Bag of worms”
– Cardiac output drop to zero
– Pulse is not palpable.
– ECG completely irregular complexes.
 ECG findings
– Completely irregular complexes
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Myocardial infarction
Interuption of blood supply
Causes death of cardiac muscle
Electrical changes in dead/ dying

cardiac muscle occur in sequence
Causes ECG changes - ST elevation

T inversion
deep / pathological Q waves
 Acute myocardial infarction

 ECG changes:
After After Hours After Days After Weeks (several days)
Minutes
ST elevation ST elevation Normalized ST
T inversion T inversion Normalized T
Deep Q Deep Q Deep Q
ST elevation:
 Right coronary artery inferior branch MI

– II / III / aVF
 Anterior descending branch of left coronary artery

– V1/ V2/ V3/ V4/ V5
 Circumflex branch of left coronary artery

– / V5 / V6 / aVL
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Acute inferior myocardial infarction
Acute anterior myocardial infarction
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Hypertrophy of cardiac muscle
Right atrial - Tall P waves
Left atrial – Bifid P waves
Ventricular - Tall R waves
Metabolic effects
Normal [k+] = 4.5 mol/dl
Remove K+ mainly by kidney
 Hyperkalemia
– Rise in K+ results tall peaked T waves.
– In kidney failures.
 Hypokalemia pnemonic (No pot, No Tea )

– Low K+ results inverted or flat T waves with prominent U waves
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SEQ
*30th batch*
2.) A 40 years old man is brought to an emergency treatment unit with a history of severe
retrosternal chest pain of 1 hour duration. His ECG is shown below.
He is diagnosed to have an acute myocardial infarction and given antiplatelets and

thrombolytic (human recombinant tissue plasminogen activator) treatment.
2.1 List two abnormalities seen in his ECG. (5 marks)

2.2 What coronary artery is most likely affected? (5 marks)
2.3 With the help of a diagram, briefly describe the regulation of the normal blood flow in the
artery mentioned in 2.2 (20 marks)
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3.) CARDIAC CYCLE
You need to know?
 Orderly depolarization wave results a contraction wave in the myocardium (excitation-

contraction coupling)
 Excitation-contraction coupling
– Results contractile response
– Begins just after the start of depolarization.
 Contraction of the chambers – systole (contraction)

 Relaxation of the chambers – diastole (relaxation)
 Atrial systole starts just after the P wave

 Ventricular systole starts near the end of the R wave & ends just after the T wave
 Contraction produces
– Sequential changes in pressures & flows blood in heart chambers & vessels.
 Blood pressures
– Systolic pressures – highest pressure during systole in aorta
– Diastolic pressures – lowest pressure during diastole in aorta
Mechanical events of cardiac cycle
 Phases
1) Late diastole – 0.36 s
2) Atrial systole – 0.1 s
3) Ventricular systole – 0.3 s
4) Early diastole – 0.04 s
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1) Late diastole
 Mitral & the tricuspid valves are opened.

 Aortic & the pulmonary valves are closed.
 Blood flows into the heart throughout diastole.
 Filling of atria & the ventricles.
 The rate of filling declines as the ventricles become distended.
 The cusps of the mitral & tricuspid valves drift toward the closed position.
 The pressure in the ventricles remains low.
2) Atrial systole
 Contraction of the atria propels additional blood (30%) into the ventricles
 But 70% of the ventricular filling occurs passively during diastole
 During atrial systole some blood regurgitate into the great veins.
3) Ventricular systole
i. Isovolumetric (isovolumic, isometric) ventricular contraction
ii. Ventricular ejection
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i. Isovolumetric ventricular contraction
 Lasts about 0.05 seconds

 At the start of ventricular systole the mitral & tricuspid valves close & aortic, pulmonary
valves remain closed.
 All the valves are closed & ventricles are closed chambers for a short period of time.
 Then, ventricles contract very little
 But, ventricular pressure rises very rapidly as the myocardium presses on the blood
 The pressure in the ventricles exceeds the pressure in the great arteries.
 During this time the cusps of AV valve bulge into atria causing a small but sharp rise in
atrial pressure.
ii. Ventricular ejection
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 When the pressure in the left ventricle exceeds aortic artery pressure, the aortic valve
opens
 When the pressure in the right ventricle exceeds pulmonary artery pressure, the
pulmonary valves open
 The phase of ventricular ejection begins
 Blood ejects into the aorta & pulmonary artery
 The intra ventricular pressure rises to a maximum & then declines before the end of
ventricular systole
 Therefore ejection is rapid at first & the slows down
 Peak left ventricular pressure is about 120 mmHg
 Peak right ventricular pressure is about 25 mmHg
 Late in systole the aortic pressure actually exceeds the ventricular pressure
 But momentum keeps the blood moving forward into the aorta
 The AV valves are pulled down by the contraction of the ventricles
 And the atrial pressure drops.
4) Early diastole
i. Protodiatole – lasts for 0.04 s
– When the ventricular muscle is fully contracted the falling ventricular pressure
drop more rapidly
– Ends when momentum of ejected blood is overcome
– The aortic & pulmonary valves close.
ii. Isovolumetric relaxation (next page)
 The AV valves, aortic & pulmonary valves are closed

 Pressure continue to drop rapidly
 When the ventricular pressure falls below the atrial pressure AV valves open
 Resulting end of the iso-volumetric relaxation
 When AV valves open ventricular filling starts.
 Ventricular filling is rapid at first
 Slows down towards the late diastole.
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Normal pressure – volume loop of the left ventricle (SEQ)
 After B (mitral valve closes), all the valves are closed and pressure rises but volume
remains constant during iso-volumetric contraction (B to C).
 Ventricular ejection in both figures occurs from C (aortic valve opens) to D (aortic
valve closes)
 With peak ventricular pressure (peak systolic pressure).
 D to A is iso-volumetric relaxation.
 Ventricular filling begins at A and ends at B.
 Ventricular relaxation is complete at A. The horizontal distance from point A to B is
the stroke volume.
 The significance of this is that area enclosed by the loop is a measure of total
ventricular work.
 Point D- the end-systolic pressure-volume point, is one measure of performance of
a ventricle.
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Important facts about cardiac cycle?
 Atrial pressure continues to rise after the ventricular systole until the AV valves open.
 Timing of the events.
– The activities of the right & left side are asynchronous

– Right atrial systole precedes the left atrial systole
– Left ventricular systole precedes the right ventricular systole
– Right ventricular ejection begins before the left ventricular ejection
 During inspiration the aortic valve closes slightly before pulmonary valve.(physiological
splitting)
 During expiration both valves close at the same time.
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 Mechanism of physiological splitting:
During inspiration intrathoracic pressure decreases
abdominal pressure increases
so,venous return ( VR ) to the right atrium is increased
right ventricular(RV) distention increases
so,RV volume increases
RV ejection takes some additional time
so, pulmonary valve closure delayed
Cardiac chamber volumes
 End diastolic volume

– The volume of the ventricles at the end of the diastole
– About 130 ml
 Stroke volume
– The volume of blood ejected from each ventricle during ventricular
ejection (with each stroke)
– About 70-90 ml at rest
 End systolic volume
– Volume of blood remains in each ventricle at the end of systole
– About 50 ml
Ejection fraction
 Percentage of blood ejected with each stroke from the end diastolic volume
EF = (Stroke volume / end diastolic volume) × 100 %

– Normally about 65%
– Valuable index of ventricular function
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Length of systole & diastole
 With change of heart rate the length of systole & diastole varies
 With tachycardia the length of cardiac cycle decreases
– Both the systolic & diastolic length decreases
– The shortening is mainly due to reduction of the length of diastole
Arterial pulse
 The blood forced into the aorta during ventricular ejection

– Moves the blood forward
– Sets up a pressure wave that travels along the arteries
– Expands the arterial wall
 This expansion is palpable as the pulse
Character of the pulse
 Slow rising pulse – aortic stenosis
 Collapsing pulse – aortic regurgitation
 Radio-femoral delay – co-arctation of the aorta
Rate, rhythm; of pulse  radial pulse by index & middle fingers

Character, volume: of pulse  carotid pulse by thumb
Atrial pressure changes
 Atrial pressure
– Rises during atrial systole.
– Starts to drop with atrial diastole.
– A transient rise is seen with isometric ventricular contraction when AV valve
cusps bulge into the atria.
– With ventricular ejection pressure drops rapidly due pulling of AV valve &
continues to drop rapidly due to atrial diastole.
– Atrial pressure rises again due to venous return in ventricular systole.
– When AV valve opens in ventricular diastole pressure drops again.
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Jugular venous pulse
 The atrial pressure changes are transmitted to the great veins

 Internal jugular vein has direct communication with RA
 These pressure fluctuations can be seen in the internal jugular veins in the neck, but it
can’t be felt
 To examine patient should be reclining at angle of 45⁰
 Why we use internal jugular vein?

– It has no valves
– Runs in less facial planes that of external jugular vein
 Produces 3 characteristics waves

– Three positive waves ‘a, c & v’
– Two descents ‘x & y’
 The ‘a’ wave – atrial systole

– Regurgitation of blood into the great veins with atrial systole
– Stoppage of venous flow in great veins.
 The ‘c’ wave – cusp bulging

– Transmitted pressure due to bulging of the cusp of AV valves during
isovolumetric ventricular contraction.
 The ‘v’ wave – venous return during ventricular systole
 The ‘x’ wave – atrial diastole

Cusps going down by ventricular ejection
 The ‘y’ wave – ventricular diastole

– Opening of tricuspid valve in ventricular diastole.
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Abnormal jugular venous pulse
 Large ‘a’ waves (cannon waves)
– Seen in complete heart block when atria contracts with closed AV valves
 Giant ‘c’ wave

– Seen in tricuspid regurgitation
 ‘a’ waves absent in

– Atrial fibrillation
 All the Jugular venous pressures rise in

– Right heart failure
– Congestive heart failure
 Raised venous pressure with no waves

– Superior vena cava obstruction (loss of connection between RA & internal
jugular vein)
SEQ
*Batch 29- Repeat*

1.2 outline the events taking place during ventricular diastole
*Batch 26 - repeat *
1.4.1 draw a clearly labeled diagram for a normal JVP tracing and mention the cardiac event
producing them
*Batch 26 - proper*
1.4 List the phases of the cardiac cycle.
1.5 Explain the left ventricular mechanical events that take place from beginning of the QRS
complex to the beginning of T wave.
*Batch 25 - proper*
1.3 Draw a clearly labelled diagram to show the pressure changes in the left ventricle and aorta
during
the phases of a cardiac cycle.
1.4 In the above diagram, indicate the opening and closure of the aortic valve.
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4.) CARDIAC OUTPUT
Definition
 The volume of blood pumped by each ventricle per each minute.
 The left ventricle’s cardiac output is the same as the right ventricle’s output.
 Measured in Liters per min (L/min).
 In a normal healthy adult male in the supine position, it is around 5L/min.
 Influenced by
o Stroke volume (SV)
o Heart rate(HR)
Stroke Volume
 The amount of blood pumped out by each ventricle during each heart beat.
EDV –ESV = SV
EDV – volume of blood that fills the ventricle during diastole. (135ml)
ESV – volume of blood remaining in the ventricle after systole. (65ml)
135ml – 65ml = 70ml
Calculation of the cardiac output
CO = Stroke volume x Heart rate
CO = 70ml/b x 72 bpm
= 5.040L/min
= (~5L/min)
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Cardiac Index (CI)
 CO increases in proportion to body surface area.
 Minute volume expressed in relation to square meter of body surface area.
 CI is CO per square meter of body surface per minute.
Cardiac Output
CI C =
Body surface area
 In an adult with a body surface area of 1.734 m2 CI is 3L/min/m2 .

 Accurate than CO for cardiac function.
Comparison with Cardiac Output Cardiac Index

adult males
Babies  
Females  
Elderly  
Cardiac Reserve
 The difference between resting and maximal CO.
 Important in exercise.
Ejection Fraction
 Fraction of EDV that is ejected out by each ventricle.
Stroke Volume
Ejection X 100 Fraction=
End Diastolic Volume
 Normally it is 60% - 65%
Identify factors that will increase the ejection fraction?

increase decrease
 When heart is beating more  Myocarditis
effectively  MI
 Heart failure
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Why does the cardiac output change? (Variations in cardiac output)
 Physiologically
– Increased oxygen consumption by the tissue causes CO to rise
– Reduced oxygen consumption causes a fall in CO
 Age – CO is less in children.CI is more than in adults due to less body surface
area.
 Sex – CO is less in females. CI is more due to less body surface area.
 After meals – CO is increased in the first one hour.
 Emotional conditions – anxiety, excitement.
 Exercise – Increase CO
 Posture – changing from recombinant to supine will decrease CO. Changing from
supine position to standing position will decreases CO.
 Pregnancy – later months of pregnancy increase CO by 40%
 Adrenaline and Noradrenaline – Increase CO
 Pathologically
– Disease can also alter CO.
– Increase CO- Thyrotoxicosis (hyperthyroidism) – Increased basal metabolic rate
Fever – increase oxidative procedure
Anemia – due to hypoxia
– Reduce CO - Hypothyroidism
Cold
Cardiac failure
Shock
Haemorrhage
Parasympathetic & sympathetic activity of heart
Parasympathetic activity Sympathetic activity

Nerve By vagus nerve ( x cranial Sympathetic ganglion
nerve )
Neurotransmitter Acetyl choline Noradrenalin
Receptor type M2 receptors Β1 receptors (mcq)
Action Keeps the HR at 72/min Increase HR
Cardiac output Normal increases
What happens to alter the cardiac output?

 Increasing the HR (Chronotropic effect)
1.) Reducing the resting vagal tone on to SA node/AV node
2.) Increase the sympathetic discharge to SA node/AV node
3.) Increase the circulating catecholamine action on the SA node/AV node
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 Increasing the stroke volume (inotropic effect)
1.) Positive inotropic effect increases contractility
2.) Negative inotropic effect reduces contractility
Factors that determine the cardiac output
1.Venous return
2.Force of contraction
3. Heart rate
4.Peripheral resistance
1. Venous Return
 Amount of blood returned to the heart from different parts of the body.
 When VR increases , EDV increases, SV increases, CO increases.
 VR is directly proportional to CO
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Factors alter venous return (VR)
Increase venous return Decrease venous return
1. Increasing venous tone 1.) Reducing venous tone

 By increasing sympathetic activity (dilatation)
 Contraction of the venous smooth muscle
2.) Standing
2. Muscle pump
 Running person 3.) Reduced blood volume
 Contraction of skeletal muscles (soleus-peripheral heart)
4.) Increased pericardial
3. Respiratory pump pressure (pericardial
 Diaphragm descends during inspiration effusion)
 -ve intra-thoracic pressure & +ve abdominal pressure
 So, during inspiration splanchnic blood pulls towards 5.) Reduced cardiac muscle
thorax stretching
4. Increased atrial contraction 6.) Gravity

 Sucks venous blood towards atria
5. Increase in blood volume
1. Force of Contraction
 CO is directly proportional to the force of contraction.
 Depends on Diastolic period
Ventricular filling
Pre load
After load
Frank Starling Law
Within physiological limits, the force of contraction of heart is directly proportional to the
initial length of muscle fibres before contraction.
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Pre load
 Amount of stretch of the cardiac muscle fibres ( ventricle) at the end of diastole just
before contraction.
 Determined by left ventricular end diastolic volume.
 It depends on Venous return and
Ventricular filling
VR increases, EDV increases, Pre load increases
Frank Starling Curve
 The LVEDV represents the preload.
 The force of contraction increases with

increasing preload until a point is
reached where the ventricle is over
stretched and the force of contraction
decreases.
 This point is the apex of the starling
curve.
 Force of contraction is not synonymous
with contractility, and for all points
along a starling curve, contractility is
equal.
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After load
 Force against which the ventricle must contract and eject blood .
 Force is determined by The arterial pressure and
Total peripheral resistance
 LV after load is determined by the aortic pressure.
 RV after load is determined by the pulmonary pressure.
 Higher aortic pressure = lower SV
 Increase after load decrease SV
 Decrease after load increase SV
1. Heart Rate
 CO is directly proportional to the heart rate.

 Increases HR Increases CO
o Chronotropic effect may be excitatory due to sympathetic activity
o May be inhibitory due to parasympathetic activity
 Marked increase in HR will increase the CO

Eg :- Vigorous exercise
 Why normally low heart rates in athletes?
– As mentioned above their SV is increased (because their thick LV myocardium)

– But CO is constant
– So, HR should go down to maintain normal CO
CO = Stroke volume x Heart rate
2. Peripheral Resistance
 CO is inversely proportional to peripheral resistance

 Resistance offered to the flow of the peripheral blood vessels.
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You need to know?
Mechanism of action of DIGOXIN & DIGITOXIN
 Reversibly inhibits the Na+/K+ ATP ase pump in myocytes

 Reduces transport of Na+ from intracellular to extracellular space
 Increase intracellular Na+
 Inhibit Na+/Ca2+ exchange
 Increased intracellular Ca2+
 Causes increase contractility
 Excessive intracellular Ca2+ - premature contractions & trigger
arrhythmias
Measuring the cardiac output
Direct Methods Indirect Methods

1. Cardiometer 1. Fick principle
2. Flowmeter 2. Indicator dilution method
3. Thermodilution method
4. Ultrasonic Doppler transducer
technique
5. Doppler Echocardiography (most
often used)
 Fick Principle
- Amount of substance taken or given = amount of blood flow/min x AV
difference
– Invasive
Modified Fick Principle

– Require surgery to measure CO
CO = Amount of substance taken or given by the organ/min / AV difference of the
substance across the organ
CO = Oxygen consumption/Arterial- venous oxygen difference
- By using O2 consumption
- By using CO2 evolved
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 Indicator dilution technique
– Inject substance to vein and measure its concentration in arterial blood
– Plotted on a logarithmic graph and calculated to volume/min
– Thermo dilution (using cold saline) is easier/ safer
 Doppler Echocardiography
– Uses ultrasound waves to produce the image of the heart.
– CO = SV x HR
– In order to access SV , it is necessary to measure flow velocity and determine the
cross sectional area.
– Aortic valve is used.
SEQ
27 R
1.3. A 25 year old man has the following recordings .
Heart rate – 72 beats per minute
Stroke volume – 60 ml
A) Calculate his cardiac output. (10 marks)
B) State the Fick principle in measuring cardiac output. (10 marks)
C) Describe the factors regulating cardiac output in a healthy young man. (30 marks)
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05) HEMODYNAMICS
Blood flow
 Measured as a volume/ unit time (cm3/sec)
 Can be measured using electromagnetic or Doppler flow meters; Plethysmography
 (functional studies using fMRI, PET scans)
Why does blood flow?

 Circulation maintained by a pressure gradient (ΔP)
 Heart pumps blood to aorta at a high pressure
 Pressure gradually falls in the circulation
– when blood enters the atria, it is at its lowest pressure
Flow (Q) = Pressure gradient (ΔP)

Resistance (R)
Q = (ΔP)/R
In the human body, this means

 Q = (ΔP)/R
 Pressure (ΔP) = Flow (Q) x Resistance (R)
 Blood pressure = Cardiac output × total peripheral resistance

(BP = CO × TPR)
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Resistance & blood flow
 Resistance ∞ Length of vessel

∞ Viscosity of blood ()
∞ 1/ radius4
4
 Poiseuille formula Flow = ΔPr
8L
Significance of the formula
 A small change in the radius of a vessel will cause a large change in the flow of blood.
4
– Flow ∞ r
– In the body, the arteriolar radius is increased to increase flow
 A rise in the haematocrit/ rise in plasma proteins and RBC stiffness causes a rise in the
viscosity () of blood.
Effects of Viscosity in small vessels

Cell free plasma (peripheral)
RBC (in center)
 Arterioles, capillaries and venules

 RBCs move to centre of vessel
 Cell free plasma at the edge of vessel
 [Fahraeus-Lindquist effect]
 Less viscosity and resistance to flow in these vessels in vivo

unless haematocrit very high
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Velocity of blood flow
 Flow
– volume per unit time (mL/sec)
– How many Litres go past point A in a second?
 Velocity (speed)
– distance per unit time (m/sec)
– How long does it take to go from A to B?
Relationship between flow & velocity
 What happens in a vessel with a narrowing?
 Velocity ∞Flow
∞ 1/Total cross sectional area Increased velocity to maintain
same volume of flow
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Velocity of flow & total cross sectional area
What happens in the body?

 Blood flows from the aorta to capillaries
 Total cross sectional area very high in capillaries
 Velocity falls from the aorta (30cm/sec) to the capillary (0.08cm/sec)
Gives time for exchange of gases, nutrients, fluids, electrolytes at

capillaries
Types of blood flow
Laminar flow Turbulent flow
• Close to vessel wall, • Movement in all
hardly any movement directions
• Highest velocity in the • Increases resistance to
middle of vessel flow
• Efficient flow • Larger ΔP to move blood
• Vessels >0.5mm
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Assessing turbulence
 Reynold’s number (Re)

– Turbulence associated >2000
 In life, turbulence causes sounds that can be auscultated (using stethoscope)
– Murmurs (and thrills) in heart
– Bruits (vessels)
Why are murmurs heard in anemia ……?
Law of Laplace
‘w’ is negligible
Prevents small vessels (e.g. Capillaries)

from collapsing
Critical closing pressure

 In small vessels, the surrounding tissue pressure > pressure inside the vessel
– Causes collapse of vessel with no flow
– e.g. Alveolar capillaries
 Happens in inactive tissue capillaries
– e.g. capillaries in Muscles at rest
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06). STRUCTURAL FEATURES OF THE CIRCULATION
Blood vessel basic structure

 Three layers
– Tunica intima
– Tunica media
– Tunica adventitia
Tunica intima Tunica media Tunica adventitia

Vascular Smooth muscle in Consist of external
endothelium circular arrangement elastic lamina &
 Secretory collagen fibers
function Contain Ca2+, K+, Cl-
 Respond to channels Prevent over
chemicals in stretching of vessel
blood Smooth muscle
 Able to responsible for Protective layer
respond to contractile ability of
changes in blood vessels
flow, stretch
Contraction-reduces
Elastic fibers (internal
elastic lamina) vessel diameter
 Constriction
Endothelial damage Relaxation- increases
cause sub-endothelial vessel diameter
plaque formation  Dilation
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Physiology of arterial circulation
Elastic arteries Muscular arteries Arterioles
EX: aorta, brachial artery  More smooth muscles  Main importance in

 elastin in internal &  Less elastin, collagen regulating the resistance in
external elastic lamina than elastic arteries the circulation.
 recoil ability  Transport function  Resistance vessels
– in systole- vessels  Resting tone – smooth
stretches & stores muscles partially  Arteriolar constriction
energy & this is released contracted under – Increase resistance
in diastole normal resting  Arteriolar dilation
– Stretch - causes energy conditions – Reduce resistance
to be stored & released  Smooth muscles are
when the force of innervated by  Very responsive to
stretching is released. sympathetic nervous stimulation
system. – Sympathetic – adrenalin NT
 Collagen fibers in media  NT= noradrenalin act – Catecholamine hormones in
& adventitia prevent on α receptors on blood
over stretching vessel smooth muscles.
( no vagal innervation to
Systole -stretching blood vessels)
 Increase sympathetic –
contract more
( VASOCONSTRICTION)
 Decrease sympathetic
Diastole-recoiling – contract less
( VASODILATION )
 Recoil tendency of blood

vessel wall help to keep
the bulk flow , to
continue to flow up
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The pulse
 Wave of pressure travelling along arteries at systole

 Causes a palpable expansion of the vessel
 Velocity greater than the flow rate for blood (very rapid moving wave)
 Pulse weak in shock

 Pulse strong when stroke volume is high (Exercise, anxiety)
Physiology of capillaries
 Single layer of endothelial cells & basement membrane

 No smooth muscle/ collagen/ elastin
 Large total surface area
 Function as exchange vessels

– Substances moved in & out of the circulation
 Pericytes surrounding endothelium
– Contractile.
– Secrete substances.
– Regulate flow between endothelial cells .
– Filtration occurs at here.
– Pericytes alters the ability of capillaries to exchange things.
 Pre capillary sphincter
– No sympathetic innervation
– Locally secreted hormones act on sphincter
Continuous capillary Fenestrated capillary

 Passage of molecules <10nm between  Holes with thin membrane cover
endothelial cells  20-100 nm molecules can pass
through it
 Vesicular transport
EX: in muscles EX: GIT / Endocrine organs
Liver – no membrane , large particles
can cross
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Microcirculation
 Blood from meta-arterioles pass via a tiny sphincter ‘pre-capillary sphincter’.

 5μm-arterial end & 9μm-venous end – allows a single red cell to pass in a thimble
shape.
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Physiology of venous circulation
Collecting venules Veins- capacitance vessels

 Single layer of smooth muscle &  Less thickness than arterial system
converge to form veins
 But lumen diameter is greater than
arterial system.
 Large veins have valves

– Aid return of blood to heart
 Can distend with blood- act as

capacitance vessels (reservoirs)
– Veins can increase volume without a
rise in the pressure
– With excessive stretching of veins
(EX: heart failure) their pressure
rises
 Contraction of veins (veno-

constriction) increases venous
return to heart
– Veins store 50% of blood
– Aided by muscle & thoracic pump
Characteristics of blood vessels
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Volume-pressure relationship of vessels
 Veins-small change in the volume, pressure doesn’t change very much
Physiology of Lymphatic system
 Drain interstitial spaces

 Vessels eventually drain to right & left subclavian veins
Right lymphatic duct  right subclavian vein

Thoracic duct  left subclavian vein
 Vessels contain valves

 Go through lymph nodes
 Differ from capillaries
– No fenestrations
– Wide gaps between endothelial cells
– ‘NO’ basal lamina
What happens to blood flow?

 Blood pumped at high pressure from left ventricle (mean 100mmHg)
 Pressure in arterial system reduces slowly
– Low pressure in veins
– Lowest pressure in atria (1-2 mmHg)
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07.) BLOOD PRESSURE
 Blood pressure means the force exerted by the blood against any unit area
of the vessel wall.
 Measured in millimeters of mercury (mmHg)
 Usually refers to arterial blood pressure.
BP
Systolic BP Diastolic BP
*Highest pressure in the *Lowest pressure in the
aorta aorta
*Occurs during systole of * Occurs during diastole
the cardiac cycle of the cardiac cycle
*Usually 120mmHg (SI *Usually 70-80 mmHg
units 16kPa) (SI units 9.3kPa)
Determination of blood pressure
Pressure = Flow x Resistance
Blood pressure = Cardiac output x Total peripheral resistance
BP = CO × TPR
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Cardiac output (CO) Total peripheral resistance (TPR)
 Cardiac output= Stroke volume x Heart rate  Determined by the arteriolar tone
CO = SV x HR (R∞1/r4)
 Mainly determined by the SV  Constriction increases mainly diastolic

BP
 Rise in SV, increase mainly systolic BP
 Dilatation reduces diastolic BP
Blood pressure evaluation
 Conveniently written as systolic pressure over diastolic pressure

120/70 mmHg
 Usually measured in the brachial artery at the level of the right atrium.
Pulse pressure
Pulse pressure (PP) = Systolic pressure –Diastolic pressure
PP =SBP-DBP
 Around 50mmHg. (120-70 = 50 mmHg)
 Increases >50mmHg physiologically, during aerobic (isotonic) exercise.
Abnormalities of the pulse pressure
Increase (collapsing pulse) Decrease (slow rising pulse)
 Arteriosclerosis  Aortic stenosis

– hardening of arteries leads to reduced
compliance
– Rise in systolic and fall in diastolic
pressure
 Aortic regurgitation
↑EDV  ↑SV  ↑CO  ↑SBP
 thyrotoxicosis
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Mean blood pressure (MBP)
 This is the average pressure during the cardiac output
 Closer to the value of diastole (DBP)
– Period of diastole is longer than systole
MBP = Diastolic pressure + 1/3 of pulse pressure
 MBP is the main determinant of adequate blood flow through tissues
Physiological variations in the blood pressure

Increase BP Reduce BP
 Age –older people have  Age-children have lower

higher BP (SBP & DBP) BP than adults
 Males  Females
 Rise in cardiac output  Sleep
(EX: Anxiety)
 Raised TPR
 Arteriosclerosis
 ‘white coat hypertension’
Effects of gravity
 BP falls above the level of the heart

 BP rises below the level of the heart
 Proportional to the vertical distance from the heart
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8.) HEART SOUNDS & MURMURS
Heart sounds
 Produced by vibration of the taught heart valves immediately after closure of the valves.
 These vibrations travel through the tissues to the chest wall.
 Opening of normal valves do not cause a sound.
1st heart sound- 2nd heart sound-‘’dub’’ 3rd heart sound 4th heart sound
‘‘lub’’
Low pitched, slightly High pitched, short Soft low pitched sound in Late in diastole.
prolonged (0.15 S). (0.12S) loud & sharp. early diastole.
Mostly pathological.
Produced by the closure Produced by aortic & Physiological in young
of tricuspid & mitral pulmonary valve closure. adults. Atrial contraction causing
valves. rapid ventricular filling on
Follows ventricular Rapid filling of ventricles a tense ventricular wall.
At the start of the systole. following AV valve
ventricular systole. opening with a little
In inspiration- elastic resistance on the
physiological splitting of ventricular wall created
the 2nd heart sound by the initially filled
(aortic component before volume of blood.
the pulmonary)
Physiological splitting
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Mechanism:
During inspiration intrathoracic pressure decreases
Abdominal pressure increases
So,venous return ( VR ) to the right atrium is increased
Right ventricular (RV) distention increases
So,RV volume increases
RV ejection takes some additional time
So, pulmonary valve closure delayed.
You must know?
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Heart murmurs
 Normal flow is lamina, non-turbulent and silent.

 Murmurs are abnormal sounds heard when there is turbulent flow with in the heart or
blood vessels.
 Lamina flow – Concentric layers of fluid moving with a high velocity at the center of the
vessel and a low velocity along the walls.
Ohm’s law
 Flow = Δ pressure/resistance
 With increasing pressure flow should increase if the resistance is static
 But with increase in pressure beyond a limit does not increase the flow in a liner
fashion. This is due to turbulence.
Reynolds number
 Point where laminar flow becomes turbulent.
 Re <2000 = lamina flow

 Re >3000= highly turbulent flow
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 Turbulence can be created by:
Narrow/Stenosed valves-
accelarated flow
Normal flow, abnormal
valves
Turbulence incompetent valves-
regurgitant/backward flow
High flow in pregnancy or

Thyrotoxicosis
Abnormal flow normal
valves
Low viscosity of blood in
anemia
Abnormal communication Patent foramen ovale/ Inter-

between heart chambers ventricular septal defect
Characteristics of murmur
1.) Loudness
2.) Quality
3.) Location
4.) Timing
1) Loudness-Depends on the turbulence of flow not the severity of the lesion

2) Quality – Pitch (frequency) of the murmur. ( low, medium or high)
3) Location – cardiac areas for Auscultation.
 Aortic area – 2nd intercostal space right sternal edge
 Pulmonary area – 2nd intercostal space left sternal edge
 Tricuspid area – 4th intercostal space left sternal edge
 Mitral area – 5th intercostal space near mid clavicular line
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Murmurs in valvular disease
Valve Abnormality Timing of murmur

Aortic or Pulmonary Stenosis Systolic
Insufficiency Diastolic
Mitral or Tricuspid Stenosis Diastolic
Insufficiency Systolic
 Timing – phase of the cardiac cycle. (IMPORTATNT)
 Systolic murmurs (between the first and second heart sounds)

1) Mid systolic
2) Late systolic
3) Pan systolic (heard throughout the systole)
 Diastolic murmurs ( between the second and the first heart sounds)
1) Early diastolic
2) Mid diastolic
3) Pre-systolic
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 Con.
Pan systolic murmur
Pan systolic murmur
Continuous murmur
Congenital heart diseases causing murmurs
 Patent Ductus Arteriosus (PDA) → Continuous Machinery murmur in both systole and
diastole.
 Septal defects associated murmur (ASD or VSD) – only systolic murmurs, 2nd
heart sound splits in ASD
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Left to right blood shunt (left side pressure > right side pressure)
Right ventricular overload
High flow through pulmonary valve
Lamina flow exceeds the critical velocity
Turbulent flow
Systolic murmur
Changes in S1 and S2 heart sounds in pathological conditions
 RBBB- Right bundle

branch block
 LBBB- Left bundle
Branch block
 ASD- Atrial septal
defect
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Conditions causing S3 and S4 heart sounds to appear
 S3 – in early diastole (rapid ventricular filling)

– High output states ( Anemia, Fever, Pregnancy, thyrotoxicosis)
– Left ventricular failure
– Mitral regurgitation
– Constrictive pericarditis
 S4 – in late diastole (atrial contraction  rapid ventricular filling on tensed
ventricular wall)
– Hypertension
– Aortic stenosis
– Hypertensive cardiomyopathy
Murmurs in valvular disease
SEQ
1) A 65 year old male with dyspnea and recurrent syncope was found to have a murmur in the
praecordium. Echocardiography confirmed a tight (severe) aortic stenosis.
1. Briefly describe the structural adaptations of the semilunar valves in
relation to its function. (15 marks)
2. Explain the basis of the murmur including its time and quality. (30 marks)
3. Briefly explain the basis of his syncopal episodes. (20 marks
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9.) CVS REGULATION
Why is the cardiovascular system (CVS) regulated?
 Adjust blood flow according to tissue needs

e.g., Increase flow to exercising muscles
 Maintain blood supply to vital organs (brain, heart) in times of
stress e.g., Bleeding (haemorrhage)
 Maintain body temperature (increase or decrease temperature)
e.g. - send blood to skin to enable heat loss
How circulatory adjustments are done? (Ganong)
 Altering the output of the pump (heart)

 Changing the diameter of the resistance vessels (arterioles):
Via autoregulation, local metabolites, vasoactive substances, and
nerves
 Altering the amount of blood pooled into the capacitance vessels (veins):
Via vasoactive substances, vasomotor nerves
Terminology
 Constriction of resistance vessels (arterioles) – vasoconstriction
 Dilation of resistance vessels – vasodilation
 Constriction of veins – venoconstriction
 Dilation of veins - venodilation
CVS regulation
Local Systemic
Neural Humoral
Short Long
term term
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Local regulation
a) Short term Reduced tissue oxygen/
1) Tissue blood flow Nutrients
 As tissue metabolism increases,

 blood flow increases
Release of vasodilator Direct
 Mechanism Substances (Indirect)
– Direct
– Indirect
Examples:
Act on meta arterioles and pre
– Increase muscle blood flow in exercise capillary sphincters (relax)
-
– Regulation of organ specific flow

(Autoregulation)
 Vital organs can maintain a constant rate of blood flow even

when the blood pressure changes (e.g., Brain, kidney), at the
expense of the circulation to the rest of the body
 As the blood pressure rises in the acute (sudden) instance, there is a rise in
blood flow.
 In the long term, the blood flow remains relatively constant between a
range of blood pressures (50-200mmHg).
This is important in the kidneys as a constant blood flow maintains the

kidney’s removal of waste matter at an optimal level.
Q=(ΔP/R)
 ΔP ↑ but, Q should be constant
So, R should↑
 To↑ R diameter of vessel should ↓
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Mechanism of auto regulation
Metabolic theory Myogenic theory
• Reduced blood flow causes • Increased blood pressure

accumulation of vasodilator stretches smooth muscle which
substances then contracts
Metabolic activities of cellular  BP

organelles 
↓
Excess pressure Stretches the
↓O2 concentration at tissue level vessel smooth muscle
↓

Release of vasodilator substances
Reflex Contraction of smooth muscles
form endothelium/ cells
↓ 
Vasodilation Vasoconstriction

Reduce blood flow to the normal level

Constant rate of blood flow
Locally acting vasoconstrictors & vasodilators
Locally acting Vasodilators Locally acting Vasoconstrictors
• Reduction of • Damaged vessels have capacity to

– Oxygen & pH vasoconstriction
• Rise in – Serotonin helps this
– Osmolality • Fall in temperature
– pCO2 (brain, skin)
– Temperature
– Potassium
– Lactate
– Histamine
– Adenosine (in cardiac muscle)
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Vasoconstrictor & Vasodilator secretions
Mediator Source Effect

Vasoconstrictors Endothelin-1 (ET-1) Endothelial cells Vasoconstrictor
Airway epithelium (most potent)
Thromboxane A2 (TA2) platelets Vasoconstriction /

platelet
aggregation
Serotonin Enterochromaffin cells vasoconstriction
(ECL cells)
– found in gastric
mucosal glands to
systemic circulation
In the analgesic
pathway
Vasodilators Prostacyclin(PGI2) Endothelial cells Vasodilation/inhibit
platelet
aggregation
Vasoactive intestinal Mucosa of GIT to Vasodilation

peptide (VIP) systemic circulation
Nitric oxide (NO) Endothelial cells Vasodilation
Carbon monoxide (CO) Endothelial cells Vasodilation
 Prostacyclin & thromboxane A2 derived from arachidonic acid (omega-6-fatty

acid) using cyclo-oxygenase pathway (COX pathway).
• COX-1 pathway: (non-inflammatory situations, always active) PGI2
• COX-2 pathway: (usually only active during inflammations) thromboxane
A2
 Both act to balance clot formation while avoiding excessive extension of clots.
(PGI2 and thromboxane A2 have opposite effects)
Endothelial cells also secrete growth factors and vasoactive substances. (lecture)
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 YOU NEED TO KNOW -Mechanism of action of aspirin?
(Refer Eicosanoids)
• Asprin is a NSAID (Non-steroidal anti-inflammatory drug), used to prevent clot

formation especially in the arterial circulation
(Eg: Prevention of heart attacks, strokes)
 Irreversible inhibition of Cyclo-Oxygenase, (COX is responsible for the
formation of both prostacyclin and thromboxane A2.)
• Aspirin alters balance towards prostacyclin.
Although the inhibition of the enzyme is irreversible, the endothelial cells replace
the enzyme rapidly. So new prostacyclin can be formed again in a short period of time.
Thromboxane A2 from platelets is inhibited for longer as the platelets last for longer and it takes
more time for new platelets to be formed (about 4 days).
• aspirin is used to prevent clot formation in patients at risk of strokes and heart
attacks (when commonly, clot formation occurs in cerebral and coronary arteries
respectively).
YOU NEED TO KNOW-Mechanism of action of NO?

• Formed by endothelial cells.
• Acts as a messenger to cause vasodilatation. (in smooth

muscle).
NO functions:
(Refer male sexual response and the role of sildenafil)
1. Cause arterial dilatation when local flow increases

– Other substances can act via NO (Ach, Bradykinin)
– Some vasoconstrictor substances also stimulate secretion of NO
2. Secreted by intact endothelium by factors released by platelet aggregation
– damaged endothelium, NO not formed – vasoconstriction occurs
3. Role in maintaining normal blood pressure
4. Vascular remodelling and angiogenesis(branches formation from a vessel)
– Role in atherosclerosis
5. Role in male sexual response
b) Long term local regulation of flow

Adaptations:
 Increase the number/ size of vessels
– Stimulated by tissue O2 requirements.
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 Collateral circulation:
– Pre-existing small vessels in the coronary circulation.
– Not important in health.
– In patients with obstructed coronary vessels (ischaemic heart disease),
they increase in size to help supply blood to parts of the heart that are
ischaemic (low supply of oxygen).
2.) Systemic regulation

a) Humoral regulation
 Chemical substances transported in blood
 Regulation at the whole-body level
 Hormones:
 Chemicals secreted by endocrine glands to the blood.
 Circulated to all the tissues of the body.
 Act on their receptors to cause an effect.
 Tissues or organs without receptors will not respond to the hormone.
Vasoconstrictors vasodilators
1)Catecholamines 1) Histamine
2)Angiotensin II 2) Prostaglandins (some types)
3)vasopressin (ADH) 3) Atrial natriuretic peptide (ANP), Ventricular
natriuretic peptide (or brain natriuretic peptide/
B-type natriuretic peptide/ Brain natriuretic
peptide: BNP)
4) Bradykinin, Kallidin: a bioactive kinin
(act locally and systemically)
5) Others (K+, citrate, acetate)
1.Catecholamines
Most potent ones:
1. Adrenaline
– from adrenal medulla
– May cause vasodilatation in skeletal muscle/ liver
- Acts on the heart to cause a positive inotropic (increased ventricular
contraction i.e., stroke volume) and chronotropic effect (increased
hear rate).
2. Noradrenaline
– Post ganglionic sympathetic neurotransmitter; mainly exerts effects via neural
regulation
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The following chart is VERY IMPORTANT:
Heart expresses mainly β1 receptors: positive ionotropic and chronotropic effect

• positive inotropic effect: increase the contraction of ventricular muscle
• positive chronotropic effect: increase the depolarisation of SA node and decrease the
AV nodal delay to increase the heart rate.
▪ Arterioles & veins mainly have (as in hepatic and skeletal muscular arterioles):
– α1, α2 receptors: vasoconstriction
– β2 receptors: vasodilatation
2. Angiotensin II
 Acts on arterioles to increase total peripheral resistance
ACE-Angiotensin
Converting enzyme
 ACE inhibitors used to treat hypertension
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 The Renin-Angiotensin-Aldosterone System (RAAS):
o Short-term effects: vasoconstriction
o Long-term effects: secretion of aldosterone
o also involved in regulating the constant blood flow to the kidney
 Renin
o secreted by the afferent arterioles of the kidney.
o converts angiotensinogen to angiotensin I.
 Angiotensin converting enzyme (ACE)

o present mainly in the pulmonary capillary endothelium.
o converts angiotensin I to angiotensin II.
o ACE inhibitors: used to treat hypertension
 Angiotensin II
o powerful vasoconstrictor.
o acts on the adrenal cortex: cause secretion of aldosterone.
o acts on hypothalamus to cause thirst and secrete vasopressin (ADH).
o Aldosterone (and angiotensin II) act to cause sodium and water
retention
 causes an increase in blood pressure.
3.)Vasopressin (ADH-Anti Diuretic Hormone)

 From hypothalamus via the posterior pituitary
 At high concentrations, act as a powerful vasoconstrictor (via V1 receptors)
o Especially on the arterioles.
o Also, on the venous system: increase return of blood to the heart.
 At low concentrations:
Anti-diuretic action: concentrate the urine by preventing water loss from our body.
(via V2 receptors)
b) Neural regulation (rapid action)

▪ Important for the global regulation of the circulation
▪ Rapid method of regulation
▪ Enables
– Distribution of blood according to body requirements
o Regulation of the heart (chronotropic and inotropic) function
o Blood vessel tone (arterial and venous)
– Rapid control of the blood pressure
– Both sympathetic and parasympathetic innervation of heart
o Only sympathetic NS innervates the blood vessels
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Factors regulating the blood pressure
 Short term regulating mechanisms

– Mainly Neural
 Long term regulating mechanisms
– Adjust the body fluid volume
– Mainly humoral ( circulating hormones )
Effect of autonomic nerves system to the CVS

Effector Sympathetic NS Parasympathetic NS
Heart  Increase heart rate  Reduces heart rate
(positive (negative
chronotropic) chronotropic)
 Increase contractility  No effect on

(positive inotropic) contractility
Blood vessels  Arteriolar constriction  Minimal effect
increases resistance
to flow ( TPR)
 Venoconstriction
increases venous
return
Effect of autonomic NS on heart

Sympathetic action on heart Parasympathetic action on heart
• Post ganglionic fibres release  Post ganglionic fibres release Acetyl

Noradrenalin choline (Ach)
• Act on 1 receptors  Act on M2 muscarinic receptors

– SAN increase rate of – SAN decrease rate of
depolarisation depolarisation
– AVN reduce delay – AVN increase delay
– Myocardium to increase – Minimal effect on
inotropic action myocardium
• Act on α1 receptors of blood vessels-
vasoconstriction
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Short term neural regulation
 Baroreceptors (IMPORTANT)
 Chemoreceptors
 Hormonal mechanisms
 Intrinsic vascular mechanisms
– Capillary fluid-shift system
– Stress-relaxation
Baroreceptors
▪ Main mechanism for regulating BP: baroreceptor mediated reflexes

o Detect stretch of large arteries (stretch reflexes BP)
o Located in the interstitium of the vessels
▪ High pressure receptors in the

– Aortic arch
– Carotid sinus (near the origin of ICA)
– The carotid sinus sends its information to the medulla using the
glossopharyngeal (IX) while the aortic arch sends information using the vagus
(X) nerve.
 Low pressure receptors

Atria
Pulmonary vessels
Baroreceptor reflex in BP regulation- an overview
 Important in the short term regulation of BP

– EX: In maintaining BP during changing position from sitting to standing
– Baroreceptors are most useful for short term regulation of BP in the
pressure range of 70 – 150 mmHg
 Prolonged elevated blood pressure (hypertension) causes re-setting of the
system (as seen in the dotted line of the graph)
 Respond to pressures 60-180mmHg (best around 100mmHg)
o Even a small change is detected and corrected by this reflex.
Earlier, to 35-45% fall in systemic BP by nearly 90 mmHg pressure at carotid

sinus.
But after resetting, only 10% fall in systemic BP by 90mmhg pressure at
carotid sinus.
To fall 35-45% systemic BP baroreceptors need nearly 125mmHg carotid sinus
pressure.
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– The baroreceptors have a constant rate of discharge. (tonic
discharge rate)
– If the blood pressure increases,
o the stretch of the baroreceptors is increased
o causes an increase in the rate of discharge of nerve impulses
in the IX and X cranial nerves.
– If the blood pressure falls below the normal level,
o reduced stretch of the baroreceptors
o reduced rate of discharge in the afferent nerves.
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Baroreceptor reflex
Neural regulation of CVS by medullary center
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Baroreceptor Afferents
(X,IX) enter nucleus
of tractus solitarius
Glutamate
Excitation of the caudal

ventrolateral medulla
(CVLM)
GABA
Inhibition of the rostral

ventrolateral medulla
(RVLM) ‘vasomotor area’
RVLM fibers descend in

‘Bulbospinal tract’ in the
interomediolateral grey
column of spinal cord
Pre ganglionic sympathetic neuron  sympathetic ganglia & Adrenal medulla

Ach
Sympathetic ganglia  Postganglionic sympathetic fibers  Arterioles or Venules / heart

Ach NE
 The information from the afferent nerves enters the nucleus of the tractus solitarius (NTS) in the medulla.
Adrenal medulla  circulating catecholamines (NE)  Arterioles or Venules / heart
 The NTS excites another part of the medulla called the caudal ventrolateral medulla (CVLM) by secreting
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 The information from the afferent nerves enters the nucleus of the tractus solitarius (NTS)
in the medulla.
 The NTS excites another part of the medulla called the caudal ventrolateral medulla (CVLM)
by secreting glutamate.
 CVLM inhibits the rostral ventrolateral medulla (RVLM)/vasomotor area via inhibitory
neurotransmitter GABA.
 Summary
Increased baroreceptors discharge inhibits the vasomotor area to reduce the sympathetic
outflow to the heart, blood vessels and the adrenal medulla (to reduce adrenaline secretion).
 Descending pathway
RVLM fibres descend in bulbospinal tract in the intermediolateral grey column of spinal cord
(Refer ANS)
Vagal connections from NTS
 NTS to vagal motor neurons

– Nucleus ambiguous
– Dorsal motor nucleus
 PNS innervation to the heart.

 Afferent: vagus nerve
 Baroreceptor impulses arriving at the
NTS are also passed to the vagal centres
o To control the parasympathetic
output to heart.
 Increased baroreceptor discharge:
o an increase in vagal output to the
heart
o reduces the vasomotor centre
sympathetic discharge to the
heart, blood vessels and adrenal
medulla.
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Neural regulation of BP (SEQ)
Elevated BP
↓
Increase stretch of the baroreceptors (BR)
↓
Increase BR stimulation
↓
Increase BR discharge
↓
Afferents from cranial nerves IX & X
↓
Nucleus of tractus-solitarius
↓ Glutamate
Excitation of CVLM
↓ GABA
Inhibition of RVLM (sympathetic output stimulate by here)
↓ ↓
Reduction in sympathetic output to CVS Increase in parasympathetic output to CVS
↓ ↓
Heart- decreased HR & Heart- decreased HR
Stroke volume (→ reduced cardiac output)
(→ reduced cardiac output)
↓
Vessels
Veins- reduced venous return  Parasympathetic stimulation no effect on
(→ reduced cardiac output) heart contractility
Arterioles- reduced resistance  No parasympathetic regulation for the
(→ reduced BP) blood vessels
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Direct afferents to RVLM
 Chemoreceptors (detect chemical composition of the blood)

– ↑CO2, ↓O2 stimulate discharge (i.e. Raise BP)
 Cerebral cortex
– Rise in BP with emotions
 Hypothalamus (causes blood pressure to rise or fall with emotions)
 Reticular formation
– Pain causes rise in BP
– prolonged pain may cause fall in BP
 Vagal afferents from lung inflation
– sinus arrhythmia
Low pressure receptors
 Atria, pulmonary arteries and veins

– function at lower pressures
– more responsive to volume changes
Other CVS reflexes
1.) Bainbridge reflex (to equalize VR to CO)

Describes a rise in atrial stretch causing an increase in sympathetic output
and a rise in the heart rate:
Transient increase of VR to the RA
↑ BP in RA
Stimulate RA stretch receptors
Direct Vagal afferents to RVLM
↑ Sympathetic activity, ↓ Parasympathetic activity to heart
↑Both HR (+ chronotropic) & cardiac contractility (+ inotropic)
↑ CO
So, VR = CO
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2.) Cushing reflex
 CNS ischaemic response - Ischemia of VMC or BP <60mmHg
Increased intracranial pressure
Cerebral ischemia - Ischemia of VMC or BP <60mmHg
Activation of sympathetic output from medullary VMC
↑HR/ ↑myocardial contractility/↑TPR - ↑BP
 Raised intracranial pressure causes high BP by Cushing reflex  stretch baroreceptors

 baroreceptor reflex activation  ↓HR ( BRADICARDIA)
Bradycardia + high SBP
EX: patients with cerebral stroke, we can see bradycardia with increased systolic BP
The valsalva manoeuvre
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 The Valsalva manoeuvre is a test that is used for testing the function of the autonomic nervous
system.
 Performed by expiration against a closed glottis.
Phase 1: increased BP
o due to an increase in intrathoracic pressure that is added to the aortic pressure.
Phase 2: fall in the blood pressure.
o The rise in intrathoracic pressure causes a decrease in the venous return.
o The reduced venous return causes a reduced stroke volume and therefore cardiac output
followed by blood pressure.
Phase 3: increased BP
o As the BP reduces in phase 2, the baroreceptor reflex is initiated to increase the
sympathetic output (baroreceptors are inhibited)
o Reduce vagal output: increased BP and HR.
Phase 4: rise in BP
o although the expiration against the glottis is released and the intrathoracic pressure
normalized, the blood pressure remain elevated for some time as the vasoconstriction
persists causing an elevation of the TPR.
SEQ
01) Briefly describe the regulation of cerebral blood flow in a healthy individual. (25 marks)
02) Describe the neural compensatory mechanism/s that operate/s under the physiological
conditions when there is an increase blood pressure. (20 marks)
03) Describe the neural regulation of blood pressure. (35 marks)
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10.) CORONARY CIRCULATION
Arterial circulation
• The perforator branches of right & left two coronary arteries supply the myocardium
• They arises from the sinuses of the aortic valve cusps
• They are patent throughout the cardiac cycle
• There are no significant anastomoses between coronary arteries, at very old age small
anastomoses can be seen
• Coronary arteries are ‘end arteries’
Venous circulation
• Most of the venous blood return to the heart via coronary sinus
• Coronary sinus drain into right atrium (RA)
• Some vessels directly empty into the heart chambers
1. The arterio-sinusoidal vessels
– Sinusoidal capillary like vessels that connect arteriole to the chambers
2. Thebesian veins
– Veins that connect capillaries to the chambers
3. Arterio-luminal vessels
– Small arteries draining directly to the chambers.
Coronary blood flow during cardiac cycle

 During systole
 Heart contracts & compresses the blood vessels.
 Also, pressure in the left ventricle LV) is higher than of aorta.
 The arteries supplying the sub-endocardial portion of the LV get compressed
during systole.
 The blood flow to the sub-endocardial portion stops during systole .
 The sub-endocardial portion gets blood supply only during diastole.
 In superficial portions get blood supply throughout the cardiac cycle.
The pressure gradients of coronary arteries
 The pressure difference between aorta & RV is higher than that of aorta & LV
(Aorta-RV) > (Aorta-LV)
 Therefore the flow is not appreciably reduced during systole for the RV
Aorta LV RV (Aorta-LV) (Aorta-RV)
Systolic 120 121 25 -1 95
pressure(mmHg)
Diastolic 80 0 0 80 80
pressure(mmHg)
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Flow of coronary arteries
When heart rate is increased (Tachycardia):
 The duration of cardiac cycle decreases

 The shortening is mainly in diastole.
 Reduction of coronary flow to the left ventricle.
 Decrease in diastole results decrease in ventricular filling.
 The left ventricular coronary flow decreases.
 Because no blood flow occurs during systole in the subendocardial portion of the left
ventricle, this region is prone to ischemic damage and is the most common site of
myocardial infarction.
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What happens to the patients with stenotic aortic valve?
 Blood flow to the left ventricle is decreased in patients with stenotic aortic valves.
 Because, the pressure in the left ventricle must be much higher than that in the aorta to
eject the blood.
 Consequently, the coronary vessels are severely compressed during systole.
 Patients with aortic stenosis are particularly prone to develop symptoms of myocardial
ischemia.
 In part because, of this compression and in part because the myocardium requires more
O2 to expel blood through the stenotic aortic valve.
 Coronary flow is also decreased when the aortic diastolic pressure is low.
Variations of coronary flow

 The coronary flow at rest is about 250ml/min.
 5% of the cardiac output.
 At rest heart extracts 70-80% of oxygen from each unit of blood.
The capacity for increasing O2 extraction from coronary blood flow is very limited.
 Oxygen delivery to cells can be increased significantly only by increasing the blood
flow
 During stress the coronary blood flow has to be increased
EX: If a patient has narrowed coronary artery and when more myocardial O2 is needed,
such as during exercise, the limited increase in flow may not be adequate to supply the
increased O2 demand because there is limited to no ability to extract more oxygen from
the coronary blood flow.
Auto-regulation of coronary blood flow

 The coronary flow shows considerable auto-regulation
 The coronary blood flow and the caliber of the arteries influenced by
– Pressures changes in the aorta (described above)
– Chemical factors
– Neural factors
 Chemical factors
 Products of metabolism cause coronary vasodilatation
– Hypoxia (↓O2) and local Increase of CO2
– H+, K+, lactate, prostaglandins, adenosine, adenine nucleotides
 Neural factors
 The β-adrenergic receptors in coronary arterioles
– Causes vasodilation
 The α-adrenergic receptors in coronary arterioles
– Causes vasoconstriction
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 Increased activity of noradrenergic nerves or an injection of nor-epinephrine results
coronary vasodilatation
– A secondary effect
– Vasodilation, due to production of vasodilator metabolites
 When the systemic blood pressure falls, the overall effect of the reflex increase in
noradrenergic discharge is increased.
 Then, coronary blood flow secondary to the metabolic changes in the myocardium at a
time when the cutaneous, renal, and splanchnic vessels are constricted.
 In this way the circulation of the heart, like that of the brain, is preserved when flow to
other organs is compromised.
Coronary artery disease
 The cholesterol plaques in the coronary arteries Causes obstruction to the blood flow
resulting myocardial ischemia
 When flow is reduced and results hypoxia to the cells results chest pain – angina
pectoris
 Many individuals have angina only on exertion, and blood flow is normal at rest. Others
have more severe restriction of blood flow and have angina pain at rest as well
 If the myocardial ischemia is severe and prolonged, irreversible changes occur in the
muscle, and the result is myocardial infarction
 MI is mostly due to rupture of the plaque

 Results thrombus formation over the plaque
 Causes complete occlusion of the coronary artery
 When myocardial cells actually die after MI, they leak enzymes into the circulation.
– CPK-MB
– Troponin T and I
– SGOT and SGPT
– LDH
 Measuring the rise in serum enzymes and iso-enzymes produced by infarcted

myocardial cells also plays an important role in the diagnosis & time of onset of
myocardial infarction.
 The ECG shows ST segment elevation in acute myocardial Infarction (acute MI)
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SEQ
19th Repeat
4. An 18 years old athlete runs a 400m relay during the Olympic games.
4.2 Briefly explain the mechanisms involved in maintaining the blood supply to his heart
muscles during the event. (25 marks)
27th Proper
1.5 List the factors regulating coronary blood flow. (10 marks)
1.6 Using a clearly labelled diagram explain the blood flow in the left coronary artery during the
cardiac cycle of a healthy individual. (25 marks)
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11.) CEREBRAL CIRCULATION
 ~15% of cardiac output goes to the brain
 A constant blood supply is needed as the brain rely on oxidative metabolism
Arterial circulation
 2 pairs of arteries form the circle of Willis

1) Internal carotid
2) Vertebral arteries
 Provides collateral circulation
 Cerebral arteries do not have cross-over of flow.
 Occlusion of a cerebral artery results in ischemia.
Venous drainage
 Via Dural sinuses and deep cerebral veins
 Special feature is that the veins are valve-less
Innervation of cerebral blood vessels

1) Post ganglionic sympathetic nerves
2) Cholinergic neurons
3) Sensory nerves
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Innervation Location of cell NT Primarily end on Effect
bodies
Post ganglionic Superior cervical Norepinephrine More proximal vasoconstriction
sympathetic ganglia Neuropeptide Y Large arteries
nerves
Parasympathetic Sphenopalatine Acetyl choline More proximal vasodilation
Cholinergic ganglia VIP Large arteries
nerves
Sensory nerves Trigeminal Substance P More distal Pain sensation
ganglia small arteries Sub. P-vasodilation
 Cerebral blood vessels are pain sensitive.
Ohm’s law
 Venous pressure in the brain is normally low. (2-5 mmHg)

 Venous pressure is mainly influenced by intra cranial pressure. (intra cranial pressure
directly effect on venous pressure of brain)
Cerebral blood flow= MAP-ICP

Resistance
Cerebral auto-regulation
 Is the ability of the brain to maintain relatively constant blood flow despite changes in
perfusion pressure.
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 Auto-regulation is maintained between the MAP of 65-140 mmHg.(ganong’s)
 Out of the range of auto-regulation cerebral blood flow is dependent on mean arterial
pressure in a linear fashion.
Regional cerebral blood flow
 In resting adult
– Grey matter has an average blood flow of 69ml/100g/min
– White matter has an average blood flow of 28ml/100g/min
– When awake the highest blood flow is to the premotor and frontal areas.
There can be marked variations of the regional blood supply of the brain
according to necessity, but the total blood flow remains constant.
Factors affecting the cerebral circulation
1. Vasomotor and sensory nerves.

2. Intra Cranial Pressure (ICP).
3. Local constriction and dilation of cerebral vessels.
4. Mean arterial and mean venous pressure at brain level.
5. Viscosity of blood.
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REPEAT CAMPAIGN |2021 Batch 30
|100
1.) Role of vasomotor nerves
 Large cerebral vessels are innervated by sympathetic and parasympathetic nerves
 Noradrenergic discharge occurs when blood pressure is markedly elevated (normally
other tissues when BP ↑  blood flow ↑)
 Then, vasoconstriction of cerebral blood vessels
 Reduces the resulting passive increase in blood flow (Plateau part of pressure flow curve
shift to right)
2.) Role of ICP

 Brain is encased in a rigid bony structure – the skull.
 Brain, CSF and blood are incompressible.
 Increase in volume in the skull increases the ICP.
 Increased ICP causes constriction of cerebral blood vessels.
 Increased ICP reduce cerebral blood flow.
 Reduced ICP increase cerebral blood flow.
↓Cerebral blood flow= MAP-↑ICP

Resistance
Cushing reflex
Increase in ICP
Compress blood vessels
Reduces blood supply to vasomotor area
Result in local hypoxia and hyperpnoea
Discharge of vasomotor area increase
Increase systemic blood pressure
Elevation of blood pressure result in baroreceptor discharge
Bradycardia ensues
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Local control of cerebral blood flow
1. Metabolic control
i. CO2 concentration
ii. H+ concentration
iii. O2 concentration
2. Myogenic response
1. Metabolic control
I. CO2 concentration
 Elevated CO2 - vasodilation due to elevated H+ in the extracellular space
 Reduced CO2 - vasoconstriction
This is used when there is cerebral edema where hyperventilation causes CO2 washout and
reduces the edema due to less cerebral blood flow.
II. O2 concentration
 Hypoxia is a potent vasodilator
 Reduced O2 causes ATP depended K+ channels to open.
– Hyperpolarization of smooth muscle cells.
– Relaxation of smooth muscle.
 Increase NO and Adenosine.  Vasodilation
2.) Myogenic response (Bayliss effect)
 Smooth muscle,
– intrinsic contraction in response to elevated systemic pressure
– Dilation in response to reduced systemic pressure.
Stretch of
artery
Vascular smooth
muscle cell
Depolarization
Ca2+ enter in to
the smooth
muscle cells
Arterial
Constriction
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Local flow
 Depending on the body part active, the blood flow increase to the corresponding part of
the brain.
 High metabolic demands of neural tissue require coordination between neuronal
activity and blood flow in the brain.
Neuronal activity ∞ Blood flow
EX:
 In subjects who are awake but at rest, blood flow is greatest in the premotor and
frontal regions.
 During voluntary clenching of the right hand, flow is increased in the hand area of the
left motor cortex and the corresponding sensory areas in the post-central gyrus.
Measuring blood flow to different parts of the brain

1. Positron emission tomography (PET)
2. Functional magnetic resonance imaging (Functional MRI)
3. Diffusion weighted MRI
PET of a person during speech
Broca’s area
Brain metabolism
 Approximately 20% of total body resting oxygen consumption happens in the brain.
 Brain is extremely sensitive to hypoxia.
 Glucose is the ultimate energy source.
 During prolong starvation brain can use lipid or amino-acid for energy.
 Either prolong hypoxia or hypoglycemia will cause severe brain damage.
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Blood brain barrier (BBB)
 Present in the endothelium throughout the brain.
 The apical tight junctions between capillary endothelial cells in the brain and between
the epithelial cells in the choroid plexus.
(More specifically the barrier in the choroid epithelium between blood and CSF /
BLOOD- CSF barrier)
Transport type in BBB Substance

Can’t transport All proteins, polypeptides, substances
bound to proteins, ions
Freely transport Water, O2 , CO2, lipophilic substances,
steroid hormones
By facilitated diffusion Glucose, Galactose, Amino acid,
Nucleotides
 Receptor mediated transport and active efflux transport has a role.

 Water movement into the brain by hydrostatic pressure is immediately apposed
(stopped) by the osmotic pressure gradient in the vascular lumen.
SEQ
22ND Proper
5.4 Briefly describe the regulation of cerebral blood flow in a healthy individual. (25 marks)
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12.) SPLANCHNIC, CUTANEOUS AND SKELETAL MUSCLE
CIRCULATION
Splanchnic Circulation
Comprises blood flow through
 Intestines
 Liver
 Spleen
 Pancreas
Receives 30% of cardiac output
Intestines
Spleen Portal vein
Pancreas
LIVER Hepatic vein
Hepatic Artery IVC
Intestinal blood flow
 Parallel circulation with extensive anastomosis.

 Local activity determines blood flow to each area.
Absorption – Villi and mucosal flow increase
Gut motility - smooth muscle blood flow increase
 Blood flow to small intestine doubles after a meal.
 Under normal conditions shunting of oxygen from the arterioles to the venules is not
harmful to the villi
 In disease conditions in which blood flow to the gut becomes greatly reduced oxygen
deficit in the tips of the villi can become so great that the villus tip suffers ischemic
death.
Factors causing vasodilation
Substances released from the mucosa

 Peptide hormones-Cholecystokinin,gastrin,secretin
 Kinins-Kallidin,bradykinin
 Adenosine
 Parasympathetic nerves – Increased glandular secretions causing a secondary effect in
increasing stomach and lower colon blood flo
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Vasoconstriction
 Sympathetic stimulation – displace blood to essential parts of the body (eg: brain and
heart) in stressful situations like exercise or shock.
 After a few minutes of vasoconstriction, the flow often returns almost to normal by
means of a mechanism called “autoregulatory escape.”
 It is the local metabolic vasodilator mechanisms due to ischemia
Spleen Circulation
Acts as a reservoir of blood

Rich in cells
Cutaneous circulation
 Sub dermal capillaries and venous plexus act as a reservoir of blood.
 Extensive arterio-venous anastomosis present in fingers, toes and palms.
 Flow can change from 1ml/100g of skin/min to 150ml/100g of skin/min.
 Important in thermal regulation.
 Increase in hypothalamic temperature causes vasodilatation.
 Noradrenergic nerve stimulation , circulating noradrenaline and adrenergic causes
vasoconstriction.
 No known neural vasodilator supply
 Vasodilator agents – Bradykinin and vasodilator metabolites
White Reaction - 15 seconds

Light pressure on the skin
(Mechanical stimulation)
Causes contraction of precapillary sphincters that drain out capillaries and small veins.
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Triple Response
Axonal reflex following firm pressure on the skin

1. Red reaction – 10 seconds
Capillaries dilate due to direct effects of pressure
2. Wheal – minutes
Increased permeability of the capillaries and post capillary venules
Local oedema
Swelling
3. Flare
Arteriolar dilation
Redness spreading out from the site of injury
Reactive hyperemia
Redness of an area of skin following reduced perfusion to the area.
Hypoxia causes vasodilation
Axon reflex
 Is a response in which impulses initiated in sensory nerves by the injury are relayed
antidromically down other branches of the sensory nerve fibres
 Transmitter released at the central termination of the sensory C fiber neurons is
substance P
 Substance P and CGRP (Calcitonin gene-related peptide) are present in all parts of the
neurons.
• Both dilate arterioles and substance
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Skeletal muscle blood flow
Even before the initiation of exercise neurally mediated vasodilation occurs.

Local mechanisms then maintain the blood flow with the start of exercise.
 Resting Muscle
low metabolic activity
blood flow is very low
4ml/100g of muscle/min
 During Exercise
The flow of blood increase to 50ml/100g of muscle/min
In athletes up to 80ml/100g of muscle/min
Muscle contraction compress the vessels and impede flow

10% of muscle contraction – compress vessel
70% of muscle contraction – complete occlusion
In rhythmic contraction the flow increase during relaxation of muscle
Acute control of skeletal blood flow - Vasodilation
 Oxygen lack theory

Lack of O2 and nutrients to vascular smooth muscles cause less contraction.
 Vasodilator theory
Adenosine, K+,CO2 , H+ ( lactic acid)
Produced due to lack of oxygen and continued metabolism despite reduced blood flow.
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Acute control of skeletal blood flow - Vasoconstriction
Noradrenaline – sympathetic stimulation
Vasopressin
Angiotensin II
Ca2+
 Active hyperemia - Vasodilation due to both vasodilatory substances and lack of O2 and
nutrients.
 During exercise active hyperemia increases muscle blood flow by x20
 This causes an increase in cardiac output
Normal adult x4-5
Athlete X 6-7
 Arteriolar and precapillary sphincter dilation increase number of capillaries x10-x100
 With dilated capillaries the distance for O2 and nutrients to diffuse reduce and surface
area increase.
 Velocity of flow reduce.
 Rise in temperature, H+ & 2,3 DPG releases more oxygen to the tissues.
 Oxygen- Haemoglobin dissociation curve shifts to the right
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13) CARDIOVASCULAR CHANGES IN EXERCISE
Type of contraction
Isotonic Isometric
 Muscle tone remains the same, but  Muscle length remains the same, but
muscle length reduces muscle tone increases
 Aerobic/Cardiovascular Exercises  Static, weight, or resistance exercises
 The muscles are relaxed in between  The muscles are tonically contracted
contractions
Eg:-Walking Eg:- Carrying a bag

Running Weightlifting
Cycling Rock climbing
Dancing Athletic throwing events
Skipping
Swimming
CVS changes in Isotonic exercises CVS changes in Isometric Exercises

Heart Rate ↑ Heart Rate ↑
Systolic BP ↑ Systolic BP↑↑
Diastolic BP slight ↑→↓ Diastolic BP ↑↑
Total Peripheral Resistance ↓ Total Peripheral Resistance ↑
Stroke Volume ↑ Stroke Volume →
Muscle Blood Flow ↑↑ Muscle Blood Flow↓
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Aerobic/Anaerobic
Aerobic Anaerobic
 Prolonged  High intensity
 Slow twitch skeletal muscles are involved  Fast twitch skeletal muscles are used
(red muscle fibers) (white muscle fibers)
(Refer skeletal muscle note) (Refer skeletal muscle note)
 In early exercise glucose used  Creatine phosphate and glucose used as
 Later free fatty acids are used fuel
 Fuels stored in muscle, adipose tissue, and  Fuels stored as Glycogen and creatinine
liver phosphate in muscles
 CO2, H2O, and energy produced  Lactic acid and energy produced
Eg:- Swimming Eg:- Sprinting

Long distance running Weightlifting
Intensity of Physical
activity
Mild, Moderate Heavy Severe
 Occurs below  Above aerobic capacity  Above aerobic capacity
aerobic  Initially lactic acid elevates  Lactic acid continues to rise.
capacity  Later gains a steady state  Unsteady state
 Lactic acid is and remain constant can Eg:-100m running
not elevated be maintained for a long
period because lactic acid level In severe exercises compensatory mechanisms
become constant start to fail when 1. Heart Rate > 180/min
Because of this diastolic time reduces and
ventricular filling reduces. So,
1.stroke volume reduces.
2.High temperature
3.pH increase caused by lactic acid
accumulation.
(This becomes the limitation of exercise)
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Cardiovascular changes in Exercise
Aim of these changes : To supply more blood active muscles, heart, lungs and skin
1. Increased venous return due to

Stroke Volume a. Increased muscle pump
Cardiac output b. Increased thoracic pump
increases c. Increased rate of circulation
d. venoconstriction
2. Increased contractility of heart muscle due to
Heart Rate a. Sympathetic activity (beta 1 receptors of
cardiac muscle)
3. Increased heart rate due to

a. Sympathetic activity (beta 1 receptors)
Maximum HR = 220/min – age

When HR > 180/min CO reduces due to decreased diastolic
Cardiovascular Redistribution of time
changes blood Heart rate increases 4 times in an untrained person and 6
times in a trained athlete
1. Reduced blood flow to some organs by vasoconstriction

a. Renal, splanchnic, and inactive muscles
2. Increased blood flow to
Increased blood flow a. Heart because increased HR and contractility
to active muscles b. Skin because increased temperature
c. Active muscle
3. Cerebral blood flow remains constant
Increased Sympathetic activity – This Muscle receives blood flow between contractions. During contractions blood
starts even before exercising when we vessels are compressed and the flow is minimum.
think to exercise (psychic stimuli) Blood vessels of the muscles are dilated by
Decreased Parasympathetic activity to the 1. Initially sympathetic activity (beta 2 receptors of vessels)
heart 2. Later it is maintained by vasodilator metabolites
a) Increased K+
b) Increased H+ due to lactic acid production in severe exercises
c) Increased temperature
d) Increased PCO2
e) Reduced PO2
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Pulsatile nature of muscle blood
flow
Main CVS changes

 Heart Rate ↑ proportionate to Level of
Exercise
 Stroke volume ↑ up to a certain level.

When Heart rate > 180/min stroke volume
decreases because the diastolic time
reduces
 Systolic Blood Pressure ↑ proportionate

to level of exercise
 Diastolic Blood Pressure can slightly

↑/↓/→(same)
 Pulse pressure ↑ significantly because

Systolic blood pressure increased
significantly
 Mean arterial pressure slightly ↑ because

increase of diastolic blood pressure was
slight
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Trained athlete Vs Untrained athlete
Trained athletes have,

1. Greater cardiac outputs
2. Greater end-systolic ventricular volumes
3. Greater stroke volumes
4. Larger hearts
5. Lower heart rates
6. Lower total peripheral resistance – (Due to recruitment of new blood vessels)
than untrained people.
Because of they have greater stroke volumes at rest, during exercises trained athletes can
increase their cardiac output without increasing their heart rate significantly.
Questions
1) Why does a sprinter can never win against a long-distance runner in a 3000m race?
2) Briefly outline the physiological basis for the following findings in a trained athlete after
a 10000m race
• Systolic blood pressure of 160mmHg (35 marks)
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14.) PHYSIOLOGY OF SHOCK
 Shock is a state of peripheral circulatory failure that is characterized by inadequate
perfusion of the peripheral tissues.
 During shock, the systolic arterial pressure is usually <90 mm Hg, and the mean arterial
pressure is <70 mmHg
 Leads to organ failure and death
Classification of shock
Hypovolemic Cardiogenic Obstructive Distributive

shock shock shock shock
Neurogenic
shock
Septic Shock
Anaphylactic
shock
1.) HYPOVOLEMIC SHOCK
 Large hemorrhages, in which one loses 30% or more of total blood volume produce
hypovolemic shock.
↓Preload  ↓ LVEDV  ↓Stretch of ventricle  ↓ SV  ↓CO  ↓Tissue perfusion
Hypovolemic Shock -Causes

 Hemorrhagic
– Trauma
– Gastrointestinal
– Retroperitoneal
 Fluid depletion (non-hemorrhagic)
• External fluid loss
– Dehydration
– Vomiting
– Diarrhea
– Polyuria
• Interstitial fluid re-distribution
– Thermal injury
– Trauma
– Anaphylaxis
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Compensatory mechanisms for hypovolemic shock
 Main target – to restore the BP
 First - circulatory control mechanisms act on the heart and blood vessels
to restore cardiac output and to increase peripheral resistance.
 Second- mechanisms of capillary exchange and fluid conservation
restore the intravascular volume.
Rapid(first) mechanisms Hemorrhage
Central blood ↓Venous

volume return (↓VR)
↓VR ↓SV
↓Atrial volume ↓CO
↓Regional
blood flow
Low pressure ↓Arterial
baroreceptor pressure
↓pH of
↓O2, ↑CO2, ↓pH brain ECF
High pressure
baroreceptors
Peripheral Central
chemoreceptors chemoreceptors
Medullary CVS
regulatory center
(Sympathetic
response)
↑Heart rate
↑Contractility Renin secretion
Arterial constriction Venous constriction
ANG II
(Described below)
↑CO ↑TPR ↑VR
↑SBP ↑DBP ↑CO
↑Arterial ↑SBP
pressure
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Secondary(slow) mechanisms
1.) Renin-angiotensin-aldosterone system (RAAS)
Hemorrhage
Reduced perfusion
of kidney
Renin ACE in lungs
Angiotensinogen in Angiotensin I Angiotensin II

blood
Potent vasoconstrictor Adrenal cortex Posterior pituitary Hypothalamic thirst

center
↑TPR ↑Aldosterone secretion ↑ADH ↑Thirst sensation
↑Na+ & water ↑Water retention ↑Water intake

retention in kidney in kidney
Restoration of blood
volume
↑ BP towards
normal
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2.) Capillary exchange
 Arteriolar constriction → Reduced capillary pressure → Fluid moves from interstitial

space to capillaries → ↑circulating blood volume
3.) Increase albumin synthesis in liver Long term

4.) Increase erythropoietin secretion from kidney regulation
5.) Increase 2,3 BPG in RBC
Clinical features of hypovolemic shock
– Narrowing of the pulse pressure.

– Sensation of faintness when sitting or standing.
– Cold and moist (“clammy”) skin.
– Rapid and weak pulse.
– Urine output drops to <25 ml/hr, even if fluid intake had been normal.
2) CARDIOGENIC SHOCK
 Reduced cardiac function from direct myocardial damage or mechanical abnormality

leading to reduced CO and BP
Causes for cardiogenic shock

 Myopathy
• Myocardial infarction (hibernating myocardium)
• Left ventricle/ Right ventricle
 Myocardial contusion (trauma)
 Myocarditis
 Cardiomyopathy
 Post-ischemic myocardial stunning
 Septic myocardial depression
 Pharmacologic
• Anthracycline cardiotoxicity
• Calcium channel blockers
 Mechanical
• Valvular failure (stenotic or regurgitant)
• Hypertrophic cardiomyopathy
• Ventricular septal defect
 Arrhythmic
• Bradycardia
• Tachycardia
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3) OBSTRUCTIVE SHOCK
 Secondary to obstruction to the cardiovascular unit.
– Tension pneumothorax
– Pericardial effusion(cardiac tamponade)
– Pulmonary embolism
– Aortic stenosis
 Leads to inadequate diastolic filling or decreased systolic function secondary to increase
in after load (RESISTANCE).
 Leads to reduce CO and BP.
Impaired diastolic filling Impaired systolic contraction
(decreased ventricular preload) (increased ventricular afterload)
 Direct venous obstruction (vena cava)  Right ventricle
– Intra-thoracic obstructive – Pulmonary embolus (massive)
tumors – Acute pulmonary hypertension
 Increased intra-thoracic pressure  Left ventricle
– Tension pneumothorax – Saddle embolus in aorta
– Mechanical ventilation (with  Aortic stenosis
excessive pressure )
– Asthma
 Decreased cardiac compliance
 Cardiac tamponade (pericardial
effusion)
4) DISTRIBUTIVE SHOCK
I. Septic (bacterial, fungal, viral) shock
II.Anaphylactic shock
III. Neurogenic shock
Septic shock
 Presence of infection associated with a systemic inflammatory response.
 Results in physiologic alterations at the capillary endothelial level.
– Activation of host defense mechanisms that result in the influx of activated
neutrophils and monocytes
– Release of inflammatory mediators (cytokines)
– Local vasodilation
– Increased endothelial permeability (leakage of capillary fluid)
Clinical features of septic shock
 Systemic vasodilation due to inflammatory mediators (cytokines)
 ↓SVR (TPR)
 ↓DBP (hypotension)
 ↓Vital organ perfusion
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As a compensation,
BP=CO×TPR
(TPR decreased so, maintain the BP, CO should increase)
 HR & CO increased
 ↑SBP
 Large pulse pressure (↑SBP-↓DBP)
 Warm extremities due to the good capillary refill
Anaphylactic shock
 Anaphylaxis is an acute, potentially fatal, multi organ system reaction caused by the
release of chemical mediators (histamine) from mast cells and basophils.
Allergen B-lymphocytes IgE Mast cells histamine vasodilation
Physiological responses to anaphylaxis mediators

– Smooth muscle spasm in the respiratory and gastrointestinal (GI) tracts.
– Vasodilation
– Increased vascular permeability.
– Stimulation of sensory nerve endings.
– Increased mucous secretion.
– Increased bronchial smooth muscle tone.
– Airway edema.
 Cardiovascular effects
– Vasodilation (decreased vascular tone)
– Capillary leakage
 Hypotension, cardiac arrhythmias, syncope, and shock can result from,
– intravascular volume loss
– Vasodilation
– Myocardial dysfunction.
 Increased vascular permeability can produce a shift of 35% of vascular volume to the
extravascular space within 10 minutes.
(Clinical features same as septic shock)
3) Neurogenic shock (spinal shock)

 Rarest form of shock
 Caused by spinal cord trauma
 Sudden loss of autonomic and motor reflexes below the injury level
– Loss of vascular sympathetic tone
 Sudden loss of peripheral vascular resistance (↓TPR)
 Leads to vasodilatation and hypotension.
 Warm skin due to dilation of blood vessels.
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Physiological basis
I. Hypotension - Loss of vascular tone below the level of injury.
Arterial vasodilation Venous vasodilation

↓TPR ↓Venous return to the RA
↓ organ perfusion ↓SV
↓DBP ↓↓CO
↓SBP
II. Bradycardia
– Loss of sympathetic input from spinal cord
– Tonic parasympathetic tone is unapposed to heart
– Treatment by atropine  inhibit parasympathetic discharge
(All the other shocks try to ↑HR (tachycardia) except neurogenic shock)
Damage to the brain & spinal cord
Loss of sympathetic tone
Parasympathetic nervous system unopposed
Uncontrolled vasodilation
Low BP
Hypo-perfusion
Neurogenic shock
Summary of shock
Type of shock CO HR SVR PCWP EDV MVO2

HYPOVOLEMIC ↓ ↑ ↑ ↓ ↓ ↓
CARDIOGENIC ↓ ↑ ↑ ↑ ↑ ↓
OBSTRUCTIVE ↓ ↑ ↑ Afterload ↑ Afterload ↑ ↓
Preload ↓ Preload ↓
SEPTIC ↑ or↓ ↑ ↓ ↔ or ↓ ↓ ↑ or ↓
ANAPHYLACTIC ↑ ↑ ↓ ↔ or ↓ ↓ ↑
NEUROGENIC ↓ ↓ ↓ ↔ ↓ ↓
PCWP-Pulmonary Capillary Wedge Pressure (back pressure to LA)
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15) HEART FAILURE
What is cardiac failure

 The heart is unable to maintain sufficient cardiac output
 To meet the demand of the body
 Despite Normal venous pressure
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Terms to understand
 Pre load- depends on venous return
 After load-peripheral resistance
 Backwards failure- failure of heart to pump blood out
 Right heart failure- right ventricular failure
 Left heart failure- left ventricular failure
 Congestive heart failure- failure of both ventricles
 Forward failure- high output failure
Inability to maintain tissue perfusion due to increased demand
Causes of heart failure

 Myocardial dysfunction
– Ischemic heart diseases
– Hypertension
– Cardiac muscle abnormalities-cardiomyopathies
 Volume overload
– Valvular regurgitations
 Outflow obstruction
– Stenosis of the valves
 High output failure
– Anaemia , thyrotoxicosis
 Constricted ventricular filling
– Cardiac tamponade
Pre load (venous return)

– remember starling’s law of a normal heart
– increase in venous return resulting
– increased EDV- increased initial fiber
length
– increased SV and increased CO
– however failing myocardium
Results reduction of ventricular
function curve
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After load
– outflow resistance
– this is the load against that each ventricle contracts
– Depends on
– systemic and pulmonary resistance
– compliance of the vessels
– volume of blood
Compensatory mechanisms in heart failure
 ventricular dilatation
 ventricular hypertrophy
 increased ionotrophy
 neurohumoral activity
 peripheral vasoconstriction
 Neurohumoral activity largely depends on the sympathetic activity
th
Manifestations of heart failure
Left heart failure

Features:
– dyspnoea
– orthopnoea
– fatigability
– paroxysmal nocturnal dyspnoea
– fine crepirations at the lung bases
Right heart faliure

Features:
– Dyspnoea
– generalised oedema-dependent oedema
– raised JVP
– ascites
– tender enlargement of liver
Congestive heart faliure

Fluid accumulation of fluid occurs in
– lungs – pulmonary oedema
– dependent parts -ankle and sacral oedema
Features:
– combination of right and left heart failures
th
High output failure
– heart is unable to meet the tissue demands
– commonly seen in
o thyrotoxicosis
o beri beri
 Pathophysiology
– rise in venous pressure-congestion of organs
– salt and water retention due to
o decreased renal perfusion
o increase in sodium and water retention
– increased renin angiotensin aldosterone secretion
– increased vasopressin secretion
th
Treatment
– Classes of drugs
– diuretics
o reduces the congestion of lungs by increasing the urine output
– ACE inhibitors
o inhibits renin angiotensin aldosterone mechanism
– digitalis
o increased myocardial contractility
th
th
th

CVS Physiology - 220505 - 061700

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CVSPHYSI

01) Electrical properties of the heart………………………………….02

03) Cardiac cycle………………………………………………………………..34

04) Cardiac output……………………………………………………………..44

06) Structural features of circulation………………………………….58

07) Blood pressure……………………………………………………………..64

08) Heart sounds and murmurs………………………………………….67

09) CVS regulation………………………………………………………………75

10) Coronary circulation……………………………………………………..92

11) Cerebral circulation……………………………………………………….97

12) Splanchnic, Cutaneous and Skeletal muscle circulation.104

13) Cardiovascular changes in exercise……………………………..109

15) Heart failure…………………………………………………………………122

Structure - function relationship of cardiac muscle

RMP of ventricular muscle

RMP Depolarization AP Propagation of AP Contraction

 Cardiac muscle action potential has 5 phases.

Cardiac muscle About 300ms

 Magnitude is determined by ECF [Na+]

 Events occur in each phase

Phase Channels get opened Channels get Events

Phase 1 Transient K+ channels Voltage gated Na+ influx decrease

Phase 2 Voltage gated Ca2+ Ca2+ influx

Phase 3 Various K+ channels Voltage gated K+ efflux

Phase 4 K+ leak channels K+ diffuse out of the cell

Excitation - contraction coupling

• Releasing of Ca2+ from SR triggers by ECF Ca2+ entry.

Cardiac muscle action potential refractory periods

 Absolute refractory period

 Relative refractory period

o Because of this long absolute refractory period tetanization of the

 Parts of the heart beat in orderly sequence

 Atrial systole (0.1 S)  Ventricular systole (0.3 S)  Diastole (0.4 S)

 During diastole all 4 chambers are relaxed (0.4 S)

The cardiac conduction system

 Capable of spontaneous discharge.

 Located in the right atrium at the opening of SVC.

2) Inter nodal atrial pathways

 Three bundles of atrial fibers. (anterior, middle, posterior)

 Only connection between atria and ventricular musculature.

 Specialized conducting fibers.

 Passes to the purkinje system

 Depolarizes the inter-ventricular

 The wave of depolarization then

Electrical changes occurs in SA node

 Normal pacemaker of the heart – SA node

 Electrical changes of SA node can describe in 3 phases.

 Parasympathetic nervous system regulation

 Effect of sympathetic stimulation

• Sympathetic innervation to SA node by R stellate ganglion.

 Effect of Parasympathetic nervous system

 Effect of sympathetic nervous system

chronotropic action & inotropic action

 chronotropic – about action of heart rate

– Negative chronotropic – decrease heart rate

 Inotropic – about force of contraction of heart

– Negative inotropic action – reduction of force of contraction.

 The surface electrode

 The surface electrodes are known as ECG leads.