CARDIOVASCULAR PHYSIOLOGY

FOR UNIVERSITY STUDENTS

S. I. OGUNGBEMI
DEPARTMENT OF PHYSIOLOGY
UNIVERSITY OF LAGOS
Cardiovascular System
 INTRODUCTION
• Cardiovascular system (CVS: aka circulatory system)
consists of the heart and blood vessels.

 The Heart
• The heart is a muscular pump with 4 chambers.
• The chambers are 2 atria and 2 ventricles.
• The ventricles are the pumps arranged in series.
• These pumps maintain continuous blood flow and
blood perfusion round the body.
The Pump
The Heart
• The 2 pumps are left ventricle (LV) which pumps blood to
systemic circulation and right ventricle (RV) which
pumps blood to pulmonary circulation.

• LV output = RV output = 5000 mL/min of blood.

• Heart beats at 70-75 times per minute i.e. heart rate.
• LV or RV output/beat = 70 mL i.e. stroke volume.
• CVS circulates blood from the heart via a network of
arteries, arterioles, capillaries to body tissues and
• Drains blood from body tissues via venules, veins and
vena cavae to the heart.
 (Vascular System)
The Vessels
Thoracic
Aorta
Superior
Vena
Cava
 Major Functions of the Cardiovascular System
• Transport and supply of O₂ from the lungs to the body
tissues.

• Extraction and transport of CO₂ from the body tissues to

the lungs.

• Absorption and transport of nutrients (digested food,

electrolytes and vitamins) from gastrointestinal tract to
the body tissues.

• Extraction and transport of waste and by-products of

cellular metabolism from body tissues to excretory
organs: kidneys, gut, liver, skin, lungs.
• Transport of hormones from endocrine organs to target
tissues/organs.
• Distribution of body heat from body’s core to its surface,
aiding temperature regulation.
• Transport of red and white blood cells, immune factors,
playing role in defense against foreign antigens, viruses,
bacteria, parasites, fungi and cancer cells.
• Perfusioning of the body tissues, aiding tissue
hydration.

 Functional Divisions of Circulatory System

• Functionally, RV runs pulmonary circulation which is
in series with LV that runs systemic circulation.
• RV is a low pressure pump which receives deoxygenated
blood from superior (SVC) and inferior (IVC) vena cavae
via the right atrium.

• RV pumps the blood via pulmonary trunk and arteries to

pulmonary capillaries surrounding the alveoli.

• The blood is then oxygenated and drained into the LV via

left atrium and pulmonary veins.

• This is the pulmonary circulation of low pressure belt

of 25 (systolic) to 10 (diastolic) mmHg.
• LV receives the oxygenated blood and pump it to the
systemic circulation via aorta, large arteries arterioles and
systemic capillaries to body tissues.

• In returns, the capillaries, venules and veins then drain

blood from the body tissues via SVC and IVC to the right
atrium.

• This is the systemic circulation of high pressure belt

(SBP: 120 and DBP: 80 mmHg).

• The heart, especially the RV and LV, provides the

propulsive force as the pump for both pulmonary and
the systemic circulations.
 Structural Function of the Heart
• The heart lies slantly in the thorax in the thorax as an
inverted conoid.

• The superior portion where blood vessels enter and leave

the heart is the BASE.

• The extremity of the left ventricle is the APEX.

• The heart is a hollow muscular organ which weighs about

300 or 350 g in adults.

• The heart muscle is specially called cardiac muscle.

• The heart is made of 4 chambers: 2 atria and 2 ventricles

which lie side-by-side in series.
• It is divided by the septum into right and left portions.

• The right portion comprises right atrium and right

ventricle.

• The left portion comprises left atrium and left ventricle.

• It is also divided into 2 atria above and 2 ventricles below

by 2 atrioventricular valves on both right and left sides.

• There are 4 valves in the heart: 2 atrioventricular valves

described above and 2 semilunar valves at the exits of
aorta on the left and pulmonary trunk on the right.

• The inlet (atrioventricular) valve and the outlet (semilunar)

valve of each ventricle lie along side one another.
• So, the 4 valves lie in the same plane in the septum
separating the atria from the ventricles.

 The 3 Layers of the Heart

• The 3 layers of the heart are:

Endocardium
Myocardium and
Epicardium

• Endocardium
– It is the inner lining of the heart.
– It continues with the endothelium (i.e. the lining of
the blood vessels).
• Myocardium
– It is the muscular layer of the heart.
– It is made up of conductive and contractile cardiac
tissues.
• Epicardium
– It is a serous layer that function as the visceral layer
of the pericardium.
• Pericardium
– It is the conical sac within which the heart lies.
– It consists of inner serous pericardium and outer
fibrous pericardium.
– Inner serous pericardium composed of visceral
(attaching the heart) and parietal (attaching the fibrous
sac) layers.
• These 2 layers allows the heart to beat in the mediastinum
with minimum friction.

• Pericardium sets a limit to the maximum size of the

ventricles and prevents excessive stretching of the cardiac
muscle fibres during ventricular filling (with blood).

• It is attached to the diaphragm, fixing the apex during each

heart beat.

• Thus, during ventricular contraction the base and the

atrioventricular ring descends towards the apex.

• This arrangement increases the size of the atria for

subsequent venous return as blood is ejected from the
ventricles.
• Cardiac Valves
• Cardiac valves are thin flaps of flexible, endothelium
covered fibrous tissues.

• They are firmly attached at the base to the fibrous valve

rings.

• There are 2 types of valves: the atrioventricular (AV)

valves and semilunar valves.

• The AV valves are the right atrioventricular (tricuspid)

valve and the left atrioventricular (bicuspid or mitral)
valve.

• Semilunar valves are the aortic and pulmonary arterial

valves
• All the 4 valves lie in the same plane in the fibrous septum
which separates the atria from the ventricles.

• The movements of these valves’ flaps are passive.

• The valve ensure unidirectional flow of blood through the

heart without backflow.

• Blood Supply to the Heart

• The right and left coronary arteries and their branches
supply blood to the heart.

• They are the 1st branches to the heart just above the
aorta.

• Coronary venous blood is drained by the coronary sinus

• Nerve Supply to the Heart

• Sympathetic and parasympathetic nerves supply the heart.

• Parasympathetic fibres supply the atria, sinus node, AV-

node and conductive tissue via vagus nerve.

• Sympathetic nerves are from T₁ to T₄ via inferior cervical

(stellate) ganglion.

• The parasympathetic supplies slow down conduction speed

and heart rate.

• Sympathetic nerves speed up electrical conduction, heart

rate and force of contraction.
• The heart also possess some sensory fibres for
cardiovascular reflexes and pain signals.

• Function Histology of the Heart

• The cardiac tissue are divided into conductive tissue and

contractile tissue in the myocardium.

• Conductive Tissue

• The conductive tissue comprises special modified nerve

cells that initiate and conduct rhythmic depolarisations of
the myocardial cells.

• These specialised tissues are:

Sinuatrial (SA) node
 Internodal tracts
Atrioventricular (AV) node
Atrioventricular bundle of His
Purkinje fibres

• SA Node is located in the wall of right atrium (beneath

the epicardium) at superior vena cava and right atrium
junction

• It contains the pace-maker cells that originate

depolarisation and each subsequent heart beat.

• AV node lies beneath the endocardium of posterior wall

of the right atrium about the insertion of the tricuspid
valve, The internodal tract connects the SA node to AV node.
• These tracts are 3:
Anterior band of Bachmann
Middle band of Wenckebach
Posterior band of Thorel

• The specialised conductive cells of AV node is arranged

interiorly in a longitudinal fashion to form bundle of
parallel fibers called AV bundle of His.

• The bundle of His divides into the right and left bundle
branches.

• Purkinje fibres branch off from the main bundle and supply
the myocardium.
• Bundle branches and their smaller branches constitute a
fast conduction pathway through which excitation
impulses are rapidly spread throughout the heart.

 The Contractile Tissues

• A cardiac muscle cell is called myocardial fibre or cardiac
myofibril

• Histology of the myocardial tissue shows that myocardial

fibre is striated as it is in skeletal muscle.

• These fibres are cylindrical in shape with central nuclei.

• In addition to this striations, myocardial fibres are

interconnected into a latticework.
• It is difficult to see where a cell ends and another begins.

• Intercalated disc separate individual myocardial fibres.

• Intercalated disc has electrical conductance of 400 units

greater than that of ordinary cardiac muscle membrane,
i.e. its resistance is ¼₀₀ unit of myocardial membrane.

• The adjacent myocardial fibre membranes fuse with each

other to form “tight junctions”.

• These tight junctions allow complete free diffusion of ions

in and out of the myocardial fibres.

• Tight junction makes the entire myocardium contracts as

if it were a large sheet of muscle – i.e. functional
syncytium.
• Action potentials from adjacent cardiac myofibrils are
conducted speedily through the intercalated discs and tight
junctions to all cardiac myofibrils.

• This leads to depolarisation of the entire heart at once.

• Subsequently, the entire ventricular myofibrils also

contract in synchrony in order to develop adequate
expulsive force to pump out blood.

• The syncytial arrangement of myocardial fibres enables the

contraction wave to rapidly spread from one myofibril to
another until the whole ventricular mass contracts at once.

• The detail histology of the heart is given under nerve-

muscle physiology.
 Note

• No nerves are involved in the spread of contraction

waves throughout the myocardium.

 Evidence

• It has been shown that series of interdigital cuts through a

piece of atrial or ventricular muscle such that could severe
any nerve running in it could not prevent synchronous
contraction.

• Despite the cuts, application of contraction waves at one

part would spread through to the whole myocardial mass
producing synchronous contraction.
 Functional Structure of the Vessels
 Blood vessels are arteries and veins
 In addition, there are also lymphatic vessels.
• In general circulation plan:
Aorta leads from the heart to supply blood and divides
to become arteries.
Arteries then divide repeatedly to become arterioles.
Arterioles divide repeatedly to become capillaries.
Capillaries unite to become venules.
Venules unite to become veins.
Veins unite to become vena cava which then returns
blood to the right atrium.
• Arteries and veins have 3-layer walls:
Tunica intima
Tunica media
Tunica adventitia

• Tunica intima is the innermost layer, composed of a super-

smooth epithelium called endothelium which continues
with endocardium of the heart.
• Tunica media is the middle layer composed of smooth
muscle
• Tunica adventitia is the outermost layer of connective
tissues.
• Aorta and large arteries are blood distributing or
conducting vessels, distributing oxygenated blood.
• They have thinner wall of smooth muscle and larger wall
of elastic tissues.
• They are stretched during systole but are elastically
recoiled during diastole.
• The elastic recoil during diastole impacts momentum to the
blood flow in the arteries (impact of 40 mm Hg).
• The elastic recoil results in diastolic pressure of 80 mm
Hg.
• The stretch/recoil cycle provides continuous blood flow in
circulation.
• Arterioles contain thick layer of vascular smooth muscles.

• These smooth muscles have sympathetic and

parasympathetic innervations.

• Smooth muscle responds to vasoactive agents like

adrenaline, noradrenaline and acetylcholine

• Arterioles are the major sources of peripheral resistance to

blood flow in circulation.

• Alterations of arteriolar radius bring about changes in

peripheral resistance, blood pressure and blood flow.

• R α ¹⁄r⁴ → R = ⁿ⁄r⁴: where R = peripheral resistance; r =

arterial radius; n = constant.
• Decrease in radius (vasoconstriction) increases peripheral
resistance (R) while increase in radius (vasodilatation)
decreases R of the arterioles.
• Decrease in R increases flow (F) and vice versa
• Increase in R or F increases mean arterial pressure (P)

• Capillaries are the smallest vessels with diameter of about

8 μm.
• They are one cell thick endothelial wall but just large
enough for an RBC to pass through at once.
• Capillaries are sites of exchange of substances between
blood and tissue cells.
• Filtration occurs at the arterial end of the capillaries
(mostly O₂ and nutrients, ions, hormones)

• Reabsorption occurs at the nervous end (removing CO ₂,

waste products and metabolites)

• Veins are blood drainage vessels, draining and returning

blood into the heart.

• They return deoxygenated blood to the heart.

• They are thinned-walled low pressure and cylindrical

distensible vessels.

• They are capacitance vessel containing about 75% of the

entire circulating blood volume.
• Some veins have one-way valves which prevent reflux of
blood flow as they drain blood against gravity.

• They possess sympathetic innervation which maintains the

venomotor tone.

• Venules are the smallest veins with less prominent

muscular walls than those of arterioles.
 PHYSIOLOGICAL PROPERTIES OF THE HEART
• Physiological properties that are peculiar to cardiac
tissues/cells are listed below as follow:
1. Spontaneous and automatic cardiac rhythmicity
2. Length-Tension relationship
3. Prolonged repolarisation of action potentials
4. Absolute refractoriness
5. Functional syncytium nature of cardiac myofibril
6. Obeys all or none law
7. Double innervation
• Note: the 6th property is common to skeletal muscle or nerve cell
and 7th property is common to some visceral tissues as well.
 Length-Tension Relationship
• If the length of a cardiac myofibril is increased, the force
of contraction also increases.

• Starling’s law states that the force of contraction of cardiac

myofibril is proportional to its extension and initial length.

• The initial length is the resting length before the extension

of the cardiac myofibril or muscle fibre.

• These fibres are extended by blood filling the ventricles i.e.

blood volume exerts tensions on the heart muscle fibres.

• In addition at resting length, these cardiac myofibrils

assume sarcomere length for maximal contraction.
• This extension by the filling blood volume stores up
potential energy which is kinetiated into contraction
(mechanical energy).

• This energy from mas to ½κε² means mas = ½κε²

• κ = extension constant

• ε = extension of the myocardial fibre

• m = mass of the myocardial fibre

• a = acceleration of the myocardial fibre during contraction.

• s = distance covered by the myocardial fibre during

contraction.
• The force of contraction is increased by positive inotropic
agents like Ca²⁺, adrenaline, noradrenaline, thyroxine etc.

• On the other hand, the force of contraction is reduced by

negative inotropic agents like K⁺, acetylcholine etc.

 Note
• Excess Ca²⁺ will make the heart to stop working at systole
(i.e. cardiac arrest at systole).

• Excess K⁺ will make the heart to stop at diastole (i.e.

cardiac arrest at diastole).
 Spontaneous and Automatic myocardial Rhythmicity
• Inherently, the heart is able to initiates its own electrical
excitation, contraction and heart beat without nervous or
humoral stimulation from any tissues outside itself.

• So the cardiac myofibrils contract (at systole) and relax (at

diastole) alternately in a rhythmic manner inherently.

• Conductive tissues which produces spontaneous excitation

and contraction are the source of this ability of the heart.

• The conductive tissues are the SA and AV nodes, bundle of

His and Purkinje fibres.
 Prolonged Repolarisation
• The action potential in the myocardial or contractile
cells lasts about 300 msec unlike the 2 msec in skeletal
muscle.

• This is due to the fact that repolarisation phase of the

action potential (AP) is prolonged in cardiac muscle cells.

• Slow influx of Ca²⁺ or slow inward Ca²⁺ current is

responsible for the prolonged repolarisation phase.

• Ca²⁺ moves slowly inside cardiomyocytes to produce the

plateau, resulting in persistent depolarisation during the
prolonged repolarisation phase of cardiac AP

• This persistent depolarisation is a positive membrane

• Ca²⁺ influx is via potential sensitive channels (PSC) of the
cardiacmyocytes which opens during electrical excitation.

• Ca²⁺ also flux in via receptor operated channels (ROC)

which are sensitive to noradrenaline, adrenaline (agonists).

• Influx of ISF Ca²⁺ stimulates the release of more Ca² ⁺ᵢ

from sarcoplasm reticulum which then induce cardiac
muscle contraction.

• Ca²⁺ channels blockers like verapramil or nifedipine

inhibit Ca²⁺ entry following depolarisation of the
myocardial cells.
 Functional Syncytium Myofibrils
• The cardial myocytes function like a syncytium.

• Because the whole ventricular or atrial myofibrils contract

at once as if they were one myofibril.

• Cardiac myofibrils possess intercalated disc, tight and gap

junctions which make them to contract as a syncytium.

 Absolute Refractoriness
• A second excitation cannot cause the cardial myocytes to
depolarise or contract while the first excitation in process.

• Therefore, the heart muscle cannot tetanise, because its

action potential (AP) is prolonged and the period of
contraction is as long as the duration of its AP.
• The prolonged absolute refractoriness makes it impossible
for the heart muscle to tetanise.

 Obeys “All” or “None” Law

• Cardiac myofibril does not possess graded excitation.

• These myofibrils are only excited to produce an AP (“all”

part of the rule) by a threshold or suprathreshold stimulus.

• On the other hand, the myofibrils are not excited by

subthreshold stimulus (the “none” part of the rule).

• Cardiac myofibrils doesn’t exhibit recruitment of fibres

with increase in stimulus strength unlike skeletal muscle.
 CARDIAC ELECTROPHYSIOLOGY
 Origin of the Heartbeat

• The 2 atria and the 2 ventricles beat in orderly rhythm as

atria systole is followed by ventricular systole.

• Systole of atria and ventricles occurs one after the other

respectively and is followed by diastole in orderly rhythm.

• The heartbeat ORIGINATES in a specialised cardiac

conducting system comprises modified nerve tissues.

• The conductive system generates and transmits electrical

current or action potential (AP) from one point to another
and to all part of the myocardium.
• The tissues that make up the conduction system are:
1.Sino-atria node (SA node)
2.3 atria internodal pathways
3.Atrioventricular node (AV node)
4.Bundle of His and its branches
5.The Purkinje system

• The SA node is the cardiac pacemaker, since it originates

AP spontaneously and automatically and spread to all
other conductive tissues and myocardium.

• Other conductive tissues and myocardium are induced in

this way to generate and transmit impulses.
• SA node discharges AP most rapidly than AV node,
conductive fibres and myocardial fibre.

• SA node firing rate superimposes those of all others,

making them to discharge at the same rate with SA node.

• SA nodal rate equals heart rate as the pacemaker.

• AP generated in the SA node spread through the atrial

pathways to the AV node.

• AV node then spread AP via His bundle and its branches.

• Finally, AP is spread to the ventricular muscles (for

contraction) via Purkinje fibres.
 Origin and Spread of Cardiac Excitation
• P (pacemaker) cells produce AP in the SA node.

• They are small round cells (with few organelles) joined

by gap junction and found in large population in SA
node.

• They are also found in AV node but in a lesser

population.

• SA nodal P cells send AP radially via the atria to

converge on the AV node through:
1. Anterior internodal tract of Bachman
2. Middle internodal tract of Wenckebach
3. Posterior internodal tract of Thorel and
• The atrial depolarisation is complete within 0.1 s.

• In the AV node, depolarisation is then sent to the ventricles

with a slow conduction of 0.1 s delay.

• Sympathetic stimulation hastens the conduction,

shortening the delay while vagal stimulation lengthens the
conduction, prolonging the delay.

• Depolarisation waves then further spread from the top of

interventricular septum in the Purkinje fibres rapidly to all
parts of the ventricles within 0.08 – 0.10 s.

• This depolarisation is so rapidly spread in the His bundle-

Purkinje fibres and ventricular muscle mass.
• Depolarisation wave is of similar shape, duration and
amplitude in His bundle-Purkinje and ventricular fibres.
• In the human hearts, ventricular depolarisation starts at the
left side of the interventricular septum, and then moves to
the right across mid-portion of the septum, spreading
down to the heart apex (base → apex).
• The wave returns along the ventricular walls to the AV
groove, from endocardial to epicardial surface and to the
posterobasal of the ventricle, pulmonary conus and
uppermost portion of the septum.

• Ventricular depolarisation is from left to right side (after

which impulses travel to the apex) while ventricular
repolarisation occurs in reverse direction (apex → base).
 Note
• Bundle of His and Purkinje fibres are normally quiet and
are just latent pacemakers.
• However, they are capable of spontaneous discharge only
if they are damaged.
• Atrial and ventricular myofibrils also do not discharge
spontaneously unless they are injured.
• Sinoatrial (SA) node discharges at 70/minute.
• Atrioventricular (AV) node discharges at 50/minute.
• Bundle of His-Purkinje fibre discharges at 45/minute.
• Ventricular myofibril discharges at 40/minute.
 Action Potentials in Cardiac Cells
• Cardiac action potentials (AP) are generated in:
a. Pacemaker or Conductive cells
b. Atrial cells and
c. Ventricular cells

• Pacemaker SA and AV nodal cells AP are similar

• Atrial, His bundle, bundle branch, Purkinje fibre and

ventricular AP are similar.

 Generation of Action Potential in Pacemaker Cells

• Pacemaker potentials are largely found in SA and AV

nodes
• Pacemaker potentials are pre-potentials that trigger another
AP following a previous AP.
• Pre-potentials are declinations of membrane potentials
from resting membrane potential (RMP: -60 mV) to firing
level (-40 mV) in pacemaker cells (magnitude of +20 mV).
• Depolarisation Phase
• After a previous AP in a pacemaker cell, h or f channels
which are permeable to Na⁺/K⁺ are opened.
• Influx of Na⁺ depolarise the pacemaker membrane – first
portion of pre-potentials, prominent in SA and AV nodes.
• Transient (T) Ca²⁺ channels are later opened to produce
Ca⁺⁺ influx (ICa²⁺) to complete the pre-potentials.
• There is also release of Ca²⁺ from sarcoplasmic reticulum
during pre-potentials.

• After the pre-potentials, longlasting (L-) Ca² ⁺ channels are

then opened to cause Ca²⁺ to produce depolarisation.

• Subsequently, pacemaker depolarisation is slow but not

rapid or sharp before the plateau.

 Repolarisation Phase
• At the peak of the pacemaker AP following the brief
plateau of ICa²⁺, there is opening of K⁺ channels.

• This then leads to increase in gK⁺ and influx of K⁺ and

subsequent repolarisation and hyperpolarisation.
• Following hyperpolarisation, IK⁺ or K⁺ influx declines to
activate h or f channels, bringing about another pre-
potential and depolarisation in the pacemaker cell.

 Effect of Cholinergic and Vagal Stimulation

1. Hyperpolarisation of pacemaker membrane with a slow
and decreased slope of pre-potential.
2. Release of acetylcholine at the nerve endings
3. Increase gK⁺ of nodal tissue cells.
4. Depolarising effect is slowing down the heart rate.
• Note: M₂ muscarinic receptor and decrease in cAMP is
responsible for these vagal effects.
 Effect of Sympathetic Stimulation
1. Speeds up gNa⁺ and gCa²⁺ via h- and T- channels
respectively.
2. Speeds up depolarisation spike frequency via L-
channels.
3. Stimulate β₁ receptors to produce increase heart rate.
4. Noradrenaline and increase cAMP facilitates opening of
L-channels.
 Further Information
• Temperature or fever increases discharge frequency of
SA and AV nodes to produce increase in heart rate.
• Digitalis depresses nodal tissues particularly on AV
• Digitalis (i.e. digoxin and digitoxin) depresses nodal
tissues particularly on AV nodes to exert vagal-like effects.
• Digitalis is a known treatment for systolic heart failure.
• It augments ventricular contractility.
• It improves left ventricular emptying and cardiac output.
• It decreases ventricular filling pressure.
• It’s useful to treat atrial fibrillation and flutter by reducing
heart rate and frequency of AP transmission through AV
node and heart rate. via
• Digoxin and digitoxin strengthens cardiac contraction
through the inhibition of Na⁺/K⁺ ATPase.
• This is achieved via greater release of Ca²⁺ and subsequent
improvement in contraction force.

• Digitalis decreases AV nodal conduction velocity in order

to improve transmission to the ventricle.

 Artificial Pacemaker

• Artificial pacemaker is invaded under the chest skin below

the clavicle to help moderate heart rate and contractility.

• It generates electric current to stimulate atria and

ventricles.

• It has a pulse generator with one or more leads, powered

by a very reliable lithium battery.
• It lasts for many years about a size of 50 kobo coin.

• The leads connect the pulse generator to the inner wall of

the heart.

• The leads are made up of insulated metal coils with small

metal electrodes that attached to the heart.

• Types of artificial pacemakers are single chamber, dual

chamber and biventricular pacemakers.

• Single chamber pacemaker sets the pace of the left

ventricle and uses 1 lead.

• Dual chamber pacemaker sets the pace of 2 heart

chambers and uses 2 leads.
• It uses atrial electrical feedbacks to set the ventricular rate.
• It is very useful in the management of heart block.
• Biventricular pacemaker uses 3 leads for right atrium,
right and left ventricles.
• Artificial pacemakers are needed in management of
bradycardia, tachycardia, heart block and heart failures,
neurogenic syncope.
• It changes the atria and ventricles to pump blood at a
normal volume and rate.
• It senses and moderates the heart natural rhythms in case
of bradycardia and tachycardia, but switches off in normal
heart condition.
 Typical Cardiac Action Potential

• Typical cardiac action potential (AP) is found in atrial and

ventricular myofibrils, His bundle and Purkinje fibres.

• Atrial and ventricular myofibrils produces no prepotentials

nor spontaneous discharge except in injurious conditions.

• His bundle and Purkinje fibre are latent pacemakers which

neither produce pre-potentials nor spontaneous discharge
except when SA and AV nodes are blocked.

• Ventricular myofbril (or myocyte) action potential is here

presented as the typical cardiac AP for atrial, His bundle
and Purkinje Cells.
• SA and AV nodes then spread depolarisation to His bundle,
Purkinje and ventricular cells to generate action potential.

• Generation of AP is discussed under 5 phases.

1. Depolarisation phase 0
2. Initial repolarisation phase 1
3. Plateau phase 2
4. Final repolarisation phase 3 and
5. RMP phase 4
 Depolarisation Phase
• As the cardiac myocyte membrane becomes excited, there
is increase in gNa⁺ and Na⁺ influx into the cardial
myocyte via the voltage gated Na⁺ channels.
• This Na⁺ influx produces depolarisation of the cardial
myocyte from RMP of -90 mV until depolarisation of +15
mV (at -75 mV of the membrane potential) is reached.

• This depolarisation of +15 mV is the firing level (FL).

• At the FL, there is a spark of Na⁺ influx because

numerous thousands of voltage-gated Na⁺ channels are
opened.

• The membrane is then further depolarised from FL to peak

potential (+35 mV) through the zero potential.

• This is depolarisation phase 0.

• The next is repolarisation phases 1, 2 and 3.

 Repolarisation Phase
• After a time lapse, an initial rapid repolarisation phase 1
is produced due to 2 events:
– Closure of voltage-gated Na⁺ channels and the
subsequent reduction in gNa⁺/Iɴₐ⁺
– Transient efflux of K⁺ via K⁺ channels.

• Instantly, gCa²⁺ increases and Ca²⁺ influx into cardial

myofibrils via voltage- and ligand-gated Ca² ⁺ channels.

• The slow Ca²⁺ influx overbalance K⁺ efflux to produce

persistent depolarisation during the repolarisation
phase.

• This persistent depolarisation owing to slow I Ca²⁺ causes

the plateau that prolong the repolarisation phase.
• This Ca²⁺ influx (from ISF) also stimulates the release of
Ca²⁺ from sarcoplasmic reticulum of the cardial myofibril.
• The resultant 1000 fold increase in ICF Ca²⁺ then brings
about the initiation of muscle contraction.
• Ca²⁺ blockers (verapramil and nifedipine) reduce influx of
Ca²⁺ (at the plateau) and the cardiac contractility.
• The final repolarisation is produced by the K ⁺ efflux via
multiple types (especially) voltage-gated K ⁺ channels.
• There is also inactivation of Ca²⁺ channels and inhibition
of Ca²⁺ influx during the final repolarisation phase.
• The membrane potential is then brought from peak
potential (+35 mV) to RMP (-90 mV).
 ELECTROCARDIOGRAMME (ECG)
• Electrocardiogramme is the extracellular recording of the
combined voltage produced from the electrical activities
of cardiac muscle cells during each cardiac cycle.

• ECG gives the algebraic sum of the cardiac action

potentials of all the cardiac muscle fibres from different
regions of the heart during each cardiac cycle.

• This characteristics sequence of potentials are generated

by the heart during each cardiac cycle.

• Since the ISF surrounding the heart is an electrolyte and

electric conductor the body is a volume conductor of
electric current.
• This cardiac voltage or potential or ECG can be picked up
on the body using extracellular electrodes, because the
body is a volume conductor of electricity.

• This cardiac voltage becomes much attenuated by the time

it reaches the surface of the skin.

• So, ECG machines picks up this cardiac voltage using

amplifiers before it is recorded on moving strip of paper.

• The paper is ruled in mm²: 10 mm = 1 mV on the voltage

(“y”) axis and 25 mm = 1 s on the interval (“x” axis).

• ECG tracing contains P, Q, R, S, T and u waves on ruled

paper with each letter wave representing a depolarisation
or repolarisation of different regions of the heart.
 Measurement of Electrocardiogramme
• ECG is measured using ECG machines.
• ECG limb leads are metal plates connected to ECG
machine that are strapped over the flat portion of the
limb.
• ECG chest leads are small metal pots connected to ECG
machine that are attached to 6 positions on the chest.
• Electrode jelly is applied on the electrodes to ensure good
electrical connection.
• The 3 types of ECG leads used in recording ECG are:
– Standard limb leads which are bipolar leads
– Augmented unipolar limb leads
 Standard Limb Leads
• An electrode connects the right leg to the earth.
• The 3 leads in standard limb leads are numbered I, II, III.
• ECG from these 3 leads are recorded by connecting the
appropriate pair of electrodes to the amplifier.
• Lead I measures ECG voltage between right arm (RA) and
left arm (LA).
• Lead II measures ECG voltage btw RA and left leg (LL).
• Lead III measures ECG voltage between LA and LL.
• Summary: lead I → RA//LA; lead II → RA//LL and lead
III → LA//LL
 Augmented Unipolar Limb Leads
• This is an alternative way of measuring ECG.

• One input of the amplifier is connected to the other 2

limbs via 2 resistors.

• This records difference between potential in 1 limb and

the mean potential of the other 2.

• aVR is the lead attached to right arm (- deflection).

• aVL is the lead attached to left arm (+ deflection).

• aVF is the lead attached to the left foot (+ deflection).

• a = augmented; V = voltage
• The augmented leads increase the size of the potential by
50% without any change in configuration from the non-
augmented records ie aV = ³/₂ of unaugmented lead.

 Unipolar Chest Leads and Limb Leads

• Chest and limb lead ECG are recorded by connecting the

amplifier between exploring chest electrodes and
resistances connected to 3 limbs as indifferent electrodes.

• The 6 chest leads with their 3 aV limb leads, making 9

leads are commonly used in clinical electrocardiography.

• Chest leads and their recordings are designated V ₁, V ₂,

V₃, V₄, V₅ and V₆ while the aV limb leads and their
recordings are designated aVR, aVL and aVF.
• Amplifier converts the 9 unipolar to augmented leads by
increasing voltage amplitude by 50% without any change
in configuration from the nonaugmented recording.

• Anatomical location of chest lead positions are as follows:

• V₁ → 4th intercostal space immediately to the right of
sternum.
• V₂ → 4th intercostal space immediately to the left of
sternum.
• V₃ → midway between V₂ and V₄
• V₄ → 5th intercostal space in the left mid-clavicular line,
corresponding to the apex of the heart.
• V₅ → 5th intercostal space in the left anterior axillary
line in the same horizontal plane as V₄.
• V₆ → 5th intercostal space in the left mid axillary line in
the same horizontal plane as V₄.
 Normal Electrocardiograph Wave Movement
• The important consideration in interpreting the
configurations of the waves in each lead depends on:
1. The sequence in which the parts of the heart are
depolarised.
2. The position of the heart in relative to the electrodes.
• The atria are located posteriorly in the chest while the
ventricles form the base and anterior surface of the
• The right ventricle is anteriolateral to the left ventricle.
• Left ventricle is posteriolateral and form the apex of heart.
o The aV Limb Leads
• aVR looks at the cavities of the ventricles.
• Atrial and ventricular depolarisations and repolarisations
move away from the exploring aVR electrodes
• Therefore P, QRS and T waves are all negative or
downward deflections in aVR lead.
• aVL and aVF leads look at the ventricles
• Atrial and ventricular depolarisations and repolarisations
move towards the exploring electrodes aVL and aVF
• Therefore P, QRS and T waves or deflections are
predominantly positive or biphasic in aVL and aVF leads.
o The Chest Leads and Standard Limb Leads
• There is no Q wave in V₁, V₂ and V₃ and initial portion
of the QRS complex (i.e. R wave) is a minor upward
wave.
• Ventricular depolarisation first moves across the mid-
portion of intraventricular septum from left to right
towards the exploring V₁, V₂ and V₃ electrodes
• Then, depolarisation wave moves down the septum and
into left ventricle, but away from electrodes to produce a
large S wave.
• Wave lastly moves along the ventricular wall and towards
• Conversely, in the left ventricular leads, (V₄−V₆), there
may be initial small Q wave.

• Q wave represents left to right septal depolarisation.

• There is also a large R wave which represents septal and

left ventricular depolarisation.

• R wave in V₄ and V₅ is followed by a moderate S wave

which represents late depolarisation of the ventricular wall
moving back towards the AV junction.

• Note: there is considerable variation in the position of

normal heart which affects ECG QRS complex in various
leads.
• Deflection of P, QRS and T waves in V₁, V₂, and V₃ are
negative as these waves of depolarisation are moving
away from the position of the V₁, V₂, and V₃ leads.

• The deflection of P, QRS and T waves in leads V₄, V₅ and

V₆ and I, II and III are similar and positive.

• These waves of depolarisation are moving toward the

position of leads V₄, V₅ and V₆ and I, II and III.

 Cardiac Vector
• An approximate mean QRS vector (electrical axis of the
heart) is often plotted by using the average QRS voltage in
each lead.
• Approximation is done by recording net difference btw the
positive and negative peaks of the QRS complex.

• The normal direction of the mean QRS vector is taken as -

30 to +110 degrees on the co-ordinate system.

• Left axis deviation is presented if the calculated axis falls

to the left of -30 degree.

• Right axis deviation is presented if the calculated axis falls

to the right of +100 degree.

• Left axis deviation mean to left ventricular hypertrophy

(LVH), but there are more reliable ECG criteria for LVH.

• Right axis deviation suggest right ventricular hypertrophy.

• The mean electrical axis of the heart is calculated from
Einthoven’s triangle.

• The mean QRS vector in I, II and III are calculated.

• The values are plotted on appropriate axis of equilateral

triangle with perpendicular bisector to the to the centre.

• The point of intersection of the vectors values is joined to

the centre of the circle by a line.

• Therefore, the angle this line makes with the horizontal is

the mean axis.

• Vectorcardiogrammes of P, QRS and T waves are now been

done electronically and projected on the screen.
 The Synchrony of Cardiac Electrical Activities
• The figure below shows the synchrony of order, timing,
strength and duration course of individual cardiac cell
action potentials (AP) relative to the ECG waves.

• Production of APs in cardiac cells are in the order of: SA

node, atrium, AV node, His bundle, bundle branches,
Purkinje fibres and ventricular myofibrils.

• Meanwhile, depolarisation and repolarisation phases of

these APs from different heart portions synchronise in
order, timing and duration with:
– One another i.e. individual APs
– ECG depolarising and repolarising waves and
– Cardiac cycle.
• SA nodal depolarisation begins the electrical activity at
say time 0 s and its repolarisation lasts till 0.22 s after.

• Depolarisation of SA node is 0.08 s earlier than atrial

depolarisation and P wave on ECG tracing.

• Atrial depolarisation starts 0.08 s after SA node and its

repolarisation lasts till 0.25 s after the depolarisation.

• Atrial depolarisation starting time correspond with that of

P wave on ECG tracing.

• AV node depolarisation begins at about 0.12 s after that of

SA node following atrial depolarisation and corresponds to
the peak of P wave.
• AV node depolarisation lasts till 0.24 s from the start of
depolarisation.

• His bundle and branches and Purkinje fibre also begin

depolarisation at 0.2, 0.22 and 0.24 s respectively
following SA node depolarisation.

• Depolarisations of these fibres occur during PR segment

(no ECG wave but isoelectric line).

• Their repolarisation last till 0.32 s after depolarisation.

• Depolarisation of ventricular muscle fibre begins at 0.24 s

after SA node depolarisation (i.e. 0.16 s after P wave
onset) and its repolarisation lasts till 0.32 s after.
• The depolarisation of His bundle, Purkinje fibre and
ventricular myofibril produce the QRS complex.

• Their persistent depolarisation phase of the prolong

repolarisation produces and corresponds to the isoelectric
line of ST segment.

• Their final repolarisation phase produces and corresponds

to T wave.

• The prolonged repolarisation also corresponds to the

ventricular systole.

• This synchrony of the electrical activities of individual

heart portion is possible owing to the syncytium property
of the heart via intercalated disc and gap junction.
 Interpretation of ECG Tracing

• P wave (+) represents atrial depolarisation, because it is

produced by atrial depolarisation.

• QRS wave (+) represents ventricular depolarisation,

because it is produced by ventricular depolariastion.

• T wave (+) represents ventricular repolarisation, because it

is produced by ventricular repolarisation.

• Q wave (-) is produced by depolarisation of the middle ⅓

of interventricular septum.

• R wave (+) is produced by lower ⅓ of interventricular

septum and lower ⅔ of right and left ventricles.
• S wave (-) is produced by upper ⅓ of interventricular
septum and upper ⅓ of right and left ventricles.
• U wave (+) is produced by depolarisation of the papillary
muscles – an inconstant finding.
• Note: – wave produced by atrial repolarisation is not normally
seen, because it is superimposed by the larger QRS complex.
– Therefore, the unseen wave of atrial repolarisation is buried in
the QRS complex.
– S wave in V₁−V₃ appears to be a mirror image of R wave in
V₄−V₆
• PR interval is the period for atrial depolarisation and
conduction of AP from atria via AV node to the ventricles.
• PR interval also measures the period for the following
events, which occur during PR interval:
1. The spread of atrial depolarisation wave to the vicinity of
AV node.
2. The delay imposed by AV node – the main delay
3. The rapid spread of depolarisation from AV bundle and
its branches

• QRS duration is the period for ventricular

depolarisation (i.e. spread of AP) and atrial
repolarisation (Q wave)

• QT interval is the period for ventricular depolarisation

plus atrial and ventricular repolarisations.

• QT then stands for the duration of the AP in the

ventricles.
• P wave amplitude is normally 0.1-0.2 mV
• R wave amplitude is normally 1 mV
• Q wave amplitude is normally 0.1-0.3 mV
• S wave amplitude is normally 0.3 mV in V₄-V₆ chest and
limb leads.
• T wave amplitude is normally 0.3 mV.
• QRS wave amplitude greater than 5 mm or 0.5 mV is
written in capital Letter e.g. Q, R and S.
• QRS wave amplitude lesser than 5 mm or 0.5 mV is
written in small letter e.g. q, r and s.
• P wave duration is about 0.1 s.
• PR interval is about 0.18 s.
• QRS duration is about 0.1 s
• QT interval is about 0.40 s
• ST interval is about 0.32 s.
• T wave duration is about 0.18 s

• A Physiologist or Physician should be able to derive the

following from an ECG tracing:
 Heart rate
 Cardiac rhythm
 Electrical axis of ECG waves/anatomical orientation of the
heart
 Heart block
 Hypertrophy/relative size of the heart
 Myocardial ischaemia
 Accelerated conduction
 Arrhythmias

o Heart Rate
• Heart rate (HR) is calculated as 25 ÷ RR interval × 60

• If RR interval = 20 mm? HR = 25 × 60 ÷ 20 mm = 75 bpm

• In normal sinus rhythm (NSR), HR ranges 70 to 75 bpm.

• HR decelerates during sleep, expiration and accelerates by

emotion, exercise, fever, inspiration.
o Cardiac Rhythm
1. The source of heart electrical activity is cardiac rhythm.
2. A sinus (or atrial) rhythm originates from the SA node.
3. A junctional rhythm originate from the AV node.
4. A ventricular rhythm originates from the ventricles.

 Characteristics of Sinus Rhythm

1. Every QRS complex is preceded by a P wave.

2. The P waves in successive cardiac cycles are of uniform

morphology with little or no variations.

3. The P waves are upright (positive) in the leads.

4. The cardiac rate does not fall below 60 or above 100 bpm
– physiologic range.

5. The PP or RR interval are constant with difference not

exceeding 0.12 s (or 3 mm).

• Conditions 1-5 is called normal sinus rhythm.

• In sinus arrhythmia, conditions 1-3 are met but the

difference in the PP or RR intervals not differ from 0.12
s.

• In sinus bradycardia, the rate is below 60 while in sinus

tachycardia, it exceeds 100 bpm.

• Atrial rhythm is practically indistinguishable from

sinus rhythm in the physiological range.
o Characteristics of Junctional Rhythm

1. In junctional rhythm, the rate is between 40 and 60 bpm.

2. Its P wave is usually inverted, preceding, coinciding with

or following QRS complex.

3. It is described as slow junctional tachycardia between 60

and 100 bpm in spite of the physiologic range.

4. Above 100 bpm, it is described as accelerated junctional

tachycardia.

5. Young adults/athletes have SAN and AVN functioning

competitively at similar rate – isorhythmic rhythm.
6. Sometimes in alternation with AVN in control and at
other times the SAN in control.
 Characteristics of Ventricular Rhythm
1. Rate is 30-50 bpm (idioventricular rhythm)
2. Absent P waves
3. Wide QRS complex with duration exceeding 0.12 s
4. Ventricular rate between 50 and 100 is described as
accelerated ventricular rhythm.
 ECG Axis of the Heart and Associated Conditions
• Electrical axis of the heart is classified as:
1. Normal axis (within 0° to +90° or -30° to +110°)
• Left axis deviation (LAD: 0° to -90° or left of -30°)

• Right axis deviation (RAD: +90° to +180° or right of

+100°)

• Indeterminate axis (-90 to -180°)

• About 97% of normal Nigerians fall in the normal range

of electrical axis.

• 2.9% of normal Nigerian fall in LAD

• 0.1% of normal Nigerian fall in RAD and

• Indeterminate QRS axis is extremely rare in normal

subjects.
• The following conditions are associated with LAD:
1. Heart block
2. Myocardial infarction or ischaemia
3. Emphysema
4. Congenital heart disease
5. Hyperkalaemia
6. Ageing
7. Male sex
• Conditions associated with RAD:
– Normal variation
– Right ventricular hypertrophy
– Right ventricular conduction defect
– Dextrocardia
– Inspiration
– Emphysema
 ECG Pathophysiology
• Abnormal Pacemakers: they arise with damage to SA or
AV nodes

• Diseased or injured atrial and ventricular myofibrils can

act as abnormal pacemakers.

• Incomplete heart block is due to slow conduction

between atria and ventricles.

• 1st degree heart block is due to prolong nodal delay (PR >
0.20 s prolong nodal delay) with P wave : QRS = 1 : 1

• However, in first degree heart block, all the atria impulses

reach the ventricles.
• In 2nd degree heart block, not all atrial impulses are
conducted to the ventricles.

• A ventricular beat may follow every 2nd or 3rd atrial beat

i.e. P wave:QRS wave = 2:1 or 3:1 block.

• In Wenckebach phenomenon: repeated sequence of beats

with progressively prolonged PR interval until a QRS and
ventricular beat is dropped.

• The PR interval that follows each QRS or dropped beat is

usually normal or slightly prolonged.

• Right or left bundle branch block is due to interruption of

His bundle with deformed and prolonged QRS (>0.1 s)
depolarisation but normal ventricular rate or P:QRS.
• Hemiblock or Fascicular block occurs on the anterior or
posterior fascicle of left bundle branch.
• Left anterior hemiblock produces abnormal LAD on ECG
whereas left posterior hemiblock produces abnormal RAD.
• Combination of fascicular and branch blocks produces
bifascicular or trifascicular block.
• Complete heart block fully interrupts conduction from
atria to the ventricle by AV nodal or infranodal block.
• The ventricle beats at idioventricular rhythm of low rate
(43/min) independently of the atria (107/min).
• Independent P and QRS wave on ECG wave with regular
PP or RR interval but with irregular PR interval.
• Ectopic beat is extra premature beat which (transiently
interrupts cardiac rhythm) is produced before normal beat.

• There exists atria, nodal and ventricular extra systole or

premature beats.

• Ectopic beat that is produced at regular but higher rate than

that of SA node could be atria, ventricular or nodal
paroxysmal tachycardia or atrial flutter.

• Atrial tachycardia is about 220/min.

• Atrial flutter rate is 200-350/min

• Atrial fibrillation is 300-500/min and there is no P but F

(saw-teeth) wave which is rapid and irregularly irregular.
 Long QT Syndrome

• It occurs when the QT interval is prolonged > 420 ms.

• It indicates heart vulnerability due to irregular

repolarisation.

• There heart is vulnerable to increase frequency of

ventricular arrhythmias and sudden death.

• It is caused by different drugs, electrolyte abnormalities

and myocardial ishaemia or congenital factor.

• Mutations of 8 different genes have been reported to

cause long QT syndrome.
• 6 caused reduced functions of various K⁺ channels by
structural deformation.

• 1 inhibits a K⁺ channel by reducing the amount ankyrin

isoform that link it to the memebrane cytoskeleton.

• 1 increases the function of cardiac Na⁺ channel.

 Ventricular Fibrillation

• The fibrillated ventricular muscle fibres contract in a

totally irregular and ineffective way.

• Ventricular fibrillation follows electric shock or ventricu-

lar extrasystole and coincides with midportion of T wave.

• Some ventricular myocardium is depolarised, incomple-

tely repolarised and completely repolarised.

• Fibrillating ventricle cannot pump blood effectively (no

heart beat or QRS wave) and that stops blood circulation.

• Fibrillation lasting more than a few minutes is fatal most

frequently in myocardial infarction.
 Cardiopulmonary Resuscitation
• Defibrillators produce electrical shocks for defibrillating a
stopped or fibrillating heart in patients.

• Cardiac output and perfusion of the coronaries can be

partially maintained by closed-chest cardiac massage.

• Defibrillators can also be implanted surgically in patients

at high risk for ventricular fibrillation.

• Defibrillators are programmed to discharge automatically

after 5-10 s of ventricular tachycardia or fibrillation.

• Cardiac massager places heel of one hand on the lower

sternum, above xiphoid process, and the heel of the other
hand on the first hand.
• Pressure is applied straight down, depressing the sternum
4 or 5 cm toward the spine.

• This procedure is done 80-100 times/minute.

• Whenever the heart suddenly stops, the pulmonary veins,

left heart and arteries still are full of oxygenated blood.

• Therefore, the attention is shifted to circulation.

• However, if respiration also stops full cardiopulmonary

resuscitation should be applied.

• In this case, cardiac compression should be alternated with

mouth-to-mouth breathing at a rate of 1 ventilation to 5
Compressions.
• Abnormalities of membrane polarisation
associated with acute myocardial infarction
• Cardiac Cycle
• Introduction
 Mechanical Phases during Cardiac Cycle
• Mechanical events of the cardiac cycle occurs during:
1. Late diastole
2. Atrial systole
3. Ventricular systole
4. Early diastole

o Events in Late Diastole

• Mitral and tricuspid valves btw atria and ventricles
opened.

• Aortic and pulmonary valves are closed.

• Blood flows into the heart throughout the diastole, filling

• Rate of filling declines as the ventricles become distended,
especially when the heart rate is low, because the cusps of
atrioventricular valves drift towards the closed position.

• The atrial pressure is 4 mm Hg which exceeds ventricular

pressure (0 mm Hg) promotes the ventricular filling.

o Events in Atrial Systole

• The 2 Atria contract during atrial systole.

• Atrial depolarisation leads to atrial contraction or systole.

• Atrial contraction produces rise in atrial pressure, increase

in AV valves (leaflet) diameter (separation) and ejection of
blood into the ventricles.
• Atrial contraction propels 30% blood into the ventricles at
⅟10 before the onset of systole.
• 70% of ventricular filling occurs passively during diastole
as a result of the pressure gradient.
• Atrial contraction narrows superior and inferior vena cavae
and pulmonary veins orifices.
• Atrial contraction is not essential for life, but the heart is a
much more efficient pump when the atria are contracting.
• The inertia of blood that moves blood towards the heart
also keep the blood in the heart.
• However, there is some regurgitation of blood into the
veins during atrial systole.
• The pressure in the atria produces a curve that shows “a”,
“c”, and “v” waves and the “x” and “y” descents.

• The “a” wave is the increase in atrial pressure produced by

atrial contraction.

• The “c” wave is the slight increase in atrial pressure

produced by ventricular contraction.

• At this “c” wave point, AV valves bulge into the atria,

producing the 1st heart sound.

• The “x” descent is caused by the pulling down of the AV

valves by the contracting ventricles.

• The “v” wave is produced by atrial filling (i.e. subsequent

• increase in atrial pressure) and reaches a peak in late
ventricular systole while the AV valves are closed.

• The “y” descent is produced by fall in atrial pressure

following opening of AV valves and ventricular filling.

• Pressure changes in the right atrium are communicated to

the great veins so that the “a”, “c” and “v” waves together
with “x” and “y” descents are seen in the jugular veins.

• Jugular venous pressure is then a useful clinical index of

functional activity of the heart, especially the right pump.

• The period between the end of “a” wave to the beginning

of another “a” following “y” descent is the atrial diastole.
• The jugular pulse wave are superimposed on the
respiratory fluctuations in venous pressure.

• Venous pressure falls during inspiration (resulting from

increased negative intra-thoracic pressure) and rises again
during expiration.

• Giant “c” wave is produced with each ventricular systole

in tricuspid valve insufficiency.

• Giant “a” wave is produced whenever the atrial contracts

while the tricuspid valve is closed.

• Atrial premature beat (or extrasystole) produces an “a”

wave whereas ventricular extrasystole beat does not.
• In complete heart block, atria and ventricles beat at
different rate, such that waves that are not synchronous
with the radial pulse are made out.

 Event in Ventricular Systole

• At the start of ventricular systole, the AV valves close.

• Ventricles initially contract little, but intraventricular

pressure rises as ventricles press the blood in it.

• This is the period of isovolumetric ventricular

contraction, lasting about 0.05 s.

• Following isovolumeric contraction, pressures in the left

and right ventricles exceed pressures in the aorta (80 mm
Hg) and pulmonary artery (10 mm Hg) respectively.
• So, aortic and pulmonary valves open and the bulging of
AV valves into atria causes a sharp rise in atrial pressure.
• Opening of the aortic and pulmonary valves begins the
phase of ventricular ejection of blood.
• Ejection of blood is rapid at first but slowing down as
systole progresses.
• The intraventricular pressure rises to a maximum and then
declines somewhat before ventricular systole ends.
• Peak left ventricular pressure is about 120 mm Hg, and
peak right ventricular pressure is 25 mm Hg or less.
• Late in systole, aortic pressure exceeds ventricular, but for
a short period momentum keeps blood moving forward
• The AV valves are then pulled down by the contractions of
the ventricular muscle, and atrial pressure drops.
• Finally, the amount of blood ejected by each ventricle per
stroke at rest is 70–90 mL.
• The end-diastolic ventricular volume is about 130 mL.
• Thus, about 50 mL of blood remains in each ventricle at
the end of systole (end-systolic ventricular volume).
• Ejection fraction is (index of ventricular function) % end-
diastolic ventricular volume (≈65%) ejected per stroke.
• Injecting radionuclide-labeled red blood cells to image
cardiac blood pool at the end of diastole and systole can be
used to calculate the ejection fraction.
 Events in Early Diastole

• After full ventricular contraction, the falling ventricular

pressure drop more rapidly: the period of protodiastole,
lasting for about 0.04 s.

• Prodiastole ends when momentum of blood is overcome

and aortic and pulmonary valves close to set up transient
vibrations in the blood and vessel walls.

• After the closure of the valves, the blood pressure

continue to drop rapidly during the period of
isovolumetric ventricular relaxation.
• Filling is rapid at first, then slows as the next
cardiac contraction approaches.
• Atrial pressure continue to rise after the end
of ventricular systole until the AV valves open,
then drops and slowly rises again until the
next atrial systole.
 Contribution of Pericardium During Cardiac Cycle
• Pericardium normally separates the heart from the rest of
thoracic viscera within the pericardial space.

• This pericardial space (of 5-30 mL clear fluid) lubricates

the heart, permitting contraction with minimal friction.

 Timing within Cardiac Cycle

• Although events on the 2 sides are similar, they are

asynchronous somewhat in that:

• Right atrial systole precedes left atrial systole, and

contraction of right ventricle starts after that of the left.
• As pulmonary arterial pressure is lower than that of aortic,
right ventricular ejection begins before that of the left.

• During expiration, the pulmonary and aortic valves close

at the same time; but during inspiration, the aortic valves
closes slightly before pulmonary valves.

• The slower closure of the pulmonary valve is due to lower

impedance of the pulmonary vascular tree.

• When measured over a period of minutes, the left

ventricular output is equal to that of right.

• Nevertheless, transient differences in output during the

respiratory cycle occur in healthy individual.
 Length of Systole and Diastole
• Cardiac muscle contracts and repolarises faster at high HR
• The duration of systole can decrease from 0.27 s at HR of
65 to 0.16 s at HR of 200 bpm.
• The reduction in systole is due to a decrease in systolic
ejection time.
• Systolic duration is much more fixed than diastolic: while
HR is increased, diastole is shortened to a greater degree.
• For example, at a HR of 65, diastolic duration is 0.62 s
whereas at the HR of 200 it is 0.14 s.
• This observation has important physiologic and clinical
implications.
• During diastole the heart muscle rests and coronary blood
flow to the sub-endocardial portions of the left ventricles.

• Most of the ventricular filling occurs in diastole.

• The filling is accurate at 180 bpm provided there is ample

venous return, producing increase in cardiac output (CO).

• At a very high rate ventricular filling is compromised to a

degree that CO falls and symptoms of heart failure.

• The highest ventricular rate possible is 400/min

theoretically.

• However, AV node does not conduct more than 230

impulses/min, because of the long refractory period
• Although, a ventricular rate of 230/min is seen only in
paroxysmal ventricular tachycardia.

 Duration of Events During Isovolumetric Ventricular

Contraction

• The events observed during the isovolumeric contraction

by using ECG, phonocardiogramme, carotid pulse
simultaneously are:

1. Electromechanical systole (QS₂)

2. Pre-ejection period (PEP)

3. Left ventricular ejection time (LVET)

• QS₂ = period from the onset of QRS complex to the
closure of aortic valves – 2nd heart sound.

• LVET = period from the beginning of carotid pressure rise

to the dicrotic notch.

• PEP = QS₂ – LVET = period for the electromechanical

events that precedes systolic ejection

• PEP ratio LVET = 0.35 normally.

• It increases without change in QS₂ when left ventricular

performance is compromised in cardiac diseases.

 Arterial Pulse
• The blood pumped into aorta during systole moves the
• Blood in the aorta forward and set up a wave that travels
along the arteries.
• This pressure expands the arterial wall as it travels and the
expansion is palpable as the pulse.
• The pulse wave travels at 4 m/s in aorta, 8 m/s in large
arteries, 16 m/s in the small arteries of young adults.
• Wave velocity is much higher than blood flow velocity.
• The pulse is felt at the wrist about 0.1 s after the peak
systolic ejection into the aorta.
• The pulse wave moves faster with advancing age, as the
arteries become more rigid.
• Pulse strength is always determined by pulse pressure.

• Pulse is weak during shock, but it is strong with large

stroke volume during exercise or histamine administration.

• Also a very high pulse pressure wave can be felt or heard

by the individual (palpitation).

• The pulse is particularly strong when the aortic valve is

incompetent (aortic insufficiency).

• Such that it can produce a force of systolic ejection

sufficient to make the head nod with each heartbeat.

• Dicrotic notch is a small oscillation on the falling phase of

pulse wave.
• It is caused by vibration of the aortic valves snap shut.

• It is visible when the pressure wave is recorded but not

palpable.

• Pulmonary artery pressure curve also has a dicrotic notch

produced by the closure of the pulmonary valves.

 Heart Sound
• There 4 heart sounds

• 1st heart sound is a low slightly prolonged “lub” sound.

• It is caused by vibration set up by sudden mitral and

tricuspid valves closure at the start of ventricular systole.
• The 1st heart sound, “lub”, has a duration of 0.15 s and a
frequency of 25-45 Hz.

• It is soft when the heart rate is low because:

The ventricles are well filled with blood and

The leaflets of the AV valves float together before

systole

• The 2nd heart sound is a shorter, high-pitched “dup”.

• It is caused by vibrations associated with pulmonary and

aortic valves closure just after the end of ventricular
systole.
• The 2nd heart sound lasts about 0.12 s with a frequency of
50 Hz.

• It is associated with diastolic phase.

• This makes it loud and sharp when DBP in the aorta is

elevated, causing the respective valves to shut briskly at
the end of systole.

• Interval between aortic and pulmonary valve closure

during inspiration is long enough for 2nd heart sound to be
reduplicated.

• This is physiologic splitting of the 2nd heart sound,

however, there are also pathophysiologic splitting in
various diseases.
• The 3rd heart sound is a soft low-pitched sound heard
about ⅓ the way through diastole in normal young adults.

• It is produced by the vibration set up by the inrush of

blood during rapid ventricular filling.

• It coincides with this period of rapid ventricular filling.

• It has a duration of 0.1 s.

• The 4th heart sound can be heard sometimes immediately

before the 1st heart sound.

• It is produced during ventricular filling by high atrial

pressure or stiff ventricles in ventricular hypertrophy.
 Murmurs or Bruits
• They are abnormal sound heard in various part of the
cardiovascular system.

• It is the sound of blood flow at a velocity above critical

velocity owing to obstruction in blood flow, becoming
turbulent.

• There are 4 major murmurs owing to:

Heart valve defects
Vascular obstruction of diseases
Septal defects
Physiological adjustment
 Heart Valve Defect Murmurs
• Murmurs are produced by turbulent flow owing to:
Narrowed valve orifice (stenosis).
Backward flow as in case of incompetent valves
(regurgitation or insufficiency).
• Murmur of a particular valve is best detected using
stethoscope over the particular valve.
Aortic and pulmonic valves murmur at the heart base.
Mitral valve murmur at the heart apex.

• Hole in the aortic valve cusp produces a loudest murmur.

It is a high-pitched musical diastolic murmur
sometimes audible without stethoscope several feet
away from patient.
• The character accentuation, and transmission of sound are
used to locate its origin in one valve or the other.
• Aortic or pulmonic stenosis murmur is heard during
systole.
• Aortic or pulmonic insufficiency is heard during diastole
• Mitral or tricuspid stenosis is heard during diastole
• Mitral or tricuspid insufficiency is heard during systole.
 Vascular Obstruction Bruits/Murmurs
• The following are examples of bruits or murmurs heard
outside the heart owing to vascular obstructions.
– Bruits heard over a large highly vascular goiter
 – Bruits heard over a carotid artery when its lumen is
narrowed and distorted by atherosclerosis
– Murmurs heard over aneurysmal dilation of aorta,
arteriovenous fistula, patent ductus arteriosus.

 Septal Defects
– Congenital interventricular septal defects produces
systolic murmurs as as blood flow from left to right
ventricle.
– Interatrial septal defects also can produce soft murmurs.

 Physiological Adjustment Murmurs

• They are normal systolic murmurs produced in:
– Children and adults without cardiovascular diseases.
– Anaemic patients owing to low blood viscosity and rapid
 Echocardiography
• Echocardiography is a noninvasive technique that does
not involved injections or insertion of catheter to evaluate
wall movements and other aspects of cardiac functions
like:
• In echocardiography, pulse of ultrasonic waves at 2.25
MHz are emitted from a transducer.
• This transducer also functions as a receiver to detect
waves reflected back from various portion of the heart.
• Reflections occur whenever and wherever acoustic
impedance changes.
• This produce a recording of the echoes displayed against
time on an oscilloscope.
• This is a record of the movements of the ventricular wall,
septum and valves during the cardiac cycle.
• Echocardiography combined with Doppler techniques can
measure blood flow velocity and volume through valves.
• It has clinical applications in evaluating and planning
therapy with patients with valvular lesions