Physiology of cardiovascular system

Physiology of the
Cardiovascular
System
By:
1

Outlines
 Introduction to CVS
 The heart
Anatomy of the heart
Chambers of the heart
Pathway of blood through the heart and lungs
Cardiac muscle and the cardiac conduction system
Innervations of the heart
Cardiac cycle
Heart sounds
Cardiac output
 Vascular Physiology
2

Introduction
• The term cardiovascular system
– refers to the passages through which the blood flows
Components of the CVS
1. The heart: Driving force(Pump) for CVS
2. Blood Vessels: Passage ways
 Arteries: Distribution channels to the organs
 Capillaries: Exchange region
 Veins: Blood reservoirs and streets for return of
blood to the heart.
3. Blood: is the transport medium.
3

General functions of the CVS
1. Transport of O2, nutrients, water, hormones, electrolytes,
and drugs.
2. Rapid washout of metabolic wastes.
4. Regulation of temperature and blood flow.
6. Contribution to defense mechanisms
4

Anatomy of the heart
Location:
– The heart is located in the thoracic cavity in the
mediastinum, the area between the lungs
– Superior surface of diaphragm
– Anterior to the vertebral column, posterior to the sternum
Size:
The heart has
• The size of a clenched fist.
6

Gross Anatomy of Heart: Frontal Section
7

The Heart
• The muscular pump that
forces the blood through
vessels made of arteries,
veins and capillaries.
• It is a dual pump that
drives blood in two
consecutive circuits,
– the systemic and
– pulmonary circulations
• Receives blood from
the rest of the body
through the vena cava.
8

Outer Surfaces Layers:
The Pericardium
• The heart is enclosed in
a double-walled sac
called the pericardium.
• Clear pericardial fluid inside
pericardium(30-50ml)
Function
Barrier to infection
Provides lubrication
Prevents sudden over
distention of chamber of
heart
9

The Layers of the Heart Wall
Epicardium
• The outermost layer of the wall of the heart is called the
epicardium.
Myocardium
• The second layer under the epicardium.
• This makes up the bulk of the heart.
• Responsible for pumping action of the heart
Endocardium
• Innermost layer of the wall of the heart.
• It is formed by a single layer of endothelial cells
• Endocardium continues as endothelium of the blood
vessels. 10

Chambers of the Heart
The heart has four chambers “two atria and two ventricles”
The Atria:
• Two thin-walled muscular sheaths,
• Blood returning to the heart is received by two superior
chambers, the right and left atria.
• Blood enters right atria from
– superior and inferior vena cavae and
– coronary sinus
• Blood enters left atria from pulmonary veins.
The Ventricles:
• Thicker-walled portion of the heart
• The right and left ventricles are the pumps that eject blood
into the arteries. 11

Cont,d
• The right side of the heart
comprises the right atrium and the right ventricle.
• The left side of the heart
comprises the left atrium and the left ventricle.
• The right atrium
receives venous blood from the systemic circulation
• The right ventricle
pumps it into the pulmonary circulation
• The left atrium:
 Receives blood from lungs by pulmonary veins.
• The left ventricle
 ejects the blood into the aorta, which then distributes the
blood to all the organs via the arterial system.
12

Pathway of Blood Through the Heart and Lungs
• Right atrium  tricuspid valve  right ventricle
• Right ventricle  pulmonary valve  pulmonary arteries
 lungs
• Lungs  pulmonary veins  Left atrium  bicuspid
valve  Left ventricle  aortic semilunar valve  aorta
 systemic circulation
14

Pathway of Blood Through the Heart and Lungs cont’d
15

Heart Valves
• Valves of the heart permit the flow of blood through heart in
only one direction.
• To pump blood effectively, the heart needs valves that
ensure a predominantly one-way flow.
• There are four valves in human heart.
Two atrioventricular valves: found between atria and the
ventricles
 Two semilunar valves: placed at the opening of blood
vessels arising from ventricles, namely systemic aorta and
pulmonary artery.
16

Types of valves
1. Atrio-ventricular-AV valves
a. Mitral (bicuspid) valve lies b/n left atrium and left
ventricle.
 They are responsible for preventing the back flow
of blood from the LV to the LA.
b. Tricuspid (three cusps) valve lies b/n Rt atrium and Rt
ventricle.
 They are responsible for preventing the back flow
of blood from the RV to RA
17

2. The semilunar valves:
• Constitute the aortic and pulmonary valves located at the
exits of the right and left ventricles.
a. Aortic valve
– allows blood to flow into the aortic tree and to the left
and right main coronary arteries.
– They prevent the back flow of blood from the aorta to
the LV.
b. Pulmonary valve
allows blood to flow into the pulmonary artery.
They also prevent the back flow of blood from PA to the
RV.
18

Cardiac Muscle and the Cardiac Conduction
System
22

Structure of Cardiac Muscle
• The heart is composed of three major types of cardiac
muscle:
Atrial muscle,
Ventricular muscle, and
Specialized excitatory and conductive muscle fibers.
• The atrial and ventricular types of muscle
– contract in much the same way as skeletal muscle,
except that the duration of contraction is much longer.
• Cardiac muscle is striated like skeletal muscle but
– it differs from Sk.m in many structural and
physiological ways.
23

Cont’d
Cardiac myocytes (muscle cells), or cardiocytes,
are relatively
– short, thick, branched cells.
– They usually have only one, centrally placed nucleus.
– The T tubules are much larger than in skeletal muscle
and
– admit supplemental calcium ions from the ECF into the
cell during excitation.
– They are joined end to end by thick connections called
intercalated discs (cell membranes that separate
individual cardiac muscle cells)
24

• Intercalated discs contain two types
of specialized junctions:
(a) Desmosomes which act like
fastens and hold the cells tightly
together
(b) Gap junctions which permit
action potentials to easily spread
from one cardiac muscle cell to
adjacent cells 26

Cont’d
• Intercalated discs : offer no obstacle to
conduction of excitation.
• Atria and ventricle behave functionally as a
– Syncytium: Excitation anywhere in
atria or ventricles spread allover
unexcited fibers.
• This two functional syncytiums allows the
atria to contract a short time ahead of
ventricular contraction.
• Potentials are conducted from the atrial
syncytium into the ventricular syncytium
through the A-V bundle.
27

In cardiac muscle, there are two types of cells:
Contractile cells &
Autorhythmic (or automatic) cells.
• Contractile cells:
99% of the cardiac muscle cells
Do not contract unless stimulated electrically by pacemaker
tissue.
Do the mechanical work of pumping.
• Autorhythmic cells:
– self-stimulating
– do not contract but specialized for initiating and
conducting the action potentials responsible for
contraction of the working cells.
– Located in the conducting systems of the heart
29

The cardiac conducting system
30

Cont’d
• Sinoatrial node (SA node)
– Normal pacemaker
– is located near the superior vena cava.
– Excitation spreads over working myocardium of atria
• Atrioventricular node (AV node):
– Located near the right AV valve.
– Only pathway for conduction to ventricles, rest of
atrioventricular boundary consist of unexcitable
connective tissue. 31

Cont’d
– Propagation briefly delayed at AV node = Important
for ventricular filling (this allows atria to empty
before ventricular contraction begins)
• Potential pacemaker (if SA node fails)
• Bundle of His.
 The atrioventricular (AV) bundle (bundle of His), a pathway
by which signals leave the AV node.
 The right and left bundle branches, divisions of the AV
bundle that enter the interventricular septum and descend
toward the apex.
32

Purkinje fibers
• Nerve like processes that
arise from the bundle
branches and then
– turn upward and
– spread throughout the
ventricular myocardium.
• They distribute the electrical
excitation to the myocytes of
the ventricles.
• They form a more elaborate
network in the left ventricle
than in the right
33

Spread of cardiac excitation
• Begins at the SA node & quickly spreads through both atria.
• Also travels through the heart's conducting system (AV
node --> AV bundle --> bundle branches --> Purkinje
fibers) through the ventricles
35

Inter nodal pathways and transmission of the
Cardiac Impulse through the Atria
• The ends of the sinus nodal fibers connect directly with
surrounding atrial muscle fibers.
• Therefore, action potentials originating in the sinus node
– travel outward into these atrial muscle fibers.
• In this way, the action potential spreads through the entire
atrial muscle mass and,
– finally, to the A-V node.
36

Delay of Impulse Conduction from the Atria
to the Ventricles
• The cardiac impulse does not travel
from the atria into the ventricles too
rapidly.
• This delay allows time for the atria
to empty their blood into the
ventricles before ventricular
contraction begins.
• It is primarily the A-V node and
adjacent conductive fibers that
delay this transmission into the
ventricles.
37

Cont’d
• The impulse, after traveling
through the internodal pathways,
– reaches the A-V node about
0.03 second after its origin in
the sinus node.
• Then there is a delay of another
0.09 second in the A-V node itself
before the impulse enters A-V
bundle, where it passes into the
ventricles.
• A final delay of another 0.04
second occurs mainly in this
penetrating A-V bundle.
38

Cont’d
• This makes a total delay of
0.16 second before the
excitatory signal finally
reaches the contracting
muscle of the ventricles.
• Cause of the Slow
Conduction
– is mainly by reduced
numbers of gap junctions
between successive cells.
39

Rapid Transmission in the Ventricular
Purkinje System
• Purkinje fibers
– Largest fibers in conduction
system
– Conduct impulse from the A-V
bundle into the ventricles.
– They transmit action potentials
at a fastest velocity of 4 to 6
m/sec.
• The rapid transmission of action
potentials is caused by
– a very high level of gap
junctions b/n successive cells. 40

Cont’d
• Once the impulse reaches the ends of the Purkinje
fibers,
– it is transmitted through the ventricular muscle
mass by the ventricular muscle fibers themselves.
41

44
 In the presence of parasympathetic tone

Cont’d
• SA node has the highest or fastest rhythm &, therefore,
– sets the pace or rate of contraction for the entire heart.
• As a result, the SA node is referred to as the pacemaker.
• Any region of spontaneous firing other than the SA node is
called an abnormal Pacemakers—“Ectopic” Pacemaker.
• If the SA node is damaged,
– an ectopic Pacemaker may take over the governance of
the heart rhythm.
– The most common ectopic Pacemaker is the AV node,
which produces a slower heartbeat.
45

Action potential on the Two Types of cells
• The action potentials that occur in these two types of
cells are a bit different:
46
Action potential of an
autorhythmic cell
Action potential of a
contractile cell

Action potential of autorhythmic Cells
• The cardiac autorhythmic cells
do not have a resting potential.
Instead, they display
pacemaker activity.
• Pacemaker potential is the
unstable resting membrane
potential in SA node.
• RMP in SA node is –55 to –60
mV. But in other cardiac
muscle fibers –85 to –95 mV.
• Pacemaker potential is a
gradual depolarization for the
SA node. 47

Ionic Basis of Electrical Activity in Pacemaker
48

Ionic Basis of Electrical Activity in Pacemaker cont’d
Pacemaker potential is due to:
• The initial part is due to slow influx of sodium ions and
the later part is due to the slow influx of calcium ions.
Depolarization:
• When the pacemaker potential reaches a threshold of - 40
mV,
– voltage-gated fast calcium channels open and Ca+2 flows in
from the ECF.
– This produces the rising (depolarizing) phase of the action
potential, which peaks slightly above 0 mV.
49

Repolarization
• It is due to the efflux of potassium ions from pacemaker
fibers.
• When repolarization is complete,
The K channels close and
The pacemaker potential starts over, on its way to
producing the next heartbeat.
• Each depolarization of the SA node sets off one heartbeat.
• When the SA node fires,
It excites the other components in the conduction system;
At rest, it fires every 0.8 second or so, creating a heart
rate of about 75 b/min.
51

Action potential In Contractile cells:
• Action potential in a
single cardiac muscle
fiber occurs in the
following phases:
1. Initial depolarization
2. Initial repolarization
3. A plateau or final
depolarization
4. Final repolarization.
52

Ionic bases of AP
Has 5- phases.
Phase-0: Depolarization caused by rapid Na-influx(Fast Na
channels open)
Phase-1: Initial repolarization due to closure of fast Na
channels and efflux of a small quantity of K ions
Phase-2: The plateau caused by Ca2+
influx
Phase-3: Repolarization caused by K+
efflux due to calcium
channels close and slow potassium channels open.
Phase-4: Resting membrane potential (−90 mv)
RMP re-established by Na-K-ATPase
53

Two types of calcium channels
• L-type calcium channels (long lasting calcium
current)
– Predominant type
– Once open, inactivated slowly, thus provide long
lasting calcium current
– Activated during upstroke (-20mV)
– Blocked by verapamil, amlodipine, diltiazen
• T-type(transient) calcium channels
– Less abundant
– Activated at more negative (-70 mV)
– Inactivate more quickly than L-type 55

Excitation-Contraction Coupling
• The mechanism that couples
– Excitation—an action potential in the plasma membrane
of the cardiac muscle cell—and
– Contraction an increase in the cell’s cytosolic calcium
concentration.
• As is true for skeletal muscle,
– the increase in cytosolic Ca concentration in cardiac
muscle is due mainly to release of Ca from the SR
• But there is a difference between skeletal and cardiac
muscle
– in the sequence of events by which the action potential
leads to increased release of Ca from the SR. 56

Cont’d
Systole(electrical):
• Spread of excitation from cell-to cell via gap junctions
• Also spread to interior via T-tubules
• During plateau phase, Ca++
permeability increases
• This Ca++
triggers release of Ca++
from SR
• Ca++
level increases in cytosol
• Ca++
binds to Troponin C
• Ca++
-Troponin complex interacts with tropomyosin (to
unlock active site between actin and myosin)
• Cross bridge cycling = contraction (systole) 57

Excitation-contraction coupling in cardiac muscle Cont’d
60

Cont’d
• Hormonal (catecholamines):
– (Phosphorylation of Ca++
channels)
– Increase Ca++
into cells by phosphorylation of Ca++
channels by cAMP dependent protein kinase
(cAMP-PK).
61

Relaxation(diastole)
– As result of Ca++
removal
• Ca++
removed By:
– Uptake by SR
– Extrusion by Na+
-Ca++
exchange
– Ca++
pump (to limited extent)
• Hormonal: catecholamines
– Inhibition of Troponin-C-Ca++ bondage by Troponin-I
and phosphorylation of phospholamban by
catecholamine
62

Cont’d
 Calcium resequestered into SR by ATP-dependent
calcium pump
 Sarco-endoplasmic reticulum calcium ATPase (SERCA) ,
that is inhibited by phospholamban.
 Inhibition action on SERCA by phospholamban
(protein) is relieved by phosphorylation
 Calcium pump remove calcium from cell
63

Cardiac glycosides
– Inhibit Na+/K+-ATPase
– Increase more Na+ in and less Na+ outside of the cell
– leads to increase in intracellular Ca++
– through the inhibiting Na+/Ca++ exchange pump (by
decreasing the availability of sodium to pump calcium
out.
– leads to enhanced contractility
64

Nature of muscle contraction
• Skeletal muscle : - Tetanic contraction possible
- Short refractory period
- Recruitment of motor units
- Summation of twitches
• Cardiac muscle : - no tetanic contraction
- prevented by long refractory period
- no summation
• Importance: Cardiac muscle must relax b/n contractions
so that the ventricles fill with blood. 66

Cardiac innervation
• Sympathetic  all parts of heart
• Parasympathetic (from vagus) –
• Mainly : SA node, Atria and AV node
• No Ventricular innervations of parasympathetic
• Strong stimulation of vagus, has no effect on ventricles
(Vagal escape or Ventricular escape)
69

Sympathetic and Parasympathetic effects
• Sympathetic stimulation
↑ HR (+ve chronotropic)
↑ force of contraction (+ve
Inotropic)
Increase slope of
pacemaker potential
• Parasympathetic stimulation
Ach opens K+
channels
Reduce slope of pacemaker
potential →↓ HR
Also hyperpolarize pacemaker
potential and reduce HR
72

Actions of the heart
• Chronotropic state: is the frequency of heartbeat or HR
• Inotropic state: Force of contraction of heart
• Bathmotropic state: refers to the excitability of cardiac
muscle
• Dromotropic state: Conduction velocity of the cardiac
conduction system
NB: SNS has positive tropic effects
PNS has negative tropic effects
75

Effects of non-physiologic environment
1. Body temperature:
Rise (eg. Fever): increases the heart rate
 Decrease: decrease contractility
2. pH:
• Acidosis: - ve Inotropic effect, due to depression of
affinity of troponin C to Ca++
severe acidosis stops heart in diastole
• Alkalosis: +inotropic effect due to increase affinity of
troponinin C to Ca++
severe alkalosis stops heart in systole
76

3.Inorganic ions:
a.Na+
Hypernatremia
• -ve inotropic effect
• Stimulate Na+
-Ca++
exchanger to take Na+
in, drive Ca++
out of
cardiac myocyte, cytosolic Ca++
level decreases
Hyponatremia: opposite effect
b. Ca++
hypercalcemia:
• Increase cytosolic Ca++
level, stronger systole & incomplete
diastole.
• If level very high, heart stop in systole (Calcium Rigor)
77

Cont’d
• Hypocalcemia:
• decrease myocardial contractility, but no serious effect
C. Potassium
• Hyperkalemia:
• Negative inotropic effect
• Marked hyperkalemia - heart stop in diastole
• Hypokalemia: weak +inotropic effect
78

Coronary Circulation
• Heart muscle is supplied by
two coronary arteries, namely
right and left coronary arteries,
which are the first branches of
aorta.
• Heart depends strongly on
aerobic metabolism
• Brief period of low oxygen:
damage to myocardium.
79

Cont’d
Right Coronary Artery
(RCA) supplies:
. RA and RV
Left Coronary Artery
divides into:
I. Circumflex Artery (CA)
supplying
. LA and
. Posterior part of LV
II. Anterior interventricular
artery supplying
. Anterior walls of both
ventricles
80

Cont’d
• Interruption of the blood supply to any part of the
myocardium can cause myocardial ischemia.
• If a large part of myocardium is involved or if the occlusion
is severe involving larger blood vessels, it leads to necrosis.
• The coronary circulation has a defense against such an
occurrence—points called anastomoses.
• where two arteries come together and combine their
blood flow to points farther downstream.
• Thus, if one artery becomes obstructed,
some blood continues to reach myocardial tissue
through the alternative route. 81

Venous Drainage from the heart
• After flowing through capillaries
of the myocardium,
• Venous drainage from heart
muscle is by:
Coronary sinus
• Drains blood from left side of
the heart and opens into RA
(draining 75%)
Anterior coronary veins
• Drain blood from right side of
the heart and open directly into
RA
82

Cont’d
Thebesian veins
• Drain deoxygenated blood from myocardium, directly
into the concerned chamber of the heart.
• Physiological shunt
83

Coronary Flow in Relation to the Cardiac Cycle
• Most organs receive more arterial blood flow when
– the ventricles contract than when they relax, but
– the opposite is true in the coronary arteries.
• The reason for this is that,
– contraction of the myocardium compresses the arteries
and obstructs blood flow.
84

Factors affecting coronary blood flow
Need for oxygen
 Metabolic factors (K, H,Adenosine,CO2)
Nervous factors.
87

Clinical conditions
Coronary Artery Disease
• It is one of the most
common and serious effects
of aging.
• Fatty deposits build up in
blood vessel walls and
– narrow the passageway for
the movement of blood.
• The resulting condition,
called atherosclerosis
– often leads to eventual
blockage of the coronary
arteries and a “heart
attack”.
88

Myocardial Infarction
• A myocardial infarction (MI) or heart attack—is the
sudden death of a patch of myocardium resulting from
ischemia , the loss of blood flow.
Causes:
A) Vascular Spasm
 Spastic contraction of the vessels
b)Atherosclerosis
 Deposition of cholesterol on the vessel wall (plague)
Atheroma: Tumors of smooth muscle cells
c)Thromboembolism
Blood clot breaks off, stops and impedes blood flow
90

Electrocardiography
Electrocardiography
• Is the technique by which electrical activities of the heart
are studied.
Electrocardiograph is the instrument (machine) by which
electrical activities of the heart are recorded.
Electrocardiogram (ECG or EKG) is the recorded tracing
(recorded copy made by the machine)
93

Cont’d
• As the heart undergoes depolarization and repolarization,
– the electrical currents that are generated spread not only
within the heart, but also throughout the body (body fluid
good conductor of current)
• A small portion of the current spreads all the way to the
surface of the body.
• If electrodes are placed on the skin on opposite sides of the
heart, electrical potentials can be recorded.
94

Difference b/n AP and ECG
Action potential
• AP is one electrical
event in a single cell
• Recorded using
intracellular electrode
Electrocardiogram
• Is summated electrical
activity of all muscle
• Recorded using
electrodes placed on
surface of body
96

Information obtained from ECG
• Anatomical orientation of the heart
• Relative size of chambers
• Origin of excitation, rhythm and conduction disturbance
• Extent, location and progress of ischemic damage
• Electrolyte disturbance
• Influence of drugs such as glycosides
• HR = 1/cycle length or (1 divided by RR duration)
Therefore, provide indirect information about heart function.
98

• A "typical" ECG tracing is shown
to the right.
• The different waves that comprise
the ECG represent the sequence
of
– Depolarization of the atria
and
– Depolarization and
repolarization of the
ventricles.
• Electrocardiogram (ECG) of the
heart is recorded from specific
sites of the body in graphic form
relating
– voltage (vertical axis) with
– time (horizontal axis). 99

ECG Conventions
• ECG paper has horizontal and vertical lines at regular
intervals of 1 mm.
• Every 5th line (5 mm) is thickened.
• Duration of the waves on X-axis.
1 mm = 0.04 sec.,5 mm = 0.20 sec.
Paper speed =25mm/sec.
• Amplitude of the waves on Y-axis.
(1 mm = 0.1 mV ,5 mm = 0.5 mV, 10mm deflection →
1mV
• Recording points = wrist, ankle, skin on chest
Right leg = ground(earth).
100

A) Waves of normal ECG
The normal electrocardiogram is composed of
• P wave,
• QRS complex, and
• T wave.
102Waves, Intervals and Segments of the a normal ECG

‘P’ wave
• ‘P’ wave is positive and the first wave in ECG.
• It is produced due to the depolarization of both atria.
• Atrial repolarization is not recorded as a separate wave in
ECG because it is obscured by the QRS complex.
• Normal duration is 0.1-0.3 second.
• Normal amplitude is 0.1 to 0.12 mV.
103

‘QRS’ complex
• Is due to depolarization of ventricles. .
• ‘Q’ wave is a small negative wave.
• It is continued as the tall ‘R’ wave, which is a positive
wave.
• ‘R’ wave is followed by a small negative wave, the ‘S’
wave.
104

Cont’d
• ‘Q’ wave is due to the depolarization of basal portion of
interventricular septum.
• ‘R’ wave is due to the depolarization of apical portion of
interventricular septum and apical portion of ventricule
• ‘S’ wave is due to the depolarization of basal portion of
ventricular muscle.
• Normal duration of ‘QRS’ complex = 0.08 - 0.10 second.
• Amplitude of ‘Q’ wave = 0.1 - 0.2 mV.
• Amplitude of ‘R’ wave = 1 mV.
• Amplitude of ‘S’ wave = 0.4 mV.
105

‘T’ wave
• ‘T’ wave is due to the repolarization of ventricles.
• Normal duration of ‘T’ wave is 0.2 second.
• Normal amplitude of ‘T’ wave is 0.3 mV.
106

U’ wave
• Small rounded, upright wave, following T wave.
• ‘U’ wave is not always seen.
• Mostly seen in slow heart rate.
• It is also an insignificant wave in ECG.
• represents repolarization of papillary muscles.
107

B. Segments – lines b/n two waves
1. P-R (P-Q) segment
 Represents the delay in the AV node
 Duration 0.04-0.13 sec
108

2) “S-T” segment
• Is the time interval between the end of ‘S’ wave and the
onset of ‘T’ wave.
• Represents the complete depolarization of ventricles.
• It is an isoelectric period.
• Normal duration is 0.08 second
109

3) T-P segment
• From end of T wave to the beginning of P wave
• Duration 0.25 sec
• The heart muscle is completely repolarized and at rest and
ventricular filling is taking place,
110

Intervals
1) P-Q or P-R Interval.
• The time between the beginning of the P wave and the
beginning of the QRS complex.
• Is the interval between the beginning of electrical excitation
of the atria and the beginning of excitation of the ventricles.
• The average P-Q interval is about 0.16 second.
111

2) Q-T Interval.
• Is the time interval between the onset of ‘QRS’ complex
and the end of ‘T’ wave.
• indicates the ventricular depolarization and
repolarization.
• It signifies the electrical activity in ventricles.
• Is about 0.35 second.
112

3) R-R interval
• Is the time interval between two consecutive ‘R’ waves.
• Signifies the duration of one cardiac cycle.
• Normal duration is 0.83 second.
Determining heart rate from the ECG
• HR = 1/ RR interval
E.g; If the ‘R-R’ interval is 1 second, the heart rate is 60 bpm.
• The normal RR interval in the adult person is about 0.83
second.
• HR= 60/0.83 times per minute=72 bpm.
113

ECG cont’d
• Firing of the autorhythmic cells, do not generate enough
electricity to reach body surface
• There fore no wave is recorded for such cells
114

Types of Electrocardiogram Recording leads
1) Bipolar
2) Unipolar: Chest leads
Augmented limb
1. Bipolar/standard limb leads:
• Record voltage b/n two
electrodes (leads) placed on
the wrists and legs. These
leads include:
Lead I= LA with RA,
measures electric potential
difference b/n LA& RA.
Lead II =LL with RA,
Lead III = LL with LA. 115

Einthoven Triangle
• Is defined as an equilateral triangle that is used as a model
of standard limb leads used to record electrocardiogram.
• Heart is presumed to lie in the center of Einthoven triangle.
• Electrical potential generated from the heart appears
simultaneously on the roots of the three limbs, ( left arm,
right arm and the left leg).
116

Einthoven Law
• If electrical potentials of any two of the three leads are
given, the 3rd
one can be determined.
• Amplitude (electrical potential) of QRS complex in one
lead can be mathematically calculated, by summing up or
subtracting the amplitude in other two leads
• Example: Amplitude of QRS in lead II = I + III
The amplitude of QRS in lead III = II – I.
117

Normal electrocardiograms recorded from the three standard
bipolar limb leads.
119

2. Unipolar leads:
A) Precordial (Chest Leads)
• ECG are recorded with one electrode
placed on the anterior surface of the
chest
– directly over the heart
• They are labeled as leads V1, V2, V3,
V4, V5, and V6
• Electrodes are placed on the chest as
shown.
• Heart surfaces are close to the chest
wall and
– each chest lead records mainly the
electrical potential of the cardiac
muscle immediately beneath the
electrode.
120

Cont,d
• QRS in V1, V2, are
negative because
– the chest electrodes
are nearer the base
of the heart
(direction of electro
negativity).
• V3 is in b/n.
• QRS of leads v4-v6 are
positive because
– they are nearer the
apex (direction of
electro positivity).
Fig. Normal electrocardiograms
recorded from the six standard chest
leads
122

B. Augmented Unipolar Limb
Leads
• A modified unipolar limb lead
• The three standard leads are:
I. aVF lead: an augmented unipolar
limb lead in which the positive
electrode is on the left leg.
II. aVL lead: an augmented
unipolar limb lead in which the
positive electrode is on the left
arm.
III.aVR lead: an augmented
unipolar limb lead in which the
positive electrode is on the right
arm.
123

Normal recordings of the augmented unipolar limb leads
• They are all similar to
the standard limb lead
recordings, except
that the recording
from the aVR lead is
inverted.
124

Placement of Electrocardiograph Leads
125

Interpretation of an ECG
General questions asked:
1. What is the heart rate?
Normal rate=60-100bpm
Faster than normal =tachycardia
Lower than normal =bradycardia
2. Is the rhythm of the heart regular?
3. Are all normal waves present in recognizable form?
4. Does a QRS complex follow each P wave?
126

Relationship of the ECG to Electrical Activity of the
Myocardium
 Red: indicates
depolarized
myocardium,
and
 Green: indicates
repolarized
myocardium.
• Arrows: indicate
the direction in
which a wave of
depolarization or
repolarization is
traveling.
127

Some examples of abnormal rhythm(arrythmias)
Arrythmia is irregular heartbeat or disturbance in rhythm of
the heart.
Abnormal cardiac rhythm can be caused by:
Shift of pacemaker from SA node to other part of the heart
Abnormal rhythmicity of the pacemaker
Blockage at different points (interference with conduction).
Abnormal pathways of transmission through the heart.
128

Sinus arrhythmia
• Sinus arrhythmia is a normal rhythmical increase and
decrease in heart rate, in relation to respiration.
• It is also called respiratory sinus arrhythmia (RSA).
• During inspiration:
HR increases
RR interval is shortened
• During expiration:
HR decreases
RR interval is prolonged
129

Principles of Vectorial Analysis
• Cardiac vector (cardiac axis)
is the direction at which
electrical potential generated in
the heart travels at an instant.
• Vector is represented by an
arrow.
• Arrow head shows the
direction
• Length of the arrow represents
the amplitude (magnitude or
voltage) of electrical potential.
133
Instantaneous mean vector
when current flows through
interventricular septum of the
heart

Direction of a Vector is Denoted in Terms of Degrees
• When a vector is exactly horizontal
& from right side towards left side
of the heart, the degree of vector is
zero.
• From this zero reference point, the
scale of vectors rotates clockwise.
• From left to right of the heart =
+1800
• From above and straight
downward= +90o
.
• Straight upward= -900
(+2700
)
134

Axis for Each Standard Bipolar Lead and Each
Unipolar Limb Lead
• The direction from negative electrode to positive electrode
is called the "axis" of the lead.
• In Lead I:
 Because the electrodes lie exactly in the horizontal
direction, with the positive electrode to the left, the axis
of lead I is 0 degrees.
• In recording lead II:
Electrodes are placed on the right arm and left leg.
Vector is from above downwards and slightly towards
left, i.e. its axis is 60°. 135

Cont’d
• In lead III, vector is from above downwards and slightly
towards right ,its axis is 120°.
• aVR, Vector is from below towards upper part of the heart
and slightly towards right at +210 degrees;
• aVF, Vector is from above downwards at +90 degrees; and
• aVL ,the vector is from below, towards upper part of the
heart and slightly towards left at –30°.
136

137
Axes of the three bipolar and three unipolar leads

Electrical vectors of atrial muscle
140

Mean Electrical Axis of the ventricles
• Is sum total of all electrical currents generated by ventricles
during depolarization.
• Current flows from base of ventricles(-ve) toward apex
(+ve).
• The mean electrical axis of the normal ventricles is 59°
• It varies between -20° and 100°.
• Electrical axis is determined from standard limb leads
(fig..below).
141

Calculation of mean QRS vector
143
An equilateral triangle is drawn
on a plain paper.
From the midpoint of each side,
perpendicular line is drawn
towards the center.
On each side of triangle, the
amplitude of QRS complex is
plotted
From the positive end of each
projected vector another
perpendicular line is drawn
towards interior of the triangle
Now an arrow is drawn between
the two meeting points.

Cont’d
144
Changes in mean electrical
axis
•Left axis deviation
 More horizontal heart
 Short obese individual
 LV hypertrophy
Left bundle-branch
block
•Right axis deviation
 More vertical heart
 Tall thin persons
 RV hypertrophy
Right bundle branch block
Mean electrical axis and axis
deviations

Axis deviation Cont’d
145
Right bundle-branch block Left bundle-branch block

Cardiac Cycle and Heart Sounds
146

The Cardiac Cycle
• The sequence of cardiac events that occurs during each beat
are called the cardiac cycle.
• The cardiac cycle consists of
– a period of relaxation called diastole, during which the
heart fills with blood, followed by a period of contraction
called systole.
• It is consists of one complete contraction and relaxation of
all four heart chambers.
• Duration of one cardiac cycle= 0.8 sec.
147

Cont’d
• Each Cardiac Cycle is initiated by spontaneous generation
of an action potential in the sinus node.
• The atria pumping blood into the ventricles before the
strong ventricular contraction begins.
• Thus, the atria act as primer pumps for the ventricles.
• The ventricles in turn provide the major source of power for
moving blood through the body’s vascular system. 148

Mechanical Events during Cardiac Cycle
Events of cardiac cycle are classified into two:
A. Atrial events:
Atrial systole
Atrial diastole
B. Ventricular events.
Ventricular systole:
Isometric contraction
Ejection period
Ventricular diastole:
Isometric relaxation
Filling (Rapid, Slow & last rapid )
149

150Atrial and ventricular events of cardiac cycle

A) Atrial events
1) Atrial Contraction (Atrial systole)
 Is also known as last rapid filling phase
 Considered as the last phase of ventricular diastole
During atrial contraction:
– Intra-atrial pressure increases by about 5 mm Hg.
– This helps for the atria eject blood into the ventricles
(Atria contribute about 20% to ventricular filling)
– The ventricular volume and pressure increase slightly
due to the atrial ejection of blood.
– Atrial contraction not essential for ventricular filling.
• Duration = 0.11sec. 152

2) Atrial diastole
This is the period during which atrial filling takes place.
Simultaneously, ventricular systole also starts.
RA receives deoxygenated blood through vena cava and LA
receives oxygenated blood through pulmonary veins.
• It lasts for about 0.7 sec.
• NB. The heart relaxes as a whole for 0.4 sec.
153

B) Ventricular events
I) Ventricular systole
1) Isometric Contraction (Isovolumetric Contraction)
• Begins shortly after the beginning of QRS.
• All valves are closed.
At this point
– the volume of the blood remains constant while the
pressure in the ventricles rises rapidly.
– The tension increases, however the A-V valves are closed
no blood flows into the atria.
• Duration = 0.05sec.
154

2) Rapid Ejection:
• As soon as the pressure in the ventricles exceeds the
pressure in the arteries,
– The semilunar valves open and
– Blood flows rapidly from the ventricle into the arteries.
– This corresponds with a sharp decrease in ventricular
volume.
• At the end of maximal ejection,
– the onset of the T wave occurs signalizing the beginning
of ventricular repolarization.
• Duration = 0.09 sec.
155

3) Slow Ejection:
• The blood is ejected slowly.
• The ventricular volumes and pressure in the arteries start
to decrease.
• At this point muscle fibers have reached a shorter length
and can no longer contract forcefully.
End systolic volume:
Is the amount of blood remaining in each ventricle at the
end of ejection period.
About 40 to 50ml per ventricles.
156

II) Ventricular diastole
1)Isometric (Isovolumetric) Relaxation:
• Characterized by decrease in tension.
• Intraventricular pressure decreases during this period.
• All valves are closed.
• The amount of blood cannot change
– because the valves at both ends of the ventricles are
closed.
157

2) Rapid Ventricular Filling:
• As soon as ventricular pressure falls below atrial
pressure
– the A-V valves open and
– There is a sudden rush of blood (which is
accumulated in atria during atrial diastole)
During this period:
– the flow of blood from the aorta to the peripheral
arteries continues and
– the aortic pressure falls slowly.
• Duration = 0.11 sec.
158

3) Slow filling phase
• After the sudden rush of blood, the ventricular filling
becomes slow.
• It is also called diastasis.
• About 20% of filling occurs in this phase.
• Duration of slow filling phase is 0.19 second.
4) Last rapid filling phase
 Occurs because of atrial systole.
 Flow of additional amount of blood into ventricles due
to atrial systole is called atrial kick.
159

End-Diastolic Volume
• Is the amount of blood remaining in each ventricle at
the end of diastole.
• It is about 110 to 120 mL per ventricle.
160

With in a cardiac cycle, it is possible to observe the
association action of the following:
 Summated ECG voltage changes,
 Myocardial contraction and relaxation,
 Opening and closing of cardiac valves,
 Pressure and volume changes,
 Heart sounds
167

The pressure Changes in the Atria
• In the atrial pressure curve, three minor pressure elevations, called
the a, c, and v atrial pressure waves, are noted.
• The a wave
– is caused by atrial contraction.
– Ordinarily, the right atrial pressure increases 4 to 6 mm Hg
during atrial contraction, and
– the left atrial pressure increases about 7 to 8 mm Hg.
171

The c wave
– Occurs when the ventricles begin to contract;
– it is caused mainly by bulging of the A-V valves backward toward
the atria because of increasing pressure in the ventricles.
The v wave
– It results from slow flow of blood into the atria from the veins
while the A-V valves are closed during ventricular contraction.
– Occurs toward the end of ventricular contraction.
172

Pressure changes during cardiac cycle
174

Heart Sounds
Four separate heart sounds (S1, S2, S3 and S4) identified by:
 Stethoscope mediated auscultation
 Phonocardiographic recording
S1: Slightly prolonged “lub” sound
– Occurs at the Isometric contraction of ventricles.
– Caused by sudden closure of AV-valves.
S2: Shorter, high pitched “ dub” sound
– Occurs at isometric relaxation of ventricles
– Caused by sudden closure of semilunar valve
– Both S1 & S2 is detected by Stethoscope
175

• S3 (sometimes): due to rapid ventricular filling
• S4 (occasionally): during atrial contraction
• Third and fourth sounds occur normally in children
(abnormal in adult)
Chest areas from which sound is best heard
176

Murmurs (bruits)
• Abnormal sounds heard in various parts of the
vascular system.
• May be caused by turbulent blood flow that is
speeding up when an artery or a heart valve is
narrowed.
Causes of murmur
177

Cardiac Output (CO)
– is defined as the volume of blood ejected from the heart
per minute.
– is a product of heart rate and stroke volume.
CO = HR x SV
• The usual resting values of CO
– for young, healthy men, resting cardiac output averages
about 5.6 L/min.
– for women, this value is about 4.9 L/min
• At typical resting values,
– CO = 75 beats/minx70 mL/beat =5,250 mL/min.
178

• Cardiac output is not constant.
• Vigorous exercise
– increases CO to as much as 21 L/min and
– up to 35 L/min in world-class athletes.
• The difference between the maximum and resting cardiac
output is called cardiac reserve.
 Cardiac Reserve = C.O during maximal exercise - C.O at
rest
E.g. 35L-5 L =30L
 Cardiac Index = Cardiac output÷ Body surface area
3.8 L/m/m2(male), 7-10% less in female
179

Ejection fraction(EF)
EF=Measurement of ventricular performance
 is fraction of EDV ejected from ventricles per beat
EF (%)= SV/EDV X 100
A healthy man has EF of 50% or more
Is primary clinical index of contractility
180

Factors Affecting Cardiac Output
1. Venous return
2. Force of contraction Directly proportional to CO
3. Heart rate
4. Peripheral resistance → Inversely proportional to CO
Venous Return
• Is the amount of blood which is returned to heart from
different parts of the body.
It is influenced by right atrial pressure.
182

Factors affecting venous return(VR)
1. Right Atrial Pressure(RAP)
• Mean pressure in the right atrium accounts 2 mmHg
• ↑RAP→↓VR
2. Resistance to venous return (RVR)
• Occurs mainly at arterioles
• The more the resistance in the arterioles lesser the VR.
3. Sympathetic stimulation:
 ↑VR by inducing venoconstriction
4. Blood volume:
 ↑Blood volume → ↑VR
183

5.Respiratory movements
• VR increases with inspiration and decreases with expiration
6. Arteriolar dilatation →↓Resistance to VR and ↑VR
7. Skeletal muscle contraction
Squeezes veins b/n muscles → ↑VR
8. Gravity
• Standing motionless for some time →Pooling of blood in
lower extremities → ↓VR → ↓C.O →hypotension →brain
ischemia → fainting episode.
184

Heart Rate
• Heart rate and cardiac output have a direct relationship
with certain limits.
• As a general rule,
– a patient with a heart rate that is too fast
–(>150/minute – not enough filling time) or
– too slow (< 50/minute - not enough rate)
–requires urgent assessment for signs and
symptoms of shock.
• Both extreme rates can be associated with inadequate
cardiac output.
185

Cont,d
• This graph illustrates the relationship
between
– heart rate and cardiac output.
• As heart rate increases, so does
cardiac output - to a certain limit.
• Cardiac output tends to fall when
– heart rate exceeds 150/minute due to
inadequate filling time.
– Low cardiac output states also occur
with low heart rates (<50/minute).
186

Force of contraction of the heart
A. Preload
• Preload is the volume or pressure in the ventricle at the end
of diastole.
• Increases the force of contraction and cardiac output.
• Preload is connected to stroke volume and cardiac output
via the Frank-Starling law.
Frank-Starling phenomenon
• Frank and then Starling demonstrated that
– The more the stretch of the heart’s chambers, the more
forceful the contraction (and indeed the greater the stroke
volume).
187

B. Afterload
• The resistance to the ejection of blood from the ventricle is
called after load.
• The higher the afterload, the more difficult a job it is for the
left ventricle to eject sufficient stroke volumes.
• As the afterload increases,
– CO and SV decreases
• The left ventricle is 3 times the thickness of the walls of the
right ventricle due to afterload.
189

Summary, Parameters that Affect Cardiac Output,
190

Regulation of cardiac output
1) Neural regulation
1.1. High centre areas:
• Pre-motor cortex, frontal lobe, part of temporal lobe,
on stimulation→↑rate and force of contraction of the
Heart and increase CO.
1.2. Cardiovascular centers In Medulla Oblongata:
• Cardioinhibitory centre:
– ↓HR→ ↓cardiac contractility and decrease CO.
• Cardioacceleratory centre:
– ↑cardiac contractility → ↑ CO.
191

Cont’d
• Autonomic innervations to the heart
Sympathetic nervous system: ↑CO
Parasympathetic nervous system:↓CO
192

2 Hormonal and Chemical Regulation
 Inotropic agents with positive effect on the heart
(Those which increases force of contraction)
–Glucagon,
–T3/T4,
–Cathecolamines
–Hypercalcaemia
 Inotropic agents with negative effect on the heart
–Hyperkalemia,
–hypocalcemia,
–acidosis,
–toxins 193

Changes in stroke volume(SV)
SV is determined by:
– Pre load→ leads to a change in EDV
– After load
– Contractility → Leads to a change in ESV
195

Cardiac function curves
Cardiac function curves are of two types:
1. Cardiac output curves
2. Venous return curves.
Cardiac output curves
• Show the relationship between cardiac output and right
atrial pressure.
• Increase RA pressure increase CO (only up to a certain
point)
• In steady state, vol. of blood left ventricle ejects as CO =
venous return. 197

When RA pressure = ∼4mmHg., CO can on longer keep
up with venous return, thus levels off.
198

Venous return curve:
• As RA pressure increases, pressure gradient decreases and
venous return decreases.
• When RA pressure negative, veins collapse, blood flow to
veins impeded (although pressure gradient has increased)
• Therefore, venous return levels off because veins have
collapsed.
199

Coupling of cardiac and vascular functions
• Cardiac output →Cardiac function and
• Venous return→ Vascular function
• When venous return is normal (5 L/minute), the cardiac
output as well as the right atrial pressure are normal.
201

Hypertrophy of the heart
1. Physiological hypertrophy
Physical exercise:
Heart wt. = 500gm. (350 gm. In sedentary)
Length and thickness of myocardial cells increased
Therefore, large vol. of blood is ejected per beat
Stroke vol. is larger & HR is slower.
204

2) Pathological hypertrophy
e.g. Aortic stenosis-unilateral hypertrophy (LV)
Degree of compensation limited
Thus myocardial fiber diameter increases,
Distance between capillaries and cell interior increases
(diffusion distance increases),
Thus inadequate O2, nutrition.
Result = heart failure (myocardial insufficiency)
205

Physiology of cardiovascular system

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