Cardiovascular Physiology

30/03/10 1
 Cardiovascular system (CVS)

CVS consists of the heart and a

series of blood vessels (arteries,

veins and capillaries).

30/03/10 2
 CVS
Function: Homeostasis through:
– Generate blood pressure.

– Ensuring one way blood flow.

– Regulating blood supply.

30/03/10 3
 Parts of the circulatory system

The circulatory system forms two circuits in series

with each other:-

- Systemic circulation (greater circulation)

- Pulmonary circulation (lesser circulation)

30/03/10 4
30/03/10 5
 Lungs
The Normal
Heart and
Regional Pulmonary
Semilunar
Circulation Valve
Aorta

Superior Left
Vena Pulmonary
Cava Artery

Left
Left Pulmonary
Atrium Veins

Right
Pulmonary Aortic Semilunar
Artery Valve
Bicuspid or
Right
Mitral Valve
Pulmonary
Veins

Tricuspid Valve

30/03/10 6
Inferior Vena Cava Septum
 Brain
The
Systemic
Circulation
Lungs
Veins (Flexible Arteries (Stiff
Compliant “Pipes”) Inflexible “Pipes”)

Precapillary
Sphincters

Liver
Stomach

Pancreas

Intestines
Kidneys

Arterioles
Skin

30/03/10 7
Muscle
 Systemic and pulmonary circulations

30/03/10 8
30/03/10 9
30/03/10 10
30/03/10 11
 Location
Heart is located in thoracic cavity in the mediastinum,
between the lungs.
The heart lies obliquely in the mediastinum with its
base directed posteriorly and slightly superiorly and
the apex directed anteriorly and slightly inferiorly.
The apex is also directed to the left so that
approximately 2/3 of the heart mass lies to the left of
midline.
The base of the heart is deep to the sternum and
extends to the 2nd intercostal space.
The apex is approximately 9 cm. to the left of the
sternum and is deep to the fifth intercostal space.
30/03/10 12
 Pericardium
Pericardium: a double layered closed sac that surrounds
the heart:
1- Fibrous pericardium: outer layer, tough, fibrous
connective tissue. Prevents over distension of the heart
and anchors it within the mediastinum. Superiorly it is
continuous with the connective tissue of the great
vessels, and inferiorly attached to the surface of the
diaphragm.
2- Serous pericardium: thin transparent inner layer.
– Parietal pericardium: part of the serous pericardium that
lines the fibrous pericardium.
– Visceral pericardium: part of the serous pericardium that
covers the heart surface.
Pericardial cavity: between the parietal and visceral
pericardium is filled with a thin layer of serous
Pericardial
30/03/10
fluid: reduces friction of the beating heart.
13
 Heart Wall
Epicardium: thin serous membrane of the
outer surface of the heart. Also called
the visceral pericardium
Myocardium: thick middle layer
composed of cardiac muscle.
Endocardium: simple squamous
epithelium over a layer of connective
tissue, continuous with all blood vessels
of the body.
30/03/10 14
 Heart Anatomy
• The heart is a strong muscular pump that contracts

and relaxes all life.

• It is the size of the fist of the hand.

• It is formed of 4 chambers:

Two thin walled low pressure reservoirs, the atria and

two thick walled pumping chambers, the ventricles.

30/03/10 15
 Functional anatomy of the heart

30/03/10 16
 Heart beat

30/03/10 17
 Heart valves
• Tricuspid valve: 3 cusps, between the right atrium and
right ventricle.
• Bicuspid valve: two cusps, between the left atrium and
left ventricle, also known as the mitral valve.
• Semilunar valves: Consists of three pocket like
semilunar cusps, the free inner borders meet in the
middle of the artery to block retrograde flow.
Aortic valve: between the left ventricle and the
aorta.
Pulmonary valve: between the right ventricle
and the pulmonary artery.

30/03/10 18
 Heart valves

30/03/10 19
 ِ V and Semilunar Valves
A

30/03/10 20
 Innervations of heart
autonomic nerve supply:
1- Sympathetic: increase activity of
whole heart.
(increase heart rate and contractility)
2- Parasympathetic: comes through
vagus nerve and decrease activity
of atria only.
(decrease heart rate)
30/03/10 21
Autonomic Innervations of the heart

30/03/10 22
 Mammalian Heart

30/03/10 23
30/03/10 24
 THE CARDIAC MUSCLE
• Cardiac muscle is formed of myocardial
muscle fibers which are elongated
branched nucleated cells, the ends of
which are joined together by intercalated
discs, forming a network.
• The intercalated discs contain gap
junctions which have low electric
resistance and allow free diffusion of
ions. Thus, excitation in one area
spreads throughout the heart.
30/03/10 25
• This permits the cardiac muscle to
contract as a whole as if it is made of a
single muscle cell or as a functional
syncytium.
• The heart is composed of 2 functional
syncytia: ATRIA AND VENTRICLES.

30/03/10 26
 THE CARDIAC MUSCLE

30/03/10 27
 GAP JUNCTIONS

30/03/10 28
 PROPRTIES OF CARDIAC
MUSCLE
• 1- EXCITABILITY

• 2- CONTRACTILITY

• 3- RHYTHMICITY

• 4- CONDUCTIVITY

30/03/10 29
 1- EXCITABILITY
• Definition: Excitability is the ability of
the cardiac muscle to respond to a
stimulus by generating an action
potential followed by a contraction.
• Cardiac muscle resting membrane
potential and action potential differ in
different parts of the heart.

30/03/10 30
 Cardiac Action Potentials

30/03/10 31
 THE A.P. OF THE
VENTRICLES

30/03/10 32
 PHASES OF VENTRICULAR
A.P.
- Phase 0: Initial rapid
depolarization.
- Phase 1: Brief initial
repolarization.
- Phase 2: Prolonged plateau.
- Phase 3: Late rapid
repolarization.
- Phase 4: Resting membrane
potential (-100 mv)
30/03/10 33
 IONIC BASIS OF VENTRICULAR
ACTION POTENTIAL
• Phase 0: Initial rapid depolarization: due to Na+ inflow
due to opening of fast Na+ channels.
• Phase 1: Brief initial repolarization: due to opening of
transient K+ channels.
• Phase 2: Prolonged plateau: due to opening of slow
Ca++ - Na+ channels.( A balance is created between
influx of Na+ and Ca+ and outflux of K+)
• Phase 3: Late rapid repolarization: due to delayed
opening of K+ channels.
• Phase 4: Resting membrane potential ( -100 mv)
30/03/10 34
30/03/10 35
 LONG REFRACTORY PERIOD
• Cardiac muscle action potential
differs from skeletal muscle action
potential.
• Cardiac action potential is
characterized by A LONG
REFRACTORY PERIOD due to
the plateau phase, during which
the heart cannot be restimulated.
• The action potential results in a
mechanical response:
contraction (systole) followed by
relaxation (diastole).

30/03/10 36
 Action Potential and Mechanical Response
Cardiac Muscle Skeletal Muscle

30/03/10 37
 NON TETANIZING PROPERTY
• The cardiac muscle has a long
refractory period (due to
plateau phase), which
coincides with the whole period
of systole.
• Thus the heart remains non
excitable for the entire
contraction phase.
• This ensures that the heart
cannot go into a sustained
state of contraction (tetanus)
which could lead to stopping of
circulation.
30/03/10 38
30/03/10 39
 2- CONTRACTILITY
• Definition: It is the ability of the cardiac muscle to
contract to pump blood.
• The heart is a strong muscular pump that contracts and
relaxes all the time day and night, and its cessation
means death.
• There are two types of muscle contraction:
a- Isometric contraction: increase muscle tension
without shortening (e.g. during early systole)
b- Isotonic contraction: Tension is constant but
muscle shortens and work is done (e.g. during
late systole when blood is ejected)

30/03/10 40
 CONTRACTILITY (cont)
• The cardiac contractility obeys two
laws:
• ALL OR NONE LAW:
If other conditions are constant, the
cardiac muscle either contracts
maximally ( if the stimulus is
adequate) or does not contract at all
( if the stimulus is inadequate)
30/03/10 41
 CONTRACTILITY (cont)
• STARLING’s LAW:
[LENGTH-TENSION RELATIONSHIP]
• The ability of the cardiac muscle to generate
force, is dependent on the initial length of the
muscle prior to contraction, i.e. end diastolic
volume (EDV).
• The greater the initial length of the muscle
fibers, the greater the force of contraction
(within limits).

30/03/10 42
 Application of STARLING LAW
If the amount of blood
returning to the heart
increases (i.e.↑venous
return)  this will stretch the
cardiac muscle fibers, i.e.
increase its length at end of
diastole (↑↑EDV: end
diastolic volume )
 increase the force of
contraction at systole 
increase stroke volume.
[ Thus, the heart will pump
out whatever volume is
delivered to it]
30/03/10 43
30/03/10 44
 3- RHYTHMICITY
• Definition: It is the ability of the cardiac
muscle to initiate its own regular impulses
(rhythm), independent of any nerve supply.
• Cause: The cardiac muscle has a specialized
excitatory conductive system, which have
the property of auto rhythmicity.
• Rate of autorhythmicity:
• SA Node: 70-80 beats/min
• AV Node: 40-60 beats/min
• Bundle of His: 30 beats /min
• Purkinje fibers: 15 beats/min (incompatible
with life)
30/03/10 45
 Excitatory Conductive system

30/03/10 46
 PACEMAKER OF THE HEART
• The area which determines the pace or rhythm of the
heart is called the pacemaker of the heart.
• The SA Node is the pacemaker of the heart because:
1- it has the highest rhythm
2- and the whole heart obeys it.
• If the SA Node is destroyed, the AV Node will be
pacemaker.
• VAGAL TONE: It is the continuous impulses in the
vagus nerve which decrease the inherent high rhythm
of the SA Node from 90-100/min to 70-80/min (the
normal heart rate)

30/03/10 47
30/03/10 48
 PACEMAKER POTENTIAL
Pacemaker cells have unique electric
properties:
• Prepotential: Unstable
membrane potential due to
slow continuous leakage of
Na+ ions into the
myocardium leads to:
spontaneous diastolic
depolarization.
• After reaching firing level,
the next action potential
follows automatically.
• No plateau is seen.

30/03/10 49
 HEART RATE is determined by
pacemaker activity of the heart (70-80/min)
• Variations in heart rate:
1- Tachycardia (Increase
HR) : sympathetic
stimulation as in
emotions, exercise,
hyperthyroidism.
2- Bradycardia (decrease
HR) : parasympathetic
stimulation as in sleep,
hypothyroidism.
30/03/10 50
 4- CONDUCTIVITY
• Definition: It is the ability of the cardiac
muscle to conduct or transmit an action
potential over the whole heart along
specialized conducting system having high
conduction velocities.
• Velocity of conduction:
• SA Node: 1 m/sec
• AV Node: 0.05 m/sec
• Bundle of His: 1 m/sec
• Purkinje fibers: 4 m/sec
30/03/10 51
30/03/10 52
 Conduction Velocity in heart

m/sec 1
1m/sec

m/sec 4
m/sec 0.05

30/03/10 53
 PROPAGATION OF CARDIAC IMPULSE
• Cardiac impulse is initiated by SA Node.
• It spreads through atria in internodal tissue at a rapid
rate to reach AV Node.
• The conduction velocity slows down in AV Node which
is known as AV Nodal delay. This delay is important
as it gives time for proper ventricular filling.
• The wave then travels rapidly down the AV bundle,
bundle branches and Purkinje fibers to all parts of the
ventricles. The fastest conductivity in Purkinje fibers is
important as it excites the whole ventricle as one unit
leading to powerful ventricular contraction.
• Block in transmission of impulse is “heart block”
30/03/10 54
30/03/10 55
 THE CARDIAC CYCLE
• Definition: The cyclic events that occur in the
heart chambers during each beat.
• As the normal heart rate is 70 beat/min, the
duration of each cardiac cycle is 60/70 = 0.8 sec
• Each cardiac cycle includes: Atrial systole 
Ventricular systole  Diastole of whole heart.
• Blood flow in the heart is determined by pressure
difference across the orifices of the heart which
leads to opening and closure of valves.
• First and second heart sounds are due to closure
of AV and semilunar valves respectively.
30/03/10 56
 STROKE VOLUME
• STROKE VOLUME:
is the volume of
blood ejected by
each ventricle per
beat.
= End diastolic
volume - End
systolic volume
= 120-50= 70 ml
30/03/10 57
 CARDIAC OUTPUT
• Cardiac output is the volume of blood
ejected by each ventricle / min
= Stroke volume x Heart rate
= 70 x 70
= 5 liter/min

30/03/10 58
30/03/10 59
 PHASES OF CARDIAC CYCLE
I- SYSTOLE
• Atrial systole: [SA Node depolarization]
The atria contract propelling the last 30% of its blood into
ventricles.
• Ventricular Systole: [Depolarization of ventricles]
1- Isometric Contraction Phase:
- Ventricular pressure>atrial pressureAV valves close.
- Now ventricles contract as a closed chamber (all valves are
closed)
- No change in volume but pressure increase.
2- Ventricular Ejection Phase:
- Ventricular pressure> aortic and pulmonary pressure
semilunar valves open.
- Now blood gushes out of ventricles into aorta and
pulmonary vessels
30/03/10 60
 PHASES OF CARDIAC CYCLE
II- DIASTOLE
• Ventricular Diastole: [Repolarization of ventricles]
1- Isometric Relaxation Phase:
- When ventricular pressure < aortic and pulmonary
artery pressure  Semilunar valves close.
- Now ventricles relax as a closed chamber (with all
valves closed)
- No change in volume but pressure decrease.
2- Ventricular Filling Phase:
- Ventricular pressure<atrial pressure AV valves open.
- Now ventricles start to fill with blood from atria.
- First 30% (rapid filling), mid 30% ( reduced filling or
diastasis), last 30% (atrial systole)
30/03/10 61
30/03/10 62
 SYSTOLE

30/03/10 63
 DIASTOLE

30/03/10 64
30/03/10 65
30/03/10 66
30/03/10 67
30/03/10 68
30/03/10 69
 ECG

30/03/10 70
 ECG Recording

30/03/10 71
 ECG Intervals and Segments

30/03/10 72
 Normal ECG Record

30/03/10 73
 ECG Leads

30/03/10 74
 ECG LEADS

30/03/10 75
30/03/10 76
30/03/10 77
 Normal ECG Recording

30/03/10 78
30/03/10 79
30/03/10 80
30/03/10 81
30/03/10 82
 ECG Abnormalities

30/03/10 83
30/03/10 84
 HEART SOUNDS

30/03/10 85
• CARDIAC MUSCLE CELLS
• Elongated branching cells with one or two
centrally located nuclei.
• Striated
• Intercalated discs
• Desmosomes
• Gap Junctions
• Autorhythmicity - cardiac muscle has the
ability to depolarize spontaneously. only
1% of the cells have this ability
30/03/10 86
 Cardiac muscle

30/03/10 87
 Intercalated discs

30/03/10 88
 CONDUCTION SYSTEM
• Sinoatrial node (SA Node): is medial to the
opening of the superior vena cava.
• Action potentials originate here and travel
across the wall of the atrium to the
atrioventricular node (AV Node) located
medial to the right atrioventricular valve.
• Action potentials pass through the AV node
and along the atrioventricular bundle, which
extends from the AV node into the
interventricular septum.
30/03/10 89
• The AV bundle divides into right and left
bundle branches, the action potential
descends to the apex of the heart along
the bundle branches.
• Action potentials are carried by Purkinje
fibers from the bundle branches up along
the ventricular walls.

30/03/10 90
 The cardiac conduction system

30/03/10 91
 CONDUCTION SYSTEM

30/03/10 92
On the left, the action potential of a contractile
cell. On the right is the action potential of an
autorhythmic cell

30/03/10 93
Ionic changes in autorhythmic cells

30/03/10 94
 Ionic changes in ventricular
muscle

30/03/10 95
30/03/10 96
 Heart sounds

30/03/10 97
 Mitral Area
• located about the apex
beat, which is usually in
the fifth intercostal
space.
• It is also called the apical,
or the left ventricular
area.
• The systolic murmur of
Mitral Regurgitation and
the diastolic murmurs of
Mitral Stenosis and
Increased Valvular Flow.

30/03/10 98
 Tricuspid Area

located at the lower

left sternal border
(LLSB).
The diastolic murmur
of Tricuspid
Stenosis.

30/03/10 99
 Pulmonary Area
• located in the second
intercostal space at
the left sternal border.
• The systolic murmur
of Pulmonic Stenosis
and the diastolic
murmur of Pulmonic
Regurgitation.

30/03/10 100
 Aortic Area
• located in the second
intercostal space at
the right sternal
margin.
• The systolic murmurs
of Aortic Stenosis and
Increased Aortic
Valve flow.

30/03/10 101
 Electrocardiography (ECG)
• It is a recording of electrical activity of
the cardiac muscle from the surface of
the skin of the thoracic cage where the
body fluid act as a good conductor from
cardiac muscle to electrodes placed on
the skin..
• The electrical activity proceed the heart
contraction.

30/03/10 102
 Basis of the ECG
• When the excitation wave begins to spread in the heart.
• The surface of the cells in the heart depolarized and
becomes negative in relative to the surrounding region.
• Thus there are two areas in the heart one excited and the
other is notexcited, and both of them act as two terminals of
the battery, one negative and the other is positive.
• This generates an electrical field throughout the body fluid.

30/03/10 103
 Basis of the ECG
• The electrical activity of the heart
starts at the SAN then spread to the
both atria and then to the both
ventricles and the surrounding
tissues.
• ECG is used to evaluate some heart
problems such as arrhythmias,
ischemia, necrosis and hypertrophy
of the heart.
30/03/10 104
• The used apparatus for recording called
electrocardiograph which has an electrode
placed on the skin and the recording obtained
from a specific point called (a lead), the
standard ECG has 12 different leads that record
the same electric events but from different
views.
• The leads are of 3 types:-
– Bipolar limb leads.
– Unipolar leads.
– Augmented unipolar leads.

30/03/10 105
 Bipolar limb leads:
• These leads measure the potential difference between
2 limbs by applying active electrodes from ECG
apparatus anywhere on the limbs (wrist or ankle).
3 different leads are recorded:-
• Lead I: It measures the potential difference between
the left arm (LA) and right arm (RA).
• Lead II: It measures the potential difference between
the left (LL) and right arm (RA).
• Lead III: It measures the potential difference
between the left leg (LL) and left arm (LA).
30/03/10 106
 Unipolar leads:
• These measure the absolute (actual)
potential at a certain point.
• This is done by applying one electrode
from electrocardiograph to the desired
point while the other electrode is made
indifference (-ve), this means that the
unipolar leads measures the potential
difference between active potential and
zero potential.

30/03/10 107
Unipolar limb leads:
It measures the absolute potential at right
arm (VR), left arm (VL) and left leg (VF).
Unipolar (V) leads:
It measures the absolute potential at 6
standard points on the anterior chest wall
(V1, V2, V3, V4, V5 andV6).

30/03/10 108
V1: At right margin of the sternum in the 4th
intercostals space.
V2: At left margin of the sternum in the 4th
intercostals space.
V3: Midway between V2 and V4.
V4: At the left midclavicular line in the 5th
intercostals space.
V5: At the left anterior axillary line at the 5th
intercostals space.
V6: At the left mid axillary line at the 5th
intercostals space.
30/03/10 109
Augmented Unipolar limb Leads:
• In this case there is magnification
of amplitudes by about 50%.
• The leads called aVR, aVL and
aVF, where a= augmented.
• The augmented leads are easier
to interpret and recorded by ECG
machines.
30/03/10 110
 Normal ECG
• Normal ECG consists of 5 main waves called
P Q R S T waves.
• These waves are separated by segments.
• Each waves start and ends at the isoelectric line.
• The QRS waves from a complex called QRS
complex.
• This normal ECG can be recorded in aVl, aVF,
V5 and V6 because the exploring electrode faces
the left ventricle.

30/03/10 111
 ECG

30/03/10 112
 ECG Components Diagram

30/03/10 113
 The P wave
• Represents atrial activation (atrial
depolarization).
• Small +ve wave.
• Its amplitude 0.1 (up to 0.25) mv.
• Its duration 0.08 (up t0 0.11)
seconds.

30/03/10 114
 Abnormalities of P- wave
• In left atrial hypertrophy (due to mitral
stenosis), the P wave become broad
and notched.
• In right atrial hypertrophy (due to
pulmonary hypertension) P wave
become tall.
• In AV nodal rhythm: P wave inverted.
• In atrial fibrillation: P wave disappear.

30/03/10 115
 The QRS complex
• Represents ventricular activation (depolarization).
• The QRS duration is the duration of ventricular
activation (0.06-0.1).
• Q wave: is –ve wave due to depolarization of
interventricular septum.
• R wave: is a large +ve wave, its amplitude is 10
mm (1 mv), caused by depolarization of the apex
and ventricular wall, it is + ve wave.
• S wave: is a –ve wave, caused by depolarization
of the posterobasal part of the left ventricle and
pulmonary conus.
30/03/10 116
 Abnormalities of QRS complex
• In ventricular hypertrophy.
• Infarction.
• Extrasystole.
• Bundle branch block.
• Electrolyte disturbance.

30/03/10 117
 T wave
• It is a +ve large blunt wave.
• Represents ventricular activation (ventricular
repolarization).
• Its amplitude 0.2 (up to 0.4) mv.
• Its duration 0.2 (up to 0.25) second.

30/03/10 118
 Abnormalities of T wave
• Inverted:
• Myocardial infraction.
• Ventricular hypertrophy.
• Extrasystole.
• Bundle branch block.
• Digitals overdosage.
• Increase amplitude:
• Sympathetic overactivity.
• Muscular exercise.
• Hyperkalmia.

30/03/10 119
 ECG Intervals and Segments

30/03/10 120
 P-R interval
• - From the start of P-wave to the start of R wave.
- Its range from 0.12 to 0.21 second.
- It means conduction of cardiac impulse through
A-V node.
Abnormalities of P-R interval:
• 1- Prolonged:
• - First degree of heart block.
• - Increased vagal tone.
• 2 - Shortened:
• - A- V nodal rhythm.
• - Sympathetic overactivity.
• - Wolff- Parkinson- white syndrome.
30/03/10 121
 Q-T interval
Start from the onset of Q wave to the end of T wave.
• Its duration 0.36- 0.24 second.
• It is called electrical systole of the heart.
T- Q interval:
• Start from the end of the T wave to the onset of the
next Q wave.
• It is called electrical diastole.
• Its duration is about 0-4 second.
Abnormalities of T-Q interval:
• It is shortened before atrial and ventricular
extrasystole.
• It is prolonged after ventricular extrasystole.
30/03/10 122
 S-T segment
- Start from the end of S wave to start of T
wave.
• Its duration is about 0.12.
Abnormalities of S-T segment:
• Its deviation upward or downward indicates
myocardial damage.

30/03/10 123
 ECG changes in myocardial infraction

30/03/10 124
 The Normal Heart - Coronary Artery Anatomy

Left Main CA

Layers of the Arterial Wall

Circumflex

Adventitia
Media
Intima
Right CA

Left Anterior Descending CA Marginal Branch Intima composed of

30/03/10 125
endothelial cells
 Left Ventricular Volumes - Definitions

End Diastolic Volume (EDV)

Volume at the end of diastole
(end of ventricular filling)

End Systolic Volume (ESV)

Volume at the end of systole
(end of ventricular contraction)

Stroke Volume (SV) = EDV - ESV Ejection Fraction

is the best
Ejection Fraction (EF) = SV indicator of heart
EDV performance and
30/03/10 disease prognosis 126
Left ventricular norm for EF: 62%
 Changes in Ventricular Volumes with Exercise
120
110
LVEDV
100
90
Left 80
Ventricular 70 LVEDV - LVESV = SV
Volume (ml) SV
60
50
40
30
20 LVESV

10

Rest 300 600 - 750 Peak

30/03/10 Exercise 127
Kg meters / min
 Definitions

• Cardiac Output: (Q) = HR X SV

• Cardiac Index = Q / body surface area
• Preload: (EDV) volume of the left ventricle at the end of diastole
(dependent on venous return & stretch of the cardiac muscle cells)
• Afterload: resistance to ventricular emptying during systole
(the amount of pressure the left ventricle must generate to squeeze
blood into the aorta)
• Frank Starling Law of the Heart: the heart will contract with greater
force when preload (EDV) is increased
• Myocardial Contractility: the squeezing contractile force that the heart
can develop at a given preload
• regulated by:
• sympathetic nerve activity (most influential)
• catecholamines (epinephrine norepinephrine)
• amount of contractile mass
30/03/10•
drugs 128
 Starlings Law of the Heart and Contractility

u contractility
SV
normal
(left ventricular contractility
performance)

d contractility
(heart failure)

Preload
(venous return)

30/03/10 129
 Influences on Myocardial Contractility

u Contractility related to :
sympathetic adrenergic nerves
catecholamines: - epinephrine
- norepinephrine

drugs: - digitalis
- sympathomimetics

d Contractility related to:

- loss of contractile mass (may be due to heart attack)
- myocardial muscle disease (cardiomyopathy)
- drugs (anesthetics, barbiturates)
30/03/10 130
 Definitions
• Arteriovenous Oxygen Difference (AVO D) the difference in oxygen
2
content between arterial and venous blood
• measured in ml% - ml O 2 / 100 ml blood

• Oxygen Consumption (VO ) - the rate at which oxygen can be used in

2
energy production and metabolism
• “absolute” measures: L O / min , ml O / min
2 2

• “relative” measures: ml O / kg body wt. / min

2

• Fick equation: VO = Q X AVO D

2 2

• Maximum Oxygen Consumption (VO ) maximum rate at which a

2max
person can take in and utilize oxygen to create usable energy
• defined as plateau of consumption rate increase
• often estimated with VO 2peak

• Myocardial Oxygen Consumption VO of mildthe heart muscle (myocardium)

2
27% - 40%
• "estimated" by RPP: HR X SBP
moderate 41% - 54%
predicted VO2max - attained VO2max
marked 55% - 68%
30/03/10 131
VO severe > 69%
• Functional predicted
Aerobic Impairment:
2max
 Definitions
• Systolic Blood Pressure (SBP) pressure measured in brachial
artery during systole (ventricular emptying and ventricular
contraction period)
• Diastolic Blood Pressure (DBP) pressure measured in brachial
artery during diastole (ventricular filling and ventricular
relaxation)
• Mean Arterial Pressure (MAP) "average" pressure throughout the
cardiac cycle against the walls of the proximal systemic
arteries (aorta)
• estimated as: .33(SBP - DBP) + DBP

• Total Peripheral Resistance (TPR) - the sum of all forces that

oppose blood flow
• length of vasculature (L)
• blood viscosity (V)
• vessel radius (r) TPR = ( 8 ) ( V ) ( L )

30/03/10
(  ) ( r4 ) 132
 Cardiovascular Hemodynamic Basics

Pressure (MAP) P aorta – P vena cava

Flow (Q) = =
Resistance (TPR) (8) (V) (L)
() (r 4)

Flow (Q) = () (Pa – Pv) (r 4) Normally Resting Q is

about 5 - 6 liters / minute
(8) (V) (L)
V = viscosity of fluid (blood) flowing through the pipe
L = length of pipe (blood vessel)
r = radius of the pipe (blood vessel)
Pa = aortic pressure
Pv = venous pressure

30/03/10 133
 Respiratory Physiology - Definitions

• Minute Ventilation (V ) - amount of air passing through the

E
lungs in one minute
• Dyspnea - breathing difficulty
• Respiratory Exchange Ratio - amount of CO 2expired by the
lungs divided by the amount of O2 extracted from the air
in the lungs (VCO2 / VO2 ).

RER = .7 r 100% fat 0% carb

RER = .85 r 50% fat 50% carb
RER = 1.0 r 0% fat 100% carb

30/03/10 134
 Neurophysiology - Definitions & Concepts
Afferent - sensory nerves - going toward spinal column
Efferent - effector nerves - going away from spinal column
Adrenergic Receptor Types
 1 stimulation r constriction of:
blood vessels visceral sphincters
bronchioles bladder
 stimulation:
vasodilatation bronchiole constriction
 1 stimulation:
u HR and contractility u renin secretion
 2 stimulation:
vasodilatation bronchiole dilation
urinary tract relaxation
relaxation of visceral smooth muscle

30/03/10 135
 Microcirculatory Anatomy – a Capillary Bed

Smooth Muscle Arteriole

Precaillary
Sphincter

Anastomosis
(Shunt)
True Capillary
With Single
Layer of
Endothelium

Metarteriole

30/03/10 136
Venule
 Development of the Driving Pressure in
the Human Cardiovascular System

Arterial 100 102

Pressure
Normal Resting Pressure
(mm Hg) 26
Driving the Blood from Left
Ventricle to Vena Cava:
Mean 7
7 102 - 2 = 100 mmHg
Circulatory
Filling 0
Pressure
7
7 6
2
Central
Venous
Pressure
(mm Hg) 0 1 5 Normal
Cardiac Output (Q) Resting
30/03/10 Cardiac 137
(Liters / min) Output
 The “Closed” Cardiovascular Mean arterial pressures in red
Hemodynamic System PO2 = 160 LV
PCO2 = .3
RV
RA LUNGS LA AORTA
PO2 = 100
(0) (13) PCO2 = 40
(3) (100)
9% of blood volume
(7)

Ohms Law: Flow (Q) = upstream pressure – downstream pressure SYSTEMIC (92)
resistance
ARTERIES
low compliance
VEINS 13% of blood volume
(CAPACITANCE VESSELS)
(20)
high compliance (40)
(2)
64% of blood volume
CAPILLARY ARTERIOLES
PO2 = 40 PCO2 = 46 BEDS
7% of blood volume

Systemic Circulation = 100 mmHg – 0 mmHg = 100 ml / sec = 6 liters / min

30/03/10
Flow (Q) 1 mmHg sec / ml 138
 Sites of
Cardiorespiratory
Control
30/03/10 139
 Cardiorespiratory Control

•Heart Rate – CNS (medulla) and neurohormone regulation

• Parasympathetic vagus control (Neurotransmitter: acetlycholine)
• Vagal control dominant at rest – withdrawn during exercise

• Sympathetic cardio–acceleration (Neurotransmitter: E and NE)

• Baroreceptor influences
• Sympathetic discharge indirectly proportional to firing rate
• Parasympathetics are directly proportional to firing rate
•d pressure r d receptor firing r u sympathetics r u HR
•u pressure r u receptor firing r u parasympath. r d HR

• Chemoreceptor influences
• Main function: protect brain from poor perfusion
•
30/03/10 u O or d CO r u parasympathetic discharge r d HR
2 2
140
 Cardiorespiratory Control

Stroke Volume – regulated by Frank Starling mechanism

• u venous return r u EDV r u stroke volume

Cardiac Output (Q) – main determinant: body O2 needs

• Autoregulated by intrinsic changes in preload, & SV

•u afterload r initial d in Q r u EDV r u SV back to normal
•u venous return r u preload r u SV

• Autoregulated by extrinsic hormonal influences

• Norepinephrine release r u HR and SV

30/03/10 141
 Cardiorespiratory Control
Blood Pressure – influenced by 3 major factors
• Total peripheral resistance
• Baroreceptor (BR) and CNS Influences
• u BP r u BR firing rate r vasodilation r d BP
• d BP r d BR firing rate r u sympathetics r u BP

• Chemoreceptor influences
• dO , u CO , d pH r
2 2 CNS stim. r vasoconstriction

• Circulating catecholamine influences

• E and NE have varying effects on TP
• E and NE usually activate α receptors r u TPR
• Fight or flight response
•Q
• Blood Volume
30/03/10 142
• Renin – Angiotensin system
 H y p o t e n s i o n
H y p o v o l e m i aH 2 O r e a b s o

r e n a l p e r f u s s y i mo n p a t h e t i cA Dt o H n e( v a s o p

a f f e r e n t a r t e Nr i oa Cl a l r d e l i v e r y t o m e s s a n g i a
s t r e t c h i n J Gm ac ce ul l sl a d e n s a c c e e l l l sl c o n t r a c
r e n i n
G F R
stretch receptor
a n g i o t e n s i n I
activation in atria, aorta,
and carotid sinuses
B L O O D P R E Sa Sn gU i Ro Et e n s i n I I t h i r s t
( v a s o c o n s t r i c t i o n ) ( t h i r s t i s m o r e s
r e g u l a t e d b y o
a l d o s t e r o n e r e c e p t o r s i n
h y p o t h a l a m u
n e g f e e d b a c k
N +a r e a b s o r p t i o n
+
( a n d K e x c r e t i o n )
Renin - Angiotensin
System of Body Fluid
E C F v o l u m e
Balance and other
n e g f e e d b a c k
Body Fluid Regulation
Mechanisms
30/03/10
r e n i n 143
 Dehydration
• Dehydration: the loss of body water and associated electrolytes
• Causes:
• Gastroenteritis (viral / bacterial infection r vomiting & diarrhea) most common
• Diseases: yellow fever, cholera,
• Excessive alcohol consumption
• Most liquors have Congeners which are toxins….they must be removed
• The clearer & better quality your liquor (vodka & gin) the less congeners
• more distillation cycles r better quality
• This removal is done by the liver (liver glucose is broken down r lethargy)
• The excess fluid is flushed out by the kidneys (u water usage r dehydration)
• Prolonged exercise without fluid replacement (heat exhaustion & heat stroke risk)
• Diabetes: hyperglycemia r u glucose excretion r u water loss r dehydration
• Shock: blood loss due to some hypotensive state
• Gastrointestinal blood loss: bleeding from ulcers or colorectal cancer 144
30/03/10
 Dehydration
• Signs & Symptoms of dehydration:
• Dry mouth, dry swollen tongue, rapid heart rate (possible chest palpitations)
• Lethargy (sluggishness), confusion
• Poor skin turgor (a pinch of skin does not spring back into position)
• Good test for ailing elderly folks
• Elevated BUN (NH metabolized in liver & excreted by kidneys (renal function test)
4

• Elevated creatinine r d GFR (kidney clearance of waste products)

• Low blood viscosity
• Headache
• Fluid loss r low blood pressure r dizziness upon standing up
• A high urinary specific gravity (comparison of density to water: 1 gram / cm )
2

• Treating Dehydration
• Sip small amounts of water
• Drink carbohydrate / electrolyte solutions: Gatorade, Pedialyte.etc
30/03/10 145
0
 Cardiorespiratory Control
Skeletal Muscle Blood Flow – autoregulated – 2 mechanisms
• Mechanism 1: Metabolic by-product vasodilation
• Usually overrides neurohormone control
• Mediated by vasodilator metabolite (VDM) buildup & removal
• Adenosine (ATP by-product), CO , H , prostaglandins
2
+

• Exercise Example – negative feedback control

• Muscle exercises r VDM’s released r u vasodilation
• u blood flow r VDM’s removed r vasoconstriction

• Mechanism 2: Myogenic response

• Involves stretch activated Ca++ channels
30/03/10 • u blood flow r vessel stretch r channel activation 146
 Cardiorespiratory Control

Exercise Systemic Blood Flow: Autonomic influences

• Sympathetic outflow & circulating catecholamines
• α activation r vasoconstriction in non - exercising tissue
• Redistribution of blood flow during maximal exercise
- NC in brain blood flow - 500 ml/min u to heart
- 11,300 ml/min u to muscle - 400 ml/min u to skin
- 500 ml/min d to kidneys - 800 ml/min d to viscera
- 200 ml/min d to various other parts of the body

30/03/10 147
 Cardiorespiratory Control
Respiration: VE = Tidal Volume X Respiratory Rate

• Controlled via the medulla respiratory center

• Peripheral chemoreceptors – not a big influence
• u blood CO content r receptor activation r u V
2 E

• d blood O content r receptor activation r u V

2 E

• Central chemoreceptors – dominant influence

• u blood CO & lactate r receptor activation r u V
2 E

• P CO r u HCO + H r H activates receptor r u V

a 2 3
¯ + +
E

• Respiratory control during exercise – no consensus

• u venous return r mechanoreceptor activation r u V E

• proprioceptor activation r u V E

• intrapulmonary receptor activation r u VE

30/03/10 148
• Minute ventilation control during exercise
 Acute Responses to Aerobic Exercise
• Oxygen Consumption (VO2)
• u VO in direct proportion to u workload (power requirement of exercise)
2

• Expressed in both relative and absolute terms

• Relative: ml O /kg/min Absolute: ml/min or L/min
2

• average VO for 40 year old male 37 ml/kg/min

2max

• Oxygen consumption linked to caloric expenditure (1 liter of O 2 consumed = 5 kcal)

• Heart Rate
• u up to 3 times resting value at peak exercise (d time spent in diastole)
180
Heart 160
Rate
140
100 HR – VO2
1.0 2.0 3.0 relationship is
Oxygen Uptake (L / min) linear until about
50 150 250 90% VO2max
30/03/10 149
Workloads (Watts)
• Stroke Volume Acute Responses
• u up to 1.5 resting value at peak exercise
• increase levels off at 40% - 50% VO2 max to Aerobic
• u in venous return r u EDV (Starling mechanism) Exercise
• d ESV eluding to an u in myocardial contractility
• u ejection fraction rest: 58% max exercise: 83%
120
Stroke
Volume 110
(ml/beat) 70
25% 50% 75%
Percentage of VO2 max

•Cardiac Output (Q)

• u up to 4 times resting value at peak exercise (u is rapid at onset, then levels
off)
• u Q r u venous return
• Venous return mediated by and related to:
• sympathetic venoconstriction
• muscle pump
30/03/10
• u inspiration r d thoracic pressure
150
• Arteriovenous oxygen difference
• Difference in [O ] between arterial and mixed venous blood
2

• Illustrated by the oxyhemoglobin desaturation curve

• u approximately 3 fold from rest to max exercise
• at rest, about 25% of arterial O is extracted
2

• at peak exercise 85% of arterial O is extracted Acute Responses

2
to Aerobic
Exercise
• Blood Pressures and Resistance to Flow
• SBP: u - failure to u signifies heart failure
• DBP: slight u or slight d or NC
• MAP: slight u
• TPR: d - mainly due to vasodilation in exercising muscle

• Coronary (Myocardial) Blood Flow

• 4.5% of Q goes to myocardium at rest and at peak exercise
• this increase is due to u MAP and CA vasodilation

• Blood Flow to the Skin

• u as exercise duration u to allow for heat dissipation
30/03/10 151
• d at max exercise to meet exercising muscle demands
 Acute Responses to Aerobic Exercise

• Minute Ventilation
•resting average: 6 Liters/min
• peak exercise average: 175 Liters/min
• respiratory rate: resting 12-18 peak exercise: 45-60
• tidal volume: resting .5 liters peak exercise: 2.25 Liters
• Plasma Volume
•blood plasma u in the interstitum of exercising muscle
• fluid shift results in a 5% u in the hemoconcentration
• blood viscosity increases

30/03/10 152
 Oxygen
Oxygen Debt
DEBT and Deficit
& Oxygen DEFICIT

“Steady State” Oxygen Deficit Oxygen Debt

VO2 (EPEOC)

VO2 Untrained or people with

certain cardiorespiratory
diseases will have larger
DEBTS and DEFICITS
Rest

Onset EXERCISE TIME Termination

AT CONSTANT
WORKLOAD
Oxygen Deficit due to:
• delay in time for aerobic ATP production to supply energy
Oxygen Debt due to:
• resynthesis of high energy pohosphates (CP, ATP)
• replace oxygen stores
• lactate conversion to glucose (gluconeogenesis)
30/03/10
• u HR, respiration, catecholamines, body temperature 153
 OBLA Respiratory Compensation
P a O 2 (hyperventilation)
P A O 2

P A C & O 2 P a C O 2

No Change in
Ventilatory and VE
V E
Metabolic
VCO2
Changes
During V C 2 O
V O2 m
Exercise a x

V O2
-
H C 3 O
p H

Increasing
30/03/10 154
workload
• Resting Effects of
NC NC
VO2 = HR x SV x AVO2diff Exercise
Training on the
due to: due to:
u time in diastole u preload Components of
d afterload the Fick
u ventricle size
u blood volume Relationship

• Submax Workload (measured at same pre-training workload)

NC NC
VO2 = HR x SV x AVO2diff

note: a d in afterload (mentioned above)

accompanied by a d in HR response translates into
a d myocardial VO2 at rest or at any workload

• Max Workload (measured at peak exercise)

NC
VO2 = HR x SV x AVO2diff

30/03/10 some studies show 155

a slight decrease
• Mean Arterial Pressure Training Adaptations
• NC at rest or during exercise
• Systolic and Diastolic Blood Pressure
•usually NC at rest or during exercise
• possible d at submaximal workload
• may d at rest in borderline hypertensives
• some studies report a mean d of about 9 mmHg
• Totalu capillarization
Peripheral Resistance and Afterload
• (more parallel circuits) r d TPR
• d TPR r d Afterload (slight – not of major significance)
• Respiratory Variables
• Respiratory Rate
• Rest: NC
• Submax exercise: d
• Max exercise: slight u
• Tidal Volume
• Rest: NC
• Submax exercise: NC or slight u
• Max exercise: slight u
• Anaerobic Threshold
• Occurs at a higher percentage of VO max
2
30/03/10
• Pre-training: 50% VO max Post-training: 80% VO max
2 2
156
• Mitochondria Training Adaptations
• u number, size and membrane surface area
• Aerobic Enzymes in Exercising Muscle
• u Krebs cycle enzymes (succinate dehydrogenase)
• u β oxidation enzymes (carnitine acyltransferase)
• u electron transport enzymes (cytochrome oxydase)
• Fatty Acid & Glycogen Utilization
• u utilization of β oxidative pathways to produce ATP
• Called the “glycogen sparring” effect
• d RER for any given submaximal workload
• u muscle glycogen stores (with high carbohydrate diet)
• No Appreciable Change in Resting Metabolic Rate
Exception: training induced u in lean muscle mass

• d Platelet Aggregation
• u Fibrinolytic Activity
• d Circulating Catecholamines
• u vagal tone r d risk of arrhythmia
• Resistance to Pathological Events
• smaller infarct size and quicker recovery
• Less of a d in ventricular function during ischemia
30/03/10 157
 "Average" Values for Sedentary and
Trained Individuals
Heart Rate
( beats / minute )

200 185 185

150

100 75
60

50

0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 158
 "Average" Values for Sedentary and
Trained Individuals
Stroke Volume
( ml / beat )

160

150 120

100 80
60

50

0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 159
 "Average" Values for Sedentary and
Trained Individuals
Cardiac Output
( liters / minute)

40
35 30
30
22
25
20
15
10 5 5
5
0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 160
 "Average" Values for Sedentary and
Trained Individuals

A-V O2 Difference
( ml%)

20
16
14
15

10
6 6

0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 161
 "Average" Values for Sedentary and
Trained Individuals

Oxygen Consumption
( liters / minute)

6
4.5
5
4 3
3
2
1 0.25 0.25
0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 162
 "Average" Values for Sedentary and
Trained Individuals
Oxygen Consumption
( ml / kg / minute)

55
60
50
38
40
30
20
10 3.5 3.5

0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 163
 "Average" Values for Sedentary and
Trained Individuals
Systolic Blood Pressure
( mm Hg)

210 206
200
134 130
150

100

50

0
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 164
 "Average" Values for Sedentary and
Trained Individuals
Diastolic Blood Pressure
( mm Hg)

90
88
86 84
84 82 82
82 80
80
78
76
74
sedentary-rest sedentary-max trained-rest trained-max

30/03/10 165
 HEART ANATOMY (EXTERNAL VIEW)

• The heart is a complex

muscular pump that
maintains oxygen and
blood circulation through
the lungs and the rest of
the body.

• The heart pumps about

7200 liters/day.

30/03/10 166
 HEART ANATOMY (CROSSECTION VIEW)

 The heart has four

chambers.
 Two atria act as collecting
reservoirs.

 Two ventricles act as

pumps.

 The heart has four valves

for:
 Pumping action of the
heart.
 Maintaining
30/03/10 167

unidirectional blood flow.

 HEART (PHYSIOLOGY)

 Deoxygenated blood returns

to the heart via the superior
and inferior vena cava, enters
the right atrium, passes into
the right ventricle, and from
here it is ejected to the
pulmonary artery.

 Oxygenated blood returning

from the lungs enters the left
atrium via the pulmonary
veins, passes into the left
ventricle, and is then ejected
to the aorta.

30/03/10 168
 VASCULAR FLUID MECHANICS
 Velocity and
pressure are
inversely related to
the cross sectional
area of blood
vessels.

 These parameters
drop in the
capillaries where
the cross-sectional
30/03/10
area is more. 169
 JUST BEFORE I LEAVE……

One of the Keys to

Happiness is having a
good health and a bad memory…

30/03/10 170
 •Is a muscle about the size of your fist
•Weighs approximately one pound
•Is located behind and slightly to the left of the breastbone
•Pumps about 5 quarts (4.7 liters) of blood every minute

30/03/10 171
30/03/10 172
The function of the heart is to circulate blood
throughout the body by:

•Pumping blood through the lungs removes carbon dioxide

and refreshes the blood with oxygen
•The oxygenated blood is pumped to the body to provide
oxygen and nutrients and to remove waste products.
•The coronary arteries are the blood vessels that supply blood
and oxygen to the heart muscle.

30/03/10 173
 Blood Supply To The Heart

2 coronary arteries branch

from the main aorta just
above the aortic valve. “No
larger than drinking straws,
they divide and encircle the
heart to cover its surface
with a lacy network that
reminded physicians of a
slightly crooked crown
(coronary comes from the
Latin coronarius, belonging
to a crown or wreath). They
carry out about 130 gallons
of blood through the heart
muscle daily.” (Clark, 119)
30/03/10 174
 Coronary Artery Disease
• Coronary artery disease 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”.

30/03/10 175
30/03/10 176
30/03/10 177
 Signs and Symptoms
• None: This is referred to as silent
ischemia. Blood to your heart may be
restricted due to CAD, but you don’t
feel any effects.
Chest
None Pain • Chest pain: If your coronary arteries
can’t supply enough blood to meet the
oxygen demands of your heart, the
result may be chest pain called angina.
• Shortness of breath: Some people may
not be aware they have CAD until they
Signs & develop symptoms of congestive heart
Symptoms failure- extreme fatigue with exertion,
shortness of breath and swelling in
their feet and ankles.
• Heart attack: Results when an artery to
your heart muscle becomes completely
blocked and the party of your heart
Shortness Heart muscles fed by that artery dies.
Of Breath Attack

30/03/10 178
 can, and
does, occur in almost any artery in the
body. But in the heart it’s effects can be
crucial. “The body depends on a strong
pumping heart to circulate life-giving
blood, and this includes to the heart
muscle itself. If the coronary arteries
become blocked, the cardiac muscle
begins to fail, and so the blood circulation
decreases, which includes the circulation
to the heart muscle itself.” (Thibodeau,
494)
30/03/10 179
30/03/10 180
 • High blood cholesterol
• High blood pressure
• Smoking
• Obesity
• Lack of physical activity

30/03/10 181
 Risk Factors
Uncontrollable
Uncontrollable
Controllable

•Sex •High blood

pressure
•Hereditary
•High blood
•Race cholesterol
•Age •Smoking
•Physical activity
•Obesity
•Diabetes
•Stress and anger
30/03/10 182
 Screening and Diagnosis

me me shows
as asu
ur res
es

c
i fi
od

ec

coronaries
sp
ele ctrical

Electro- blo Stress Coronary

cardiogram Test Angiography

ar t

Sit
he

es
es su

of
to
l s pp
pu ly
Narrowi
ng in
im

30/03/10 183
 •Blood tests: used to evaluate kidney and
thyroid function as well as to check
cholesterol levels and the presence of
anemia.
•Chest X-ray: shows the size of your heart
and whether there is fluid build up around the
heart and lungs.
•Echocardiogram: shows a graphic outline of
the heart’s movement
•Ejection fraction (EF): determines how well
your heart pumps with each beat.
30/03/10 184
• Many people are able to manage coronary
artery disease with lifestyle changes and
medications.

• Other people with severe coronary artery

disease may need angioplasty or surgery.

30/03/10 185
30/03/10 186
 Arterial Blood Pressure
It is the lateral pressure exerted by
blood on the walls of aorta and
arteries.
• Ejection of blood into the aorta by the left ventricle
results in a characteristic aortic pressure pulse.
• The peak of the aortic pressure pulse is termed the
systolic pressure (Psystolic).
• The lowest pressure in the aorta is termed the
diastolic pressure (Pdiastolic).
• The difference between the systolic and diastolic
pressures is the aortic pulse pressure.
• The mean aortic pressure (MAP) is the average
pressure (geometric mean) during the aortic pulse
cycle
30/03/10 187
As the aortic pressure pulse travels down the
aorta and into distributing arteries, there are
characteristic changes in the systolic and
diastolic pressures, as well as in the mean
pressure.
As the pressure pulse moves away from the
heart, the systolic pressure rises and the
diastolic pressure fall.
There is also a small decline in mean arterial
pressure as the pressure pulse travels down
distributing arteries due to the resistance of the
arteries.
30/03/10 188
• Therefore, when arterial pressure is
measured using a sphygmomanometer
(i.e., blood pressure cuff) on the upper
arm, the pressure measurements
represent the pressure within the brachial
artery, which will be slightly different than
the pressure measured in the aorta or the
pressure measure in other distributing
arteries.

30/03/10 189
 Measurements of Blood Pressure
1- Direct Method
• The most accurate means for measuring blood
pressure is directly within an artery (intra-arterial)
using a catheter.
• But because this method is invasive, it is neither
practical nor appropriate for repeated measurements
in non-hospital settings, or for large-scale public
health screenings.
2- The mercury-filled sphygmomanometer
• The usual method of measurement, therefore, is a
noninvasive means that uses a sphygmomanometer,
which includes either a column of mercury or
pressure-registering gauge.
30/03/10 190
 Physiological factors affecting Arterial Blood pressure
Age:
• New born: 80/40 mmHg
• 4 years: 100/65 mmHg.
• Adults: 120/80 mmHg
• After that: Gradually increase due to increase elasticity of arteries.
Sex:
• Children: have equal Blood pressure.
• Adults before 45 years: male more than female.
• Adults after 45 years: the diastolic B.P. is more in female than males.
Race: ABP in oriental is less than in European and American.
Gravity: B.P. in upper parts of the body is more than the lower parts
especially during standing.
Meals: Digestion increases the arterial blood pressure.
Emotions and exercise: increase the arterial blood pressure.
Sleep: Deep quiet sleep decrease A.B.P., while sleep with dreams
increase
30/03/10 A.B.P. 191
 Factors that Affect Blood
Pressure
• Blood pressure is affected by several factors:
• 1- Cardiac output.
• 2- Peripheral resistance
• 3- Vessel elasticity
• 4- Blood volume

30/03/10 192
 1- Cardiac Output
It is the amount of blood pumped by the left
ventricle per minute.
It keeps the arteries full of blood.
An increase in cardiac output results in increased
blood pressure.
Anything that decreases cardiac output also
decreases blood pressure, because there is less
pressure on the vessel walls.
Cardiac Output = Heart Rate X Stroke Volume
Anything that affects heart rate or stroke volume
affects cardiac output and thus blood pressure.
30/03/10 193
 Regulation of Cardiac Output
• The cardiac output is regulated by two
forces:

• Intrinsic (Frank-starling
mechanism).
• Extrinsic (autonomic
nervous system).
30/03/10 194
 Intrinsic control
• Increased end-diastolic volume = increased
strength of cardiac contraction and increased
stroke volume
• This increase in strength of contraction due to
an increase in end-diastolic volume (the volume
of blood in the heart just before the ventricles
begin to contract) is called the Frank-Starling
law of the heart:
• Increased end-diastolic volume
= increased stretching of cardiac muscle
= increased strength of contraction
=30/03/10
increased stroke volume 195
30/03/10 196
 Extrinsic control
• Increased sympathetic stimulation,
increased strength of contraction of
cardiac muscle
Mechanism
• sympathetic stimulation cause release
of norepinephrine which increase
permeability of muscle cell membranes
to calcium and calcium diffuses through
more cross-bridges and causes stronge
contraction
30/03/10 197
 Extrinsic control

30/03/10 198
 2- Peripheral Resistance
One of the main factors that affect blood
pressure is peripheral resistance.
• Blood cells and plasma encounter resistance
when they contact blood vessel walls.
• If resistance increases, then more pressure is
needed to keep blood moving.
Three main sources of peripheral resistance:
• a. Blood vessel diameter
• b. Blood viscosity
• c. Total vessel length
30/03/10 199
 a- Vessel Diameter
• Vessel diameter affects peripheral
resistance.
• As a diameter of a tube gets smaller, a
greater proportion of the fluid is in
contact with the wall of the tube.
Therefore resistance to flow is increased
and pressure rises.
• Larger diameter, same volume, less
pressure.
Smaller diameter, same volume, more
pressure.
30/03/10 200
Vasomotor Fibers
• Constriction of blood vessels raises blood pressure.
• Vessel diameter is actively regulated by vasomotor
fibers, sympathetic nerve fibers that innervate the
vessel's smooth muscle layer.
• Vasomotor fibers release norepinephrine, a
powerful vasoconstrictor.
• A vasoconstrictor is a substance that causes blood
vessels to constrict.
Vasoconstrictors
• Blood vessel diameter is also regulated by blood-
borne vasoconstrictors.
• (Epinephrine, Angiotensin II, Vasopressin)

30/03/10 201
 b- Viscosity of blood
Blood viscosity affects peripheral resistance.
• Viscosity is related to the thickness of a fluid.
The greater the viscosity, the less easily molecules slide
past one another and the more difficult it is to get the fluid
moving and keep it moving.
• Because of this greater resistance to flow, a greater
pressure is required to pump the same volume of viscous
fluid.
• The hematocrit is the percentage of red blood cells in the
total blood volume.
• The hematocrit affects blood viscosity and therefore
resistance to flow.
• The more viscous the blood, the greater resistance it
encounters and the higher the blood pressure.
• The hematocrit can increase when there are more red
blood cells or less plasma in the blood.
• The hematocrit can decrease when there are fewer red
blood cells or more plasma.
30/03/10 202
 c- Vessel Length
• Total vessel length affects peripheral
resistance.
• Increased fatty tissue requires more
blood vessels to service it and adds to
the total vessel length in the body.
• The longer the total vessel length, the
greater the resistance encountered,
and the greater the blood pressure.
30/03/10 203
 3 - Vessel Elasticity
• Besides peripheral resistance, blood vessel
elasticity also affects blood pressure.
• A healthy elastic artery expands, absorbing the
shock of systolic pressure.
• The elastic recoil of the vessel then maintains
the continued flow of blood during diastole.
• When an individual has arteriosclerosis,
arteries become calcified and rigid, so they
can't expand when the pulse wave of systolic
pressure passes through them
30/03/10 204
 4 - Blood Volume
Blood volume affects blood pressure.
• When there is a greater volume of fluid, more fluid
presses against the walls of the arteries resulting in
a greater pressure.
• When there is less volume there is less pressure.
• Reduced blood volume (for example due to excessive
sweating) reduces blood pressure short term. Long
term homeostatic mechanisms compensate, bringing
blood volume and blood pressure back up to
normal levels.
• Increased blood volume (for example due to water
retention from excessive salt intake) increases blood
pressure short term. Long term homeostatic
mechanisms compensate, bringing blood volume and
blood pressure back up to normal levels.

30/03/10 205
 Regulation of arterial blood pressure
Blood pressure is maintained
at a constant level within a
narrow limit to ensure an
adequate flow of blood to
the tissue especially the
vital organs e.g. heart, brain
and kidney.
30/03/10 206
 Regulation of arterial blood pressure 2
• Blood pressure=cardiac output X peripheral resistance

Thus the regulation of arterial blood

pressure depend upon the previous
two factors through two
mechanisms:-
1- Nervous
2- hormonal

30/03/10 207
 Regulatory mechanisms
• 1- immediately acting mechanisms.

• 2- intermediately acting mechanisms.

• 3- Long term acting mechanisms.

30/03/10 208
 immediately acting mechanisms
• Starts: within a seconds.
• Lasts: hours.
• Type: Nervous.
• Mechanism:
– Stimulation of baroreceptors in the aortic arch
or carotid sinus by changes of blood pressure
between 60mmHg and 200mmHg blood
pressur.
– Stimulation of chemoreceptors in the aortic
body or carotid body by changes of blood
pressure between 40mmHg and 60mmHg
blood pressure.
30/03/10 209
 1- immediately acting mechanisms

30/03/10 210
 Control of blood pressure

30/03/10 211
 2- intermediately acting mechanisms.
• Starts: within half of hour.
• Lasts: hours to 3-4 days.
• Type:
• Mechanism:
– Fluid shift mechanism.
– Stress relaxation mechanism.

30/03/10 212
 3- Long term acting mechanisms
• Starts: within half an hour.
• Lasts: days, months, or even years.
• Type: hormonal.
• Mechanisms:
– 1- Renin mechanism.
– 2- Aldosterone mechanism.
– 3- Antidiuretic hormone mechanism.

30/03/10 213
30/03/10 214
 SHORT-TERM CONTROL OF ARTERIAL BLOOD PRESSURE
THE SENSORY ARM
sinus nerve
Arterial blood pressure is controlled by a to CN IX
Int
negative feedback process carotid
Ext
Carotid sinus and aortic arch baroreceptors carotid
respond to changes of blood pressure. vagus
Carotid nerve
sinus baro- CN X
receptor
100
Integrated nerve activity

sinus
% maximum

nerve vagus
nerve Aortic arch
baroreceptor

Afferent nerve firing reflects both

the rate of change of blood
0
pressure during the pulse and the
30/03/1060 110 200 215
arterial pressure, mm Hg mean level
 SHORT-TERM CONTROL OF ARTERIAL BLOOD PRESSURE
THE EFFERENT ARM
Medullary cardiovascular
centres regulate the
efferent Receptor Medullary
arm via the autonomic afferents cardiovascular
nervous system. centres
When activated:
Sympathetic fibres innervate sympathetic parasympathetic
• arterioles - vasoconstriction
• the s.a. node - tachycardia
• myocardium - positive inotropy

Parasympathetic (vagal) fibres

innervate
• the s.a. node - bradycardia

Vagal tone to the s.a node predominates

30/03/10 216
 THE BARORECEPTOR REFLEX - AN EXAMPLE
CORRECTION OF POSTURAL HYPOTENSION

On standing up venous return falls Effect of gravity on

Cardiac output diminishes
Arterial blood pressure is reduced
Baroreceptor afferent firing reduced
venous return
Preload diminished
- Starling’s Law
Subject possibly feels faint
as cerebral flow is reduced
Due to reduced arterial B.P.

Medullary centres inhibition reduced

Increased sympathetic tone to Vasoconstriction Tend to

arterioles restore
Reduced vagal tone to s.a. Tachycardia arterial
node blood
Increased
30/03/10
myocardial sympathetic tone Raised stroke work 217
pressure
 IMBALANCE OF FORCES AT A CAPILLARY - OEDEMA
Osmotic imbalance

Reduction of Π c - Π i reduces absorption and increases net water

loss from the plasma
mmHg
35 Area 1 > Area 2

25
1 Πc-Πi

2
15

arteriolar venular Pc - Pi

This may be due to:

reduction of plasma protein (Π c) - e.g. reduced albumin production; raised urinary
loss30/03/10 218
 IMBALANCE OF FORCES AT A CAPILLARY - OEDEMA
Hydraulic imbalance
Increase of Pc - Pi increases filtration and thereby net water loss from the plasma

mmHg
35 Area 1 > Area 2

25
1
Πc-Πi
2
15

arteriolar venular Pc - Pi

This is generally due to an increase of Pc.Note that the venular end rises more than the
arteriolar end as postcapillary resistance is less than precapillary resistance
Factors that raise venous pressures will therefore increase Pc - e.g. congestive heart
30/03/10 219
failure, venous compression
THE BALANCE OF FORCES AT A PULMONARY CAPILLARY
In a pulmonary capilllary hydraulic pressures are much less

mmHg The smaller value of Pc is

35
due to the reduced pressure
generated by the right
Πc-Πi ventricle.
25
Pc - Pi < Π c - Π i along the
entire capillary. Thus there
Absorption
is no filtration of fluid.
15
This ensures that the
Pc - Pi extravascular space is
5 arteriolar venular relatively fluid free
minimising the diffusion
distance between alveolus
and capillary.
30/03/10 220
 Shock
• Shock is an abnormal
reduction in cardiac output
to the point that not enough
blood is being circulated to
supply all of the cells in the
body with adequate oxygen
and nutrients.
30/03/10 221
• Shock is a severe
condition that occurs
when not enough blood
flows through the body,
causing very low blood
pressure, a lack of urine,
and finally cell and tissue
damage.
30/03/10 222
 Types of shock

1- Cardiogenic.
2- Hypovolemic.
3- Distributive.
4- Obstructive.
30/03/10 223
 1- Cardiogenic Shock
This type of shock is caused by sever
depression of myocardial contractility.
• Cause:
Myocardial infarct (MI; a “heart attack”).
A myocardial infarct is an area of dead
cardiac muscle fibers that were killed
when their blood supply was interrupted,
usually because the artery supplying them
with blood became occluded (plugged).
30/03/10 224
If more than about 40% of the left
ventricle’s muscle fibers stop
functioning, the remaining cardiac
muscle fibers are unable to eject enough
blood from the left ventricle to keep
cardiac output within homeostatic limits,
and the person will usually go into
cardiogenic shock.
• About 5 – 10% of all MI victims go into
cardiogenic shock, which has a mortality
rate of 80 – 90%.
30/03/10 225
Manifestations of the cardiogenic shock
1- dyspnea,
2- cheyne-stock respiration.
3- edema.
4- confusion.
5- lack of concentration.
6- rapid week pulse.
7- low blood pressure.
8- pale cold skin.
9- sweating,
30/03/10 226
 2- Hypovolemic Shock
Hypovolemic shock develops when the
volume of blood in the circulatory
system falls below normal limits.
If the volume of blood in the
cardiovascular system is reduced,
there will be less blood for the heart to
pump and, all else being equal, less
blood for the heart to pump will result in
less blood being pumped
( = reduced cardiac output).
30/03/10 227
If the reduction in blood volume is
great enough, cardiac output may
be reduced enough to put a
person into shock.
A loss of 10 – 15 % of one’s total
blood volume is sufficient to
induce at least a mild state of
hypovolemic shock in most
persons.
30/03/10 228
 Examples of hypovolemic shock:
• a- Hemorrhagic Shock
• b- Burn shock
• C- Internal bleeding
• D- Dehydration
30/03/10 229
 Hemorrhagic Shock
• Hemorrhage – loss of blood – is probably the
most obvious cause of hypovolemic shock.
• A serious wound, especially one that severs a
large artery, can result in loss of sufficient
blood to put a person into shock.
• The degree, or depth, of hypovolemic shock is
directly related to the amount of blood loss, as
are the symptoms and the hazards of
remaining in a state of shock for a period of
time.
30/03/10 230
 b- Burn shock
• It is a hypovolemic shock
which follows extensive
burns.
• It is due to loss of plasma
from the burned skin.
30/03/10 231
 C- Internal bleeding
Loss of blood from the body.
Loss of blood from the cardiovascular
system can occur internally, as well as
externally.
For example, hypovolemic shock is a
serious risk following blunt force
trauma to the chest or abdomen
This is because the force of the blow can
rupture the aorta, spleen, or liver.
30/03/10 232
 D- Dehydration 1
A reduction in blood volume sufficient to cause
shock can occur in other ways that don't
involve hemorrhage For example,
dehydration resulting from any number of
causes can reduce the blood volume enough
to induce hypovolemic shock.
Vomiting and/or diarrhea, particularly in
infants, can quickly result in dangerous
degrees of dehydration.

30/03/10 233
 D- Dehydration 2
This is why cholera is such a deadly disease. The
cholera bacterium, to facilitate its spread to
other hosts, produces a toxin that does nothing
more than make the capillaries of the intestinal
tract lining highly permeable to water.
This results in massive efflux of water from the
blood into the lumen of the intestine which, in
turn, induces severe diarrhea.
The resulting water losses are so rapid that it's
very difficult to replace them quickly enough to
prevent death due to dehydration.

30/03/10 234
 Signs and Symptoms Hemorrhagic Shock

1- Palpitations.
2- dizziness.
3- tachycardia.
4- Cold clammy skin.
5- Sweating.
6- oliguria.
7- breathing difficulty.
8- Anuria ( = no urine production)
Deficient blood supply to brain and heart
Brain and heart damage leading to death.
30/03/10 235
 3- Distributive Shock
• As the term “distributive” implies, this form of
shock develops when the cardiac output
(which is usually normal in this case) is not
being distributed properly to the organs that
need it.
• There are a variety of causes of distributive
shock, but they all have one thing in
common:
- a massive dilation of the blood vessels –
especially the veins – throughout the body,
with the result that blood tends to pool in the
vessels an not reach the capillaries rapidly
enough.
30/03/10 236
• In addition, certain causes of distributive
shock also trigger mechanisms that make
the capillaries very leaky to plasma (the
liquid fraction of the blood).
• This results in a significant fraction of the
plasma leaking out into the extracellular
spaces ( = edema), where it’s no longer
available for circulation by the heart. The
resulting hypovolemia makes the situation
even worse.

30/03/10 237
 Causes of Distributive shock
a- Septic Shock
• The most common form of distributive shock is
septic shock, which results directly from some
sort of infection, usually bacterial (sepsis means “a
toxic condition resulting from infection”). In some
cases, the body responds to sepsis with a massive
reaction that is essentially allergic in nature. Cells
throughout the body release a variety of
compounds that trigger the general vasodilatation
and plasma loss that produce the shock state.
•

30/03/10 238
b- Anaphylactic Shock
• Anaphylactic shock is similar to septic shock
in that it also involves the generalized
vasodilatation and increased capillary
permeability that severely reduces blood
supply to the tissues, but the cause is not
a bacterial infection.
• The most common causes of anaphylaxis
and the resulting shock are foods (especially
peanuts), drugs (especially penicillin and
aspirin), insect stings (especially bees,
wasps, and ants), blood transfusions, and
even exercise.
30/03/10 239
c- Neurogenic Shock
• This form of shock involves the nervous system.
• The basic cause of neurogenic shock is
generally a massive inhibition of both the
Excitatory and Inhibitory portions of the Vasomotor
Center. Now,
• Well, the problem is that inhibition of the Excitatory
Portion of the
• Vasomotor Center also results in vasodilatation
throughout the body, due to inactivation
of the tonic vasoconstrictor neurons that are
normally being stimulated by the Excitatory
Vasomotor Center
30/03/10 240
• This vasodilatation, coupled with the
decreased cardiac output, typically results
in a drastic reduction in blood flow to the
brain, a reduction sufficient to lead to
damage within a relatively short time.
• The two principal causes of neurogenic
shock are trauma to the medulla (say,
from a head injury), spinal cord injuries,
and general anesthetics.

30/03/10 241
 4- Obstructive Shock
• This is an unusual form of shock that results
when pressure on the heart prevents it from
filling or pumping effectively.
• The most common causes of obstructive
shock are pneumothorax (air in the chest
cavity) or cardiac tamponade (compression
of the heart by fluid or blood in the pericardial
space)

30/03/10 242
30/03/10 243
30/03/10 244