Cvs introduction ms 2020

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MAGDI AWAD SASI
CVS PHYSIOLOGY
2nd year medicine
MAGDI AWAD SASI 2020

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Learning Objectives
 List the properties of cardiac muscle
 List the possible pacemakers tissues of the cardiac muscle.
 Define the rhythamicity and account for its myogenic origin.
 Illustrate the pacemaker potential.
 Discuss the ionic basis of pacemaker potential .
 Discuss the factors affecting rhythamicity
 Describe the autonomic supply of the heart & its function

Circulation Reviewed
 Heart – "four chambered"
– Right atrium & ventricle
– Pulmonary circuit
– Left atrium & ventricle
– Systemic circuit
 Blood Vessels – "closed circulation"
– Arteries –from heart
– Capillaries– cell exchange
– Veins – to heart
3MAGDI AWAD SASI 2020

Heart Chambers
 Atrium (R & L):
receive blood
(entryway)
 Ventricle (R &
L): pump blood
out
 Septum: wall
between atria &
ventricles
 Valves: prevent
backflow of blood
Right Side
Left Side

Double Circulation Loop
 Pulmonary circuit:
blood to/from
lungs
 Systemic circuit:
blood to/from all
body tissues
5

The Anatomy of the Heart
 The Heart Wall and Cardiac Muscle Tissue
Figure 12-4(c)6

The Anatomy of the Heart
 Cardiac Muscle Cells
– Shorter than skeletal muscle fibers
– Have single nucleus
– Have striations (sarcomere organization)
– Depend on aerobic metabolism
– Connected by intercalated discs
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings 7MAGDI AWAD SASI 2020

Cardiac Muscle
 Branching cells
 One/two nuclei per cell
 Striated
 Involuntary
 Medium speed contractions

PHYSIOLOGIC
CHARACTERISTICS OF THE
CONDUCTION CELLS
 AUTOMATICITY
 EXCITABILITY
 CONDUCTIVITY
 RHYTHMICITY
 CONTRACTILITY
 TONICITY

 Automaticm: ability to initiate an electrical impulse
 Conductiblity: ability to transmit an electrical impulse
from one cell to another
 Excitability: ability to respond to an electrical impulse
 Refractoriness: cardiac muscle can not be exited during
the whole period of systole and early part of diastole. This
period prevents waves summation and tetanus
 Contractility: Contractility is the ability of the cardiac
muscle to contract. In this way flowing of blood is provided.
Functional properties of the heart

Functional properties of the heart
• F
Excitability
Automatism
Conductibility
Refractoriness
Contractility

N.B.
-conductivity is measured by P-R interval in the ECG
and
a-c interval in jugular venous pulse wave.

CARDIAC MUSCLE
 ATRIAL MUSCLE
 VENTRICULAR MUSCLE
 SPECIALISES EXCITATORY
&CONDUCTIVE MUSCLE FIBERS

Define the rhythamicity and account for its myogenic
origin.
 Autorhythmic Cells
– __non-contractile_________
– Initiate and conduct action potentials
responsible for contraction.
– Located in the SA node, AV node, Bundle of
His, Purkinje fibers.
 Contractile Cells
– 99% of the cardiac muscle cells

Electrical Activity of Heart
 Heart beats rhythmically as result of action
potentials it generates by itself Two specialized
types of cardiac muscle cells
A. Contractile cells
• 99% of cardiac muscle cells
• Do mechanical work of pumping
• Normally do not initiate own action potentials
B. Autorhythmic cells
• Do not contract
• Specialized for initiating and conducting action potentials
responsible for contraction of working cells
C. CONDUCTIVE TISSUE

Sherwood’s Human Physiology 9-11 (9-8 6th Edition)
Specialized Conduction System
► Sinoatrial (SA)
node.
► _Pacemaker___
_
► Cells exhibit
autorhythmicity.

1 - Sinoatrial node (SA node)
2 - Atrioventricular node (AV node)
3 – Bundle of His
4 - Right & Left Bundle Branches
which lead to Purkinje Fibers

Electrical Signals from “Pacemaker” Cells
Drive the Heart’s Contractions
 Cardiac conduction system:MYOGENIC
independent of the nervous system
– Sinoatrial (SA) node: cardiac pacemaker
– Atrioventricular (AV) node:

Rhythmicity (automaticity):
It is the ability of cardiac muscle to contract in a
regular constant manner w/out nerve supply.
♥ It’s myogenic in origin (i.e. not neurogenic).
♥ Its initiated by the ‘pacemaker’ of the ht, the
SA- node.

The pacemaker of the heart:
= the SA- node.
♥ Contains the P- cells, which are probably the
actual pacemaker cells.
♥ Has the fastest rhythm (rate of discharge) of all
parts of the heart, 90 impulses/min.
its fibers have an unstable RMP.
♥ Has spontaneous (w/out stimulation)
depolarization, up to firing level.
?

The pacemaker potential
♥ The pacemaker cells are characterized by
having an unstable membrane potential.
♥ Its RMP is ( -60 mV).
♥ This is the basis for automaticity

Na+
K+Na+
K+
-60 mV
RESTING
THRESHOLD
-0
Gradually
increasing PNa
AUTOMATICITY

Pacemaker Pre-potential:
♥ Due to gradual state of depolarization:
■ Steady  in K+ permeability
( K+ efflux), leading to
 intracellular negativity.
■ Causing spontaneous leakage
of membrane to Na+ w/out
stimulation.
 (-60 mV to -55 mV).
■ Which causes op of voltage
gated transient Ca2+ channels,
leading to some Ca2+ influx.
 (-40 mV).
?
-6

AUTORHYTHMICITY( PACE MAKER
POTENTIAL)

Pacemaker Action potential (AP)
♥ Pacemaker Depolarization:
– Opening of long lasting (fast) Ca2+ channels.
• More Ca2+ influx  till reaching the potential, i.e. firing
level point  leading to depolarization.
– Opening of VG Na+ channels ? also contribute to
the upshoot phase of the AP.
-6

♥ Pacemaker Repolarization:
– Opening of VG K+ channels.
• K+ diffuses outward (efflux), … (so +vity will go out of cell).
♥ Pacemaker Hyperpolarization:
■ excessive K+ effllux,
(This will lead to hardship of K+ efflux in 2nd depolarization).
 Ectopic pacemaker:
– Pacemaker other than SA node:
• If APs from SA node are prevented from reaching these
areas, these cells will generate pacemaker potentials.
-6

Automaticity
Hiss bungle – 30-40 /min
SA-node – 60-90 /min
AV – node – 40-60 /min
Purkinje fibers - <20 /min

Components of the Conduction System
 Sinoatrial Node (Part I):
– The pacemaker
– Self -excitatory.
– Basic rhythm of the heartbeat.
– Crescent shaped and is about15 X5 mm .
– Right atrium near the entrance of vena cava.
– Impulses 70-80 / minute without any nerve
stimulation from brain.

SA NODE PACEMAKER BECAUSE
1) Highest frequency of discharge
 Other cells with low frequency of
discharge called latent or potential
pacemakers.
 Abnormal or ectopic pacemakers
Become pacemaker when:
Develop rhythmical discharge rate that
is more rapid than SA node
 Develop excessive excitability
 Blockage of transmission of the
impulses from the SA node to other
parts of the heart
2) Of overdrive suppression:
The greater rhythmicity of the SA
node forces the other automatic
cells to fire off at a faster rate
than their natural discharge rate.
This causes depression of their
rhythmicity.
SA node rhythmical discharge
rate = 70-80/min
AV node = 40-60/min
P fibers = 15-40/min

 Even more distally the bundles ramify into
Purkinje fibers (named after Jan Evangelista
Purkinje (Czech; 1787-1869)) that diverge to
the inner sides of the ventricular walls.
 Propagation along the conduction system
takes place at a relatively high speed once it is
within the ventricular region, but prior to this
(through the AV node) the velocity is
extremely slow.

Chronotropism
Chronotropism means an influence on
the heart rate.
A +ve chronotropic factor (or effect) is
one that increases the heart rate.
A –ve chronotropic factor (or effect) is one
that decreases the heart rate.

1. Chemical factors
Adrenaline and noradrenaline are
released into the blood under
conditions of stress.
Both substances have a +ve
chronotropic effect.

2. Physical factors
Arise in body temperature by 1 °C increases
the heat rate by 20 beats/minute.
The rise in body temperature increase the
heart rate by increasing the permeability of
the membrane to Ca++ during the pacemaker
potential and increasing the speed of ionic
fluxes across the membrane during the
action potential.
The only physiological condition that rises
body temperature above the normal resting
range is muscular exercise.

3. Conductivity
Impulses can spread easily between
cardiac muscle fibers.
Yet, conduction in the heart is normally
carried out by the specialized conducting
system to ensure the spread of the
excitation wave from the S-A node to all
over the heart in certain pattern.

What are the Factors affecting rhythmicity?
1. Nervous factors :
A. Vagal stimulation
increase K+ efflux. Decrease Ca++ influx
B. Sympathetic stimulation
decrease K+ efflux.increase Ca++ influx
2. Effect of temperature
A- moderate warming ->increase HR
B- Excessive warming and cooling
decrease HR

MAGDI AWAD SASI 2020 39
 3. Effect of drugs:
I-Digitalis—decrease HR act like Ach.
II-Hormones as thyroxin and catecholamines
increase HR
III-Cholinergic drugs  decrease HR.
 4. Effect of pH :
 Alkalosis → increase HR
 Acidosis → decrease HR
 (Alkalaemia or acidaemia) producing cardiac
arrhythmias
 5. Blood gases :
Sever O2 lack or CO2 excess → decrease HR
.

Why digitalis used in the treatment
of heart failure?
Because Digitalis— increase contractility.
 But it
1. Decrease HR
2. Decrease conductivity.
3. Increase excitability in high doses
extra systole

6. Effect of
extracellular ions
• Na+:-
Excess Na+ ions depress
the cardiac activity
(membrane
hyperpolarization)
•-Low Na+ ions, slow the
diastolic depolarization of
SA node and
•reduces rhythmicity.
-60
-70
Excess K+ or
•Decrease K+ → increase
•the slope of the prepotentials →
increase rhythmicity.
K+

•Excess Ca++ strengthen the myocardial contractility,
•favoring systole  leads to stoppage of the heart in systole
•Ca++ rigor).
-Low Ca++ → increase rhythmicity
Ca++:-

 7- Ischaemia ( decrease blood flow to
the heart), and bacterial toxins depress
automaticity.

Scheme of the conduction system of
the heart
1 – sine-atrial node ;
2 - atrial bundle of Bachmann ;
3 - interstitial conducting paths (
Bachmann’, Venkebah’, Torel’ );
4 atrioventricular node ;
5 – Hiss bundle;
6 - right bundle of Hiss bundle;
7 - anterior branch of the left
bundle of Hiss bundle;
8 - posterior branch of the left
bundle Hiss bundle;
9 - bundle of Kent ;
10 - James’ bundle ;
11 - Maheym’ bundle. 44MAGDI AWAD SASI 2020

CONDUCTIVITY
spread of excitation
 Excitation – originates from the SA node
 Conduction velocity in atrial muscle = 0.3 to 0.5 m/sec
 Conduction is faster in the interatrial
 bundles (presence of specialized conduction fibers)
 0.03 m/sec internodal pathway to AV node
 0.09 m/sec AV node itself
 0.04 m/sec penetrating AV bundle
 Total delay in the AV nodal and AV bundle system = 0.13 m/sec +
0.03 m/sec from SA to AV node = 0.16 m/sec

Atrio-ventricular Node
– Located in the bottom of the right atrium near
the septum.
– Cells in the AV node conduct impulses more
slowly, so there is a delay as impulses travel
through the node.
– this allows time for atria to finish contraction
before ventricles begin contracting.

Cause of slow conduction in the transitional,
nodal, and penetrating AV bundle fibers:
 1) Their sizes are considerably smaller than
the sizes of the normal atrial muscle fibers.
 2) All these fibers have RMP that are much
less negative than the normal RMP of other
cardiac muscle.
 3) Few gap junctions connect the successive
muscle cells in the pathway.

Important functional
characteristics of the A-V node
The A-V node is characterized by:
Very slow conductivity----This delay allows the atria to
finish with their systole before passing the impulse to
the ventricles to start ventricular systole.
Long absolute refractory period after conducting an
impulse:
This limits the number of impulses that can be
transmitted from the atria to the ventricles to 230
impulse/min. This protects the ventricles from
receiving high frequency of impulses from the atria.

Atrioventricular Bundle
 A.K.A. “Bundle of His”
– From the AV node,
impulses travel
through to the right
and left bundle
branches
– These branches extend
to the right and left
sides of the septum
and bottom of the
heart.

The one-way conduction in the A-V
bundle
The A-V bundle conducts impulses
only in one direction, i.e. from the A-
V node to the bundle branches.
This prevents the reentry of impulses
from the ventricles into the atria.

• Propagation from the AV node to the ventricles is
provided by a specialized conduction system.
Proximally, this system is composed of a common
bundle, called the bundle of His (after German
physician Wilhelm His, Jr., 1863-1934).
• More distally, it separates into two bundle
branches propagating along each side of the
septum, constituting the right and left bundle
branches. (The left bundle subsequently divides
into an anterior and posterior branch.) .

Atrioventricular Bundle
Continued….
– These branch a lot to
form the Purkinje
fibers that transmit the
impulses to the
myocardium (muscle
tissue)
– The bundle of His,
bundle branches and
Purkinje fibers transmit
quickly and cause both
ventricles to contract
at the same time
– Like a “phone tree”

Excitation reaches the Bundle of His
 Velocity of conduction =3-4 m/sec
 Increased magnitude of the AP;
 increased velocity of phase 0 depolarization;
 increased duration of the AP
 Excitation transmitted to the RBB and LBB and fascicles
then to the ventricular muscle

Lastly,
 As the ventricles contract, blood is forced out
through the semilunar valves into the pulmonary
trunk and the aorta.
 After the ventricles complete their contraction
phase, they relax and the SA node initiates
another impulse to start another cardiac cycle.

Remember:
■ Intrinsic rhythmicity of denervated SA- node is  90
impulses/min, while that of AV- node is  60
impulses/min.
■ However, vagal tone controls SA- node to become 70
impulses/min, & AV- node to 40 impulses/min.
■ If SA- node activity is depressed by a disease, AV-
node takes over & becomes the pacemaker instead,
leading to bradycardia.

references
 Ross & Pawlina, Histology: A Test and
Atlas, 5th ed.
 William F.Ganong review of medical
physiology

References
 Human physiology by Lauralee
Sherwood, 7th edition
 Text book physiology by Guyton
&Hall,12th edition
 Text book of physiology by Linda .s
contanzo,third edition

Thank you!

Cvs introduction ms 2020

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