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Transcript
12-Mar-17
Cardiovascular
System
Prof Dr Waqas Hameed
HOD, Physiology
Pak Int’l Med Colg
A Businessman with heart attack
•
A 55 years old businessman got a Myocardial infarction.
Timely treatment was given and he was saved. However
it was noted by the physician that his heart rate has
dropped to just 40 beats per minute.
•
He was all right when he was lying in bed but on the
second day when he tried to go to washroom he
collapsed and felt dizziness. The cardiologist advised to
put ‘an artificial pace maker’ to control his heart rate.
Immediately!
•
•
What is the problem with this patient?
How will artificial pacemaker help him?
Electrical Activity of the Heart
1
12-Mar-17
Electrical Activity of Heart
• Heart beats rhythmically - result of action potentials it
generates itself (autorhythmicity)
• Two specialized types of cardiac muscle cells
– Contractile cells
 99% of cardiac muscle cells
 Do mechanical work of pumping
 Normally do not initiate own action potentials
– Autorhythmic cells
 Do not contract
 Specialized for initiating & conducting action potentials
responsible for contraction of working cells
Membrane Ion Channels in Cardiac
Muscle
 Fast Na+ channels
 Slow Na+ - Ca++ channels
 K+ channels
2
12-Mar-17
Action Potential in Contractile Muscle
Autorhythmicity
 Action Potential is generated by specialized heart cells
itself
 This generation of action potential is rhythmic
 It spreads to the whole heart by specialized cardiac
muscle
 It leads to Rhythmic Contraction of Heart (Heart Beat)
Sinoatrial Node / Sinus Node
 small, flattened, ellipsoid
strip of specialized cardiac
muscle
Size:
3 mm wide, 15 mm long &
1 mm thick
Location:
 superior posterolateral
wall of right atrium
 immediately below &
slightly lateral to the
opening of superior vena
cava
3
12-Mar-17
SA Node to AV Node
 Anterior
 Middle
(tract of Wenckebach)
 Posterior (tract of Thorel)
 Anterior Interatrial Band
(Bachmann’s bundle)
connects right atria with left
Intrinsic Cardiac Conduction System
Approximately 1% of cardiac muscle cells are autorhythmic rather
than contractile
70-80/min
40-60/min
20-40/min
4
12-Mar-17
Special Property of Autorhythmic Cells
(Drift & Fire)
• (Please Recall that the Nerve & Skeletal Muscle cells have a
constant Resting Membrane Potential)
‘Fire’
 Cardiac Muscle cells do not have Resting Potential
 Instead they have PACEMAKER POTENTIAL
DRIFT to
threshold
‘f ’ channels: ‘ f ’ from funny
T-Type Ca++ Channels: “Transient” Ca++ Channel
L-Type Ca++ Channel: “Longer Lasting” Ca++ Channel
P: Permeability
S-A Node
(sinoatrial node)
 Their membrane potential slowly depolarizes between the
two action potentials (drifts to threshold), when the
threshold for action potential generation is reached, the
membrane generates an impulse(fires)
 An autorythmic cell membrane’s slow drift to threshold is
called pacemaker potential
Atrioventricular Node
Internodal pathways
 posterior wall of right atrium
A-V Node
(atrioventricular node)
 immediately behind the
tricuspid valve
A-V bundle
Left & Right bundle
branches of Purkinje
fibers
5
12-Mar-17
Conducting System of Heart
6
12-Mar-17
7
12-Mar-17
Targets of Cardiac Excitation
 Atrial Excitation & Contraction should be complete
before the onset of ventricular contraction
 Excitation of cardiac muscle fibers should be coordinated
to ensure that each heart chamber contracts as a unit
(syncytium) to pump efficiently
 The pair of atria & the pair of ventricles should be
functionally coordinated so that both members of the
pair contract simultaneously
Autorhythmic Cells: Initiation of Signals
8
12-Mar-17
Pacemaker & Action Potentials of Heart
Conduction between the Atria & the
Ventricles
• Action potential cannot be transferred from atria to
ventricles at any other place except for AV Node
• Slow conduction across AV Node – ventricular filling
• Atria completely depolarize, contract & empty into
ventricles
• delay of impulse at AV Node - AV Nodal delay
Control of Excitation & Conduction in Heart
 Role of the Purkinje System:
– Efficient fast conducting system - ensures very fast
spread of impulse in all portions of ventricles
A-V Nodal delay = 0.13 sec
A-V Node = 0.09 sec
A-V bundle = 0.03 sec
– Effective & Synchronous pumping by ventricles is
achieved only by this system
9
12-Mar-17
10
12-Mar-17
Abnormal Pacemakers “Ectopic” Pacemaker
Pacemaker elsewhere than SA Node
 abnormal sequence of contraction
 debility of heart pumping
Site:
 most frequently at the A-V node
 penetrating portion of the A-V bundle
Stokes-Adams syndrome
A-V block occurs
• atria continue to beat at the normal rate of rhythm of the
sinus node
• new pacemaker usually develops in the Purkinje system of
the ventricles
• new rate b/w 15 to 40 beats/ min
• Purkinje fibers had been “overdriven” by the rapid sinus
impulses
• Gap of 5 to 20 seconds; ventricles fail to pump blood
• Person faints after first 4 to 5 seconds
Action potential
in cardiac
contractile cell
Travels down
T tubules
Entry of small
amount of Ca2+
from ECF
Addition of
Ca+2 initiates
contraction
Release of large
amount of Ca2+
from sarcoplasmic
reticulum
Cytosolic
Ca2+
Troponin-tropomyosin complex
in thin filaments pulled aside
Removal of
Ca+2 causes
relaxation
Cross-bridge cycling between
thick and thin filaments
Thin filaments slide inward
between thick filaments
Contraction
11
12-Mar-17
Control of Excitation & Conduction in the
Heart
• Cardiac Nerves
Heart rate
– Sympathetic Stimulation
• Distributed to all parts of the heart
• Sympathetic stimulation releases “norepinephrine”
that increases permeability of cardiac cells for Na+ &
Ca++ ions
Sympathetic
activity
(& epinephrine)
Parasympathetic
activity
– ↑’s rate of sinus nodal discharge
– ↑’s the rate of conduction at all levels
– ↑’s force of contraction
Control of Excitation and Conduction in the Heart
(contd.)
Pacemaker Function
• Cardiac Nerves
– Parasympathetic Stimulation
• Parasympathetic supply (Vagus Nerve) mainly
distributed to SA & AV nodes
• Parasympathetic
stimulation
releases
‘acetylcholine’ - causes increased leakage of K+
causing hyperpolarization of cardiac cells leading
to:
- Decreased Heart rate
- Slowed impulse transmission in ventricular
muscle fibers leading to decreased
rate of heart pumping
12
12-Mar-17
Sympathetic and Parasympathetic
 Sympathetic – speeds heart rate by  Ca++ & I-f channel
flow
 Parasympathetic – slows rate by  K+ efflux &  Ca++ influx
13