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LIU Chuan Yong 刘传勇 Institute of Physiology Medical School of SDU Tel 88381175 (lab) 88382098 (office) Email: liucy@sdu.edu.cn Website: www.physiology.sdu.edu.cn. Section 2. Electrophysiology of the Heart. CARDIAC ELECTROPHYSIOLOGY. Two kinds of cardiac cells.

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slide1

LIU Chuan Yong

刘传勇

Institute of Physiology

Medical School of SDU

Tel 88381175 (lab)

88382098 (office)

Email: liucy@sdu.edu.cn

Website: www.physiology.sdu.edu.cn

section 2

Section 2

Electrophysiology of the Heart

slide4

Two kinds of cardiac cells

1, The working cells.

Special property: contractility

slide5

2, Special conduction system

including the

Sinoatrial node, Atrioventricular node,

Atrioventricular bundle (bundle of His),

and Purkinje system.

Special property: automaticity

a cell

Na+

Cl-

Cl-

Cl-

K+

K+

Na+

Cl-

Cl-

Na+

Na+

K+

K+

Na+

Cl-

Cl-

Cl-

Cl-

K+

Cl-

K+

Cl-

Na+

Cl-

Cl-

K+

Cl-

Na+

Lipid bilayer

membrane

Na+

Cl-

Cl-

K+

A Cell

0 mV

- X mV

K+

equilibrium
Equilibrium
  • The process of ions diffusing and changing the membrane voltage will continue
  • until the membrane potential attains a value sufficient to balance the ion concentration gradient.
  • At this point the ion will be “in equilibrium”.
  • What is this potential?
the nernst potential
The Nernst Potential

An ion will be in equilibrium when the membrane potential is:

where [X]o and [X]i are the external and internal concentrations of the ion; R, T, and F are thermodynamic constants such that (at 37 °C):

The Nernst

Potential

for example
For Example...
  • Typically, [K]o = 4 mM and [K]i = 140 mM
    • so VK = 61*log(4/140) = - 94 mV
    • i.e. a cell with these normal K concentrations and ONLY a K-selective ion channel will have a membrane potential of -94 mV
  • Likewise, [Na]o = 140 mM and [Na]i = 10 mM
    • so VNa = 61*log(140/10) = + 70 mV
    • i.e. a cell with these normal Na concentrations and ONLY a Na-selective ion channel will have a membrane potential of +70 mV
action potentials from different areas of the heart fast and slow response

0

0

mv

mv

-90mv

-90mv

0

mv

-80mv

ACTION POTENTIALS FROM DIFFERENT AREAS OF THE HEARTFast and Slow Response

ATRIUM

VENTRICLE

SA NODE

time

electrophysiology of the fast ventricular muscle
ELECTROPHYSIOLOGY OF THE FAST VENTRICULAR MUSCLE

AMP

+20

1

To oscilloscope

2

0

3

0

mv

Cardiac Cell

4

-90

0

300

t (msec)

slide14

General description

Resting potential: -90mv

Action Potential

Phase 0: rapid depolarization, 1-2ms

Phase 1: early rapid repoarization, 10 ms

Phase 2: plateau, slow repolarization, the potential is around 0 mv. 100 – 150ms

Phase 3, late rapid repolarization. 100 – 150 ms

Phase 4 resting potentials

+20

1

2

0

3

0

mv

4

-90

0

300

t (msec)

ion channels in working muscle
Ion Channels in Working Muscle
  • Essentially same in atrial and ventricular muscle
  • Best understood in ventricular cells
ion channels in ventricular cells
Ion Channels in Ventricular Cells
  • Voltage-gated Na+ channels
  • Inward rectifier K+ channels
  • L-type Ca2+ channels
  • Several Voltage-gated K+ channels
cardiac na channels
Cardiac Na+ Channels
  • Almost identical to nerve Na+ channels (structurally and functionally)
    • very fast opening (as in nerve)
    • has inactivation state (as in nerve)
    • NOT Tetrodotoxin sensitive
  • Expressed only in non nodal tissue
  • Responsible for initiating and propagating the action potential in non nodal cells
slide18

+20

1

2

0

3

0

mv

4

-90

0

300

t (msec)

inward rectifier i k1 structure
Inward Rectifier (Ik1) Structure

Note: No “voltage sensor”

P-Region

Extracellular

Fluid

M1

M2

membrane

Inside

H2N

HO2C

inward rectification
Inward Rectification

K+

K+

K+

K+

Mg2+

Mg2+

Extracellular solution

Intracellular Solution

K+

K+

K+

-80 mV

-30 mV

K+

K+

role for inward rectifier
Role for Inward Rectifier
  • Expressed primarily in non nodal tissues
  • Sets resting potential in atrial and ventricular muscle
  • Contributes to the late phase of action potential repolarization in non nodal cells
slide24

+20

1

2

0

3

0

mv

4

-90

0

300

t (msec)

cardiac voltage gated k channels

Inactivating K channels (ITO)

“Ultra-rapid” K channels (IKur)

“Rapid” K channels (IKr)

“Slow” K channels (IKs)

Cardiac Voltage-gated K Channels
  • All structurally similar to nerve K+ channels
  • ITO is an inactivating K+ channel- rapid repolarization to the plateau
  • IKur functions like nerve K+ channel- fights with Ca to maintain plateau
  • IKr, IKs structurally and functionally complex
cardiac ca 2 channels
Cardiac Ca2+ Channels
  • L-type
  • Structurally rather similar to Na channels
  • Some functional similarity to Na channels
      • depolarization opens Ca2+ channels
  • Functionally different than Na channels
      • slower to open
      • very slow, rather incomplete inactivation
      • generates much less current flow
role of cardiac ca 2 channels
Role of Cardiac Ca2+ Channels
  • Nodal cells
    • initiate and propagate action potentials- SLOW
  • Non nodal cells
    • controls action potential duration
    • contraction
ca 2 channel blockers and the cardiac cell action potential
Ca2+CHANNEL BLOCKERS AND THE CARDIAC CELL ACTION POTENTIAL

DILTIAZEM 地尔硫卓

ACTION POTENTIAL

CONTROL

10 µMol/L

30 µMol/L

10

30

CONTROL

10

FORCE

30

TIME

ion channels in atrial cells

0

0

mv

mv

-90mv

-90mv

Ion Channels in Atrial Cells
  • Same as for ventricular cells
  • Less pronounced plateau due to different balance of voltage-gated Ca2+ and K channels

ATRIUM

VENTRICLE

phase 0 of the fast fiber action potential

Na+

Na+

m

m

m

A

B

h

h

-65mv

-90mv

Na+

Na+

m

m

C

D

h

h

0mv

+20mv

Na+

m

E

h

+30mv

PHASE 0 OF THE FAST FIBER ACTION POTENTIAL

Chemical

Gradient

Electrical

Gradient

ion channels in ventricular muscle

Inactivating K channels (ITO)

“Ultra-rapid” K channels (IKur)

“Rapid” K channels (IKr)

“Slow” K channels (IKs)

Voltage-gated

Na Channels

Voltage-gated

Ca Channels

200 msec

IK1

Ion Channels in Ventricular Muscle

0

Ventricular muscle

membrane potential (mV)

-50

ion channels in ventricular muscle34
Ion Channels in Ventricular Muscle

Current

Na Current

Ca Current

IK1

ITO

IKur

IKr

IKs

slide36

Ion Channels in Purkinje Fibers

  • At phase 4, the membrane potential does not maintain at a level,
  • but depolarizes automatically – the automaticity
  • (Phase 0 – 3) Same as for ventricular cells
  • (Phase 4) Plus a very small amount of If (pacemaker) channels
slide37

Activated by negative potential (at about -60 mv during Phase 3)

  • Not particularly selective: allows both Na+ and K+
the sa node cell
The SA node cell
  • Maximal repolarization (diastole) potential, –70mv
  • Low amplitude and long duration of phase 0. It is not so sharp as ventricle cell and Purkinje cell.
  • No phase 1 and 2
  • Comparatively fast spontaneous depolarization at phase 4

A, Cardiac ventricular cell

B, Sinoatrial node cell

sa node action potential
SA Node Action Potential

Voltage-gated Ca+2 channels

Voltage-gated K+ channels

0

SA node membrane potential (mV)

No inward-rectifier

K+ channels

-50

If or pacemaker channels

200 msec

sa node cells
SA Node Cells

Current

Ca Current

K currents

If

(pacemaker current)

looking at the pacemaker currents
LOOKING AT THE PACEMAKER CURRENTS

voltage

iK

if

ionic currents

iCa

slide43

AV Node Action Potentials

  • Similar to SA node
  • Latent pacemaker
  • Slow, Ca+2-dependent upstroke
  • Slow conduction (delay)
  • K+-dependent repolarization

0

AV node membrane potential (mV)

SA node

-50

AV node

200 msec

fast and slow response rhythmic and non rhythmic cardiac cells
Fast and slow response, rhythmic and non-rhythmic cardiac cells
  • Fast response, non –rhythmic cells: working cells
  • Fast response, rhythmic cells: cells in special conduction system of A-V bundle and Purkinje network.
  • Slow response, non-rhythmic cells: cells in nodal area
  • Slow response rhythmic cells: S-Anode, atrionodal area (AN), nodal –His (NH)cells
ii electrical properties of cardiac cells

II Electrical Properties of Cardiac Cells

Excitability, Conductivity and Automaticity

slide47

(1) Refractory Period

+25

1

RRP

0

-25

2

3

0

-50

Transmembrane Potential

4

ARP

-75

-100

-125

0

0.1

0.2

0.3

Time (msec)

  • Absolute Refractory Period – regardless of the strength of a stimulus, the cell cannot be depolarized.
  • Relative Refractory Period – stronger than normal stimulus can induce depolarization.
refractory period
Refractory Period
  • Absolute Refractory Period (ARC): Cardiac muscle cell completely insensitive to further stimulation
  • Relative Refractory Period (RRC): Cell exhibits reduced sensitivity to additional stimulation
slide49

Na+ Channel Conformations

Another Non-conducting

conformation

(a while after more

depolarized potentials)

Non-conducting

conformation(s)

(shortly after more

depolarized potentials)

Conducting

conformation

(at negative potentials)

Open

Inactivated

Closed

Outside

IFM

Inside

IFM

IFM

refractory period50
Refractory Period
  • The plateau phase of the cardiac cell AP increases the duration of the AP to 300 msec,
  • The refractory period of cardiac cells is long (250 msec).
    • compared to 1-5 msec in neurons and skeletal muscle fibers.
refractory period51
Refractory Period
  • Long refractory period prevents tetanic contractions
  • systole and diastole occur alternately.
  • It is very important for pumping blood to arteries.
slide52

Comparison of refractory period and summation

in cardiac and skeletal muscle fibers

supranormal period

Absolute

S.N.

Rel

Supranormal period:
  • The cells can be restimulated and the threshold is actually lower than normal.
  • Occurs early in phase 4 and is usually accompanied by positive after-potentials as some potassium channels close.
  • Can be source of reentrant arrhythmias especially when phase 3 is delayed as in long Q-T syndrome
skeletal vs cardiac muscle contraction
Skeletal Vs. Cardiac muscle contraction
  • Impulse generation: Intrinsic in cardiac muscle, extrinsic in skeletal muscle
  • Plateau phase: Present in cardiac muscle, absent in skeletal muscle
  • Refractory period: long in cardiac muscle, shorter in skeletal muscle
  • Summation: Impossible in cardiac muscle, possible in skeletal muscle
slide57

Extra-stimulus

  • premature excitation
  • premature contraction

 compensatory pause

automaticity autorhythmicity
Automaticity (Autorhythmicity)
  • Some tissues or cells have the ability to produce spontaneous rhythmic excitation without external stimulus.
  • Different intrinsic rhythm of rhythmic cells
    • Purkinje fiber, 15 – 40 /min
    • Atrioventricular node 40 – 60 /min
    • Sinoatrial node 90 – 100 /min
      • normal pacemarker
      • latent pacemarker
      • ectopic pacemarker
automaticity autorhythmicity60
Automaticity (Autorhythmicity)
  • The mechanism that SA node controls the hearts rhythm (acts as pacemaker) rather than the AV node and Purkinje fiber
    • The capture effect
    • Overdrive suppression
3 factors determining automaticity
(3) Factors determining automaticity
  • Depolarization rate of phase 4
  • Threshold potential
  • The maximal repolarization potential
flow of cardiac electrical activity action potentials

SA node

Pacing (sets heart rate)

Atrial Muscle

0.4m/s

AV node

0.02 m/sDelay

Purkinje System

4m/sRapid, uniform spread

Ventricular

Muscle

1m/s

Flow of Cardiac Electrical Activity (Action Potentials)
characteristics of conduction in heart
characteristics of conduction in heart
  • Delay in transmission at the A-V node (150 –200 ms) – sequence of the atrial and ventricular contraction – physiological importance
  • Rapid transmission of impulses in the Purkinje system – synchronize contraction of entire ventricles – physiological importance
2 factors determining conductivity
(2) Factors determining conductivity
  • Anatomical factors
  • Physiological factors
anatomical factors
Anatomical factors
  • A.Gap junction between working cells
    • functional atrial and ventricular syncytium
multi cellular organization
Multi-cellular Organization

= Gap Junction Channel

anatomical factors72
Anatomical factors
  • A. Gap junction between working cells and functional atrial and ventricular syncytium
  • B. Diameter of the cardiac cell – conductive resistance – conductivity
physiological factors
Physiological factors
  • A. Slope of depolarization and amplitude of phase 0
    • Fast and slow response cells
  • B. Excitability of the adjacent unexcited membrane
slide74

III. Neural and humoral control of the cardiac function

  • Vagus nerve and acetylcholine (Ach)
  • Vagus nerve :
  • release Ach from postganglionic fiber
  • M receptor on cardiac cells
  • K+ channel permeability increase
  • but Ca 2+ channel permeability decrease
ach on atrial action potential
ACh on Atrial Action Potential

(  ) K+ Conductance (Efflux)

0 mv

Voltage

- 90mv

Time

slide76

1) K+ channel permeability increase

  • resting potential (maximal diastole potential) more negative
  • excitability decrease
ion channels in ventricular muscle77

Inactivating K channels (ITO)

“Ultra-rapid” K channels (IKur)

“Rapid” K channels (IKr)

“Slow” K channels (IKs)

Voltage-gated

Na Channels

Voltage-gated

Ca Channels

200 msec

IK1

Ion Channels in Ventricular Muscle

0

Ventricular muscle

membrane potential (mV)

-50

slide78

2) On SA node cells,

  • K+ channel permeability increase
  • the depolarization velocity at phase 4 decrease + maximal diastole potential more negative
  • automaticity decrease
  • heart rate decrease
  • Negative chronotropic action
sa node action potential79
SA Node Action Potential

Voltage-gated Ca+2 channels

Voltage-gated K+ channels

0

SA node membrane potential (mV)

-50

If or pacemaker channels

200 msec

slide81

Ca2+ channel permeability decrease

  • myocardial contractility decrease
  • negative inotropic action
role of cardiac ca 2 channels82
Role of Cardiac Ca2+ Channels
  • Nodal cells
    • initiate and propagate action potentials- SLOW
  • Non nodal cells
    • controls action potential duration
    • contraction
slide83

4) Ca2+ channel permeability decrease

  • depolarization rate of slow response cells decrease
  • conductivity of these cell decrease
  • negative dromotropic action
sa node action potential84
SA Node Action Potential

Voltage-gated Ca+2 channels

Voltage-gated K+ channels

0

SA node membrane potential (mV)

No inward-rectifier

K+ channels

-50

If or pacemaker channels

200 msec

slide85

2. Effects of Sympathetic Nerve and catecholamine on the Properties of Cardiac Muscle

  • Sympathetic nerve release norepinephrine from the postganglionic endings;
  • epinephrine and norepinephrine released from the adrenal glands
  • binding with β1 receptor on cardiac cells

 increase the Ca2+ channel permeability 

slide86

Ca2+ channel permeability increase:

  • Increase the spontaneous depolarization rate at phase 4
  • automaticity of SA node cell rise
  • heart rate increase

Positive chronotropic action

slide87

Ca2+ channel permeability increase:

  • Increase the depolarization rate (slope) and amplitude at phase 0
  • increase the conductivity of slow response cells

Positive dromotropic action

  • Increase the Ca2+ concentration in plasma during excitation
  • myocardial contractility increase

positive inotropic action

slide89

Effect of autonomic nerve activity on the heart

Region affected Sympathetic Nerve Parasympathetic Nerve

Increased rate of diastole depolarization ; increased cardiac rate

Decreased rate of diastole depolarization ; Decreased cardiac rate

SA node

Increase conduction rate

Decreased conduction rate

AV node

Decreased strength of contraction

Increase strength of contraction

Atrial muscle

Ventricular muscle

Increased strength of contraction

No significant effect

slide90

IV The Normal Electrocardiogram (ECG)

Concept: The record of potential fluctuations of myocardial fibers at the surface of the body

the heart
The Heart

is a pump

has electrical activity

(action potentials)

generates electrical

current that can be measured

on the skin surface (the ECG)

currents and voltages
At rest, Vm is constant

No current flowing

Inside of cell is at constant potential

Outside of cell is at constant potential

A piece of cardiac muscle

inside

------------------------------

++++++++++++++++++

outside

-

+

Currents and Voltages

0 mV

currents and voltages94
During AP upstroke, Vm is NOT constant

Current IS flowing

Inside of cell is NOT at constant potential

Outside of cell is NOT at constant potential

A piece of cardiac muscle

AP

inside

++++------------------------

------++++++++++++++

outside

current

-

+

Currents and Voltages

An action potential propagating

toward the positive ECG lead

produces a positive signal

Some positive

potential

more currents and voltages

During Repolarization

A piece of totally depolarized

cardiac muscle

A piece of cardiac muscle

inside

inside

+++++++++++++++++++

-------------------------------

------------+++++++++++

outside

Vm not changing

No current

No ECG signal

+++++++-------------------

outside

current

Some negative potential

-

+

More Currents and Voltages

Repolarization spreading toward

the positive ECG lead produces

a negative response

the ecg
The ECG
  • Can record a reflection of cardiac electrical activity on the skin- EKG
  • The magnitude and polarity of the signal depends on
    • what the heart is doing electrically
      • depolarizing
      • repolarizing
      • whatever
    • the position and orientation of the recording electrodes
cardiac anatomy

Internodal

conducting

tissue

Cardiac Anatomy

Superior

venacava

Pulmonary

veins

Atrioventricular (AV) node

Left atrium

Sinoatrial (SA)A node

Atrial muscle

Mitral valve

Tricuspid valve

Purkinje

fibers

Ventricluar

muscle

Inferior

vena cava

Descending aorta

flow of cardiac electrical activity

Atrial muscle

Internodal

conducting

fibers

Atrial muscle

Flow of Cardiac Electrical Activity

SA node

AV node (slow)

Purkinje fiber

conducting system

Ventricular muscle

conduction in the heart

Superior

venacava

Pulmonary

veins

AV node

Left atrium

SA node

Atrial muscle

Mitral valve

Specialized

conducting

tissue

Tricuspid valve

Purkinje

fibers

Ventricluar

muscle

Inferior

vena cava

Descending aorta

Conduction in the Heart

approx. 0.44 s

0.12-0.2 s

SA

node

Atria

AV

node

Purkinje

Ventricle

2 the normal ecg

approx. 0.44 s

0.12-0.2 s

QT

PR

R

T

Atrial muscle

depolarization

P

Q

S

Ventricular

muscle

repolarization

Ventricular muscle

depolarization

2. The Normal ECG

Right Arm

“Lead II”

Left Leg

action potentials in the heart

approx. 0.44 s

0.12-0.2 s

QT

PR

Superior

ECG

venacava

Aorticartery

SA

Pulmonaryartery

Pulmonary

veins

AV node

SA node

Left atrium

Atrial muscle

Mitral valve

Atria

Specialized

conducting

Interventricular

septum

tissue

Tricuspid valve

Purkinje

fibers

Ventricluar

muscle

Inferior

vena cava

Descending aorta

Action Potentials in the Heart

AV

Purkinje

Ventricle

3 uses of the e c g
3. Uses of the ECG
  • Heart Rate
  • Conduction in the heart
  • Cardiac arrhythmia
  • Direction of the cardiac vector
  • Damage to the heart muscle
  • Provides NO information about pumping or mechanical events in the heart.