genesis and spreading of cardiac impulses

CARDIAC IMPULSESGenesis and transmission of

CARDIAC IMPULSES

Pondicherry universityDepartment of Biochemistry and Molecular Biology

Conduction System• Auto-rhythmic Fibers : Specialized cardiac muscle

fibers called which has an inherent and rhythmicalelectrical activity. Automaticity and rhythmicity.

• Sinus Node ( SA node) : Sinoatrial node, a smallflattened ellipsoid strip, 3mm wide -15mm long –1mm thick -3 to 5µm diameter, Located in superiorposterolateral wall of R.atrium, near opening ofsuperior vena cava. Connected directly to atrial musclefibres. Capability of self-excitation.

• Internodal pathway: Connects between two nodes

• Auto-rhythmic Fibers : Specialized cardiac musclefibers called which has an inherent and rhythmicalelectrical activity. Automaticity and rhythmicity.

• Sinus Node ( SA node) : Sinoatrial node, a smallflattened ellipsoid strip, 3mm wide -15mm long –1mm thick -3 to 5µm diameter, Located in superiorposterolateral wall of R.atrium, near opening ofsuperior vena cava. Connected directly to atrial musclefibres. Capability of self-excitation.

• Internodal pathway: Connects between two nodes

• Atrioventricular Node (AV Node) : Less GapJunctions between nodal cells, more resistance.Comparatively slow conduction.

• A-V Bundle / Bundle of His : Impulses travels onlyin one direction.

• Purkinje Fibers: Very high permeability gapjunctions. velocity of 1.5 - 4.0 m/sec (6x that ofventricular muscle & 150x in A-V nodal fibers).Synchronize Right and Left ventricular contraction

Cont..Conduction System• Atrioventricular Node (AV Node) : Less Gap

Junctions between nodal cells, more resistance.Comparatively slow conduction.

• A-V Bundle / Bundle of His : Impulses travels onlyin one direction.

• Purkinje Fibers: Very high permeability gapjunctions. velocity of 1.5 - 4.0 m/sec (6x that ofventricular muscle & 150x in A-V nodal fibers).Synchronize Right and Left ventricular contraction

cont.. Conduction System

Parts of Conducting System Velocity of impulse

Atrial Muscle 0.3 m/sec

Ventricular Muscle 0.3 – 0.5m/sec

AV Node 0.05 m/sec

Cont..Conduction System

AV Node 0.05 m/sec

Internodal fibers 1m/sec

Left & Right Bundle Branches 2 m/sec

Purkinje Fibers 1.5 - 4 m/sec

Are cardiac action potentials different?

SA NODE ACTION POTENTIAL (AP)

• Found in SA nodal cells. These cells has no trueresting potential. Their potential is called asPacemaker potential (-60mV)

• Depolarizing is primarily by slow Ca++ currentsinstead of by fast Na+ currents.

• No fast Na+ channels and currents operating inSA nodal cells. This results gradualdepolarization. Hence called as slow responseaction potential

• Pacing rate is 100 times/minute

• Found in SA nodal cells. These cells has no trueresting potential. Their potential is called asPacemaker potential (-60mV)

• Depolarizing is primarily by slow Ca++ currentsinstead of by fast Na+ currents.

• No fast Na+ channels and currents operating inSA nodal cells. This results gradualdepolarization. Hence called as slow responseaction potential

• Pacing rate is 100 times/minute

Cont…SA NODE AP

F-type Sodium channel(Funny type)Voltage gated

Potassium channel

Types of Channels

SA Nodal Cell

T- type Calcium Channel(Transient type)

L- type Calcium Channel(Long lasting type)

Na+

Threshold

Na+

• F –type Sodium channel openscausing inward movement of Na+.

• Depolarization in membrane potential• Responsible for inherent leakiness ofNa+ in SA node. (Automaticity)• These channels works at -60 mVinstead of -90 mV in normal Na+

channels. Hence called as funnychannels/ funny currents

Na+

Threshold

Na+

Ca2+ (T)

• Around -50 mV Voltage gated T- typeCa2+ channel opens. (T-Transient)• As the potential become positive theiractivity decreases.• Active for very short time.•Na+ permeability decreases graduallywith increase in potential positively.

Na+

Threshold

Na+

Ca2+ (L)

• This gradual depolarization is knownas a Pacemaker potential .•Around -40 mV Voltage gated L- typeCa2+ channel opens. (L-Long lasting)• Active for long time.• Ca2+ movement through this channelis not rapid, making slower rate ofdepolarization.

Ca2+ (T)

Na+

Threshold

Na+

•Voltage gated T- type Ca2+ channelcloses.• As the potential become positive andtheir activity decreases.• L- type Ca2+ channel primarilyresponsible for depolarization• Na+ permeability is considerably lessdue to high positive potential.

Ca2+ (L)

Na+K+

Threshold

Na+K+

•Voltage gated L- type Ca2+ channelcloses.• Voltage gated K+ channel opens.• Out ward movement of K+ ion causinghyperpolarization• hyperpolarized state is necessary forpacemaker channels to becomeactivated.

Na+

Threshold

Na+

• Voltage gated K+ channel becomeinactive as the potential becomenegative again.• a slow decline in the outwardmovement of K+

• Na+ F- type channel become prominentand cycle repeats

SA NODE AP : Summary

AV Node AP

• Similar to AP of SA Node.• determined primarily by changes in slow

inward Ca++ and K+ currents, and do notinvolve fast Na+ currents.

• have intrinsic pacemaker activity produced bythe same ion currents as in SA nodal cells.

• Pacing rate is 40 – 60 times /minute

• Similar to AP of SA Node.• determined primarily by changes in slow

inward Ca++ and K+ currents, and do notinvolve fast Na+ currents.

• have intrinsic pacemaker activity produced bythe same ion currents as in SA nodal cells.

• Pacing rate is 40 – 60 times /minute

Myocyte AP• Found in muscle cells heart• Unlike nodal cells myocytes have a true resting

membrane potential (-90 mV)• Threshold voltage of -70 mV cause rapid

depolarization.• Types of channels

- Fast Na+ channel- L- type Ca2+ channel- Transient Outward K+ channel- Voltage – gated K+ channel- K+ leaky channel

• Found in muscle cells heart• Unlike nodal cells myocytes have a true resting

membrane potential (-90 mV)• Threshold voltage of -70 mV cause rapid

depolarization.• Types of channels

- Fast Na+ channel- L- type Ca2+ channel- Transient Outward K+ channel- Voltage – gated K+ channel- K+ leaky channel

K+

•K+ leaky channel is open at resting membrane potential-90 mV

Na+ entersFast Na+ channel


Na+

• fast Na+ channel opensaround -70 mV• Rapid depolarization due tofast Na+ channels



Na+

• Transient outward K+channel become activemaking a small repolarizationof +5 mV.

K+


Ca2+ entersL-type Ca2+ channel


Ca2+

• Repolarization is delayed andthere is a plateau phase in theaction potential.•Ca2+ inward = K+ outward

K+




Ca2+

• Transient outward K+channels closes• Membrane potentialdepolarizes to about -40 mV



K+ exitsVoltage gated K+channel


K+ K+


• Ca2+ channel got inactivated• hyperpolarization (-55 mv) happensdue to voltage gated K+ channel.• K+ leaky channel become activated






K+

Outflow of K+ restores the negative resting membrane potential (-90 mV).

Myocyte AP: summary

• action potential in non-pacemaker cells is primarilydetermined by relative changes in fast Na+, slowCa++ and K+ currents.

• Fast sodium channel opens around -70 mV, allows rapiddepolarization, rate of depolarization is higher thannodal cells.

• After 1msec fast sodium channel closes. Ca2+ channelsopens around -5 mV and stays open for 0.25sec

• During plateau phase Ca2+ move from the interstitialfluid into the cytosol. This inflow causes even moreCa2+ to pour out of the sarcoplasmic reticulum and T-tubules into the cytosol .This helps in musclecontraction

• At the end of plateau of AP, Ca influx stops while effluxinto sarcoplasmic reticulum & T-tubules occur &contraction ends

Myocyte AP and Contraction• action potential in non-pacemaker cells is primarily

determined by relative changes in fast Na+, slowCa++ and K+ currents.

• Fast sodium channel opens around -70 mV, allows rapiddepolarization, rate of depolarization is higher thannodal cells.

• After 1msec fast sodium channel closes. Ca2+ channelsopens around -5 mV and stays open for 0.25sec

• During plateau phase Ca2+ move from the interstitialfluid into the cytosol. This inflow causes even moreCa2+ to pour out of the sarcoplasmic reticulum and T-tubules into the cytosol .This helps in musclecontraction

• At the end of plateau of AP, Ca influx stops while effluxinto sarcoplasmic reticulum & T-tubules occur &contraction ends

Transmission of cardiac impulses

AV nodal DelayPart of conducting

systemReasons for delay Delay

(sec)AV node less number of gap

junctions0.09 sec

AV bundle Resistance in AV bundle 0.04 sec

Internodal pathways Transmission time 0.03 secInternodal pathways Transmission time 0.03 sec

• A total delay of 0.16 sec. This allows time for the atria to empty theirblood into the ventricles before ventricular contraction begins. Thisincreases the efficiency of the pumping action of the heart.

• It is primarily the AV node and it’s adjacent fibers that delay thistransmission into the ventricles

Parts of conducting system Pacing rate

SA Node 75 times/min

AV Node 60-50 times/min

Bundle of His & Purkinje fibers 20-30 times/min

Who is the real pacemaker?

Bundle of His & Purkinje fibers 20-30 times/min

• The discharge rate of the sinus node is faster than discharge rate of either the A-Vnode or the Purkinje fibers.

• the sinus node discharges again before either the A-V node or the Purkinje fibers canreach their own thresholds

• rate of rhythmical discharge in SA Node is faster than any other part

Reference

• Widmaeir. P.E, Raff.H, Strang .T.K- Vander’s Human Physiologythe mechanisms of body function. 11th edition. McGraw-HillHigher Education

• Gerard J. Tortora, Bryan Derrickson. Principles of Anatomy andPhysiology, 13th Edition. John Wiley & Sons, Inc.

• Kim E. Barrett, Scott Boitano, Heddwen L. Brooks, Susan M.Barman, Ganong’s Review of Medical Physiology, 23rd edition.McGrawHill Medical

• Arthur C. Guyton, John E. Hall. Text Bookof Medical Physiology11th Edition. Elsevier Saunders, Elsevier Inc

• Widmaeir. P.E, Raff.H, Strang .T.K- Vander’s Human Physiologythe mechanisms of body function. 11th edition. McGraw-HillHigher Education

• Gerard J. Tortora, Bryan Derrickson. Principles of Anatomy andPhysiology, 13th Edition. John Wiley & Sons, Inc.

• Kim E. Barrett, Scott Boitano, Heddwen L. Brooks, Susan M.Barman, Ganong’s Review of Medical Physiology, 23rd edition.McGrawHill Medical

• Arthur C. Guyton, John E. Hall. Text Bookof Medical Physiology11th Edition. Elsevier Saunders, Elsevier Inc

genesis and spreading of cardiac impulses

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