HEART ELECTROPHYSIOLOGY
Sunday, June 1, 2025 1:58 PM
Intrinsic conduction of the heart
Key Concepts:
• Electrophysiology: The study of electrical properties of biological cells and tissues.
• Automaticity: The intrinsic ability of the heart to spontaneously depolarise itself and trigger action potentials. These action
potentials are spread throughout the entire myocardium to trigger muscle contraction. This ability doesn't depend on the
nervous system for its basic function.
Myocardium Components:
The myocardium (the muscle layer of the heart) is made up of two main components:
1. Nodal Cells:
○ These are non-contractile cells.
○ They are the cells that generate automaticity.
○ They can spontaneously depolarise and generate action potentials.
○ Examples include the SA node, AV node, AV bundle (bundle of His), bundle branches (left and right), and Purkinje fibres.
○ These cells set a rhythm or pace for the heart.
2. Contractile Cells:
○ These cells consist of contractile proteins like actin, myosin, troponin, and tropomyosin.
○ They also contain the sarcoplasmic reticulum.
○ They make up the large portion of the heart.
○ These are the cells that generate the force that pushes blood out of the heart.
Intrinsic Cardiac Conduction System (Pathway of Action Potentials):
The normal conduction pathway starts with the pacemaker of the heart:
1. SA Node (Sinoatrial Node):
○ Located in the superior component of the right atrium, just beneath the superior vena cava.
○ It is a crescent-shaped structure composed of nodal cells.
○ It is the pacemaker and sets the sinus rhythm.
○ The SA node generally sets the pace at around 60 to 80 beats per minute on its own, without extrinsic nervous system
influence.
○ Action potentials generated by the SA node are spread out.
2. Bachmann's Bundle:
○ A specialized structure connecting the SA node (in the right atrium) to the left atrium.
○ It allows electrical potentials from the SA node to activate/depolarise the left atrium.
3. Internodal Pathway:
○ Fibers coming from the SA node that stimulate different parts of the right atrium.
○ Both Bachmann's bundle and the internodal pathway ultimately converge onto the AV node.
4. AV Node (Atrioventricular Node):
○ A second important structure that receives all action potentials from the SA node (via internodal pathways and Bachmann'
bundle).
○ Located running from the right atrium into the interventricular septum.
○ Acts as a connection/gateway between the atria and ventricles.
○ The AV node introduces a delay of about 0.1 seconds before sending action potentials down to the bundle of His.
○ Significance of the delay: It allows time for the atria to contract and empty their blood into the ventricles before the
ventricles contract. This coordinated contraction is essential for efficient blood pumping.
○ Reasons for the delay: The AV node has fewer Gap Junctions compared to other nodal cells, which slows down ion flow. It
fibers also have a smaller diameter, which reduces conduction speed.
5. Bundle of His (AV Bundle):
○ Receives action potentials from the AV node.
○ Located in the interventricular septum.
6. Bundle Branches:
○ The bundle of His conducts impulses into two bundle branches: the right bundle branch (going to the right myocardium)
and the left bundle branch (going to the left myocardium).
7. Purkinje Fibres:
○ Specialised structures that branch off the bundle branches and dig into small components of the myocardium.
○ They supply different components within the myocardium and trigger the myocardium to contract.
Cellular Electrophysiology:
The heart's electrical activity is driven by ion movement across the cell membrane.
• Intercalated Discs: Structures connecting cardiac cells together. They are composed of Gap Junctions and Desmosomes.
Cardiovascular system Page 1
, • Intercalated Discs: Structures connecting cardiac cells together. They are composed of Gap Junctions and Desmosomes.
○ Gap Junctions: Channels (made of connexin proteins) that allow ions to pass directly from cell to cell. They are the
communication gateway between nodal cells, other nodal cells, and contractile cells.
○ Desmosomes: Structural proteins (like cadherin, desmoplakin, actin) that act as adhesion molecules, keeping cells tightly
connected and preventing separation during stretching.
• Functional Syncytium: Because cardiac muscle cells are interconnected by Gap Junctions, ions flow rapidly between them,
causing them to depolarise and contract as a unit or not contract at all. This unit contraction is called the action of the functional
syncytium.
Nodal Cell Action Potential (SA node):
Nodal cells (like the SA node) have a different action potential compared to contractile cells. They do not have a stable resting
membrane potential.
1. Slow Depolarisation (Pacemaker Potential):
○ Starts around -60 mV.
○ Funny Sodium Channels: Leaky channels that allow sodium (Na+) to slowly leak into the cell, making the inside more
positive.
○ As the membrane potential approaches threshold (around -55 mV), T-type Calcium Channels open. These allow calcium
(Ca2+) to flow in slowly, further depolarising the cell.
2. Rapid Depolarisation:
○ When the membrane potential reaches threshold (-40 mV), L-type Calcium Channels open.
○ Calcium floods into the cell very powerfully, causing rapid depolarisation.
○ The membrane potential rises quickly to about +40 mV.
3. Repolarisation:
○ At around +40 mV, the L-type Calcium Channels shut off.
○ Potassium (K+) Channels open powerfully, allowing potassium to exit the cell.
○ Losing positive potassium ions causes the inside of the cell to become more negative, leading to repolarisation.
○ The membrane potential drops towards -60 mV.
4. Return to Beginning:
○ Around -60 mV, the potassium channels close, and the funny sodium channels start opening again, beginning the next cycle
of slow depolarisation.
Contractile Cell Action Potential:
Contractile cells (like ventricular myocytes) have a stable resting membrane potential and a different action potential shape compared
to nodal cells.
1. Phase 4 (Resting Membrane Potential):
○ Stable resting membrane potential between -85 to -90 mV.
○ Maintained primarily by the slow leak of potassium ions.
○ Positive ions (cations like sodium and calcium) flowing from nodal cells via Gap Junctions cause the membrane potential to
rise towards threshold.
2. Phase 0 (Rapid Depolarisation):
○ When the membrane potential reaches threshold potential (around -70 mV), voltage-gated Sodium (Na+) Channels blast
open.
○ Sodium floods into the cell very fast, causing rapid depolarisation.
○ The membrane potential rises quickly to about +10 mV.
3. Phase 1 (Initial Repolarisation):
○ At around +10 mV, the voltage-gated Sodium Channels inactivate (close).
○ Some Potassium (K+) Channels open, allowing potassium ions to exit the cell.
○ A little bit of calcium might also start slowly trickling in through calcium channels.
○ More potassium leaves than calcium enters, causing a slight drop in membrane potential from +10 mV to around 0 mV.
4. Phase 2 (Plateau Phase):
○ Hitting 0 mV stimulates L-type Calcium Channels to become more active and open powerfully.
○ Calcium (Ca2+) flows into the cell.
○ At the same time, Potassium (K+) is still leaving the cell.
○ Because positive ions are entering (Ca2+) and positive ions are leaving (K+) at roughly equal rates, the membrane potential
plateaus for a relatively long period (about 250 milliseconds) around 0 mV.
○ This plateau is crucial because the calcium influx during this phase triggers muscle contraction.
5. Phase 3 (Repolarisation):
○ The L-type Calcium Channels start closing.
○ Potassium (K+) Channels open even more powerfully, allowing potassium ions to aggressively exit the cell.
○ With calcium influx reduced and potassium efflux increased, the inside of the cell becomes increasingly negative, leading to
rapid repolarisation.
○ The membrane potential drops back down to the resting membrane potential of -85 to -90 mV.
Excitation-Contraction Coupling (How action potential leads to contraction):
Cardiovascular system Page 2
Sunday, June 1, 2025 1:58 PM
Intrinsic conduction of the heart
Key Concepts:
• Electrophysiology: The study of electrical properties of biological cells and tissues.
• Automaticity: The intrinsic ability of the heart to spontaneously depolarise itself and trigger action potentials. These action
potentials are spread throughout the entire myocardium to trigger muscle contraction. This ability doesn't depend on the
nervous system for its basic function.
Myocardium Components:
The myocardium (the muscle layer of the heart) is made up of two main components:
1. Nodal Cells:
○ These are non-contractile cells.
○ They are the cells that generate automaticity.
○ They can spontaneously depolarise and generate action potentials.
○ Examples include the SA node, AV node, AV bundle (bundle of His), bundle branches (left and right), and Purkinje fibres.
○ These cells set a rhythm or pace for the heart.
2. Contractile Cells:
○ These cells consist of contractile proteins like actin, myosin, troponin, and tropomyosin.
○ They also contain the sarcoplasmic reticulum.
○ They make up the large portion of the heart.
○ These are the cells that generate the force that pushes blood out of the heart.
Intrinsic Cardiac Conduction System (Pathway of Action Potentials):
The normal conduction pathway starts with the pacemaker of the heart:
1. SA Node (Sinoatrial Node):
○ Located in the superior component of the right atrium, just beneath the superior vena cava.
○ It is a crescent-shaped structure composed of nodal cells.
○ It is the pacemaker and sets the sinus rhythm.
○ The SA node generally sets the pace at around 60 to 80 beats per minute on its own, without extrinsic nervous system
influence.
○ Action potentials generated by the SA node are spread out.
2. Bachmann's Bundle:
○ A specialized structure connecting the SA node (in the right atrium) to the left atrium.
○ It allows electrical potentials from the SA node to activate/depolarise the left atrium.
3. Internodal Pathway:
○ Fibers coming from the SA node that stimulate different parts of the right atrium.
○ Both Bachmann's bundle and the internodal pathway ultimately converge onto the AV node.
4. AV Node (Atrioventricular Node):
○ A second important structure that receives all action potentials from the SA node (via internodal pathways and Bachmann'
bundle).
○ Located running from the right atrium into the interventricular septum.
○ Acts as a connection/gateway between the atria and ventricles.
○ The AV node introduces a delay of about 0.1 seconds before sending action potentials down to the bundle of His.
○ Significance of the delay: It allows time for the atria to contract and empty their blood into the ventricles before the
ventricles contract. This coordinated contraction is essential for efficient blood pumping.
○ Reasons for the delay: The AV node has fewer Gap Junctions compared to other nodal cells, which slows down ion flow. It
fibers also have a smaller diameter, which reduces conduction speed.
5. Bundle of His (AV Bundle):
○ Receives action potentials from the AV node.
○ Located in the interventricular septum.
6. Bundle Branches:
○ The bundle of His conducts impulses into two bundle branches: the right bundle branch (going to the right myocardium)
and the left bundle branch (going to the left myocardium).
7. Purkinje Fibres:
○ Specialised structures that branch off the bundle branches and dig into small components of the myocardium.
○ They supply different components within the myocardium and trigger the myocardium to contract.
Cellular Electrophysiology:
The heart's electrical activity is driven by ion movement across the cell membrane.
• Intercalated Discs: Structures connecting cardiac cells together. They are composed of Gap Junctions and Desmosomes.
Cardiovascular system Page 1
, • Intercalated Discs: Structures connecting cardiac cells together. They are composed of Gap Junctions and Desmosomes.
○ Gap Junctions: Channels (made of connexin proteins) that allow ions to pass directly from cell to cell. They are the
communication gateway between nodal cells, other nodal cells, and contractile cells.
○ Desmosomes: Structural proteins (like cadherin, desmoplakin, actin) that act as adhesion molecules, keeping cells tightly
connected and preventing separation during stretching.
• Functional Syncytium: Because cardiac muscle cells are interconnected by Gap Junctions, ions flow rapidly between them,
causing them to depolarise and contract as a unit or not contract at all. This unit contraction is called the action of the functional
syncytium.
Nodal Cell Action Potential (SA node):
Nodal cells (like the SA node) have a different action potential compared to contractile cells. They do not have a stable resting
membrane potential.
1. Slow Depolarisation (Pacemaker Potential):
○ Starts around -60 mV.
○ Funny Sodium Channels: Leaky channels that allow sodium (Na+) to slowly leak into the cell, making the inside more
positive.
○ As the membrane potential approaches threshold (around -55 mV), T-type Calcium Channels open. These allow calcium
(Ca2+) to flow in slowly, further depolarising the cell.
2. Rapid Depolarisation:
○ When the membrane potential reaches threshold (-40 mV), L-type Calcium Channels open.
○ Calcium floods into the cell very powerfully, causing rapid depolarisation.
○ The membrane potential rises quickly to about +40 mV.
3. Repolarisation:
○ At around +40 mV, the L-type Calcium Channels shut off.
○ Potassium (K+) Channels open powerfully, allowing potassium to exit the cell.
○ Losing positive potassium ions causes the inside of the cell to become more negative, leading to repolarisation.
○ The membrane potential drops towards -60 mV.
4. Return to Beginning:
○ Around -60 mV, the potassium channels close, and the funny sodium channels start opening again, beginning the next cycle
of slow depolarisation.
Contractile Cell Action Potential:
Contractile cells (like ventricular myocytes) have a stable resting membrane potential and a different action potential shape compared
to nodal cells.
1. Phase 4 (Resting Membrane Potential):
○ Stable resting membrane potential between -85 to -90 mV.
○ Maintained primarily by the slow leak of potassium ions.
○ Positive ions (cations like sodium and calcium) flowing from nodal cells via Gap Junctions cause the membrane potential to
rise towards threshold.
2. Phase 0 (Rapid Depolarisation):
○ When the membrane potential reaches threshold potential (around -70 mV), voltage-gated Sodium (Na+) Channels blast
open.
○ Sodium floods into the cell very fast, causing rapid depolarisation.
○ The membrane potential rises quickly to about +10 mV.
3. Phase 1 (Initial Repolarisation):
○ At around +10 mV, the voltage-gated Sodium Channels inactivate (close).
○ Some Potassium (K+) Channels open, allowing potassium ions to exit the cell.
○ A little bit of calcium might also start slowly trickling in through calcium channels.
○ More potassium leaves than calcium enters, causing a slight drop in membrane potential from +10 mV to around 0 mV.
4. Phase 2 (Plateau Phase):
○ Hitting 0 mV stimulates L-type Calcium Channels to become more active and open powerfully.
○ Calcium (Ca2+) flows into the cell.
○ At the same time, Potassium (K+) is still leaving the cell.
○ Because positive ions are entering (Ca2+) and positive ions are leaving (K+) at roughly equal rates, the membrane potential
plateaus for a relatively long period (about 250 milliseconds) around 0 mV.
○ This plateau is crucial because the calcium influx during this phase triggers muscle contraction.
5. Phase 3 (Repolarisation):
○ The L-type Calcium Channels start closing.
○ Potassium (K+) Channels open even more powerfully, allowing potassium ions to aggressively exit the cell.
○ With calcium influx reduced and potassium efflux increased, the inside of the cell becomes increasingly negative, leading to
rapid repolarisation.
○ The membrane potential drops back down to the resting membrane potential of -85 to -90 mV.
Excitation-Contraction Coupling (How action potential leads to contraction):
Cardiovascular system Page 2
