Cardiovascular | Electrophysiology | Intrinsic Cardiac Conduction System

Name: Cardiovascular | Electrophysiology | Intrinsic Cardiac Conduction System
Uploaded: 2017-08-03T18:42:36.000Z
Duration: 1 h 36 min 1 s

Introduction to Electrophysiology

In this section, the speaker introduces the topic of electrophysiology and explains why it is important in understanding the functioning of the heart.

The Heart's Intrinsic Ability - Automaticity

The heart has the unique ability to depolarize itself without relying on the nervous system.

This intrinsic ability is known as automaticity.

Automaticity allows the heart to spontaneously depolarize and trigger action potentials that spread throughout the myocardium (muscle layer of the heart), leading to contraction.

Components of Myocardium

The myocardium is composed of two types of cells: nodal cells and contractile cells.

Nodal cells are non-contractile cells responsible for generating automaticity and action potentials. Examples include SA node, AV node, AV bundle (bundle of His), bundle branches, and Purkinje fibers.

Contractile cells make up a major portion of the myocardium and consist of contractile proteins such as actin, myosin, troponin, tropomyosin, and sarcoplasmic reticulum. They generate force for pumping blood out of the heart.

Pacemaker Cells - SA Node

This section focuses on pacemaker cells called SA nodes and their location within the heart.

Location of SA Node

The SA node is located in the superior part of the right atrium, just beneath the superior vena cava.

It appears as a crescent-shaped structure consisting of nodal cells.

Function of SA Node

The SA node acts as a pacemaker by setting what is known as sinus rhythm.

Sinus rhythm refers to a normal heart rate range between 60 to 80 beats per minute generated by the SA node without any external innervation.

Summary and Conclusion

This section provides a summary of the key points discussed in the video.

Electrophysiology is crucial for understanding the heart's intrinsic ability to depolarize itself (automaticity) and trigger action potentials.

The myocardium consists of nodal cells responsible for generating automaticity and contractile cells responsible for contraction.

The SA node, located in the right atrium, acts as a pacemaker by setting sinus rhythm.

Sinus rhythm refers to the normal heart rate range of 60 to 80 beats per minute generated by the SA node without external innervation.

Timestamps are approximate and may vary slightly.

New Section

This section discusses the normal conduction pathway of the heart, including the SA node, Bachmann's bundle, internodal pathways, and the AV node.

Normal Conduction Pathway

The SA node generates action potentials to trigger the heart to beat at a rate of 60-80 times per minute. It is located in the right atrium.

The SA node sends electrical signals to the left atrium through a specialized structure called Bachmann's bundle. This allows for depolarization of both atria.

Internodal pathways connect different parts of the atria and stimulate various areas. They eventually converge onto the AV node.

The AV node is an important structure located near the interventricular septum. It acts as a gateway between the atria and ventricles. Some action potentials from Bachmann's bundle reach the AV node as well.

New Section

This section explains how the AV node functions and its significance in delaying action potentials.

Function of AV Node

Action potentials from Bachmann's bundle and internodal pathways converge onto the AV node.

The AV node has a delay of approximately 0.1 seconds before sending action potentials down through the interventricular septum to the bundle of His.

This delay allows time for atrial contraction before ventricular contraction, ensuring efficient blood flow through proper coordination between chambers.

New Section

This section discusses microscopic reasons for why nodal cells in the AV node have numerous gap junctions.

Microscopic Reasons for Gap Junctions in AV Node

The AV node consists of a bundle of nodal cells that are rich in gap junctions.

Gap junctions allow ions to pass from cell to cell, facilitating the conduction of electrical signals through the AV node.

New Section

This section discusses the cardiac conduction system and the flow of electrical signals through different structures in the heart.

Cardiac Conduction System

The cardiac conduction system consists of several structures that facilitate the transmission of electrical signals in the heart.

The SA node, or sinoatrial node, is the pacemaker of the heart and initiates the electrical impulses. It is located at the superior vena cava's opening into the right atrium.

From the SA node, the electrical signal travels through internodal pathways to reach the AV node, or atrioventricular node. There is a 1-second delay at this point to allow time for atrial contraction before ventricular contraction.

The AV node has fewer gap junctions and smaller diameter muscle fibers compared to other structures, resulting in a slower conduction speed.

After passing through the AV node, the electrical signal enters a bundle called the bundle of His or AV bundle. From there, it divides into right and left bundle branches.

The right bundle branch conducts signals to the right myocardium, while the left bundle branch conducts signals to the left myocardium.

Finally, small branching units called Purkinje fibers distribute electrical signals throughout different parts of the myocardium, triggering contraction.

New Section

This section further explains how each structure in the cardiac conduction system contributes to generating action potentials.

Nodal Cell and Contractile Cell Communication

Nodal cells are connected via gap junctions, allowing ions to pass from cell to cell within nodal tissue. This facilitates coordinated electrical activity.

Gap junctions also exist between nodal cells and contractile cells, enabling the flow of ions from nodal cells to contractile cells. This helps initiate depolarization in contractile cells.

New Section

The focus now shifts to understanding how action potentials are generated within nodal and contractile cells.

Nodal Cell Action Potentials

Nodal cells have a unique property called automaticity, allowing them to spontaneously generate action potentials without external stimulation.

These action potentials are generated due to the interplay of various ion channels, including calcium and potassium channels.

Contractile Cell Action Potentials

Contractile cells are responsible for the actual contraction of the heart muscle. They generate action potentials through a different mechanism compared to nodal cells.

The action potential in contractile cells involves the opening and closing of sodium, potassium, and calcium channels, leading to depolarization and repolarization phases.

New Section

This section explores the cellular connections between nodal and contractile cells.

Cellular Connections

Gap junctions play a crucial role in connecting nodal cells with each other as well as with contractile cells. They allow ions to flow between these cell types, facilitating coordinated electrical activity.

Funny Sodium Channels and Calcium Channels

This section explains the role of funny sodium channels and calcium channels in nodal cells, focusing on their impact on membrane potential.

Funny Sodium Channels

Funny sodium channels are leaky channels in nodal cells that allow a slow influx of sodium ions into the cell.

Nodal cells do not have a stable resting membrane potential, but generally have a membrane potential around -60 millivolts.

The opening of funny sodium channels causes the inside of the cell to become more positive due to the influx of positive sodium ions.

As the membrane potential approaches the threshold potential (around -55 millivolts), t-type calcium channels open, allowing calcium ions to enter slowly.

Calcium Channels

T-type calcium channels open around -55 millivolts when stimulated by the influx of sodium ions.

The combined effect of funny sodium channels and t-type calcium channels leads to further depolarization of the cell.

When the threshold potential (-40 millivolts) is reached, l-type calcium channels open, resulting in a rapid influx of calcium ions.

The influx of calcium ions causes a significant increase in membrane potential, reaching approximately +40 millivolts.

Overall Result

The activation of funny sodium channels and subsequent opening of t-type and l-type calcium channels lead to depolarization of nodal cells.

This depolarization does not require nervous system functioning and contributes to cellular activity.

Impact on Contractile Cells

This section explores how the depolarization caused by ion channel activity affects contractile cells through gap junctions.

Accumulation

The depolarization in nodal cells results in an accumulation of positive charges within these cells.

Impact on Contractile Cells

Gap junctions connect nodal cells with contractile cells.

The depolarization of nodal cells spreads through gap junctions to the contractile cells.

This depolarization triggers the contraction of the contractile cells, leading to muscle activity.

Summary

This section provides a summary of the key points discussed in the transcript.

Funny sodium channels in nodal cells allow a slow influx of sodium ions, leading to membrane depolarization.

T-type calcium channels open as the membrane potential approaches the threshold potential, further contributing to depolarization.

L-type calcium channels open at the threshold potential, causing a rapid influx of calcium ions and significant membrane depolarization.

The depolarization in nodal cells spreads through gap junctions to contractile cells, triggering muscle contraction.

Timestamps are provided for each section and bullet point.

Desmosomes and Gap Junctions in Cardiac Cells

This section discusses the role of desmosomes and gap junctions in cardiac cells, focusing on their structure and function.

Desmosomes

Desmosomes are special structural proteins that tightly connect cardiac cells.

They consist of various proteins, including catenins for cell-to-cell communication and attachment plaques.

Desmosomes act as adhesion molecules, keeping the cells tightly connected.

Gap Junctions

Gap junctions are protein connections between nodal cells and contractile cells in the heart.

These connections allow positive ions to move from cell to cell through gap junctions.

The influx of positive ions helps bring the membrane potential closer to threshold potential.

Intercalated Discs

When gap junctions and desmosomes combine, they form intercalated discs.

Intercalated discs are composed of a network of gap junctions and desmosomes connecting cardiac cells.

Depolarization and Resting Membrane Potential

This section explains depolarization in cardiac cells and discusses resting membrane potential.

Depolarization Process

Positive ions entering the contractile cell through gap junctions bring the resting membrane potential closer to threshold potential.

Threshold potential is approximately -70 millivolts within these cells.

Voltage-gated sodium channels open at threshold potential, allowing sodium ions to flow into the cell rapidly.

The influx of sodium ions causes the inside of the cell to become highly positive.

Sarcolemma and Wave-like Movement

The sarcolemma is the muscle cell membrane in cardiac cells.

As positive charges move across the sarcolemma, a wave-like movement occurs around the muscle cell membrane.

New Section

This section discusses the process of depolarization in a cell, focusing on the opening and closing of different channels and the movement of ions.

Depolarization Process

At approximately positive 10 millivolts, sodium channels open and sodium ions start entering the cell, causing depolarization.

Along with sodium channels, calcium channels also open slightly, allowing a small amount of calcium to enter the cell.

As depolarization continues, more calcium channels open and calcium ions start flowing into the cell along with sodium ions.

When the membrane potential reaches positive 10 millivolts, sodium channels close (inactivate).

Potassium channels then open up as the cell becomes highly depolarized at positive 10 millivolts. Potassium ions start leaving the cell.

As potassium ions leave, there is a slight drop in membrane potential from around 10 millivolts to zero.

At zero millivolts, voltage-gated calcium channels become more active and allow an influx of calcium ions into the cell.

Simultaneously, potassium ions continue to leave the cell while calcium ions enter. This results in a plateau phase where there is no significant change in membrane potential for about 250 milliseconds.

New Section

In this section, additional details about ion movements during depolarization are discussed.

Ion Movements during Depolarization

During depolarization, positive calcium ions enter the cell through L-type calcium channels.

At the same time, potassium ions continue to leave the cell.

The simultaneous movement of positive ions entering (calcium) and leaving (potassium) results in no significant change in membrane potential.

This plateau phase lasts for about 250 milliseconds, during which the cell remains depolarized or plateaued.

New Section

This section introduces the phases of depolarization and provides terminology related to ion movements.

Phases and Terminology

The depolarization phase where sodium ions enter the cell is referred to as phase zero.

The subsequent drop in membrane potential due to potassium channels opening and potassium leaving is called phase one.

The plateau phase, where calcium enters and potassium continues to leave, is not assigned a specific phase number.

The transcript does not provide further information beyond this point.

New Section

This section explains how calcium ions trigger the release of other calcium ions in muscle cells.

Calcium-induced Release Mechanism

Calcium ions flow into the cell through a structure called T tubules.

These calcium ions then move to a specialized organelle called the sarcoplasmic reticulum.

Within the sarcoplasmic reticulum, calcium-sensitive channels are present. One of these channels is called the ryanodine receptor type II.

When there is an increase in calcium levels, the ryanodine receptor opens up and releases more calcium ions into the sarcoplasm.

Role of Calcium in Muscle Contraction

Calcium binds to a protein called troponin, which consists of three components: troponin C, troponin T, and troponin I.

The binding of calcium to troponin C changes its shape and allows for interaction between myosin and actin proteins.

This interaction leads to an increase in cross bridges between myosin and actin, resulting in muscle contraction.

Synchronization of Muscle Cells

Muscle cells are interconnected through gap junctions, allowing for rapid signal transmission.

When one muscle cell receives a signal, neighboring cells also depolarize simultaneously, leading to synchronized action.

New Section

This section discusses the concept of a functional syncytium in the myocardium and how cells reach their resting state.

How Cells Contract as a Unit

The myocardium contracts as a unit due to gap junctions between cells, creating a functional syncytium.

Reaching Resting State

Voltage-gated calcium channels close at positive 40 millivolts, leading to the opening of potassium channels. Potassium exits the cell, causing it to become more negative and repolarize.

As potassium ions leave the cell, it becomes more negative and reaches the resting membrane potential around negative 60 millivolts. However, this potential is not stable. Sodium channels start opening again around negative 60 millivolts, leading to repolarization.

During the plateau phase, calcium ions enter the cell while potassium ions exit. Calcium ion channels eventually close, preventing excessive muscle contraction.

To replenish calcium levels and allow for muscle rest, calcium is pumped back into the sarcoplasmic reticulum (SR) through special channels that require ATP. Sodium can also help move calcium back into the SR through secondary active transport.

Calcium can be pumped out of the SR into the extracellular fluid using ATP-dependent primary active transport mechanisms involving proton exchange or sodium movement down its concentration gradient. This process replenishes calcium levels outside of the cell and inside the SR.

New Section

This section explains how calcium is moved against its concentration gradient to maintain proper levels inside and outside of cells.

Moving Calcium Against Concentration Gradient

Special black channels in the sarcoplasmic reticulum (SR) pump calcium back into the SR, requiring ATP and often involving proton exchange.

Red channels can also help pump calcium back into the SR by utilizing sodium movement down its concentration gradient. This is an example of secondary active transport.

The same channels that move calcium into the SR can also pump it out into the extracellular fluid, again using ATP-dependent primary active transport mechanisms. Sodium movement down its concentration gradient assists in this process.

The transcript provided does not include any further sections or timestamps beyond this point.

New Section

This section discusses the movement of potassium and calcium ions in the heart muscle, leading to changes in membrane potential.

Potassium and Calcium Ion Movement

The potassium channels start moving out more aggressively, causing a loss of positive ions.

Without counteracting calcium ions, the membrane potential drops until it reaches resting membrane potential.

At resting membrane potential, there is a brief period where the membrane stays rested.

Ions from neighboring cells can leak into the cell via gap junctions, triggering the threshold potential.

Phase two is known as the plateau phase, involving both calcium and potassium channels.

Phase four is characterized by no sodium or calcium ion movement, with only slow leakage of potassium ions to maintain stable resting membrane potential.

New Section

This section explains how the intrinsic ability of the heart communicates through its muscle fibers.

Intrinsic Ability of the Heart

The intrinsic ability refers to how the heart muscle functions without external influences.

Understanding electrophysiology helps comprehend this intrinsic ability.

Part two will delve into extrinsic innervation and its impact on heart rate regulation.

New Section

This section explores the extrinsic innervation of the heart and its effects on heart rate.

Extrinsic Innervation of the Heart

Extrinsic innervation can modify the baseline intrinsic ability of the heart.

It can increase heart rate above basal rate or decrease it below basal rate (bradycardia).