Building on our understanding of cardiac cells, let’s explore how their electrical activity translates into the heart’s mechanical performance and how this is reflected on an electrocardiogram (EKG).
The Sinoatrial (SA) Node and the P Wave
The Sinoatrial (SA) node is the heart’s primary pacemaker, located in the right atrium.
Initiating the Impulse: The SA node generates an electrical impulse that spreads across the atria. Note that the impulse generated by the SA node is not seen on an EKG!
Atrial Contraction: This impulse causes the atrial myocardial cells to depolarize and contract, pushing blood into the ventricles.
EKG Representation: The atrial depolarization is represented by the P wave on an EKG. The P wave reflects the electrical activity from the start to the finish of atrial depolarization. The P-wave is best interpreted in leads II and V1.
In II, the initial part of the P-wave represents the conduction in the right atrium, the terminal part represents conduction in the left atrium, and the middle part represents conduction in both atria.
In V1, the initial positive deflection reflects right atrial depolarization while the terminal negative deflection reflects the left atrial depolarization. More on this as we go on.
The Atrioventricular (AV) Node: The Gatekeeper
After the atria contract, the electrical impulse reaches the Atrioventricular (AV) node.
Impulse Delay: The AV node slows down the impulse, ensuring that the ventricles have enough time to fill with blood before they contract. This gives the atria enough time to complete contracting and filling the ventricles.
Regulation: The AV node is influenced by the autonomic nervous system. Sympathetic stimulation (e.g., during exercise or stress) can speed up conduction, while parasympathetic stimulation (e.g., during rest) can slow it down.
The Bundle of His, Bundle Branches, and Purkinje Fibers
From the AV node, the impulse travels to the ventricles via specialized pathways.
Bundle of His: This pathway divides quickly into the right and left bundle branches.
Right Bundle Branch: The right branch carries the impulse through the right side of the inter-ventricular septum and the right ventricle.
Left Bundle Branch: The left bundle further divides into the septal fascicle, depolarizing the inter-ventricular septum from left to right, the anterior fascicle sweeping the anterior surface of the left ventricle, and the posterior fascicle covering the posterior surface of the left ventricle.
These branches branch out into countless Purkinje fibers that deliver the electrical cues to the ventricular myocardium.
Purkinje Fibers: These fibers spread throughout the ventricles, allowing rapid transmission of the impulse.
Coordination: This electrical network ensures that both ventricles contract simultaneously and efficiently.
The QRS Complex: Ventricular Depolarization
The depolarization of the ventricles is captured on the EKG as the QRS complex– As the name suggests, it may have several waves.
Components:
Q Wave: The first negative deflection, if any. In a normal EKG, the initial small negative deflection of the QRS complex reflects the interventricular septum’s depolarization by the septal fascicle of the left bundle branch. This usually moves from left to right across the inter-ventricular septum.
R Wave: The first positive deflection, if any, indicating the main phase of ventricular depolarization. If there’s a second upward deflection, that’s termed the R′ (R-prime).
S Wave: A negative deflection following the R wave, representing the final phase of ventricular depolarization.
QS Complex: If the only deflection is negative, we call it a QS wave.
Because the left ventricle has significantly more muscle than the right ventricle, most of the electric activity we see in the QRS complex of a normal heart is from the left ventricle’s electrical activity.
Significance: The shape and size of the QRS complex provide vital information about ventricular health and conduction pathways.
Small waves may be represented in a lower-case letter and large waves in an upper-case letter. So qR implies a small Q-wave and a prominent R-wave.
Refractory Period
After depolarization, the myocardial cells take a short break, a refractory period where they’re immune to further stimulation.
Absolute refractory period: From the end of QRS to the early to mid T wave, when cardiac cells have not fully recovered and a premature beat cannot cause another beat.
Relative refractory period: The mid to end of the T wave, when cardiac cells are “hyper-polarized” and a premature beat can initiate depolarization. This causes an R-wave to fall on a T-wave (the R on T phenomenon) which could trigger a life-threatening ventricular arrhythmia such as ventricular tachycardia or ventricular fibrillation.
Repolarization and the T Wave
After depolarization and following the refractory period, the ventricles repolarize, returning to their resting state.
Repolarization Process: Ventricular myocardial cells restore their negative internal charge.
EKG Representation: This phase is shown as the T wave on the EKG.
Importance: The T wave indicates that the heart muscle is ready for the next heartbeat.
The Complete EKG Cycle
An EKG cycle reflects the entire process of a heartbeat.
P Wave: Atrial depolarization and contraction.
PR Interval: Delay at the AV node.
QRS Complex: Ventricular depolarization and contraction.
ST Segment and T Wave: Ventricular repolarization.
In our previous articles, we explored the various types of cardiac cells and their roles in sustaining the heart’s rhythm. Now, we’ll delve deeper into the intricate ways these cells communicate to ensure the heart functions in a coordinated and timely manner. This complex communication is essential for the heart’s ability to efficiently pump blood throughout the body.
We needn’t understand the intricacies of the process to understand what we see on an EKG. Instead, just a few principles would suffice:
Visualizing Electrical Activity with Electrocardiogram (EKG/ECG)
The heart’s electrical activity can be monitored and recorded using an electrocardiogram.
How EKG Leads Detect Electrical Activity
Depolarization Toward a Lead:
When a wave of depolarization moves toward a positive electrode, it produces an upward (positive) deflection on the EKG.
Depolarization Away from a Lead:
When it moves away from a positive electrode, it results in a downward (negative) deflection.
Repolarization:
The opposite occurs during repolarization; moving toward a lead causes a negative deflection, and moving away causes a positive deflection.
Multiple Leads:
By placing electrodes in different positions, we can view the heart’s electrical activity from various angles, providing a comprehensive picture.
EKG Waves Correspond to Cardiac Events
P Wave: Represents atrial depolarization.
PR Interval: Time from the onset of atrial depolarization to the onset of ventricular depolarization.
QRS Complex: Reflects ventricular depolarization (Atrial repolarization is lost in the QRS complex since the voltage is much smaller compared to the voltage of the QRS, in case you wondered where that went!).
T Wave: Indicates ventricular repolarization.
If you are a curious learner who wants to understand the intricacies, keep reading!
Our cells, when resting, are polarized- they are negatively charged on the inside. The obvious question then is:
Why Are Cells Negatively Charged Inside?
There is an uneven Ion Distribution Across the Cell Membrane
Inside the Cell:
High concentration of potassium ions (K⁺).
Presence of large, negatively charged molecules like proteins and DNA that cannot cross the cell membrane.
Outside the Cell:
Higher concentration of sodium ions (Na⁺) and chloride ions (Cl⁻).
Selective Permeability of the Cell Membrane
The cell membrane acts as a selective barrier, allowing certain ions to pass through more easily than others. This permeability depends on:
The types of ions.
The types of active channels.
The membrane potential (how negative the inside of the cell is).
Other regulatory factors.
The Sodium-Potassium Pump (Na⁺/K⁺-ATPase)
The sodium-potassium pump is critical in maintaining the cell’s negative internal charge. It uses energy (ATP) and pumps 3 sodium ions (Na⁺) out of the cell and brings 2 potassium ions (K⁺) into the cell. In essence, more positive charges are pumped out than brought in, keeping the inside of the cell negative. Without this pump, ion concentrations would eventually equalize, eliminating the membrane potential necessary for cellular functions.
Importance of the Negative Internal Charge
Electrical Signaling:
The difference in charge across the membrane (resting membrane potential) is crucial for generating action potentials- the electrical signals that enable nerve impulses and muscle contractions.
A pacemaker cell depolarizes spontaneously and becomes more positive on the inside- when this happens, the cell next to it follows suit, and then the next, and so on.
The Pacemaker Cells: Setting the Heart’s Rhythm
Pacemaker cells are responsible for initiating the heart’s rhythmic contractions. This is because they have the highest intrinsic frequency (i.e., they beat the fastest and hence set the pace). The cells in the SA node have the highest intrinsic frequency of all the pacemaker cells and normally set the pace for the heart.
Unstable Resting Membrane Potential
Unlike most other cells, pacemaker cells do not have a stable resting membrane potential (other cells such as skeletal muscles and cardiac myocytes have a stable resting membrane potential unless they are stimulated)
They exhibit automaticity– even without being stimulated, the membrane potential gradually becomes less negative until it reaches the threshold to trigger an action potential.
The automaticity in the pacemaker cells drives depolarization or the loss of polarization within the cell (so the inside of the cell starts losing the excess negative charge).
Key Ion Channels in Pacemaker Cells and the process of depolarization
a. “Funny” Channels
Activation:
Open spontaneously when the membrane potential is hyper-polarized (more negative), around -60 mV.
Function:
Allow a slow influx of sodium ions (Na⁺) and a minimal efflux of potassium ions (K⁺).
Effect:
Causes gradual depolarization as more sodium enters than potassium exits.
b. T-Type Calcium Channels (Transient-Type)
Activation:
Open as the membrane potential becomes less negative, around -50 mV.
Function:
Permit a brief influx of calcium ions (Ca²⁺).
Effect:
Further depolarizes the cell, bringing it closer to the threshold for an action potential.
c. L-Type Calcium Channels (Long-Lasting)
Activation:
Open when the membrane potential reaches the threshold, around -40 mV.
Function:
Allow a rapid and significant influx of calcium ions (Ca²⁺).
Effect:
Generates the upstroke of the action potential, fully depolarizing the cell.
Repolarization: Resetting the Pacemaker Cell so the inside is negative again
Closure of L-Type Calcium Channels:
As the cell is fully depolarized, the L-type channels close and this stops the influx of calcium ions.
Opening of Voltage-Gated Potassium Channels:
Allows potassium ions (K⁺) to exit the cell.
Result:
The membrane potential becomes more negative, returning to its hyperpolarized state (~ -60 mV).
Cycle Restarts: Continuous Rhythmic Activity
Reactivation of Funny Channels:
Once the membrane potential is hyperpolarized, funny channels reopen, and the cycle begins anew.
Autonomous Rhythm:
This process enables the heart to beat continuously without conscious input.
How Pacemaker Signals Spread Through the Heart
Depolarization of the SA Node
The action potential originates in the sinoatrial (SA) node pacemaker cells.
While many cells in the heart can serve as pacemakers, the SA node has the highest rate and sets the pace.
Note: Under most conditions, pacemaker and conducting cells have automaticity—cardiac myocytes typically don’t.
Conduction from cell to cell
The electrical impulse spreads through the heart from one cell to another via gap junctions.
Gap junctions are specialized structures that form direct connections between neighboring cells, allowing the exchange of ions. When one cell depolarizes, connected cells also depolarize because of a flow of positive charges from one cell to the next!
Subsequently the entire atria depolarize.
Atrioventricular (AV) Node
The impulse reaches the AV node, where it is briefly delayed to allow the ventricles time to fill with blood as the atria complete contracting.
His-Purkinje System
The impulse travels down the Bundle of His, divides into right and left bundle branches, and eventually spreads through the Purkinje fibers.
Ventricular Contraction
The ventricles depolarize and contract in a coordinated manner, effectively pumping blood to the lungs and the rest of the body.
But what causes the activated myocytes to contract?
Depolarization and repolarization of myocytes and Excitation- Contraction Coupling
The heart pumps blood through a sequence of electrical and mechanical events that cause the myocytes to contract. These events connect electrical signals(depolarization and repolarization) to muscle contraction in a process called excitation-contraction coupling (ECC). Here’s a simple explanation:
Electrical Excitation: Depolarization
How It Happens:
Trigger: Depolarization starts when a neighboring cell’s action potential triggers the opening of voltage-gated sodium channels (Na⁺).
Sodium Influx: Voltage-gated sodium (Na⁺) channels open, allowing sodium ions to rush in. This changes the inside of the cell from negative (-90 mV) to positive (+20 mV).
Calcium Influx (Plateau Phase): L-type calcium channels open, letting calcium ions (Ca²⁺) enter. This happens after the initial sodium rush and keeps the membrane potential near 0 mV for a short time.
Purpose: This electrical signal prepares the muscle cell for contraction by triggering the release of calcium.
Linking Electrical to Mechanical: Excitation-Contraction Coupling
What Happens? The calcium that enters during the plateau phase acts as a “trigger” for contraction. Here’s how it works:
Calcium Enters the Cell: L-type calcium channels in the cell membrane allow a small amount of calcium into the cell.
Calcium-Induced Calcium Release: The small calcium influx activates ryanodine receptors (RyR) on the sarcoplasmic reticulum (SR), a storage site for calcium inside the cell. This causes a large release of calcium into the cytoplasm.
Calcium Binds to Troponin: Calcium attaches to troponin, a protein on muscle fibers. This moves another protein called tropomyosin, uncovering binding sites on actin (muscle filaments).
Cross-Bridge Formation: Myosin, another muscle protein, attaches to actin and “pulls” to shorten the muscle fiber, creating the contraction.
Electrical Reset: Repolarization
What Happens? After the contraction, the cell must return to its resting state so it’s ready for the next heartbeat. This is called repolarization.
How It Happens:
Closing of Calcium Channels: L-type calcium channels close, stopping calcium from entering the cell.
Potassium Efflux: Potassium (K⁺) channels open, letting potassium exit the cell. This removes positive charge from inside, making the cell more negative again.
Restoration: The sodium-potassium pump (Na⁺/K⁺-ATPase) and calcium pumps reset the ion levels, returning the cell to its original state (-90 mV inside).
Relaxation: Stopping Contraction
What Happens? Once repolarization begins, the heart muscle relaxes.
How It Happens:
Calcium Removed from the Cytoplasm: Calcium is pumped back into the sarcoplasmic reticulum (by SERCA pumps) or out of the cell (by calcium pumps or Na⁺/Ca²⁺ exchangers).
Troponin Releases Calcium: Without calcium, troponin allows tropomyosin to block the actin binding sites again.
No Cross-Bridges: Myosin can no longer bind to actin, so the muscle relaxes.
The Whole Process at a Glance
Electrical Signal (Depolarization): Sodium and calcium rush into the cell, “activating” it.
Trigger for Contraction (ECC): Calcium released from storage inside the cell allows actin and myosin to interact, causing contraction.
Resetting the Cell (Repolarization): Calcium stops entering, potassium leaves, and the cell returns to its resting state.
Relaxation: Calcium is removed, the contraction ends, and the muscle relaxes.
The cycle repeats…
Comparison: Pacemaker Cells vs. Cardiac Myocytes
Feature
Pacemaker/ Conduction Cells
Cardiac Myocytes (Contractile Cells)
Resting Membrane Potential
Unstable (gradually depolarizes from ~-60 mV)
Stable (~-90 mV)
Main Depolarization Ion
Calcium ions (Ca²⁺)
Sodium ions (Na⁺)
Action Potential Speed
Slow
Fast
Action Potential Shape
No plateau phase
Plateau phase present
Spontaneous Activity
Yes (automaticity)
No (requires stimulation from pacemaker cells)
Main Function
Initiate and propagate electrical impulses
Contract to pump blood
Key Takeaways
Pacemaker Cells:
Automaticity allows them to set the heart’s pace.
Use calcium ions for depolarization.
Lack a plateau phase in their action potential.
Cardiac Myocytes:
Rely on rapid sodium influx for depolarization.
Have a plateau phase due to sustained calcium influx, which prolongs the contraction.
Require stimulation from pacemaker cells to initiate contraction.
Summary
Understanding how cardiac cells communicate and synchronize their activity helps us appreciate the complex processes that keep our hearts beating efficiently.
Negative Internal Charge: Essential for generating and propagating electrical signals in cardiac cells.
Pacemaker Cells: Use specialized ion channels to spontaneously depolarize and set the heart’s rhythm.
Coordination of Heartbeats: Electrical impulses spread from pacemaker cells to contractile cells, ensuring synchronized contractions.
The human heart is a marvel of biological engineering, beating tirelessly to pump blood throughout the body. This incredible feat is made possible by different types of cardiac cells, each playing a unique role in maintaining the heart’s rhythm.
In this article, we’ll explore the three main types of cardiac cells: pacemaker cells, electrical conducting cells, and myocardial cells.
Pacemaker Cells: The Heart’s Natural Pace-Setters
Pacemaker cells are specialized cells responsible for generating the electrical impulses that set the heart’s rhythm. Think of them as the conductors of an orchestra, initiating each heartbeat by “striking the first note.” The most prominent group of pacemaker cells is located in the Sinoatrial (SA) node, situated in the right atrium of the heart.
Intrinsic Rhythm: The SA node typically fires at a rate of 60 to 100 times per minute, aligning with a normal resting heart rate.
Adaptive Rate: Pacemaker cells adjust their firing rate based on the body’s needs. For example, during exercise, they increase the heart rate to supply more oxygen-rich blood to muscles; during rest, they slow down.
Hierarchy of Pacemakers: While many cardiac cells have the potential to act as pacemakers, the cells in the SA node usually set the pace because they fire the fastest.
Electrical Conducting Cells: The Heart’s Communication Network
Once the pacemaker cells generate an electrical impulse, it needs to be rapidly transmitted throughout the heart. This is where electrical conducting cells come into play.
Impulse Transmission: These cells efficiently carry the electrical signal from the pacemaker cells to the rest of the heart muscle.
Synchronization: By ensuring the impulse reaches appropriate parts of the heart quickly, they coordinate the contraction of the atria and then the ventricles, maintaining a harmonious heartbeat.
Myocardial Cells: The Heart’s Muscle Powerhouses
Myocardial cells are the muscle cells of the heart responsible for its contraction and relaxation.
Contraction Mechanism: When stimulated by an electrical impulse, myocardial cells release calcium ions inside the cell. This triggers the cells to contract, pumping blood out of the heart.
Systole and Diastole: The rhythmic contraction and relaxation of myocardial cells correspond to systole(contraction phase) and diastole (relaxation phase).
Electrical Conduction: Although their primary function is mechanical, myocardial cells can also conduct electrical impulses, albeit more slowly than specialized conducting cells.
Backup Pacemakers: In certain situations, myocardial cells can take over pacemaker functions if the primary pacemaker cells fail.
The Electrical Cycle: Depolarization and Repolarization
Understanding the electrical properties of cardiac cells is key to comprehending how the heart functions.
Resting State: In their resting state, cardiac cells have a negative charge inside compared to the outside.
Depolarization: When an electrical impulse occurs, this charge reverses, becoming positive inside. This change spreads from cell to cell, much like a wave, leading to the contraction of the heart muscle.
Repolarization: After contraction, cells return to their resting negative charge in a process called repolarization, preparing them for the next heartbeat.
Visualizing the Heart’s Electrical Activity: The Role of EKG
The heart’s electrical activities can be recorded and visualized using an electrocardiogram (EKG or ECG).
EKG Tracing: By placing electrodes on the skin, an EKG captures the electrical signals produced by the heart, displaying them as waves on a graph.
Diagnostic Tool: EKGs are essential for diagnosing various heart conditions, as they reveal abnormalities in heart rhythm and electrical conduction.
