Cardiac Action Potentials Made Easy: Summit, Plummet, Climb, Continue
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Example Case
A male patient presents after a syncopal episode 30 minutes ago. He states he was at home cooking dinner when he began to feel lightheaded. The next thing he remembers is waking up on the kitchen floor.
He admits he has been experiencing intermittent palpitations for the past 2 days. You are concerned his syncopal episode could be from a cardiac conduction abnormality. You begin to recall the conduction system along with the types of cardiac action potentials that occur in the myocardium.
Cardiac Action Potential
An action potential is a change in voltage across a cell membrane, specifically a rise in voltage followed by a fall.
Action potentials are used to send information throughout the body, and they are also necessary for some types of cells to function as they trigger intracellular processes (such as contraction of muscle cells).
Cells that use action potentials are also called excitable cells and include: neurons, muscle cells (skeletal, cardiac, and smooth), cardiac pacemaker cells (specialized cardiac muscle cells), and endocrine cells to name a few.
This post will focus on the action potentials of cardiac pacemaker cells and cardiac muscle cells (non-pacemaker cells).
Understanding cardiac action potentials becomes clinically relevant when using antiarrhythmic drugs or managing conduction disorders.
EZmed always provides an easy way to remember medical topics.
In this post you will learn a simple catchphrase that will help you understand everything you need to know about cardiac action potentials including the different phases and what ions are involved.
Cardiac Conduction System
Let’s first begin by briefly recapping the cardiac conduction system.
Make sure to check out the EZmed blog that makes the conduction system easy! Conduction System of the Heart: The Electrical Pathway
There are 2 main processes that occur in the heart: cardiac conduction (pacemaker cells) and cardiac contraction (non-pacemaker cardiac muscle cells).
Of note: cardiac muscle cells are also called cardiac myocytes, cardiomyocytes, or myocardiocytes.
Pacemaker Cells
The pacemaker cells are specialized cardiac myocytes that are capable of generating spontaneous action potentials and are responsible for cardiac conduction.
Pacemaker cells are primarily located in the sinoatrial (SA) node and atrioventricular (AV) node.
However, they are also present in other parts of the conduction system including the bundle of His, right and left bundle branches, and Purkinje fibers.
The inherent pacemaker rate of the SA node is faster than the other pacemaker cells, and for that reason the SA node generates the initial action potential in a normal functioning heart.
If the SA node becomes suppressed, then the other pacemaker cells are capable of generating spontaneous action potentials but at a slower heart rate.
The SA node is located in the back of the right atrium near the superior vena cava entry.
The action potential generated by the SA node will travel through the right atrium and to the left atrium through Bachmann’s bundle, thereby depolarizing the atria and leading to atrial contraction.
The impulse then travels to the AV node, located at the base of the right atrium, via an internodal pathway.
Conduction velocity is slowed through the AV node long enough to allow for atrial contraction and movement of blood from the atria to the ventricles before ventricular contraction occurs.
From the AV node, the impulse will travel through the bundle of His and down the right and left bundle branches.
The right bundle branch is responsible for depolarizing the right ventricle, and the left bundle branch is responsible for depolarizing the left ventricle.
The bundle branches terminate into Purkinje fibers which also help stimulate the ventricular myocardium to contract.
In a normal functioning heart the SA node generates the action potential that will ultimately lead to cardiac contraction. The action potential travels to the AV node, through the bundle of His, into the right and left bundle branches, and lastly through the Purkinje fibers.
Non-Pacemaker Cardiac Myocytes
The non-pacemaker cardiac myocytes are the contractile cardiac muscle cells that are responsible for atrial and ventricular contraction, and they make up the bulk of the myocardium.
Since the contractile myocytes do not generate spontaneous action potentials like the pacemaker cells do, their action potentials are generated when neighboring cardiac myocytes are depolarized or when pacemaker cells stimulate them.
Cardiac Action Potentials
The action potentials between non-pacemaker cells (such as atrial and ventricular myocytes) and pacemaker cells (such as the SA node and AV node) are similar but slightly different.
Let’s discuss each one below while providing an easy way to remember the material.
Atrial and Ventricular Myocytes
“Summit, Plummet, Continue, Plummet”
Let’s first discuss the action potentials of non-pacemaker cardiac myocytes - the contractile cardiac muscle cells that contract the atria and ventricles.
All you need to memorize is the following phrase: “summit, plummet, continue, plummet”.
Through this simple catchphrase, you have just learned all of the action potential phases and the ion channels involved.
Here’s how:
“Summit” = Sodium = Phase 0
When a cardiac myocyte becomes stimulated, the resting membrane potential (-90 mV) becomes more positive and an action potential is generated if the threshold (-70 mV) is met.
The action potential will first “summit” as the voltage across the cell membrane becomes more positive.
This is referred to as depolarization and it is phase 0 of the action potential.
What ion is going to be involved in depolarizing the cell?
Here’s where the catchphrase is helpful.
Summit starts with the letter “S”, and this will help you remember when the action potential summits it is sodium involved.
In order for the cell to become more positive and depolarize, will sodium ions enter the cell or exit it?
They will need to enter the cell.
And this is exactly what occurs during phase 0 of the cardiac myocyte action potential.
Sodium ion channels open when the threshold cell membrane voltage is met, and an influx of sodium ions into the cell leads to depolarization.
Phase 0 = “Summit” phase of action potential = Sodium ion influx
Phase 0 is the “summit” phase in which the voltage across the cell membrane becomes more positive (depolarizes) due to the influx of sodium ions.
Plummet = Potassium = Phase 1
As the cell becomes more positive from the influx of sodium ions, these sodium channels begin to close thereby reducing the influx of sodium.
The action potential will then “plummet” as the voltage across the cell membrane becomes slightly more negative.
This causes the cell to slightly repolarize and is phase 1 of the action potential.
What ion is going to be involved in repolarizing the cell?
Again, here is where the catchphrase comes in hand.
Plummet starts with the letter “P”, and this will help you remember when the action potential plummets it is potassium involved.
In order for the cell to become more negative and repolarize, will potassium ions enter the cell or exit it?
They will need to exit the cell.
And this is exactly what occurs during phase 1 of the cardiac myocyte action potential.
The sodium channels from phase 0 have closed thereby reducing the influx of sodium ions, and the potassium channels are open leading to an efflux of potassium ions and a slight repolarization of the cell.
Phase 1 = “Plummet” phase of action potential = Potassium ion efflux
Phase 1 is a slight “plummet” phase in which the voltage across the cell membrane becomes slightly more negative (repolarizes) due to the efflux of potassium ions.
Continue = Calcium = Phase 2
After slight rerpolarization has occurred in phase 1, the action potential will then “continue” as the voltage across the cell membrane stays fairly constant.
This plateau in the voltage is phase 2 of the action potential.
If potassium is exiting the cell, then there needs to be another positive ion entering the cell to keep the action potential level and counteract the loss of positive charge.
Which ion will this be?
Again, use the catchphrase.
Continue starts with the letter “C”, and this will help you remember when the action potential continues it is calcium involved.
We know that when calcium enters muscle cells it will lead to contraction.
And this is exactly what occurs during phase 2 of the cardiac myocyte action potential.
L-type calcium channels are open, and an influx of calcium ions into the cell leads to myocyte contraction. This contraction will lead to systole of the heart.
Phase 2 = “Continue” phase of action potential = Calcium ion influx
Phase 2 is the “continue” phase in which the voltage across the cell membrane remains constant (contraction) due to calcium influx that counteracts potassium efflux.
Plummet = Potassium = Phase 3
After myocyte contraction has occurred in phase 2, the action potential will then “plummet” again as the voltage across the cell membrane becomes negative.
This is referred to as repolarization and is phase 3 of the cardiac myocyte action potential.
We know from phase 1 that plummeting will involve the efflux of potassium ions.
And this is exactly what occurs during phase 3 of the cardiac myocyte action potential.
The calcium channels have now closed thereby reducing the influx of calcium, and the potassium channels are open leading to an efflux of potassium ions and repolarization of the cell.
Phase 3 = “Plummet” phase of action potential = Potassium ion efflux
Phase 3 is the major “plummet” phase in which the voltage across the cell membrane becomes more negative (repolarizes) due to the efflux of potassium ions.
Resting Phase = Phase 4
After the cell has repolarized, it is now back at its resting membrane potential.
This is phase 4 of the cardiac myocyte action potential in which the cell is at rest until the next stimulus occurs.
The heart is in diastole during phase 4 as there is no action potential being generated to lead to contraction.
Phase 4 is when the cell is at rest and the voltage remains at a fairly constant level (resting membrane potential) until the next stimulus generates an action potential.
Pacemaker Cells: SA and AV Node
“Climb and Plummet”
Now that we have a good understanding of the action potentials of the non-pacemaker cardiac myocytes, let’s discuss those of the pacemaker cells - the specialized cardiac muscle cells that lead to conduction.
These specialized pacemaker cells are primarily found in the SA and AV node, along with the rest of the conduction system (bundle of His, bundle branches, Purkinje fibers).
All you need to memorize is the following phrase: “climb and plummet”.
Through this simple catchphrase, you have just learned all of the action potential phases and the ion channels involved with pacemaker cells.
Here’s how:
Climb = Calcium = Phase 0
Unlike the non-pacemaker cardiac myocytes, the pacemaker cells have the ability to spontaneously generate an action potential.
They do not require an external stimulus, and their cell membrane at “rest” slowly becomes more positive on its own (discussed below during phase 4).
Once the threshold cell membrane voltage is met, then an action potential is generated.
The action potential will first “climb” as the voltage across the cell membrane becomes more positive.
This is referred to as depolarization and it is phase 0 of the action potential (similar to non-pacemaker cardiac myocytes).
What ion is going to be involved in depolarizing pacemaker cells?
Use the catchphrase.
Climb starts with the letter “C”, and this will help you remember when the action potential climbs it is calcium involved.
In order for the cell to become more positive and depolarize, will calcium ions enter the cell or exit it?
They will need to enter the cell.
And this is exactly what occurs during phase 0 of the pacemaker cell action potential.
Calcium channels open and an influx of calcium ions into the cell leads to depolarization.
Phase 0 = “Climb” phase of action potential = Calcium ion influx
We can see how phase 0 of pacemaker cells differs from atrial/ventricular myocytes.
Depolarization of atrial/ventricular myocytes is a result of sodium ions entering the cell (“summit”), whereas depolarization of pacemaker cells is the result of calcium ions entering the cell (“climb”).
Phase 0 is the “climb” phase in which the voltage across the cell membrane becomes more positive (depolarizes) due to the influx of calcium ions.
Plummet = Potassium = Phase 3
There is no phase 1 or phase 2 of pacemaker cell action potentials as they are not muscle cells and do not need to contract.
They are conduction cells and only need to depolarize and repolarize over and over. This will lead to SA automaticity and AV conduction.
As the cell becomes more positive from the influx of calcium ions in phase 0, these calcium channels begin to close thereby reducing the influx of calcium.
The action potential will then “plummet” as the voltage across the cell membrane becomes more negative.
This causes the cell to repolarize and is phase 3 of the action potential.
We know from non-pacemaker myocytes that a plummet/repolarization phase is due to the efflux of potassium ions out of the cell.
This is the case for the plummet phase of pacemaker cells as well.
Calcium channels have closed and potassium channels are open leading to an efflux of potassium ions and repolarization.
Phase 3 = “Plummet” phase of action potential = Potassium ion efflux
Phase 3 is the “plummet” phase in which the voltage across the cell membrane becomes more negative (repolarizes) due to the efflux of potassium ions.
“Resting” Phase = Phase 4
Unlike the atrial/ventricular myocytes, pacemaker cells do not have a true “resting phase”.
During phase 4, the pacemaker cells continue to become more positive due to baseline influx of positive ions until a threshold voltage (-40 mV) is met thereby generating the next action potential.
Phase 4 occurs when the voltage across the cell membrane slowly becomes more positive until the next action potential is generated.
Practical Applications
Antiarrhythmics
The various phases of the action potentials of cardiac muscle cells and pacemaker cells provide opportunity for medications to act, and this is exactly how antiarrhythmics work.
There are 4 different classes of antiarrhythmics including: sodium channel blockers (Class I), beta blockers (Class II), potassium channel blockers (Class III), and calcium channel blockers (Class IV).
Each class of medication functions by blocking different phases of the cardiac myocyte and pacemaker cell action potentials.
Pathology
Problems with the conduction system of the heart can lead to heart blocks or dysrhythmias.
Conduction disorders can affect the SA node (sick sinus syndrome), the AV node (1st, 2nd, and 3rd degree AV blocks), and the bundle branches (right or left bundle branch blocks).
There are also disorders of the ion channels that can lead to long QT syndrome and Brugada syndrome.
Regulation
The autonomic nervous system influences cardiac action potentials.
Increased sympathetic activity stimulates beta adrenergic receptors in the heart to increase heart rate and cardiac contractility by increasing the slope of phase 4 in pacemaker cells and augmenting phase 2 in non-pacemaker cells respectively.
Parasympathetic activity stimulates the muscarinic cholinergic receptors in the heart to normalize heart rate by slowing the rate of depolarization.
Conclusion
Hopefully this helped you better understand cardiac action potentials.
Remember “summit, plummet, continue, plummet” for non-pacemaker cardiac myocytes (such as atrial and ventricular myocytes).
Atrial and ventricular myocyte action potentials have a phase 0 (summit = sodium in), phase 1 (plummet = potassium out), phase 2 (continue = calcium in), phase 3 (plummet = potassium out), and phase 4 (resting phase).
Remember “climb and plummet” for pacemaker cells (such as SA node and AV node).
Pacemaker cell action potentials do not have a phase 1 or 2 as there is no need for contraction. Their action potentials have a phase 0 (climb = calcium in), phase 3 (plummet = potassium out), and phase 4 (“resting” phase).
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https://www.nhlbi.nih.gov/health-topics/conduction-disorders
http://www.pathophys.org/physiology-of-cardiac-conduction-and-contractility/
https://www.cvphysiology.com/Arrhythmias/A010