Pharmacology - ANTIARRHYTHMIC DRUGS (MADE EASY)
Summary
TLDRThis lecture delves into the world of antiarrhythmic drugs, explaining the heart's electrical system and how it controls the heartbeat. It covers the role of specialized cells, the conduction system, and the action potential differences between pacemaker and cardiac muscle cells. The script also explores arrhythmias, their mechanisms, and the Vaughan Williams classification of antiarrhythmic drugs, detailing the function and effects of each class. Additionally, it touches on other agents like Digoxin, Adenosine, and Magnesium Sulfate, concluding with their applications in treating various cardiac conditions.
Takeaways
- ๐ The heart's pumping action is controlled by its electrical system, involving specialized cells that generate and transmit electrical impulses to the cardiac muscle.
- ๐ The cardiac conduction system consists of five elements: the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, bundle branches, and Purkinje fibers, which coordinate the heart's rhythm.
- ๐ The normal heart rhythm is initiated by the SA node and is represented on an electrocardiogram (ECG) by the P wave for atrial contraction, the PR interval for AV node delay, the QRS complex for ventricular contraction, and the T wave for ventricular recovery.
- ๐ Cardiac cells are divided into contractile cells that generate force for heart contraction and conducting cells that initiate electrical impulses, with the latter exhibiting automaticity.
- ๐ก๏ธ The action potential of pacemaker cells differs from that of cardiac muscle cells, with pacemaker cells having a resting membrane potential of about -60 mV and undergoing a unique depolarization process.
- ๐ซ Arrhythmias are deviations from the normal heart rhythm, classified as bradyarrhythmias (<60 bpm) or tachyarrhythmias (>100 bpm), with the latter involving mechanisms like abnormal automaticity, triggered activity, and reentry.
- ๐ก๏ธ Vaughan Williams classification categorizes antiarrhythmic drugs into four classes based on their primary mechanism of action, influencing sodium and calcium channels, and potassium channels, among others.
- ๐ Class 1 antiarrhythmics, such as Procainamide, Quinidine, and Disopyramide, work by blocking sodium channels to slow down depolarization and are used for various arrhythmias but can cause adverse effects.
- ๐ก๏ธ Class 2 drugs are beta blockers that reduce heart rate and contractility, useful for arrhythmias caused by increased sympathetic activity, with examples like Propranolol and Metoprolol.
- ๐ Class 3 agents, including Amiodarone and Dronedarone, block potassium channels to prolong the action potential and are effective against atrial fibrillation and ventricular tachyarrhythmias but can have significant side effects.
- ๐ฐ Class 4 drugs, like Verapamil and Diltiazem, block calcium channels to slow conduction in the SA and AV nodes, treating supraventricular tachycardia and atrial fibrillation.
- ๐ฟ Other antiarrhythmic agents not fitting into the Vaughan Williams classes include Digoxin, which enhances contractility and slows AV node conduction, Adenosine for acute supraventricular tachycardia, and Magnesium Sulfate for specific arrhythmias like torsades de pointes.
Q & A
What are antiarrhythmic drugs and why are they important?
-Antiarrhythmic drugs are medications used to treat abnormal heart rhythms, or arrhythmias. They are important because they help regulate the heart's electrical system, ensuring the heart beats at a normal rhythm and preventing potentially life-threatening conditions.
What is the role of the sinoatrial (SA) node in the heart's electrical system?
-The SA node serves as the heart's natural pacemaker, initiating the electrical signals that cause the atria to contract and push blood into the ventricles. It is the starting point of the cardiac conduction system.
How does the cardiac conduction system consist of five elements?
-The cardiac conduction system is made up of the sinoatrial node (SA node), atrioventricular node (AV node), bundle of His, bundle branches, and Purkinje fibers. These elements work together to generate and transmit electrical signals for the heart's contractions.
What is the significance of the P wave, Q wave, R wave, S wave, and T wave on an electrocardiogram (ECG)?
-The P wave on an ECG represents atrial depolarization and the beginning of atrial contraction. The Q wave indicates the start of ventricular depolarization. The R wave is the peak of ventricular depolarization, the S wave follows and represents the end of depolarization. Lastly, the T wave represents the recovery phase of the ventricles as they repolarize.
What are the two types of cardiac cells and their functions?
-There are contractile cells, which generate force for heart contractions and make up most of the atrial and ventricular walls, and conducting cells, which initiate the electrical impulses controlling heart contractions.
What is automaticity and why is it important in the heart?
-Automaticity is the ability of certain cardiac cells, particularly in the SA node, AV node, bundle of His, and Purkinje fibers, to spontaneously initiate an action potential. It is important because it allows the heart to maintain a regular rhythm without external stimulation.
What are the three basic mechanisms responsible for the initiation of tachyarrhythmias?
-The three mechanisms are abnormal automaticity, triggered activity, and reentry. Abnormal automaticity occurs when cells become more permeable to sodium, leading to increased automaticity. Triggered activity involves abnormal leakage of positive ions causing afterdepolarizations. Reentry is a loop of electrical activation circulating through heart tissue, often due to an accessory pathway.
How does the Vaughan Williams classification categorize antiarrhythmic drugs?
-The Vaughan Williams classification divides antiarrhythmic drugs into four classes based on their dominant mechanism of action: Class 1 (sodium channel blockers), Class 2 (beta blockers), Class 3 (potassium channel blockers), and Class 4 (calcium channel blockers).
What are the potential adverse effects of class 1 antiarrhythmic drugs?
-Class 1 antiarrhythmic drugs can cause adverse effects such as blurred vision, headache, tinnitus, and in some cases, they may even cause arrhythmias themselves. The specific side effects can vary depending on the drug within this class.
How do class 2 antiarrhythmic drugs, such as beta blockers, affect the heart?
-Class 2 antiarrhythmic drugs, which are beta blockers, work by acting on beta-1 receptors to prevent the action of catecholamines on the heart. This results in decreased heart rate, reduced contractility, and slowed conduction through the AV node.
What is unique about sotalol among class 3 antiarrhythmic drugs?
-Sotalol is unique because it has both potassium channel blocking activity, like other class 3 drugs, and beta receptor blocking activity. This dual mechanism makes it effective for treating certain types of arrhythmias.
How does Digoxin work and what are its main uses?
-Digoxin works by inhibiting the sodium-potassium pump, leading to increased intracellular calcium which enhances myocardial contractility. It also stimulates the parasympathetic system, slowing sinus node discharge rate and AV node conduction. It is used particularly for patients with heart failure and atrial fibrillation.
What is the primary indication for Adenosine and what are its common side effects?
-Adenosine is primarily indicated for the acute treatment of supraventricular tachycardia. Its common side effects include chest pain, flushing, and hypotension due to its very short duration of action and need for IV administration.
What is the role of Magnesium Sulfate in treating arrhythmias?
-Magnesium Sulfate is effective for treating certain types of arrhythmias, such as torsades de pointes and those induced by Digoxin. Its precise mechanism is not fully understood, but it is known to play a role in the transport of sodium, potassium, and calcium across cell membranes.
Outlines
๐ Introduction to Antiarrhythmic Drugs
This paragraph introduces the topic of antiarrhythmic drugs, explaining the heart's electrical system and how it controls the pumping action. It details the components of the cardiac conduction system, including the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, bundle branches, and Purkinje fibers. The normal heart rhythm is described, starting from the SA node and culminating in the contraction of the ventricles, represented by the P wave, PR interval, QRS complex, and T wave on an electrocardiogram. The paragraph also distinguishes between contractile and conducting cells in the heart, emphasizing the automaticity of the latter and the role of the SA node as the primary pacemaker. It concludes with a comparison of action potentials in pacemaker cells versus heart muscle cells, highlighting the unique depolarization and repolarization processes in pacemaker cells.
๐ Understanding Cardiac Muscle Cells and Arrhythmias
The second paragraph delves into the action potential of cardiac muscle cells, contrasting it with that of pacemaker cells. It describes the resting membrane potential of cardiac muscle cells and the phases of an action potential, including the rapid depolarization (phase 0), the brief dip (phase 1), the plateau (phase 2), and repolarization (phase 3). The concept of arrhythmias is introduced as deviations from the normal heart rhythm, with classifications into bradyarrhythmias and tachyarrhythmias based on heart rate. The paragraph then focuses on the mechanisms of tachyarrhythmias, including abnormal automaticity, triggered activity, and reentry, providing examples such as Wolff-Parkinson-White syndrome and atrioventricular nodal reentry tachycardia (AVNRT).
๐ก๏ธ Vaughan Williams Classification of Antiarrhythmics
This paragraph discusses the Vaughan Williams classification of antiarrhythmic drugs, which categorizes them into four classes based on their primary mechanism of action. Class 1 drugs are explained as sodium channel blockers that slow down the rate of depolarization and conduction velocity. They are further subdivided into three subclasses: Class 1A, which prolongs the action potential and effective refractory period; Class 1B, which shortens the action potential and effective refractory period; and Class 1C, which markedly depresses phase 0 depolarization. Specific drugs and their uses, as well as potential adverse effects, are mentioned for each subclass. The paragraph also notes the risk of proarrhythmic effects with Class 1 agents.
๐ Exploring Class 2 to 4 Antiarrhythmic Drugs
The fourth paragraph continues the discussion on antiarrhythmic drugs, starting with Class 2, which includes beta blockers that act on beta-1 receptors to decrease heart rate and contractility. Examples of beta blockers and their uses are provided. Class 3 drugs are described as potassium channel blockers that increase the duration of the action potential and effective refractory period, with Amiodarone being highlighted for its broad effectiveness and potential adverse effects. Class 4 drugs are characterized by their action on calcium channels, slowing conduction in the SA and AV nodes. Verapamil and Diltiazem are mentioned as examples. The paragraph concludes with a brief mention of other antiarrhythmic agents like Digoxin, Adenosine, and Magnesium Sulfate, setting the stage for further discussion.
๐ Additional Antiarrhythmic Agents and Their Mechanisms
The final paragraph provides insights into Digoxin, Adenosine, and Magnesium Sulfate, which do not fit neatly into the Vaughan Williams classification. Digoxin is explained as an inhibitor of the sodium-potassium pump, leading to increased intracellular calcium and enhanced contractility, and its use in heart failure and atrial fibrillation is noted. Adenosine is described as a nucleoside that stimulates A1 receptors, reducing automaticity and conduction velocity, and is used for acute supraventricular tachycardia with brief mention of its side effects. Magnesium Sulfate's role in arrhythmia treatment, particularly for torsades de pointes and Digoxin-induced arrhythmias, is highlighted, despite its mechanism being less understood. The paragraph ends with a thank you note to the viewers.
Mindmap
Keywords
๐กAntiarrhythmic drugs
๐กCardiac conduction system
๐กSinoatrial node (SA node)
๐กElectrocardiogram (ECG/EKG)
๐กAction potential
๐กAutomaticity
๐กArrhythmia
๐กVaughan Williams classification
๐กBeta blockers
๐กPotassium channels
๐กCalcium channels
Highlights
Introduction to antiarrhythmic drugs and the heart's electrical system.
Description of the five elements of the cardiac conduction system.
Explanation of the normal heart rhythm and its representation on an electrocardiogram.
Differentiation between contractile and conducting cardiac cells.
Importance of the SA node as the heart's natural pacemaker.
Potential for other conduction tissues to become latent pacemakers.
Comparison of action potentials in pacemaker cells versus cardiac muscle cells.
Role of electrolyte ions in generating action potentials in the heart.
Mechanisms of arrhythmias including abnormal automaticity, triggered activity, and reentry.
Overview of the Vaughan Williams classification of antiarrhythmic drugs.
Function of class 1 antiarrhythmic drugs and their subclasses.
Use of class 2 antiarrhythmic drugs as beta blockers in arrhythmia treatment.
Class 3 antiarrhythmic drugs' impact on potassium channels and action potential duration.
Class 4 antiarrhythmic drugs' effect on calcium channels and heart conduction.
Discussion of other antiarrhythmic agents like Digoxin, Adenosine, and Magnesium Sulfate.
Digoxin's mechanism of action through the inhibition of the sodium-potassium pump.
Adenosine's unique role in treating acute supraventricular tachycardia.
Magnesium Sulfate's effectiveness in treating specific arrhythmias despite an unclear mechanism.
Transcripts
in this lecture I'm going to talk about antiarrhythmic drugs so let's get right
into it as you may already know the pumping action of the heart is
controlled by the heart's electrical system the heart contains specialized
cells that are able to create their own electrical impulses and send them to the
cardiac muscle causing it to contract now the cardiac conduction system is
made up of five elements number one the sinoatrial node SA node for short number
two the atrioventricular node AV node for short number three the bundle of His
number four the bundle branches and number five the Purkinje fibers so the
normal heart rhythm begins when electrical signals are sent from the SA
node the signal from the SA node causes the atria to contract pushing blood
through the open valves into the ventricles on the typical
electrocardiogram this is represented by the P wave next electric signal arrives
at the AV node and is briefly delayed so that the contracting atria have enough
time to pump all the blood into the ventricles this is represented by the
line between the P and the Q wave at this point the signal travels to the
bundle of His into the bundle branches this is represented by the Q wave and
finally this signal travels through the Purkinje fibers which causes the
ventricles to contract and thus pump blood from the right ventricle into the
lungs and from the left ventricle into the rest of the body this is represented
by the R and S wave the last T wave represents the recovery of the
ventricles now cardiac cells can be divided into
two types first contractile cells which make up most of the walls of the atria and
ventricles and when stimulated they generate force for contraction of the
heart and the second type conducting cells which initiate the electrical impulse
that controls those contractions now while contractile fibers can't generate an
action potential on their own the conducting fibers are capable of
spontaneously initiating an action potential by themselves they exhibit
so-called automaticity the conducting cells are primarily concentrated in the
tissues of the SA node AV node bundle of His and Purkinje fibers now normally SA
node reaches threshold potential the fastest which is why it serves as the
natural pacemaker of the heart when the SA node drives the heart rate the cells
of AV node bundle of His and Purkinje fibers do not express automaticity or in
other words their spontaneous depolarization is suppressed however
under certain conditions when activity of the SA node becomes suppressed or the
firing rate of these other conducting tissues becomes faster one of them can
become the new pacemaker of the heart this is why the AV node bundle of His
and Purkinje fibers are called latent pacemakers now before we move on let's
take a closer look at the action potential of the pacemaker cells versus
the heart muscle cells as there are some important differences between them so in
the heart each cardiac cell contains and is
surrounded by electrolyte fluids the main ions responsible for the electrical
activity within the heart are sodium calcium and potassium
when cardiac cells are stimulated by an electrical impulse their membrane's
permeability change and ions move across the membrane thus generating an action
potential so now the membrane potential in the pacemaker cells starts at about
negative 60 millivolt when spontaneous flow of sodium mainly
through slow sodium channels and opening of the voltage-gated T-type calcium
channels continue slow depolarization this is referred to as phase 4
once threshold potential of about negative 40 millivolt is reached the
voltage-gated L-type calcium channels open calcium rushes in and rapidly
depolarizes cell to about positive 10 millivolts this is referred to as phase 0
finally the L-type calcium channels
close and the voltage-gated potassium channels open which allows potassium
ions to escape thus repolarizing the cell back to negative 60 millivolts this
is referred to as phase 3 after this the cycle just repeats itself
also note that there is no phase 1 or phase 2 in the action potential of the
pacemaker cells okay so now let's take a look at the action potential of the
cardiac muscle cells unlike pacemaker cells the cardiac muscle cells have
resting membrane potential of about negative 90 millivolts
due to the constant outward leak of potassium through the inward-rectifier
channels this resting phase is referred to as phase 4 now when an action
potential is triggered in a neighboring cell the voltage-gated sodium channels
open and sodium rushes in causing a rapid depolarization to about positive
40 millivolts this is referred to as phase 0 at this point the sodium
channels become inactivated and other voltage-gated channels begin to open
mainly potassium channels which allow potassium to escape thus bringing about
a small dip in membrane potential this is referred to as phase 1 now
something that I didn't mention is that during depolarization at phase 0
voltage-gated L-type calcium channels began to open slowly allowing calcium
enter into the cell so now with the positive potassium ions leaving and the
positive calcium ions steadily coming in we have this electrically balanced
ion exchange which keeps the membrane potential on a plateau this is
referred to as phase 2 lastly the plateau phase is followed by
a rapid repolarization referred to as phase 3 which is caused by a gradual
inactivation of the calcium channels and continuous outflow of potassium
this brings the membrane potential back to the resting phase 4 so now let's
switch gears and let's talk about arrhythmias so what is arrhythmia well
arrhythmia is simply a deviation of heart from a normal rhythm so normal
heart rhythm will have a heart rate of between 60 to 100 beats per minute with
each beat generated from the SA node each cardiac impulse will also propagate
through normal conduction pathway with normal velocity now arrhythmias are
generally classified based on heart rate as bradyarrhythmias when the rate
is below 60 beats per minute or tachyarrhythmias when the rate is above
100 beats per minute however in order to understand pharmacology of antiarrhythmic
drugs we need to focus on mechanisms of tachyarrhythmias so there are three
basic mechanisms responsible for the initiation of tachyarrhythmias first
abnormal automaticity also referred to as enhanced automaticity this occurs when
the cell membrane becomes abnormally permeable to sodium
during phase 4 which results in increase in the slope of phase 4
depolarization this can cause other cells to accelerate their automaticity and
thus generate impulses faster than the SA node the second mechanism is called
triggered activity triggered activity involves the abnormal leakage of
positive ions into the cardiac cell leading to this bump on the action
potential called afterdepolarization these afterdepolarizations can occur
during phase 2 3 or 4 and if they have sufficient magnitude they can
trigger premature action potentials now the third mechanism of
tachyarrhythmias is called reentry example of this is wolff-parkinson-white
syndrome in which an extra or so-called accessory pathway exists between the
upper and lower chambers of the heart so normally the electrical signal travels
from the SA node to AV node to bundle branches and once it reaches the
Purkinje fibers it stops and waits for another signal from the SA node
now when the accessory pathway appears the signal travels through this pathway
from ventricles back to atria causing them to contract before SA node fires
again this creates this abnormal loop of electrical activation circulating
through a region of heart tissue causing tachyarrhythmia another example of
reentry is atrioventricular nodal reentry tachycardia AVNRT for short
so typically there are two anatomic pathways for carrying signal through the
AV node first pathway is called the fast pathway because it allows fast
conduction however it has a long refractory period meaning it recovers
slowly on the other side this second pathway is called the slow pathway
because it only allows slow conduction and because of that it has short
refractory period meaning it recovers fast so now the signal comes down from
the SA node and then it splits and travels fast through the fast pathway
and slow through the slow pathway so the fast pathway signal reaches the common
pathway on the other end well before the slow pathway signal gets there from
there the fast pathway signal spreads to the ventricles as well as up the slow
pathway where it hits the slow signal causing it to terminate
now if a premature beat occurs at the time when the fast pathway signal is
still in the refractory period the signal will travel down the slow pathway
as the slow signal approaches the common pathway fast pathway comes out of
refractory period so now the slow signal spreads to the ventricles and it also
travels up the fast pathway but let's not forget that the slow pathway has a
short refractory period so by the time the signal reaches the top the
slow pathway is ready to conduct another signal so what ultimately happens here
is that this signal continues to circle around sending fast impulses which
result in tachycardia now let's move on to discussing the actual antiarrhythmic
drugs so most commonly used classification of antiarrhythmics is the
Vaughan Williams classification which groups most antiarrhythmics into four
classes based on their dominant mechanism of action now let's discuss
each of these classes so first we have class 1 drugs which work mainly by
blocking sodium channels in the open or inactivated state inhibition of sodium
channels decreases the rate of rise of phase 0 depolarization and slows
conduction velocity class 1 drugs are subdivided into three subclasses
according to their effect on the cardiac action potential first we have class 1A
drugs which moderately depress the phase 0 depolarization by blocking fast
sodium channels they also prolong repolarization by blocking
some potassium channels so what we'll see with class 1A agents is prolonged
action potential and prolonged effective refractory period the agents in this
class include Procainamide Quinidine and Disopyramide these agents are used in
the treatment of a wide variety of arrhythmias
such as ventricular tachycardias and recurrent atrial fibrillation adverse
effects include blurred vision headache and tinnitus which may occur with large
doses of Quinidine and some anticholinergic effects which may occur
with the use of Disopyramide secondly we have class 1B drugs which have
relatively weak effect on the phase 0 depolarization due to minimal blockade
of fast sodium channels however these agents shorten repolarization by
blocking sodium channels that activate during late phase 2 of the action
potential so what we'll see with class 1B agents is shorten duration of
action potential and shorten effective refractory period the agents in this
class include Lidocaine and Mexiletine which are mainly used in the treatment
of ventricular arrhythmias when it comes to adverse effects Lidocaine can cause
CNS toxicity including seizures while Mexiletine can cause nausea and
vomiting now the third and the last subtype that we have is class 1C drugs
which are powerful fast sodium channel blockers which depress the phase 0
depolarization markedly they also inhibit the His-Purkinje conduction
system with a limited effect on repolarization and refractory period the
agents in this class include Flecainide and Propafenone which are mainly used in
the treatment of refractory ventricular arrhythmias when it comes to adverse effects
the most common ones include dizziness blurred vision and nausea also something
that I haven't mentioned yet is that one of the risk associated with the class 1
agents actually all of them is that they have potential to actually cause
arrhythmias themselves so weighing the risk versus benefit is very important before
initiating therapy with these agents now let's move on to class 2
antiarrhythmic drugs so agents in this class act on the beta-1 receptors
preventing the action of catecholamines on the heart so class 2 agents
are simply beta blockers beta blockers depress sinus node automaticity and slow
conduction through the AV node which results in decreased heart rate and
decreased contractility examples of beta blockers commonly used for arrhythmia
are Propranolol Metoprolol Atenolol and Esmolol now Esmolol unlike the other
beta blockers is somewhat special in that it's given intravenously in an
emergency acute arrhythmias and the reason for that is that it has fast
onset of action and very short half-life which allows it to be titrated rapidly
when necessary so the bottom line is that beta blockers are good choice for
treatment of arrhythmias provoked by increased sympathetic activity and if
you want to learn more about them check out my other videos about adrenergic
receptors and beta blockers now let's move on to class 3 antiarrhythmic
drugs so class 3 agents work mainly by blocking the potassium channels that
are responsible for the Phase 3 repolarization this leads to increase in
duration of action potential and increase in effective refractory period
the agents in this class include Amiodarone Dronedarone Sotalol
Dofetilide and Ibutilide there are mainly used in treatment of
supraventricular and ventricular tachyarrhythmias as well as atrial fibrillation
and flutter the most widely used drug in this class is Amiodarone which
is very effective for the treatment of these aforementioned arrhythmias
Amiodarone has multiple actions and besides blocking potassium channels
Amiodarone also blocks sodium channels calcium channels and even some alpha and
beta receptors unfortunately Amiodarone is also associated with many adverse
effects such as pulmonary fibrosis blue-grey skin discoloration neuropathy
hepatotoxicity corneal microdeposits and because it contains iodine
Amiodarone also can cause thyroid dysfunction
leading to hypo or hyperthyroidism lastly due to its long
half-life Amiodarone can linger in many tissues for months after discontinuation
of therapy now on the other hand we have Dronedarone which is derivative of Amiodarone
it's less lipophilic and has shorter half-life it also
doesn't contain iodine so in general it has better side effect profile unfortunately
in many cases Dronedarone doesn't seem to be as effective as Amiodarone
now Sotalol is a unique drug in this class because it not only has potassium
channel blocking activity but also beta receptor blocking activity
lastly Dofetilide and Ibutilide are the most selective potassium channel
blockers in this class however they're also most likely to cause arrhythmias
themselves and therefore are typically initiated in the inpatient setting only
now let's move on to class 4 antiarrhythmic drugs so class 4 agents work
by blocking voltage-sensitive calcium channels during depolarization
particularly in the SA and AV nodes which results in slower conduction in
these tissues and reduced contractility of the heart the agents in this class
include Verapamil and Diltiazem which are the nondihydropyridine calcium
channel blockers unlike dihydropyridines which act primarily in the
periphery causing vasodilation nondihydropyridines are much more selective
for the myocardium and therefore they show antiarrhythmic actions Verapamil and
Diltiazem are most commonly used in treatment of supraventricular
tachycardia and atrial fibrillation and now before we end this lecture I wanted
to briefly discuss some other antiarrhythmic agents that do not quite
fit into any of the classes that we covered thus far and these are
Digoxin Adenosine and Magnesium Sulfate so
let's talk about Digoxin first and in order to understand how it works let's
picture a cardiac cell under resting conditions sodium slowly leaks into the
cell and potassium leaks out however during an action potential additional
sodium enters in along with calcium and additional potassium leaves the cell so
at some point we have this imbalance that has to be restored and this
restoration is accomplished by pumps such as sodium-potassium ATPase which
transports sodium ions to the outside of the cell and potassium to the inside of
the cell and we also have sodium-calcium exchanger which removes calcium from the
cell in exchange for sodium and as a side note here keep in mind that
sodium-calcium exchanger can carry sodium and calcium in both directions so now what
happens when Digoxin comes around is that it inhibits sodium-potassium pump
by binding to the potassium binding site this results in the increase in
intracellular sodium which then in turn causes the sodium-calcium exchanger to
pump sodium out and bring more calcium in now this increase in intracellular
calcium leads to enhanced myocardial contractility Digoxin also
stimulates parasympathetic system which increases activity of the vagus nerve
this results in the slowing of sinus node discharge rate and decreased
conduction through the AV node these actions make Digoxin particularly useful
for patients with both heart failure and atrial fibrillation now let's talk about
the second agent which is Adenosine unlike all the other agents Adenosine is
a naturally occurring nucleoside it works by stimulating A1 type
adenosine receptors on the atrium as well as on the SA node and AV node which
results in decreased automaticity decreased conduction velocity and
prolonged refractory period due to its very short duration of action
adenosine has to be administrated by IV its main indication is an acute
supraventricular tachycardia one of the biggest benefits of Adenosine is that
it's relatively non-toxic with the most common side effects being chest pain
flushing and hypotension now finally let's talk about our third agent which
is Magnesium Sulfate Magnesium Sulfate plays an important role in transport of
sodium potassium and calcium across the cell membranes unfortunately its precise
mechanism of action for treating arrhythmias is largely unknown however
what we know is that Magnesium Sulfate administered intravenously is very
effective for treatment of torsades de pointes and Digoxin induced
arrhythmias and with that I wanted to thank you for watching I hope you
enjoyed this lecture and as always stay tuned for more
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