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Review of Electro-Cardiac physiology
Note that the different tissues have very different electrical characters.

The slope of phase 0 is different (Atria 1m/s, AV 0.1 m/s, His/Purk 1-2m/s, Vent 0.4 m/s) depending on which ions are moving etc...

There is an effectrive Refractory period (ERP) during which it is unlikely to get another action potential (generally form phase 0 until just after the start of phase 3). For fast fibers it is about the same length as the action potential, for slow fibers however the ERP is normally longer than the AP duration. This is b/c Na fibers recover faster than the Ca channels used in slow fibers.

Phase 4 is steady in those tissues with no automaticity, however it slowly rises to threshold according to the intrinsic rate in the nodal tissues.

A cardiac arrhythmia is defined as any abnormality in rate, regularity or site of origin of cardiac impulse or a disturbance in conduction rate or pattern. It canbe broken down into abnormalities in impulse generation and abnormalities in impulse conduction. Many factors can precipitate an arrhythmia: ischemia, hypoxia, acidosis, alkalosis, electrolyte abnormalities, etc.

Normal timing of the EKG:
PR interval ~ 0.18 sec
QT interval ~ 0.4 sec
ST interval ~ 0.32 sec

Typical Ion concentrations:
Ion out/in/eq
Na- 145/10/+50mv
K - 4/150/-90mv
Ca- 2/10^-7/+140
Fast Response Fibers Vs. Slow Response Fibers
Fast fiber damage can convert them into slow fibers and can create new foci for pacemaking.

We examine the difference as a function of excitability. This is expressed as 1/(resting potential - threshold potential). It leads us to understand that slow fibers are more excitable than the fast, so it protects the heart from ectopic foci developing from a 2nd action potential.

Fast response (Non-pacemaker) fibers:

Phase 0; rapid depolarization
sodium influx

Phase 1; rapid (or initial) repolarization to plateau inactivation of sodium channels,
transient potassium efflux, some chloride current

Phase 2; sustained repolarization, plateau calcium influx ((slower than Na but similar in that they both have 2 gating mechanisms)
), some slow potassium efflux

Phase 3; rapid (or final) repolarization to diastolic resting level
potassium efflux, inactivation of "slow" calcium channel

Phase 4; diastolic resting level, reestablishing ionic disequilibrium
sodium-potassium (3 Na out/2 k in) ATPase pump; sodium-calcium exchanger (Ca also stored in sarcoplasmic reticulum).


Slow response (Pacemaker) fibers

Phase 0; depolarization - calcium influx
Phase 3; repolarization - potassium efflux
Phase 4; slow diastolic depolarization (big difference between fast and slow, decrease in K efflux, Na leakage in, toward the end Ca influx).
Normal Sinus Rhythm
P - QRS - T wave. Normal is about 70 BPM
Sinus Bradycardia
Supraventricular
May be as low as 60 per minute. Can be a result of athletic conditioning, hypothermia, vagal overtone, etc.
Paroxysmal Atrial Tachycardia (PAT)
Supraventricular
Sinus on the left, and then all of a sudden the heart goes into the atrial arrhythmia, may increase up to 150 BPM due to an ectopic focus in the atrium (not the ventricle)
Sinus Taccycardia
Supraventricular
The Sa node is still controlling the beat but it is >150 BPM. May be due to sympathetic overtone e.g. Pheochromocytoma causing overrelease of epinephrine, or hyperthyroidism. Pregnancy, hyperthermia, etc...
Atrial Flutter
Supraventricular
Atria beating at about 300 BPM. Sawtooth pattern in which there is 2 P waves for each QRST complex. The AV node is protecting the ventricle, so it only beats at half the rate of the Atria.
Atrial Fibrillation
Supraventricular
No effective contraction of the atria, blood is passivel flowing from A to V. Only every certain # of beats will get though. 300-600 atrial beats per minute.
Premature Ventricular Contraction (PVC)
Ventricular
Least serious of the 3. "feels like my heart skipped a beat." An ectopic focus in the ventricle leads to an extra beat. Every heart does that once in a while but too many can lead to V-Tac
Vantricular Tachycardia
Ventricular
The ventricle takes over the beat. It is rapid. CO drops significantly, can lead to V-Fib.
Ventricular Fibrillation
Ventricular
No effective contraction of the ventricles. Will quickly lead to death if not corrected.
Types of Arrhythmias
Cardiac arrhythmias can be divided based on their site of origin:

(1) Supraventricular arrhythmias include sinus bradycardia/tachycardia,
atrial flutter/fibrillation and paroxysmal supraventricular tachycardia

(2) Ventricular arrhythmias include PVCs, ventricular tachycardia and ventricular fibrillation.
Mechanisms of Antiarrhythmic Agents
Blockade of Sodium Channels-
Some of the oldest original drugs. Affects phase 0.

Blockade of Sympathetic Autonomic Effects on the Heart (B-adrenergic receptor blockers)

Prolongation of Effective Refractory Period (Potassium Channel Blockers)

Blockade of Calcium Channels
Classification of Antiarrhythmic Drug
See Chart
Classes of Antiarrhythmic Drugs
Drugs either are sodium channel blockers, B-blockers, prolong the refractory period (K+ channel blockers) or are Ca2+ channel blockers. They are generally state depedant (prefer channels in either the active or inactive state) and do not bind well to resting channels. This is the source of drug selectivity. The drugs also takes time to work, so that if the heart tissue is cycling normally the drus may not bind, so that again we select for diseased tissue.

Class I - Sodium Channel Blockers
Ia slows phase 0 and also prolongs the ERP by blocking K channels, so they prolong AP duration.

Ib shortens Phase 3

Ic markedly slows phase 0. Most potent Na blockers, and most specific.

Class II - Antisympathetic Drugs - B-Blockers. Supresses phase 4 (slow conduction across AV node as well)

Class III - Prolong the Action Potential, K+ channel Blockers. Prolong phase 3

Class IV - Calcium Channel Blockers. Shortens actions potentials, major effect on the SA/AV node.

V- Miscellaneous including Digoxin, adenosine, Mg, K.
Nervous Inputs to the Heart
A. Parasympathetic - Vagal nerve -
Acetylcholine (muscarinic M2 receptors), Decreases SA firing rate, Decreases AV node conduction.

B. Sympathetic -norepinephrine B-1 receptor.
Increases SA firing rate, Increases conduction in AV node.
Wolf-Parkinson-White Syndrome
An alternate pathway from atria to ventricles which by passes the AV node

Ventricles not protected from atrial tachyarrhythmias

Normally we slow down the AV node to protect the ventricles form atrial tachycardias, but this would exacerbate the condition so that we have to use alternatives to the normal tx regimen.
Class I drugs
General Info:
Again, these drugs will effect ALL channels, but they are more selective for disease. They may cause arrhythmias.
They all inhibit Na channels, and may also be consideren to have local anesthethic activity.

Mechanism:
Sodium channels exist in three states: 1) closed or resting, 2) open or active, 3) inactive or refractory. The length of time that channels remain inactive is a function of the membrane potential; as the membrane potential becomes more negative Na+ channels return to the resting state faster. Drugs in class I bind to the open or inactive states of Na+ channels but do not bind to resting channels. Channels that have a class I drug bound tend to remain in the inactive state longer. The more selective drugs bind to inactive channels only. They in effect decrease conduction velocity by decreasing rate of phase 0 depolarization. Most of drugs in class I have a greater effect on the Na+ channels in abnormal tissue than they do in normal tissue.

Class I is divided into subclasses:

IA Prolong action potential -Moderate phase 0 depression, prolong QT interval (due to K channel effects). They prefer active/inactive channels equally. They all have similar direct effects, but differ in antimuscarininc activity and side effects (disopyramide > quinidine > Procainamide). Useful mostly for Ventricular and a few supraventricular arrhythmias.

IB Small phase 0 depression - Shortens the action potential in Purkinje cells -Little effect on other cardiac cells Greatest effects on abnormal cardiac cells -i.e. selective. Prolongs the refractory period (prolongs AP in diseased tissue). Fewest side effects, little effects on EKG. Prefers inactive channels, and thus has little effect on phase 0. Used only for Ventricular arrhythmias.

IC No effect on action potential - Strong phase 0 depression. Strongly prefer active channels. Broaden QRS the most, little effect on AP duration. Useful mostly for Ventricular and a few supraventricular arrhythmias.

IA-
Quinidine
Procainamide
Disopyramide

IB-
Quinidine
Procainamide
Disopyramide

IC-
Flecainide
Propafenone

***Treatment of the elderly is more challenging. Half lives of many of the drugs used increase including quinidine, procainamide and lidocaine
Class II Drugs
Class II (B-Blockers...*=cardioselective)-likely the only ones we should use for PVC's at all. Can be used for supraventricular and ventricular arrhythmias.

Propranolol
Esmolol * - short acting
Atenolol *
Metoprolol* etc.
Class III drugs
Class III (prolongs action potential)- With the exception of Ibutilide (supraventricular only) they are useful both for Supra and Ventricular arrhythmias.

Amiodarone
Bretylium
Sotalol
Ibutilide
Dofetilide
Class IV drugs
Class IV (Ca++ channel blockers)- Used for supraventricular arrhythmias

Verapamil
Diltiazem
Other Useful Anti-arrhythmia drugs
Digoxin
Edrophonium
Phenylephrine
Atropine
Isoproterenol
Potassium
Magnesium
Quinidine
Class: Ia (from cinchona tree, also tx's malaria)

Major Cardiac Effects:
These drugs slow conduction and prolong the refractory period and the QRS interval. The prolongation of the QRS is due K+ channel blockade. They decrease the firing of ectopic pacemakers. The decrease in rate of conduction can convert a unidirectional block into a bi-directional block and prevent reentry. The effect of these drugs is greater on partially depolarized cells. They have some calcium channel activity which can result in depression of nodal tissue.

Pharmacokinetics:
All can be given orally. Quindine is 80% bound to albumin and thus can displace digoxin from albumin.

Major Side Effects:
Cardiac side Effects –
Excessive prolongation of the QT interval (>30%) may lead to torsade de pointes. Avoid widening QRS greater than 30%. They can cause excessive slowing of conduction throughout the heart. They directly depress the SA node (sick sinus syndrome...do not give to bradycardics).

Antimuscarinic effects -
These drugs inhibit the action of the vagal input to the heart. But their relative activity in this respect is not the same. The antivagal effects can overcome the direct effects on nodal tissues so that these drugs can actually increase the sinus rate depending on dose.
Disopyramide > Quinidine > Procainamide

Extra Cardiac Effects-
GI effects - nausea, vomiting, diarrhea – 1/3 to 1/2 of patients
Cinchonism - headache, dizziness and tinnitus
Digitalis toxicity – Albumin displacement of Dig, increases effective conc.
When given i.v. can cause severe hypotension

Therapeudic Use:
Used to maintain normal sinus rhythm in atrial fibrillation or flutter. Sometimes ventricular tachycardia. Mainly used in a heart with an arrhythmia that is otherwise normal (not damaged). Shown to increase sinus rhythm in patients but to increase mortality in the same patients.
Avoid the use of quinidine in “Sick Sinus Syndrome”.
Procainamide
Class: IA

Major Cardiac Effects:
These drugs slow conduction and prolong the refractory period and the QRS interval. The prolongation of the QRS is due K+ channel blockade. They decrease the firing of ectopic pacemakers. The decrease in rate of conduction can convert a unidirectional block into a bi-directional block and prevent reentry. The effect of these drugs is greater on partially depolarized cells. They have some calcium channel activity which can result in depression of nodal tissue.

Pharmacokinetics:
Oral, Procainamide is shortest acting (3-4) and is thus given as a sustained release preparation.

Major Side Effects:
Cardiac side Effects –
Excessive prolongation of the QT interval may lead to torsade de pointes. Avoid widening QRS greater than 30%. They can cause excessive slowing of conduction throughout the heart. They directly depress the SA node.

Antimuscarinic effects -
These drugs inhibit the action of the vagal input to the heart. But their relative activity in this respect is not the same. The antivagal effects can overcome the direct effects on nodal tissues so that these drugs can actually increase the sinus rate depending on dose.
Disopyramide > Quinidine > Procainamide

Extra Cardiac Effects-
Lupus like syndrome (1/3 of patients on long term therapy, reversable)
Minor Effects - Nausea, Rash, Fever. More likely than quinidine to produce cardiac failure in toxic doses.


Therapeudic Use:
Length of use limited by side effects. The drug of second choice after lidocaine for sustained ventricular arrhythmias after acute myocardial infarction.
Disopyramide
Class: IA

Major Cardiac Effects:
These drugs slow conduction and prolong the refractory period and the QRS interval. The prolongation of the QRS is due K+ channel blockade. They decrease the firing of ectopic pacemakers. The decrease in rate of conduction can convert a unidirectional block into a bi-directional block and prevent reentry. The effect of these drugs is greater on partially depolarized cells. They have some calcium channel activity which can result in depression of nodal tissue.

Pharmacokinetics:
Oral Administration

Major Side Effects:
Cardiac side Effects –
Excessive prolongation of the QT interval may lead to torsade de pointes. Avoid widening QRS greater than 30%. They can cause excessive slowing of conduction throughout the heart. They directly depress the SA node.

Antimuscarinic effects -
These drugs inhibit the action of the vagal input to the heart. But their relative activity in this respect is not the same. The antivagal effects can overcome the direct effects on nodal tissues so that these drugs can actually increase the sinus rate depending on dose.
Disopyramide > Quinidine > Procainamide

Extra Cardiac Effects:
Antimuscarinic - Atropine-like symptoms - dry mouth, blurred vision, constipation etc. More strongly negative inotropic and can give heart failure.

Therapeudic Use:
Only approved for ventricular arrhythmias. Used if quinidine and procainamide are poorly tolerated or not effective.
Lidocaine
Class: IB

Major Cardiac Effects:
Lidocaine's action is more directly limited to Na+ channels. It tends to be more selective in its effects than other Class I drugs. Has greater effect on diseased (depolarized) tissue than on normal tissue. Has less effect on atrial tissue, which has shorter action potentials, and thus sodium channels spend less time in the inactive state.

Pharmacokinetics:
Extensive first pass effect - only 3% of oral lidocaine enters the plasma. Half life is 1-2 hr. when given intavenously.

Major Side Effects:
Cardiotoxicity-
Lidocaine is the least cardiotoxic and safest of all currently used antiarrhythmic drugs. Worsens ventricular arrhythmias in less than 10% of patients. May suppress cardiac output in some heart failure patients.

Other side effects-
Same as other local anesthetics, i.e. neurologic (tremor, light headedness nausea etc)

Therapeudic Use:
Normally only used in emergency situations. Agent of choice to suppress ventricular tachycardia and prevents ventricular fibrillation after cardioversion.
Not effective against atrial arrhythmias
Mexiletine (tocainide)
Class: IB

Major Cardiac Effects:
Structurally related to lidocaine but designed to minimize first pass metabolism and thus can be given orally. Electrophysiologic and antiarrhythmic actions are similar to those of Lidocaine. It has a longer half-life.

Pharmacokinetics:

Major Side Effects:
Neurologic side effects- tremor nausea blurred vision lethargy.

Therapeudic Use:
Flecainide
Class: IC

Major Cardiac Effects:
Potent Na+ channel blocker with activity on activated channels
It slows the conduction velocity but have little effect on action potential duration.
It has no antimuscarinic action.

Pharmacokinetics:

Major Side Effects:
Cardiotoxicity-
Increased mortality post-myocardial infraction. The use of flecainide in post myocardial infarction patients has been questioned. CAST trial.

Other Side Effects – blurred vision

Therapeudic Use:
Patients with normal heart but have supraventricular arrhythmias.
Propafenone
Class: IC

Major Cardiac Effects:
similar action on sodium channels as flecainide.

Pharmacokinetics:

Major Side Effects:
Cardiotoxicity -
Risk of worsing arrhythmias

Side effects – metallic taste and constipation

Therapeudic Use:
Supraventricular arrhythmias
Moricizine
Class: IC

Major Cardiac Effects:
similar action on sodium channels as flecainide.

Pharmacokinetics:

Major Side Effects:
Cardiotoxicity -
Risk of worsing arrhythmias

Side effects – dizziness and Nausea

Therapeudic Use:
Ventricular Arrhythmias
Supraventricular arrhythmias
Propanolol
Class: II

Major Cardiac Effects:
Action of these drugs is chiefly due to blocking the action of catecholamines on the heart which tend to make the heart more excitable and thus less stable. Decrease activity of nodal tissue and thus can slow the sinus rate and depress AV conduction.

Propanolol and some other -blockers also have membrane effects especially in higher concentrations that are similar to the effects of quinidine and are probably due to blockade of sodium channels.

Pharmacokinetics:

Major Side Effects:

Therapeudic Use:
suppress premature ventricular contractions (PVC)s, including those induced by digitalis; can also suppress supraventricular tachycardia.
Atenolol
Class: II

Major Cardiac Effects:
Action of these drugs is chiefly due to blocking the action of catecholamines on the heart which tend to make the heart more excitable and thus less stable. Decrease activity of nodal tissue and thus can slow the sinus rate and depress AV conduction. This is a cardioselective B1 blocking agent.

Pharmacokinetics:

Major Side Effects:
asthma, negative inotropic, heart failure in patients with left ventricle insufficiency.

Therapeudic Use:
suppress premature ventricular contractions (PVC)s, including those induced by digitalis; can also suppress supraventricular tachycardia.
Metoprolol
Class: II

Major Cardiac Effects:
Action of these drugs is chiefly due to blocking the action of catecholamines on the heart which tend to make the heart more excitable and thus less stable. Decrease activity of nodal tissue and thus can slow the sinus rate and depress AV conduction. This is a cardioselective B1 blocking agent

Pharmacokinetics:

Major Side Effects:
asthma, negative inotropic, heart failure in patients with left ventricle insufficiency.

Therapeudic Use:
suppress premature ventricular contractions (PVC)s, including those induced by digitalis; can also suppress supraventricular tachycardia.
Esmolol
Class:

Major Cardiac Effects:
Action of these drugs is chiefly due to blocking the action of catecholamines on the heart which tend to make the heart more excitable and thus less stable. Decrease activity of nodal tissue and thus can slow the sinus rate and depress AV conduction. This is a SHORT-ACTING cardioselective B1 blocking agent used for acute arrhythmias.

Pharmacokinetics:

Major Side Effects:
asthma, negative inotropic, heart failure in patients with left ventricle insufficiency.

Therapeudic Use:
**used for accute arrhythmias. Suppress premature ventricular contractions (PVC)s, including those induced by digitalis; can also suppress supraventricular tachycardia.
Amiodarone
Class: III

Major Cardiac Effects:
Has Class IA, II and IV activity
Blocks K+ channels thus prolongs the action potential duration. Blocker of Na+ channels in inactive state. Weak Ca2+ channel blocker and adrenoreceptor blocker. Good inhibitor of abnormal automaticity. It slows the sinus rate and AV conduction velocity. This combination of effects gives amiodarone high efficacy and low chance of causing torsade de pointes.

Pharmacokinetics:
(half life = 13-103 days or more) Depends on the body load of amiodarone which accumulates without saturation in all body organs

Major Side Effects:
Cardiotoxicity-
Bradycardia, heart block, heart failure

Other side effects-
Due to the deposition of this drug in organ tissue.
These include neurologic and GI problems. Skin deposits result in photodermatitis. May cause thyroid dysfunction, liver necrosis and lung fibrosis.

Therapeudic Use:
***Most effective drug for prevent of atrial fibrillation and Ventricular tachycardia or fibrillation. Used to maintain normal sinus rhythm in atrial fibrillation. Prevents recurrent ventricular tachycardia. No increase in mortality has been seen.
Bretylium
Class: III

Major Cardiac Effects:
Lengthens action potential duration and effective refractory period. Shown experimentally to increase the strength of stimulation needed to induce ventricular fibrillation.
It causes depletion of catecholamines from sympathetic neurons thus after initial administration acts similar to a class II drug.

Pharmacokinetics:
IV use only in the USA

Major Side Effects:
Cardiotoxicity-
In the initial phase of administration catecholamine release is occurring and thus bretylium can precipitate arrhythmias.

Other side effects-
Postural hypotension
Nausea and vomiting

Therapeudic Use:
Rarely used. In emergencies after lidocaine and cardioversion have failed.
Sotalol
Class: III

Major Cardiac Effects:
Non-selective B-blocking and Class III activities

Pharmacokinetics:
Orally available with minimal metabolism

Major Side Effects:
Cardiotoxicity-
Torsade de pointes up to 6%

Therapeudic Use:
Supraventricular and life threatening ventricular arrhythmias.
Ibutilide
Class: III

Major Cardiac Effects:
Prolongs action potential in cardiac tissue by delaying repolarization by blockade of a portion of the K+ current and activating a slow, inward sodium current.

Pharmacokinetics:
Given IV

Major Side Effects:
Cardiotoxicity-
Side effects torsade de pointes 4-8% Treatment should be initiated in a hospital setting monitoring for excessive QT prolongation.

Therapeudic Use:
Newly approved for termination of atrial fibrillation (30% success i.v.) or flutter (50% success i.v.)
Dofetilide
Class: III

Major Cardiac Effects:
Potent Inhibitor of the delayed rectifier K channel

Pharmacokinetics:
Orally Available

Major Side Effects:
Cardiotoxicity-
Side effects torsade de pointes 1-3% Treatment should be initiated in a hospital setting monitoring for excessive QT prolongation.. No increased mortality was detected in clinical trials.

Therapeudic Use:
Newly approved for termination of atrial fibrillation (30% success i.v.) or flutter (50% success i.v.).
Used to sustain sinus rhythm after conversion of atrial fibrillation or atrial flutter via cardioversion.
Verapamil (diltiazem)
Class: IV

Major Cardiac Effects:
Verapamil is the prototype - other one in use is diltiazem. Blocks both active and inactive Ca2+ channels. Effects are mainly limited to nodal cells. It slows the sinus rate and slows conduction through the AV node. There may be a small reflex increase in sinus rate due to hypotensive action.
Suppresses abnormal automaticity induced by digoxin. Causes peripheral vasodilatation.

Pharmacokinetics:
Can be given orally but in larger doses since it is 80% metabolized by first pass effect.

Major Side Effects:
Cardiaotoxic-
AV block, Sinus arrest(Contraindicated in patients with a diseased sinus node, sinus sick syndrome, or AV block), Some evidence of increased incidence of arrhythmias (most people take them for hypertension, and thus those pt's are at greater risk for arrhythmias).

Extracardiac-
Constipation, hypotension, Some Neurological effects.

Therapeudic Use:
Atrial tachycardias; slows the ventricular rate in atrial fibrillation or flutter.
Adenosine
Adenosine directly inhibits AV nodal conduction with mild effect on the SA node. Enhanced K+ conduction and inhibition of cAMP-induced Ca2+ influx. *****Drug of choice for rapid management of paroxysmal supraventricular tachycardia. High efficacy (90-95%) and short duration of action (less than 10 sec half-life), Injectable. No time to cause side effects.
Magnesium/Potassium
Magnesium - used in patients with digitalis induced arrhythmias that have lowered blood magnesium levels. Also found to have antiarrhythmic effects torade de pointes with normal serum magnesium levels.
Potassium used in digitalis-induced arrhythmias especially if serum K+ is low.

Antibodies can also be used for Dig arrhythmias.
Digoxin (digitalis)
): used to slow ventricular rate in atrial fibrillation or flutter. Often effective in supraventricular tachycardia. Frequent cause of arrhythmias. Contraindicated in Wolf-Parkinson-White syndrome.
Edrophonium/Phenylephrine/Atropine/Isoproterenol
Edrophonium: Promuscarinic- often converts supraventricular tachycardia
Phenylephrine: A1 Agonist- reflex bradycardia. Also converts supraventricular tachycardia but can cause sinus arrest.
Atropine: Antimuscarinic- used in severe sinus bradycardia or AV block
Isoproterenol: Beta-agonist used in severe sinus bradycardia or AV block
Sodium Channel Review
M gate = activation gate (closed at rest)

H gate = inactivation gate (open at rest, but closes until recovery)
CAST study
Class IC were thought to be very specific, so we did
Cardiac Arrhythmic Supression Trial-
They took S/p MI patients and put half on Flecainide and half on placebo. The findings were that those on the drug had double the mortality rate of those on placebo. They casued so many arrhythmias that the pt's were better off without it.

Note that in contrast, Class II's have been shown to have positive effects of mortality S/P MI.
Non-Pharmacological Interventions
If we feel an arrhythmia, what can we do...

1. Simulate baroreceptors to increase vagal tone by holding our breath and massaging our carotids

2. Cardioversion (paced electrical currents to restore rhythm)

3. Electrical Defribulation