Transcript Arrhythmia 315

Arrhythmia
Arrhythmias are abnormal beats of the heart.
Types of arrhythmias include:
According to heart rate :
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Heartbeats that are too slow ( bradycardia)
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Heartbeats that are too fast (tachycardia)
According to etiology
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Delayed after depolarization
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Heart block
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Abnormal pacemaker (Ectopic foci)
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Reentry circus movement
Risk Factors
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Excess caffeine ,stress ,tobacco use ,alcohol use
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Digitalis overdose
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High blood pressure & coronary artery disease
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Heart muscle damage after heart attack (MI)
Action Potential In Conducting and Non Conducting Tissues
Heart Action Potentials
Three ion channels regulate Action Two ion channels regulate firing
from SA node:
Potential of non pacemaker cells
“fast” Na+ channels: phase O
“slow” Ca+ channels: phase
O
K+ channels: phase 1,2,3
K+ channels: phase 3
Ca++ channels: phase 2
membrane leakiness: phase 4
Symptoms:
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•
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Some arrhythmias may occur without any symptoms. Others may cause
noticeable symptoms, such as:
Fainting
Dizziness, sensation of light-headedness
Palpitations
Sensation of a missed or extra heart beat
Shortness of breath & chest pain
Etiology of arrhythmias
1. Delayed after depolarization
Non pacemaker cells (non conducting fibers) normally have a stable phase 4 (i.e.
they do not fire unless they receive a signal from the pacemakers)· In certain
condition, non conducting cells have a slow, rising phase 4, which allows them
to fire without a signal from the pacemaker. It is due to an increase in
intracellular Ca2+ ·
An increased intracellular Ca2+ occur in :
• A. Use of cardiac glycosides
• B. Increased sympathetic tone (adrenergic stress)
• C. Myocardial ischemia
3. Abnormal pacemaker (Ectopic foci)
• The pacemaker is the tissue which has the fastest rate of firing
Normally, this is the SA node· Sometimes, other nodal or conducting
tissues in the heart can assume the role of pacemaker
• The main predisposing factors are
a-β adrenoceptor stimulation: causes increase in Ca2+ levels
b- Myocardial ischemia: There is a reflex increase in sympathetic tone as a result of poor
perfusion. This increase in sympathetic tone increases Ca2+ levels· Also, ischemia affects
the Na+/K+ pump which requires ATP to extrude Na+ out of the cell. If this pump fails to
work (due to lack of ATP) Na+ concentrations increase in the cell, resulting in
depolarization
4. Heart block
• Damage to nodal tissue, most commonly AV node (e.g. during a
myocardial infarct or in case of digitalis toxicity), this prevents
conduction of the signal to other parts of the heart· The areas of the
heart which normally rely on normal SA node signal start to beat
independently, under the action of their own pacemakers.
Bradycardia
Asystole (Heart arrest)
Tricky one…
3rd Degree Heart Block (HB Type III)
or
Atrial fierlation
How Would You Know????
Atrial Fibrillation
Atrial fibrillation is the most common abnormal heart rhythm in
older people. In atrial fibrillation, the atria may be contracting at
greater than 300 beat per minutes. However, only some of these
electrical signals travel down the conduction pathway and
stimulate the ventricles. Consequently, the heart rhythm is
irregular and erratic
Atrial Flutter
In atrial flutter, unlike atrial fibrillation, the atrial rate
tends to be regular at 200 beats per minute. Like atrial
fibrillation, there is virtually always some degree of AV
block, such that the ventricular rate is usually around
150 beats per minute; in fact, atrial flutter can be
confused with sinus tachycardia at 150 beats per minute.
Ventricular Tachycardia
Ventricular tachycardia may give rise to symptoms such as
palpitations, shortness of breath, or light headedness,
depending upon the rate of the arrhythmia, its duration,
and the underlying heart disease. loss of consciousness
(syncope) or sudden death also may occur. Tachycardia
rates between 110 and 150 may be tolerated even if
sustained for minutes to hours. However, faster rates (>180
beats per minute) may cause drops in arterial pressure and
produce syncope.
Supraventricular tachycardia
Atrioventricular Reentry Tachycardia (Wolfe-Parkinson-White
Syndrome).
Atrioventricular reentry tachycardia requires the participation of both atrium and
ventricle and a piece of conducting tissue bridging the atrium and ventricles
outside of the AV node. This extra piece of tissue is called an accessory pathway.
The accessory pathway is an extra piece of conducting heart muscle with which
the patient is born. In atrioventricular reentry tachycardia, the two pathways
of the reentry circuit can be composed of one accessory pathway and the AV
node or it can be made up of two accessory pathways without the participation
of the AV node .
Ventricular Fibrilation
Ventricular fibrillation results when multiple sites in
the ventricles fire impulses very rapidly in an
uncoordinated fashion. The ventricles cease to
pump blood effectively, thereby stopping the
circulation of blood. Death follows within a few
minutes, unless a normal rhythm is restored with
emergency treatment.
Treatment
Antiarrhythmic Medications
These will help slow down or speed up your
heart rate, or return your heart rhythm to
normal , depending on your need.
Electrical Cardioversion or Defibrillation
These treatments involve placing paddles on
the chest. An electrical current is passed
through the chest wall to the heart, in order
to re-set its electrical circuits, and attempt to
return the heart rhythm to normal.
Defibrillators
Defibrillators
- Defibrillators are devices that deliver an electric shock to the
heart to terminate an abnormal rhythm and allow the normal
rhythm to resume
-ICDs are need for better treatments for individuals with life-threatening arrhythmias. As
the rate of sudden death in individuals without ICDs who were treated with medications,
coronary artery bypass, or angioplasty is up to 30-40% annually
-They are used in: Patients who have survived at least one episode of cardiac arrest due to a
ventricular tachyarrhythmia and Patients who have recurrent, poorly tolerated ventricular
tachycardia.
Drug class Classifications:
The antiarrhythmic agents are often classified using a
system loosely based on the channel or receptor involved. This
system specifies four classes, usually denoted by Roman numerals
I through IV:
I. Sodium channel blockers
that are subdivided into 3 subgroups, IA, IB, and IC
II. Beta adrenoceptor blockers
III. Potassium channel blockers
IV. Calcium channel blockers
A miscellaneous class includes adenosine, digitalis, potassium
iod, and magnesium ion.
Class I - sodium channel blocking drugs
all of them behave like local anesthetics.
These agents are frequently subdivided according to their effects
on action potential duration
Class IA agents (prototype: quinidine) prolong the action
potential.
Class IB drugs shorten the action potential in some cardiac
tissues (prototype: lidocaine).
Class IC drugs have no effect on action potential duration
(prototype: flecainide).
Sodium channel conformational states
3 states:
resting: closed, can be opened
activated: open and ions moving
inactivated: closed and can not be opened
Mechanism of action:
Useful sodium channel-blocking drugs bind to their receptors much more readily
when the channel is open or inactivated than when it is fully repolarized and
recovered from its previous activity.
Ion channels in arrhythmic tissue spend more time in the open or inactivated
states than do channels in normal tissue. Therefore, these antiarrhytmic drugs
block channels in abnormal tissue more effectively than channels in normal tissue.
As a result, antiarrhythmic sodium channel blockers are state dependent in their
action, ie, selectively depressants on tissue that is frequently depolarizing (eg,
during a fast tachycardia) or is relatively depolarized during rest (by hypoxia).
Drugs with classIA action:
Quinidine ,procainamide, and disopyramide
Quinidine
C a r d i a c effects:
A-V depressant :negative inotropic
increase action potential (AP) duration
E x t r a c a r d i a c effects:
quinidine possesses alpha adrenoceptor-blocking properties
that can cause vasodilation and a reflex increase in HR.
Toxicity:
-Quinidine has antimuscarinic actions in the heart that inhibit
vagal effects. This can overcome some of its direct membrane
effect and lead to increased sinus rate and increased
atrioventricular conduction. This action can be prevented by
prior administration of a drug that slows atrioventricular
conduction (verapamil, a beta-blocker, digitalis).
-One type of arrhythmia, called torsade de pointes, is
particularly associated with quinidine.
-Hyperkalemia usually exacerbates the cardiac toxicity of class
I drugs.
2-Procainamide
The electrophysiological effects of procainamide are similar
to those of quinidine.
Procainamine ´s cardiotoxic effects are similar to those of
quinidine. The most troublesome adverse effect is a syndrome
resembling lupus erythematosus and usually consisting of
arthralgia and arthritis. Approximately one-third of patients
receiving long-term procainamide therapy develop this
syndrome.
Drugs with class IB actions:
Lidocaine
- is the prototype IB drug. This drug affects ischemic or
depolarized Purkinje and ventricular tissue and has little effect
on atrial tissue; the drug reduces action potential duration.
-It is useful in acute ventricular arrhythmias, especially those
involving ischemia, eg, following myocardial infarction.
-Atrial arrhythmias are not respondsive unless caused by
digitalis.
Mexiletine, tocainide and phenytoin have similar effects.
Toxicity:
Typical local anesthetic toxicity CNS stimulation, including
convulsions; allergy (usually rashes but may extend to
anaphylaxis).
These drugs may also precipitate arrhythmias, but this is less
common than with class IA drugs. Hyperkalemia, however,
increases cardiac toxicity
Drugs with class IC action:
Encainide (recently withdrawn), and propafenone
These drugs have no effect on ventricular action potential duration
Flecainide
It is effective in both atrial and ventricular arrhythmias:
(a) refractory ventricular tachycardias that tend to progress to VF at unpredictable
times, resulting in "sudden death
(b) certain supraventricular arrhythmias.
Toxicity:
more likely than other antiarrhythmic drugs to exacerbate or precipitate
arrhythmias (proarrhythmic effect). For this reason, the class IC drugs are limited
use.
. Hyperkalemia increases the cardiac toxicity of these agents.
CLASS II (BETA-BLOCKERS)
Their mechanism in arrhythmias is primarily cardiac beta blockade
and reduction in cAMP, which results in the reduction of both
sodium and calcium currents and the suppression of abnormal
pacemakers.
Esmolol
a very short-acting beta-blocker for intravenous
administration, is used almost exclusively in acute surgical
arrhythmias.
Propranolol, metoprolol, and timolol
are commonly used as prophylactic drugs in patients who
have has a myocardial infarction. These drugs provide a
protective effect for two years or more after the infarct.
CLASS III (POTASSIUM CHANNEL BLOCKERS)
They cause prolongation of the action potential duration by blockade of
potassium channels that are responsible for the repolarization of the action
potential.
AP prolongation results in an increase in effective refractory period and
reduces the ability of the heart to respond to rapid ectopic beats
Amiodarone
most effective antiarrhythmic drug.
broad spectrum: it blocks sodium, calcium, and potassium
channels and beta adrenoceptors.
Toxicity
Thyroid dysfunction (hyper- or hypothyroidism), paresthesias,
tremor, microcrystalline deposits in the cornea and skin, and
pulmonary fibrosis. Amiodarone rarely causes new arrhythmias.
CLASS IV (CALCIUM CHANNEL BLOCKERS)
Verapamil is the prototype. Diltiazem is also effective
Nifedipine and the other dihydropyridines are not useful as
antiarrhythmics, probably because they decrease arterial
pressure sufficiently to evoke arrhythmias.
These agents cause a state-dependent selective depression
of calcium current in tissues that require the participation of
L-type calcium channels.
Calcium channel blockers were drugs of choice in
atrioventricular nodal reentry (also known supraventricular
tachycardia) until adenosine became available. Their major
use now is in the prevention of these nodal arrhythmias.
• Potassium ion:
Potassium depresse ectopic pacemakers, including
those caused by digitalis toxicity. Hypokalemia is
associated with increased incidence of arrhythmias,
especially in patients receiving digitalis. Conversely,
excessive potassium levels depress conduction and, if
abnormal, normalized.
• Magnesium ion:
Magnesium has not been as well studied as
potassium but appears to have similar depressant
effects on digitalis-induced arrhythmias.
Examples of Antidysrhythmic drugs