Arrhythmia

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Arrhythmia

• Arrhythmias are abnormal beats of the heart.
• Types of arrhythmias include
• According to heart rate
• Heartbeats that are too slow ( bradycardia)
• Heartbeats that are too fast (tachycardia)
• According to etiology
• Delayed after depolarization
• Heart block
• Abnormal pacemaker (Ectopic foci)
• Reentry circus movement
• Risk Factors
• Excess caffeine ,stress ,tobacco use ,alcohol use
• Digitalis overdose
• High blood pressure coronary artery disease
• Heart muscle damage after heart attack (MI)

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• Action Potential In Conducting and Non
  Conducting Tissues

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Heart Action Potentials

• Two ion channels regulate firing from SA node
• slow Ca channels phase O
• K channels phase 3
• membrane leakiness phase 4

Three ion channels regulate Action Potential of
non pacemaker cells fast Na channels phase
O K channels phase 1,2,3 Ca channels
phase 2
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• Symptoms
• 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

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• 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-ß 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.

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Bradycardia

• Asystole (Heart arrest)

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Tricky one
3rd Degree Heart Block (HB Type III) or Atrial
fierlation How Would You Know????
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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

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• 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.

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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 (gt180 beats per minute) may cause drops in
  arterial pressure and produce syncope.

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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.

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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.

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• 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.

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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.

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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.
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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).
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Sodium channel conformational states

• 3 states
• resting closed, can be opened
• activated open and ions moving
• inactivated closed and can not be opened

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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
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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.
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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.
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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
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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.
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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.
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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.
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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.
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• 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.

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Examples of Antidysrhythmic drugs