cardiac arrhythmias are abnormal heart rhythms that occur when the electrical signals controlling the heart beat are not working properly. these can include tachycardia ,Bradycardia,atrial fibrillation and more.

1. ARRHYTHMIA
DIAGNOSIS AND MANAGEMENT
HARESH A DESAI

2. These are drugs used to prevent or treat
irregularities of cardiac rhythm.
Nearly 3 out of 4 patients of acute MI & about
half of those given a GA exhibit at least some
irregularities in cardiac rhythm.
Arrhythmias are most common cause of
sudden cardiac death.
Abnormal automaticity or impaired
conduction or both = card arrhythmias.

3.  Cardiac action potential –when a stimulus
reaches the cardiac cell, specific ions move
into & out of the cell eliciting an action
potential. (divided into 4 phases )
 Phase 0 –is the rapid depolariation of the cell
mem in which – fast entry of Na into the cell
through Na channels.( followed by
repolarisation )

4.  Phase-1 is a short, initial rapid repolarisation
due to efflux of K ions.
 Phase- 2 is a prolonged plateau phase due to
slow entry of Ca ions in to the cell through the
Ca channels.(cardiac cell differs from other
cells in having this phase of action potential.
 Phase- 3 is a second period of rapid
repolarisation with K ions moving out of the
cell.

5.  Phase-4 is the resting phase during which K
ions return into the cell while Na & Caions
move out of it & the resting membrane
potential is restored.
 During Phase 1 &2, the cell does not
depolarise in response to another impulse,
i.e. it is in absolute refractory period. But in
Phase 3 & 4, the cell is in relative refractory
period &may depolarise in response to
impulse.

7. Arrhythmia Presentation
 Palpitation.
 Dizziness.
 Chest Pain.
 Dyspnea.
 Fainting.
 Sudden cardiac death.

8. Etiology
 Physiological
 Pathological:
 Valvular heart disease.
 Ischemic heart disease.
 Hypertensive heart diseases.
 Congenital heart disease.
 Cardiomyopathies.
 Carditis.
 RV dysplasia.
 Drug related.
 Pericarditis.
 Pulmonary diseases.
 Others.

9. Arrhythmia Assessment
 ECG
 24h Holter monitor
 Echocardiogram
 Stress test
 Coronary angiography
 Electrophysiology study

10. Mechanism of Arrhthmogensis
1. Disorder of impulse formation.
a) Automaticity.
b) Triggered Activity.
1) Early after depolarization.
2) Delayed after depolarization.
2. Disorder of impulse conduction.
a) Block – Reentry.
b) Reflection.
3. Combined disorder.

11.  Types of arrrythmias-
 1 EXTRASYSTOLES (ES)
 2 PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA (PSVT)
 3 ATRIAL FLUTTER (AFL)
 4 ATRIAL FIBRILLATION (AF)
 5VENTRICULATTACHYCARDIA
 6TORSADES DE POINTES

13. SINUS TACHYCARDIA
 Rate: 101-160/min
 P wave: sinus
 QRS: normal
 Conduction: normal
 Rhythm: regular or slightly irregular
 The clinical significance of this dysrhythmia depends on the
underlying cause. It may be normal.
 Underlying causes include:
 increased circulating catecholamines
 CHF
 hypoxia
 PE
 increased temperature
 stress
 response to pain
 Treatment includes identification of the underlying cause and
correction.

15. SINUS BRADYCARDIA
 Rate: 40-59 bpm
 P wave: sinus
 QRS: Normal (.06-.12)
 Conduction: P-R normal or slightly prolonged at slower rates
 Rhythm: regular or slightly irregular
 This rhythm is often seen as a normal variation in athletes, during
sleep, or in response to a vagal maneuver. If the bradycardia
becomes slower than the SA node pacemaker, a junctional rhythm
may occur.
 Treatment includes:
 treat the underlying cause,
 atropine,
 isuprel, or
 artificial pacing if patient is hemodynamically compromised.

17. SINUS ARRHYTHIMIA
 Rate: 45-100/bpm
 P wave: sinus
 QRS: normal
 Conduction: normal
 Rhythm: regularly irregular
 The rate usually increases with inspiration and decreases with
expiration.
 This rhythm is most commonly seen with respiration due to
fluctuations in vagal tone.
 The non respiratory form is present in diseased hearts and
sometimes confused with sinus arrset (also known as "sinus pause").
 Treatment is not usually required unless symptomatic bradycardia is
present.

19. PAROXYSMAL ATRIAL
TACHYCARDIA
 Rate: atrial 160-250/min: may conduct to ventricles 1:1, or 2:1, 3:1,
4:1 into the presence of a block.
 P wave: morphology usually varies from sinus
 QRS: normal (unless associated with aberrant ventricular
conduction).
 Conduction: P-R interval depends on the status of AV conduction
tissue and atrial rate: may be normal, abnormal, or not measurable.
 PAT may occur in the normal as well as diseased heart.
 It is a common complication ofWolfe-Parkinson-White syndrome.
 This rhythm is often transient and doesn't require treatment.
 However, it can be terminated with vagal maneuvers.
 Digoxin, antiarrhythmics, and cardioversion may be used.

21. ATRIAL FIBRILLATION
 Rate: atrial rate usually between 400-650/bpm.
 P wave: not present; wavy baseline is seen instead.
 QRS: normal
 Conduction: variableAV conduction; if untreated the ventricular
response is usually rapid.
 Rhythm: irregularly irregular. (This is the hallmark of this
dysrhythmia).
 Atrial fibrillation may occur paroxysmally, but it often becomes
chronic. It is usually associated with COPD, CHF or other heart
disease.
 Treatment includes:
 Digoxin to slow the AV conduction rate.
 Cardioversion may also be necessary to terminate this rhythm.

23. VENTRICULAR TACHYCARDIA
 Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm
 P wave: obscured if present and are unrelated to the QRS complexes.
 QRS: wide and bizarre morphology
 Conduction: as with PVCs
 Rhythm: three or more ventricular beats in a row; may be regular or
irregular.
 Ventricular tachycardia almost always occurs in diseased hearts.
 Some common causes are:
 CAD
 acute MI
 digitalis toxicity
 CHF
 ventricular aneurysms.
 Patients are often symptomatic with this dysrhythmia.
 Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.
 Electrical countershock is the intervention of choice if the patient is
symptomatic and rapidly deteriorating.
 Some pharmacological interventions include lidocaine, pronestyl, and
bretylium.

25. Antiarrhythmia Agents

26. CLASSIFICATION
 Rate: usually between 150 to 220/bpm,
 P wave: obscured if present
 QRS: wide and bizarre morphology
 Conduction: as with PVCs
 Rhythm: Irregular
 Paroxysmal –starting and stopping suddenly
 Hallmark of this rhythm is the upward and downward deflection of theQRS
complexes around the baseline.The term Torsade de Pointes means "twisting
about the points."
 Consider itV-tach if it doesn’t respond to antiarrythmic therapy or treatments
 Caused by:
 drugs which lengthen the QT interval such as quinidine
 electrolyte imbalances, particularly hypokalemia
 myocardial ischemia
 Treatment:
 Synchronized cardioversion is indicated when the patient is unstable.
 IV magnesium
 IV Potassium to correct an electrolyte imbalance
 Overdrive pacing
Class Action Examples Side Effects
1A Fast sodium channel blocker
varies depolarization and
action potential duration
Quinidine,
procainamide,
disopyramide
Class: nausea,
vomiting
Quinidine: hemolytic
anemia,
thrombocytopenia,
tinnitus
Procainamide: lupus
1B lignocaine,
Mexiletine
Lidocaine: dizziness,
confusion, seizures,
coma
Mexiletine: tremor,
ataxia, rash
1C Flecainide,
Propafenone
Flecainide: pro-
arrhythmia, nausea,
dizzyness
2 beta-blockers SA node & AV
node conduction
Propranolol,
metoprolol
Class: CHF,
bronchospasm,
bradycardia,
hypotension
3 Prolong action potential by
blocking K+ channels
Amiodarone,
sotalol
Amiodarone:
hepatitis, pulmonary
fibrosis, thyroid
disorders, peripheral

27. Class 1A agents: Procainamide, quinidine
Uses
Wide spectrum, but side effects limit usage
Quinidine : maintain sinus rhythms in atrial fibrillation and
flutter and to prevent recurrent tachycardia and
fibrillation
Procainamide: acute treatment of supraventricular and
ventricular arrhythmias (no longer in production)
Side effects
Hypotension, reduced cardiac output
Proarrhythmia (generation of a new arrhythmia) eg.

28. Class 1B agents: Lignocaine, phenytoin
Uses
acute : Ventricular tachycardia and fibrillation (esp.
during ischemia)
Not used in atrial arrhythmias or AV junctional
arrhythmias
Side effects
Less proarrhythmic than Class 1A (less QT effect)
CNS effects: dizziness, drowsiness

29. Class 1C agents: Flecainide, propafenone
Uses
Wide spectrum
Used for supraventricular arrhythmias (fibrillation
and flutter)
Premature ventricular contractions (caused
problems)
Wolff-Parkenson-White syndrome
Side effects
Proarrhythmia and sudden death especially with
chronic use (CAST study)
Increase ventricular response to supraventricular
arrhythmias

30. Class II agents: Propranolol, esmolol
Uses
treating sinus and catecholamine dependent tachy
arrhythmias
converting reentrant arrhythmias in AV
protecting the ventricles from high atrial rates (slow AV
conduction)
Side effects
bronchospasm
hypotension

31. Class III agents: Amiodarone, sotalol, ibutilide
Sotalol
Uses
Wide spectrum: supraventricular and ventricular
tachycardia
Side effects
Proarrhythmia, fatigue, insomnia
AMIODARONE- highly lipophilic long acting antiarrythmic drug
with multiple actions.
Prolong APD & QT interval with blocking K+ channels.
Preferentially blocks inactivated Na+ channels.
Partially inhibits myocardial ca+ channels , has noncompititive
beta adrenergic blocking property.

32. Class III agents: Amiodarone, sotalol, ibutilide
Amiodarone
Uses
Very wide spectrum: effective for most arrhythmias
Side effects: many serious that increase with time
Pulmonary fibrosis
Hepatic injury
Increase LDL cholesterol
Thyroid disease
Photosensitivity
May need to reduce the dose of digoxin and class 1
antiarrhythmics

33. Class IV agents: Verapamil and diltiazem
Uses
control ventricular rate during supraventricular
tachycardia
convert supraventricular tachycardia (re-entry around
AV)
Side effects
Caution when partial AV block is present. Can get
asystole if β blocker is on board
Caution when hypotension, decreased CO or sick sinus
Some gastrointestinal problems

34. Additional agents
Adenosine
Administration
rapid i.v. bolus, very short T1/2 (seconds)
Cardiac effects
Slows AV conduction
Uses
convert re-entrant supraventricular arrhythmias
hypotension during surgery, diagnosis of CAD
Magnesium
treatment for tachycardia resulting from long QT

35. Additional agents
Digoxin (cardiac glycosides)
Mechanism
enhances vagal activity, inhibits Na/K ATPase
 refractory period, slows AV conduction
Uses
treatment of atrial fibrillation and flutter
Atropine
Mechanism
selective muscarinic antagonist
Cardiac effects
blocks vagal activity to speed AV conduction and
increase HR