cardiac arrythmias

1. CARDIAC ARRYTHMIAS
AND
MANAGEMENT
MODERATOR- DR VIKAS GOEL
PRESENTER- DR PRATIMA

2. DEFINITION
Cardiac arrhythmias are a group of conditions in which the heart beats with an irregular or
abnormal rhythm.
Arrhythmia /dysrhythmia: abnormality in the site of origin of impulse, rate, or conduction
Arrhythmias may be described based on ---
(1)rate (bradycardia or tachycardia),
(2) rhythm (regular or irregular),
(3)origin of impulse (supraventricular, ventricular, or artificial pacemaker),
(4) impulse conduction (atrioventricular, ventriculoatrial or block),
(5) ventricular rate, or
(6) special phenomena (e.g., preexcitation).

3. Arrhythmia pathogenesis
• Disorder of impulse formation:
o Abnormal Automaticity.
• Triggered Activity.
o Early after depolarization.
o Delayed after depolarization.
• Disorder of impulse conduction:
o Impulse Block
o Re - entry phenomena

4. Abnormal automaticity
The SA node is the heart’s natural pacemaker
Any impulses fired from elsewhere in the heart before or concurrently with SA node
firing can lead to premature heartbeats or sustained abnormal heartbeats.
Problems associated are
o sinus tachyarrhythmia
o sinus bradyarrhythmia
o Abnormality in site of impulse generation ,ectopic foci
o Escape rhythms

5. Triggered activity
This is an abnormal secondary upstroke which occur only after a normal initial or
“triggering“ upstroke or action potential.
These secondary upstrokes are called after-depolarization's
This may be of two types–
o Early after depolarization o Delayed after depolarization

6. Abnormal impulse conduction
● Conduction block may occur due to depression of impulse conduction at AV node
& bundle of His, due to vagal influence or ischaemia .
Types :
1st degree heart block – slowed conduction
2nd degree block – some supraventricular complex not conducted
3rd degree block – no supraventricular complex are conducted
Re-entry phenomena
● The most common mechanism of reentry is based on the model originally
proposed by Erlanger and Schmitt and later modified by Wit.2
● This model postulates the presence of a ring or loop of cardiac tissue that is
functionally separate from neighboring tissue and the presence of transient or
permanent unidirectional block in a portion of the loop.

7. It can be of two types-
I. Anatomically defined re-entry
● E.g, bundle branches, fibrosis, dual pathways, atrioventricular node (plus
accessory pathway) Wolf Parkinson White syndrome (wpw)
II. Functionally defined re-entry
● Mostly seen in patients with ischemic heart disease
Re-entry phenomena(anatomical)

8. Classification of arrhythmias
Abnormal heart pulse formation
● Sinus arrhythmia
● Atrial arrhythmia
● Atrioventricular junctional arrhythmia
● Ventricular arrhythmia
Abnormal heart pulse conduction
● Sinus-atrial block
● Intra-atrial block
● Atrio-ventricular block
● Intra-ventricular block
Abnormal heart pulse formation and conduction

9. CAUSES & RISK FACTORS
● Coronary artery disease.
● Electrolyte imbalances in your blood (such as sodium or potassium).
● Structural changes of the heart
● Scarring of the heart, often the result of a heart attack
● Healing process after heart surgery.
● Hypertension (high blood pressure)
● Diabetes
● Drug abuse
● Excessive coffee consumption
● Hyperthyroidism (an overactive thyroid gland)
● Mental stress
● Smoking
● Some dietary supplements &some herbal treatments

10. Symptoms of tachycardia
● breathlessness (dyspnea)
● dizziness
● syncope (fainting, or nearly fainting)
● fluttering in the chest
● chest pain
● lightheadedness
● sudden weakness
Symptoms of bradycardia
● angina (chest pain)
● trouble concentrating
● confusion
● difficulties when exercising
● dizziness
● fatigue (tiredness)
● lightheadedness
● palpitations
● shortness of breath
● syncope (fainting or nearly fainting)
● diaphoresis, or sweating

11. Investigations
● blood and urine tests
● EKG (electrocardiogram)
● Holter monitor - a wearable device that records the heart for 1-2 days
● echocardiogram
● chest X-ray
● heart catheterization

12. Management of arrhythmias
● Pharmacological therapy.
● Cardio version.
● Pacemaker therapy.
● Surgical therapy
● Interventional therapy
Pharmacologic Rationale & Goals
The ultimate goal of antiarrhythmic drug therapy:
● Restore normal sinus rhythm and conduction
● Prevent more serious and possibly lethal
arrhythmias from occurring.
Antiarrhythmic drugs are used to:
● decrease conduction velocity
● change the duration of the effective refractory
period(ERP)
● suppress abnormal automaticity

13. Mechanisms of Anti-arrhythmic drugs
To suppress automaticity
↓ Rate of phase 0
↓ Slope of phase 0
↑ Duration of ERP(effective refractory
period)
Resting membrane potential more negative
Abolishing reentry
Slow conduction
↑ ERP
Anti arrhythmic drugs
Anti-tachycardia agents
Anti-bradycardia agents
Anti-tachycardia agents
VaughamWilliams classification
Class I : sodium channel blocker
Class II : ß-receptor blocker
Class III : Potassium channel blocker
Class IV : Calcium channel blocker
Others: Adenosine

14. Class I – Na+ channel blockers
The primary action of these class of drugs is
o To limit the conductance of Na+ across the cell membrane
o Reduce the rate of phase 4 depolarization
They are further divide into three subclasses
o Subclass IA
o Subclass IB
o Subclass IC

15. Na+ channel blockers(subclass IA)
● Less use in clinical practice
● The anti arrhythmic drugs include
● quinidine
● procainamide.
● are open state Na+ channel blockers.
● This class of drugs moderately delay
the channel recovery.
● They suppress the AV conduction and
prolong refractoriness
Na+ channel blockers(subclass IB)
● block the Na+ channels more in inactivated
than in open state, but do not delay
channel recovery.
● have little or no effect at slower heart
rates, and more effects at faster heart
rates
● do not change or may decrease the action
potential duration.
● Class IB drugs tend to be more specific for
voltage gated Na channels than Ia
● E.g Lidocaine - Mexiletine
● Perfect to ventricular tachyarrhythmia

16. Cardiac Na+ channel
Na+ channel blockers(subclass IC)
● Most prominent action is on open state
Na+ channels and have the longest
recovery time
● delay conduction and prolong the P-R
interval, broaden the QRS complex
● have minimal effect on action potential
duration
E.g Moricizine – Propafenone
● Can be used in ventricular and/or supra-
ventricular tachycardia and extrasystole.
● This class of drug has high proarrhythmic
potential

17. Class II – β1 adrenergic blocking agents
● are conventional beta blockers act by blocking the effects of catecholamines
at the β1- adrenergic receptors, thereby decreasing sympathetic activity on
the heart.
● They decrease conduction through the AV node.
● They prolong PR interval, but no effects on QRS or QT interval
● E.g. Propranolol - Metoprolol
● Perfect to hypertension and coronary artery disease patients associated
with tachyarrhythmia

18. Class III – K+ channel blockers
● acts by prolonging repolarization.
● Not affect the sodium channel, so conduction velocity is not decreased.
● The prolongation of the action potential duration and refractory period,
combined with the maintenance of normal conduction velocity, prevent re-
entrant arrhythmias.
● Class III agents have the potential to prolong the QT interval of the ECG
● E.g Amiodarone - Bretylium

19. Class IV- calcium channel blockers
● The primary action of this class of drug is to inhibit Ca2+ mediated slow inward
current.
● They decrease conduction through the AV node, and shorten phase two (the
plateau) of the cardiac action potential.
● As they reduce the contractility of the heart, so may be inappropriate in heart failure.
● They slow sinus rhythm, prolong PR interval, no effect on QRS complex
● E.g. Verapamil - Diltiazem
● used in supraventricular tachycardia

20. ● Others
• Adenosine-
be used in supraventricular tachycardia
● Digoxin:-
Used to control ventricular rate in AF – AFL -PSVT
Adenosine
Endogenously produced important chemical mediator used in PSVT
Mechanism:
Activation of Ach sensitive K+ channel causes membrane hyperpolarization of SA
node and results in
● depression of SA node
● slowing of AV conduction and shortening of action potential in atrium indirectly
reduces CA++ current in AV node with depression of reentry in PSVT.

21. Anti-bradycardia agents
● ß-adrenic receptor activator:
● Isoprenaline
● Epinephrine
● M-cholinergic receptor blocker:
● Atropine
● Non-specific activator:
● Aminophylline
Non-drug therapy
1-Cardioversion:
● For tachycardia especially
hemodynamic unstable patient
2-Radiofrequency catheter ablation
(RFCA):
● For those tachycardia patients (SVT,
VT, AF, AFL)
3-Artificial cardiac pacing:
● For bradycardia, heart failure and
malignant ventricular arrhythmia
patients.

23. Radiofrequency catheter ablation

24. Artificial cardiac pacing

25. Management of different types of arrythmia
Premature beats
● Premature beats are the most common type of arrhythmia.
● Premature beats that occur in the atria are called premature atrial contractions, or PACs
and those that occur in the ventricles are called premature ventricular contractions
● PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol,
cigarettes, or medications.
● Treatment is rarely necessary

26. Sinus tachycardia
● Sinus tachycardia is a heart rhythm originating from the SA node with an elevated rate of
impulses, defined as a rate greater than 100 beats/min in an average adult.
● Sinus tachycardia is usually a response to normal physiological situations, such as
exercise and an increased sympathetic tone with increased catecholamine release—
stress, fright, flight,anger
● Treatment not required for physiologic sinus tachycardia.
● Underlying causes are treated if present.

27. Paroxysmal supraventricular tachycardia
Here the heart rate ranges from 160 – 250 beats per min
There are 2 common types
1) Atrio ventricular reciprocating tachycardia
2) AV nodal reentrant tachycardia
AV Nodal Reciprocating Tachycardia
● Patients with AVRT have been born with an extra, abnormal electrical connection in the
heart.
● In AVRT, the extra connection, which is often called an accessory pathway, joins one of
the atria with one of the ventricles
● In some patients with AVRT, the accessory pathway is capable of conducting electrical
impulses in both directions while in other patients the accessory pathway can only
conduct electrical impulses in one direction or the other

28. ● This difference turns out to be important. In most patients with AVRT, the impulses
can only go across the accessory pathway from the ventricle to the atrium.
● Patients in whom the impulses can travel across the accessory pathway in the
other direction - from the atrium to the ventricle - are said to have Wolff-Parkinson-
White (WPW) syndrome
Wolf Parkinson White Syndrome
● An abnormal band of atrial tissue connects the atria and the
ventricles and can electrically bypass the normal conducting
pathways
● A reentry circuit develops causing paroxysms of tachycardia.
● Drug treatment : flecainide, amiodarone or disopyramide
● Digoxin and verapamil are contraindicated
● Transvenous catheter radiofrequency ablation is the treatment
of choice

29. AV nodal Re-entrant Tachycardia
● AVNRT develops because of the presence of two electro-physiologically distinct pathways
for conduction in the complex AV node.
● The fast pathway in the more superior part of the node has a longer refractory period,
whereas the pathway lower in the AV node region conducts more slowly but has a shorter
refractory period.
● As a result of the inhomogeneities of conduction and refractoriness, a reentrant circuit can
develop in response to premature stimulation.

30. Management of PSVT
Acute Management
● If the patient is hemodynamically stable, vagal maneuvers e.g carotid massage ,
can be successfully employed. If not successful, the administration of IV
adenosine frequently does so.
● Intravenous beta blockade or calcium channel therapy should be considered as
second-line treatment.
● Patients with hemodynamic instability require emergency cardioversion.
Long-term management
● It includes ablation of the accessory pathway.
● Also, verapamil, diltiazem & β-blockers are effective in 60- 80% of patients.

31. Atrial Flutter
● Atrial flutter is a macro-reentrant arrhythmia identified by flutter waves, often best seen
in the inferior leads at 250 to 350 beats/min
● Patients often present with a 2:1 atrioventricular conduction with a ventricular rate of
150 beats/min
● Here the electrical signals come from the atria at a fast but even rate, often causing the
ventricles to contract faster and increase the heart rate.
● When the signals from the atria are coming at a faster rate than the ventricles can
respond to, the ECG pattern develops a signature "sawtooth" pattern, showing two or
more flutter waves between each QRS complex

32. Treatment
● For acute paroxysm : Cardioversion
● Recurrent paroxysms may be prevented by class Ic and class III agents
● The treatment of choice for patients with recurrent atrial flutter is radiofrequency
catheter ablation
Atrial fibrillations
● Atrial fibrillation is the most common sustained narrow complex Tachyarrhythmia .
● It is marked by disorganized, rapid, and irregular atrial activation. The ventricular
response to the rapid atrial activation is also irregular
● Typically the pulse rate will vary between 120 and 160 beats per minute

33. ● The ECG shows normal but irregular QRS complexes,fine oscillations of the baseline
(so-called fibrillation or f waves) and no P waves
The most important risk factors-
● structural heart disease
● valvular heart disease
● left ventricular hypertrophy
Acute management of AF
● Cardioversion rates delivered
synchronously with the QRS complex
typically are >90%.
● Pharmacologic therapy to terminate AF
is less reliable.
● Oral and/or IV administration of
amiodarone or procainamide has only
modest success.
● Patients are anticoagulated ( warfarin)
for 4 weeks before cardioversion

34. Ventricular tachycardia
Ventricular tachyarrhythmia is defined as three or more consecutive ectopic beats at a
rate more rapid than 100 beats/min
● This is a potentially life-threatening arrhythmia because it may lead to ventricular
fibrillation, asystole, and sudden death.
● A condition in which an electrical signal is sent from the ventricles at a very fast but
often regular rate.
● If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained
ventricular tachycardia.
● If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular
tachycardia

35. Sustained ventricular tachyarrhythmia also is traditionally classified as
● Monomorphic (one site of origin) or
● polymorphic (two or more sites of origin).
1-Monomorphic ventricular tachyarrhythmia
usually results from reentry, and the site of
reentry depends in part on the type of heart
disease.
● In patients with coronary artery disease,
the reentry circuit is usually located in
ventricular myocardium,
● whereas in dilated cardiomyopathy with
left bundle branch block,bundle branch
reentry is common.
2-polymorphic ventricular tachyarrhythmia may
occur in acquired states that produce a marked
prolongation of the Q-T interval.
Treatment
● In hemodynamically compromised
:emergency asynchronous
defibrillation is done
● If hemodynamically stable:
intravenous therapy with class I
drugs or amiodarone .
● VT in patients with structural heart
disease is now almost always
treated with the implantation of an
ICD to manage anticipated VT
recurrence

36. Ventricular fibrillation
● A condition in which many electrical signals are
sent from the ventricles at a very fast and erratic
rate. As a result, the ventricles are unable to fill
with blood and pump.
● This rhythm is life-threatening because there is
no pulse and complete loss of consciousness.
● It requires prompt defibrillation to restore the
normal rhythm and function of the heart.
Treatment
● Basic and advanced cardiac life
support is needed
● Implantable cardioverter-
defibrillators (ICDs) are firstline
therapy in the management of these
patients

37. Torsades pointes
● This is a type of short duration tachycardia that reverts to sinus rhythm spontaneously.
● It may be Congenital or due to Electrolyte disorders and certain Drugs
● It may present with syncopal attacks and occasionally ventricular fibrillation.
● QRS complexes are irregular and rapid that twist around the baseline. In between the
spells of tachycardia the ECG show prolonged QT interval

38. Treatment:
● correction of any electrolyte disturbances
● stopping of causative drug
● atrial or ventricular pacing
● Magnesium sulphate for acquired long QT interval
● IV isoprenaline in acquired cases
● B blockers in congenital types
● Patients who remain symptomatic despite conventional therapy and those with a strong
family history of sudden death usually need ICD therapy

39. Sinus Bradycardia
● Physiological variant due to strong vagal tone or atheletic training.
Rate as low as 50 at rest and 40 during sleep
● Common causes:
● Hypothermia,
● hypothyroidism,
● Drug therapy with beta blockers,
● digitalis and other antiarrhythmic drugs.
● Acute ischemia and infarction of the sinus node (as a complication of acute myocardial
infarction).

40. Sick sinus syndrome
● Sick sinus syndrome is a group of arrhythmias caused by a malfunction of the
sinus node
● A condition in which the sinus node sends out electrical signals either too slowly
or too fast. There may be alternation between too-fast and too-slow rates.
● This condition may cause symptoms if the rate becomes too slow or too fast for
the body to tolerate.
● Artificial pacemakers have been used in the treatment of sick sinus syndrome.
● Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias
respond well to medical therapy.
● However, because both bradyarrhythmias and tachyarrhythmias may be
present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia.
● Therefore, a pacemaker is implanted before drug therapy is begun for the
tachyarrhythmia

41. Atrio ventricular block
● First degree heart block
● PR interval is lengthened beyond 0.20 seconds.
● In first-degree AV block, the impulse conducting from atria to ventricles through the AV
node is delayed and travels slower than normal
● Seldom of clinical significance, and unlikely to progress

42. Second degree A-V Block
A- Mobitz type I (Wenckebach phenomenon):
● Gradually increasing P-R intervals culminating in
an omission.
● When isolated, usually physiological and due to
increased vagal tone and abolished by exercise
and atropine.
B- Mobitz type II:
● The P wave is sporadically not conducted.
● Occurs when a dropped QRS complex is not
preceded by progressive PR interval
prolongation.
● Pacing is usually indicated in Mobitz II block,
whereas patients with Wenckebach AV block
are usually monitored

43. Third degree A-V Block
● Common in elderly age groups due to idiopathic bundle branch fibrosis.
● Other causes include coronary heart disease, calcification from aortic valve, sarcoidosis
or it may be congenital.
● ECG shows bradycardia, P wave continues which is unrelated to regular slow
idioventricular rhythm.
● Treatment is permanent pacing.

44. Thank you