Arrhythmia Presentation By HAZHAR NANAKALE PHARMACOLOGIST AMITY UNIVERSITY DELHI-INDIA

1. ARRHYTHMIA
Hazhar Faisal Abdullah
M.Pharm (Pharmacology) 2nd Sem
Faculty of Pharmacy
Amity University
DELHI-INDIA

2. DEFINATION:
■ Cardiac arrhythmia/cardiac
dysrhythmia/irregular heart beat is a group of
condition in which the heart beat is irregular, too
fast or too slow.

3. ABNORMAL RHYTHM:
CAN BE OF TWO EXTREME FORMS:
1. Bradycardia - Cardiac beats below 60
beats per minute .
2. Tachycardia – Cardiac beat above 100
beats per minute.

5. ETIOLOGY (CAUSES):
■ Coronary artery disease.
■ Electrolyte and pH imbalances in your blood (such as sodium or
potassium).
■ Changes in your heart muscle.
■ Injury from a heart attack.
■ Healing process after heart surgery.
■ Irregular heart rhythms can also occur in "normal, healthy"
hearts.
■ Ischemic Heart Disease
■ Neurogenic and drug influences
■ Others

6. (SYMPTOMS)
■ Palpitation (make you feel like your heart is beating too hard or too fast
characterized by awareness of cardiac muscle contractions in the chest )
■ Dizziness.
■ Shortness of breath or chest pain Dyspnea.
 Sincope or Fainting (a short loss of consciousness and muscle strength)
 Unstable haemodynamic condition.
 Abnormal pulse.
 Precipitation of cardiac failure.
■ Sudden cardiac death
■ Swelling
■ Exercise Intolerance

7. Normal cardiac rhythm:
For normal cardiac rhythm:
I. Heart rate should be 80-100
II. Impulse should originate from SA node
III. Cardiac impulse should propagate through normal
conduction pathway
IV. Normal velocity

9. CARDIAC ACTION POTENTIAL:
■ FAST CHANNEL AP SLOW CHANNEL AP

10. CARDIAC CONDUCTION AND ECG:
 Cardiac cycle
 P wave = atrial depolarization
 PR interval = pause between atrial and
ventricular depolarization
 QRS = ventricular depolarization
 T wave = ventricular depolarization
 U wave=Perkinje fiber repolarization

11. Mechanism of Arrhythmias
1) Enhanced/ectopic pacemaker activity
2) After depolarisation
i. Early after-depolarisation
ii. Delayed after depolarisation
3) Reentry
i. Circus movement type
ii. Microentry circuit
4) Increased/decreased automaticity

13. 1-ENHANCED/ECTOPIC
PACEMAKER ACTIVITY
■ An ectopic pacemaker or ectopic foci is an excitable groups of cells that causes the
premature heart beat outside the normally functioning SA node of human heart....
– Results due to pathological increase in phase 4 slope - accelerated pacemaker
rate
– May result from current of Injury
– Physiology: ACh reduces such pacemaker rate – by decreasing phase 4 and
hyperpolarization
– Ventricular wall cells may also show such pace maker activity – due to ischemia.

16.  Blockage of Conduction from SA node
 AV node Blockage
Causes
• Ischemia
• Fibrosis (the thickening and scarring of connective tissue, usually as a result of injury or
damage)
• Viral Infection
RESULTS in HEART ATTACK

17. 2-AFTER DEPOLARISATION:
These are secondary depolarisation accompanying a normal or
premature action potential.
 EARLY AFTER DEPOLARISATION:
repolarisation during phase 3 AP is interrupted and membrane
potential oscillates.
If the amplitude of oscillation is sufficiently large, neighbouring tissue is
activated and series of impulses are propagated

18. CONTINUE..
■ EAD are frequently associated with long QT interval.
■ They result from depression of delayed rectifier K+ ion.
 DELAYED AFTER-DEPOLARISATION:
• After attaining RMP a secondary deflection occurs which may reach
threshold potential and initiate a single premature AP.
• Result from a Ca+ overload.

19. Becaues an AP is needed to trigger after depolarisation, arrhythmia based on
these have been called triggered arrhythmias.

20. 3-REENTRY:
■ Due to primarily to abnormality of conduction, an impulse may
recirculate in the heart and cause repetitive activation without need
for any new impulse to be generated.
■ One of the causes of the most arrhythmias
■ Normally, impulses propagate in synchronized manners
■ But, here one impulse reenters and re-excites areas of heart more
than once – no need for new impulse generation
■ Re-entering of impulses may be
1. Anatomically defined reentry – Circus movement type
2. Functionally defined reentry - Microentry circuit

21. A- CIRCUS MOVEMENT TYPE:

22. 2.Re-entryTachycardias
 Atrial Fibrillation

23. B- MICRO ENTRY CIRCUIT:

24. 4-INCREASED OR DECREASED
AUTOMATICITY or Fractionation of Impulse:
 Increased Vagal activity – Atrial ERP (effective refractory period )brief and
inhomogeneous
 Premature impulses get conducted by fibers having short ERP – then to
the fibers with longer ERP and so on
 Asynchronous activation of atrial fibers – inhomogeneity – Atrial
fibrillation etc.

25. Classification of Arrhythmia:
 NORMOTROPIC
• Sinus tachycardia
• Sinus bradycardia
• Sinus arrhythmia
 ECTOPIC
• Heart block
• Extrasystole
• Paroxysmal tachycardia
• others

26. Arrhythmia Conditions - Clinically
■ Extrasystole: premature beats due to abnormal automaticity/after
depolarization – AES, VES or AV nodal ES
■ Paroxysmal Supraventricular Tachycardia (PSVT): Sudden onset of atrial
tachycardia 150-200/minute (1:1), reentry phenomenon (AV node)
■ Atrial Flutter: 200-350/minute (2:1 to 4:1 AV block), reentrant circuit in right
atrium
■ Atrial Fibrillation: Asynchronous activation of atrial fibres 350-550/min with
irregular 100 to 160 ventricular beats – due to electrophysiological
inhomogenicity of atrial muscles (bag of worms)
■ Ventricular tachycardia: 4 or more consecutive extrasystole of ventricles –
monomorphic or polymorphic
■ Ventricular Fibrillation: rapid irregular contractions – fatal (MI,
electrocution)
■ Torsades de pointes: polymorphic ventricular tachycardia, rapid
asynchronous complexes, rise and fall in baseline of ECG
■ Atrio-ventricular Block (A-V Block): vagal influence or ischaemia - 1st, 2nd
and 3rd degree – slowed conduction, drop beat and no

27. 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 catecholamine's
 CHF
 hypoxia (oxygen deficiency)
 increased temperature
 stress
 response to pain
■ Treatment includes identification of the underlying cause and correction.

29. 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,
 artificial pacing if patient is hemodynamically compromised.

31. 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.

33. 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 of Wolfe-Parkinson-White syndrome.(WPW is
caused by the presence of an abnormal accessory electrical conduction
pathway between the atria and the ventricles. Electrical signals traveling down
this abnormal pathway (known as the bundle of Kent) may stimulate the
ventricles to contract prematurely)
■ This rhythm is often transient and doesn't require treatment.
 However, it can be terminated with vagal maneuvers.
 Digoxin, antiarrhythmics, and cardioversion (is a procedure that uses external
electric shocks to restore a normal heart rhythm) may be used.

35. ATRIAL FIBRILLATION:
■ Rate: atrial rate usually between 400-650/bpm.
■ P wave: not present; wavy baseline is seen instead.
■ QRS: normal
■ Conduction: variable AV 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.

37. 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.

39. TORSADE DE POINTES:
■ Rate: usually between 150 to 220/bpm,
■ P wave: may be 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 the QRS complexes around the baseline.
The term Torsade de Pointes means "twisting about the points."
■ Consider it V-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

41. VENTRICULAR FIBRILLATION:
■ Rate: unattainable
■ P wave: may be present, but obscured by ventricular waves
■ QRS: not apparent
■ Conduction: chaotic electrical activity
■ Rhythm: chaotic electrical activity
■ This dysrhythmia results in the absence of cardiac output.
■ Almost always occurs with serious heart disease, especially acute MI.
■ The course of treatment for ventricular fibrillation includes:
 immediate defibrillation and ACLS protocols.(Advanced cardiac life
support (ACLS) in adults)
 Identification and treatment of the underlying cause is also needed.

43. HEART BLOCK
■ DEPRESSED CONDUCTION OF IMPULSE FROM ATRIA TO VENTRICLES
■ AV NODE BECOMES DEFECTIVE AND IMPULSES (P-WAVES) ARE BLOCKED FROM BEING
TRANSMITTED TO VENTRICLES
■ FIRST DEGREE
■ SECOND DEGREE
TYPE I
TYPE II
■ THIRD DEGREE

44. 1° HEART BLOCK
■ PR INTERVAL > 0.20 SECONDS
■ CAUSES: MAY BE NORMAL VARIANT
INFERIOR WALL MI
DRUGS: DIGOXIN
VERAPAMIL
■ TREATMENT:
MONITOR
OBSERVE FOR SYMPTOMS

45. 2° HEART BLOCK
■ ONE OR MORE P-WAVES ARE NOT CONDUCTED THROUGH THE
VENTRICLE
■ HEART RATE - VENTRICULAR RATE SLOW TO NORMAL
ATRIAL RATE MAY BE 2 – 4 X’s
FASTER THAN VENTRICULAR
 PRI becomes progressively longer until drops QRS

46. 3° HEART BLOCK
(COMPLETE HEART BLOCK)
■ ATRIAL IMPULSES & VENTRICULAR RESPONSE
ARE IN TOTAL DISASSOCIATION
■ P-WAVES ARE SEEN & ARE IRREGULAR
■ QRS COMPLEX ARE SEEN & ARE IRREGULAR
(ESCAPE RHYTHM)
■ NO CORRELATION BETWEEN P-WAVES & QRS
(RATE IS SLOW) – independent rhythms

47. NSR(Normal sinus rhythm) vs 3RD Degree Block

48. 3° HEART BLOCK
(COMPLETE HEART BLOCK)
■ TREATMENT
PACEMAKER
TEMPORARY
OR
PERMANENT

49. Diagnosis of Arrhythmia:
■ Medical history
■ Physical examination
■ Laboratory test

50. Anti-arrhythmia Agents:
■ Anti-tachycardia agents
■ Anti-bradycardia agents

51. TREATMENT:Anti-tachycardia agents

52. 5-Others: Adenosine, Digital

53. Anti-bradycardia agents
■ Isoprenaline
■ Epinephrine
■ Atropine
■ Aminophylline

54. Non-drug therapy:
■ Cardioversion: For tachycardia especially hemodynamic
unstable patient
■ Radiofrequency catheter ablation (RFCA): For those
tachycardia patients (SVT, VT, AF, AFL)
■ Artificial cardiac pacing: For bradycardia, heart failure
and malignant ventricular arrhythmia patients.

55. CLASS 1:Na+ CHANNEL BLOCKERS
FURTHER CLASSIFIED INTO:
• Class 1a-
Eg:quinidine,procainamide,disopyramide
• Class 1b-Eg:lidocaine
• Class1c-Eg:propafenone

57. Quinidine:
■ Dextroisomer of Quinine: Na+ channel blocking and antivagal action
■ Actions:
 Inhibition of Na channel – slanted O phase and Decreases phase 4
 Prolongation of APD – due to K+ channel block
 Increase in ERP – due to delay in Na+ and K+ channel recovery
 Net result is delay in conductivity and increase in refractoriness
 Fall in BP – direct cardiac depression
 Other actions include – alpha blockade, decreased skeletal muscle contractility,
uterine contractions, vomiting and diarrhoea etc.
 Kinetics: well absorbed orally, half life – 10 Hrs
 Uses:
 Broad spectrum antiarrhythmic
 Atrial fibrillation and flutter, prevention of PSVT and prevention of ventricular
tachycardia
 Adverse effects: Not used now for adverse effects like Proarrhythmia (torsades de pointes), sudden
cardiac arrest or VF, cinchonism, angioedema, vascular collapse etc.
 Available as 200, 300 mg tabs. And 300 mg/ml Injections

58. Procainamide:
■ Procaine derivative (amide)
■ Identical action with quinidine except:
– Minimal antivagal action
– Lesser suppression of ectopic automaticity
– Lesser depression of contractility and AV conduction
– No alpha blocking action
■ Kinetics:
– Absorbed orally and bioavailability is 80%
– Metabolized in liver to N-acetyl-procainamide (NAPA) – blocks K channel and prolongs
repolarization
■ Dosage – 250 mg tabs and 1gm/ml injections
– Antiarrhythmic – 0.5 to 1 gm oral followed by 0.25-0.50 mg every 2 Hrs
■ Uses: Mainly for monomorphic VTs and to prevent recurrences
■ ADRs: Hypersensitivity, flushing, hypertension, torsedes de pointes and CNS
symptoms – mental confusion, hallucinations and weakness

59. Lidocaine (Lignocaine) :
■ Popular antiarrhythmic and also local anaesthetic (membrane stabilizing action)
■ Lowest potency for Na+ channel inactivated state – ECTOPIC Foci
– Enhance phase – 4 depolarization in partially depolarized or stretched PF – After
depolarization antagonized – no effect on SAN
– Practically no action on Atrial fibres
– Rate of 0 phase in AVN and ventricles – not affected
– Reduction in APD in PF and ventricular myocardium
■ Actions:
– Selective action on partially depolarized and cells with long APD – normal ventricular and
conducting fibres – not affected
– Suppression of automaticity in ectopic foci (reentry) – one way or two way block
– Enhanced phase-4 depolarization in partially depolarized
– Little effects on cardiac contractility and arterial BP

60. ■ Kinetics: Ineffective orally, given IV lasts for 10-20 minutes. Therefore given as IV bolus
50-100 mg followed by 20-40 mg every 10-20 minutes. Half-life prolonged in CHF (coz.
Vd decreases) and 70-80% metabolized by liver
■ Adverse effects: Neurological – drowsiness, paresthesia, blurred vision, nystagmus and
fits etc.
– No proarrhythmic effects – no cardiotoxicity
■ Uses: 50-100 mg bolus and 10-20 mg every 20 minutes
– 1st line of drug in Arrhythmia following acute MI and cardiac surgery
– Prevention of ventricular tachycardia
– Digitalis toxicity – no AV block
■ LA lignocaine Vs Antiarrhythmic lignocaine ?

61. CLASS 2:β BLOCKERS

62. ■ Drugs used are beta-blockers: Propranolol, Sotalol, Esmolol and
Acebutlol
■ Suppression of adrenergically mediated activity
■ Propranolol - Membrane stabilizing effect like quinidine on heart –
high doses – clinical dose: cardiac adrenergic blockade
■ Clinical doses (antiarrhythmic effect) - Block beta-1 receptor in
heart and decreases heart rate
1. Decrease in phase 4 depolarization and automaticity in SA node,
AVN, PF and other ectopic foci (Adrenaline causes ventricular ES
and fibrilation by increasing the phase 4 depolarization !!!)
2. Prolongation of ERP of AVN – impede AV conduction

63. Uses of Propranolol:
■ Arrhythmias associated with increased sympathetic activity – sinus
tachycardia, atrial extrasystoles provoked by emotion and exercise
■ Less effective in PSVT than adenosine and verapamil
■ Propranolol is used to treat sympathetically mediated arrhythmias -
phaeochromocytoma and halothane anaesthesia
– Sinus tachycardia, atrial and nodal extrasystole and nodal
extrasystole provoked by exercise
Does not abolish AF or Afl but decreases ventriculsar rate
■ Reduce mortality after MI – anti-ischaemic action
■ Esmolol IV – quickly terminates AF and fluttter and used in
emergency control of arrhythmia due to anaesthetics

64. CLASS 3:K+ channel blockers

65. ■ Class III drugs K channel blockers prolong repolarization (increase
refractoriness) by blocking outward potassium conductance
– Prolongation of Cardiac action potential
– Increased ERP
■ Drugs – Amiodarone Ibutilide, dofetilide, sotalol (II + III action) and
bretylium
■ Bretylium is used only in life threatening arrhythmias

66. Amiodarone:
Long acting and highly lipophillic and Iodine containing compound
MOA: - multiple actions
1. Blocking of delayed rectifier K+ channel – prolongs APD
2. Weak class I (lidocaine like) – depresses conducton in partially depolarized and
long APD
3. II (beta- blocker) – NC alpha and beta; and class IV actions
4. Also direct coronaray and peripheral vasodilator
■ Overall – Slowed conduction and supressed automaticity
Kinetics: Incompletely and slowly absorbed – daily oral dose is given for several days
for actions to develop, t1/2 = 3-8 weeks
Dose: 400-600 mg/day p.o for many days followed by 100-200 mg/day as maintenance
(100-300 mg slow IV)

67. Amiodarone:
Uses:
■ Most tachyarrhythmic conditions – ventricular and supraventricular
■ Recurrent VT and VF
■ WPW syndrome
Adverse effects:
■ Photosensitization – skin pigmentation
■ Peripheral neuropathy – weak shoulder and pelvic muscles
■ Myocardial depression – bradycardia
■ Pulmonary alveolitis and fibrosis – kept below 200 mg
■ Corneal micro deposits – on long term use
■ Hypothyroidism, goitre – inhibition of T4 to T3
Drug Interactions: Digoxin and warfarin (reduced renal clearance)

68. CLASS 4:calcium channel blockers

69. ■ Three important classes:
– Phenylalkylamines – hydrophillic Verapamil
– Dihydropyridines – lipophilic Nifedepine
– Benzothiazepines – hydrophilic Diltiazem
■ Verapamil and diltiazem: are useful in Arrhythmia
■ Relatively selective AV nodal L-type calcium channel blockers –
depression of Ca++ mediated depolarization and delay recovery
– Slows SA node automaticity
– reduced phase 4 depolarization in SAN and PF – extinction of
latent pacemakers and DAD
– Prolongation of AVN ERP – reentry terminated
– Negative ionotropic action

70. ■ Uses: Verapamil
1. PSVT:
■ For termination of attack – 5 mg IV over 2-3
minutes (reflex bradycardia)
■ For prevention of attack 60-120 mg orally tds
2. Reduce ventricular rate in Atrial fibrillation (AF) and
Atrial flutter – with digitalis

71. Others: Adenosine, Digital
Adenosine:
■ Endogenously produced important chemical mediator used in PSVT
■ MOA:
– Activation of ACh sensitive K+ channel - membrane hyperpolarization of
SA node (G-protein coupled adenosine receptor A1)
– depression of SA node and also slowing of AV conduction
– shortening of action potential in atrium and reduced excitability
– Also indirectly reduces Ca++ current in AV node – depression of reentry
in PSVT

72. ■ Very short half life – 20-30 sec. - Uptake by RBCs and endothelial cells
(5-AMP and inosine)
■ Administered intravenously – available as free base or ATP
– 6 - 12 mg/ATP 10 - 20 mg given as a rapid intravenous bolus
(administered over a 1-2 second period)
– If the first dose does not result in elimination of the supraventricular
tachycardia within 1-2 minutes - 12 mg should be given as a rapid
intravenous bolus
■ ADR: chest tightness, dyspnoea, fall in BP and flushing etc.

74. REFERENCES:
 The pharmacological basis of therapeutics by goodman and gilman’s
 Essentials of medical pharmacology by KD Tripathi.
 Clinical pharmacy and therapeutics by walker whittlesea.
 Basic and Clinical Pharmacology Katzung 13 Edition
 Pharmacotherapy Handbook - Ninth Edition by Barbara G.
Wells (Author), Joseph T. Dipiro (Author), Terry L. Schwinghammer (Author)
 www.youtube.com - Pathophysiology of Cardiac Arrhythmias by Andrew Wolf
 Wikipedia
 http://www.rnceus.com/ekg/ekgsecond2.html
 ACLS Guidelines 2005
 www.EMS-ED.net
 http://www.doctorshangout.com/forum/topics/acls-algorithms-1

75. ThankYou