DR NIKUNJ R SHEKHADA (MBBS,MS GEN SURG DNB CTS SR)

1. CARDIAC ARRHYTHMIAS
BY DR NIKUNJ
(CTS RESIDENT STAR HOSPITAL)
(Coordinator:DR P.SATYENDRANATH PATHURI)
(3/9/2018)

2. • The heart has a conduction system separate from any other system
• The conduction system makes up the PQRST complex we see on paper
• An arrhythmia is a disruption of the conduction system
• Understanding how the heart conducts normally is essential in understanding and
identifying arrhythmias
• SA Node
• Inter-nodal and
• inter-atrial pathways
• A-V Node
• Bundle of His
• Perkinje Fibers

3. SA Node
• The primary pacemaker of the heart
• Each normal beat is initiated by the SA node
• Inherent rate of 60-100 beats per minute
• Represents the P-wave in the QRS complex or atrial depolarization (firing)
P wave: the sequential activation (depolarization) of the right and left atria

4. AV Node
• Located in the septum of the heart
• Receives impulse from inter-nodal pathways and holds the signal before sending
on to the Bundle of His
• Represents the PR segment of the QRS complex
• Represents the PR segment of the cardiac cycle
• Has an inherent rate of 40-60 beats per minute
• Acts as a back up when the SA node fails
• Where all junctional rhythms originate

5. QRS Complex
• Represents the ventricles depolarizing (firing) collectively. (Bundle of His and
Perkinje fibers)
• Origin of all ventricular rhythms
• Has an inherent rate of 20-40 beats per minute

6. The Normal ECG
P
Q
R
S
T
QTPR
0.12-0.2 s approx. 0.44 s
Atrial muscle
depolarization
Ventricular muscle
depolarization
Ventricular
muscle
repolarization
Heart Rate: 60 - 90 bpm
PR Interval: 0.12 - 0.20 sec
QRS Duration: 0.06 - 0.10 sec
QT Interval (QTc < 0.40 sec)
SA Node discharge = 60 – 100 / min
AV Node discharge = 40 – 60 min
Ventricular Tissue discharge = 20 – 40 min
• Heart rate (state atrial and ventricular, if different)
• PR interval (from beginning of P to beginning of QRS)
• QRS duration (width of most representative QRS)
• QT interval (from beginning of QRS to end of T)
• QRS axis in frontal plane

7. CARDIAC ARRHYTHMIAS
• An abnormality of the cardiac rhythm is called a cardiac arrhythmia.
• Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no
symptoms at all.
• There are two main types of arrhythmia:
• 1. bradycardia: the heart rate is slow (< 60 b.p.m.)
• 2. tachycardia: the heart rate is fast (> 100 b.p.m.).
• Tachycardias are more symptomatic when the arrhythmia is fast and sustained. Tachycardias are
subdivided into
• supraventricular tachycardias, which arise from the atrium or the atrioventricular junction.
• Ventricular tachycardias, which arise from the ventricles.

8. SINUS RYTHM
• The normal cardiac pacemaker is the sinus node
• its rate of discharge is controlled by the autonomic nervous system;
• sympathetic system increases heartrate.
• parasympathetic system decrease heartrate.
• Normal sinus rhythm is characterized by P waves that are upright in leads I, and II
of the ECG,but inverted in the cavity leads AVRand V1.

10. SINUS ARRHYTHMIA
• Fluctuations of autonomic tone result in phasic changes of the sinus discharge
rate.
• During inspiration,parasympathetic tone falls and the heart rate quickens,
• expiration the heart rate falls.
• This variation is normal, particularly in children and young adults
• Typically sinus arrhythmia results in a regularly irregular pulse
•

11. ARRHYTHMIA FORMATION
• Arrhythmias can arise from problems in the
 Sinus node
 Atrial cells
 AV junction
 Ventricular cells.
• Arrhythmias caused by 2 mainmechanism:
 Automaticity
 Re-entry

12. SA NODE PROBLEMS
• SA Node can:
• fire too slow :Sinus Bradycardia
• fire too fast :Sinus Tachycardia

13. SINUS BRADYCARDIA
• A sinus rate of less than 60 b.p.m.during the day or less than 50 .m. at night is
known as sinus bradycardia.
• CAUSES
• Physiological
 In athletes
 During sleep
• Pathological
 Extrinsic causes: Hypothermia, hypothyroidism,cholestatic jaundice and raised
intracranial pressure. Drug therapy with beta-blockers,digitalis and other anti
arrhythmicdrugs. Neurally mediated syndromes
 Intrinsic causes: Acute ischaemia and infarction of the sinus node (as a
complication of acute myocardial infarction). Chronic degenerative changes such
as fibrosis of the atrium and sinus node (sick sinus syndrome)

14. TREATMENT
• Identification & treatment of the cause
• Acute symptomatic bradycardia responds to atropine o.6 mg i.v.
• Temporary pacemaker in symptomatic bradycardia if there isreversible cause
• Permenant pacemaker in symptomatic irreversible cause.

15. SINUS TACHYCARDIA
• Resting sinus rate of more than 100b.p.m. is known as sinus tachycardia.
• Causes:
• Non cardiac Acute
 1. Fever
 2. Hypovolemia
 3. Pain
 4. Infection
 5. Exercise
 6. Emotion/anxiety
• Cardiac :HF with compensatoy tachycardia
• Treatment of the cause
• Symptomatic sinus tachycardia can be reduced with beta-blocker and/or Verapamil

16. ATRIAL CELL PROBLEMS
• Atrial cells can:
• fire occasionally from a focus
• Premature Atrial Contractions(PACs)
• Fire continuously due to a looping re-entrant circuit
• Atrial Flutte

17. ATRIAL CELL PROBLEMS
• Atrial cells can also:
• fire continuously from multiple foci or
• fire continuously due to multiplemicro re-entrant “wavelets” Atrial Fibrillation
•

18. ATRIAL TACHYARRHYTHMIAS
• Atrial tachyarrhythmias including atrial fibrillation, atrial flutter, atrial
tachycardia and atrial ectopic beats all arise from the atrial
myocardium.They share common etiologies
CAUSES
• Cardiac
 Hypertension
 Congestive heart failure
 Coronary artery disease andmyocardial infarction
 Cardiomyopathy: dilated,hypertrophic
 Myocarditis and pericarditis
 Wolff-Parkinson-White syndrome
 Sick sinus syndrome
 Cardiac tumours
 Cardiac surgery.

19. ATRIAL TACHYARRHYTHMIAS
Non-cardiac
 Thyrotoxicosis
 Phaeochromocytoma
 pneumonia, COPD
 pulmonary embolism
 hypokalaemia
 Alcohol abuse
 Caffeine & smoking
 Idiopathic

20. ATRIAL FLUTTER
• It is a condition in which atrial rate typically between 250 and 350 beats per
minute.• The ECG shows regular saw tooth-like atrial flutter waves (F waves)
between QRS complexes
• Clinical features:
• Palpitation
• Reduced COP leads to fatigue,weakness, coolness of the skin
• In adequate coronary perfusion may cause angina, inadequate cerebral perfusion
may lead to dizziness or syncope.

21. Management
• DC cardioversion at < 50J as initial treatment of choice
• Procainamide 15 mg/kg over 60 minmaintainace1–4 mg/min can be given for
cardioversion
• Verapamil to slow ventricular response
• Digitalis with beta-blocker or calcium channel blocker may be given to slow
ventricular rateif electrical or pharmacological cardioversionis not possible
• Amiodarone 15 mg/min for 10 min, 1 mg/minfor 6 h to restore sinus rhythm and
prevent reccurence of atrial flutte
• radiofrequency catheter ablation.

22. ATRIAL FIBRILLATION
• Atrial fibrillation is a continuous, rapid(300-600 per minute) activation of the atria.
• The atria beats rapidly and ineffectively , the ventricles respond at irregular
intervals giving the characteristic irregularly irregular pulse.
• •ECG• Absent P wave• Fine oscillation of baseline(fibrillation waves)• QRS rhythm
is rapid & irregular.
• CLINICAL FEATURES
• Palpitation
• if ventricular response is rapid,COP may fall resulting in Symptoms of pulmonary
congestion (dyspnea, orthopnea& PND)Symptoms of inadequate peripheral
perfusion (angina,dizziness & syncope)
• Systemic embolism (stroke, leg pain & abdominal pain)

23. Management
• When atrial fibrillation is due to an acute precipitating event such as alcohol
toxicity,chest infection or hyperthyroidism, the provoking cause should be treated.
• Strategies for the acute management of AF are ventricular rate control or
cardioversion (±anticoagulation).
• Ventricular rate control is achieved by drugs which block the AV node.
• while the cardioversion is achieved electrically by DC shock or medically either by
intravenous infusion of an anti-arrhythmic drug such as a class Ic or a class III agent
or by taking an oral agent previously tested in hospital and found to be safe in a
particular patient (pill-in-pocket approach).

24. ELECTRICAL DC CARDIOVERSION
• If pt is unstable due to fast ventricular rate & presents in shock,severe
hypotension, pulmonary edema or ongoing MI.
• the risk of thromboembolism is high if atrial fibrillation persist more than 48 hrs.
• Conversion to sinus rhythm can beachieved by electrical DC cardioversion 200 J,
then 2 × 360 Jin about 80% of patients

25. RATE CONTROL
• In less unstable pt or those at highrisk of thromboembolism due to cardioversion
• Rate control is usually achieved by a combination of Digoxin, beta-blockers or
calcium-channel blockers (Verapamil or diltiazem).
• The ventricular rate response is generally considered controlled if the heart rate is
between 60 and 80beats per minute at rest and 90 and115 beats per minute
during moderate exercise
• If rate control is unsuccessful and duration of atrial fibrillation is morethan 2-3
days then perform transoesophageal echocardiography to look for atrial thrombus,
if there is no thrombus then cardiovert the pt,in case of presence of thrombus give
anticoagulation for 4 wks before& 4 wks after cardioversion

26. • Two strategies are available for the long-term management of atrialfibrillation:
• 1. rhythm control (anti arrhythmicdrugs plus DC cardioversion plus warfarin)
• 2. rate control (AV nodal slowing agents plus warfarin)
• Elective cardioversion :First anticoagulate the pt for 4 wks.
• Pharmacological cardioversion by using amiodarone 300-400mgtwice daily for 2-
4wks then 200mgdaily . Anticoagulation should be continued.
• Radiofrequency VA node ablation& insertion of permanent pacemaker should be
used in resistant cases with no drug works

27. AV JUNCTIONAL PROBLEMS
• The AV junction can:
• fire continuously due to a looping re-entrant circuit
• block impulses coming from the SA Node Paroxysmal Supraventricular Tachycardia
• AV Junctional Blocks

28. SUPRAVENTRICULAR TACHYCARDIA (SVT)
• This is a tachycardia occurring in episodes with rate of 140-240, as ar esult of re-
entry or rapidly firing ectopic focus in the atria or AV node. It may last from few
seconds to many hours (if untreated)
• Predisposing factors:
 Anxiety
 Excess tobacco or coffee
 Hyperthyroidism
 Exertion
 Alcohol
• Clinical features
 Pt feels that has suddenly start tobeat fast (palpitation).
 Fainting, breathlessness, dizziness,neck pulsation, central chest pain,and
weakness•
 polyuria is some time a feature.
 ECG shows tachycardia with normalQRS complex.

29. Management
• Acute management In the absence of heart disease , serious side effects are rare,
and most attacks break spontaneously.
• Terminate attack if cardiac failure,syncope or anginal pain develops or if there
underlying cardiac or coronary disease
• vagotonic maneuvers
 Carotid sinus message
 Valsalva maneuver
 facial immersion in cold water
 Pressure on eyes
 Self inducing vomiting
 Breath holding
 Lowering the head between the knees

30. • Drugs
 If physical manoeuvres have not been successful,
 intravenous adenosine 6mg bolus, if no response within 1-2 minutes 2nd&3rd
12mg should be given.
 verapamil 5-10 mg i.v. over 5-10minutes Maintenance 2.5–10 mg/h.
 Beta blokers ismolol 500microg/kg within one minute follwed by 25-
200microg/min
• Beta blocker and digoxin are less commonly used•
• Amiodarone is not required for termination of attack, it is used for prevention of
occurrence.
• if pt hymodynamically unstable or if adenosine or veramapil are contraindicated or
in effective ,Synchronized DC cardioversion should be performed.
• Long-term management Verapamil, diltiazem, and beta-blockers have proven
effective in 60-80% of patients.
• If drug therapy is not effective then perform electrophysiological evaluation and
perform catheter mediated ablation

31. HEART BLOCK OR CONDUCTION BLOCK
• may occur at any level in the conducting system.
• Block in either the AV node or the His bundle results in Atrioventricular (AV)
block,whereas block lower in the conduction system produces bundle branch block
• Atrioventricular block There are three forms:
• First-degree AV block
• This is simple prolongation of thePR interval to more than 0.22 s.Every atrial
depolarization is followed by conduction to the ventricles but with Delay of
conduction may be within atrium, AV node, bundle of his or bundle branches.

32. SECOND-DEGREE AV BLOCK
• This occurs when some P waves conduct and others do not. There are several
formsThere are three types:-
• I. Mobitz I block (Wenckebach blockMobitz I block)is progressive PR interval
prolongation until a P wave fails to conduct.
• The PR interval before the blocked P wave is much longer than the PR interval
after the blocked P wave
•

33. • Mobitz II block occurs when a dropped QRS complex is not preceded by
progressive PR interval prolongation

34. 2 : 1 or 3 : 1 (advanced) block
• It may present as either type I or type II AV block in which there are 2 p waves or 3
to each QRS complex.
• If PR interval is prolonged and QRS is narrow then it is type I.
• if PR normal and QRS is wide then it is type II 2nddegree AV block
•

35. THIRD-DEGREE (COMPLETE) AV BLOCK
• Complete heart block occurs when all atrial activity fails to conduct to the
ventricles.
• In patients with complete heart block the etiology needs to be established.
Cardiac action is maintained by spontaneous escape rhythm

36. BUNDLE BRANCH BLOCK
• The His bundle gives rise to the right and left bundle branches.
• The left bundle subdivides into the anterior and posterior divisions of the left
bundle.
• Various conduction disturbances can occur.
• Normal Impulse Conduction: Sinoatrial node,AV node, Bundle of His, Bundle
Branches, Purkinje fibers
• So, depolarization of the Bundle Branches and Purkinje fibers are seen as the QRS
complex on the ECG.Therefore, a conduction block of the Bundle Branches would
be reflected as a change in the QRS complex
• With Bundle Branch Blocks you will see two changes on the ECG. QRS complex
widens (> 0.12 sec). QRS morphology changes
• Why does the QRS complex widen? When the conduction pathway is blocked it
will take longer for the electrical signal to pass throughout the ventricles

37. Right Bundle Branch Blocks
• QRS morphology is characteristic For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those leads overlying the right ventricle (V1
and V2).V1Rabit ear (M)
• Causes of right bundle branch block :It is a normal finding in 1% of young
adults and 5% of elderly adults.
• Congenital heart disease.
• Pulmonary disease.
• Acute myocardial infarction.
• Cardiomyopathy.
• Conduction system fibrosis.

38. LEFT BUNDLE BRANCH BLOCK
• QRS morphology is characteristic For LBBB the wide QRS complex assumes a
characteristic change in shape in those leads opposite the left ventricle (right
ventricular leads -V1 and V2).Broad,deep S waves
•
Causes of left bundle branch block
• Left ventricular outflow obstruction
• Aortic stenosis
• Hypertension
• Coronary artery disease
• Acute myocardial infarction•
• Severe coronary disease (two- to -three-vessel disease)

39. Ventricular ectopic rhythms
• Ventricular ectopic beats
• Ventricular tachycardia
• Ventricular fibrillation
• Ventricular Conduction Normal Signal moves rapidly through the ventricles
• Abnormal Signal moves slowly through the ventricles

40. VENTRICULAR CELL PROBLEMS
• Ventricular cells can:
• fire occasionally from1 or more foci :Premature Ventricular Contractions(PVCs)
• fire continuously from multiple foci
• fire continuously due to a looping re-entrant circuit Ventricular Tachycardia

41. VENTRICULAR TACHYCARDIA
• Ventricular tachycardia is defined as three or more consecutive
• usual rate is 160-240/min with regular rhythm.
• Ventricular tachycardia is either non-sustained (lasting < 30sec) or sustained.
• Pt may C/O Palpitation, dyspnea,dizziness or syncope
• CUASES
• Acute MI
• Myocarditis
• Dilated cardiomyopathy
• Hypertrohic cardiomyopathy
• Chronic ischemic disease
• Mitral valve prolapse
• ECG show a rapid ventricularrhythm with broad abnormal QRS complexes

42. TREATMENT
• Treatment may be urgent, depending on the haemodynamic situation.
• If thepatient is haemodynamically compromised (e.g. hypotensive or pulmonary
oedema) emergency DC cardioversion may be required.
• On the other hand, if the blood pressure and cardiac output are well maintained first-
line drug treatment consists of lidocaine(50-100 mg i.v. over 5 minutes) followed by a
lidocaine infusion (2-4 mg i.v. perminute).
• if VT not suppressed by lidocaine then give I.V amiodarone (150mgover 10min followed
by 360mg over6hrs then 540mg over18hrs followedby 20-80mg/kg/min infusion ).
• DCcardioversion is necessary if medicaltherapy is unsuccessful.
• Chronic recurrent VT
• Sustained VT :Treatment of choice is implantable cardioverter-defibrillator device(ICD).
• Non sustained VT: Beta blockers reduce the incidence of sudden death by40-50.
amiodarone may be beneficial. implantable cardioverter-defibrillator device
•

43. Ventricular fibrillation
• This is very rapid and ineffecti veventricular activation which produce no pulse.
Therefore pt is pulseless and rapidly becomes unconscious and respiration ceases.
• Causes
 MI
 Electric shock
 Hypokalemia
• Clinical features:
• Loss of consciousness within seconds
• Pulse absent• Respiration ceases.
• ECGshows shapeless oscillations
• Management: Electrical defibrillation.
• If it not availablethen perform CPR.
• In survivors of VT if cause is not revrsible, then ICD is 1st line therapy to manage
further episodes

44. Thank you