Cardiac arrhythmias

1. Assistance Prof. Dr .Ghazi F. Haji
Cardiologist
Arrhythmias

3. A cardiac arrhythmia
@is a disturbance of the electrical rhythm of the
heart
@Arrhythmias are might be occur in :
1- structural heart disease
2-healthy heart.
A heart rate > 90/min is tachycardia
heart rate < 60/min is a bradycardia.

4. Mechanisms of tachycardia
• Increased automaticity..
• Re-entry. (Most tachyarrhythmias are due to re-
entry).
• Triggered activity..
Mechanisms of Bradycardia may be due to:
• Reduced automaticity, e.g. sinus bradycardia.
• Blocked or abnormally slow conduction, e.g. AV block

5. Classification of arrhythmia ;
1- Supraventricular (Narrow QRS complex )
(sinus ,atrial .junctional)
2-Ventricular (wide ,bizzar QRS complex)
Sometime :supraventricular with wide QRS
complex
 1-BBB
 2-accessory conduction

6. Noticeable arrhythmia symptoms
may include:
A fluttering in your chest
A racing heartbeat (tachycardia)
A slow heartbeat (bradycardia)
Chest pain
Shortness of breath
Lightheadedness
Dizziness
Fainting (syncope) or near fainting
Polyurea

7. Sinus rhythm :
@Sinus arrhythmia : change in heart rate during respiration
(increase in inspiration VS expirat)occur in
children,autonomic neuropathy
@Sinus bradycardia :
 In -atheletic -sleep
 MI.
 Sinus node dysfunction(sick sinus syndrom(tachy-brady
syndrome)
 hypothyroidism,hypothermia,cholestaesis juandic
 increase intracranial pressure .
 drugs (b-blocker .calcium channel blocker .antiarrhythmic
drugs)
Treatment : (if asymptomatic –no treatment .if symptomatic -
atropin) pacemaker if not response

8. @Sinus tachycardia: (physiological ,pathological)
The upper limit of normal rate for sinus tachycardia is
thought to be 220 bpm minus age.
 cause by anxiety ,fever. anemia. thyrotoxosis
.phaeochrmocytoma .pregnancy .heart failure
,drugs(sympathomametic ,b-agoinst like
ventolin,butadinie )
 Treatment :if asymptomatic not need treatment
 if ymptomatic :treated depend on types , onset and
hemodynamic status

9. Atrial rhythm :
#Atrial ectopic beat (extrasystolic ,premature beat)
no symptoms or sensation of a missed beat or an
abnormally strong beat.
The ECG –shows a premature but otherwise
normal
QRS complex; if visible, the preceding P wave has
a
different morphology
Treatment ;avoid coffee.tea,stress@ .b blocker

10. Atrial tachycardia
@Atrial tachycardia caused by sinoatrial disease or
digoxin toxicity.
@It produces a narrow complex tachycardia with
abnormal P-wave morphology.
@Treatment :
β-blockers
class I or III anti-arrhythmic drugs
.Catheter ablation.

11. Atrial flutter
due to a large (macro) re-entry circuit, usually within the
RA encircling the tricuspid annulus.
The atrial rate is approximately 300/min, and is usually
associated with 2:1, 3:1 or 4:1 AV block.
The ECG shows saw-toothed flutter waves .

12. Management
Treatment :
1-Carotid sinus pressure or intravenous adenosine may help
to establish the diagnosis
2-Digoxin, β-blockers or verapamil can be used to control the
ventricular rate .
3-direct current (DC) cardioversion or by using intravenous
amiodaron
4-Beta-blockers or amiodarone can also be used to prevent
recurrent episodes of atrial flutter.
5-Catheter ablation offers a 90% chance of complete cure

13. Atrial fibrillation
@Atrial fibrillation (AF) is the most common
sustained cardiac arrhythmia, with an overall
prevalence of 0.5%,The prevalence rises with
age,
@Due to multiple re-entry circuits looping around
the atria.
@‘irregularly irregular’ pulse.
The ECG -irregular QRS complexes; there are no
P waves.
@AF can be classified
Paroxysmal –self terminated within 7days
Persistent –last more than 7 days
Permanent- if not terminated or relapse within

14. @structural remodelling occurs with atrial fibrosis and
dilatation that further predispose to AF
@ AF is often completely asymptomatic
@AF can cause palpitation, breathlessness and
fatigue. In patients with poor ventricular function or
valve disease it may precipitate or aggravate
cardiac failure
.@A fall in BP may cause lightheadedness, and chest
pain may occur with underlying coronary disease.
@AF is associated with significant morbidity and a
twofold increase in mortality

15. Common causes of atrial
fibrillation
• Coronary artery disease
(including acute MI)
• Valvular heart disease,
especially rheumatic mitral valve disease
• Hypertension
• Sinoatrial disease
• Hyperthyroidism
• Alcohol
• Cardiomyopathy
• Congenital heart disease
• Chest infection
• Pulmonary embolism
• Pericardial disease
• Idiopathic (lone AF)

16. Management
Assessment of patients with newly diagnosed AF
includes
a full history, physical examination, 12-lead ECG,
echocardiogram,thyroid function tests. ect
The goal of treatment:
1-restore sinus rhythm
2-prevent recurrent episodes of AF,
3-, minimize the risk of thromboembolism

17. Paroxysmal atrial fibrillation
1-not necessarily require treatment.
2-Beta-blockers are normally used
Beta-blockers reduce the ectopic firing that normally initiates AF.
3-Class Ic drugs such as propafenone or flecainide, are also
effective at
preventing episodes but should not be given to patients with
coronary disease or left ventricular dysfunction
.4-Amiodarone is the most effective agent for preventing AF but
its side-effects restrict its use to patients
.@Digoxin and verapamil are not effective drugs for preventing
paroxysms of AF,
If no response or because of side effects of drugs –can do
5-Cardiac ablation -Ablation prevents AF in
approximately 70% of patients. Complication s are
*small risk of embolic
*stroke or cardiac tamponade.

18. Persistent and permanent atrial
fibrillation
There are two options for treating persistent AF:
$= rhythm control: attempting to restore and
maintain sinus rhythm
$=rate control: accepting that AF will be permanent
and
$=prevent embolic complications.

19. Rhythm control. An attempt to
restore sinus rhythm
Attempts to restore and maintain sinus rhythm are
most successful
1- if AF has been present for < 3 months
2-the patient is young
3- no important structural heart disease.

20. 1-Immediate DC cardioversion after the administration of
intravenous heparin is appropriate if AF has been present for
< 48 hours.
2-Chemical cardioversion is performed with drugs, such
as amiodarone, dronedarone, procainamide, dofetilide, ibutili
de, propafenone, or flecainide.(Vernakalant, an
investigational drug)
In other situations, >48h AF--DC cardioversion deferred until
the patient has been established on warfarin, with an
international normalised ratio (INR) > 2.0 for a minimum of 4
weeks,.
3-Anticoagulation should be maintained for at least 3 months
following successful cardioversion
Concomitant therapy with amiodaroneor β-blockers may
reduce the risk of recurrence.
4-Catheter ablation( radiofrequency ablation The Maze
procedure)

21. Rate control. If sinus rhythm
cannot be restored, treatment
should be directed at maintaining an appropriate
heart rate.
@Digoxin, β-blockers or rate-limiting calciu m
antagonists such as verapamil or diltiazem
@catheter ablation+a permanent pacemaker
must be implanted beforehand. This is known as
the ‘pace and ablate’ strategy.

22. Prevention of thromboembolism
Loss of atrial contraction and left atrial dilatation
cause stasis
of blood in the LA and may lead to thrombus
formation
in the left atrial appendage. This predisposes
patients to
stroke and other forms of systemic embolism.
@warfarin (target INR 2.0–3.0) reduces the risk of
stroke by about two-thirds,
@aspirin reduces the risk of stroke by only one-
fifth
.

23. CHA2DS2-VASc
1
Congestive heart failure
C
1
Hypertension>
140/90
H
2
Age>75y
A2
1
Diabetes
D
2
Prior
Stroke or TIA or thro
mboembolism
S2
1
Vascular
diseasesVascular
disease (e.g.
peripheral artery
disease, myocardial
V
1
Age 65-74y
A
1
Sex category (female )
Sc

24. consideration
Anticoagulant
Risk
Score
Aspirine dialy
None or aspirin
low
0
Aspirine dialy or
riase to INR2-3
Aspirine ,warfarin or
other
moderate
1
Riase INR 2-3
Warfarin or other
anticoagulant
dabigatran, rivaroxaban
and apixaban
Moderate
to high
2 or
more

25. Quiz
1-describe the ECG
2- What are the treatment

26. Supraventricular’ tachycardias
(SVT) is a narrow QRS complex :
Atrioventricular nodal re-entrant tachycardia
(AVNRT)(120-240/m)
@This is due to re-entry in a circuit involving the AV
node and its two right atrial input pathways: a ‘fast’
pathway and ‘slow’ pathway .
@It tends to occur in hearts that are otherwise normal
and episodes may last from a few seconds to many
hours.
1-a fast heart beat and may feel faint or breathless.
2-Polyuria,
The ECG usually shows a tachycardia with normal QRS
complexes

27. Supraventricular tachycardia

28. Management
Treatment is not always necessary.
@ carotid sinus pressure or other
Measures that increase vagal tone (e.g. Valsalva
manoeuvre)
@Intravenous adenosine or verapamil
@Suitable alternative drugs
include β-blockers or flecainide.
@In severe haemodynamic compromise, the
tachycardia
should be terminated by DC cardioversion
@If episodes are frequent or disabling, prophylactic
oral therapy with a β-blocker or verapamil may be
indicated.
@Catheter ablation offers a high chance ofcomplete

29. Wolff–Parkinson–White syndrome
and atrioventricular re-entrant
tachycardia(AVRT)
@In these conditions, an abnormal band of
conductingTissue connects the atria and ventricles. is
known as an accessory pathway.
50%-concealed accessory pathway - does not alter the
appearance of the ECG in sinus rhythm.
50%--conduction takes place partly through the AV node
and partly through the accessory pathway-short PR
interval and a ‘slurring’ of the QRS complex, called a
delta wave known as Wolff Parkinson–White
syndrome.

30. . @. It should be treated as an emergency,
usually with DC cardioversion.
@If atrial fibrillation occurs, it may produce
a dangerously rapid ventricular rate
because the accessory pathway lacks the
rate-limiting properties of the AV node .
@Prophylactic anti-arrhythmic drugs, such
as flecainide, propafenone or amiodarone ,
can also be used. Catheter ablation is first-
line treatment in symptomatic patients and
is nearly always curative
@Digoxin and verapamil shorten the
refractory period of the accessory pathway
and should be avoided.

31. Ventricular tachy arrhythmias
@Ventricular ectopic beats(extrasystoles, premature
beats)
ventricular ectopic beats are premature, broad and
bizarre
The complexes may be unifocal or multifocal
. ‘Couplet’ and ‘triplet’ ‘bigeminy’.
@Ectopic beats produce a low stroke volume because
left ventricular contraction occurs before filling is
complete.
@The pulse is therefore irregular, with weak or missed
beats
.@ Patients are usually asymptomatic but may complain
of an irregular heart beat, missed beats or abnormally
strong beats.

32. Ventricular ectopic beats in otherwise healthy
subjects
increases with age. disappear with exercise.
@Treatment is not necessary unless the patient is
highly symptomatic, in which case β-blockers can be
used.
@investigations such as an echocardiogram (looking
for structural heart disease) and an exercise stress
test (to detect underlying ischaemic heart disease).

33. Ventricular ectopic

34. Ventricular ectopic beats
associated
with heart disease
@acute MI . Persistent, frequent (> 10/hour) ventricular
ectopic beats in patients who have survived the acute
phase of MI indicate a poor long-term outcome.
Other than β-blockers, anti-arrhythmic drugs do not
improve and may even worsen prognosis.
..
Treatment should be directed at the underlying condition.

35. Ventricular tachycardia (VT)
@The common causes of VT include
acute MI,
cardiomyopathy
@chronic ischaemic heart disease particularly when it
is associated with a ventricular aneurysm or poor left
ventricular function.
@It is caused by abnormal automaticity or triggered or
by re-entry within.
@Patients may complain of palpitation or symptoms of
low cardiac output, such as dizziness, dyspnoea or
syncope.
The ECG shows tachycardia with broad, abnormal QRS
complexes with a rate > 120/min .
VT may be difficult to distinguish from SVT with bundle
branch block or pre-excitation(WPW syndrome).

36. Wide QRS
Narrow QRS

37. @idioventricular rhythm (‘slow’ VT) at a rate only slightly
above the preceding sinus rate and below 120/ min.
These episodes often reflect reperfusion of the infarct
territory and may be a good sign. They are usually
self-limiting and asymptomatic, and do not require
treatment.
@(‘normal heart VT’), usually because of abnormal
automaticity in the right ventricular outflow tract or one
of the fascicles of the left bundle branch. The
prognosis is good and catheter ablation can be
curative

38. Management
@Synchronised DC cardioversion is the treatment of choice
if systolic BP is < 90 mmHg.
@intravenous amiodarone may be given as a bolus followed
by a continuous infusion
@Intravenous lidocaine can be used but may depress left
ventricular function, causing hypotension or acute
heartfailure.
@ Hypokalaemia, hypomagnesaemia, acidosis and
hypoxaemia should be corrected.
@Beta-blockers .
@ Class Ic anti-arrhythmic drugs should not be used for
prevention of VT in patients with ischaemic heart disease
In patients at high risk of arrhythmic death (e.g. those with
poor left ventricular function, or where VT is associated
with haemodynamic compromise), the use of an
implantable cardiac defibrillator is recommended .

39. in
the differential diagnosis of broad-complex
tachycardia
@History of MI
• AV dissociation (pathognomonic)
• Capture/fusion beats (pathognomonic,)
• Extreme left axis deviation
• Very broad QRS complexes (> 140 ms)
• No response to carotid sinus massage or i.v.
adenosine

40. Torsades de pointes (ventricular
tachycardia) Polymorphic VT
@The ECG shows rapid irregular complexes that
oscillate from an upright to an inverted position and
seem t twist around the baseline as the mean QRS
axis changes
@degenerate into ventricular fibrillation
@During periods of sinus rhythm, the ECG will usually
show
a prolongeQT interval (> 0.42 s at a rate of 60/min).
.@The arrhythmia is more common in women and is
often
triggered by a combination of aetiological factors (e.g.
QT-prolonging medications and hypokalaemia).

41. Causes of long QT interval and torsades de
pointes
Bradycardia
Electrolyte disturbance
• Hypokalaemia
• Hypomagnesaemia
• Hypocalcaemia
Drugs
• Disopyramide (and other class Ia anti-arrhythmic drugs, p. 573)
• Sotalol, amiodarone (and other class III anti-arrhythmic drugs)
• Amitriptyline (and other tricyclic antidepressants)
• Chlorpromazine (and other phenothiazines)
• Erythromycin (and other macrolides)
Congenital syndromes
• LQT1: gene affected KCNQI: K+ channel, 30–35%
• LQT2: gene affected HERG: K+ channel, 25–30%
• LQT3: gene affected SCNSA: Na+ channel, 5–10%
• LQT4–12: rar

42. @Thecongenital long QT syndromes are a family of
genetic disorder.
@Treatment should be directed at the underlying
cause. Intravenous magnesium should be given in
all cases.
@Atrial pacing.
@Intravenous isoprenaline is a reasonable alternative
to
pacing.
.@ Beta-blockers are effective at preventing syncope
in patients with congenital long

43. Sinoatrial disease (sick sinus syndrome)
@occur at any age but is most common in older
people.
@The underlying pathology involve fibrosis,
degenerative changes or ischaemia of the SA(sinus)
node.
@may present with palpitation, dizzy spells or
syncope, due to intermitten tachycardia,
bradycardia, or pauses with no atrial or ventricular
activity (SA block or sinus arrest)
@A permanent pacemaker.

44. Common features of sinoatrial
disease
Sinus bradycardia
• SA block (sinus arrest)
• Paroxysmal atrial tachycardia
• Paroxysmal atrial fibrillation
• AV block

45. Atrioventricular and bundle
branch
block
First-degree AV block
In this condition, AV conduction is delayed so the
PR
interval is prolonged (> 0.20 s;). It rarely causes
symptoms.

47. Second-degree AV block.
In Mobitz type I second-degree AV block :there is
progressive lengthening of successive PR intervals
culminating in a dropped beat.. This is known as
Wenckebach’s phenomenon and is usually due to
impaired conduction in the AV node itself..
In Mobitz type II second-degree AV block -the PR
interval of the conducted impulses remains constant
but some P waves are not conducted. This is usually
caused by disease of the His–Purkinje system and
carries a risk of asystole.
.

48. Third-degree (complete) AV block
When AV conduction fails completely, the atria and
ventricles
beat independently (AV dissociation, ) Complete AV
block -produces a slow (25–50/min), regular pulse
that,.
.
Cannon waves may be visible in the neck and the
intensity of the firstheart sound varies due to the loss
of AV synchrony

49. Aetiology of complete AV block
Congenital
Acquired
• Idiopathic fibrosis
• MI/ischaemia
• Inflammation
Acute (e.g. aortic root abscess in infective
endocarditis)
Chronic (e.g. sarcoidosis, p. 708; Chagas disease,
p. 354)
• Trauma (e.g. cardiac surgery)
• Drugs (e.g. digoxin, β-blocker)

50. Stokes–Adams attacks
Episodes of ventricular asystole may complicate
complete
heart block or Mobitz type II second-degree AV
block, or occur in patients with sinoatrial disease
This may cause recurrent syncope or ‘Stokes–
Adams’ attacks.A typical episode is characterised by
sudden loss of
consciousness that occurs without warning and results
in collapse..

51. AV block complicating acute MI
Acute inferior MI is often complicated by transient AV
block because the RCA supplies the AV node.
if the patient remains well, no treatment is required.
Symptomatic second- or third-degree AV block may
respond to atropine(0.6 mg i.v., repeated as
necessary) or, if this fails, a temporary pacemaker.
In most cases the AV block will resolve within 7–10
days.
Second- or third-degree AV heart block complicating
acute anterior MI indicates extensive ventricular
damage
involving both bundle branches and carries a poor
prognosis.

52. Bundle branch block and hemiblock
Conduction block in the right or left bundle branch
can occur as a result of many pathologies,
including
Ischaemic or hypertensive heart disease or
cardiomyopathies
.
This causes delayed conduction into the LV or RV,
broadens the QRS complex (≥ 0.12 s) and
produces
the characteristic alterations in QRS morphology

53. Right bundle branch block (RBBB can occur in healthy
people but left bundle branch block (LBBB) often
signifies important underlying
heart disease.
The combination of right bundle branch and left anterior
or posterior hemiblock is known as bifascicular block

54. Common causes of bundle branch
block
Right bundle branch block
• Normal variant
• Right ventricular hypertrophy or strain, e.g. pulmonary
embolism
• Congenital heart disease, e.g. atrial septal defect
• Coronary artery disease
Left bundle branch block
• Coronary artery disease
• Hypertension
• Aortic valve disease
• Cardiomyopathy

55. Anti-arrhythmic drug therapy

56. Classification of anti-arrhythmic drugs
according to effect on the intracellular
action potential
Class I: membrane-stabilising agents (sodium channel blockers)
(a) Block Na+ channel and prolong action potential
• Quinidine, disopyramide
(b) Block Na+ channel and shorten action potential
• Lidocaine, mexiletine
(c) Block Na+ channel with no effect on action potential
• Flecainide, propafenone
Class II: b-adrenoceptor antagonists (b-blockers)
• Atenolol, bisoprolol, metoprolol, I-sotalol
Class III: drugs whose main effect is to prolong the action potential
• Amiodarone, d-sotalol
Class IV: slow calcium channel blockers
• Verapamil, diltiazem
N.B. Some drugs (e.g. digoxin and adenosine) have no place in this
classification, while others have properties in more than one class:
e.g. amiodarone, which has actions in all four classes.

57. Other anti-arrhythmic drugs
Atropine sulphate (0.6 mg i.v., repeated if necessary
to
a maximum of 3 mg).

58. Adenosine. Must be given intravenously. It
produces transient AV block lasting a few seconds.
Adenosine is givenas an intravenous bolus, initially 3
mg over 2 seconds If there is no response after 1–2
minutes, 6 mg should be given; if necessary, after
another 1–2 minutes, the maximum dose of 12 mg
may be given.
Patients should be warned that they may experience
short-lived and sometimes distressing flushing,
breathlessness and chest pain. Adenosine can
cause bronchospasm and should be avoided in
asthmatics; its effect are greatly potentiated by
dipyridamole and inhibited by theophylline and other
xanthines.

59. Response to intravenous
adenosine
Arrhythmia Response
Supraventricular tachycardia Termination
Atrial fibrillation, atrial flutter Transient AV
block
Ventricular tachycardia No effect

60. Digoxin. A purified glycoside from the European
foxglove, Digitalis lanata, which slows conduction and
prolongs the refractory period in the AV node..
Digoxin is largely excreted by the kidneys, and the
maintenance dose should be reduced in children, older
People and those with renal impairment.
It is widely distributed and has a long tissue half-life (36
hours), so that effects may persist for several days after
th last dose..

61. Therapeutic procedures
External defibrillation and cardioversion
This will interrupt any arrhythmia and produce a brief
period of asystole -that is usually followed by the
resumption of sinus rhythm.
Defibrillators deliver a DC, high-energy, short-duration
shock via two metal paddles coated with conducting
jelly or a gel pad, positioned over the upper right
sternal edge andthe apex.
Modern units deliver a biphasic shock, during which the
shock polarity is reversed mid-shock. This reduces
the total shock energy required to depolarise the
heart.

62. Electrical cardioversion
This is the termination of an organised rhythm such
as AF or VT with a synchronised shock, usually under
general anaesthesia.
The shock is delivered immediately after detection of
the R wave,
High-energy shocks may cause chest wall pain post-
procedure, so if there is no urgency it is appropriate to
begin with a lower-amplitude shock
(e.g. 50 joules), going on to larger shocks if necessary.
-

63. Catheter ablation
The technique has revolutionised the management
of
many arrhythmias and is now the treatment of
choice for
AVNRT and AV re-entrant (accessory pathway)
tachycardias,
when it is curative in > 90% of cases.
Focal atrialtachycardias and atrial flutter can also
be eliminated by radiofrequency ablation,

64. Temporary pacemakers
. Permanent pacemakers

65. Implantable cardiac defibrillators
(ICDs)
Primary prevention
• After MI, if LV ejection fraction < 30%
• Mild to moderate symptomatic heart failure on optimal
drug
therapy, with LV ejection fraction < 35%
Secondary prevention
• Survivors of VF or VT cardiac arrest not due to
transient or
reversible cause
• VT with haemodynamic compromise or significant LV
impairment (LV ejection fraction < 35%)

66. Cardiac resynchronisation
therapy (CRT)
CRT improves symptoms and quality of life, and
reduces mortality in patients with moderate to
severe symptomatic heart failure who are in sinus
rhythm, with left bundle branch block and LV
ejection fraction ≤ 35%.’

67. Quiz
What are the treatment of SVT ?
Enumerate the causes of complete heart block?

68. Thanks a lot