2010

[CARDIAC ARRHYTHMIAS &

AMANI Al-ZAYANI

ANTI-ARRHYTHMIC DRUGS]
Dr. Akhtar Husain
 CARDIAC ARRHYTHMIAS

Arrhythmia is an abnormal rhythm of the heart

Two terms (arrhythmias & dysrhythmias)  both mean the same
 Very common. (i.e. normal people can have arrhythmias)
 Non-specific. (i.e. any arrhythmia can happen in any heart disease & many arrhythmias
can occur even without a structural heart disease)
i.e. Just because a patient having an arrhythmia it does not mean that the patient
has a heart disease
 May or may not be symptomatic. (i.e. a patient with an arrhythmia may be
symptomatic, other patient with the same arrhythmia may not be symptomatic)
 Often intermittent. (comes & goes ) e.g. if somebody says I get palpitations and you
examine the patient he’s perfectly normal & you do ECG & it’s perfectly normal, but
still he may have arrhythmias at the time of the palpitation and this may be every day,
once a month, once in 10 years. Lasting for 2 seconds, 1-2 minutes or lasting for many
hours.
 May or may not need treatment.
 Diagnosis only by ECG. What you need to do is  to have an ECG done at the time of
the symptom

This is a conduction pathway from the SA

node to the AV node  bundle of His  left
bundle branch + right bundle branch

 In order for the p wave to have normal

configuration it must start from the SA
node

If the atrial activity starts from

somewhere else  then the p wave would be
abnormal

 In order for the QRS to be normal  it

has to follow the previously mentioned
pathway

If it doesn’t follow this pathway  then the

QRS would be abnormal

Normal ECG:

CARDIAC ARRHYTHMIAS & ANTI-ARRHYTHMIC DRUGS Page 2

12 leads  6 limb leads + 6 chest leads
P wave: small positive wave before the QRS, positive in all leads except in aVR, sometimes V1 it will
be negative, Otherwise it’s positive.
Each small square = 0.04 second
PR interval = 0.12 -0.20 seconds  up to 5 small squares
Rate= divide 300 by number of big squares between 2 consecutive QRS complexes
Rhythm:

So this is the normal sinus

rhythm  because the rate
around 70 & each QRS is
preceded by a normal p wave.
HR < 60  sinus bradycardia
HR > 100  Sinus tachycardia

Sinus tachycardia:
Occurs whenever there’s a sympathetic
activity:
1. Nervous
2. Exercise
3. High fever
4. hypoxia
5. shock
6. anxiety
Sinus tachycardia per se is not
dangerous, and it does not need
treatment, but you need to look at the
underlying cause & treat accordingly,
but don’t treat sinus tachycardia itself

Sinus Bradycardia:
Can occur normally or due to certain drugs like
Sinus arrhythmia: this is also a beta blockers, or as a feature of hypothyroidism
normal thing due to the change Sinus bradycardia per se doesn’t need treatment.
of the vagal tone with respiration However, you should treat severe symptomatic
bradycardia (i.e. if the patient dizzy or faint & the
Most of the time doesn’t need rate may be 25- 30 (if it’s above 40 there’s usually
treatment no problem, if it gets low the patient gets dizzy
and faint  treat with pacemaker
 All severe (rate <40 bpm) and symptomatic
Premature Atrial contractions: PAC:
bradyarrhythmias need to be treated with
It can occur in any disease, and it is not usually dangerous and it does not need any treatment.
permanent pacemaker implantation.
However it can precipitate supra ventricular tachyarrhythmia (SVT or AF), but otherwise
generally we don’t treat it. (almost never you need to treat PACs)
CARDIAC ARRHYTHMIAS & ANTI-ARRHYTHMIC DRUGS 3 Page

It may or may not be symptomatic. If asymptomatic  don’t treat

If Symptomatic  treat because the patient is aware of it & it’s uncomfortable or because it
caused SV tachyarrhythmias
If treatment needed use class IA, IC, class II
 PVC:
QRS looks totally bizarre because it’s not going through
the normal pathway & no p wave preceding it.
Treatment:
 If patient is asymptomatic and has no underlying
heart disease, no treatment is needed.
 But if he’s symptomatic & has underlying has
disease then you may need to treat it
 For acute patients in CCU: lidocaine IV,
procainamide IV or amiodarone.
 For long term: class IA, IC, II, amiodarone.

Atrial bigeminy:

This is alternating Sinus (normal)

and PACs (i.e. one normal (red
arrow), one PAC ( blue arrow))

NL- PAC- NL- PAC

Bigeminal PVCs: ventricular

bigeminy:
Sinus – PVC- Sinus – PVC

A: SUPRAVENTRICULAR TACHYARRHYTHMIAS
With all the supraventricular tachyarrhythmias there are 2 things in common:
1- QRS is narrow
2- rate is fast

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4 types:
1. Sinus tachycardia: 100-200 bpm
2. Paroxysmal SVT: 150-250 bpm
3. Atrial Flutter: 250-350 (usually 300) bpm
4. Atrial Fibrillation: >350 bpm

Q: if the rate is 170 bpm is it sinus tachycardia or P. SVT?

1- Sinus tachycardia:
Although we say that in sinus tachycardia the range is up to 200 bpm, but mostly it goes up
to 120 -130, it can reach up to 200 in certain cases.
1. Children. The rate of sinus tachycardia is age dependent. So, you can reach sinus
tachycardia at a rate of 200 bpm but that is more in children, but in adult it doesn’t
(it usually less reaches to 160-180 maximum)
2. Severe stress. In order to have really fast sinus tachycardia (e.g. 160) it has to be
a very severe stress (e.g. high grade fever, severe bronchial asthma with hypoxia,
patient is going to shock d/t GI bleeding..etc)
N.B in sinus tachycardia, regardless of the rate you would see a clear cut p wave
2- Paroxysmal supraventricular tachycardia:
This is a totally deferent situation
 The rate is about 180 bpm (very fast)
 No clear cut P waves are seen, no real P waves.
But sometimes with difficulty you may see a P
wave.
 Regular QRS
 Very regular & it comes in attacks
 Very common arrhythmia (roughly 1 case /week
in ER)
 Very sudden onset, sudden offset

e.g. In case of sinus tachycardia in a patient who has a baseline rate of 70 -80 then it goes
up gradually to 100- 110 – 120 – 150 - 140 - 160 bpm & when it comes down it will come
down also in a gradual manner (160 – 140 -120 – 110…) . However in paroxysmal SVT a
patient of a baseline of 70 suddenly within one beat jumps to 180 bpm (very sudden onset)

 Usually seen in relatively young people with no underlying heart disease and no
obvious stress
 Presentation: Patient would have palpitations, he will be very nervous coming to ER.
But otherwise his temperature is normal, no GI bleeding, no bronchial asthma
attack & he’s otherwise ok. So you need to reassure the patient, there’s nothing to
worry about it is not dangerous

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 Treatment: It is easy to treat (converts fast)
1. Conversion
 Conversion to normal sinus rhythm (NSR): by vagal stimulation (e.g. carotid sinus
massage, valsalva maneuver, put the face in cold water)
 If fails:  IV adenosine 6-12 mg or verapamil 5-10 mg IV, electrical cardioversion.
Adenosine is a normal substance in the body (ATP, ADP all are adenosine), it has a very
short half life (less than one minute), so you give a bolus adenosine & it may convert
SVT
 If the patient is hemodynamically unstable & the drugs don’t work you can do DC shock
(rare)  almost always it will convert by Carotid Sinus massage or adenosine)
2. Prevention
If a patient comes for the 1st time with SVT or he has it once a year or once / 5 years 
you don’t need to give prophylaxis
If it happened frequently like several times a month or everday & the patient is bothered
 give prophylaxis
 Prophylaxis: class IA, IC, II, amiodarone, verapamil, digoxin.
You may also use Ablation therapy
3- Atrial flutter:
The atrial activity is called a flutter
wave & it would be at a rate of 300 bpm,
however the AV node cannot conduct
this fast so, the ventricular rate would
be slower.
[flutter]: [ventricular rate] ratio would
be 
2: 1 , 3:1 or 4:1 in other word there are
2 flutter waves and 1 QRS , or
3 flutter & 1 QRS
4 flutter & 1 QRS
(this is variable conduction)
Accordingly atrial rate of 300 bpm with corresponding ventricular rate of 150, 100 or 75)
The flutter waves are exactly the same shape and the same size. (saw-toothed
appearance)
 Atrial flutter is with variable rate, so it is irregular

Carotid
CARDIACsinus massage or IV
ARRHYTHMIAS adenosine may help DRUGS
& ANTI-ARRHYTHMIC to establish the diagnosis by temporarily increasing the
6
Page

degree of AV block and revealing the flutter waves.

This patient has atrial flutter and CSM was done  and you get only flutter waves no QRSs  because
of complete block.
  Atrial flutter usually occurs with underlying heart disease
 It is not a stable arrhythmia  atrial flutter will eventually become atrial
fibrillation
 the ONLY way to treat atrial flutter is DC shock (Electrical cardioversion) 
convert it by DC shock
Treatment:
Not a stable arrhythmia- converts to atrial fibrillation.
Electrical cardioversion (50-100 J)  50 J is usually enough
Prophylaxis: class IA, IC, II, amiodarone. (usually we don’t give any prophylaxis)
4- Atrial fibrillation:
There’s no definite P wave, just wiggles wiggles wiggles (zig-zagging) of different sized
It’s totally irregular
Extremely important arrhythmia
It is the commonest chronic arrhythmia  and it can stay there for life long
Commonly seen in: [ CAD, hypertensive HD, RHD (esp. MS), pericarditis, thyrotoxicosis,
Cardiomyopathy]  so any heart disease
But remember
1. Mitral stenosis  very common in MS
2. Thyrotoxicosis  as a non cardiac condition that may cause AF

Treatment:
First step: slow ventricular rate
With digoxin, verapamil, beta blocker.
 If the patient has CHF  use Digoxin (you shouldn’t use beta blocker or verapami in
a patient with CHF because it will make CHF worse
 If the patient has Thyrotoxicosis  use Beta blocker
 Other patients  use either beta blocker or verapamil
Second step: Ask yourself should I convert it or not?
 If a patient has a chronic AF> 6 months, or if the patient has large left atrium  then
you cannot convert it
 If it is a recent onset in the past 48 hrs  then you convert either by DC shock
(electrical cardioversion) or class IA drugs (IV procainamide) or IV amiodarone

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It has to be (<48 hrs) because one of the complications of AF is thrombo-embolic
phenomena  a clot in the left atrium that can embolize
If more than 48hr  you have to anticoagulate before cardioversion for 3 weeks at least
(3 wks before cardioversion) & 4 weeks after cardioversion

Prophylaxis: class IA, IC, amiodarone

 If the patient has chronic AF the patient should be on anticoagulation with warfarin
Because they have high incidence of left atrial thrombus.

B: VENTRICULAR TACHYARRHYTHMIAS
1. Ventricular tachycardia
2. Ventricular fibrillation

1. Ventricular tachycardia:

We talked about PVCs earlier:

We have isolated PVCs, also 2 PVCs may come
together  this is called complex or coupled
PVCs
3 PVCs or more together  this is called
ventricular tachycardia

If you have ventricular tachycardia lasting less than 30 sec.  we call it non sustained VT
If you have ventricular tachycardia lasting more than 30 sec.  we call it sustained VT

 Wide QRS -Fast rate

- Almost always occurs with underlying heart disease & it is more dangerous
The condition of the patient depends on:
1. how bad the heart (the left ventricular function)

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 2. how fast the rate
E.g. if the heart was in a poor condition & the rate is 160 bpm  the patient may be
in shock & there may be no pulse, no blood pressure  you do immediate
cardioversion
But if the rate is not fast, the heart is in a relatively good condition  the patient
may tolerate it ..
So in a patient with ventricular tachycardia  he may or may not get
hemodynamically unstable
- The danger about VT is  that it will not stay for a long time it will convert into
ventricular fibrillation & you know VF= sudden death (unstable arrhythmia)

Treatment:
 If hemodynamically stable: lidocaine, procainamide, amiodarone. (IV)
 If unstable: electrical cardioversion.
 Prophylaxis: class IA, IB, IC, class II, amiodarone.
2. Ventricular Fibrillation:

 It is totally bizarre
 There is no pattern
 You can’t see QRS or T waves
 Very dangerous
 Potentially reversible if you
give DC shock
 Anybody with heart disease can have it at any time

VF = Sudden death (it is the commonest cause of sudden death)

Whenever you here that someone went to sleep & didn’t get up in the morning  this is VF
Somebody in the office collapses & dies  VT

In case of VT if you look at the patient he’s like a dead person  no pulse no blood
pressure & no respiration & no response  However if you give DC shock right away within
5-7 minutes  then the patient can survive
If you delay it  the heart may function again but you may get brain damage

Treatment
 Sudden death, but reversible if defibrillation (200-400 J) is done within a few
minutes.
 Prophylaxis same as VT.

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C: ATRIOVENTRICULAR BLOCKS:

1. First degree AV block (PR>0.20secs)

2. Second degree Mobitz type I
3. Second degree Mobitz type II
4. 2:1 AV block
5. Third degree (Complete AV block)

1-First degree AV block (PR>0.20secs)

 It is prolonged PR interval
 but every P wave is followed by a QRS
 NL PR  0.12- 0.20 sec (up to one large
square)
 No treatment needed
 It is seen in: (some drugs e.g. digitalis,
inferior wall MI, Rheumatic fever)

2-Second degree: Mobitz type I

 Prolonged PR  the next one is longer
PR  then more longer PR  then it
drops out of a QRS
 Commonly seen in:
1- acute inferior MI
2- digitalis toxicity
 it can go into complete heart block but
usually Mobitz type I doesn’t need
treatment

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 after a while from the inferior MI  it can recover by itself

3-Second degree Mobitz type II

 All the PRs are the same (no progressive prolonation as in Mobitz I), but every once
in a while a P wave is not conducted (QRS complexes are dropped)
 This is more dangerous
 Usually requires a pacemaker
4- 2:1 AV block
2 P wave + 1 QRS

5- Third degree (Complete AV block)

 The P wave & the QRS are totally
dissociated
 It is associated with dizziness &
fainting
 Required permanent pacemaker
implantation

WPW Syndrome (wolff Parkinson

White syndrome)= preexcitation
syndrome:
Short PR & delta wave

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The worst things that can happen to these patient is AF which looks like Ventricular
tachycardia with a very fast ventricular rate & it can lead to sudden death.

Treatment:
 Electrical cardioiversion.
 Flecainide, amiodarone for long term therapy.
 Radiofrequency ablation therapy of the accessory pathway.

ANTI-ARRHYTHMIC DRUGS

The problem with anti-arrhythmic drugs

1- They are not very effective
2- They have very serious side effects
3- All Anti-arrhythmic drugs are proarrhythmic i.e. they cause arrhythmia themselves

Classification

Class I: Sodium channel blockers:

A. Quinidine, Procainamide, Disopyramide.
B. Lidocaine, Mexiletene,Tocainide, Phenytoin.
C. Flecainide, Encainide
Class II: Beta Blockers.
Class III: Prolong Action Potential: Amiodarone, Bretylium.
Class IV: Calcium channel blockers: Verapamil, Diltiazem. (not all CCB have anti-
arrhythmic effect, but some of them)

Quinidine - Ia

 Dosage: 200-300 mg q 6 hrs. po

 It can’t be given IV
 Indications: effective against both SV & V tachyarrhythmias
1. PAC’s, PVC’s
2. SVT, VT
3. AF  (in conversion & prophylaxis).
 Side effects: (the commonest is Diarrhea)
Cinchonism – vertigo, visual dist., diarrhea, vomiting, tinnitus, abdominal cramps.
Cardiac S/Es:
1- proarrhythmia,

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 2- Increases the ventricular rate in atrial fibrillation.
E.g. let’s say someone has a ventricular rate of 140 bpm, if you use quinidine
the rate jumps to 160 -180 bpm  this is dangerous
But we already said we can use it in AF ??
What you do is first slow the rate (give medicine that slows the rate)
Once the rate is 70 or so, then you can add quinidine (but don’t add
Quinidine if the rate is very fast.
3- Interaction with digoxin.
4- Prolongs QRS & QT intervals.
Procainamide – Ia

 Can be given both orally or IV (that what makes it different than Quinidine)
 The problem with procainamide it has a very short half life, so you have to
give it every 3 hours & this is not practical  that’s why we don’t use
procainamide very much
 Dosage: 250-500mg q 3 hrs. po. 1 Gm iv followed by 2-4 mg per minute.
 Indication: vent. & supraventricular arrhythmias. Same as quinidine
 Side effects: Most important S/E is drug induced SLE  that’s another reason
why we don’t use it commonly
GI, prolongs QRS & QT, proarrhythmic, increased VR in AF.
Sometimes a patient comes with a lot of PVCs & PACs  so we give IV procainamide

Disopyramide – Ia

 Given orally
 Dosage: 100-200mg q 6hrs po
 Indications: same as quinidine.
 You should know the  Side effects: the most important S/E is Anticholinergic
effect  dryness, blurred vision, urinary retention, glaucoma
 Others GI- N&V, diarrhea, abd. Pain,
 Cardiac-
1. -ve inotropic effect  it will make the CHF worst
2. proarrhythmic,
3. prolongs QRS & QT

Lidocaine – Ib

 Only given IV, can’t be given orally

 Dosage: 50-100mg bolus followed by 1-5mg/min.
 Indications: Effective only in ventricular arrhythmias.
 Side effects are neurological:

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 Paresthesia, drowsiness, agitation, disorientation, muscle twitching, convulsions
proarrhythmic effect.
 Half life 100 minutes
 Dose should be Reduce dose in CHF and liver disease.  if you give the regular
dose the patient will get convulsions

Tocainide and Mexiletene – Ib

 Tocainide and Mexiletene are similar to Lidocaine in action, indication & side
effects but they are used orally.
 No one will ask you about it =)

Phenytoin – Ib

 Phenytoin is an antiepileptic drug. It is mainly used in arrhythmias due digoxin

toxicity.

Flecainide – Ic

 It is a very important anti-arrhythmic drug & very effective

 Dosage: 50-300mg po bid
 Indications: ventricular and SV arrhythmias, especially useful in WPW syndrome.
 Side effects: the most important thing is that it makes CHF worst
dizziness, blurred vision, headaches, nausea, proarrhythmia.

Propranolol - II

 Dosage: oral 10-120mg q 6hrs. 1-3 mg IV

 Indications: ventricular and SV arrhythmias, especially useful for slowing of
ventricular rate in AF- especially if the AF is d/t  thyrotoxicosis.
 Side effects: bradycardia, AV block, hypotension, CHF.
Fatigue, bronchospasm, nightmares, impotense, cold extremities.

Amiodarone - III

 It is very effective but it has serious S/Es

 Can be given orally & IV
 Dosage: 800mg daily for one week loading.  Then 200-400mg daily maintenance.
 Half life 10-60 days.

CARDIAC ARRHYTHMIAS & ANTI-ARRHYTHMIC DRUGS Page 14

  Indications: SV & vent. Arrhythmias.
 Can be safely used in CHF patients. (imp)
 Side effects: particularly important is pneumonitis
Photosensitivity, corneal microdeposits, hepatic dysfunction, hypo &
hyperthyroidism, proarrhythmia, SB, AV block, hypotension, tremors, ataxia,
Drug interactions (digoxin,warfarin)  so lower the dose when used with them

Verapamil – IV
 Can be given orally as well as IV
 Dosage: 80 mg q 6-8 hrs po. 5-10 mg IV.
 Indications: only effective for supraventricular arrhythmias
It’s main use is to Convert P. SVT to normal sinus rhythm and to slow VR in AF.
No effect on ventricular arrhythmias.
 Side effects: It will make the CHF worst
sinus bradycardia, hypotension, edema, constipation.

Drug t1/2 Route Indications S/E Effect

on CHF
Quinidine Only orally SV & V MC  diarrhea
Can’t be It increases VR
given IV in AF
Procainamide very short orally or IV both SV & V drug induced
half life SLE
increased VR in
AF
Disopyramide Given orally Anticholinergic Worsen
effect
-ve inotropic
effect
Lidocaine Half life Only given Effective only Neurological Reduce
100 IV, can’t be in ventricular dose in
minutes given orally arrhythmias CHF

Mexiletene,Toc Used orally // // //

ainide
Flecainide oral SV & V Worsen
WPW Synd.
propranolol orally & IV SV & V
Slows VR in AF
Amiodarone Up to 60 orally & IV SV & V Pneumonitis safely

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 days Drug interaction used in
CHF
patients.
Verapamil orally & IV only effective Worsen
for SV, slow
VR in AF

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