E.
Salami
Cardiac
Arrhythmias +
Anti-arrhythmic
Drugs
SYMPTOMS:
- arrhythmia = the actual etiology
- Palpitation = the actual awareness of the
heartbeat
- skipping of beats
- pounding
- racing heart
- BADNESS: Hypotension, decreased LOC,
chest pain, Shortness of breath, sudden
syncope
IN GENERAL:
• Fast or slow?
• ventricular or supra-ventricular?
• Compromised or not?
• Does arrhythmia need management?
• What is underlying substrate predisposition?
• What is the trigger?
• will arrhythmia recur?
KEY ECG PEARLS
- Rhythm: What you read in Dubin’s “every p
has a QRS and every QRS has a p” IS
WRONG. You can meet that rule AND still not
have sinus rhythm.
- p wave axis - the axis normal if the P is
positive in Lead I, Lead II, and aVF
- make sure the p waves have the same
morphology - more than 3 p wave shapes
and they are FAST - its likely a multifocal
atrial tachycardia ( multiple foci of electrical
impulse in the atria that override the SA
node), if they are NORMAL RATE its
wandering pacemaker ( the SA node
doesn’t always control the rate, other foci
alternately take over the electrical impulse)
- THEN look for AV association
- Intervals and Blocks:
- Look at V1 if its POSITIVE and the QRS is
widened its a RBBB, if it is NEGATIVE and
the QRS is wide then its a LBBB
- Extreme Axis deviation (Lead I and II are
down) + concordance + AV dissociation =
V Tach
- LBBB hall marks - monophasic deep S
wave in V1, RSR ( bunny ears) in V4 and
Monophasic upward R in V5/V6
- Axis Deviation:
- Left Axis deviation - look for Q waves! Only
two things cause this… old inferior MI or
Left anterior fascicular blocks ( “faulty
wires” - one thread away from BBB)
- Right axis deviation - look for Q waves!
Either old lateral MI or left posterior
fascicular block.
- Intervals:
- The better approach to AV blocks! think
about it like this….
- 1st degree AV block = delayed AV
condition i.e. prolonged PR interval
- 2nd Degree AV block = intermittent AV
conduction i.e. a “flickering light bulb”, see
GROUPED BEATING
- Mobits I - look for the PR interval of the
beat just before the dropped beat and the
one that comes right after the heart starts
again…
- Different Lengths? Mobitz I
(Wenchebach)
- Same size? Mobitz II
- 3rd Degree AV block = NO AV conduction
i.e * look at the RR interval! this will be
REGULAR despite whatever the P waves
are doing.
BRADYARRHYTHMIAS
Sinus Bradycardia
Caused by……
- Drugs - digoxin, beta blockers, calcium
channel blockers, amiodarone
- Increased vagal tone
- Metabolic - sepsis, myxedema, hypothermia,
hypoxia
- OSA
- increased ICP
- if asymptomatic - watch and wait
- Symptomatic - atropine, beta one agonists
(dopamine and epinephrine)
Sick Sinus Syndrome
- may see sudden sinus brady, sudden
tachyarrhythmia, alternating tachyarrhythmia/
bradyarhythmia ( tachy-brady)
 E. Salami

- Hard to treat with medications - when you
control the tachycardia with beta blockade or
CCB you get an unacceptably low heart rate
- Treatment - Permanent pacemaker to ensure
the heart rate never goes too low and treat the
tachycardia with CCB/BB/Dig
The AV Blocks ( See ECG pearls above!)
Grade 1 - long PR, more than one big square
Tx: rarely needs treatment.
Grade 2, Mobitz I - Caused by AV node issues -
ischemia (AV node starved for O2), inflammation
(myocarditis, cardiac surgery), high vagal tone.
Worse with carotid massage and better with
atropine.
Tx: Rarely need long term treatment
Grade 2, Mobitz II - repetitive dropped beats.
This is a His-Purkinje issue. Either ischemia,
infiltrative disease, inflammation with surgery.
Tx: Usually progresses to third degree - need
pacing.
Grade 3 - complete AV node and ventricular
dissociation. Marching P waves. Junctional
rhythm or ventricular rhythm depending.
TACHYARRHYTMIAS
Approach: Is it REGULAR? Are there P WAVES?
Is the QRS NARROW or WIDE?
These critical questions will help you organize
your approach.
SUPRAVENTRICULAR TACHYCARDIAS
patient to find the cause. Generally it's gradual in
onset, usually <150 for rate
Tx: Treat the cause
Atrial Tachycardia - something other than the
SA node is causing a discharge - seen in CAD,
COPD; usually <150 HR
TX: Beta Blockers, CCB, vagal manouvres,
adenosine
MAT - different P wave morphologies and a fast
rate. Look in Lead I, II, aVF to see if the p waves
are all the same and positive - if no and its fast,
think MAT; usually <150 and irregular
Tx: BB, CCB
Flutter - saw tooth pattern, fast and SUPER
regular rate usually hovering around 150 ( specific
conduction ratio)
TX: Beta Blocker, CCB, Digoxin,
A Fib - irregularly irregular, can be normal rate or
rapid a fib. *See the A fib summary sheet for
targeted management in detail
PEARL: A fib + Delta waves = pre-excitation A
fib, DO NOT GIVE ADENOSINE! the A fib can
convert to V fib by delaying the AV node and
making the aberrant impulses go down the
accessory pathway.
Tx: In general - if you see the A fib come on and/
or they are unstable - synchronized cardio
version. If starting point for the A fib is
undetermined there is a risk of
thromboembolic stroke with cardio version.
Therefore you need to rate control and
anticoagulate first. Then you can cardiovert. In a
rush? Get a TEE to rule out LV thrombus.

Regular Irregular

P Waves Sinus Tachy, Atrial Multifocal atrial

Tachy tachycardia (MAT)

Flutter Waves Atrial Flutter - Flutter with

usually a rock variable block
steady rate of
150** AVNRT - not a p wave to be seen and a fast
regular rate (>150)? Think about AVNRT. This is a
No P waves AVNRT - super A Fibrillation
fast (heart rate in short circuit in the AV node. Theres a slow
the 200s) pathway that depolarizes fast and a fast pathway
that depolarizes slow - usually starts with a PAC
down the slow pathway and depolarizes up the
Sinus Tachy - can be caused by anything from fast pathway, this causes a vicious circle
pain to sepsis, drugs to anemia; assess the

(literally) —> and there impulse just circles in AV
node and causes a rapid rate.
Clues: typically women in their 40s, see an RSR’
in V1 and a P wave thats buried AFTER the QRS
and distort it. This rhythm has an on or off
switch - sudden onset, or nothing at all with
vagal stimulation.
TX: Vagal manouvres, CCB, adenosine
AVRT - this is a short circuit with an accessory
tract. This is different from AVNRT which DOES
NOT HAVE ONE.
Signal originates in the AV and then the impulse
goes back up through the extra pathway.
WPW - accessory pathway + pre-excitation =
WPW pattern and the delta wave. What’s going
on here? “In WPW syndrome, because of the
physiologic delay of conduction in the AV node,
conduction from the atrium reaches the adjacent
ventricle initially via the accessory pathway (AP),
which normally has no conduction delay, and a
part of ventricle is pre-excited, resulting in a
slurred upstroke at the initiation of the QRS
complex, known as the delta wave.” - (Epocrates
explained it better than I ever could)
VENTRICULAR TACHYCARDIA
Ventricular tachycardia
- Defined as bpm >100, QRS > 120 ms
- Three categories: monomorphic (consistent
pattern), polymorphic (multiple wave forms),
bidirectional (axis changes beat to beat)
- Sustained if > 30 beats of it and hemodynamic
collapse within 30 sec of onset
E. Salami
- commonest cause - CAD; your post ACS
patients have a HIGH risk of this sudden death
rhythm, other things that can cause it include
cardiomyopathy, infiltrative autoimmune
diseases (e.g. cardiac amyloid/sarcoid, Chagas
disease), anything that stretches/distorts/
causes ischemic changes to the electrical
anatomy of the heart
- MANAGEMENT - ACLS** - pulseless Vtach is
the cardiac arrest algorithm and Vtach with a
pulse is the symptomatic tachycardia
algorithm. If Torsades (sinusoidal pattern) -
check K+ and stabilize with calcium gluconate,
begin shifting with insulin and start elimination
with either Kayexelate/lasix/dialysis if severe.
- Pearl - be on the look out for these patterns
on the telemetry in post ACS patients. On
CCU it was very common to see patients go
into several beats of Vtach following large
infarcts. These arrhythmias can be treated
with medical management or implanted
devices depending o the aetiology and
stratified risk.
SVT with Abberancy
- Look at previous ECGs - this the best way to
determine whether this is a true blue Vtach or a
conduction abnormality with a fast rate.
Common aberrant patterns include:
- LBBB with tachycardia
- Rate dependent BBB - this is when the
BBB appears when the patient has a fast
heart rate. The patient QRS will normalize
at slower rates, treat this with standard
antiarrhythmics ( see chart*).
- Antidromic AVRT - discussed above; you have
a wider QRS as the unusual activation of the
pathways goes through the accessory pathway
first and goes back up to the node via the
physiologic His-Purkinje system
- NOTE: Orthodromic AVRT - here, antegrade
conduction to the ventricles occurs over the
AV node and retrograde conduction is over
the accessory pathway, the QRS complex
will be narrow.
- BOTTOM LINE:
- If stable - treat like the ACLS pathway and
with anti arrhythmic drugs +/- pacemaker or
defibrillator depending on ethology
- If unstable and pulse present - ACLS tacky
algorithm
- If pulseless - ACLS cardiac arrest algorithm
 E. Salami

Anti-Arrhythmic Drugs

Class Mechanism Indications Adverse effects Typical Drugs/Doses

I - Sodium Block fast sodium channels -
Channel Phase 0; no effect on nodal tissue
Blockers which depends on calcium
channels
IA - depress sodium channels and
slow conduction
IB - Block sodium channels in the
inactivated state, better for
tachyarrhythmia
IC - block open sodium channels,
dissociate slowly in diastole, good
for SVT
Reentry Syndromes - works well for
these as it suppress the
depolarization velocity of non nodal
tissues
Brugada Syndrome
Ventricular tachyarrhythmias
Atrial Fib
IA - anticholinergic toxicity, lupus-
like syndrome (procainamide),
enhanced digitalis effect (quinidine),
risk of torsades des poimtes
( quinidine)
IB - pulmonary fibrosis with some
agents (tocainide)
IC - can cause Life threatening
Vtach due to use dependence, the
higher the rate the less the drug can
dissociate the more pro-arrhythmic
activity; generally used with the aid
of the pacemaker for back up;
negative inotropes so don’t use in
decompensated heart failure
IA
Procainamide (V arrhythmia) -
500 to 600 mg administered as a
slow infusion over 25 to 30
minutes THEN 2 to 6 mg/minute
by continuous infusion
Quinidine
IB
Lidocaine - IV, intraosseous (IO):
Initial: 1 to 1.5 mg/kg bolus. If
refractory VF or pulseless VT,
repeat 0.5 to 0.75 mg/kg bolus
every 5 to 10 minutes (maximum
cumulative dose: 3 mg/kg).
Follow with continuous infusion
(1 to 4 mg/minute) after return of
perfusion
Mexilitine

IC
Flecanide - Initial: 50 to 100 mg
every 12 hours; increase by 50
mg twice daily at 4-day intervals;
maximum: 400 mg/day
Propafenone

II - Beta Inhibit sympathetic activity through
Blockers inhibition of the beta adrenergic
receptors
Bread and Butter of the CCU -
confer survival benefit for the
ACS patients and Heart failure
patients
Slow SA node/ectopic pacemakers
as well as increase the refractory
period of the AV node
Fatigue
Hypotension
Heart block if overdosed
Contraindicated in Acute heart
failure
Bronchoconstriction - ask about
asthma/obstructive lung disease
Metoprolol
50 mg PO BID to start for angina
Rapid Afib - IV 2.5-5mg q 2-5
min over 15 minutes to reduce
rate
Heart failure - 25 mg PO daily

Carvediliol -

Heart Failure - 3.125 mg PO BID,

increase to 6.25 mg Po BID, then
tartrate up every 2 weeks to max
dose [ is <85 kg maximum of 25
mg, if > 85kg max dose of 50
mg]

Bisoprolol - 2.5-5mg PO daily

III - Pottasium Block Pottasium channels —> Treatment of Ventricular Prolong the QT and can cause Amiodarone (most commonly
Channel Blocking depolarization = tachyarrhythmias - think ACLS TORSADES - sotalol and ibutilide used) - IV 150 mg over 10
Blockers prolonging the refractory period of can do this at slower rates minutes then 1mg/min got 6
cardiac cells Termination of rapid A fib or A flutter especially hours and then 0.5 mg per min
- chemical cardio version for 18h

Dronedarone, Ibutilide,
Dofetilide, Sotalol, vernakalant

IV - Calcium Block calcium channels and slow Non dihydropyrimadines - used for
Channel AV conduction, prolong AV angina, hypertension and
Blockers depolarization thus addressing arrhythmias such as A Fib (better
reentrant lesions tolerated than beta blockers for rate
control).
Dihydropyramindines - used for
HTN primarily due to vasodilatory
effect.
Non Di —> negative chronotropic
effect so think twice about using
these in acute heart failure;
excessive bradycardia, impaired
electrical conduction, don’t use with
beta blockers
Di —> headache, flishing, reflex
tachycardia, hypotension edema
Non-Di
Verapamil
A Fib —> IV 0.075 - 0.15 mg/kg
over 2 minutes then additional
bolus of 10 mg
PO 180-480 mg once daily
Angina —> 80-120 mg PO TID
Diltiazem
Dilt XR - 120 mg PO daily
Acute A fib: 0.25 mg/kg actual
body weight over 2 minutes,
then additional bolus of 0.35mg/
kg over 2 minutes
Di
Nifedipine
Angina; 10 mg PO TID - DO
NOT USE IN ACUTE MI
HTN emergency - 10 mg; may
repeat with a 20 mg dose in 20
minutes if needed
 E. Salami

RESOURCES
1. Life in the Fast Lane: https://
lifeinthefastlane.com/ccc/arrhythmias/
2. Pocket Medicine 4th Edition
3. Epocrates Online: https://
online.epocrates.com/diseases/40024/Wolff-
Parkinson-White-syndrome/Etiology
4. Dr. Hanninen - ward notes, ECG teaching
5. UpToDate: Wide QRS complex tachycardias:
Causes, epidemiology, and clinical
manifestations
6. UpToDate: Myocardial action potential and
action of antiarrhythmic drugs
7. Images:
1. https://ecg-educator.blogspot.com/
2016/02/wolff-parkinson-white.html
2. Wikipedia