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Arrhythmias

★ Objectives:
1. Identify the common arrhythmias
2. Know the differential diagnosis of heart rhythm disorder.
3. Learn the treatment modalities and diagnosis of atrial fibrillation.
4. Know the risk stratification of atrial fibrillation patient.

★ Resources used for this lecture:

​ Slides, Davidson's, Kumar, Step-up, Kaplan CK, ​DR. HERSI CLASS NOTES

​ ​ Done by:​ Amirah Bin Zuair​ &​ Rawa Alohali Contact us at:​[email protected]
​ Revised by:​ Team leaders
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Our lecture is mainly about Atrial fibrillation, but in our teamwork we mentioned the
other types for the sake of completion.. s ​ o your main focus should be on Afib!
If you don't have time just jump to ​page 8​ where Afib is.

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Introduction
Normal heartbeat is initiated by an electrical discharge from the Sinoatrial node (SA) passess
through the atrium to the Atrioventricular node (AV) then to the ventricles . The Atria and
ventricle depolarize sequentially as the electrical charge passes through them.
So Sinus node acts as the pacemaker of the h​eart.

Arrhythmias
A disturbance in the electrical rhythm of the heart is called Arrhyth​mia or Dysrhythmia “is the
true terminology​”​. Arrhythmias are often caused by structural heart disease, but may also occur
because of abnormal conduction or depolarization in an otherwise healthy heart.
Arrhythmias are classified based on the​ ​origin​ and ​rate​.
Origin​ based classifications are :
1- Supraventricular ​“above the ventricle”​:
A.Sinus : Electrical charges originate in the sinus node (SA) .
B.Atrial : Electrical charges begin in the atrium from foci other than the normal SA node.
Junctional : Electrical charges originate from the Atrioventricular area.
2- Ventricular : Electrical charges originate from the ventricles .
Rate​ based classifications are :
1- Bradycardia : heart rate less than 60 beats/min.
2- Tachycardia : heart rate more than 100 beats/m​in.

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 1- Bradyarrhythmias
Symptoms​: ​-Could be asymptomatic-
Decrease of cardiac output leads to dizziness, cool extremities, shortness of breath, fainting, mental status
alteration.

AV Block​ ​VIDEO
Sinus
Bradycardia Second degree
First degree Third degree
Mobitz 1 Mobitz 2

1. P wave fail to
“Wenckebach”
conduct​ without -​No
Prolonged PR a preceding PR correspondence
-Sinus rate​ less than 60 bpm. -PR interval
interval caused by prolongation. between P waves
Characteristics -Normal finding in ​athletes. prolongation till
delay in the AV 2. ​QRS suddenly and QRS complex.
-Side effect of antiarrhythmics. the​ P wave fail
node. drop. -Complete block
to conduct.
-His-purkinje (AV dissociation)
-AV node block
system block.

Atropine
Treatment No treatment required. Pacemaker.
Blocking the vagal stimulation-

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2- Tachyarrhythmias
Symptoms​:
Decrease of cardiac output leads hypotension, syncope, blurred vision, dizziness shortness of breath.
- Chest pain/ Palpitations
- Anxiety / Nervousness

★ Ventricular Tachycardia
Rapid and repetitive firing of three or more ventricular contractions at rate of more than 120 bpm.
Less common than atrial but much more sever.
Causes:​ Commonly ischemic heart diseases.
ECG findings:​ (FAT & FAST) Wide and bizarre QRS complexes.

Treatment:
✓ Stable patient​ : IV Amiodarone, Lidocaine or Procainamide.
✓ Unstable patient​ “Chest pain, SOB, Hypotension and confusion”:​ Synchronized cardioversion.

★ Ventricular Fibrillation
Multiple foci in the ventricles fire rapidly and usually preceded by ventricular tachycardia.
○ BP unmeasurable / absent heart sounds
○ Unconscious patient
○ Serious case if not treated leads to sudden death.
ECG findings: ​ No P waves identified + No QRS Identified

Treatment​:
Immediate defibrillation and CPR,​ if persisten​t IV epinephrine or vasopressin​ If fails ​antiarrhythmics.
Implantable defibrillator when cardioversion is successful.

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Atrial Tachycardia: ​Rarely associated with hemodynamic1 compromise because cardiac output is largely dependent upon ventricular output.
Look for the following finding in the history to suggest an atrial arrhythmias :
✓ Palpitation
✓ Exercise intolerance or dyspnea
✓ Embolic stroke
The most likely diagnosis even before EKG is Atrial fibrillation, since it’s the most common.

Let's go briefly over the least common atrial tachycardias first:

★ Atrial Flutter
One irritable automaticity focus in the atria fires regularly at about 250-350 bpm, and the long refractory period
in the AV node allows only one out of every two or three atrial flutter waves to conduct to the ventricles, so the
ventricular rate is 125-150 bpm.

Causes:
✓ Heart disease ( heart failure commonly)
✓ COPD
✓ Atrial septal defect
ECG findings:​ ​ Saw-tooth baseline ( QRS complex after 2 or 3 p waves )

Treatment :​ ​Same as Atrial Fibrillation.

✓ Hemodynamically unstable patient:​ Synchronized cardioversion (shock)
✓ Hemodynamically​ ​stable​ ​patient​: Rate control - Elective cardioversion-, Anticoagulation ​(depending
on CHAD VAS score)​- Refer for Ablation2 .

1
​Relating to the flow of blood within the organs and tissues of the body.
2
During the procedure, small wires called electrodes are placed inside your heart to measure your heart's electrical activity. When
the source of the problem is found, the tissue causing the problem is destroyed.To prevent the abnormal rhythms from moving
through the heart.

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 ★ Paroxysmal Supraventricular Tachycardia
Arrhythmia caused by re-entry of the impulses with abrupt onset and termination, divided to two types:

AV Nodal Reentrant Tachycardia Orthodromic AV Reentrant Tachycardia

-30%
-60%, most common. -An accessory pathway called a
Characteristics -Two pathways within the AV node. “concealed bypass tract” conducts impulses ​retrogradely from the
(one fast the other slow) ventricles to the atria.
Causes​:​ Ischemia / Digoxin toxicity.

ECG findings Narrow QRS + no discernible P waves Narrow QRS + P wave which may be discernible or may not

-Stimulate vagus delay by carotid sinus massage (or breath holding / head immersion in cold water/ valsalva
Treatment maneuver) followed by IV Adenosine (act by decreasing SA and AV nodal activity).
-If episodes are recurrent and symptomatic → ablation is preferred

VIDEO

★ Wolff-Parkinson-White Syndrome
An accessory pathway of conduction from atria to ventricles through the bundle of kent. It may lead to paroxysmal
supraventricular tachycardia alternating with ventricular tachycardia or atrial flutter and fibrillation​. Three things can make
you recognise it:
1- SVT alternating with ventricular tachycardia.
2- SVT get worse with digoxin or diltiazem.
3- Observing Delta wave on ECG.
ECG findings:​ Short PR interval ​+ delta ​waves (upward deflection before QRS) + wide QRS complex.
● Most accurate test is Electrophysiology studies (EP).

Treatment​: ​Procainamide ( Avoid digoxin / beta blockers /

calcium channels blockers) or Radiofrequency catheter
ablation.

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 ★ Atrial fibrillation (AF):
Uncoordinated atrial activation with subsequent decline of atrial function​.

● Very common ⅓ of cases of arrhythmias are AFib.

● Common in elderly above 50 years, always think of secondary causes “​pulmonary or alcohol” ​if young​.
● AF​ is associated with significant morbidity and a two-fold increase in mortality that are largely
attributable to the effects of th​e underlying heart disease and the risk of Thromboembolic events
(most feared> cerebral embolism “stroke”).

Characterised by:
● Rapid (350-600 bpm) & irregular atrial rhythm.
● Reduced filling of the left and right ventricle.
● Cardiac output can be reduced. (causing unstable hemodynamic status)
● Conduction of most impulses from atria to ventricles is blocked at AV node.
● Contraction of ventricles can be: -either-
✓ Irregular and rapid (110-180 bpm) → tachycardia
✓ Irregular and slow (<50 bpm) → bradycardia
✓ Norma​l
Note:​ If the ventricles did response for 350-600 beats from atrium (SA) → no time for ventricular filling→ no
Cardiac output→ no BP → collapse→ death. (That’s why AV node is smart and always trying to compensate by
blocking most impulses coming from the atrium)

The ventricular respons​e to AF depends on to Atrial craziness depends on:

Electrophysiologic properties of AV node, the level of vagal and sympathetic tone, and the action of drugs.

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 So A fib is a supraventricular tachyarrhythmia characterized by​ ​uncoordinated atrial activation​ ​with subsequent
decline of atrial function​. ​On the​ ECG,​ t​here is replacement of consistent P waves by f​ ibrillatory waves​ ​that vary in
size, shape, and timing (​ 350-600 beats/min), associated with an irregular, frequently rapid ventricular response
(irregularly,irregular)​

Mechanisms of the initiation of AF:

1. Ectopic beats, often arising from the pulmonary veins that triggers AF.
2. Re-entry within the atria maintains AF, with multiple interacting reentry circuits operating
simultaneously.

AF causes remodelling: “ AF begets AF” ‫​وﺣﺪة ﺗﻮﻟﺪ وﺣﺪة‬

Electrophysiological changes​ occur in the atria within a ​few

When AF persists for a period of ​months​,​ ​structural
hours ​of the onset of AF that tend to maintain fibrillation:
electrical remodelling. remodeling ​occurs with ​atrial fibrosis and dilation​ that
further ​predispose​ to AF.
(by shortening refractory period)

● Many episodes of AF resolve spontaneously.

● Over time AF tends to become persistent or permanent.
*​AF for a year is different than AF for a day, this dictates how to treat the patient.

Common Causes of AF:

Non-Cardiac Causes:
Cardiac Causes:
● HTN ● Pulmonary:
● Ischemic heart disease ○ COPD
● MI ○ Pneumonia
● Pericarditis ○ Pulmonary embolism
● Pericardial trauma ● Metabolic
● Valvular heart disease: ● Thyroid disease:
○ Rheumatic: ○ Hyperthyroidism OR Hypothyroidism
✓ mitral stenosis ● Electrolyte disorder
○ Non-rheumatic: ● Toxic:
✓ Aortic stenosis ○ Alcohol ​“Younger”
✓ Mitral regurgitation ● Systemic illness:
● Cardiomyopathy ○ Sepsis
● Post-coronary bypass surgery ○ Malignancy
○ DM

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 Different classifications of AF

“Based on Time”

Long-standing
First diagnosed Paroxysmal Persistent Permanent
persistent AF

-Not been diagnosed -Most cases -​Prolonged -Continues AF -More the one year and does
before within 48 hours, episodes ​>7 days lasting for ​one year not respond to
may continue to 7 that can be or more. cardioversion.
-Irrespective of
days. terminated by
severity nor duration -When it’s decided to -Paroxysmal AF will become
electrical or adopt a rhythm permanent as the ​underlying
-Self terminating
chemical strategy. disease ​process that disposes to
cardioversion. AF​ progress.

Note: About 50% of all patients with paroxysmal AF and 20% of patients with persistent or permanent AF have structurally
normal hearts; this is known a​s ‘lone atrial fibrillation’.

“Based on the Cause”

Lone OR Primary Secondary Non-valvular

AF without clinical/ECG evidence of Associated with ​cardiopulmonary Not associated with damage to the heart
cardiopulmonary disease disease. valves.

Patient that has valvular disease should automatically be given → Anticoagulants.

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 Diagnosis of AF:
■ Signs and symptoms:​ ​ ​(elderly with SOB, dizziness and palpitations consider AF)

Symptoms vary according to: irregularity / rate of ventricular response, functional status, AF duration, patient factors, and comorbidities..

Sign/symptom Cause

Irregularly irregular pulse

Irregular heart-beat
Palpitations

Fatigue
Diminished exercise capacity
Decreased cardiac output
Breathlessness (dyspnoea)
Weakness (asthenia)

Dizziness and fainting (syncope) Hypotension

Chest pain (angina) Cardiac ischaemia

Thromboembolic TIA, stroke ​* Might be the first presentation. Increased risk of clot formation

■ ECG findings:
Irregularly irregular rhythm, no identifiable P waves​ t​here is replacement of consistent P wave​ ​by ​fibrillatory waves ​that
vary in ​size, shape, and timing ​(350-600 beats/min), associated with an irregular, frequently rapid ventricular response​. “AF
ECG may show-Left ventricular hypertrophy, Pre-excitation, Bundle branch block or Prior MI”

Atrial Fibrillation Normal

Heart rate Tachyarrhythmia Normal

Rhythm Irregular Regular

P wave No P wave P waves

Baseline Irregular basline Steady Base line

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Investigations of AF:
■ Transthoracic Echocardiography​ ​(​To rule out cardiac diseases​)
Used to identify: ​Size and functioning of atria and ventricles,Ventricle hypertrophy,
Pericardial disease and Valvular heart disease.
Note: it’s the only way to be 99% sure that there is no clots in (LAA)

■ Laboratory tests ​Important parameters to assess include:

Thyroid function​,Renal function, Hepatic function, Serum electrolytes and Complete blood
coun.

■ Holter monitoring ​(Portable ECG device ​“recorder”​):

Continuous monitoring for a short period of time (typically 24 hours)
Useful for: ​Detecting asymptomatic AF​, Evaluating patients with paroxysmal AF, Associating
symptoms with heart rhythm disturbance​ and Assessing response to treatment.

■ Transoesophageal echocardiography ​(for Selected patients):

useful for: ​Accurate assessment of risk of stroke)​, Sensitive detection of atrial thrombi>
(Particularly th​e left atrial appendage, as it is the most common site of thrombi in patients
with AF)

■ Exercise testing.
■ Chest radiography:​ ​allows evaluation of the lung parenchyma and identifies coexisting lung
disease.

Management of AF
Two general approaches are used for managing AF:
(1) Ventricular ​rate control.​ (considered alone for patients with little symptoms of arrhythmias)
(2) Rhythm control. ​(for patients who are experiencing consequences of arrhythmias.. ex.SOB,HF.)
+ Anticoagulation​ to reduce the risk of stroke in patients with AF >​>​The CHA2DS2VASc Index

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 Treatment options for AF D​ epending on the condition of the patient we will treat:
1- Acute​ ​AF​:​ A) Hemodynamically ​unstable​ patient → immediate electrical cardioversion to sinus rhythm.
Note: All patients who go for cardioversion “regardless of the case” should take anticoagulants, why? ،‫ﻣﻮ اﻟﻮاﺣﺪ أول ﻣﺎﯾﻘﻮم ﻣﻦ اﻟﻨﻮم ﯾﻜﻮن ﻣﻔﺠﻮع‬
‫وﯾﺠﻠﺲ ﻓﺘﺮة ﻋﻠﻰ ﻣﺎ ﯾﺴﺘﻮﻋﺐ وﯾﻤﺎرس ﻧﺸﺎﻃﻪ ﻃﺒﯿﻌﻲ‬. Atrial is not mechanically functioning > Blood stasis > Thrombus formations.
B) Hemodynamically ​stable​ patient: Three things you have to achieve.

Prevention of Thromboembolism “Stroke” Maintenance of Sinus Rhythm

Control of Heart Rate
(Depending on CHADVASc ★ ) (after rate control is achieved)

AF present>48 hours, risk of embolization during cardioversion is

significant. Anticoagulate patient for 3 weeks
​before​ and 4 weeks ​after​ cardioversion
-To avoid waiting 3 weeks for anticoagulation, obtain a TEE to -Determine the pulse in a Use pharmacological cardioversion only if
patient with AF. if its too rapid, electrical cardioversion fails or is not
image the left atrium, if no thrombus is present, start IV heparin it must be treated
and perform cardioversion within 24 hours feasible.
.(target rate is 60 to 100 bpm)
-An INR of 2 to 3 is the anticoagulation range.
less than 2 indicate clot and more than 3 indicate bleeding

Pharmaceutical​:
Pharmaceutical​: most effective when initiated
Pharmaceutical​: • Ca2+-channel blockers ( within 7 days of AF onset).
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•Warfarin (INR must be checked regularly) In asthmatics •Antiarrhythmic drugs
•Aspirin (​LEAST effective, but has no interaction, no INR​) •B-blockers – Class IA / IC
•Dabigatran,Apixaban (​no interaction, no INR​) In CAD – Class III: e.g. ​Amiodarone
•Rivaroxaban •Digoxin Best effective, but not first line due to
*Last 3 drugs are mostly used now.. (if BP is very low and cannot be complications. It can be given to elderly
tolerated at rest ​last choice​) •Flecainide •Propafenone
S​afer, less side effect, given to Youngers

Non-Pharmaceutical​:
Non-Pharmaceutical​: •Ablation
Non-Pharmaceutical​:
•Removal/isolation of •Surgery (MAZE)
•Ablate/Pacing. -Electrical shocks
left atrial appendage e.g. WATCHMAN​®​ device or surgery
Direct-current cardioversion

2- Chronic AF:
A) Rate control: With ​•​Beta-blockers or​ ​• Ca2+-channel blockers •Digoxin if BP is low.
B) Anticoagulation (use CHADSVASc score)
- Patient with ‘lone’ AF under age 60 > no need for anticoagulation therapy(low risk of emboli).
- Treat all other patients with chronic anticoagulation (warfarin).

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​Warfarin inhibits the ​vitamin K​-dependent synthesis of biologically active forms of the ​calcium​-dependent ​clotting​ ​factors ​II​, VII,
IX​ and ​X​, as well as the regulatory factors ​protein C​, ​protein S​, and protein Z. it is contraindicated for pregnancy and has a high
food-drug interaction (green leaves ‫)ﻛﺮاث‬

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★ Prevention of Thromboembolism “Stroke” cont.
When to know your patient should or shouldn’t take antithrombotics?
By using Stroke Risk Score for Atrial Fibrillation: ​ The CHA2DS2-VASc Index
C​ongestive heart failure or LVEF < 35% 1

H​ypertension 1

A​ge >75 years 2

D​iabetes mellitus 1

S​troke/TIA/systemic embolism 2

V​ascular Disease (MI/PAD/Aortic plaque) 1

A​ge 65-74 years 1

S​ex ​c​ategory (female) 1

> 2 : Moderate-High risk ​“Give ​anticoagulant ​Give Warfarin”

0-1 : Low risk​ ​ ​“ ​No anticoagulant​”

Example:
78 year old ​female with history of​ DM and ​HTN.
calculate her CHADSVASc score, and determine her mangement?
Age = 2 , Female = 1, DM= 1, HTN= 1 SO 2+1+1+1=​ 5
Her score is 5, so she’s high risk, we give Warfarin

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 TEE-guided cardioversion: acute study design

Difference between Cardioversion and Defibrillation :

Cardioversion Defibrillation

Delivery of a shock​ in synchrony ​with QRS complex to Delivery of a shock​ not in synchrony with QRS complex,
terminate dysrhythmias. to convert dysrhythmias to normal sinus rhythm.

Summ​ary of the management plan

in Acute AF:

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MCQs

1- An active 78-year-old female has been followed for hypertension

but presents with new onset of mild left hemiparesis and the finding of atrial fibrillation on ECG.
She had been in sinus rhythm six months earlier. Optimal treatment
by hospital discharge includes anti-hypertensives plus :
a. Close observation
b. Permanent pacemaker
c. Aspirin
d. Warfarin (Coumadin)
e. Subcutaneous heparin

2- A 36-year-old white female nurse comes to the ER due to a sensation

of fast heart rate, slight dizziness, and vague chest fullness. The following
rhythm strip is obtained which shows :

a. Atrial fibrillation
b. Atrial flutter
c. Supraventricular tachycardia
d. Ventricular tachycardia

3- The initial therapy of choice in this stable patient is :

a. Adenosine 6 mg rapid IV bolus
b. Verapamil 2.5 to 5 mg IV over 1 to 2 minutes
c. Diltiazem 0.25 mg/kg IV over 2 minutes
d. Digoxin 0.5 mg IV slowly
e. Lidocaine 1.5 mg/kg IV bolus
f. Electrical cardioversion at 50 joules

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4- A 65-year-old man with diabetes, on an oral hypoglycemic, presents
to the ER with a sports-related right shoulder injury. His heart rate was
noted to be irregular and the following ECG obtained. The best immediate
therapy is :

A. Atropine
B. Isoproterenol
C. Pacemaker
D. Electrical cardioversion
E. Digoxin
F. Diltiazem
G. Observation

5- In the ICU, a patient suddenly becomes unresponsive, pulseless, and

hypotensive, with cardiac monitor indicating ventricular tachycardia. The
crash cart is immediately available. The first therapeutic step should be
A. A precordial thump
B. Lidocaine 1.5 mg/kg IV push
C. Epinephrine 1 mg IV push
D. Defibrillation with 200 joules
E. Defibrillation with 360 joules

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6- A patient has been in the cardiac care unit with an acute anterior
myocardial infarction. He develops the abnormal rhythm shown below.
You would :

A. Give digoxin
B. Consult for pacemaker
C. Perform cardioversion
D. Obtain digoxin level
E. Give lidocaine

Q: What’s the difference between Atrial flutter and fibrillation?

● Flutter is regular rhythm whereas fibrillation irregular.
● Flutter usually goes back into sinus rhythm or deteriorates into fibrillation

ANSWERS
1- D
2-C
3- A
4- G
5- D
6-B

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