This document provides an overview of tachyarrhythmias. It begins by defining arrhythmia and tachycardia. It then discusses the etiology, pathogenesis and mechanisms of tachycardia. It describes the different types of tachyarrhythmias including supraventricular tachycardia involving the atria, AV node, and ventricular tachycardia. For each type, it provides details on definition, signs and symptoms, ECG findings, etiology, and treatment approaches. It specifically addresses atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, Wolff-Parkinson-White syndrome, premature ventricular contractions, ventricular tachycardia, and ventricular fib

1. Tachyarrhythmia
By Lara Masri
4th year medical student
Source: step up to medicine 5th ed

2. 1- Arrhythmia
• Definition
• Etiology
• Pathogenesis
• mechanisms of tachycardia
2- Tachyarrhythmia
• Supraventricular tachyarrhythmia
• Atrial
• AV nodal
• Ventricular tachyarrhythmia

3. Cardiac arrhythmias
Definition:
A cardiac arrhythmia is defined as a disturbance of the electrical rhythm of the heart.
 A heart rate of more than 100/min is called a tachycardia, and a heart rate of less
than 60/min is called a bradycardia.
Etiology:
Cardiac arrhythmias are often a manifestation of structural heart disease but may
also occur because of abnormal conduction or depolarization in an otherwise healthy
heart.

4. Pathogenesis
Cardiac arrhythmias usually occur as the result of pathology affecting the conducting system
of the heart.
 The cardiac cycle is normally initiated by an electrical discharge from the SA node, this
impulse travel through the atrial conduction system to depolarize atria via internodal
tracts to depolarize right atrium which are ; posterior (thorel), middle (wenckebach) and
anterior tracts and via the bachmann bundle [from the anterior internodal tract] to
depolarize the left atrium, once the impulse reach AV-node, it will travel through his
purkinjie system to depolarize the ventricles.
 The sinus node regulated by the autonomic nervous
system; vagal activity decreases the heart rate and
sympathetic activity increases heart rate through
cardiac sympathetic nerves and circulating
catecholamine.

6. There are three main mechanisms of tachycardia:
Increased automaticity;
The tachycardia is produced by spontaneous depolarisation of an ectopic focus in
the atria, atrioventricular junction or ventricles, often in response to
catecholamines. Single depolarisations lead to atrial, junctional or ventricular
premature (ectopic) beats, repeated depolarisation leads to tachycardia.
Re-entry;
The tachycardia is initiated by an ectopic beat and sustained by a re-entry circuit.
Most tachyarrhythmias are caused by re-entry.
Triggered activity;
This can cause ventricular arrhythmias in patients with coronary artery disease. It
is a form of secondary depolarisation arising from an incompletely repolarised cell
membrane.

8. Tachyarrhythmia
Ventricular
PVC
Ventricular
Tachycardia
Ventricular
fibrillation
Supraventricular
Atrial
Sinus
Tachycardia
PAC MAT
Atrial
flutter
Atrial
fibrillation
Nodal
AVRT AVNRT

9. 1. Supraventricular tachyarrhythmia
 narrow QRS complex < 120 ms
- An increase in sympathetic activity, HR > 100 bpm
- Signs & symptoms: palpitation, SOB, Chest pain, Light-headedness
- Etiology:
- Normal response to emotions such as fear, pain and Anxiety
- Exercise
- Hyperthyroidism
- Structural heart diseases, HF and MI
- Pulmonary embolism
- Anemia
- Hypovolemia
- albuterol, decongestants, and substance withdrawal.

10. ECG findings
• Regularity: Regular
• HR: >100 bpm
• P wave: Present
• QRS complex: <0.12
• PR interval: Normal
Management:
- Treat the underlying cause, such as with oxygen , antibiotics, pain-killers or
fluid.
- B blocker
- CCB

11. - Very similar to premature ventricular contractions; Which is an early beat arises within
the atria, firing on its own.
- It is caused by a single site of micro-reentry outside the SA-node. (focal one site)
- Causes include adrenergic excess, drugs, alcohol, tobacco, electrolyte imbalances,
ischemia, hypoxia, and infection.
- Signs & symptoms: palpitation, SOB, and chest pain
- Characteristics:
• Paroxysmal
• Self limited and coming on suddenly
• Increase with age normally

12. ECG findings
• Regularity: Irregular
• HR: >100 bpm
• P wave: Early P wave
• QRS complex: normal or small
• PR interval: Normal or Prolonged
Management
- antiarrhythmic drugs such as β-blocker and Non- dihydropyridine CCB

13. - Irregular rhythm, with 3 or more different p-wave morphology (p-wave different height
and width) and variable PR and RR intervals
- Etiology:
- Patient with COPD or COPD exacerbations
- Electrolyte disturbance like ↓K+
- Sepsis due to catecholamine surge
- HF
- Management:
- First line treatment is to treat the underlying cause (treat COPD), if not
relieved then give the patient antiarrhythmic drugs such as β-blocker
and Non- dihydropyridine CCB.
- Electrical cardioversion is ineffective and should not be used

14. - Atrial flutter is caused by a “re-entrant rhythm” in either atrium. This is where the
electrical signal recirculates in a self-perpetuating loop due to an extra electrical
pathway in the atria.
- The signal goes round and round the atrium without interruption. This stimulates atrial
contraction at 300 bpm.
- The signal makes its way into the ventricles every second lap due to the long refractory
period of the AV node, causing 150 bpm ventricular contraction.
- Associated Conditions:
• Hypertension
• Ischaemic heart disease
• Cardiomyopathy
• Thyrotoxicosis

15. Signs and symptmos:
1. Can be asymptomatic
2. Palpitation
3. dyspnea
4. Fatigue
5. Increase in atrial thrombus formation  [ atria are not pumping properly so
the blood stay stagnant in the atria and the thrombus formed  Once
thrombus formed can send emboli to different arteries in the body so we can
see systemic embolization.
ECG findings
• saw-tooth waves
• Regular rhythm
• narrow QRS complex
• Saw-tooth flutter waves are best seen in the inferior leads (II, III, aVF)
Treatment
• Rate/rhythm control with beta blockers or cardioversion
• Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
• Radiofrequency ablation of the re-entrant rhythm
• Anticoagulation.

17. - Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and
irregular.
- This due to disorganised electrical activity that overrides the normal, organised
activity from the sinoatrial node.
- Irregular irregular pulse and HR up to 170 bpm
Symptoms

18. ECG findings
• Regularity: Irregular irregular
• Atrial rate: >400 bpm
• Variable ventricular rate
• P wave: absent
• Fibrillation waves present
• PR interval: cant measured
• QRS complex: Narrow
Etiology
Most common causes of AF (remember that AF affects SMITH)
• Sepsis
• Mitral valve pathology (stenosis or regurgitation)
• Ischaemic heart disease
• Thyrotoxicosis
• Hypertension

19. Atrial fibrillation types:
• Paroxysmal AF
• Persistent AF
• Long standing persistent AF
• Permanent AF
• Lone AF
Complications:
1. Hemodynamic Instability
2. Cardiomyopathy
3. HF
4. Stroke or embolism
Ashman phenomenon in AF:
Occurrence of wide QRS complexes that follow a short R-R interval preceded by a
long R-R interval.
Its most commonly observed during AF when there are frequent episodes of long-
short R-R cycle lengths.

22. Treatment of AF symptomatic stable patient;

23. Treatment of AF symptomatic unstable patient;
Unstable= -SOB - Chest pain - Low BP - Altered mental status

24. - Type of Paroxysmal supraventricular tachycardia as the accessory pathway involves
both atria and ventricles outside the AV node.
- The impulses can take different pathways to polarize the heart in order to contract,
then the heart will be contracting much more, that’s why we have tachycardia
- The impulse just taking the accessory pathway ( additional electrical conduction
pathway) start looping between the accessory pathway and normal pathway, keep
sending impulses to the ventricles and the atria cause much more contraction, that’s
why called re-entry tachycardia.

25. Two types of AVRT: - Orthodromic- AVRT
- Antidromic- AVRT
Orthodromic -AVRT;
- Most commonly associated with WPW syndrome.
- Retrograde conduction via accessory pathway
- Anterograde conduction via AV nodal pathway.
- The tachyarrhythmia starts and ends abruptly
Antidromic- AVRT;
- Not associated with WPW syndrome.
- Retrograde conduction via AV nodal pathway
- Anterograde conduction via accessory pathway.

27. ECG Findings:
 Regular rhythm
 VR 200-300 bpm
 Orthodermic AVRT:
• P waves are buried in the QRS complex
• Narrow QRS because the impulse doesn't go through the AV node so it
doesn’t get slowdown so the atria and ventricles are depolarized faster.
• Short PR interval
 Antidromic AVRT:
• P wave precedes QRS
• Wide QRS
• Long PR interval

28. - Extra electrical pathway connecting the atria and ventricles.
- Normally there is only one pathway connecting the atria and ventricles (AV) node. The extra
pathway that is present in Wolff-Parkinson-White syndrome is often called the Bundle of
Kent.
- Bypasses AV node.
- Congenital disease occur due to failure of maturation of the insulating around AV ring.
- Autosomal dominant
- Depending on presentation → WPW pattern & WPW syndrome
WPW pattern → only include ECG characteristics
WPW syndrome → include ECG characteristics & signs & symptoms
- Signs & symptoms: Palpitations, syncope, sudden cardiac dead

29. ECG characteristics,
Delta wave  represents the early peak citation of the ventricle muscle
Short PR  the impulse by passing the normal AV-node pathway, thus
conduct to ventricles very fast.
Wide QRS  the impulse travelling through accessory pathway and
excitation of ventricles that caused by impulse travel through AV-node
pathway.
Therapy;
•The best initial therapy to control tachyarrhythmia in WPW is one of the following:
Procainamide
 Ibutilide
 Flecainide
 Amiodarone (no longer given because it has a B-blocker effect thus block
AV-node, increase risk to progress to V.Fib)

30. o Type of Paroxysmal supraventricular tachycardia, due to a small re-entrant loop within AV
node.
o When the impulse travels from the SA-node & need to go to AV-node → in the AV-node
itself it can take two pathways either slow pathway or fast pathway, and then it travels down
to purkinje system to depolarize the ventricles.
 Premature beat reaches the AV-node & starts looping between the slow & the fast pathways,
as it loops it keep sending impulses to the ventricle → depolarize & contract
 (HR > 200 bpm)
o • Most common cause of PSVT, usually in middle
aged women.

31.  Depending on which pathway this premature signal take
→→ Typical & atypical AVNRT
Typical AVNRT:
 Seen in 80-90% cases.
 Aka SLOW – FAST type.
 Anterograde conduction to ventricles via slow pathway
 Retrograde Conduction to atria via fast pathway .
ECG findings:
- short PR interval.
- Regular rhythm
- retrograde P-wave ( fused with QRS)  Pseudo R wave in V1 + Pseudo S wave in inferior
leads.
Atypical AVNRT:
 Seen in 10-20% cases.
 Aka FAST– SLOW type.
 Anterograde conduction to ventricles via fast pathway
 Retrograde Conduction to atria via slow pathway
ECG findings:
- Long PR interval.

32. Management
of AVRT &
AVNRT
Unstable
patient
Immediately cardioverting
Stable
patient
1- Decrease AVN
conduction via vagal
maneuvers
* Valsalva
* Carotid
massage
Ice water face
immersion
2- Adenosine IV or Non-
dihydropyridine CCB or B-
blockers or Digoxin

33.  Wide QRS complex > 120 ms
- It is an early beats fires on its own from a focus in the ventricle and then spreads to the
other ventricle
- Patient complain of skipped beats (palpitations) or asymptomatic
- Etiology;
• Structural heart diseases; e.g. HF, LVH, MI
[ injured myocardium can generate re-entrance circuit in the ventricles]
• Ectopic focal beats in ventricles due to ↓K+ and ↓Mg+; in patients who take loop
and thiazide diuretics
• Hypoxemia in emphysema and COPD patients
• Hyperthyroidism
• TCA and Digoxin drugs
 PVCs can be completely normal finding.

34. - If the patient has palpitation >> diagnose with ECG ‘’best initial diagnostic test’’
- ECG findings: Additional beats and wide QRS
• These beats are generated in the ventricle without being precede by P-wave;
because the impulse that cause this additional QRS complex is generated from
the ventricles, not coming from SA node.
- In case that the patient presents with signs and symptoms and PVCs are>10% of all beats
 put the patient on drug therapy:
- β-Blockers
- Non-dihydropyridine Ca-channel blocker
(Diltiazem & Verapamil)

35. - Defined as rapid and repetitive firing of three or more PVCs in a row, at a rate
of between 100-250 bpm
* Two types upon duration:
- Non-sustained  lasts < 30 sec
- Sustained  lasts > 30 sec [more dangerous- a life threatening]
• Two types upon morphology of QRS complexes:
- monomorphic uniform QRS complexes
- polymorphic varying QRS complexes
- In the sustained type the patient presents with ;
 Palpitation
 Chest pain
 Hypotension
 Syncope
 Can progress to ventricular fibrillation that lead to death
- Etiology : - CAD with prior to MI is the most common cause
- Structural heart diseases e.g. HF, LVH, MI
- Long QT syndrome  inherited channelopathies
- TCA drugs overload

36. Bidirectional VT

37. Diagnosis:
1) ECG; wide and bizarre QRS complex- if normal perform exercise stress test.
2) Echocardiogram; to look for any structural heart disease.
Managing:
 If the patient has HF -> first optimize the therapy for HF following the guide line
detected medical therapy (GDML)
 Implant ICD (implantable cardiovolter defibrillator) -> in patients with sustained
ventricular tachycardia and structural heart disease.
 If the patient had ICD and on β-blocker and still have signs and symptoms -> add
anti-arrhythmic drugs as Amiodarone.

38. Brugada Criteria for VT:
- Used to differentiate between VT and supraventricular tachycardia with aberrancy.
Classical Criteria for VT:
1. AV dissociation
2. Capture or fusion beats
3. -ve or +ve concordance
4. Tachycardia QRS more narrow
than Sinus QRS

39. Emergency
Check the pulse
Yes “Stable”
Stop the V-Tach
with Antiarrhythmic
drugs.
No
Follow the ACLS
protocol
Yes “unstable”
Need to perform
synchronize cardio
version

40. Advanced cardiac life support (ACLS)
Adult Cardiac Arrest
Initial treatment of VT/VF
• Shockable rhythm;
• Defibrillate immediately
• Continue CPR for 2 min
• Obtain intravenous / intraosseous access
• Consider advanced airway, end-tidal carbon dioxide tension
• Administer vasopressor (epinephrine 3-5min)
• Check pulse and rhythm every 2 min, as follows;
- If shockable, administer amiodarone after second defibrillation attempt
- Rotate chest compressors
- Identify and treat reversible causes

41. - A type of rapid polymorphic ventricular tachycardia in the setting of QT prolongation.
- Characterized by: - HR (160-250)bpm
- Congenital or acquired long QT-syndromes
QTc for men >450 ms
QTc for women >470 ms
- Irregular R-R interval
-Starts suddenly and stops suddenly -> can lead to V-fib which lead to
sudden cardiac death.
- Etiology : most common are Hypokalemia, AV block, Severe IHD
- Treat with MgSO4 (magnesium sulphate); even if patient has normal Mg.
- LQT syndromes; include Jervell and Lange-Nielsen syndrome and Romano-Ward syndrome.

42. Risk factors of Torsades de pointe;

43. - Ventricular fibrillation is a rapid disorganized rhythm; ventricles don’t contract properly
and cant push blood out of heart, due to multiple foci in the ventricles fire rapidly, so
there is no cardiac output and no detectable BP.
- Etiology: structural heart disease like ischemic heart diseases and TCA overdose
- Divided after acute MI in two types:
1a= within 10 min after MI
1b = within 1 hr. after MI
- Patient will present with sudden syncope of sudden cardiac arrest.
- Check pulse => if he doesn’t have pulse follow the ACLS protocol.

44. ECG features:
• Ventricular rate betw 150-599 bpm
• Irregular rhythm
• Bizarre, irregular, random waveforms
• NO identifiable P waves or QRS complexes or T waves.
Predictors of Primary VF in periinfarction period:
• STEMI
• Early replarization on ECG
• Hypokalemia
• SBP < 120 mmHg
• Larger infarcts
• Male sex
• Smoking
 If VFib is not associated with acute MI, recurrence rate is high (up to 30%
within the first year)