Tachy arrhythmia

1. MECHANISM OF TACHYARRYTHMIAS
SUPRAVENTRICULAR TACHYCARDIA AND ITS TREATMENT

2. Definition
• Heart rate >100 beats/min is called tachycardia
• Evaluation is based on 3 ECG findings :
- duration of QRS complex
- uniformity of R-R interval
-characteristics of atrial activity

4. MECHANISM OF TACHYARRYTHMIAS:
• Tachyarrythmias can be generated from sources above or below
bundle of his
• Those whose mechanism involves tissue above the bundle of his are
called Supraventricular tachycardias

5. • Tachyarrhythmias originating
> At or above the AV node - narrow QRS complex
>Below the AV node -wide QRS complex Tachycardia
• Tachyarrhythmias - 3 mechanisms:
1)Enhanced automaticity in normal conduction tissue or in an ectopic
focus
2)Re entry of electrical potentials through abnormal pathways
3)Triggering of abnormal cardiac potentials due to after depolarizations

6. REENTRY PATHWAYS
• Reentry pathways account for most premature beats and
tachyarrhythmias
• Extra pathways impulses can be conducted at different velocities
• Extra pathways called accessory tracts can exist around the AV node
and can conduct impulses to the ventricles bypassing the AV node
and normal infra nodal conduction tract.

8. • Increased Automaticity: The SA node spontaneously discharges at a rate of 60-
100bpm
• Other pacemakers can be accelerated and overdrive the SA node as a result of
disease states or iatrogenic influence such as drug toxicity
• Cardiac automaticity result from repetitive firing of a focus other than the sinus
node
• Dysrhythmias resulting from an ectopic focus often have a gradual onset and
termination

9. TRIGGERING BY AFTERDEPOLARIZATIONS
• Afterdepolarization are oscillations in membrane potential that occur
during or after repolarization.
• Triggered dysrhythmias associated with early afterdepolarizations are
enhanced by a slow heart rate and are treated by accelerating the
heart rate with positive chronotropic drugs or pacing
• Triggered dysrhythmias associated with delayed afterdepolarizations
are enhanced by fast heart rates and can be suppressed with drugs
that lower the heart rate

10. Mechanisms of arrhythmia

11. SINUS TACHYCARDIA
• Normal sinus rhythm in a patient at rest is under the control of the
sinus node , which fires at a rate of 60-100bpm
• Sinus rhythm exceeds 100bpm it is considered Sinus Tachycardia
• ECG shows normal P wave before every QRS complex
• It is caused by acceleration of SA node discharge due to either
sympathetic stimulation or parasympathetic suppression

12. PERIOPERATIVE CAUSES OF SINUS TACHYCARDIA
• PHYSIOLOGIC INCREASE IN SYMPATHETIC TONE
• Pain
• Anxiety
• Light anesthesia
• Hypovolemia or anemia
• Arterial hypoxemia
• Hypotension
• Hypoglycemia
• Fever or infection

13. • PATHOLOGIC INCREASE IN SYMPATHETIC TONE
• Myocardial ischemia or infarction
• Congestive heart failure
• Pulmonary embolus
• Hyperthyroidism
• Pericarditis
• Pericardial Tamponade
• Malignant hyperthermia
• Ethanol withdrawal
• Drug induced - Atropine or glycopyrollate,Sympathomimetic
drugs,Caffeine,Nicotine, Cocaine or amphetamine

15. TREATMENT OF SINUS TACHYCARDIA
• 1)Treat underlying cause
• 2)Avoidance of vagolytic drugs such as pancuronium, ensuring
adequate depth, maintenance of euvolemia, correction of
hypercarbia, hypoxia
• 3)Beta blocker to decrease heart rate and decrease myocardial
oxygen demand

16. CLASSIFICATION OF SVT
I)AV NODE DEPENDENT
• a)AV nodal reentry tachycardia: Reentry within the AV node
• b)AV reentry tachycardia: Re entry includes accessory pathway
• c)Accelerated idionodal rhythm: Due to increased automaticity

17. II)AV NODE INDEPENDENT
a)Atrial flutter – macro circuits reentry confined to atria
b)Atrial fibrillation – multiple rentry confined to atria
c)Unifocal atrial tachycardia
d)Multifocal atrial tachycardia
e)Others- sinus node re entry tachycardia

18. AV NODE DEPENDENT SVT
SVT from AV node
Blocking AV node with vagal
manoeuvres or adenosine
Terminate SVT
AV NODE INDEPENDENT SVT
SVT from atria
Blocking AV node will not
terminate SVT but slow the
ventricular rate

19. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
• It is a tachyarrhythmia with average heart rate of 160-220bpm
initiated and sustained by tissue at or above the AV node
• Most common type of PSVT is AV nodal reentry tachycardia
• Older than 65yrs are at greater risk
• AVNRT is commonly due to reentry circuit in which there is
anterograde conduction over the slower AV nodal pathway and
retrograde conduction over a faster accessory pathway

21. SYMPTOMS
Palpitations , Light headedness, Dizziness ,fatigue ,chest discomfort
TREATMENT
• Avoid triggering factors
• Hemodynamically stable pt: vagal manoeuvres(Carotid sinus massage,
Valsalva manoeuvre)
• Adenosine,Calcium channel Blockers ,betablockers- Terminate PSVT
• Unresponsive to drugs-Electrical cardioversion

24. PALS

25. AV NODAL REENTRY TACHYCARDIA
• Re entry confined to AV node
• Regular Narrow complex tachycardia 140-220bpm
• P waves not seen they are buried in the QRS complexes
• Narrow QRS complex <120ms reflects rapid activation of the
ventricles via normal his purkinje system
• Symptoms-Palpitations, shortness of breath, dizziness,syncope
• Not usually associated with structural heart disease

26. AVNRT
1)Hidden P waves in ORS
complex
2) P wave is seen
sometimes seen after QRS
complex
Pseudo s in lead II
Pseudo r in lead V1

27. CHRONIC THERAPY: Beta blocker,catheter ablation

28. AV REENTRY TACHYCARDIA
(WPW syndrome)
• Reentry pathway:
AV node+ Accessory pathway
(through bundle of kent)

30. TREATMENT
• PRE EXCITED TACHYCARDIA :
- Adenosine used with caution
- Verapamil , diltiazem , digoxin : class 3
• LONG TERM THERAPY :
- Sotalol
- Propafenon
• PILL IN THE POCKET :
-Diltiazem 120 mg + propranolol 80 mg
PREVENTION
• Radiofrequency ablation of accessory pathway is usually curative

31. ACCELERATED IDIONODAL RHYTHM
• Increased automaticity of the AV junction(Above the inherent
discharge rate of 40-60beats/min
• There will be synchronization of two pacemakers so called
isorhythmic dissociation
• ECG:narrow complexes on the ECG at a regular rate (60-130bpm)
• P wave either fixed to the QRS
• It is associated with structural heart disease especially following
Inferior MI

32. MULTIFOCAL ATRIAL TACHYCARDIA
• Form of SVT that demonstrates the presence of multiple ectopic atrial pacemakers
• Atrial rhythm is between 100 and 180bpm
• Seen in patients with acute exacerbation of chronic lung disease , CHF, metabolic derangements,
electrolyte abnormalities

33. TREATMENT
1)Supplemental oxygen
2) treat underlying condition
RATE CONTROL:
• Magnesium sulfate 2g IV (in 50 ml saline)over 15 mins followed by
6 gms IV (in 500 ml saline) over 6 hours by infusion –Decreases atrial
ectopy, converting MAT to sinus rhythm
• Verapamil 0.25-5 mg IV over 2 min , repeated every 15-30 mins , total
dose of 20 mg , slows the ventricular rate and will convert to sinus
rhythm

34. ATRIAL FIBRILLATION
• Most common sustained cardiac dysrhythmia
• Most common in Congestive cardiac failure, coronary artery bypass
grafting , Critically ill patients
• Idiopathic AF <60yrs of age-Good prognosis
SYMPTOMS
1)Fatigue
2)Weakness,palpitations
3)Hypotension,syncope,angina pectoris
4)Shortness of breath,orthopnea

36. DEFINITIONS OF ATRIAL FIBRILLATIONS
• PAROXYSMAL AF-Terminates with or without treatment within 7days
• PERSISTENT AF -Sustained for >7days
• LONGSTANDING AF-AF for >12months
CAUSES
• Ischemic ,Valvular heart disease
• Pericarditis
• Hypertension,cardiac failure
• Thyrotoxicosis,alcohol abuse

37. ECG
• Tachycardia in range of 250-600 beats/min
• Irregularly irregular rhythm
• No discrete p waves
• Narrow QRS complex
• Fibrillatory waves –incomplete contraction of atria

38. AF ASSOSCITAED WITH
• Adverse haemodynamic effects:
- Rapid ventricular rate
- atrial asystole
- increase pulmonary capillary wedge pressure
- Stroke volume , Cardiac Output decline
• Systemic embolism , stroke
• Tachycardiomyopathy -Reversible global cardiomyopathy secondary
to rapid heart rate

39. TREATMENT
• Goals

41. • New onset AF converts to Normal sinus rhythm within 24-48hrs
• If AF is hemodynamically unstable the treatment is synchronized
cardioversion at 100-200J (Biphasic)
• Can be increased to 100J maximum of upto 400 J
• Electrical cardioversion is most effective method for converting AF to
normal sinus rhythm and is indicated in patients with coexisting symptoms
of heart failure ,angina , hemodynamic instability
• Digoxin-Ventricular rate control(But it will not convert AF to NSR)
• Side effects of digoxin therapy-AV block , ventricular ectopy

42. • Drug induced cardioversion : in cases of uncomplicated AF , refractory to
rate control –
*AMIODARONE : 150 mg IV over 10 mins , repeat if needed , infuse at
1mg/min for 6 hr, followed by 0.5 mg/min for 18 hr
*IBUTILIDE : 1 mg IV over 10 mins, repeated once if necessary
• Short term Side effects of AMIODARONE: Bradycardia, Hypotension,
Phlebitis at the site
• Long term side effects: Visual ,thyroid dysfunction, Pulmonary toxicity,skin
discolouration
• Patients with chronic AF –Anticoagulants

44. ATRIAL FLUTTER
• Organized atrial rhythm with an atrial rate of 250-350bpm with
varying degrees of AV block
• The rapid P waves create a SAWTOOTH appearance on ECG and are
called FLUTTER WAVES(Lead II,III,aVF,V1)
• Atrial flutter occur in association with an acute exacerbation of a
chronic condition such as pulmonary disease, Acute MI, ethanol
intoxication , Thyrotoxicosis
• If atrial flutter is hemodynamically significant,the treatment is
cardioversion
• <50J (Monophasic)is adequate to convert the rhythm to sinus

45. • Patients with atrial flutter lasting longer than 48hours should receive
angticoagulant therapy
• Ventricular rate control-Goal of therapy
• Drugs for ventricular rate control-Amiodarone,diltiazem,verapamil

46. THANK YOU