Arrythmia

tachy-arrhythmia
How to present in EKG(一)
 Identify atrial activity (P wave)
 Is there P wave present?
 normal P waves?: ectopic P waves, F wave of
Atrial flutter or Fibrillation wave of Af?
 Are all P waves in single lead looks similar?
 What is the atrial rate? Is it regular or irregular?
 Identify ventricular activity (QRS complex)
 Is QRS of normal duration? (broad or narrow)
 If QRS is broad, is it aberrant conduction or
ventricular ectopic??
(Compare QRS morphology between tachycardia and
sinus rhythm)
 What is the ventricular rate? Is it regular or irregular?
 How to present in EKG(二)

 Evaluate AV conduction: analyze the relation

between P and QRS.
Is each P wave related to a QRS? Is there evidence of
AV dissociation? (Including fusion and capture beat)?
If PR interval < 0.10 sec or > 0.40 sec, the QRS
complex is probably not produced by the preceding P
wave.
Is each P wave conducted to the ventricle (1: 1
conduction)??
Is the AV conduction speed (PR interval) normal?
Is there evidence of group beating (Wenckebach
phenomenon)??
Heart rate?

Sinus rate:60~100
Atrium rate:
AV node rate:
Ventricular rate:
Etiology of arrythmia
Organic heart disease
 Af (eg. mitral valve disease, COPD with atrium dilation)
 Ventricular arrhythmia (eg. CAD, CMP)
 AV block (eg. Aortic stenosis with Lev's disease, CAD)

Non-organic heart disease

 Systemic disease
 Hyperthyroidism (Sinus tachycardia, Af).
 Pheochromocytoma.
 Infection.
 Hypoxemia, Hypercapnia.
 Acid-base disturbance.
 Electrolyte imbalance: K, Mg, and Ca.
 Drugs: Digitalis, Anti-arrhythmic drug, Catecholamine.
Methylxanthines....
 Genetic: Long-QT syndrome ( → Torsades de pointes ).
Tachycardia
--classifications

Suproventricular tachycardia
Sinus: sinus tachycardia
Atrium: atrial flutter, atrial fibrillation, MAT
AV node and accessory pathway: AVRT,
AVNRT
Ventricle: ventricular tachycardia,
ventricular flutter, ventricular fibrilation,
torsa de points
 Tachycardia
---pathophysiology

Deranged automaticity
Triggered activity
Reentry (three condition must be met)
Two functionally distinct conducting pathways
Unidirectional conduction block in one of the
pathways
A differential in the conduction rates in the
pathway
Supraventricular tachyarrhythmias
---sinus tachycardia

Sinus tachycardia
May be high as 200 beats per minutes (bpm)
Reflects an underlying process, metabolic state,
or medication effect
Treat underlying disease為優先。
Supraventricular tachyarrhythmias
---atrial fibrillation

 the most common cause of irregularly

irregular rhythm.
 Causes：
HCVD, CAD, VHD, hyperthyroidism, one Af (no
structural heart Disease), cardiac surgery
 Classifications:
Paroxysmal: terminates spontaneously
Persistent: sustained or terminates /p cardioversion.
Permanent: cardioversion not attempted or indicated.
Supraventricular tachyarrhythmias
---atrial fibrillation

 Prognosis
Ischmic stroke in non-rheumatic Af：1. 5% per year and
one of every 6 patients
Ischemic stroke in rheumatic Af：17 folds c/w general
population and 2. 5 times greater than non-rheumatic Af
 Clinical presentation：
may be asymptomatic, palpitations, SOB, new
thromboembolic stroke
 In EKG:
P wave rate > 350 BPM ( f wave, fibrillation ) with
irregular RR interval.視 ventricular response 可分成
Slow ( < 60 BPM ), Moderate ( 60 ~ 100 BPM ) 及 Rapid
( > 100 BPM )
Supraventricular tachyarrhythmias
---atrial fibrillation

 Treatment:
 If unstable,(chest pain, pulmonary edema,
hemodynamic change) DC cardioversion
 Thromboembolic risk management：
 High risk (older than 65 years, DM, HTN, CHF
prior stroke, or TIA)
  warfarin and INR of 2 to 3
 Low risk (not high risk)
  aspirin or warfarin皆可
 Rate control V.S rhythm control
Supraventricular tachyarrhythmias
---atrial fibrillation
 Rate control: more important
 digitalis, β blocker, Ca blocker ( 但是假如有 Accessory pathway
時只能用procainamide )
 AV node ablation with pacemaker implantation
 Digoxin is ideally used in patients with decreased LV function or
a contraindication to β blocker or Ca blocker.
 Rhythm control:
 Electrical cardioversion (from 100 Joule upward) or chemical
cardioversion (Quinidine, Amiodarone, Procainamide, ... ) if Af is
of recent onset and LA size < 5 cm。但 Af 發生若已超過 48
hours , 需先給予 anticoagulation 3 周, cardioversion 後續給 4 周；
若無法等anticoagulation 3 周，可先用heparin and TEE排除atrial
thrombus，cardioversion 後給 4 周 warfarin。
 Chemical cardioversion優先考慮。
 Propafenone should not used in patients with CAD or any other
structural heart disease.
 Amiodarone：建議治療前需有baseline eye examination, liver
function tests, thyroid function tests and CXR
Supraventricular tachyarrhythmias
---atrial flutter
 Saw-tooth p wave (F wave) , P rate 250 - 350 BPM.
 Causes：如同atrial fibrillation
 Typical AF showed classic negatively directed
sawtooth waveform in inferior leads and is a macro-
reentry in a counter-clockwise rotation (CCWR).
 Therapy：
 Medical therapy：
 Rate control with digoxin, Ca channel blocker and β blocker.
 Class IA drugs
 DC cardioversion: 25-50 J起跳
 Radiofrequency ablation is curative.
Supraventricular tachyarrhythmias
---Paroxysmal atrial tachycardia (AT) with variable block
 P wave axis and morphology is different from
sinus rhythm.
 Intraatrial reentry: radiofrequency ablation is the
therapy of choice.
 Automatic atrial tachycardia:
 有warm-up phenomenon (tachycardia
accelerates after its initiation)
 Radiofrequency ablation is the therapy of
choice.
 Triggered atrial tachycardia: 可能為digitalis
toxicity
Supraventricular tachyarrhythmias
---MAT
 至少出現3種不同的 P wave.
 多在有COPD 病人發生.
 降低Heart rate可用Isoptine，但治療原則
為 control underlying disease and
maintenance of K and Mg balance
Supraventricular tachyarrhythmias
---Ectopic atrial arrythmia

來自coronary sinus or lower atrium, P 只有

一種但不正常, PR 短, QRS 正常
Supraventricular tachyarrhythmias
--PSVT (Paroxysmal Supraventricular tachycardia)

AVNRT (Atrioventricular nodal reciprocating

tachycardia) (RP<100 ms)
 條件：Dual AV nodal pathway ( Fast β & Slow
α) with uni-directional block , often initiated by
a premature complex.
 Typical ( Slow- fast ) : Fast pathway 被 block ,
impulse 經由 slow pathway 下傳再經 fast pathway 回
傳, EKG 只見QRS Complex (P 被埋在QRS 裏面) 或 P
緊跟在 QRS 之後.
 Atypical ( Fast-slow ) : Slow pathway 被 block ,
impulse 經由 fast pathway 下傳再經 slow pathway 回
傳, EKG 可見 QRS Complex and inverted P.
Supraventricular tachyarrhythmias
--PSVT (Paroxysmal Supraventricular tachycardia)
AVRT (Atrioventricular reciprocating tachycardia)
(RP >100 ms)
 Causes: concealed accessory pathway (not
detectable with surface EKG
 WPW syndrome最常見。
 Therapy：
 Radiofrequency ablation: mainstay of therapy
 Medication: adenosine, β blocker, Ca channel blocker,
and digoxin
 DC cardioversion
Supraventricular tachyarrhythmias
--Preexcitation syndromes
 7-10%與Ebstein’s anomaly有關。
 WPW syndrome (Wolff-Parkinson-White syndrome):
 Incidence 1.5 / 1000
 Accessory pathway又叫Kent bundle
 Short PR (<120 ms) + δ wave + Wide QRS by EKG (>120 ms) +
clinical PSVT attack
 Mahaim reentry tachycardia: LBBB morphology with LAD
 Therapy：
 Emergency management of acute tachycardia
 Normal QRS duration: Vagal maneuvers adenosine or
verapamil amiodarone
 Wide QRS duration: IV procainamide or amiodarone (Lidocaine,
CCB, β blocker, and digoxin should be avoided)
 Long-term management：radiofrequency ablation, amiodarone,
propafenone.
Ventricular tachyarrhythmias
--Ventricular tachycardia (VT)

3 or more QRS complexes of ventricular

origin with rate > 100 bpm
Nonsustained VT：duration < 30 seconds
without hemodynamic change
Differentiating SVT with aberration from
VT
Ventricular tachyarrhythmias
--Ventricular tachycardia (VT)
 Therapy：
 Unstable DC cardioversion
 Medical therapy: IV lidocaine or procainamide or amiodarone
 Correct reversible cause
 Ischemia, Electrolyte abnormalities(k, Ca), Bradycardia.
Hypotension, Offending agents
 Prevention treatment:
 Antiarrhythmics角色仍未定。
 Class III agents較好
 ICD (implantable cardiac defibrillator): 已於MADIT and AVID trial
證明效果優於medication therapy.
 Radiofrequency ablation eleminate the slow conducting
pathway in a reentrant circuit
Ventricular tachyarrhythmias
-- Torsades de points (TDP)
A type of polymorphic VT with an undulating appearance
 Causes：Prolonged QT interval
 Etiology
 Congenital long QT syndrome
 Drug (such as class IA drugs, haloperidol, TCA, erythromycin, baktar,
cisapride, some antihistamie with ketoconazole)
 Bradycardia
 Ionic contrast media
 Hypokalemia, hypomagnesemia, hypocalcemia
 Subarachnoid hemorrhage (SAH)
 Therapy：
 DC cardioversion (since 50-100 J)
 Treat underlying disease
 β blocker and lidocaine may be useful, though the latter is
inconsistently effective.