7. • Automaticity
- Depolarizes
spontaneously
about 70 times
per minute> thus
HR 70
- Controlled by
sympathetic and
parasympathetic
- No RMP , means
the SA node fires
continuously to
maintain CO.
7
10. Pathophysiology of tachyarrhythmia
1. Increased Automaticity
• Autonomic nervous system (sympathetic)
• Drugs – sympathomimetics :
methamphetamine, cannabis, cocaine
2. Triggered Activity
• Early after depolarization (during phase 3)
• Delayed after depolarization (during phase 4)
• LQTC , TdP
3. Rentry
• AF/AFL
• AVNRT – functional reentry
• AVRT – anatomical reentry
Wolf Parkinson white syndrome
10
11. • Tachycardia : heart rate above 100 beats per minute
• symptomatic tachycardia generally involves rates over 150 beats per
minute unless underlying ventricular dysfunction exists
• The fundamental approach
• First, determine if the patient is unstable.
UNSTABLE ARRYTHMIA
• Hypotension
• Altered mental status
• Sign of shock – cool peripheries, poor pulse volume, crt>2sec
• Ischemic chest pain
• Acute Heart Failure symptoms
• If instability is present and appears related to the tachycardia, treat
immediately with synchronized cardioversion unless the rhythm is sinus
tachycardia.
• IF STABLE DO 12 LEAD ECG FOR correct identification of the arrhythmia
11
14. SYNCHRONISED CARDIOVERSION
• LOW ENERGY SHOCK that uses a sensor to deliver electricity
that is synchronized with the peak of the QRS complex (the
highest point of the R-wave).
• When shock button pushed, there will be a delay in the shock.
During this delay, the machine reads and synchronizes with the
patients ECG rhythm. This occurs so that the shock can be
delivered with or just after the peak of the R-wave in the
patients QRS complex.
• Synchronization avoids the delivery of shock during cardiac
repolarization (t-wave). If the shock occurs on the t-wave
(during repolarization), there is a high likelihood that the shock
can precipitate VF.
14
15. 15
PSA SHOULD BE GIVEN
BEFORE CARDIOVERSION
• MIDAZOLAM 0.1MG/KG
• FENTANYL 1 MCG/KG
18. Sinus Tachycardia
• P wave present followed by QRS
• Regular rhythm with ventricular
rate >100 beats per minute.
• Many precipitating event
18
19. • Secondary Sinus tachycardia :
• Principle of mx : treat the underlying causes
19
Sinus Tachycardia
• Normal (physiologic) sinus tachycardia:
• automaticity in the sinoatrial node is increased due to increased in
sympathetic input (leading to stimulation of beta-adrenergic
receptors) and parasympathetic withdrawal.
20. Atrial Fibrillation
• Absent of P wave
• Irregular RR interval
• Due to multiple re-entrant wavelets
conducted
• Many precipitating event
• HR 60-100 RATE
CONTROLLED AF
• HR 100-149 AF WITH
Rapid ventricular
response (RVR)
• HR>150 FAST AF
20
21. AF with rapid ventricular response
• Irregular narrow-complex tachycardia at ~135 bpm
• Coarse fibrillatory waves in V1 21
22. 22
Fast AF
• Irregular narrow-complex tachycardia at ~170 bpm
• Coarse fibrillatory waves in lead ii
23. • Electrical chaos in the atria due to
simultaneous existence of multiple re-
entry circuits that generate impulse
waves which propagate through the
atria. These impulse waves collide with
each other and with refractory cells,
which fragments the waves and causes
additional chaos.
• Initiation of AF Needs
• Trigger
• Driver (maintenance)
• Multiple Risk factors esp aging, leads to
degeneration of the myocardium and
conduction cells. that promote triggers
and drivers.
• Paroxysmal/new AF are due to one or a
few ectopic foci which can be ablated.
• Long standing AF > more foci > more
trigger/driver > atrial remodeling >
Chronic AF. (ablation less effective)
23
27. • Direct suppression of the AV node conduction to increase effective refractory
period and decrease conduction velocity - positive inotropic effect, enhanced
vagal tone, and decreased ventricular rate to fast atrial arrhythmias.
27
33. Pre -excited AF
• Rate > 200 bpm
• Irregular rhythm, with
extremely high rates in
some places — up to
300 bpm (this is too
rapid to be conducted
via the AV node)
• Wide QRS complexes
due to abnormal
ventricular
depolarisation via AP
• variation in QRS
morphology
33
35. inverted flutter waves in
leads II, III, aVF
• Atrial Flutter with 2:1 Block
• for every two atrial beats, there is one ventricular beat indicated by the QRS
complex. Therefore, the atrial flutter in the electrocardiogram is 2:1
ATRIAL FLUTTER
35
38. • In some cases, presenting with 2:1
AV block, the diagnosis of atrial
flutter may not be obvious on the
ECG.
• In these situations, i.v. adenosine
may increase the degree of AV block
and reveal the typical ECG pattern.
• However, adenosine can produce a
rebound increase in AV conduction
to 1:1 and may also precipitate AF.
• Thus, it should only be used if
deemed necessary for diagnosis and
resuscitation equipment is available.
Rate control should be the first step
in very symptomatic patients with
rapid ventricular rates.
38
40. • ABSENT OF P WAVE
• REGULAR
40
AV Nodal Re-entry Tachycardia (AVNRT)
41. AV Nodal Re-entry Tachycardia (AVNRT)
• This is the commonest cause of palpitations in patients with
structurally normal hearts
• paroxysmal ,occur spontaneously or upon provocation with exertion,
caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics
(amphetamines)
• Regular
41
44. • Slow-Fast (Typical) AVNRT:
• Narrow complex tachycardia at ~
150 bpm
• No visible P waves
• There are pseudo R’ waves in V1-2
45. • Fast-Slow (Uncommon) AVNRT:
• Narrow complex tachycardia ~ 120 bpm.
• Retrograde P waves are visible after each QRS complex — most evident in V2-3.
46. Fast-Slow AVNRT:
• Narrow complex tachycardia ~ 135 bpm.
• Retrograde P waves following each QRS complex — upright in aVR and V1; inverted in
II, III and aVL.
47. Mx of AVNRT
• Vagal maneuvers are techniques used to
increase vagal parasympathetic
1. Carotid sinus massage – increase firing of carotid
sinus baroreceptor
• This action triggers the baroreceptor reflex, which results
in increased parasympathetic output to the heart via the
vagus nerve (cranial nerve X).
• Avoid in carotid bruit > STROKE
2. Modifies Valsava maneuver
• ADENOSINE 6mg >12mg > 18mg
• SYNCHRONISED CARDIOVERSION
47
48. • 37 (17%) of 214
standard Valsalva
manoeuvre achieved
sinus rhythm
• compared with 93
(43%) of 214 in the
modified Valsalva
manoeuvre group
48
49. - Depressing sinoatrial node automaticity and atrioventricular node conduction
- extremely short half-life
- injected as rapidly as possible into a proximal vein followed immediately by a 20 mL
saline flush and elevation of the extremity to ensure the drug enters the central
circulation before it is metabolized.
Adenosine has very short plasma half-life due to enzymatic deamination to inactive
inosine being achieved in seconds, with clinical effects complete within 20-30s. Thus,
repeat administration is safe within 1 min of the last dose. 49
53. • Most common due to
underlying WPW syndrome
• AVRT happens in patient with
underlying AP such as WPW
• Anatomical rentry point
• Two types
• Orthodromic avrt –most
common
• Antidromic avrt – diificult to diff
between VT
53
AV Re-entry Tachycardia (AVRT)
54. WPW
• Sinus rhythm with a very short PR interval (< 120 ms)
• Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave
• Tall R waves and inverted T waves in V1-3 — changes are due to WPW
54
55. Wolff–Parkinson–White syndrome
• AV node connects the atria and the ventricles , accessory
pathway(AP) is found in approximately 1 in 1000 persons.
• In normal heart AV node delays transmission of impulse from sa
node, however in WPW impulse travels fast thru AP.
• location of the AP
• 53% left free ventricular wall
• 36% posteroseptal
• 8% right free ventricular wall
• 3% anteroseptal
55
56. • SHORT PR INTERVAL FAST CONDUCTION
THRU AP
• DELTA WAVE + WIDE QRS COMPLEX DUE
TO SLOW CONDUCTION
• via direct muscle-to-muscle (slow)
conduction, producing an initial slurred
“delta” wave and wide QRS 56
• NO DELTA WAVE
AND QRS
NORMAL AS
IMPLUSE DOWN
THRU AV NODE
NOT THRU AP
• RETROGRADE P
WAVE
• DELTA WAVE +
WIDE QRS AS
IMPULSE TRHU AP
• P NOT ALWAYS
VISIBLE
58. Orthodromic AVRT
• Regular, narrow complex tachycardia at 180 bpm
• The QRS complexes are narrow because impulses are being transmitted in an orthodromic direction (A -> V)
via the AV node
• Retrograde P waves are visible in V1 (see first beat), and quite clearly in lead III (notch at beginning of T
wave), with a long RP interval 58
60. • Regular WCT
• DDX : Monomorphic VT , Antidromic AVRT witH WPW, SVT with
aberrancy
60
61. • Post syn cardioversion due to unstable Regular WCT
• Sinus rhythm with a very short PR interval and widespread delta waves.
• This confirms the initial ECG was antidromic reciprocating tachycardia.
61
64. MULTIFOCAL AT
64
ATRIAL TACHYCARDIA
FOCAL AT
• single ectopic focus
• Regular rhythm
• Unifocal, identical P waves
• Atrial rate > 100 bpm
• Abnormal P wave morphology and
axis (e.g. inverted in inferior leads)
due to ectopic origin
• multiple ectopic foci within the atria.
• rapid, irregular rhythm
• with at least three distinct
morphologies of P waves on the
surface ECG.
• difficult to distinguish multifocal AT
from AF on the rhythm strip, so a 12
lead ECG is indicated to confirm the
diagnosis.
65. • NC REGULAR TACHYCARDIA
• Each QRS complex is preceded by an abnormal P wave — biphasic in V1; inverted in the
inferior leads II, III and aVF; and inverted V3-V6
• P wave morphology is consistent throughout 65
FOCAL AT
66. • NC IRREGULAR TACHYCARDIA
• Rapid, irregular rhythm with multiple P-wave morphologies (best seen in the rhythm strip).
• Right axis deviation, dominant R wave in V1 and deep S wave in V6 suggest right ventricular hypertrophy due to cor pulmonale. 66
MULTIFOCAL AT
68. Accelerated ventricular rhythm
(idioventricular rhythm)
• Regular rhythm with rate at 60–100 beats per minute. As in ventricular rhythm the QRS complex is wide with
discordant ST-T segment and the rhythm is regular (in most cases).
• Idioventricular rhythm starts and terminates gradually. primarily seen after reperfusion in an occluded
coronary artery.
• Fusion and capture beats
• Usallly self limiting
68
70. idioventricular rhythm with AV dissociation and wide QRS complexes occurring at a rate faster than the sinus rate but slower than 100 bpm
• Regular rhythm
• Rate typically 50-120 bpm
• Three or more ventricular complexes; QRS duration > 120ms
• Fusion and capture beats
70
71. Junctional tachycardia
• impulses are occasionally
discharged in the
atrioventricular node or by cells
near the node.
• The cells in the atrioventricular
node itself may start discharging
impulses during ischemia or
when sa node impulses blocked
• The atria will be activated in the
opposite direction, which is why
the P-wave will be retrograde.
71
72. Junctional Tachycardia
• Narrow complex tachycardia at 115 bpm
• Retrograde P waves — inverted in II, III and aVF; upright in V1 and aVR
• Short PR interval (< 120 ms) indicates a junctional rather than atrial focus
72
73. • Ventricular tachycardia (VT) may emerge due to increased/abnormal
automaticity, re-entry or triggered activity. All types of myocardial
cells may be engaged in initiation and maintenance of this
arrhythmia.
• VT can degenerate into ventricular fibrillation.
73
Ventricular Tachycardia
75. BRUGADA
FORMULA
• TO DIFFERENTIATE SVT AND
VT
• AS MX DIFFFERENT
• SVT RESPONDS TO AV NODAL
BLOCKERS SUCH AS
ADENOSINE
• HOWEVER, ADENOSINE MAY
PRECIPITATE HEMODYNAMIC
INSTABILITY IN VT > VFIB
75
76. Ventricular Tachycardia
• WC
• Positive/ Negative Concordance (in V1-V6)
negative concordance likely VT
• Extreme Axis Deviation
• Dominant initial R wave in Avr
• Capture Beat + Fusion Beat
• Complete AV Dissociation
• Josephson Sign/Brugada Sign
• Rabbit ear sign (in V1/V2)
76
77. 77
• Capture beats. A capture beat (once called “Dressler beat”) is a normal QRS
complex, identical to the sinus QRS complex, occurring during the VT at a
rate faster than the VT. The term capture beat indicates that the normal
conduction system has momentarily captured control of ventricular
activation from the VT focus .
• Fusion and capture beats are more commonly seen when the tachycardia
rate is slower. These beats do not alter the rate of the VT, although a
change in the preceding and subsequent RR intervals is frequently
observed.
80. Monomorphic VT:
• Classic monomorphic VT with uniform QRS complexes
• Indeterminate axis
• Very broad QRS (~200 ms)
• Notching near the nadir of the S wave in lead III = Josephson’s sign
80
81. • Monomorphic VT:
• Very broad QRS complexes (~ 200 ms) with uniform morphology
• Fusion and capture beats are seen in the rhythm strip
• Brugada’s sign is present: the time from the onset of the QRS complex to nadir of S wave is > 100 ms (best seen in V6)
81
82. Aberanncy
• Aberrant conduction is not a
mechanism of arrhythmia; it is a
ventricular conduction disturbance.
• cardiac cells must repolarize rapidly in
order to be excitable by the time the
next action potential arrives.
• if component of the ventricular
conduction system not have
repolarized by the time the next
impulse reaches the ventricles, the
impulse will be blocked there and give
rise to aberrant conduction
• Aberrant conduction occurs when the
length of the cardiac cycle is changed
without a compensatory change in the
length of the refractory period.
82
83. VT vs SVT with aberrancy
• WCT should be presumed to be VT in the absence of contrary
evidence.
• This conclusion is appropriate both because VT accounts for up to
80% of cases of WCT and because making this assumption guards
against inappropriate and potentially dangerous therapy.
• As noted, the IV administration of drugs used for the treatment of
SVT (verapamil, diltiazem, or beta-blockers) can cause severe
hemodynamic deterioration in patients with VT and can even provoke
VF and cardiac arrest. Therefore these drugs should not be used when
the diagnosis is uncertain.
• Treat as SVT with aberrancy ONLY when diagnosis is certain.
83
91. • A prolonged QT reflects prolonged
myocyte repolarisation due to ion
channel malfunction.
• This prolonged repolarisation
period also gives rise to early
after-depolarisations (EADs)
• TdP is initiated when a PVC occurs
during the preceding T wave,
known as ‘R on T’ phenomenon.
91
92. 1. Congenital long QT syndromes
caused by mutations in cardiac
ion channels.
2. Acquired long
QT syndrome due to
secondary causes.
92
97. Unstable fast AF
Syn cardioversion 200j
• 62 y/o female u/l IHD. Presented with palpitation and presyncope.
• o/e drowsy Bp 82/55 HR 180
• Diagnosis and mx ?
97
QUIZ 1
98. • 55 female presented with fever , palpitation and GI losses. She also
complains for neck swelling for few years and defaulted treatment.
• o/e agitated ,febrile ,irregular good pv
• T 39 Bp 145/70 hr 110-120
• Lungs clear, no edema
98
QUIZ 2
99. 1. WHAT IS ECG SHOWING?
2. CLINICAL DIAGNOSIS ?
3. MANAGEMENT ?
4. NAME ANTI-ARRHYTHMIAC DRUG THAT SHOULD BE AVOIDED IN THIS PATIENT? 99
1. AF RVR HR 100
2. THYROID STORM
BW SCORE :70
3. IV HCT 200MG
PTU 1000MG
LUGOLS IOIDINE 10
DROPS (1 HR AFTER
PTU)
IV PROPRANOLOL / IV
ESMOLOL
4. AMIODARONE
100. quiz 3
• 42 y/o male
p/w
palpitation
and
presyncope
• Bp 80/35
• Hr 120-130
• Spo2 98
• Diagnosis?
• Mx?
• Wht went
wrong?
100
101. • Idiopathic Fascicular VT:
Broad-complex complex
tachycardia with modest
increase in QRS width
(~120 ms)
• RBBB morphology (RSR’
in V1)
• Left axis deviation (-90
degrees)
• Narrow-complex capture
beat (complex #6)
• Several dissociated P
waves are seen in the
lead II rhythm strip
(associated with the 3rd,
10th, 14th, 18th and
22nd QRS complexes)
• VERAPAMIL SENSITIVE VT
101
Diagnosis?
QUIZ 4
