MALIGNANT ARRHYTHMIAS: ECG IDENTIFICATION

1
MALIGNANT ARRHYTHMIASECG IDENTIFICATION

• DR.SIVAKUMAR ARDHANARI MD

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.co
m
2
(No Transcript)
3
Normal sinus rhythm

• Impulse formation beginning in the sinus node
• At frequencies between 60 to 100 per minute
• P is always upright in I, II and aVF and inverted
  in aVR
• Though rhythm is regular, minor variation in PP
  interval exists longest and shortest PP differlt
  0.16 except in sinus arrhythmia

4
Normal sinus rhythm

• Every P is followed by a QRS complex
• Every QRS is preceded by a P wave
• P and its following QRS is separated by fairly
  regular PR interval
• TO BE VERY PRECISE P AND QRS ARE IN SIMPLE
  HARMONY

5
(No Transcript)
6
NORMAL ECG
7

• When the rhythm deviates from the above said
  normalcy it is called ARRHYTHMIA
• Broadly it is classified as brady and tachy
  arrhythmia
• Arrhythmogenesis may be due various causes

8
(No Transcript)
9

• Some arrhythmias are considered MALIGNANT
• Because if not properly and immediately treated,
  it can be LETHAL to the sufferer
• This is important in understanding the concept of
  SUDDEN CARDIAC DEATH

10
(No Transcript)
11
SUDDEN CARDIAC DEATH
12
Anatomy of the conduction system
13
Anatomy of the conduction system

• Sinus node-
• RCA (55-60)
• left circumflex (40-45)artery
• AV node-
• RCA (85-90)
• left circumflex (10-15) artery

14
ACUTE RVMIIWMI
15
Anatomy of conduction system

• The conduction system is densely innervated by
• Cholinergic fibers- parasympathetic
• Adrenergic fibers- sympathetic
• This is important in understanding
• variability of cardiac function with autonomic
  influence
• effect of parasympathetic stimulation in
  terminating arrhythmias

16
BRADYARRHYTHMIAS

• Sinus nodal
• Sinus bradycardia
• Sinus arrhythmia
• Sinus pause/arrest
• Sinoatrial exit block
• Sick sinus syndrome
• AV nodal blocks
• First degree
• Second degree(MOBITZ type 1 and 2)
• Complete heart block

17
SINUS ARREST
18
SICK SINUS SYNDROME
19
ATRIO VENTRICULAR BLOCK

• I degree -conduction time prolonged all
  impulses are conducted
• II degree -2 forms
• Mobitz type I (WENCKEBACH)- progressive
  lengthening of conduction time until an impulse
  is failed to be conducted
• Mobitz type II- occasional or repetitive sudden
  block in conduction without prior measurable
  lengthening of conduction time
• Complete or III degree -no impulses are conducted

20
FIRST DEGREE AV BLOCK
21
FIRST DEGREE HB
22
IWMIFIRST AV BLOCK
23
21 AV BLOCK
24
COMPLETE AV BLOCK

• Occurs when no atrial activity is conducted to
  the ventricles
• So atria and ventricles are controlled by
  independent pacemakers
• One type of complete AV dissociation
• Ventricular focus is usually just below the site
  of block
• If focus near HIS bundle the rhythm is more stable

25

• CHB can occur at various levels
• AV Node-usually congenital-40-60 bpm
• Bundle of HIS
• Purkinje sys-usually acquired-

26
COMP HEART BLOCK
27
COMP HB
28
CHB
29
CHB
30
IWMICHB
31
APPROACH TO TACHYCARDIA
32
ATRIAL FLUTTER

• F waves rapid regular undulations
• SAW TOOTH APPEARANCE
• Atrial rate250-350 bpm
• Rate regularity of ventricles variable and
  depend on AV conduction sequence
• QRS may be normal or abnormal as a result of
  preexisting intraventricular conduction defect or
  aberrancy

33
ATRIAL FLUTTER
34
ATRIAL FLUTTER
35
ATRIAL FLUTTER
36
(No Transcript)
37
SVT VS VT
38

• Differentiating a VT from SVT can be difficult at
  times
• Golden rule in ER
• ANY WIDE QRS TACHYCARDIA IS VENTRICULAR
  TACHYCARDIA UNTIL PROVED OTHERWISE ESPLY WHEN
  THE PATIENT HAS A STRUCTURAL HEART DISEASE

39
Diagnosis of VT

• Arises distal to the bifurcation of the HIS
  bundle
• Diagnosis is by the occurrence of a series of 3
  or more consecutive, abnormally shaped PVCs whose
  duration exceeds 120 ms, with ST-T vector
  pointing opposite the major QRS deflection

40
VENTRICULAR ECTOPICS
41

• RR can be exceedingly regular or can vary
• Atrial activity can be independent of ventricular
  activity or can be depolarized retrograde (VA
  association)

42

• Fusion beats and capture beats provide the
  maximum support for the diagnosis of VT
• FUSION BEATS-activation of ventricles from 2 foci
• CAPTURE BEATS- capture of the ventricle by
  supraventricular rhythmwith normal confguration
  of the captured QRS at intrvl shorter than
  tachycardia in question- indicates origin of
  impulse is supraventricular

43
FUSION AND CAPTURE BEATS
44

• QRS contours can be
• Unchanging (MONOMORPHIC)
• Vary randomly (POLY OR PLEOMORPHIC)
• Vary repetitively (TORSADES DE PONTES)
• Vary in alternative cplxs (BIDIRECTIONAL)

45
MONOMORPHIC VT
46
POLYMORPHIC VT
47
TORSADES DE POINTES
48
TYPES OF VT

• VT can be
• SUSTAINED- lasting longer than 30 seconds or
  requiring termination due to hemodynamic collapse
• NON SUSTAINED- stops spontaneously within 30
  seconds

49
NON-SUSTAINED VT
50
SUSTAINED VT
51
HYPER ACUTE EXT ALMI
52
DIGITALIS EFFECT
53
PROLONGED QT(U) INTERVAL
54
Ventricular flutter fibrillation

• Represent severe derangement of heart beat that
  usually terminate fatally within 3-5 mts if
  corrective measures are not undertaken promptly.

55
VENTRICULAR FLUTTER

• Manifested as sine wave in appearance
• Regular large oscillations occurring at a rate of
  150-300(usually 200)/min

56
VENTRICULAR FLUTTER
57
VENTRICULAR FIBRILLATION

• Irregular undulations of varying contour
  amplitude
• Distinct QRS, ST or T are absent
• Fine amplitude fibrillatory waves (0.2mV) with
  prolonged VF worse prognosis confused with
  asystole

58
VENTRICULAR FIBRILLATION
59
(No Transcript)
60
(No Transcript)