The presentation was given at SEMICON 2018 at MUMBAI on 16.03.2018 [ PG Refresher course in Emergency Medicine]

1. ECG for Emergency
physician
Dr.Venugopalan P P
DA,DNB,MNAMS,MEM-GW
Director & Lead Consultant -Emergency Medicine(Aster DM Health care )
PG Teacher -NBE

2. Contents
• Case scenarios
• Rhythm strip
• Rapid fire

3. Case 1
• 54 year old chronic smoker presented ED
with generalised tiredness and palpitation
and missed beats . Initial vitals Pulse 89/
mt- irregular,BP 156/88 moof Hg, SpO2 94
in RA, RR 26/ mt and normal Temp.

4. ECG

5. Your findings?
• Rhythm irregular
• No P wave
• Wide and bizarre QRS
• T Inverted
• RR interval equal
VPC

6. Diagnostic criteria
Premature Ventricular Complex.
Rhythm that is irregular, with heart rate that is the underlying
rate.
P wave is absent
PR interval is not measurable
QRS is typically wide (> 0.10 sec)
QRS isBizarre appearance.
T Wave is inverted
Compensatory Pause

8. Ventricular Ectopics
Two PVCs together are
termed a couplet
Three PVCs in a row
with a fast rhythm is
ventricular tachycardia.

9. What are the
• Rate more than 10 / mt
• Bigemini
• Trigemini
• Multifocal
• R on T phenomenon

10. Bigemini
Trigemini

11. R on T

12. R on T -Zoom In

13. Case 2
• 58 year old man presented to ED with non specific chest
discomfort and diaphoresis
• Initial vitals HR 56/ mt, BP- 70/ 50 mm of Hg ,RR 28/mt,
SpO2 - 87 in Room air

15. What are the findings ?
• Rate 56 / mt
• Normal rhythm
• Normal P wave
• QRS - Normal
• QRS follows P wave
• Normal PR interval
• ST elevation in leads
II,III,aVF
• ST depression in
• leads I and aVL

16. What is your diagnosis?
Which artery is involved ?
What are the special problems ?
• Inferior wall MI
• Likely RCA proximal block
• Need Primary Angioplasty or
• re-vascularization therapy
• Hypotension, RV dysfunction ,
• Complete heart block
• Caution : with nitrates

17. LAD
1 st Diagonal
Circumflex
RCA
Coronary arteries and `ecg
LCA

19. Case 3
A 30-year old female with a history of Conn’s
syndrome secondary to bilateral adrenal
adenomas presents in ED with generalised
weakness and muscle pains after a change in
her medications.

21. Findings
• Sinus rhythm at around 70 bpm
• Normal axis
• PR interval 200ms (upper limit of
normal)
• Long QT (640ms, QTc 700ms)
• Widespread down sloping ST
depression / T wave inversion
• Prominent U waves, especially in the
precordial leads

22. What is it?
Markedly prolonged QT interval
Widespread ST depression
T wave inversion
Prominent U waves
Pathognomonic of severe
hypokalaemia.

23. This patient
• Potassium was 1.7 mmol/L (she had
recently stopped taking her
spironalactone).
• The muscle pain was rhabdomyolysis
secondary to hypokalaemia.
• She was treated in the high-dependency
area for 3 days on a continuous potassium
drip and made a good recovery.

24. Zoom in …

25. Case 4
• 25 year old man turned up in health
check up
• He had one or two episode of
palpitation
• Normal vitals

26. What is it?

27. Short PR interval
Delta wave
Tall R wave in V1
Wide QRS

30. Tall R
wave
in V1

31. Case 5
• 45 year old lady presented to ED with
generalised weakness
• Known case of DM,Hypertension ,CKD
• On dialysis , interrupted the last schedule

32. What is it?

33. K+

35. What is next?

36. Case 5
A 36-year old marathon runner presenting to the
ED with acute gastroenteritis.
He was completely asymptomatic at the time the
ECGs were taken, with normal blood pressure and
no chest pain, palpitations or dizziness.
Electrolytes were normal.

37. What is it?

38. ECG findings
• Accelerated idioventricular rhythm (AIVR) at
around 60 bpm
• Multiple sinus capture beats
• Isorhythmic AV dissociation:
Sinus P waves are buried in the QRS complexes
and T waves at a similar rate to the ventricular
rhythm
• Sinus arrhythmia, with variation in the PP interval
of up to 0.2 s

39. Why it is so?
• Competing sinus and idio-ventricular
pacemakers are present.
• There is underlying sinus arrhythmia,
with sinus capture occurring when the
sinus rate exceeds the idio-ventricular
rate.

40. Mechanism
The likely mechanism of the AIVR in this patient is enhanced
automaticity of an ectopic pacemaker in the ventricles coupled
with sinus bradycardia and sinus arrhythmia due to athletic
training.
Athletic training leads to changes in the autonomic nervous system,
with increased resting vagal tone and decreased sympathetic
tone.
This hyper vagotonic state causes suppression of impulse
generation by the SA node and propagation by the AV node.
Athletic individuals will commonly exhibit sinus bradycardia and low-
grade AV blocks (e.g. 1st degree heart block, Mobitz I).

41. Pacemaker potential
There are pacemaker cells at various sites throughout
the conducting system, with each site capable of
independently sustaining the heart rhythm. The rate of
spontaneous depolarisation of pacemaker cells
decreases down the conducting system:
• SA node (60-100 bpm)
• Atria (< 60 bpm)
• AV node (40-60 bpm)
• Ventricles (20-40 bpm)

42. Case 6
An 18-year old male is brought to ED by ambulance
following a generalised seizure at home. He has a
further witnessed seizure en route in the ambulance.
By the time of arrival to ED he is comatose with a
GCS of 3 and poor respiratory effort. Pupils are
symmetrically dilated. Blood sugar is normal. BP is
70/40.

43. ECG

44. ECG Finding
• Regular broad complex tachycardia
• Rate 130 bpm
• Right axis deviation (+120 degrees)
• Hidden P waves buried in the ST-segments /
T waves (best seen in leads II, aVF). These
could be retrograde P waves from a
junctional / ventricular rhythm or sinus P
waves with an extremely long PR interval
(360ms)

45. ECG Finding
• Very broad QRS complexes (160ms)
• Terminal R wave in aVR > 3mm; R/S ratio in
aVR > 0.7
• Atypical RBBB pattern in V1-2 (bizarre
morphology with left rabbit ear higher than the
right)
• QT 400ms with markedly prolonged QTc 590
ms
• Non-specific T wave abnormalities with T-wave
inversions in V1-2 & lead III

46. What is the diagnosis?
The combination of
Tachycardia
QRS and QTc prolongation
Right axis deviation
Terminal R wave in aVR > 3mm
Highly specific for poisoning with sodium-channel
blocking drugs, in particular the tricyclic
antidepressants.

47. TCA OD presentation
• Sedation and coma
• Seizures
• Hypotension
• Tachycardia
• Broad complex dysrhythmias
• Anticholinergic syndrome
This patient had attempted suicide by deliberate self-poisoning with around 35mg/kg of
Doxepin (a tricyclic antidepressant) an hour prior to presentation

48. Cardio toxic effects
Tricyclics mediate their cardio toxic effects
1-Blockade of myocardial fast sodium channels (QRS
prolongation, tall R wave in aVR) 2.Inhibition of
potassium channels (QTc prolongation)
3.Direct myocardial depression
4.Other toxic effects
Blockade at(A) Muscarinic (M1),(B)Histamine (H1) and
(C )α1-adenergic receptors.

49. •QRS > 100 ms is predictive of
seizures
•QRS > 160 ms is predictive of
ventricular arrhythmias (e.g. VT)
Degree of QRS broadening on the ECG is
correlated with adverse events:

50. Risk assessment - Doxipen
OD
• < 5 mg/kg — Minimal symptoms
• 5-10 mg / kg — Drowsiness and mild
anticholinergic effects; major toxicity not
expected
• > 10 mg / kg — Potential for all major toxic
effects to occur within 1-2 h of ingestion
• > 30 mg / kg — Severe toxicity with pH-
dependent cardio toxicity and coma > 24 h

51. Quick management tips
• Administer IV sodium bicarbonate 100 mEq
(1-2 mEq / kg); repeat every few minutes until BP
improves and QRS complexes begin to narrow.
• Intubate as soon as possible.
• ? Hyperventilate to maintain a pH of 7.50 – 7.55
• Once the airway is secure, place a nasogastric
tube and give 50g (1g/kg) of activated
charcoal.
• Treat further seizures with IV benzodiazepines
(e.g. diazepam 5-10mg).

52. Quick management tips
• Treat hypotension with a crystalloid bolus (10-20
mL/kg).
• Unsuccessful in restoring BP then consider starting
vasopressors (e.g. noradrenaline infusion).
• If arrhythmias occur, the first step is to give more
sodium bicarbonate. Lidocaine (1.5mg/kg) IV is
a second line agent once pH is > 7.5.
• Avoid Ia (procainamide) and Ic (flecainide)
antiarrhythmics, beta-blockers and
amiodarone as they may worsen hypotension
and conduction abnormalities

53. Alarming Rhythm
strips…

54. Rhythm strip 1

55. What is it?
• Runs of tachycardia interspersed with long
sinus pauses (up to 6 seconds).
• The sinus rate is extremely slow, varying
from 40 bpm down to around 10 bpm in
places.
• Sinus beats are followed by paroxysms of
junctional tachycardia at around 140 bpm.
sick sinus with the “tachy-brady” syndrome

56. What will you do next?
This patient needs a pacemaker, stat!
Admit to a monitored bed on a coronary care
unit.
Commence temporary pacing via external
pads or pacing wire until a permanent
pacemaker can be arranged.

57. Rhythm strip 2
What is it?

58. Interpretation
• Six beats of sinus rhythm at 90 bpm.
• The 7th beat is a premature atrial complex
(PAC) with different morphology P, QRS
and T waves, which initiates a run of a
supra ventricular tachycardia at 150bpm.
• The onset of the SVT is typical of an AV-
nodal re-entry tachycardia (AVNRT),
although with the rate of 150bpm, atrial
flutter with a 2:1 block is also a possibility.

59. What is next?
• Scrutinise the 12-lead ECG for flutter
waves.
• Try adenosine (or vagal stimuli such as a
Valsalva manoeuvre or carotid massage);
this should unmask any flutter waves and
may convert AVNRT to sinus rhythm.
• Flutter may require DC cardioversion or
treatment with anti-arrhythmics (e.g.
amiodarone).

60. Rhythm Strip 3
What is it?

61. What is it ?
A narrow complex tachycardia is
interrupted by a run of polymorphic VT,
which rapidly deteriorates
into ventricular fibrillation.

62. What is next ?
• DC shock [ 200 J Biphasic or 360 Joule Mono phasic ]
• Start CPR - ACLS

63. Rhythm strip 4
What is it?

64. What is it ?
• Sinus rhythm, or possibly ectopic atrial
rhythm (biphasic / inverted P waves in lead
II)
• Rate of 90 bpm
• Prolonged QTc interval of 540 ms (greater
than half the R-R interval)
• Ventricular ectopics with ‘R-on-T’
phenomenon
• The second ventricular ectopic initiates a
run of torsades de pointes

65. What is next?
• DC cardioversion if unstable.
• Load with magnesium (e.g. 2 g over 1-2
minutes) and start a magnesium infusion.
• Correct hypokalemia.
• Consider:
◦ Overdrive pacing to achieve a
ventricular rate of 90-120 bpm.
◦ Isoprenaline infusion ?

66. Rhythm strip 5
What is it?

67. •AV-nodal re-entry tachycardia
(AVNRT) at 140 bpm
•A pause in the middle of the strip
with several ventricular escape
complexes
•Cardioversion to sinus rhythm at
90 bpm at the end of the strip
Typical ECG recording of a patient receiving
a bolus of adenosine for AVNRT.

68. Rapid fire…….

69. What is it?
Complete heart block

70. What is it ?
Atrial Flutter

71. What is it ?
Sinus Arrest

72. What is it?
Multifocal Atrial Tachycardia -MAT

73. What is it ?
Bundle branch block

74. What is it?
Ventricular Fibrillation

75. What is it ?
Pacemaker Rhythm - AV sequential

76. What is it ?
Second degree Heart block - Type 1

77. What is it?
Pace maker rhythm - Single chambers - Atrial

78. What is it ?
Sinus Arrhythmia

79. What is it ?
Atrial Fibrillation

80. What is it ?
First degree Heart block

81. What is it ?
Supra ventricular Tachycardia

82. What is
Electrocardiograph?
Thank you so much for your patient listening
drvenugopalppp@gmail.com
Ans: ECG Machine