ECG for toxicology beginners

1. step by step approach
By
Kerolus E. Shehata
• PGY-III IM Resident, Ain-Shams University
• ECFMG certified

2. Objectives
1. Define the clinical importance of ECG in toxicology.
2. Illustrate the procedure of and the ECG waves.
3. Describe how to comment on a strip of ECG as regards
to heart rate and rhythm.
4. Demonstrate some changes of ECG in toxicology.

3. The electrocardiogram (ECG) is a graphic recording of the
electrical potentials produced by the cardiac tissue.
The ECG is recorded by applying electrodes to various
locations on the body surface and connecting them to a
recording apparatus.
Although the heart has four chambers, from the electrical
point of view it can be thought of as having only two, because
the two atria contract together and then the two ventricles
contract together.

4. ECG, procedure & electrode placement

5. ECG leads
There are 12 ECG leads:
The 6 (limb) standard leads can be thought as looking at
the heart in a vertical plane.
The 6 (chest) Leads looks at the heart in a horizontal
plane.
The 12 lead ECG sees the heart from 12 different views
allowing a panoramic assessment of any disruption in the
cardiac electrical activity.
The limb leads sees the heart from the vertical plane.
 the chest leads in the horizontal plane.

6. Limb leads (Bipolar & augmented)
• Bipolar leads (I, II, III): +ve & -ve poles of the lead are located on the limbs (RA, LA, LL)
• Augmented leads (aVR, aVL, aVF): +ve poles are located on the limbs as the bipolar leads, but the machine use the
Wilson's central terminal as their negative pole.

7. Chest (Precordial) leads
• The 6 precordial electrodes act as the +ve
poles for the 6 corresponding precordial
leads: (V1:V6).
• Wilson's central terminal is used as the –ve
pole.
• Wilson’s central terminal: the average
measurement from the electrodes placed
on RA, LA, and LL indicating the average
potential across the body.

8. Spatial orientation of EKG leads

9. N.B: It’s important to understand which leads represent which part of the
heart. This allows you to localize pathology to a particular heart region

10. Electrical impulse formation occurs within the conduction
system of the heart.
Excitation of the muscle fibers throughout the myocardium
results in cardiac contraction.
Four electro-physiologic events involved in the genesis of the
ECG:
•Impulse formation
•Transmission of the impulse
•Depolarization
•Repolarization

11. Basic cardiac electrophysiology
In the electric circuit, electrons move from areas where there are excess
of –ve charges to areas where there are a deficiency (or +ve charge) i.e.
from the negative electrode to the positive electrode.
The same works in the heart, electric current moves from the –ve
electrode of the lead to the +ve one determining the direction of the
lead.
When the electric impulse moves in the same direction of the lead
(towards the +ve electrode), a positive deflection is graphed on the
machine in that specific lead.
When the electric impulse moves in the opposite direction of the lead
(towards the –ve electrode), a negative deflection is graphed on the
machine in that specific lead.
When the electric impulse moves perpendicular to the lead, a biphasic
deflection is graphed on the machine in that specific lead.
The voltage amplitude is directly related to the mass of tissue
undergoing depolarization or repolarization.

12. Normal 12-lead ECG

13. Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
Although the heart has four
chambers, from the electrical
point of view it can be thought
of as having only two, because
the two atria contract together
and then the two ventricles
contract together.

14. The normal ECG

15.  Standard voltage sensitivity calibration: each 1 mV gives a 10 mm (1 cm) deflection.
 Standard paper speed: 25 mm/second
 Each small square = 1 mm X 1 mm = 40 msec. = 0.04 sec.
 Each large square = 5 mm X 5 mm = 200 msec. = 0.2 sec.
 Each minute (60 sec.) = 300 large square = 1500 small square

17. Terminology
Waveform: Movement away from the baseline in either a positive or negative direction
Segment: A line between wave forms
Interval: A waveform and a segment
Complex: Consists of several waveforms

18. Q: Why do we usually use lead II as the rhythm strip?
A: to determine the source of the cardiac pacemaker, we must
determine the presence or absence of (P) wave. The direction of
atrial depolarization is almost exactly parallel to the lead II, so a it
is the best lead to see the (P) wave.

19. Electro physiologic event Normal criteria
P wave
A small positive deflection
before QRS complex
Atrial depolarization
Normal P wave is no more
than 2.5 mm (< 0.25 mV)
tall and less than 2.5 small
squares in width (100
msec.) in any lead.

20. Electro physiologic event Normal criteria
PR interval
From beginning of P
To beginning of Q
The time the electrical
impulse takes to travel from
the SA node to ventricles. It
is, therefore, a good estimate
of AV node function
Duration 120 – 200 msec.
i.e. ≤ big square = (3 – 5
small squares)

21. Electro physiologic event Normal criteria
QRS complex
From beginning of Q
To end of S (J point)
Ventricular depolarization
Duration < 120 msec. (< 3
small squares)

22. Electro physiologic event Normal criteria
T wave Ventricular Repolarization
Normal T wave follows the
direction of the main QRS
deflection. Amplitude is < 5 mm
(1 large square) in limb leads &
< 10 mm (2 large squares) in
chest leads)

23. Electro physiologic event Normal criteria
ST segment
From J point
To beginning of T
It represents the interval between
ventricular depolarization and
repolarization when myocardial
contraction occurs. Represents
Phase 2 in the myocardial action
potential.
Isoelectric (flat)

24. Electro physiologic event Normal Criteria
QT Interval
From beginning of Q
To end of T wave
Reflects the total duration of
depolarization &
repolarization i.e. the time it
takes for your heart to contract
and then refill with blood
before beginning the next
contraction.
< 440 msec. (2 large and
1 small squares = 11
small squares)
• The QT shortens at faster
heart rates.
• The QT lengthens at slower
heart rates.

25. Schematic representation of normal ECG

26. What is rhythm?

27. What is rhythm?
The word “rhythm” is used to refer to the
part of the heart which is controlling the
activation sequence. The normal heart
rhythm, with electrical activation beginning in
the SA node, is called: sinus rhythm
Since the SA node pacing the heart,
therefore: (P) wave must be present, round,
upright, and before every "QRS" complex in a
ratio of 1:1.
Criteria for normal sinus rhythm
•P wave precedes every QRS complex
•The rhythm is regular, but varies slightly during respirations
•The rate ranges between 60 and 100 beats per minute
•The P waves maximum height at 2.5 mm.
•The P wave is positive in I and II, and biphasic in V1

28. Is the rhythm regular or
irregular?

29. – To determine if the ventricular rhythm is regular or irregular, measure
the distance between 2 consecutive R-R intervals and compare that
distance with the other R-R intervals.
– For atrial rhythm, measure the distance between 2 consecutive P-P
intervals.

30. Normal sinus rhythm
Rate 60-100 beats per minute
Rhythm • Atrial: Regular = same P-P intervals
• Ventricular: Regular = same R-R intervals
P wave Uniform in appearance, upright, normal shape, one preceding
each QRS complex. 2.5 mm in amplitude and 2.5 small squares
in width.
PR interval 120 – 200 msec. (< 1 Large square)
QRS < 120 msec. (3 small boxes)
If greater than 120 msec. in duration, the QRS is termed “wide”

31. How to calculate the heart rate?

32. Rule of 300 & 1500
“only for regular rhythms”
𝑯𝑹 =
𝟑𝟎𝟎
𝐍𝐮𝐦𝐛𝐞𝐫 𝐨𝐟 𝒃𝒊𝒈 𝐬𝐪𝐮𝐚𝐫𝐞𝐬 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝟐 𝒄𝒐𝒎𝒑𝒍𝒆𝒙𝒆𝒔
𝑯𝑹 =
𝟏𝟓𝟎𝟎
𝐍𝐮𝐦𝐛𝐞𝐫 𝐨𝐟 𝒔𝒎𝒂𝒍𝒍 𝐬𝐪𝐮𝐚𝐫𝐞𝐬 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝟐 𝒄𝒐𝒎𝒑𝒍𝒆𝒙𝒆𝒔
Or
Heart rate = 300/6 = 50 beats/min
5 64321
Paper speed = 25 mm/sec. = 5 large sq. = 25 small sq./sec.
In one minute: 1500 mm/sec. = 300 Large sq. = 1500 small sq./min.
IF each 1 large sq. there is an impulse, so in 300 large sq. (1 min.), the
rate would be 300/min. If each 2 large sq. there are 2 impulses, so
the rate would be 150/min…etc.

33. Rule of 6 seconds
“for both regular & irregular rhythms”
 Number of QRS complexes in 6 seconds (30 large squares ) X 10
 Number of QRS complexes in 10 seconds (50 Large squares) X 6
7 QRS complexes in 6 seconds
= heart rate 70 beats /min

34. Sinus tachycardia: Pulse > 100 bpm
Sympathomimetics: increase sympathetic tone → enhancing AV conduction
E.g. norepinephrine, cocaine, and amphetamines
Anticholinergics: antagonism of acetylcholine released from the vagus nerve onto the
sinus node enhancing its rate of firing
E.g. Atropine, first-generation antihistamines, and TCAs
1 2

35. Sinus bradycardia: Pulse < 60 bpm
1. Depression of the Cardiovascular control center: benzodiazepines, ethanol, and
clonidine.
2. Increase in AV nodal delay: Calcium channel blockers, B adrenergic antagonists, and
cardioactive steroids (Digitalis).
3. Cholinergics ( agents increasing Ach): Carbamates or organophosphorus compounds
The bradycardia produced by cardioactive steroids is typically accompanied by signs of
“digitalis effect” including PR prolongation and ST segment depression (Sagging)

36. Some ECG changes in toxicology

37. P wave
Abnormalities of the P wave occur with agents that
decrease the automaticity of the sinus node
e.g. Beta blockers, Calcium channel blockers.
P wave is absent in rhythms with sinus arrest, such as
occurs with drugs that increase the parasympathetic flow
such as Digitalis and cholinergics.

38. P-R interval
Agents that decrease intra-trial or atrioventricular (AV) nodal
conduction cause marked lengthening of the PR interval until
such conduction completely ceases (Complete heart block)
At this point, the P wave no longer relates to the QRS complex;
this is AV dissociation or complete heart block.
Drugs include:
Ca channel blockers (Verapamil & Diltiazem)
B-blockers (antagonizing adrenergic receptors)
Cardioactive steroids (enhancing vagal tone)

39. Heart block: First degree
Prolonged PR interval > one big square (5 small squares)
but constant

40. Heart block: First degree
Prolonged PR interval > one big square
but constant

41. Heart block: Second degree (Mobitz type I)
PR interval lengthens progressively with successive beats
until one P wave is not conducted at all.
Cycle then repeats itself

42. Heart block: Second degree (Mobitz type II)
The PR interval is fixed and normal but occasionally a P wave fails to
produce a QRS complex. Defect reaches the Bundle of His.
QRS complex is NORMAL in shape and duration

43. Complete Heart block: Third degree
(A-V dissociation)
There is no relationship between P waves and QRS
P waves > QRS complexes
Slow regular wide complexes (idio-ventricular rhythm)
Variable PR interval from beat to another

44. QRS complex
Widening of the QRS complex:
This is often a result of the effect of drugs that block fast sodium
channels.
Examples: cyclic antidepressants, quinidine, phenothiazines, amantadine,
diphenhydramine, carbamazepine, and cocaine.
QRS > 100 msec. = Indication of NaHCO3 & Predictive of seizures
QRS > 120 msec. = Predictive of Ventricular arrhythmias
In tricyclic
antidepressant (TCA)
poisoning, this
finding has both
prognostic and
therapeutic value.

46. ST segment
I- Displacement of the ST segment from its baseline
Characterizes myocardial ischemia (stress pattern) or infarction
This may occur in patients who are poisoned by :
1.Poisons that cause vasoconstriction:
• Cocaine
• Other B adrenergic agonists
• Ergot alkaloids
2.Any poisoning that results in profound hypotension or hypoxia.

47. ST segment…Cont’d
II- Sagging ST segments
Characteristic effects of cardioactive steroids
Occurs due to repolarization abnormalities
In addition with PR prolongation, are commonly described as the
“digitalis effect”
They are found in
both patients with
therapeutic drug
concentrations and
in cardioactive
steroids (Digoxin)
poisoning.
“Salvador Dali’s mustache”

48. T wave
I- Hyperacute T wave (peaked)
Amplitude > Big square (5 mm) (tall, tented)
> 2/3 amplitude of R wave
Agents causing hyperkalemia e.g. NSAID, ACEIs,
Succinylcholine, acute digoxin intoxication…etc.

49. T wave…Cont’d
II- Flat T wave:
Amplitude < 0.5 mm
(decreased amplitude)
Agents causing
hypokalemia e.g.
Insulin, beta blockers,
thiazides, furosemide,
theophylline,…etc.
Sequential development of ST-T wave changes of hypokalemia.

50. QT interval
Prolonged QT interval : > 11 small squares
Reflects an increase in the time period that the heart is
“vulnerable” to the initiation of ventricular dysrhythmias
Drugs: TCA, Phenothiazines, antihistaminics,antiarrhythmics
Electrolytes: Hypokalemia, hypocalcemia

52. Case No. (1)
A 6 year old child presented to ED one hour after ingestion of unknown plant in the farm.
He appears flushed, disoriented with apparent visual hallucinations. His temp. B.P: 110/75,
R.R: 18, Temp. 38.7 C. ECG was done.
Q1: What is the heart rate?
Q2: How about the rhythm?
Q3: What is the most probable ingested plant?
Q4: Name 3 drugs that can cause similar ECG findings.

53. Case No. (2)
26 year old female presented to ED 3 hours after suicidal ingestion of her father’s
antihypertensive medication. She looks dizzy with B.P: 80/50, Temp. 36.9 C. Hemodynamic
stabilization was done. Her ECG showed:
Q1: What is the heart rate?
Q2: How about the rhythm?
Q3: Are there any changes in the ECG waves, intervals & segments?
Q4: Name three possible drugs that can cause similar ECG findings.

54. Case No. (3)
A 67 year old chronic renal failure patient presented to ED with history of abdominal
distension & limb weakness over the last 2 days. He has missed his last 3 dialysis sessions.
B.P: 125/75, Temp. 37.3 C. ECG showed:
Q1: What is the heart rate & rhythm?
Q2: Are there any changes in the waves, intervals & segments of the ECG?
Q3: what is the possible explanation of the ECG findings?
Q4: What is the medication indicated immediately for such conditions?
Q4: Name 3 drugs that can cause similar ECG findings.

55. Case No. (4)
A 29 year old female psychiatric patient presented to ED 4 hours after suicidal ingestion of
her medication. She was dizzy and confused. Her B.P: 115/70, Temp. 38 C. Hemodynamic
stabilization was done and ECG showed:
Q1: What is the heart rate and rhythm?
Q2: Are there any changes in waves, intervals & segments of the ECG?
Q3: What is the most probable ingested drug?
Q4: What is the medication indicated for such condition?

56. Thank
you