The document discusses the early detection of lethal arrhythmias and the interpretation of ECG changes, explaining the electrical activities of the heart during depolarization and repolarization. It details the components of the ECG, including waves and intervals, as well as different rhythms and heart blocks, emphasizing the clinical significance of each and their management in acute coronary syndrome. Treatment protocols for various arrhythmias and the importance of monitoring and patient evaluation are also highlighted.

1. Early detection of lethal arrythmias
& interpretation of ECG changes
Dr Prudhvi Krishna

2. ELECTRICITY OF HEART
Contraction of any muscle is associated with
electrical charges called depolarization.
These changes can be detected by electrodes
attached to the surface of the body.
Although the heart has 4 chambers, from the
electrical point it is having only 2.

3. DEPOLARIZATION AND REPOLARIZATION

4.  Electrical activity of depolarization and
repolarization can be recorded by ECG.
 When we record electrical activity, we get a
waveform i.e. ECG waves.

5. 5
Electrical Events of the Cardiac Cycle
 Each wave or interval represents
depolarization or repolarization of
myocardial tissue.
 P wave represents depolarization
of atria which causes Atrial
contraction.
 QRS complex reflects
depolarization of ventricles which
causes contraction.
 T wave reflects repolarization of
muscle fibers in ventricles.

6. Basic ECG Components
▪ Segments are flat lines, do not include waves.
▪ Intervals include at least one wave.
 P Wave, PR segment, PR Interval
 QRS Complex
 QT Interval
 ST Segment
 T wave
 U wave

7. P Wave
 P wave – small, round
deflection on the ECG
 Right atrial
component
 Left atrial component
 Normal amplitude
 < 0.25 mV (2.5 mm)
 Normal duration
 0.04 – 0.12 sec

8. P Wave form in standard lead II
 P wave is best seen in
lead II because the
frontal plane P wave
axis is directed to the
positive pole of the
lead.

9. P Wave form in lead V1
 P wave is usually studied in lead V1.
 P wave in lead V1 is biphasic, initial
positivity and terminal negativity .
Reason:
1 .The SA node is situated in the right atrium
that activated first.
▪ The Rt. Atrium is situated anteriorly and is
also anterior to left atrium.
▪ The vector of right atrial activation is thus
directed anteriorly and is slightly to the left
that is towards the electrode of lead V1.
This lead will record intial positive wave.

10. P Wave form in lead V1
2.
▪ Left atrial activation begins slightly later
than Rt atrial activation overlaps the with
the terminal activation of rt atrium.
▪ Since the Lt atrium is situated posteriorly
, the left atrial vector is also directed
posteriorly . This vector is directed away
from the lead V1 , this leads to shallow
negative deflection.

11. P Wave
 In sinus rhythm when the SA node is the
pacemaker, the mean direction of atrial
depolarization (the P wave axis) points
downward and to the left, in the general
direction of lead II and away from lead
aVR.
 P wave is always positive in lead II and
always negative in lead aVR during sinus
rhythm indicating normal.

12. 12
PR segment
 Represents atrial repolarization.
 Usually isoelectric.
 Amount of elevation or depression relative to the TP
segment (end of T wave to beginning of P wave)
 Normal : Elevation < 0.5mm
Depression < 0.8mm

13. 13
PR Interval
 Time interval from onset of Atrial depolarization to onset of ventricular
depolarization.
 From the beginning of the P wave to the first deflection of the QRS complex.
 Delay allows time for the atria to contract before the ventricles contract.
Normal PR interval: 0.12 – 0.20 seconds

14. QRS Complex
 Represents depolarization of ventricular muscle
cells.
 Measure in seconds, from the beginning to the
end of the QRS complex.
 Normal QRS duration: < 0.10 seconds
 Q wave septal
depolarization
 R wave early ventricular
repolaization
 S wave late ventricular
repolarization.

15. Q wave
 First downward deflection .
▪ Septal depolarization.
 Why Q wave is negative?
 Activation of ventricles begins in the left subendocardial region of
the lower third of the interventricular septum spreading
transversely from left to right.
 It is opposed by smaller activation force from right to left occurs
almost at same time, which is of smaller force dominated by left
side force leading to effective vector that is directed from left to
right.

16. Why Q wave is negative?
2

17. QRS complex
▪ R wave :first upward deflection.
early ventricular depolarization
Why R wave is
positive?

18. QRS complex
▪ S wave : late ventricular depolarization,

19. QRS NOMENCLATURE
▪ Not every complex have all three waves.

20. QRS COMPLEX
▪ In lead V1,there is rS pattern
▪ In lead V6,there is qR pattern.

21. QT Interval
 The QT interval represents the total time required for both
depolarization & repolarization of the ventricles to occur.
 It is measured from the beginning of QRS complex to the end of T
wave.
 The normal QT interval ranges from 0.35 to 0.44 seconds.

22. ST Segment
 End of ventricular depolarization (QRS complex) to start of ventricular
repolarization (T wave)
 Represents early repolarization of the ventricles.
 Usually isoelectric, but may vary from 0.5mm below to 1mm above baseline.
 Nonspecific ST segment: Slight (< 1mm) ST segment depression or elevation.

23. J point
 The point where the QRS complex joins the ST
segment. It represents the approximate end of
depolarization and the beginning of repolarization of
ventricle.

24. T wave
 T wave represents the end
of repolarization of the
ventricles
 It is normally oriented in
the same direction as the
QRS complex.
 The normal T wave is
asymmetric with the first
half moving more slowly
than the second half.

25. U Wave
 Its significance is unknown, but may represent further repolarization of
ventricles vs repolarization of Purkinje fibers.
 When present, U wave manifests as a small deflection following the T wave.
 It is observed in chest leads.
 It may be upright in patients with hypokalemia or inverted in patients with
ischaemia.

26. Sinus Rhythms
▪ Originate in the SA node
▪ Normal sinus rhythm (NSR)
▪ Sinus bradycardia (SB)
▪ Sinus tachycardia (ST)
▪ Sinus arrhythmia
▪ Inherent rate of 60 – 100
▪ Base all other rhythms on deviations from
sinus rhythm

27. Sinus Rhythm

28. Sinus Bradycardia

29. Sinus Tachycardia

30. Sinus Arrhythmia

31. Atrial Rhythms
▪ Originate in the atria
▪ Atrial fibrillation (A Fib)
▪ Atrial flutter
▪ Wandering pacemaker
▪ Multifocal atrial tachycardia (MAT)
▪ Supraventricular tachycardia (SVT)
▪ PAC’s
▪ Wolff–Parkinson–White syndrome (WPW)

32. A - Fib

33. A - Flutter

34. Wandering Pacemaker

35. Multifocal Atrial Tachycardia (MAT)
(Rapid Wandering Pacemaker)
• Similar to wandering pacemaker (< 100)
• MAT rate is >100
• Usually due to pulmonary issue
• COPD
• Hypoxia, acidotic, intoxicated, etc.
• Often referred to as SVT by EMS
• Recognize it is a tachycardia and QRS is narrow

36. SVT

37. PAC’s

38. Wolff–Parkinson–White - WPW
▪ Caused by an abnormal
accessory pathway
(bridge) in the conductive
tissue
▪ Mainly non-symptomatic
with normal heart rates
▪ If rate becomes
tachycardic (200-300)
can be lethal
▪ May be brought on by stress
and/or exertion

39. Wolff–Parkinson–White
(AKA - Preexcitation Syndrome)

40. AV/Junctional Rhythms
▪ Originate in the AV node
▪ Junctional rhythm rate 40-60
▪ Accelerated junctional rhythm rate 60-
100
▪ Junctional tachycardia rate over 100
▪ PJC’s
▪ Inherent rate of 40 - 60

41. Junctional Rhythm

42. Accelerated Junctional

43. Junctional Tachycardia
Often difficult to pick out so often identified as “SVT”

44. PJC’s
Flat or inverted P Wave
or P wave after the QRS

45. Ventricular Rhythms
▪ Originate in the ventricles / purkinje fibers
▪ Ventricular escape rhythm (idioventricular) rate
20-40
▪ Accelerated idioventricular rate 42 - 100
▪ Ventricular tachycardia (VT) rate over 102
▪ Monomorphic – regular, similar shaped wide QRS
complexes
▪ Polymorphic (i.e. Torsades de Pointes) – life
threatening if sustained for more than a few seconds
due to poor cardiac output from the tahchycardia)
▪ Ventricular fibrillation (VF)
▪ Fine & coarse
▪ PVC’s

46. Idioventricular

47. Accelerated Idioventricular

48. VT (Monomorphic)

49. VT (Polymorphic)
Note the “twisting of the points”
This rhythm pattern looks like
Ribbon in it’s fluctuations

50. VF

51. PVC’s

52. R on T PVC’s

53. R on T PVC’s cont.
▪ Why is R on T so bad?
▪ Downslope of T wave is the relative refractory period
▪ Some cells have repolarized and can be stimulated again to
depolarize/discharge
▪ Relatively strong impulse can stimulate cells to
conduct electrical impulses but usually in a slower,
abnormal manner
▪ Can result in ventricular fibrillation
▪ Absolute refractory period is from the beginning of the QRS
complex through approximately the first half of the T wave
▪ Cells not repolarized and therefore cannot be
stimulated

54. Synchronized Cardioversion
▪ Cardioversion is synchronized to avoid the refractory period of
the T wave
▪ The monitor “plots” out the next refractory period in order to
shock at the right moment – the safe R wave
▪ With a QRS complex & T wave present, the R wave can be
predicted (cannot work in VF – no wave forms present)

55. A/V Heart Blocks
▪ 1st degree
▪ A condition of a rhythm, not a true rhythm
▪ Need to always state underlying rhythm
▪ 2nd degree
▪ Type I - Wenckebach
▪ Type II – Classic – dangerous to the patient
▪ Can be variable (periodic) or have a set
conduction ratio (ex. 2:1)
▪ 3rd degree (Complete) – dangerous to the patient

56. Atrioventricular (AV) Blocks
▪ Delay or interruption in impulse conduction in
AV node, bundle of His, or His/Purkinje system
▪ Classified according to degree of block and
site of block
▪ PR interval is key in determining type of AV block
▪ Width of QRS determines site of block

57. AV Blocks cont.
▪ Clinical significance dependent on:
Degree or severity of the block
Rate of the escape pacemaker site
▪ Ventricular pacemaker site will be a slower
heart rate than a junctional site
Patient’s response to that ventricular rate
▪ Evaluate level of consciousness /
responsiveness & blood pressure

58. 1st Degree Block

59. 2nd Degree Type I

60. 2nd Degree Type II (constant)
P Wave PR Interval QRS Characteristics
Uniform .12 - .20 Narrow & Uniform Missing QRS after
every other P wave
(2:1 conduction)
Note: Ratio can be 3:1, 4:1, etc. The higher the ratio, the “sicker” the heart.
(Ratio is P:QRS)

61. 2nd Degree Type II (periodic)
P Wave PR Interval QRS Characteristics
Uniform .12 - .20 Narrow & Uniform Missing QRS after
some P waves

62. 3rd Degree (Complete)

63. How Can I Tell What Block It Is?
63

64. Helpful Tips for AV Blocks
▪ Second degree Type I
▪ Think Type “I” drops “one”
▪ Wenckebach “winks” when it drops one
▪ Second degree Type II
▪ Think 2:1 (knowing it can have variable block like 3:1,
etc.)
▪ Third degree - complete
▪ Think completely no relationship between atria and
ventricles

65. Goal of Therapy
▪ Is rate too slow?
▪ Speed it up (Atropine, TCP)
▪ Is rate too fast?
▪ Slow it down (Vagal maneuvers, Adenosine, Verapamil)
▪ Blood pressure too low?
▪ Is there enough fluid (blood) in the tank?
▪ Improve contractility of the heart (dopamine, Epinephrine)
▪ Are the ventricles irritable?
▪ Soothe with antidysrhythmic (Amiodarone, Lidocaine)

66. Treatments for Rhythms
▪ As always… treat the patient NOT the
monitor
▪ Obtain baseline vitals before and/or
during ECG monitoring
▪ Identify rhythm and determine
corresponding SOP to follow
▪ Helpful to have at least one more person verify strip
▪ Obtain patient history & OPQRST of
current complaint

67. Transcutaneous Pacing
▪ No response to doses of atropine
▪ Unstable patient with a wide QRS
▪ Set pacing at a rate of 80 beats per minute in
the demand mode
▪ Start output (mA) at lowest setting possible (0)
and increase until capture noted
▪ Spike followed by QRS complex
▪ Consider medications to help with the chest
discomfort

68. Tachycardias
▪ Can be generally well tolerated rhythms
OR
▪ Can become lethal usually related to the heart rate
and influence on cardiac output
▪ Ask 2 questions:
▪ Is the patient stable or unstable?
▪ If unstable, needs cardioversion
▪ If stable, determine if the QRS is narrow or wide
▪ QRS width drives decisions for therapy in stable
patient

69. ST ELEVATION
▪ EKG changes are
significant when they
are seen in at least two
contiguous leads
▪ Two leads are
contiguous if they look
at the same area of the
heart or they are
numerically
consecutive chest leads

70. ST Elevation Evaluation
▪ Locate the J-point
▪ Identify/estimate where the isoelectric line is
noted to be
▪ Check the standardized 2mm mark at the far left or
beginning of each row of the EKG strip
▪ Compare the level of the ST segment 0.4 seconds
after the J point to the isoelectric line
▪ Elevation (or depression) is significant if more than
1 mm (one small box) is seen in 2 or more leads
facing the same anatomical area of the heart (ie:
contiguous leads)

71. Measuring for ST Elevation
▪ Find the J point
▪ Is the ST segment >1mm
above the isoelectric line in 2
or more contiguous leads?

72. Acute Coronary Syndrome
Stable
Patient Alert
Skin warm and dry
Systolic BP>100 mmHg

Aspirin 324 mg by mouth

Nitroglycerine 0.4 mg SL
May be repeated every 5 min
If pain persists following 2 doses, advance to Morphine Sulfate

Morphine Sulfate 2mg IVP
Slowly over 2 minutes
May repeat every 2 minutes as needed, to a maximum total dose of 10 mg

Transport
Unstable
Altered Mental Status
Systolic BP< 100 mmHg

Aspirin 324 mg by mouth, if pt can
tolerate

Contact Medical control

Monitor and Transport
Note: ASPIRIN my be withheld if patient is reliable and states has taken within 24 hours
Routine Medical Care
12 Lead ECG and transmit, if available

73. Patient Presenting with Coronary Chest Pain
– AMI Until Proven Otherwise
▪ Oxygen
▪ May limit ischemic injury
▪ New trends/guidelines coming out in 2011 SOP’s
▪ Aspirin - 324 mg chewed (PO)
▪ Blocks platelet aggregation (clumping) to keep clot
from getting bigger
▪ Chewing breaks medication down faster & allows for
quicker absorption
▪ Hold if patient allergic or for a reliable patient that
states they have taken aspirin within last 24 hours

74. Acute Coronary Syndrome
Medications cont.
▪Nitroglycerin - 0.4 mg SL every 5
minutes
▪ Dilates coronary vessels to relieve vasospams
▪ Increases collateral blood flow
▪ Dilates veins to reduce preload to reduce workload of
heart
▪ Watch for hypotension
▪ If inferior wall MI (II, III, aVF), contact Medical Control prior to
administration
▪ If pain persists after 2 doses, move to Morphine
▪ Check for recent male enhancement drug use (ie:
viagra, cialis, levitra)
▪ Side effect could be lethal hypotension

75. Acute Coronary Syndrome
Medications cont.
▪Morphine - 2 mg slow IVP
▪ Decreases pain & apprehension
▪ Mild venodilator & arterial dilator
▪ Reduces preload and afterload
▪ Given if pain level not changed
after the 2nd dose of nitroglycerin
▪ Give 2mg slow IVP repeated every 2 minutes as
needed
▪ Max total dose 10 mg

76. Thank you