This document provides an overview of 12-lead electrocardiogram (ECG) interpretation for myocardial infarction (MI). Key points covered include: the phases of the cardiac action potential; principles of Einthoven's triangle and augmented lead interpretation; proper 12-lead placement; identifying ST segment elevation/depression; differentiating STEMI from NSTEMI; reciprocal changes; locations of artery involvement based on lead findings; and treatment considerations for STEMI. Common STEMI mimics and the importance of differentiating MI from conditions like left ventricular hypertrophy are also discussed.

1. By. Devon Fuller EMT-P
12 Lead Interpretation

2. • Action potential of myocardial tissue and areas of ischemia/ infarction
• Proper 12 lead placement and augmented leads
• Wave formation and pathology
• Recognize and diagnose ectopic and idiopathic segments
• Recognize st-segment elevation and depression
• Differentiate between STEMI and Non-STEMI
• Learn areas of ischemia/ infarction and reciprocal changes
• 6 most common STEMI mimickers
• Learn diagnose ectopic rhythms using axis and axis deviation
• Sgarbossa Criteria
• 15 lead and right side 12 lead placement
• Uncommon 12 lead presentation
• Medications and arrhythmias
Introduction

3. • Occurs in 4 phases (some interpret 3 or 5)
• Sodium (Na+)- influx creates depolarization
• Calcium (Ca2+)- Controls the STRENGTH of depolarization
• Potassium (K+)- influx repolarizes (resets) the action potential
• Resting state average -90mV, then depolarization lifts to approx. +40mV
• During resting state, the outside of the cell is MORE positive than the
inside of the cell meaning by default, the inside of the cell is negative
• During depolarization, the inside of the cell becomes MORE positive than
the outside resulting in contraction
Action Potential

4. • Na+ begins to slowly enter the cell until around -70mV, then it enters the
cell rapidly increasing voltage to approx. +40 (phase 0)
• This influx causes K+ to rapidly leave the cell which is where the voltage
decreases (phase 1)
• As this occurs, Ca2+ begin to enter the cell resulting in NO difference in
voltage (plateau phase, Also Phase 2)
• Once depolarization occurs, the cell begins to switch again, causing Na+
and K+ to leave and Ca2+ to be reabsorbed out of the cell back to resting
state (phase 3 and 4)
Action Potential

5. Action Potential

6. Einthovens Triangle
• “White on right, smoke over fire”
• Negative to positive
• Flow of conduction towards a positive lead
• Augmented leads AVR, AVL, AVF
• Augmentation refers to voltage change
• Voltage change through leads allows
additional segments to be captured on 12
lead

7. Augmented Leads
• Lead voltage changes to reflect positive lead
• Augmentation results in variable deflection
• When voltage moves TOWARDS a positive lead, always a POSITIVE deflection
• When voltage moves AWAY from a positive lead, shows a NEGATIVE deflection
• AVR is NOT a useless lead

8. Lead Placement
• V1: 4th intercostal space right of sternum
• V2: 4th intercostal space left of sternum
• V3: Midway between v2 and V4
• V4: Midclavicular line left side
• V5: Anterior Axillary line same level of V4
• V6: Midaxllary line same level of V5

9. • Measured in milliseconds and millimeters/ millivolts
Time and Size

10. Time and Size
• 0.1 mV = 1 mm (height)
• 1 small box= 0.04 seconds
(width)
• 1 highlighted box= 0.2 seconds
• 5 highlighted boxes =1 second
• 0.5 mV = 5 mm
• Height and width used to
determine additional ectopy
during cardiac rhythm
• Based on location of isoelectric
line

11. Isoelectric line
• Base electrical line on ECG
• Used to determine elevation or
• Depression
• Dependent on upward and
• Downward deflection of QRS
• Registered in time and mV

12. Isoelectric Line
• Elevation determined by positive deviation from isoelectric line
• Depression determined by negative deviation from isoelectric line
• ST-Segment can be above or below but the J-point must be determined to
diagnose elevation or depression

13. The “Quick 6”
• Half of a 12 lead
• Shows a reflection of basic leads and
augmented leads
• May show possible areas of infarction/
ischemia
• Will not show PRI/ QRS/ QT segment
timing
• 12 lead is still the standard for diagnosis

14. The 12 Lead

15. •Shows time and elevation in exact sequence
•Considered always reliable
•Do NOT go by the computer interpretation of the rhythm, that’s why you
were trained to manually interpret
Normal range
•PRI- 0.12-0.20 seconds
•QRS- 0.04-0.12 seconds
•QT- Females- 340-400 MS
Males- 330-390 MS
• Prolonged QT segment begins over the limit of gender
Numbers?

16. QT-Segment

17. Normal vs. Abnormal

18. •Can be typical or atypical
•Caused by CAD
•Can also be caused by coronary artery spasms
•Angina is brought on by stress, vigorous activity or by nothing at all
•Typical presents with frequency and is predictable
•Atypical presents with no rhyme or reason and is often not relieved by nitro
or positioning
•Regardless of the cause, all angina patients need a 12 lead to rule out STEMI
•CAD is the leading cause of STEMI in the WORLD
Angina

19. 12 Lead Reflection

20. “ I See All Leads”

21. • Lie Lie Say All
• Alternative to diagnosis of 12 lead
• Not often used but other providers will use this method alone, or in
conjunction with ISAL to determine proper diagnosis
• Follows the appropriate pattern of 12 lead without skipping over additional
leads for completion
• For remainder of the slides, we will be looking at BOTH methods for
determination using ISAL as primary
“LII-LI-SSA-ALL”

22. Arteries of Viewing
• The "LCX", or left circumflex artery is an artery of the heart. It follows the left part of the coronary sulcus,
running first to the left and then to the right, reaching nearly as far as the posterior longitudinal sulcus. Can also
include the low lateral leads V5-V6
• The right coronary artery originates above the right cusp of the aortic valve, travels down the right atrioventricular
groove, and branches into the posterior descending artery and the right marginal artery.
• The left coronary artery arises from the aorta above the left cusp of the aortic valve and feeds blood to the left side
of the heart. It is also known as the left main coronary artery and the left main stem coronary artery. An occlusion
to this artery is often called “the widowmaker”.

23. Artery’s Affected

24. Inferior Leads
• Leads II, III, and AVF
• Reflect the circuit flow of the inferior/
partial posterior of the heart
• Main focus on RCA and additional
arterial flow from the same

25. Septal Leads
• Leads V1 and V2
• Views the junction/bifercation
of the LAD and Circumflex
artery
• Most proximal portion of the
left and right coronary arteries

26. Anterior Leads
• V3 and V4
• Most anterior portion of the
LAD
• Often defined as the
“widowmaker”
• 27% mortality rate
• Supplies the greatest amount
of blood to the largest muscle
portion of the heart

27. Lateral Leads
• V5 and V6
• Most distal portion of the
LAD and attached arterial
flow

28. Reciprocal Leads
• Any lead or group of leads that oppose primary lead viewed
• Not needed or necessary to presume infarction or diagnose a STEMI
• Strong confirmation of STEMI when present
• Can NOT be used as a “rule out” option

29. Reciprocal Change

30. Reciprocal Change

31. J-Point
• Determined by the Joining of
the QRS and ST segment
• Can be elevated or depressed
• Sometimes is hard to
determine location
• Follow the standard rules of
interpretation to find the J-
Point

32. J-Point
• With all 12 lead interpretation of suspected ischemia or infarction, first
find the J-Point on the most Isoelectric lead
• Remember that the J-Point is the connection of the S wave and the T
wave.

33. J-Point
• Once you find the J-Point, simply draw a line through the 12 all
leads and connect the J-Points

34. • Technically defined as any negative deflection that precedes an R wave
• It does not have to be a negative deflection to be present however.
• The Q-wave can be isoelectric
• Q-wave represent normal left to right depolarization of the interventricular
septum
• Most commonly seen in lateral leads (I, AVL, V5, V6)
• Not normal variant if seen in anterior septal leads (V1-V4)
• Most common cause of q-wave pathology and presence in anterior septal
leads is incorrect limb lead placement
Q-wave pathology

35. • Presence of pathological q-waves usually indicate current or prior
myocardial infarction
• Q-wave is considered pathological if:
 > 40ms wide
 > 2mm deep
 > 25 % of the QRS complex
 Seen in the anterior septal leads
• If any of these are seen and there is no ST elevation or depression, a high
probability of prior MI is present.
• Can be seen in hypertrophic cardiomyopathy and myocardial rotation as
well
Pathological Q-Wave

36. Pathological Q-Wave
 > 40ms wide
 > 2mm deep
 > 25 % of the QRS complex
 Seen in the anterior-septal
leads
The pathological Q-Wave
will NOT form until 1-2
hours into a STEMI. If it’s
presence is there, you now
know how much time the
muscle has been infarcting.

37. Ischemia VS Infarction

38. Ischemia VS. Infarction
• Ischemia is noted by ST-Depression
• Infarction is noted by ST-Elevation
• The higher the ST-Elevation, the worse
the infarction is
• Reciprocal change is known as the area
of ischemia opposite area of infarction
• As shown in the figure, infarction has
an evolution from start to finish of the
area
• Once the evolution is finished, the
cardiac muscle is PERMANENTLY
damaged
• Best pre-hospital treatment is MONA
• Morphine
• Oxygen
• Nitro
• Aspirin

39. • ST-elevated myocardial infarction
• Must be at least 1 mm elevation in 2 CONTIGUOUS leads
• Contiguous leads are any set of leads the reflect the same area, or are next
to the same area
STEMI
• *V6 and Lead I are contiguous*
• V2 and V3
• V4 and V5

40. STEMI VS NSTEMI

41. ST Elevation Patterns
ST elevation in stemi can be reflected either concave,
convex, or obliquely straight

42. • *Smile for me*- The smile of the st-segment means NO STEMI
• *Frown means down*- The frown is in indication or st-segment elevation
STEMI

43. • Area of infarction is reflected by the area of ST-Elevation
• Reciprocal changes are NOT needed to diagnose a STEMI in the field
• Be careful of the STEMI mimickers
• As long as you have 1 mm elevation in 2 or more CONTIGUOUS leads, a
STEMI can be diagnosed
STEMI-Location

44. Inferior MI
• ST-Elevation in leads II,III, and AVF
• Reciprocal changes in leads I and AVL
 KEY NOTE!!!
 Inferior AMI have shown an 88% probability to lead with either an
Inverted or depressed AVL PRIOR to the infarct presenting.
•If AVL is inverted or depressed, an AMI may be on the way

45. Septal MI
• Elevation in leads V1 and V2
• Note elevation in anterior leads as well
• Septal most often present in anterior MI as well
• Reciprocal changes noted?

46. Anterior MI
• ST-Elevation noted in leads V3 and V4
• Note the elevation in leads V1 and V2
• Anterior and Septal mi often correlate with each other
• Reciprocal changes?

47. Lateral MI
• Low Lateral AMI
• High Lateral AMI

48. • Universal in nature
• Deep, depressive, substernal chest pain/
pressure not relieved or reproducible
• Levine sign
• Pain in left or right arm, shoulders,
neck, jaw
• Weakness upon exertion
• Nausea
• Diaphoresis
• Ashen grey skin
• Rule of thumb, if pain above the naval,
do a 12 lead
Classic Presentation

49. Inferior Presentation
• In majority of population, 90% SA and AV node blood flow comes from the
RCA
• Conduction deficits/ delays
• Brady-arrhythmias
• Sinus Bradycardia
• Sinus Exit Block
• 1st degree heart block
• Hypotension
• Treat hypotension with fluid but DO NOT OVERTREAT
• May result in pulmonary edema
• Morphine and Nitro combined will drop pressure, both vasodilate
• Treat but keep pressure sustainable for cognition

50. • Most often the LCA occluded partially or fully
• Dull pressure that turns to crushing chest pain
• Pain radiates into the left arm
• Numbness or tingling sensation in fingers
• Pt may appear ashen grey or diaphoretic
Septal Presentation

51. • LCA / Circumflex occlusion, may be both
• Crushing, substernal chest pain
• Pain radiating into the left arm, right arm, or both
• Pain may appear in the shoulders and jaw
• Nausea
• Vomiting
• Diaphoresis
• Tingling or complete numbness in the fingers
• Shortness of breath
• Weakness upon exertion of any kind
• Near syncopal or positive syncopal episodes
• “Feeling of impending doom”
Anterior Presentation

52. • May have a combined presentation of both Anterior and Inferior wall MI
• Weakness upon exertion
• Pain radiating to one or both arms
• Syncope or near syncopal episodes
• Hypotension
• Brady-arrhythmias
• New heart blocks
• Most common presentation of new Bundle Branch Blocks
Lateral Presentation

53. Combination STEMI
• STEMI can occur in more than 1 area
• A “combination STEMI” is a STEMI that has ST-elevation in more than the
traditional leads yet are still contiguous
• Anterioseptal STEMI- Anterior and septal lead have ST-Elevation
• Anteriolateral STEMI- Anterior and lateral leads have ST-Elevation
• Inferiolateral STEMI- Inferior and lateral leads have ST-Elevation
• Global AMI- ALL leads have ST-Elevation other than AVR which will be
depressed
• Some STEMIs will have more than one area with additional involvement
• Eg- “Anterioseptal with lateral involvement”
• This indicates that the elevation is continuing through more than 1 area or
view of the 12 lead

54. Combination STEMI
• Inferiolateral AMI

55. Combination STEMI
• Anteriolateral AMI

56. Combination STEMI
• Anterioseptal AMI

57. • Continue to monitor ABC
• Initiate IV if available
• Continue with serial 12 leads
• ASA is a NESSICITY
• O2 via cannula (wave form capnography if indicated)
• IV fluid to maintain adequate blood pressure
• Nitro PRN
• Morphine is indicated for pain management
• Rapid transport to PCI facility
Treatment

58. • Obtain SAMPLE and OPQRST
• Be prepared for the worst
• AMI is the most common cause of acute Congestive Heart Failure
• Treat with CPAP if indicated (bp, hr, waveform capnography)
• Be cautious with Morphine and Nitro especially in Inferior AMI due to
rapid decrease in blood pressure
• Be cautious with patient allergic to aspirin
• Notify the receiving hospital early of STEMI activation and expected
arrival time
• Note area of infarct and ischemia/ reciprocal changes if available
• Remember you DO NOT have to have reciprocal changes to diagnose a
stemi
Considerations

59. • STEMI MIMICKERS!!
• TOP 6
 LVH
 LBBB
 Hyperkalemia
 Early Repolarization
 Pericarditis
 PACED
Could it be?

60. • Left Ventricular Hypertrophy
• Left ventricle is larger requiring more electrical conduction to depolarize
• This results in a longer QRS complex than normal
• Seen in the precordial leads
• Determination is selective
• Find largest QRS complex in either lead V1 or V2
• Add to the largest complex in lead V5 or V6
• If the number is greater than 30 mm, LVH is present
• If the largest QRS complex in V1 or V2 is greater than 30, LVH is present
LVH

61. •Most often referred to as athletic heart syndrome
•Often caused by aerobic exercise and strength training
•Is not a disease
•Is usually a marker for disease
•Any disease that causes an increase in afterload over time that causes the
heart to increase contractility strength, therefore increasing the myocardium
•Causes are referred to as hypertrophic cardiomyopathies
Aortic stenosis
Aortic insufficiency
Chronic hypertension
LVH

62. LVH

63. • Left Bundle Branch Block
• Left main conduction path is injured or blocked
• This results in a “lightning” effect
• The current must come back and re-route itself down the left ventricle to
complete conduction in the myocardium
• QRS must be negative deflection in lead V1 and greater than 0.12 ms
(3 small boxes)
• Was considered impossible to diagnose a STEMI in the presence of a
LBBB
• Sgarbossa criteria now used to diagnose STEMI when LBBB is present
LBBB

64. LBBB vs RBBB

65. LBBB vs RBBB

66. • LBBB
• Can NOT call STEMI w/o
sgarbossa
• Negative deflection in V1
• QRS greater than 0.12
• May or may not present with R
prime wave
LBBB vs RBBB
• RBBB
• CAN call a STEMI
• Positive deflection in V1
• QRS greater than 0.12 ms
• Typically presents with R prime
wave (RsR)

67. • Clinical presentation
• Nausea
• Dyspnea
• Fatigue and weakness
• Chest pain
• Muscle paralysis
• Parasthesias
• Palpitations
• Absent DTR
• New LBBB
• Late signs include- bradycardia, lethargy/ unconsciousness, bradypnea, flat
t-waves, death
Hyperkalemia

68. • MURDER
• Muscle cramps
• Urine abnormalities
• Respiratory distress
• Decreased cardiac contractility
• Ecg changes
• Reflexes
Hyperkalemia

69. • Increased serum potassium levels in the blood
• Often found in renal impaired/ failure patients
• ECG reflects peaked T waves
• Pay close attention to the QRS segment as it will begin to get wider
• Do NOT confuse this with hypernatremia where the QRS remains the same
or gets more NARROW as the T waves begin to peak
Hyperkalemia

70. Hyperkalemia

71. • Goal is to displace potassium and sodium in the blood
• REMEMBER THE SODIUM POTASSIUM PUMP
• Influx of sodium will offset the higher potassium load to be reabsorbed into the
kidneys for excretion
• IV access (bilaterally if available)
• CBIGKD
• Calcium gluconate
• Bicarbonate
• Insulin
• G (glucose) D50
• Kayexalate- Sodium polystyrene sulfonate. If total body potassium is an issue
• Dialysis
Hyperkalemia Treatment

72. • Typically seen in adolescent males who lead a physically active life
• May present in any male under 50
• Also called “high J-point” or “early take off”
• Etiology is still not completely understood but was once believed to be
benign in possibility of cardiac disease. This is no longer the case.
• More recent reports have suggested an association between ER and an
increased risk for arrhythmic death and idiopathic ventricular fibrillation
• Some level of increased risk of sudden cardiac death has been reported in
persons with ER.
Early Repole (not so benign)

73. • The relatively high prevalence of the ER pattern in the general population
(5 to 13 percent) in comparison to the incidence of idiopathic VF
(approximately 10 cases per 100,000 population) means that the ER pattern
will nearly always be an incidental ECG finding with no clinical
implications.
• A primary arrhythmic disorder such as idiopathic VF due to ER is far more
likely when associated with syncope or resuscitated sudden cardiac death
in the absence of other etiologies
• If seen in males 50-70, consider acute infarct
• Rarely seen in patients over 70
Early Repole (not so benign)

74. • Presentation
• PR depression
• St depression in AVR with T wave inversion
• Barbed “fish hook” appearance as a J-point with ST elevation in all leads
Early Repole cont.

75. Early Repole
•“Barbed fish hook” appearance on the ST segment
•Will almost always have ST depression and inverted T wave in AVR

76. • Clinical presentation
• Chest pain radiating to the back that is typically relieved by sitting forward
(to relieve pressure on the myocardium)
• Dry cough
• Fever
• Fatigue
• History of infection
• SHARP chest pain
• Often clinically misdiagnosed as STEMI
• Diffuse ST-elevation
• Often with Pr-depression
• Most commonly presents with t-wave inversion or ST depression in AVR
Pericarditis

77. Pericarditis

78. •Very common STEMI mimicker
•Additional voltage used to supercharge the muscles externally for cardiac
contraction
•Often results in elevation and depression
Paced Rhythm

79. • A numerical representation of the MAJOR direction of electrical flow
through myocardium
• Ranges from 0 to -180 degrees
• Proper range is from -30 to +90
• Referred to as “normal axis”
• Deviation from the normal axis is referred to as “axis deviation” (go figure
right?)
• Deviation can be physiological, pathological or extreme
• Extreme is a significant sign of life threatening cardiac abnormality or
rhythm
The Axis

80. Axis Measurments

81. • Several methods are in use today, we will focus on these 3
• Quadrant method
 Utilizes lead I and AVF
• Lead method
 Utilizes Lead I and II
 Tri-lead method
• Utilizes leads I, II, and III
Determining Axis

82. • LEAD I LEAD AVF QUADRANT AXIS
• Positive Positive Left Lower Quadrant Normal
• Positive Negative Left Upper Quadrant Possible LAD
• Negative Positive Right Lower Quadrant RAD
• Negative Negative Right Upper Quadrant ERAD
Quadrant Method

83. Quadrant Method
• Lead I- Positive
• Lead AVF- Positive
• Quadrant- Lower Left
• Axis- Normal

84. Quadrant Method
• Lead I- Positive
• Lead AVF- Negative
• Quadrant- Left Upper
• Axis- LAD

85. Quadrant Method
• Lead I- Negative
• Lead AVF- Positive
• Quadrant- Right Lower
• Axis- RAD

86. Quadrant Method
• Lead I- Negative
• Lead AVF- Negative
• Quadrant- Right Upper
• Axis- ERAD

87. • Determined by looking at leads I and II
• If the QRS is positive in lead I, it is roughly in the same direction as lead I
• If the QRS is in the same direction as lead II, it puts the axis in roughly the
same direction of lead II
• If leads I and II are BOTH positive, it places the axis in the area of -30 and
+ 90, meaning normal axis variant
Lead Method

88. •Also referred to as the “rapid-axis” method
•Utilizes the lead method with addition of lead III for better determination
TRI-Lead Method

89. • Left or Right
• Can be physiological or pathological
• Caused by a number of factors
Deviation

90. • May be a normal variant
• Conduction issues
 Left anterior block
 LVH
 LBBB
 Prior mechanical shift (surgery, lung disease, etc)
 Inferior AMI
 WPW
 Idioventricular rhythms ie. V-tach or accelerated idioventricular
 Atrial septal defects
LAD

91. • Causes
 Left posterior fascicular block
 RVH
 Lung disease (acute or chronic)
 Ventricular ectopy
 Hyperkalemia
 Sodium-channel blocker toxicity
 WPW
 May also be a normal variant for children or adults with mechanical
shifting of the heart
RAD

92. Physiological LAD
Lead I- positive, Lead II- BIPHASIC, Lead III- Negative

93. Pathological LAD
Lead I- Positive, Lead II- Negative or R wave more negative than positive q
wave, Lead 3- same criteria as lead II

94. RAD

95. •ERAD- Extreme right axis deviation
•Physiological vs pathological LAD
•Physiological left axis deviation- typically between 0 and -30
•Pathological left axis deviation- -30 to -90
•Axis deviation can be skewed due to left or right bundle branch blocks
•Be careful when using axis for complete diagnosis as the number do not lie,
however they can confuse
Extreme Axis

96. •Often seen in wide complex tachycardias (V-tach)
•Is possible to have a wide complex tachycardia that mimics v-tach but
brought on by “F” waves (flutter waves)
Extreme Axis

98. ERAD

99. •FINALLY!!
•Used to diagnose a STEMI in the presence of a LEFT bundle branch block
AND a paced rhythm
•Criteria simple to follow
•We as a prehospital provider in our local area can NOT utilize this tool as of
yet (2016)
•The criteria has increased in usage and accuracy for the past few years and is
being taught to medical providers globally
•The rules are continuing to be modified every year by new clinical evidence
and presentations
•What you learn today may NOT be in effect tomorrow
Sgarbossa Criteria

100. Sgarbossa Criteria:
• ST Elevation ≥ 1 mm and concordant with QRS complex
• ST segment depression ≥ 1 mm in lead V1, V2, V3
• ST elevation ≥ 5mm and discordant with QRS complex
•IF #1 and #2 are present, 98% probability of STEMI
•NEW rules has been added to update the parameters of Sgarbossa
•If positive concordance in ANY lead with the presence of a LBBB, Sgarbossa
criteria has been met
• ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive
discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave
Sgarbossa

101. Sgarbossa

102. Is it Sgarbossa?

103. Is it Sgarbossa?

104. Is it Sgarbossa

105. • Some common medications and drugs can cause cardiac arrhythmias
• Most over the counter medications are relatively harmless
• Stimulant drugs and medications are the most common type to cause an
arrhythmia (usually sinus tach)
• Illicit drug use can either speed up or slow down the heart
• Common household items can also cause an arrhythmia (fertilizer, cleaning
materials)
• Most drugs that stimulate the sympathetic nervous system can cause a short
lived arrhythmia, but will usually subside due to a relatively short half-life
Medication Problem?

106. • Caffeine
• Tobacco
• Alcohol
• Cold and cough medications
• Appetite suppressors (stimulants)
• ADHD medications
• Antiarrhythmic medications (paradoxical arrhythmias from medications)
• Tricyclic antidepressants
• Beta Blockers (primarily for blood pressure)
• Cocaine, marijuana, methamphetamines
Common medications and drugs

107. • Most stimulant drugs are dopaminergic (releasing or involving dopamine
as a neurotransmitter)
• These drugs will stimulate the release and inhibit the reuptake of
dopamine, leaving it at the synaptic cleft
• This leads to an increase in energy and a feeling of alertness and
concentration
• Norepinephrine is released as an additional catecholamine along with
dopamine which leads to the increase in heart rate and contractility
• If these drugs are taken too much or abused, the heart rate can increase to a
dangerous level
• The overstimulation of the sympathetic nervous system cause a fluctuation
and lowers parasympathetic response, this leads to an additional side effect
of not wanting to eat
Stimulants

108. • Caffeine
• Tobacco
• Alcohol
• Appetite suppressors
• Cocaine
• Methamphetamines
• ADHD medications
Stimulant Types

109. Sinus Tachycardia

110. • Amitriptyline (Elavil)
• Amoxapine
• Clomipramine (Anafranil)
• Desipramine (Norpramin)
• Doxepin (Sinequan)
• Imipramine (Tofranil)
• Nortriptyline (Pamelor)
• Protriptyline (Vivactil)
Tricyclic Antidepressants

111. • Increase levels of norepinephrine and serotonin
• Block the action of acetylcholine
• Can cause sedation and block histamines as well
• TCA have sodium-channel blocking properties which increase quickly in high
doses
• This causes a prolongation of the Q-T segment on an ECG
• Using the ECG and tracing the Q-T Segment can give you a better time frame
on potential cardiac arrhythmias
• Most common late stage arrhythmias are V-Fib and Torsades De Pointes
• Best initial treatment via IV is sodium bicarb, NOT for the sodium channel
issue alone but to alkalize the blood stream for protein synthesis and reduced
bioavailability of the drug
• This increases elimination of the drug
• Calcium Can be given as well (through a different, or well flushed line) to open
calcium channels and promote sodium availability
Tricyclics Cont

112. • A separate reason they are called “TCA’S”
• Mnemonic
• T-Thrombocytopenia- decrease in platelet count, increase in platelet
deficiency
• C-Cardiac- AMI, arrhythmia, stroke
• A-Anticholinergic effects- Exact opposite of SLUDGE, everything hot
• S-Seizures
• All signs and symptoms of TCA overdose
• Pay attention to the ECG changes during a suspected TCA overdose
Tricyclics Cont.

113. • Toxicity usually is apparent within the first hour after ingestion
• New onset of all complexes widening
• Prolonged PRI, QRS and QT segments
• Prolonged PRI is usually the latest sign and high indication of inevitable V-
Fib
• Prolonged QT is usually the first ECG change in an overdose
TCA ECG Changes

114. • These rules apply inconsideration of Sodium Channel Blocker overdose
• QRS > 100ms (0.10s) in lead II
• Terminal R wave in AVR > 3mm
• R-S ratio > 0.7s AVR
• Patients will often be Tachycardic however, the P waves will be hidden in
the prior T wave due to elongation of the PRI
TCA ECG Rules

115. TCA ECG

116. •Gives additional views of the heart anterior and posterior
•Leads V7, V8, V9, V4R, V5R, V6R
•V7- between V6 and V8
•V8- Midscapular on the same line as V7 and V6
•V9- Between the spine and V8
•V4R- Midclavicular in opposite intercostal space as V4
•V5R- Between V4R and V6R on same plane
•V6R- Midaxillary right side
15 Lead / Right Sided Lead Placement

117. Posterior 12 Lead

118. Posterior AMI

119. Right Leads
•When doing V4R-V6R, simply
write “R” after the appropriate V
leads

120. 15 Lead

121. 15 Lead V4R-V6R

122. •12leads are not just for diagnostic properties of a STEMI
•Additional ectopy can be viewed and assist in a diagnosis for life threatening
ailments either acute or chronic
•Brugadas syndrome
•Acute pulmonary embolism
•Hypernatremia
•Right Ventricular Hypertrophy
•Dewinters STEMI
What is That?

123. •An aberrant conduction abnormality that causes sudden cardiac death
•Leading cause in SUDS (sudden unexplained death syndrome)
•Genetic abnormality of the sodium ion pump channels
•SCN5A- influx flow sodium ion channel that fails which results in prolonged,
untreatable V-fib
•Can be viewed on a 12 lead in the V-Leads
Brugadas Syndrome

124. •3 different types of ECG patterns
•Type 1 has a coved type ST elevation with at least 2 mm (0.2 mV) J-point
elevation a gradually descending ST segment followed by a negative T-wave
•Type 2 has a saddle back pattern with a least 2 mm J-point elevation and at
least 1 mm ST elevation with a positive or biphasic T-wave. Type 2 pattern
can occasionally be seen in healthy subjects
•Type 3 has either a coved (type 1 like) or a saddle back (type 2 like) pattern
with less than 2 mm J-point elevation and less than 1 mm ST elevation. Type 3
pattern is not rare in healthy subjects
Brugadas Syndrome

125. Brugadas Syndrome

126. Brugadas Syndrome 1
Coved type ST elevation with at least
2 mm (0.2 mV) J-point elevation a
gradually descending ST segment
followed by a negative T-wave

127. Brugadas Syndrome 2
Saddle back pattern with a least
2 mm J-point elevation and at least
1 mm ST elevation with a positive
or biphasic T-wave. Type 2 pattern
can occasionally be seen in healthy
subjects

128. Brugadas Syndrome 3
Either a coved (type 1 like) or a
saddle back (type 2 like) pattern
with less than 2 mm J-point
elevation and less than 1 mm ST
elevation. Type 3 pattern is not rare
in healthy subjects

129. •The clot that won’t break
•Usually acute in nature with severe difficulty breathing though lungs are
clear
•Often misdiagnosed and treated due to its acute nature and inability of the
prehospital provider to administer fibrinolytics or perform surgery to remove
the clot
•If suspected, look at the 12 lead
•Deemed “S1, Q3, T3”
•Also known as McGinn-White sign
Acute PE

130. Acute PE
•Large deflection of the S wave in lead I
•Presence of a Q wave in lead III
•Inverted T wave in lead III
•Signals the presence of right heart strain
due to overuse/ occlusion of Pulmonary
Artery

131. •Often seen in the elderly
•Hypokalemia can mimic hypernatremia and vise versa
•Serum potassium levels may be normal in comparison to the sodium levels
•Initially present the same way in a 12 lead but subtle differences can be
examined
•Always obtain a SAMPLE from EVERY patient to determine the nature of
the 12 lead
•Hypernatremia begins to present with prolonged QT segments due to the
delay in repolarization from the potassium influx
•This is the PRIMARY difference between Hypokalemia and Hypernatremia
Hypernatremia

132. Hypernatremia

133. Hypernatremia
Hypernatremia

134. •Right ventricular hypertrophy
•Increase in myocardium of the right ventricle
•Often caused by
Pulmonary hypertension
Tetrology of the fallot
Pulmonary valve stenosis
Pulmonic regurgitation
VSD
High altitude
Cardiac fibrosis
COPD
Athletic heart syndrome
RVH

135. •Peaked P wave in lead II
•Right axis deviation in the presence of disease that causes RVH
•R wave in AVR > 5mm OR
•R wave in AVR > Q in AVR
•ST segment depression AND T wave inversion in right precordial leads
•Any one of the following in V1
R/S ratio > 1 and negative T wave
qR pattern
R > 6mm, or S < 2mm, or rSR` with R` > 10mm
RVH

136. RVH

137. •The de Winter ECG pattern is an anterior STEMI equivalent that presents
without obvious ST segment elevation.
•Key diagnostic features include ST depression and peaked T waves in the
precordial leads.
•The de Winter pattern is seen in ~2% of acute LAD occlusions and is under-
recognised by clinicians.
•Unfamiliarity with this high-risk ECG pattern may lead to under-treatment
(e.g. failure of cath lab activation), with attendant negative effects on
morbidity and mortality.
DeWinters STEMI

138. •Tall, prominent, symmetric T waves in the precordial leads
•Upsloping ST segment depression >1mm at the J-point in the precordial leads
•Absence of ST elevation in the precordial leads
•ST segment elevation (0.5mm-1mm) in aVR (told yeah it wasn’t useless)
•“Normal” STEMI morphology may precede or follow the deWinter pattern
DeWinters Criteria

139. •MAY present atypically with no symptoms of cardiac issues
•Most common complication of Diabetes is CAD
•Many patients with Diabetes present with no angina or “silent” AMI
•This is primarily found in patients with persistent higher than normal levels
of serum glucose
•Most often these patients with have “diabetic nerve pain” and will not be able
to feel the consistent pressure from angina due to either the medications they
take, the exact location of nerve damage, the bodies pH, the particular tissue
involved and ability to function homeostatically, or prior injury resulting in
dead or weakened nerve supply to the area.
Diabetes

140. Lets Wrap it UP

141. •Remember to always do a SAMPLE/ OPQRST on your patients
•Make sure the leads go on the appropriated areas for the best picture possible
•Remember the difference between benign elevation and malignant elevation
•A smile is what we want, frowns are bad
•Each lead reflects a particular section of the heart, if you need other angles
the 15 lead can very useful
•Not every STEMI will show up, but it may be calculated with the numbers
provided by the machine
•Some STEMIs are NOT STEMIs, at least 6 you know can be false
•Sgarbossa may change criteria, but the single concordant lead will remain
•12 leads can help you determine a course of action for treatment if all else
gives no answers
Summary

142. •lifeinthefastlane.com/ecg-library/de-winters-t-waves/
•AHA.ORG
•12leadblogspot.com
•Ekgtoday.net
•12leads.com
•Wikipedia
•McGraw Hill Paramedic
•Nancy Carolines Life in the Streets- Paramedic edition
•Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U
waves, and the QT interval: a scientific statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American
College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the International
Society for Computerized Electrocardiology. Circulation 2009; 119:e241.
•WASSERBURGER RH, ALT WJ. The normal RS-T segment elevation variant. Am J Cardiol 1961;
8:184.
•Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early
repolarization. N Engl J Med 2008; 358:2016.
References