ECG Review

1
ElectrocardiographyReview
Jeffrey Groom, PhD, CRNA, ARNP Technology for
Anesthesiology Nursing FIU Anesthesiology Nursing
Program
2
Electrical Conduction System
3
Electrical Flow and ECG
4
Electrical Flow and ECG
-

5
Electrical Flow and ECG
-

6
Electrical Conduction System
II
7
Electrical Conduction System
12 Lead ECG Inferior II, III, aVF Septal V1
V2 Anterior V3 V4 Lateral V5 V6 High
Lateral I, aVL
8
12 Lead ECG
I
aVR
V1
V4
II
V2
V5
aVL
III
aVF
V3
V6
9
12 Lead ECG Rhythm Strip - Interpretation
ST Monitor
10
12 Lead ECG

• RATE
• RHYTHM
• INTERVALS
• AXIS
• HYPERTROPHY
• ISCHEMIA -INFARCT

11
RATE
12
RHYTHM

• Regular or Irregular
• P waves
• QRS
• Ratio (P QRS)

13
INTERVALS

• PR Interval
• lt 1 box WNL
• gt 1 box Prolonged
• QRS Interval
• lt ½ box WNL
• gt ½ box Prolonged
• QT Interval
• lt ½ R-R WNL
• gt ½ R-R Prolonged

14
PR INTERVALS

• SHORT
• Ectopic Atrial Pacing site
• Junctional rhythm (inverted P in II)
• PROLONGED
• Conduction delay from SA through AV

15
QRS INTERVALS

• RIGHT Bundle Branch Block
• V1 rsR or M shape
• I V6 qRs and wide terminal S
• LEFT Bundle Branch Block
• V1 negative QRS
• I V6 wide upright QRS
• Intraventricular Conduction Delay
• Wide QRS not patterned as above
• Secondary ST changes T opposite S

16
Normal Sinus Rhythm
17
RIGHT Bundle Branch Block
RIGHT Bundle Branch Block V1 rsR or M
shape I V6 qRs and wide terminal S
18
RIGHT Bundle Branch Block

• Depolarization Septal gtLVgtRV
• Intermittent RBBB 2nd to rapid rate (ST, AF,
  Af, SVT)
• Permanent RBBB 2nd to MI, PE, PHtn
• RBBB Pattern RVH, PWMI, WPW
• RBBB usually hemodynamically stable, unless
• SOB Chest Pain New RBBB
• Acute AWMI RBBB gt 3rd Degree Block

19
LEFT Bundle Branch Block
LEFT Bundle Branch Block V1 negative QRS I V6
wide upright QRS
20
LEFT Bundle Branch Block

• Depolarization- RBB gt Septal gt RV gt LV
• Left Axis Deviation (? LVH)
• LBBB 2nd to pathology
• Transient MI, CHF, Myocarditis, Toxicity
• Permanent MI, Valve dz, HTN, LVH
• LBBB usually hemodynamically stable
• Acute AMI LBBB gt 3rd block
• Symptomatic Patient with Primary ST-T changes
• LBBB SWAN gt risk for 3rd block

21
QT INTERVALS

• QRS to end of T Prolonged gt than ½ R-R length
• Increased vulnerability to malignant ventricular
  arrhythmias, syncope, and sudden death.
• Causes
• Drugs (antiarrhythmics, tricyclics,
  phenothiazines, and others)
• Electrolyte abnormalities ( K, Ca, Mg)
• CNS disease (especially subarrachnoid hemorrhage,
  stroke, trauma)
• Hereditary LQTS (e.g., Romano-Ward Syndrome)
• Coronary Heart Disease (some post-MI patients)

22
AXIS
Leads I and aVF
23
AXIS DEVIATION
- 90
0
180
90
24
NORMAL AXIS
25
LEFT AXIS DEVIATION
26
RIGHT AXIS DEVIATION
27
AXIS DEVIATION
LEFT Axis Deviation
RIGHT Axis Deviation

• LVH
• LBBB
• WPW
• High diaphram, pregnancy
• WNL obese, elderly

• RVH
• RBBB
• LV PVCs
• Pulmonary- emphysema, PE
• WNL thin, young

28
AXIS DEVIATION
LEAD II AXIS PATHOLOGIC
lt - 300 NO
- 300 Borderline
gt 300 YES
29
HYPERTROPHY
LEFT VH
RIGHT VH

• LAD
• V1,2 deep S andV5,6 tall R gt35mm
• aVL R gt 12mm
• Secondary ST depress
• Most frequently seen with hypertension

• RAD
• V1 R V6 S gt10mm
• V1 rSr (incomplete RBBB)
• Secondary ST depress
• Usually will be seen with pulmonary pathology

30
LEFT HYPERTROPHY
31
RIGHT HYPERTROPHY
32
R Wave Progression

• Causes of Poor R Wave Progression (PRWP)
• LVH or RVH
• Pulmonary disease
• Anterior or anteroseptal MI
• Conduction defects
• Cardiomyopathy
• Chest wall deformity
• Normal variant
• Lead misplacement

33
ISCHEMIA - INFARCT QRST
12 Lead ECG Inferior II, III, aVF Septal V1
V2 Anterior V3 V4 Lateral V5 V6 High
Lateral I, aVL
34
ISCHEMIA - INFARCT QRST

• Ignore aVR
• Look at Qs in all leads
• Look for normal R progression
• Look at ST and T in all leads
• Look for patterns by lead group

35
EVOLUTION of INFARCT
A. Normal ECG prior to MI B. Hyperacute T wave
changes - increased T wave amplitude and width
may also see ST elevation C. Marked ST elevation
with hyperacute T wave changes (transmural
injury) D. Pathologic Q waves, less ST elevation,
terminal T wave inversion (necrosis) (Pathologic
Q waves are usually defined as duration
gt0.04 s or gt25 of R-wave amplitude) E.
Pathologic Q waves, T wave inversion (necrosis
and fibrosis) F. Pathologic Q waves, upright T
waves (fibrosis)
36
ISCHEMIA - INFARCT QRST
37
Acute Coronary Syndromes (ACS)

• ST-segment elevation myocardial infarction
  (STEMI),
• Unstable angina,
• Non-ST-segment elevation myocardial infarction
  (NSTEMI)

ACS is disruption plaques in the coronary
vasculature that release pro-coagulatory
products, causing platelet activation, adhesion,
and aggregation and resulting in thrombus
formation.
38
Acute Coronary Syndromes (ACS)

• 1. MONA
• 2. STEMI - reperfusion may be reestablished by
• pharmacologic agents antiplatelet and
  fibrinolytic (30 min)
• primary percutaneous coronary intervention (PCI)
  (90 min)
• coronary artery bypass graft surgery
• 3. NSTEMI reperfusion for Sx high risk patients

39
ISCHEMIA - INFARCT QRST
40
Inferior Wall MI
Pathologic Q waves and evolving ST-T changes in
leads II, III, aVF Q waves usually largest in
lead III, next largest in lead aVF, and smallest
in lead II Fully evolved inferior MI (note
Q-waves, residual ST elevation, and T inversion
in II, III, aVF)
41
Inferior Wall MI
42
Anterioseptal Wall MI

• Q, QS, or qrS complexes in leads V1-V3 (V4)
• Evolving ST-T changes
• Fully evolved anteroseptal MI (note QS waves in
  V1-2, qrS complex in V3, plus ST-T wave changes)

43
Anterioseptal Wall MI
44
Lateral Wall MI

• Lateral Wall (typical MI features seen in V5 and
  V6
• High Lateral MI (typical MI features seen in
  leads I and/or aVL)
• Example note Q-wave, slight ST elevation, and T
  inversion in lead aVL

45
High Lateral Wall MI
46
ST Segment Changes
47
ST Segment Changes

• Intrinsic myocardial disease (e.g., myocarditis,
  ischemia, infarction)
• Drugs (e.g., digoxin, quinidine, tricyclics, and
  others)
• Electrolyte abnormalities of K, Mg, Ca
• Neurogenic factors (e.g., stroke,
  hemorrhage,tumor)
• Metabolic factors (hypoglycemia,
  hyperventilation)
• Atrial repolarization (e.g., at fast heart rates
  the atrial T wave may pull down the beginning of
  the ST segment)
• Ventricular conduction abnormalities and rhythms
  originating in the ventricles

48
2nd ST Segment Changes

• "Secondary" ST-T Wave changes are normal ST-T
  wave changes solely due to alterations in the
  sequence of ventricular activation.
• ST-T changes seen in bundle branch blocks
  (generally the ST-T polarity is opposite to the
  major or terminal deflection of the QRS)
• ST-T changes seen in fascicular block
• ST-T changes seen in nonspecific IVCD
• ST-T changes seen in WPW preexcitation
• ST-T changes in PVCs, ventricular arrhythmias,
  and ventricular paced beats

49
Primary ST Segment Changes

• "Primary" ST-T Wave Abnormalities (ST-T wave
  changes that are independent of changes in
  ventricular activation and that may be the result
  of global or segmental pathologic processes that
  affect ventricular repolarization)
• Ischemia, injury and infarction
• Drug effects (e.g., digoxin, quinidine, etc)
• Electrolyte abnormalities (e.g., hypokalemia)
• Inflammation (pericarditis)
• Neurogenic effects (e.g., subarrachnoid
  hemorrhage causing long QT)

50
Primary ST Segment Elevation

• Ischemic Heart Disease
• Acute transmural injury - as in next example of
  acute anterior MI
• Persistent ST elevation after acute MI suggests
  ventricular aneurysm
• ST elevation may also be seen as a manifestation
  of Prinzmetal's (variant) angina (coronary artery
  spasm)
• ST elevation during stress testing suggests
  extremely tight coronary artery stenosis or spasm
  (transmural ischemia)

51
Transmural Acute Anterior MI
52
Primary ST Segment Elevation

• Other Causes
• Left ventricular hypertrophy (in right precordial
  leads with large S-waves)
• Left bundle branch block (in right precordial
  leads with large S-waves)
• Advanced hyperkalemia
• Hypothermia (prominent J-waves)

53
Primary ST Segment Depression

• Normal variants or artifacts
• Pseudo-ST-depression (wandering baseline due to
  poor skin-electrode contact)
• Physiologic J-junctional depression with sinus
  tachycardia (most likely due to atrial
  repolarization)
• Hyperventilation-induced ST segment depression

54
Primary ST Segment Depression

• Ischemic heart disease
• ST segment depression characterized below
• Upsloping" ST depression is not an ischemic
  abnormality

55
Primary ST Segment Depression

• Ischemic heart disease
• Subendocardial ischemia (exercise induced or
  during angina attack)
• Non Q-wave MI
• Reciprocal changes in acute Q-wave MI (e.g., ST
  depression in leads I aVL withacute inferior
  MI)

56
Non-Ischemic ST Depression

• RVH (right precordial leads) or LVH (left
  precordial leads, I, aVL)
• Digoxin effect on ECG
• Hypokalemia
• Mitral valve prolapse (some cases)
• CNS disease
• Secondary ST segment changes with IV conduction
  abnormalities (e.g., RBBB, LBBB, WPW, etc)

57
Infarction Time Line

• ACUTE Infarction (0 to 24 hours)
• ST Elevation
• Q small or absent
• T inversion minimal or absent
• Reciprocal ST depression

58
Infarction Time Line

• RECENT Infarction (24 hours-wk)
• ST Elevation minimal or absent
• Q present-small or large
• T inversion present
• Reciprocal ST depression minimal or absent

59
Infarction Time Line

• OLD Infarction (over a wk)
• ST elevation absent
• Q present small or large
• T inversion minimal or absent
• Reciprocal ST depression absent

60
Infarction Time Line
Acute Anterior Wall Infarction
61
Infarction Time Line
Old Inferior Wall Infarction
62
Infarction Time Line
Acute Inferior Wall Infarction
63
Infarction Time Line
Old Inferior Wall Infarction Atrial Fib PVCs
64
12 Lead ECG

• RATE
• RHYTHM
• INTERVALS
• AXIS
• HYPERTROPHY
• ISCHEMIA -INFARCT

65
Arrhythmia Review

• Six Second ECG Review Web Site
• http//www.skillstat.com/ECG_Sim_demo.html