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History taking and physical examination > ECG abnormalities 2 > Flashcards

ECG abnormalities 2 Flashcards

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1
Q

Inherited Arrhythmia Disorders

A
  1. LQTS - Long QT syndrome
  2. SQTS Short QT Syndrome
  3. The Brugada syndrome
  4. ARVC - Arrhythmogennic Right Ventricular Cardiomyopathy
  5. CPVT - Catecholaminergic Polymorphic Ventricular Tachycardia
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2
Q

LQTS types

A
  1. LQT1 -> KCNQ1 gene mutation, potassium channel, early onset broad T wave, usually part of Jervell and Lange-Nielsen syndrome (JLNS) -> with bilateral sensorineural hearing loss
  2. LQT2 -> KCNH2 gene mutation, potassium channel, bifid, low amplitude T waves
  3. LQT3 -> SCN5A mutation, sodium channel, long isoelectric ST segments with late-appearing T wave, sudden cardiac death during sleep
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3
Q

LQTS diagnosis

A
  1. Suspition -> cQT > 460 ms (usually > 480 ms)
  2. Rule out secondary causes of LQT
  3. Schwarz score (LQTS scale) > 3 or mutation of one of the responsible genes
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4
Q

Causes of LQT

A
  1. Genetic
  2. Electrolyte imbalance -> hypokalemia, Hypocalcemia, Hypomagnesemia
  3. Drugs: antyarrhythmic, Antibotics, Antipsychotics, H1 antagonists, other
  4. Cardiac conditions: MI, Cardiomyopathy, Myocarditis, bradycardia
  5. Endocrine: hypothyroidism, hyperparathyroidism, pheochromocytoma, hyperaldosteronism
  6. Intracranial disorder: SAH, stoke, thalamic hematoma, encephalitis, head injury
  7. Malnutrition
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5
Q

LQTS treatment and frequency and onset

A

1/2000, onset usually 5-15

  1. β-blokers (Nadolol, Propranolol)
  2. ICD
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6
Q

SQTS

A
  1. suspect when QT<360 ms (usually < 300)
  2. Cause: gain of function mutation of potassium channel or Ca channel -> more rapid repolarization
  3. Arrhythmias: AF, polymorphic VT, SCD
  4. treatment: Quinidine or Sotalol or ICD
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7
Q

Brugada syndrome ECG

A

-> in V1-V3
Type I -> ST elevation (usually in J point) ≥0.2 mV with coved ST segment with ST segment decreasing -> to negative T wave
Type II -> High J-point eleviation ≥2mm, saddleback ST first decreasing (but > 1mm above baseline) but T wave positive or biphasic
Type III -> J point eleviation ≥ 2 mm with ST elevation < 1mm (saddleback), positive T wave

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8
Q

Brugada syndrome causes and diagnosis

A
  1. Mutations of sodium channel gene (most common SCN5A) -> predisposition for reentry
  2. Diagnosis: ECG, can wax and wane -> augmentation: sodium channel blockers: Flecainide, Ajmaline, Procainamide
  3. Cardiac arrest often in bed, at night, can be provoked by febrile illness
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9
Q

Brugada syndrome treatment

A
  1. Quinidine
  2. ICD
  3. Avoidance of drugs elevating ST
  4. Quick management of fever
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10
Q

ARVC

A
  1. Genetic fibrofatty replacement of cardiac muscle of RV -> reentry
  2. Inverted T waves or Epsilon wave in V1-3
  3. Most common arrhythmias: PVC, VT, VF
  4. Treatment: avoidance of sports, β-blokers, Amiodarone, ICD, ablation
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11
Q

CPVT

A
  1. Mutation of gen codung ryanodine receptore RyR2
  2. Onset in childhood with syncope due to polymorphic VT
  3. ECG: PVC, bidirectional VT
  4. Treatment: avoidance of physical exercise, β-blokers, ICD, left cardiac sympathetic denervation
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12
Q

Subendocardial ischemia typical leads

A

Typically in:

  1. leftward: I, aVL, V4, V5, V6
  2. inferiorly oriented: II, III, aVF

V1-V3 depression -> almost never seen -> can mean either RV subendocardial ischemia (it resolves in the minutes following exercise or stress) or more typical LCX transmural ischemia (lateral wall)

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13
Q

Subendocardial ischemia ECG pattern

A
  1. ST depression >0,1 mV -> from J point horizontal or downsloping (upsloping can normal or abnormal when it remains depressed)
  2. T wave -> juction of ST with T wave depressed but the terminal part of T wave usually remains positive (but T wave can be inverted)
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14
Q

ECG criteria for transmural ischemia

A

A) significant elevation of ST segment at J point:

  1. ≥ 0.1 mV in any lead exept V2 and V3
  2. in leads V2 and V3 -> ≥ 0.25 mV in men < 40 yo, ≥ 0.2mV in men ≥40 yo, ≥ 0.15 in women

B) Depression of ST at J point ≥ 0.1 mV in at least 2 out of 3 leads: V1-V3

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15
Q

Eleviation of ST causes

A

Electrolites (Hyperkaliemia)
LBBB
Early repolarization (benign)
Ventricular hypertrophy
A3 -> Arrhyrhmia (VT, Brugada), Aneurysm of LV, Aortic dissection
T -> TBA - Traumatic brain injury or Takotsubo disease
Infarction
Osborn waves (hypothermia)
Non-artherosclerotic vasospasm (Prinzmetal angina)

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16
Q

Equivalents of STEMI (signs allowing to diagnose STEMI without additional criteria)

A
  1. new LBBB with addition criteria
  2. Posterior MI
  3. LMCA Occlusion
  4. Wellen’s Syndrome
  5. De Winter’s T Waves
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17
Q

Equivalents of STEMI new LBBB criteria

A

LBBB criteria + 1 of:

  1. ST elevation ≥ 0.1 mV in a lead with upward QRS complex
  2. ST depression ≥ 0.1 mV in V1, V2, or V3
  3. ST elevation ≥ 0.5 mV in a lead with downward (discordant) QRS complex

QS in V1-V4 or Q in V5 or V6 can suggest new or past MI

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18
Q

Posterior MI

A
  1. RCA (90%), LCX (10%)
  2. V2, V3 -> ST depression ≥ 0.05 mV
  3. Usually broad, prominent and tall R waves in V1-V2 (R≥S, R ≥ 40ms)
  4. V7-V9 ST elevation ≥ 0.05 mV
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19
Q

LMCA Occlusion

A
  1. ST elevation in aVR with diffuse (at least 8) ST depressions
20
Q

Wellen’s Syndrome

A
  1. Deeply-inverted or biphasic T waves in V2-3 (V1-V4) with or without ST elevation
  2. Suggests critical LAD occlusion
21
Q

De Winter’s T Waves

A
  1. Precordial ST-segment depression at the J-point
  2. Tall, peaked, symmetric T waves in the precordial leads
  3. Suggest LAD occlusion
22
Q

ECG localization of STEMI

A
  1. Anteroseptal (LAD, diagonal) -> V1-V2
  2. Anteroapical (distal LAD) -> V3-V4
  3. Anterolateral (LAD or LCX) -> V5-V6
  4. Lateral (LCX) -> I, aVL
  5. Inferior (PDA) -> II, III, aVF -> + in 1/3 RV ischemia
  6. Posterior (PDA) -> ST depressions in V1-V3 with tall R waves, V7-V9 ST elevation
  7. RV (RCA, acute/right marginal artery) -> VR3-VR4, suggested by eleviation of ST in V1
23
Q

Inferior wall STEMI

A
  1. RCA: mainly PDA and LCX (if dominant)
  2. ST eleviation in II, III, aVF
  3. Usually ST depression in I, aVL when RCA is dominant or V1-V3 when LCX is dominant
  4. Always exclude right-ventricular ischemia by RV leads (V2R-V6R) -> present in 1/3, suggested by eleviation of ST in V1
24
Q

Anterior wall STEMI

A
  1. Anteroseptal (LAD) -> V1-V2
  2. Anteroapical (distal LAD) -> V3-V4
  3. Anterolateral (LAD or LCX) -> V5-V6
  4. Usually with ST elevation in I, aVL
  5. Usually also ST depression in III, aVF
  6. LMCA Occlusion -> ST elevation in aVR with diffuse (at least 8) ST depressions
  7. proximal LAD -> V1-V4 (or to V6), I, aVL
25
Q

Progression of STEMI ECG waves and segements with time

A
  1. Increase in T wave amplitude, tombstoning
  2. ST elevation -> Pardee waves
  3. Q waves (takes several hours to days to develop) and decreasing R wave amplitude
  4. Invertion of T waves (negative), ST return to isoelectric
26
Q

Posterior wall previous infaction

A
  1. Nondominant LCX

2. V1 and V2 abnormally large R waves

27
Q

Heart amyloidosis ECG

A
  1. Low voltage of all waveforms in the limbs leads
  2. Marked left-axis deviation (LAFB)
  3. Pseudo infact changes
  4. A prolonged AV conduction time
28
Q

Acute pericarditis ECG

A

STAGE 1 -> because inflammation involves epicardial myocardium

  1. Widespread ST elevations, often horizontal or upward
  2. Upright T waves
  3. PR depression (50%)

STAGE 2

  1. ST return to normal
  2. T waves become inverted
29
Q

Pericardial effusion and chronic constriction ECG

A
  1. Low voltage
  2. Widespread ST-elevation
  3. Total electrical alternans -> alternating high and low voltages of all ECG waveforms between cardiac cycles within a given lead
  4. T-wave inversion
  5. AF in 1/3
30
Q

Cor Pulmonale (Pulmonary hypertension, RV overload features) ECG

A
  1. RV dilation/ hypertrophy
  2. RBBB
  3. Rightward axis devation
  4. P pulmonale
31
Q

PE ECG

A
  1. Tachycardia
  2. Nonspecific ST and T changes
  3. Negative T waves in V2-V4
  4. QR in V1
  5. SIQIIITIII -> rarely
  6. Acute Cor Pulmonale, RV overload -> rarely, in massive PE
32
Q

COPD and emphysema (chronic cor pulmonale) ECG

A
  1. Tall P waves in leads II, III and aVF
  2. Prolonged PR and ST depression in II, III and aVF
  3. Dextrogram
  4. Low voltage of QRS in precordial leads (especially V4-6)
33
Q

Intracranial hemorrhage ECG

A
  1. Widening and inversion of T waves in precordial leads
  2. Prolongation of QTc
  3. Bradyarrhythmias
34
Q

Hypothyroidism in ECG

A
  1. Low voltage of all waveforms
  2. Widespread inverted T waves without ST devation
  3. Sinus bradycardia (PR and QT prolongation)
35
Q

Hyperthyroidism in ECG

A
  1. Increased amplitude of all waveforms

2. Sinus tachycardia or AF

36
Q

Hypothermia in ECG

A
  1. Osborn waves -> deflections at the J point at the same direction as QRS complex -> height roughly proportional to the degree of hypothermia
  2. PR and QT prolongation
  3. Widening of QRS
37
Q

Hypokaliemia in ECG

A

LUFTP -> Low K - U waves, Flattened T, Prolongation of QTc

  1. Flattening or invertion of T wave
  2. ↑ prominence of U waves
  3. ↑ of QTc (and sometimes PR interval)
  4. Slight depression of ST segment

-> hyperpolarization
+ often premature beats and sustained tachyarrhythmias, tordases de pointes
ALKALOSIS

38
Q

Hyperkaliemia in ECG

A
  1. Tall, peaked T waves (from 5.5 mM)
  2. Loss or flattening of P waves (from 6.5 mM)
  3. Widened QRS (from 7 mM)
  4. ↓ of QTc
  5. ↑ of PR
  6. Sine wave appearance (K levels 7-8 mM)

-> decrease of potential, AV blocks, VF, Asystolia
ACIDOSIS

39
Q

Hypocalcemia in ECG

A
  1. ↑ QTc

2. Sometimes with terminal T wave inversion

40
Q

Hypercalcemia in ECG

A
  1. ↓ QTc

2. Extreme -> increased amplitude of QRS

41
Q

Digitalis effect on ECG

A
  1. Coved ST-segement depression -> “Salvador Dali sagging” appearance
  2. Flattened T wave
  3. ↓ QTc interval
42
Q

Tricyclic Antidepressant (TGA) ECG

A
  1. Wide QRS complex

2. ↑ of QTc

43
Q

Class 1 Antiarrhythmics on ECG

A

1A -> ↑ of QTc, ↓ T wave and ↑ U wave amplitude toxicity -> prolongation of QRS
1B -> usually no effect on ECG
1C -> broadening of QRS, without affecting interval between J point and T wave

44
Q

Class 2, 3, 4 Antiarrhythmics on ECG

A 
2 and 4 -> sinus bradycardia, ↑ PR
3 -> ↑QTc (Amiodaron has class 1, 2, 3 effect)
45
Q

Low voltage of ECG

A

total amplitude of QRS < 0.7 mV in all limb and < 1 mV in all precordial

History taking and physical examination (12 decks)

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