ECG abnormalities 2 Flashcards
Inherited Arrhythmia Disorders
- LQTS - Long QT syndrome
- SQTS Short QT Syndrome
- The Brugada syndrome
- ARVC - Arrhythmogennic Right Ventricular Cardiomyopathy
- CPVT - Catecholaminergic Polymorphic Ventricular Tachycardia
LQTS types
- 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
- LQT2 -> KCNH2 gene mutation, potassium channel, bifid, low amplitude T waves
- LQT3 -> SCN5A mutation, sodium channel, long isoelectric ST segments with late-appearing T wave, sudden cardiac death during sleep
LQTS diagnosis
- Suspition -> cQT > 460 ms (usually > 480 ms)
- Rule out secondary causes of LQT
- Schwarz score (LQTS scale) > 3 or mutation of one of the responsible genes
Causes of LQT
- Genetic
- Electrolyte imbalance -> hypokalemia, Hypocalcemia, Hypomagnesemia
- Drugs: antyarrhythmic, Antibotics, Antipsychotics, H1 antagonists, other
- Cardiac conditions: MI, Cardiomyopathy, Myocarditis, bradycardia
- Endocrine: hypothyroidism, hyperparathyroidism, pheochromocytoma, hyperaldosteronism
- Intracranial disorder: SAH, stoke, thalamic hematoma, encephalitis, head injury
- Malnutrition
LQTS treatment and frequency and onset
1/2000, onset usually 5-15
- β-blokers (Nadolol, Propranolol)
- ICD
SQTS
- suspect when QT<360 ms (usually < 300)
- Cause: gain of function mutation of potassium channel or Ca channel -> more rapid repolarization
- Arrhythmias: AF, polymorphic VT, SCD
- treatment: Quinidine or Sotalol or ICD
Brugada syndrome ECG
-> 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
Brugada syndrome causes and diagnosis
- Mutations of sodium channel gene (most common SCN5A) -> predisposition for reentry
- Diagnosis: ECG, can wax and wane -> augmentation: sodium channel blockers: Flecainide, Ajmaline, Procainamide
- Cardiac arrest often in bed, at night, can be provoked by febrile illness
Brugada syndrome treatment
- Quinidine
- ICD
- Avoidance of drugs elevating ST
- Quick management of fever
ARVC
- Genetic fibrofatty replacement of cardiac muscle of RV -> reentry
- Inverted T waves or Epsilon wave in V1-3
- Most common arrhythmias: PVC, VT, VF
- Treatment: avoidance of sports, β-blokers, Amiodarone, ICD, ablation
CPVT
- Mutation of gen codung ryanodine receptore RyR2
- Onset in childhood with syncope due to polymorphic VT
- ECG: PVC, bidirectional VT
- Treatment: avoidance of physical exercise, β-blokers, ICD, left cardiac sympathetic denervation
Subendocardial ischemia typical leads
Typically in:
- leftward: I, aVL, V4, V5, V6
- 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)
Subendocardial ischemia ECG pattern
- ST depression >0,1 mV -> from J point horizontal or downsloping (upsloping can normal or abnormal when it remains depressed)
- 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)
ECG criteria for transmural ischemia
A) significant elevation of ST segment at J point:
- ≥ 0.1 mV in any lead exept V2 and V3
- 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
Eleviation of ST causes
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)
Equivalents of STEMI (signs allowing to diagnose STEMI without additional criteria)
- new LBBB with addition criteria
- Posterior MI
- LMCA Occlusion
- Wellen’s Syndrome
- De Winter’s T Waves
Equivalents of STEMI new LBBB criteria
LBBB criteria + 1 of:
- ST elevation ≥ 0.1 mV in a lead with upward QRS complex
- ST depression ≥ 0.1 mV in V1, V2, or V3
- 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
Posterior MI
- RCA (90%), LCX (10%)
- V2, V3 -> ST depression ≥ 0.05 mV
- Usually broad, prominent and tall R waves in V1-V2 (R≥S, R ≥ 40ms)
- V7-V9 ST elevation ≥ 0.05 mV
LMCA Occlusion
- ST elevation in aVR with diffuse (at least 8) ST depressions
Wellen’s Syndrome
- Deeply-inverted or biphasic T waves in V2-3 (V1-V4) with or without ST elevation
- Suggests critical LAD occlusion
De Winter’s T Waves
- Precordial ST-segment depression at the J-point
- Tall, peaked, symmetric T waves in the precordial leads
- Suggest LAD occlusion
ECG localization of STEMI
- Anteroseptal (LAD, diagonal) -> V1-V2
- Anteroapical (distal LAD) -> V3-V4
- Anterolateral (LAD or LCX) -> V5-V6
- Lateral (LCX) -> I, aVL
- Inferior (PDA) -> II, III, aVF -> + in 1/3 RV ischemia
- Posterior (PDA) -> ST depressions in V1-V3 with tall R waves, V7-V9 ST elevation
- RV (RCA, acute/right marginal artery) -> VR3-VR4, suggested by eleviation of ST in V1
Inferior wall STEMI
- RCA: mainly PDA and LCX (if dominant)
- ST eleviation in II, III, aVF
- Usually ST depression in I, aVL when RCA is dominant or V1-V3 when LCX is dominant
- Always exclude right-ventricular ischemia by RV leads (V2R-V6R) -> present in 1/3, suggested by eleviation of ST in V1
Anterior wall STEMI
- Anteroseptal (LAD) -> V1-V2
- Anteroapical (distal LAD) -> V3-V4
- Anterolateral (LAD or LCX) -> V5-V6
- Usually with ST elevation in I, aVL
- Usually also ST depression in III, aVF
- LMCA Occlusion -> ST elevation in aVR with diffuse (at least 8) ST depressions
- proximal LAD -> V1-V4 (or to V6), I, aVL
Progression of STEMI ECG waves and segements with time
- Increase in T wave amplitude, tombstoning
- ST elevation -> Pardee waves
- Q waves (takes several hours to days to develop) and decreasing R wave amplitude
- Invertion of T waves (negative), ST return to isoelectric
Posterior wall previous infaction
- Nondominant LCX
2. V1 and V2 abnormally large R waves
Heart amyloidosis ECG
- Low voltage of all waveforms in the limbs leads
- Marked left-axis deviation (LAFB)
- Pseudo infact changes
- A prolonged AV conduction time
Acute pericarditis ECG
STAGE 1 -> because inflammation involves epicardial myocardium
- Widespread ST elevations, often horizontal or upward
- Upright T waves
- PR depression (50%)
STAGE 2
- ST return to normal
- T waves become inverted
Pericardial effusion and chronic constriction ECG
- Low voltage
- Widespread ST-elevation
- Total electrical alternans -> alternating high and low voltages of all ECG waveforms between cardiac cycles within a given lead
- T-wave inversion
- AF in 1/3
Cor Pulmonale (Pulmonary hypertension, RV overload features) ECG
- RV dilation/ hypertrophy
- RBBB
- Rightward axis devation
- P pulmonale
PE ECG
- Tachycardia
- Nonspecific ST and T changes
- Negative T waves in V2-V4
- QR in V1
- SIQIIITIII -> rarely
- Acute Cor Pulmonale, RV overload -> rarely, in massive PE
COPD and emphysema (chronic cor pulmonale) ECG
- Tall P waves in leads II, III and aVF
- Prolonged PR and ST depression in II, III and aVF
- Dextrogram
- Low voltage of QRS in precordial leads (especially V4-6)
Intracranial hemorrhage ECG
- Widening and inversion of T waves in precordial leads
- Prolongation of QTc
- Bradyarrhythmias
Hypothyroidism in ECG
- Low voltage of all waveforms
- Widespread inverted T waves without ST devation
- Sinus bradycardia (PR and QT prolongation)
Hyperthyroidism in ECG
- Increased amplitude of all waveforms
2. Sinus tachycardia or AF
Hypothermia in ECG
- Osborn waves -> deflections at the J point at the same direction as QRS complex -> height roughly proportional to the degree of hypothermia
- PR and QT prolongation
- Widening of QRS
Hypokaliemia in ECG
LUFTP -> Low K - U waves, Flattened T, Prolongation of QTc
- Flattening or invertion of T wave
- ↑ prominence of U waves
- ↑ of QTc (and sometimes PR interval)
- Slight depression of ST segment
-> hyperpolarization
+ often premature beats and sustained tachyarrhythmias, tordases de pointes
ALKALOSIS
Hyperkaliemia in ECG
- Tall, peaked T waves (from 5.5 mM)
- Loss or flattening of P waves (from 6.5 mM)
- Widened QRS (from 7 mM)
- ↓ of QTc
- ↑ of PR
- Sine wave appearance (K levels 7-8 mM)
-> decrease of potential, AV blocks, VF, Asystolia
ACIDOSIS
Hypocalcemia in ECG
- ↑ QTc
2. Sometimes with terminal T wave inversion
Hypercalcemia in ECG
- ↓ QTc
2. Extreme -> increased amplitude of QRS
Digitalis effect on ECG
- Coved ST-segement depression -> “Salvador Dali sagging” appearance
- Flattened T wave
- ↓ QTc interval
Tricyclic Antidepressant (TGA) ECG
- Wide QRS complex
2. ↑ of QTc
Class 1 Antiarrhythmics on ECG
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
Class 2, 3, 4 Antiarrhythmics on ECG
2 and 4 -> sinus bradycardia, ↑ PR 3 -> ↑QTc (Amiodaron has class 1, 2, 3 effect)
Low voltage of ECG
total amplitude of QRS < 0.7 mV in all limb and < 1 mV in all precordial
