ECG Midterm (Ben) Flashcards
What are the signs of necrosis in MCI?
- Pathological Q waves
- QS complexes
- Poor R progression
What are the criteria for a pathological Q wave in MCI?
- longer than 0.04 sec
- greater than 0.4 mV
- greater than 25% size of R wave
Where is it normal to see QS complexes?
aVR and V1
How does “poor R progression” look in MI?
What kind of MI might it indicate?
- R waves remain very small in V3/4
- Rs are a bit bigger, but still smaller than expected in V5/6
- can indicate actue anterior MI even in the absence of pathological Q waves
What is the main sign of lesion in the progression of an MCI?
(How does it often look? In what leads?)
ST elevation
- often as T-en-dome in various leads__
- inverse in aVL
- may have clear S wave
What is the main sign of ischemia in MCI progression?
How is this sign different in different stages?
T wave abnormalities
- hyperacute - high Ts hidden “en dome”
- acute - biphasic Ts
- subacute - coronary T (img below)
- old - inverse T
What are the 4 stages of MI progression as seen in an ECG?
And their approximate durations?
- Hyperacute - symptom onset until ~4 hours
- Acute - first 48-72 hours
- Subacute - 10 days
- Chronic/End-stage/Old/Definitive - past 10 days
What are the signs of hyperacute stage MI progression?
Ischemia and lesion only, so…
- ST elevation + T abnormality = T-en-dome
What are the ECG signs of acute stage MI?
Necrosis has begun, so…
- Pathological Q waves + poor R progression
- T-en-dome
- Sometimes biphasic T dips down after the “dome”
What is the ECG sign of subacute stage MI?
Necrosis has leaked K+ into the tissues, leading to…
- Coronary T waves - deep, peaked, symmetrical
- less lesion may mean less ST elevation
What are the ECG signs of definitive/old MI?
K+ elevation subsides, so…
- Coronary T disappears, but…
- Ischemia = primary repolarization abnormalities, including flat/negative Ts
- Necrosis = persistent patho-Q waves and smaller R waves in V3-6
Where can inferior infarcts be seen?
Occlusion of what artery usually causes them?
Other things to note with inferior infarcts?
leads II / III / aVF
occlusion of RCA
(reciprocals in anterior/left leads)
(Q waves may not persist)
Where can lateral infarcts be seen?
Occlusion of what artery usually causes them?
leads I / aVL / V5 / V6
(may see reciprocals in inferior leads)
circumflex artery occlusion
Where can anterior infarcts be seen?
How might they appear different than infarcts elsewhere?
Occlusion of what artery causes them?
in precordial leads, will see poor R progresson
may not see pathological Q waves
may see reciprocals in inferior leads
LAD occlusion
Where can posterior infarcts be seen?
They are often seen with what else?
reciprocal signs in precordial leads
(especially V1)
often seen with inferior infarcts (because both supplied via RCA)
What are the normal ID times in leads V1/V2?
in V5/V6?
What can prolongation mean?
- V1/2 - 0.04 sec
- V5/6 - 0.06 sec
- prolongation means BBB in the corresponding side (V1/2 = RBBB, V5/6 = LBBB)
How can LV hypertrophy be confirmed?
Sokoloff Index
- biggest R in V5/6 + deepest S in V1/2
- biggest R + deepest S > 3.5 mV (35 mm)
- (or axis < 10 degrees with positive aVL > 2 mV)
What are the signs of LBBB?
- wide QRS (> 0.12 s)
- broad/notched R waves in I + aVL
- broad rS or QS complexes in V1-4
What are the signs of RBBB?
- wide QRS
- M complex (rSR’) and ID > 0.04 s in V1/V2
- deep, wide S in left lateral leads
What is seen in any kind of BBB?
- wide QRS (≥ 0.12 sec)
- secondary repolarization abnormalities
- supraventricular impulses
- (differentiate it from PVCs / V.Tach)
How long is a normal QT interval?
0.35 - 0.44 seconds
What do polymorphic P waves of 3 or more forms indicate?
Multifocal Atrial Tachycardia if > 100 bpm
Wandering Atrial Pacemaker if < 100 bpm
How can an incomplete BBB appear on ECG?
BBB wave morphology (M complex or notched Rs) without the usual QRS wideness
What are the two types of WPW syndrome and how are they differentiated?
Look at V1, if QRS is…
- negative = Type B = bundle on right
-
positive = Type A = bundle on left
- (remember “apple”, APL = A-Positive-Left)
What is the ID point?
And ID time?
- ID point - where the QRS turns down for the last time
- ID time - interval btwn start of QRS and ID point, indicating how long ventricular depol. takes to reach the area of the heart under the electrode in question
- ID time can help diagnose BBBs or ventricular hypertrophy
What are the normal ID times for…
right side chest leads (V1/2)
left side chest leads (V5/6)
- Right-side: < 0.04 s
- Left-side: < 0.06 s
What 3 things can cause a discordant T wave?
- Normally repolarization occurs subepi- to subendocardially, opposite the direction of depolarization, resulting in a positive T wave…
- Depolarization of subepicardium first - as seen in VPC, then repolarization follows in same direction and T wave is opposite QRS
- Ion channel functional change - as in ischemia/angina, changing the variation in subepi-/subendo- AP length that normally results in proper repolarization directionality
- K+ channel composition change - as seen in cell stress, showing up as coronary T in subacute infarct, develops slowly + lasts longer
What is the acronym for causes of arrhythmia?
HIS DEBS
- Hypoxia - makes myocardium irritable
- Ischemia/Irritability - MCI/angina/ viral myocarditis
- Sympathetic Stim. - hyperthyroid/stress/exercise
- Drugs - esp. antiarrhythmics
- Electrolyte Issues - esp. hypokalemia
- Bradycardia - ex: sick sinus syndrome
- Stretch - hypertrophy/dilation
What causes atrial flutter?
How does it look and why?
- Usually via re-entry cycle around tricuspid
- P wave direction depends on direction of cycle rotation
- Shows 250-300 P waves/min; most blocked by AV node
- Rythm is regular + block is usually 2:1
What causes atrial fibrillation?
How does it look and why?
- multiple re-entry circuits –> 500+ impulses/min
- no P waves –> “F waves”
- irregular random RR intervals
How does multifocal atrial tachycardia look and why?
- irregular and 100-200 bpm
- polymorphic P waves of at least 3 forms, b/c they originate from different foci
- sometimes has no visible Ps in limb leads
How does a “wandering atrial pacemaker” differ from multifocal atrial tachycardia?
it is < 100 bpm and usually has 2-3 consecutive beats per different P morphology
How does paroxysmal atrial tachycardia look?
Why does it occur?
- 100-200 bpm and regular
- Can have 2 forms:
- enhanced automaticity of an atrial ectopic focus (may see ramping up/down of HR)
- atrial re-entry circuit AKA “atypical atrial flutter” (starts abruptly)
How does paroxysmal supraventricular tachycardia look?
What usually causes it?
What are some of its ECG features?
And how can you treat it?
- 150-250 bpm + irregular
- via AV node re-entry loop (known as AV Nodal Re-entry Tachy, AVNRT)
- pseudo-R’ - in V1 due to a superimposed retrograde P wave
- pseudo-S - less common, lead II/III retrograde P buried in QRS
- treat with carotid massage
How does a premature ventricular contraction (PVC) look?
What usually follows it?
What is the name for it if it alternates with sinus beats regularly?
- a sudden, wide + abnormal QRS
- may not show in all leads, but most QRS > 0.12 s
- compensatory pause usually follows; an interpolated PVC may fall btwn 2 normally conducted beats
- 1-to-1 with normal beat = bigeminy, 2:1 trigeminy, etc.
- can trigger v.tach or v.fib during MI !
PVCs are fairly common, but when are they particularly dangerous (5 times … first 2 are most important)
- During MI - can trigger v.tach or v.fib
- R-on-T - when VPC R wave superimposes on previous T, can cause TdP Tachy
- Frequent - incr. chance of dangerous tachys
- Many consecutive - same
- Multiform - diff shapes/origins
How does ventricular tachycardia look?
What are its 2 forms based on duration + 2 forms based on ECG appearance?
- 100-200 bpm + can be slightly irregular
- 3 or more VPCs in a row = v.tach
- non-sustained = < 30 s; sustained = > 30s
- ECG can appear uniform (healed infarct) or polymorphic (acute ischemia/infarct, ion issues, long QT)
How does ventricular fibrillation look?
- can be coarse (ECG jerks around irregularly) or fine (ECG gently squiggles)
- no true QRS complexes seen
- is “preterminal” + requires cardiopulmonary resuscitation or defibrillation
How does Torsade de pointes tachycardia look?
How does it arise?
- a unique v.tach in which the QRS complexes “spiral” around the baseline, changing axis and amplitude
- preceded by short-long-short R-R sequence
- is set off when a PVT lands on the previous T wave (R-on-T), usually due to a long QT
What are 4 causes of long QT?
- Genetic
- Electrolyte - hypocalcemia/-kalemia/-magnesemia
- Acute MI - long QT develops during event
- Drugs - anti-arrhythmics, tricyclics, antifungals/antihistamines when taken with macrolides/quinolones
What is a 1st degree AV block?
- long PR (> 0.2 s)
- every P still creates a QRS
What is a 2nd degree, Mobitz Type 1/Wenckebach AV block?
- progressively longer PR eventually leading to a missed QRS
- due to a block within AV node
- usually every 3rd/4th P is blocked (3:2 or 4:3 ratio)
What is a 2nd degree, Mobitz Type 2 AV block?
- constant PR interval, often long, sometimes normal
- one unconducted P, sometimes in cycles but often variable
- block is below AV node
What is a 2nd degree, 2:1 type AV block?
- every second P is without a QRS
- often treated with pacemaker
- can also be considered a Mobitz 1 or 2 with 2:1 ratio (depending on whether PR is increasing or constant)
What is a 3rd degree AV block?
- no P waves conducted to ventricles (AKA “total” block)
- ventricles generate “escape rhythm” @ 35-45 bpm
- P waves have separate rhytm @ 60-100 bpm
- no relation between the two rhythms
What is a high degree AV block?
How is it distinguished from 3rd degree?
- blocking of consecutive P waves
- P:QRS ratio of 3:1 or higher
- results in very slow ventricular rate
- capture and fusion beats help distinguish it from 3rd degree
What are 3 important things to check when diagnosing an arrhythmia via ECG?
- Are normal P waves present?
- Are QRS complexes narrow?
- Are Ps and QRSs related?
In diagnosing arrhythmia via presence of normal P waves…
what can the various ECG signs indicate?
(3 things)
- Normal P waves - arrhythmia likely of atrial origin
- Abnormal P wave axis - indicates retrograde activation of atrial muscle (from atrial/nodal/ventricular focus)
- No P waves - indicates subatrial (nodal/ventr.) rhythm
In diagnosing arrhythmia via width of QRS complexes…
what can different widths indicate?
(2 things)
- Normal (<0.1 s) - origin of rhythm @ or above AV node
- Wide - origin of rhythm likely in ventricles (except in pre-excitation syndromes)
In diagnosing arrhythmia via P-QRS association…
what can different ECG signs indicate?
(2 things)
- When P + QRS are related: sinus/atrial rhythm origin
- When unrelated: “AV dissociation” … usually either 3rd degree AV block or v.tach
