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Y Pathophys I > ECG Midterm (Ben) > Flashcards

ECG Midterm (Ben) Flashcards

1
Q

What are the signs of necrosis in MCI?

A
  • Pathological Q waves
  • QS complexes
  • Poor R progression
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2
Q

What are the criteria for a pathological Q wave in MCI?

A
  • longer than 0.04 sec
  • greater than 0.4 mV
  • greater than 25% size of R wave
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3
Q

Where is it normal to see QS complexes?

A

aVR and V1

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4
Q

How does “poor R progression” look in MI?

What kind of MI might it indicate?

A
  • 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
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5
Q

What is the main sign of lesion in the progression of an MCI?

(How does it often look? In what leads?)

A

ST elevation

  • often as T-en-dome in various leads_​_
  • inverse in aVL
  • may have clear S wave
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6
Q

What is the main sign of ischemia in MCI progression?

How is this sign different in different stages?

A

T wave abnormalities

  • hyperacute - high Ts hidden “en dome”
  • acute - biphasic Ts
  • subacute - coronary T (img below)
  • old - inverse T
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7
Q

What are the 4 stages of MI progression as seen in an ECG?

And their approximate durations?

A
  1. Hyperacute - symptom onset until ~4 hours
  2. Acute - first 48-72 hours
  3. Subacute - 10 days
  4. Chronic/End-stage/Old/Definitive - past 10 days
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8
Q

What are the signs of hyperacute stage MI progression?

A

Ischemia and lesion only, so…

  • ST elevation + T abnormality = T-en-dome
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9
Q

What are the ECG signs of acute stage MI?

A

Necrosis has begun, so…

  • Pathological Q waves + poor R progression
  • T-en-dome
  • Sometimes biphasic T dips down after the “dome”
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10
Q

What is the ECG sign of subacute stage MI?

A

Necrosis has leaked K+ into the tissues, leading to…

  • Coronary T waves - deep, peaked, symmetrical
  • less lesion may mean less ST elevation
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11
Q

What are the ECG signs of definitive/old MI?

A

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
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12
Q

Where can inferior infarcts be seen?

Occlusion of what artery usually causes them?

Other things to note with inferior infarcts?

A

leads II / III / aVF

occlusion of RCA

(reciprocals in anterior/left leads)

(Q waves may not persist)

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13
Q

Where can lateral infarcts be seen?

Occlusion of what artery usually causes them?

A

leads I / aVL / V5 / V6

(may see reciprocals in inferior leads)

circumflex artery occlusion

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14
Q

Where can anterior infarcts be seen?

How might they appear different than infarcts elsewhere?

Occlusion of what artery causes them?

A

in precordial leads, will see poor R progresson

may not see pathological Q waves

may see reciprocals in inferior leads

LAD occlusion

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15
Q

Where can posterior infarcts be seen?

They are often seen with what else?

A

reciprocal signs in precordial leads

(especially V1)

often seen with inferior infarcts (because both supplied via RCA)

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16
Q

What are the normal ID times in leads V1/V2?

in V5/V6?

What can prolongation mean?

A
  • V1/2 - 0.04 sec
  • V5/6 - 0.06 sec
  • prolongation means BBB in the corresponding side (V1/2 = RBBB, V5/6 = LBBB)
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17
Q

How can LV hypertrophy be confirmed?

A

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)
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18
Q

What are the signs of LBBB?

A
  • wide QRS (> 0.12 s)
  • broad/notched R waves in I + aVL
  • broad rS or QS complexes in V1-4
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19
Q

What are the signs of RBBB?

A
  • wide QRS
  • M complex (rSR’) and ID > 0.04 s in V1/V2
  • deep, wide S in left lateral leads
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20
Q

What is seen in any kind of BBB?

A
  • wide QRS (≥ 0.12 sec)
  • secondary repolarization abnormalities
  • supraventricular impulses
    • (differentiate it from PVCs / V.Tach)
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21
Q

How long is a normal QT interval?

A

0.35 - 0.44 seconds

22
Q

What do polymorphic P waves of 3 or more forms indicate?

A

Multifocal Atrial Tachycardia if > 100 bpm

Wandering Atrial Pacemaker if < 100 bpm

23
Q

How can an incomplete BBB appear on ECG?

A

BBB wave morphology (M complex or notched Rs) without the usual QRS wideness

24
Q

What are the two types of WPW syndrome and how are they differentiated?

A

Look at V1, if QRS is…

  • negative = Type B = bundle on right
  • positive = Type A = bundle on left
    • (remember “apple”, APL = A-Positive-Left)
25
Q

What is the ID point?

And ID time?

A
  • 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
26
Q

What are the normal ID times for…

right side chest leads (V1/2)

left side chest leads (V5/6)

A
  • Right-side: < 0.04 s
  • Left-side: < 0.06 s
27
Q

What 3 things can cause a discordant T wave?

A
  • Normally repolarization occurs subepi- to subendocardially, opposite the direction of depolarization, resulting in a positive T wave…
  1. Depolarization of subepicardium first - as seen in VPC, then repolarization follows in same direction and T wave is opposite QRS
  2. Ion channel functional change - as in ischemia/angina, changing the variation in subepi-/subendo- AP length that normally results in proper repolarization directionality
  3. K+ channel composition change - as seen in cell stress, showing up as coronary T in subacute infarct, develops slowly + lasts longer
28
Q

What is the acronym for causes of arrhythmia?

A

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
29
Q

What causes atrial flutter?

How does it look and why?

A
  • 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
30
Q

What causes atrial fibrillation?

How does it look and why?

A
  • multiple re-entry circuits –> 500+ impulses/min
  • no P waves –> “F waves”
  • irregular random RR intervals
31
Q

How does multifocal atrial tachycardia look and why?

A
  • 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
32
Q

How does a “wandering atrial pacemaker” differ from multifocal atrial tachycardia?

A

it is < 100 bpm and usually has 2-3 consecutive beats per different P morphology

33
Q

How does paroxysmal atrial tachycardia look?

Why does it occur?

A
  • 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)
34
Q

How does paroxysmal supraventricular tachycardia look?

What usually causes it?

What are some of its ECG features?

And how can you treat it?

A
  • 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
35
Q

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
  • 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 !
36
Q

PVCs are fairly common, but when are they particularly dangerous (5 times … first 2 are most important)

A
  1. During MI - can trigger v.tach or v.fib
  2. R-on-T - when VPC R wave superimposes on previous T, can cause TdP Tachy
  3. Frequent - incr. chance of dangerous tachys
  4. Many consecutive - same
  5. Multiform - diff shapes/origins
37
Q

How does ventricular tachycardia look?

What are its 2 forms based on duration + 2 forms based on ECG appearance?

A
  • 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)
38
Q

How does ventricular fibrillation look?

A
  • can be coarse (ECG jerks around irregularly) or fine (ECG gently squiggles)
  • no true QRS complexes seen
  • is “preterminal” + requires cardiopulmonary resuscitation or defibrillation
39
Q

How does Torsade de pointes tachycardia look?

How does it arise?

A
  • 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
40
Q

What are 4 causes of long QT?

A
  • Genetic
  • Electrolyte - hypocalcemia/-kalemia/-magnesemia
  • Acute MI - long QT develops during event
  • Drugs - anti-arrhythmics, tricyclics, antifungals/antihistamines when taken with macrolides/quinolones
41
Q

What is a 1st degree AV block?

A
  • long PR (> 0.2 s)
  • every P still creates a QRS
42
Q

What is a 2nd degree, Mobitz Type 1/Wenckebach AV block?

A
  • 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)
43
Q

What is a 2nd degree, Mobitz Type 2 AV block?

A
  • constant PR interval, often long, sometimes normal
  • one unconducted P, sometimes in cycles but often variable
  • block is below AV node
44
Q

What is a 2nd degree, 2:1 type AV block?

A
  • 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)
45
Q

What is a 3rd degree AV block?

A
  • 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
46
Q

What is a high degree AV block?

How is it distinguished from 3rd degree?

A
  • 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
47
Q

What are 3 important things to check when diagnosing an arrhythmia via ECG?

A
  1. Are normal P waves present?
  2. Are QRS complexes narrow?
  3. Are Ps and QRSs related?
48
Q

In diagnosing arrhythmia via presence of normal P waves…

what can the various ECG signs indicate?

(3 things)

A
  1. Normal P waves - arrhythmia likely of atrial origin
  2. Abnormal P wave axis - indicates retrograde activation of atrial muscle (from atrial/nodal/ventricular focus)
  3. No P waves - indicates subatrial (nodal/ventr.) rhythm
49
Q

In diagnosing arrhythmia via width of QRS complexes…

what can different widths indicate?

(2 things)

A
  • Normal (<0.1 s) - origin of rhythm @ or above AV node
  • Wide - origin of rhythm likely in ventricles (except in pre-excitation syndromes)
50
Q

In diagnosing arrhythmia via P-QRS association…

what can different ECG signs indicate?

(2 things)

A
  • When P + QRS are related: sinus/atrial rhythm origin
  • When unrelated: “AV dissociation” … usually either 3rd degree AV block or v.tach
51
Q
A

Y Pathophys I (3 decks)

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