Y Pathophys I > ECG Midterm (Ben) > Flashcards

ECG Midterm (Ben) Flashcards

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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?

Study These Flashcards
A

0.35 - 0.44 seconds

22
Q

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

Study These Flashcards
A

Multifocal Atrial Tachycardia if > 100 bpm

Wandering Atrial Pacemaker if < 100 bpm

23
Q

How can an incomplete BBB appear on ECG?

Study These Flashcards
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?

Study These Flashcards
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
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
26
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**
27
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... 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
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
29
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
30
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
31
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
32
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
33
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)
34
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**
35
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 !
36
PVCs are fairly common, but when are they particularly dangerous (5 times ... first 2 are most important)
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
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)
38
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
39
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_
40
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
41
What is a **1st degree AV block**?
* long PR (\> 0.2 s) * every P still creates a QRS
42
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)
43
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_
44
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)
45
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
46
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
47
What are 3 important things to check when diagnosing an arrhythmia via ECG?
1. **Are normal P waves present?** 2. **Are QRS complexes narrow?** 3. **Are Ps** **and QRSs related?**
48
In diagnosing arrhythmia via presence of normal P waves... what can the various ECG signs indicate? (3 things)
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
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)
50
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
51
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