EKG Changes Flashcards

Question

Electrolyte changes - NOT done, will be many slides. Go to the other parts of OneNote to complete this one (NOT the master EKG page for these)

Answer 1

A

Reciprocal changes from ST elevation MI use the mnemonic PAILS:
- Posterior STEMI → Anterior ST depression
- Anterior STEMI → Inferior ST depression
- Inferior STEMI → Lateral ST depression
- Lateral STEMI → Septal ST depression
Septal STEMI → Posterior ST depression

‘PAILS’ = Posterior, Anterior, Inferior, Lateral, Septal leads:
- if see ST elevation in A (anterior leads), look for reciprocal ST depression in next letter over, I (inferior leads). Means MI due to LAD.
- Same story w/others. Read it P→S.
Don’t worry about ‘Posterior’ part yet.

Answer 2

A

Axis Deviation:
Hand method:

Hold both hands up like “don’t shoot”
- Left hand = Lead I
- Right hand = Lead aVF
- (-) QRS in that lead = move hand down in that lead

□ Normal = both hands up
□ LAD = only left hand up
□ RAD = only right hand up
□ SRAD = both hands down

Nml -30 → +90
LAD -30 → -90
RAD +90 → ±180
SRAD ±180 → -90

Answer 3

A

Atrial enlargement (both RAE and LAE) -

Look at P WAVE
▪ Lead II = parallel to P wave, so large ⊕ deflection;
▪ Lead V1 = ⊥ to P wave, so biphasic deflection, so easily separate right & left atrial components

Answer 4

A

*common cause: severe lung disease
*rightie tallie, and “fit tall ‘P’ under tall P wave”

1) P > 0.25mV i.e. 2.5 small boxes [inferior leads: II, III, aVF]
2) P > 0.1mV [septal leads: V1 or V2]
3) Possible RAD

Answer 5

A

*common cause: mitral valve disease
*lefty long, and “fit long ‘M’ under long P wave

1) Notched P > 0.12sec [inferior leads]
2) P negative terminal force component (2nd half; downward part of biphasic V1 wave) > 1x1 boxes [V1]
3) NOT usually see any axis deviation, cuz LA is already normally electrically dominant

Answer 6

A

Ventricular Hypertrophy (both RVH and LVH)

look at QRS COMPLEX

A few important notes:
- BBB precludes the Dx of Ventricular Hypertrophy - BBB’s affect size & appearance of R waves, so criteria for
- Ventricular Hypertrophy can NOT be diagnosed by EKG if BBB is present
Additionally, Dx of MI can be extremely difficult in presence of LBBB

Answer 7

A

*think of COPD, uncorrected congenital HD

1) RAD > +100° - especially note that lead I QRS must be more [-] than ⊕
2) Diminished or reversed R-wave progression - R waves larger as progress V5→V1, instead of normal V1 (smallest) → V5 (largest). Similarly:
- R>S [V1], and S>R [V6] (“SR6” sounds like sports car)
- R > 0.7mV [V1]

Answer 8

A

*think systemic HTN, valvular disease

Key points:
- The left ventricle hypertrophies in response to pressure overload secondary to conditions such as aortic stenosis and hypertension
- There are numerous voltage criteria for diagnosing LVH, summarized below
- The most commonly used are the Sokolow-Lyon criteria: Sum of (S wave depth in V1 or V2) + (tallest R wave height in V5 or V6) is > 35 mm
- Voltage criteria must be accompanied by non-voltage criteria to be considered diagnostic of LVH:
LV ‘strain’ pattern: ST segment depression and T wave inversion in the left-sided leads

Answer 9

A

AVB (Atrioventricular Block)
- 1st Degree AVB
- 2nd Degree AVB:
Mobitz Type I (Wenckebach)
Mobitz Type II
- 3rd Degree AVB

Answer 10

A

PR Interval > 0.2 sec, but P:QRS still 1:1

Answer 11

A

PR widens with each beat until you skin (“drop”) a beat

Usually a certain ratio of P:QRS, such 3:2 or 4:3 (ie, 3 P’s for every 2 QRS’s)

Treatment:
- if ASYMPTOMATIC, then NO TREATMENT!
- if YES symptoms, then treat reversible causes (eg, electrolyte abnormalities), and if no reversible causes then place a PACEMAKER

Answer 12

A

Normal, constant PR that is NOT >0.2 sec, and it does NOT widen with each beat (so not 2nd degree Mobitz type I [Wenkcebach])

ACUTE treatment:
- if stable, then just monitor with transcutaneous pads IN PLACE but NOT pacing
- if hemodynamically UNSTABLE, then +/- beta blockers with transcutaneous or transvenous pacing, and treat anything like coronary ischemia

CHRONIC treatment:
- if NO reversible causes are identified (and treated, with resolved of the Mobitz Type II), then PERMANENT PACEMAKER

Answer 13

A

aka Complete heart block. Complete electrical dissociation of the atria and ventricles

Answer 14

A

STABLE 3rd degree AVB ==> PPM (permanent pacemaker)

UNSTABLE 3rd degree AVB:
1) Atropine
2) Transcutaneous pacing
3) Dopamine gtt at 5 mcg/kg/minute, up to 20
4) Dobutamine gtt at 2 to 5 mcg/kg/minute, up to 20
5) Transvenous pacing - this is really where you’re going anyways, cuz the second you start transcutaneous pacing you’re starting to place a central line so that you can get the more reliable transvenous pacing going

Answer 15

A

William Marrow
- Rabbit Ears RSR1’s

Answer 16

A

1) LBBB
2) RBBB
3) LAFB / Anterior Hemiblock
4) Posterior Hemiblock of Left Bundle (NOT commonly discussed)
5) Bifasicular Block = RBBB + Anterior or Posterior Hemiblock

note: Right Bundle (RB) does NOT divide into separate fascicles. Therefore, “HB” only applies to Left Bundle (LB)

Answer 17

A

Right Bundle (RB) does NOT divide into separate fascicles. Therefore, “HB” only applies to Left Bundle (LB)

Unlike a full on RBBB or LBBB in which the QRS is > 0.12 sec, with Anterior and Posterior HB the QRS is normal

Anterior HB (LAFB) = LAD with no other cause of LAD present
- Normal OR diseased hearts

Posterior HB = RAD with no other cause of RAD present
- ONLY diseased hearts

Answer 18

A

Combo of a RBBB plus either an Anterior or Posterior HB. So it’s going to have a WIDE QRS and RSR’ in V1 or V2 (the RBBB), and LAD (for LAFB) or RAD (for posterior HB)

RBBB + anterior HB:
- QRS widened > 0.12sec
- RSR’ (V1, V2)
- LAD

RBBB + posterior HB:
- QRS widened > 0.12 sec
- RSR’ (V1, V2)
- RAD