2013-08-28&29 Electrophysiology and EKG Interpretation

Question 0

What factors alter speed of SA firing?

Answer 0

Sped up by: sympathetic stimulation; parasymp antagonism (vagal blockade)

Slowed down by: vagal stim; symp blockade; Ca2+ channel blockers (verapamil and diltiazem but not nifedipine)

Question 1

What makes P-cells unique?

Answer 1

Slow fiber conduction in SA and AV nodes. Made possible by Ca2+.

Question 2

What makes fast conduction fibers unique?
What moves in each phase?
Which part of the EKG is associated with each phase?

Answer 2

Found in His-Purkinje

0) fast Na+ influx = depolarization = QRS
1) small K+ efflux
2) Ca2+ influx = plateau (allows for muscle contraction) = ST
3) K+ efflux depolarization = T wave
4) RMP maintained by Na/K ATPase

Question 3

Normal vs. abnormal His-Perkinje automaticity

Answer 3

normal H-P automaticity occurs when there is no AP delivered from either the SA or AV nodes;

abnormal H-P automaticity occurs with: hypoxia, digitalis toxicity, hypokalemia

Question 5

What is a normal P-R interval?

Answer 5

< 0.20 sec (one large square)

**If any longer = 1° heart block

Question 6

What is a normal Q-T interval?

Answer 6

Q-T interval should be < 1/2 R-R interval=

**Longer may mean Hereditary Long Q-T Syndrome

Question 7

Normal QRS duration?

Answer 7

< 0.12 sec (3 small squares)

**Longer = BBB

Question 8

Which two leads do you look at for deviation? What’s the trick to do it quickly? How do you determine degrees of deviation?

Answer 8

Look at I and aVF w/ “thumb test”:

• -both thumbs up = nl
• -left up, right down = L.A.D.
• -left down, right up = R.A.D.
• -both down = extreme R.A.D.

You can use trig by measuring the net deflection in I and aVF to calculate OR look for most isoelectric limb lead and refer to a cheat sheet.

Question 9

Findings of LAE?

Answer 9

Left Atrial Enlargement:

• -V1: depth of 2nd half of biphasic P is >1mm deeper and >1mm long
• -II: P duration >0.12

Question 10

Findings of RAE?

Answer 10

Right Atrial Enlargement;

• -V1: height of 1st half of biphasic P is increased; (if >2.5mm in any limb lead suspect RAE)
• -II: P is >3mm tall

Question 11

Which leads for BBB? What general finding?

Answer 11

V1 (or V2) and (V5 or) V6
QRS ≥ 0.12sec
R, R’ pattern

Question 12

LBBB findings

Answer 12

• *mimics LVH and inferior wall infarct
  1. QRS ≥ 0.12s
  2. bunny ears (R, R’) in left chest leads (V5 and V6)

Question 13

RBBB findings

Answer 13

1. QRS ≥ 0.12s

2. valley (R-S-R’) in right chest leads (V1 or V2)

Question 14

What are the fasicles?

Answer 14

1. The RBBB
2. the Ant. Div of the LBBB
3. The Post Div. of the LBBB

Question 15

(Left) Anterior hemiblock

Answer 15

LAD
Q1S3
nl or slightly wide QRS

Question 16

(Left) Posterior hemiblock

Answer 16

R.A.D.
S1Q3
nl or slightly widened QRS

Question 17

LVH findings?

Answer 17

S1 depth + R5 height ≥ 35mm (Dubin Criteria)

• -incr QRS voltage in I, aVL, V5 and V6
• -“strain pattern” = ST-depression over affected area(s)
• -(maybe L.A.D. and/or LAE)

Question 18

RVH findings?

Answer 18

R.A.D.

• -incr QRS voltage esp. in R chest leads (V1 and V2) w/ R decreasing from V1->V6
• -“strain pattern” = ST-depression over affected area(s)

Question 19

pathologic Q wave

Answer 19

= transmural infarction

will be ≥ 0.04sec (one small box) and at least 1/4 the height of the R wave

Question 20

Anterior Infarct - artery? see Q waves in?

Answer 20

Anterior Descending Br of L coronary a.

–Q waves in V1-V4

Question 21

Inferior Infarct - artery? see Q waves in?

Answer 21

Posterior descending branch (of RCA in 90% of pts)

–Q waves in II, III, aVF

Question 22

Lateral infarct - artery? see Q waves in?

Answer 22

Circumflex branch of LCA

–Q waves in I, aVL, V5, V6

Question 23

Infarction vs. Ischemia

Answer 23

Infarction = dead tissue w/ hallmark Q wave
ischemia = still viable; ST depression or elevation

Question 24

What causes ST changes?

Answer 24

Ischemia interferes with ATP-dep K+ and Ca2+ pumps

**Don’t understand super well!

Question 25

ST depression vs. elevation

Answer 25

ST-depression = subendocardial ischemia; created when ischemic tissue is behind normal tissue

• -similar to the “strain pattern in LVH” which likely also is due to ischemia;
• -also seen in V5/V6 in LBBB

ST-elevation = transmural ischemia; created when ischemic tissue is in front of nl tissue

• *will be more bowed upward in acute MI
• -also seen in V1/V2 of LBBB;
• -also seen in pericarditis w/ STE in multiple leads not confined to a coronary territory

Question 26

What is the progression of changes in STEMI?

Answer 26

secs: ST-depression - subendocardial ischemia
mins: Peaked T - earliest sign of transmural ischemia

mins-hrs: ST-elevation - acute transmural ischemia, still potentially reversibly though usually progresses to infarct

hrs: ST-elev + T-inver - subendocard has infarcted

hrs-days: ST-elev + T-inver + Q-wave - transmural infarct

months: ST-elev goes away, still have T-inver and Q-wave
years: T-inver goes away, still have Q-waves

Question 27

What is the standard approach to EKG interpretation?

Answer 27

1. Rate - tachy if >100, brady if = incr risk of V tach)
2. Axis - deviation (I and aVF; to ° of ∆: find isoelectric limb lead and use chart); rotation (find iso chest lead; should be V3/V4)
3. Hypertrophy - P wave for LAE/RAE; R Wave in V1-V4 for RVH; S1 + R5 for LVH)
4. Infarction: Look for ST-dep, ST-elev, T-inver, and Q-waves in all leads

Question 28

What causes ST changes in

Answer 28

myocytes depolarize in diastole

1. less O2, less ATP, less Na/K-ATPase
2. leakage of K+ out of cells which depolarizes them (not 100% sure why) and causes arrhythmias, conduction problems and EKG ∆s
   - –EKG ∆s because you are making a dipole: the depolarized cells and the polarized cells
   * *ST elevation is ACTUALLY depression of everything else!

Question 29

What are classical signs of a positive stress test?

Answer 29

subendocardial ischemia causes ST-depression