Ekgs

Front 1

how might you calculate the the voltage criteria in LVH (left ventricular hypertrophy)

Back 1

look at S in V1 and R in V5 and if it is over 35 then you probably have LVH

Front 2

what kind of AV block involves a prolonged PR interval and continuously declining frequency of QRSs

Back 2

first degree

Front 3

what happens in LV hypertrophy to the ST segment

Back 3

ST strain
hypertophy produces ST segment depression (subendocardial hypoxia in the hypertophied ventricle)

Front 4

why might you get an enlarged P wave's negabie component in V1 with LVH

Back 4

due to left atrial enlargement (LAE)
it is defined if the P wave is negative in V1 at least 1mm deep and at least .04 seconds long)
if the you have RVH then the initial (positive component) of the P wave would be larger.
remember diphasic P waves are a sign of hypertrophy

Front 5

what happens to the QRS duration in LVH

Back 5

it is greater than .09 seconds

Front 6

each criteria for LVH is assigned points. There are 6 criteria. what are they and how many points is assigned to each

Back 6

1. voltage criteria - 3pts
2. ST depressoin - 3 pts
3. LAE - 3 pts
4. L axis devation - 2 pts
5. QRS duration over .09 sec - 1 pt
6. intrinsicoid deflection - 1 point
if points are over 4 is probable LVH and if its 5 pts - it is definated as LVH

Front 7

what kind of deviation do you get with RVH

Back 7

Right axis deviation (negative QRS in lead I)

Front 8

how do evaluate the voltage in RVH

Back 8

you compare the relative sizes os R and S waves in V1 and V6. the waves will be great in right leads should be greater

Front 9

what is the right ventricular "strain" pattern

Back 9

ST-T depression in right sided leads

Front 10

explain what is meant by a Q wave infarction

Back 10

a pathological Q wave is one that is at least .04 seconds wide and at least 1/4the the magnitude of the remaining R wave. An infarct large enough to produces this is called a Q wave infarction or an transmural infarction.
a small infarct is called a non-Q wave or nontransmural infarction.

Front 11

an Anterior MI (Left anterior descending artery) will produce pathological Q waves in what leads

Back 11

V1 - V4

Front 12

An inferior MI involves what artery and produces pathological Q waves in what leads

Back 12

posterior descending artery

pathological Q waves in II, III, aVF

Front 13

A lateral MI involves what artery and produces pathological Q waves in what leads

Back 13

I,aVL, V5, V6

Front 14

how does infarcted muscle versus ischemic muscle affect an ECG differently

Back 14

infarcted muscle is dead - it has large Q wave and possible St elevation. ischemic mscle is still viable and will show depression of the ST (also in subendocardial infarct)

Front 15

5 causes for spontaneous depolarization of the His Purkinje fibers (fast fibers)

Back 15

1. Increased Sympathetic Tone (drugs, anxiety, etc)
2. Hypolalemia
3. Hypoxia or ischemia
4. Digitalis toxicity
5. Atrial Enlargement

Front 16

what ST segment characterisitic is seen in someone with typical angina

Back 16

ST-depression - sign of subendocardial ischemia.

Front 17

T wave inversion happens when?

Back 17

with ischemia (symmetrical)
LVH (assymetrical)

Front 18

how do you check for a BBB

Back 18

look for RR' in right (v1,v2)and left chest leads (v5,v6)

Front 19

what is the first sign of transmurel ischemia

Back 19

a peaked symmetrical T wave

also seen in hyperkalemia

Front 20

a q wave indicating necrosis would have what measurements on an ECG

Back 20

at least 1 mm wide and 1/3 the amplitude or more of the QRS

Front 21

what EKG characterisitics persist after an infarction

Back 21

T wave inversion disappears over months and Q waves remain as evidence of prior infarction

Front 22

W/ a LBBB you would see a wide positive QRS (>.12 seconds)with RR' in what chest leads

Back 22

V5 and V6

for a RBBB you would look for this in V1 and V2

Front 23

LBBB can mimic on the EKG what other three differential diagnosis

Back 23

LVH
anterior infarction
inferior infarction
so these diagnosis cannot be made in the presense of LBBB

Front 24

in order to make the diagnosis of a BBB you need a QRS that is at least how many squares wide

Back 24

3 (.12 secs)

Front 25

what chest lead do you want to check first if you suspect hypertrophy

Back 25

v1
P waves for atrial H
R waves for RVH
S waves depth in V1 + R wave in V5 for LVH

Front 26

what are the two left chest leads

Back 26

V5 and V6

Front 27

If there is a R,R' in the right chest leads V1 and V2 then there probably is a

Back 27

Right Bundle Branch Block

Front 28

The EKG pattern for RBBB and LBBB can often be confused with what other EKG detectable pathology

Back 28

the ventricular complexes in Ventricular tachycardia

Front 29

if the P wave is diphasic then we know

Back 29

there is atrial enlargement

or even if the P wave is not diphasic if it is higher than 2.5 mm

Front 30

if the initial componenet of diphasic P wave in lead V1 is larger than the terminal portion then what atria is enlarged

Back 30

right

if the terminal portion is larger in V1 then its left atrial enlargment

Front 31

In V1 - which is larger the S wave or the R wave

Back 31

S (pointing down). The R wave is small. Of course if you have Right ventricular hypertrophy you will have a large R wave pointing up

Front 32

what does Reentry mean

Back 32

premature stimulus reaches two pathways of differing excitability.

Front 33

In pts with Wolff-Parkinson-White (WPW) syndrome what two pathways are present and which one is slow vs fast and shoter vs longer refractory

Back 33

1. A-V node (slow conduction velocity and shorter refractory period)
2. Bundle of Kent is fast conduction and longer refractory period

Front 34

what does the "delta wave" represent?

Back 34

in pts with WPW. the bundle of kent conducts fast and the A-V node conduction follows shortly after via the normal His Purkinje route

the two wave fronts merge, producing a "fusion beat"

Front 35

what is the most common trigger of WPW circuit

Back 35

atrial premature beat APB

Front 36

how might the impulse in WPW go back to conducting down the right pathway

Back 36

if when the impulse arrives at the A-V node the bypass tract is still in a refractory period (it does have a longer refractory period) then the abnormal impulse will be forced to travel back through the A-V node.

if then the normal impulse which is slower reaches the Av node (which is now in repolarization) it will propagate retrogradely back to the atrium

Front 37

why might you see an inverted P wave in lead II in pts with WPW

Back 37

backward depolarization of the atrium. the slow normal impulse reaches the AV node but the AV node is still in the refractory period due to early depolarization by the faster abnormal impulse which has reached the node first. t

Front 38

Why is PSVT sustainable over days (150-250)

Back 38

slow AV nodal conduction makes the re-entrant tachycardia possible because it allows enough time for each part of the circuit to recover excitability before the impulse reaches it. -

Front 39

three conditions for all re-entrant tachycardias

Back 39

1. anatomically distinct pathways
2. slow conduction
3. Diff refractory periods

Front 40

how might you terminate an AV nodal reentrant tachycardia?

Back 40

carotid massage
drugs (AV nodal blockers) which usually work by shortening the refractory period