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40 Cards in this Set

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  • Back
how might you calculate the the voltage criteria in LVH (left ventricular hypertrophy)
look at S in V1 and R in V5 and if it is over 35 then you probably have LVH
what kind of AV block involves a prolonged PR interval and continuously declining frequency of QRSs
first degree
what happens in LV hypertrophy to the ST segment
ST strain
hypertophy produces ST segment depression (subendocardial hypoxia in the hypertophied ventricle)
why might you get an enlarged P wave's negabie component in V1 with LVH
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
what happens to the QRS duration in LVH
it is greater than .09 seconds
each criteria for LVH is assigned points. There are 6 criteria. what are they and how many points is assigned to each
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
what kind of deviation do you get with RVH
Right axis deviation (negative QRS in lead I)
how do evaluate the voltage in RVH
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
what is the right ventricular "strain" pattern
ST-T depression in right sided leads
explain what is meant by a Q wave infarction
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.
an Anterior MI (Left anterior descending artery) will produce pathological Q waves in what leads
V1 - V4
An inferior MI involves what artery and produces pathological Q waves in what leads
posterior descending artery

pathological Q waves in II, III, aVF
A lateral MI involves what artery and produces pathological Q waves in what leads
I,aVL, V5, V6
how does infarcted muscle versus ischemic muscle affect an ECG differently
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)
5 causes for spontaneous depolarization of the His Purkinje fibers (fast fibers)
1. Increased Sympathetic Tone (drugs, anxiety, etc)
2. Hypolalemia
3. Hypoxia or ischemia
4. Digitalis toxicity
5. Atrial Enlargement
what ST segment characterisitic is seen in someone with typical angina
ST-depression - sign of subendocardial ischemia.
T wave inversion happens when?
with ischemia (symmetrical)
LVH (assymetrical)
how do you check for a BBB
look for RR' in right (v1,v2)and left chest leads (v5,v6)
what is the first sign of transmurel ischemia
a peaked symmetrical T wave

also seen in hyperkalemia
a q wave indicating necrosis would have what measurements on an ECG
at least 1 mm wide and 1/3 the amplitude or more of the QRS
what EKG characterisitics persist after an infarction
T wave inversion disappears over months and Q waves remain as evidence of prior infarction
W/ a LBBB you would see a wide positive QRS (>.12 seconds)with RR' in what chest leads
V5 and V6

for a RBBB you would look for this in V1 and V2
LBBB can mimic on the EKG what other three differential diagnosis
LVH
anterior infarction
inferior infarction
so these diagnosis cannot be made in the presense of LBBB
in order to make the diagnosis of a BBB you need a QRS that is at least how many squares wide
3 (.12 secs)
what chest lead do you want to check first if you suspect hypertrophy
v1
P waves for atrial H
R waves for RVH
S waves depth in V1 + R wave in V5 for LVH
what are the two left chest leads
V5 and V6
If there is a R,R' in the right chest leads V1 and V2 then there probably is a
Right Bundle Branch Block
The EKG pattern for RBBB and LBBB can often be confused with what other EKG detectable pathology
the ventricular complexes in Ventricular tachycardia
if the P wave is diphasic then we know
there is atrial enlargement

or even if the P wave is not diphasic if it is higher than 2.5 mm
if the initial componenet of diphasic P wave in lead V1 is larger than the terminal portion then what atria is enlarged
right

if the terminal portion is larger in V1 then its left atrial enlargment
In V1 - which is larger the S wave or the R wave
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
what does Reentry mean
premature stimulus reaches two pathways of differing excitability.
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
1. A-V node (slow conduction velocity and shorter refractory period)
2. Bundle of Kent is fast conduction and longer refractory period
what does the "delta wave" represent?
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"
what is the most common trigger of WPW circuit
atrial premature beat APB
how might the impulse in WPW go back to conducting down the right pathway
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
why might you see an inverted P wave in lead II in pts with WPW
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
Why is PSVT sustainable over days (150-250)
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. -
three conditions for all re-entrant tachycardias
1. anatomically distinct pathways
2. slow conduction
3. Diff refractory periods
how might you terminate an AV nodal reentrant tachycardia?
carotid massage
drugs (AV nodal blockers) which usually work by shortening the refractory period