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35 Cards in this Set
- Front
- Back
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Define Normal Sinus Rhythm on ECG. (4)
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Every P followed by QRS.
Every QRS followed by P Upright P in I, II, and III PR b/t .12 and .2s |
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Give me the normal ranges for:
PR interval QRS width QT interval |
PR = .12-.20sec
QRS = <.10s QT = .35-.45s |
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How does RV Hypertrophy manifest on EKG chest leads? Axis? Understand why!
LV? Chest Leads? Axis? ECG analysis has a high _____ and a low______ for LVH when echo is used as the standard. |
R > S in V1... slowly becoming less prominent --> V4
RAD May show inverted T-wave in V5-V6 (the ones over the LV) (S in V1) + (R in V5 or V6) >/= 35mm or R in aVL > 11mm or R in I > 15mm LAD high specificity, low sensitivity |
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Time from atrium to ventricle is illustrated in the ECG by what?
First phase 0 to last phase 0 in ventricular cells? Reploarization w/i the ventricle? |
PR duration
QRS duration QT interval |
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How should you measure the QT interval? How about in a-fib?
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3-to-5 consecutive beats and average it.
No consensus.. can try over 10 beats average. |
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Vz the progression of QRS complexes in normal sinus rhythm for V1-V6.
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R wave becomes progressively taller, and S becomes progressively less deep.
(p90 of Lilly) |
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Pts w/ a BBB or a PPM (permanent pace maker) can have an abnormally ______ QRS cmplx?
QT interval varies ____ with HR? What is the JT interval? When should it be used? |
wide.
Inversely QT-QRSD; to evaluate QT interval in pts with a wide QRS complex |
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QRS widening .10-.12 indicates what? >.12?
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widened QRS 0.10-0.12 sec
(2.5-3 small boxes) >0.12sec (3 small boxes) |
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LBBB shows what on EKG? Why?
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initial polarization of the left septum (usually the first thing to go), doesn't happen. Thus, the initial spike of depolarization is directed at V6 (LV) not V1 (RV). This means you'll have no Q in V6, and have a Q in V1 (where there isn't supposed to be one).
LV waits till the end to depolarize, so you'll see a Rprime that is higher than R in V6, with a small dip (most of RV depolarization is now at ~90deg to V6 = v.small neg) inbetween. The exact opposite is observed in V1 (inverted two peaks). |
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fascicular blocks (also known as hemiblocks) can cause large changes in ______?
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mean ECG axis.
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Left Anterior fascicular block (LAFB) results in what on ECG? Why?
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LAD of greater than 45 deg from norm.
small Q in leads aVL and I Small R in inferior leads (II, III, aVF) Normally, conduction via the left ant and left post fascicles is simultaneous, such that LV depolarization is a uniform process. In this case, the block means that depolarization spreads entirely from the unaffected fascicle. (p101 in Lilly) |
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Left Posterior Fascicular block (LPFB) on ECG? Is this more or less common than LAFB?
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RAD
Small R (no Q) in aVL and I Small Q in inferior leads Less common. (p101 lilly) |
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Do LAFB and LPFB widen the QRS?
FBs are picked up on which types of leads? L and R BBB? |
not significantly, no.
limb leads precordial leads |
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What is the hallmark of transmural MI on ECG?
What are the characteristics of this entity? In which leads does it appear? Are they permanent? |
pathologic Q wave
length > 1 small box height >25% of total height of QRS The ones that reflect the anatomic site of MI (overlying the MI)... this is b/c the dead tissue doesn't conduct, so the lead picks up activity going AWAY from it on the other side of the heart. This is usually less strong than the local current (hence the normal Q wave). Yes, they don't go away over time, generally speaking. |
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Which location does NOT show a pathological Q wave upon MI? Why?
How do we detect this then? What also shows this, and how can we differentiate? |
Posterior wall.
There are no leads on the back. look for tall R-wave in V1-V2, b/c they should be recording the *opposite* of what leads on the back would show. Of course, the effect here of a little less decrease in the R wave then normal (hence it's higher) is smaller than the effect we'd see if we had a lead on the back. RVH - MI won't cause RAD usually. |
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How can you differentiate b/t RVH and posterior wall MI?
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MI won't cause RAD, though both will cause large R in V1-V2.
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If a pathological Q wave appears in one lead, is it Dx?
What about Q-waves in aVR? |
No, it must appear in 2+ leads in the combinations listed.
Disregarded b/c conduction is usually directed away from the right arm, so that's not a big deal. |
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In the presence of LBBB, can pathological Q waves be used to Dx MI? Why or why not?
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No. the abnormal depolarization in that condition renders our analysis too muddy.
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What is the meaning of transmural infarct?
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That means that the entire thickness of the heart wall is involved in the area of infarct - it is these conditions in which pathological Qwaves show.
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Do pathological Qwaves develop when the MI is not transmural, but only involves the subendocardial layers of the myocardium? What do we thus call these MIs?
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not usually, no, b/c the remainder of cells can generate some electrical activity.
non-Q wave MIs. |
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Can pathological Q waves distinguish b/t acute MI and one from long ago? Can anything else make this distinction?
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No, b/c the change is permanent.
Yes, ST and T wave abnormalities. |
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Upon MI, what is the initial abnormality in the ST segment? Does this show up before or after pathQ?
What happens next? (1-2 days later, several days later, weeks-months later) |
elevation w/ a peaked appearance in the T-wave.
Before. first 1-2 days after: ST remains elevated and T-wave inverts. Several days later, the ST segment returns to normal, but the T wave stays inverted. weeks-months: whole thing should return to normal (except Q). |
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If the ST seg length and T wave don't eventually return to normal post-MI, what can this indicate?
What is seen in leads opposite the site of MI re: ST & T? |
A bulging fibrotic scar (ventricular aneurysm) has developed @ the site of the infarction.
can see *reciprocal changes*, e.g. depression of MI |
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Transmural MI may cause _____, giving the false appearance of ST segment elevation (height wise).
Non-Q infarct? These observations are consistant with diastolic or systolic current theory? |
a downward shift of the baseline potential over the MI due to some cells around the infarct being unable to fully repolarize, thus seeming more negative than normal, fully repolarized areas.
since the ECG leads only record relative position, this can --> ST elevation. Shift the baseline up b/c the cells around the infarct now generate a current towards the uninjured outside of the heart. - **gives the appearance of ST depression!! (important for Dx) Diastolic. |
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Explain ST elevation re: systolic current theory.
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infarct shortens APs in cells affected, as a result, they repolarize faster than neighboring cells --> generating gradient b/t the two zones --> electrical current TOWARDS the ischemic area = ST elevation in the leads overlying MI>
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Does the Q-wave vs nonQ infarct distinction have a clinical importance? Can we take our time making this distinction?
How is it done then, if the Q-wave takes a while to appear? For the purposes of such decisions, how do we label our two Dx choices? |
Yes, Tx is different.
No, gotta do it quickly because Tx is diff. Gotta use ST seg elevation. acute ST-elevation MI non-ST elevation MI (see depression) |
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In non-Q-wave MI, what is seen in the leads overlying the infarct?
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ST depression, rather than elevation. Baseline --> shifted upward --> appearance of ST seg depression.
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On which lead is RA enlargement best seen? How is it seen?
LA enlargement? |
Lead II
will show a taller than 2.5mm initial component of the P-wave Lead I Will show a larger than normal (1mm x 1mm) negative deflection in the second part of the P-wave. |
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Which disorder can cause an inverted T-wave that has a gradual downslope and a very steep return (making it asymmetrical) on leads V5 and V6?
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LVH
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Diphasic P-wave can indicate...
P-wave > 2.5mm? |
atrial enlargement due to volume overload
Right atrial enlargement |
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Pt presents with LAD.
normal QRS, ST, and T. Tall R on lateral limb leads (I, aVL) Deep S on inferior Limb leads (III, aVF, II) |
LAFB, if not other cause can be found.
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Pt presents with RAD, to which there is no ready attributable cause.
QRS, ST, and T are normal R waves are tall on the inferior leads S waves are deep on the lateral leads. |
LPFB, if no other attributable cause can be found for the RAD.
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What is the "money" lead to look at if you see a >.12s QRS?
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V1, looking for a BBB.
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RBBB causes what? why?
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On V1, you'll see a double-peak R, with the second (R1) being usually higher than the first. This is due to the two ventricles depolarizing "out of phase."
On V6, you'll see a the inverse (mountain surrounded by a moat). Can see deepened S on lateral limb leads. Understand why. |
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LBBB causes what? why?
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loss of septal initial conduction. first current the V1 sees is negative. then a positive deflection while the RV depolarizes, then and bigger Negative deflection when the LV finally depolarizes.
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