8. Electrocardiography Flashcards
what defines normal sinus rhythm
a P wave for every QRS, rate 60-100, P waves with normal configuration: upright in II, negative or biphasic in V1.
if PR interval is < 5 mm, what is the cause?
1st degree AV block, usually due to slow conduction in the AV node
if QRS is < 3 mm, what is the cause?
consider a bundle branch block
what should the Q-T interval be like?
should be less than half the R to R length. if not, prolonged QT.
what would define LAD?
positive in I, negative in aVF
what would define RAD?
negative in I
normal axis looks like what, in what leads?
positive in I, positive in aVF
with hypertrophy, how will the axis vector change?
will point more towards the point of hypertrophy
with infarct, how will the axis vector change?
will point away from point of ischemia
best leads for analysis of P wave?
II and V1
what will we see in lead II if there is RAE?
in lead II, RAE increases the height of the P wave.
what will we see in lead II if there is LAE?
in lead II, LAE will increase the duration of the P wave
what will we see in lead V1 if there is RAE?
tall initial positive deflection
what will we see in lead V1 if there is LAE?
wide and deep negative deflection (1mm by 1mm)
a QRS interval of > 3 mm –> what?
His bundle delay, bundle branch block
in terms of the functioning of the heart, what does LBBB create?
delay in activation of the L side of the heart.
in terms of the functioning of the heart, what does RBBB create?
delay in activation of the R side of the heart
key points for LBBB
- wide QRS
- predominantly + complex in V6, neg in V1
key points for RBBB
- wide QRS
- RSR’ complex in V1 (rabbit ears)
- ST-T depression in leads with late QRS positivity
what does lead I look like with left anterior hemiblock?
predominantly positive QRS, left axis deviation
what does lead I look like with left posterior hemiblock?
predominantly negative QRS, right axis deviation
why does hypertrophy lead to higher voltage?
the mass of muscle being depol is increased
LVH increases QRS voltage in what leads?
I, aVL, V5, V6
RVH increases QRS voltage in what leads?
V1, V2, aVF, III
what is a strain pattern?
ST segment depression in the leads over the affected ventricle. prob result of subendocardial hypoxia in hypertrophied ventricle.
formula for LVH, and other criteria?
- SV1 and RV5 >35
- lateral ST segment depression/strain
- LAD
- LAE
criteria for RVH?
- RAD (QRS in Lead 1 is neg)
- incr voltage in right-sided leads
- R ventricular strain pattern (ST segment in R sided leads)
define a pathological Q wave
at least 1/4 the magnitude of the remaining R wave
infarction: ECG appearance?
QRS abnormality, relatively large Q wave
ischemia: ECG appearance?
ST deviation
subendocardial ischemia (mild): ST segment will look like what?
down-sloping. like a strain pattern
downsloping ST depr is also associated with what?
ventricular hypertrophy, prob reflects sustained subendocardial hypoxia in the thickened myocardium.
transmural ischemia (mild): ST segment will look like what?
upsloping and elevated - tombstone sign
transmural ischemia of the anterior wall is almost due to what?
obstruction of the LAD artery
what does a peaked T-wave indicate?
earliest sign of acute transmural ischemia in STEMI, likely due to potassium leaking into myocardial interstitium
what is the most observed sigh of acute transmural ischemia? what timeframe does it present at?
ST elevation. appears at min to hours. still potentially reversible at this point.
what does a T wave inversion indicate?
likely due to subendocardial infarction. occurs after more prolonged ischemia. usually seen with tombstone sign.
what is the earliest evidence of actual infarction?
within hours-days, Q wave will appear. not reversible
what happens as the transient ischemia resolves?
the ST seg returns to baseline. still have a Q wave, T seg inversion.
years after a STEMI, what will the EKG look like?
only the pathological Q waves. T wave inversion will correct, and ST elev will return to baseline.
