ICL 2.3: Introduction to ECG Basic Principles Flashcards
how do you approximate heart rate from an EKG?
300 divided by the number of big boxes between R waves
how much time is one little box? big box?
40 msec
200 msec (5 little boxes)
what is an ectopic rhythm?
any PQRS rhythm that doesn’t meet sinus criteria
sinus criteria is:
1. P in front of every QRS
- (+) in lead I and II, (-) in lead V1
- 60-100 bpm
what is the effect of adenosine on the heart?
it temporarily stops AV conduction
what is the effect of atropine on the heart?
- increases AV node conduction
2. prolongs sub AVN conduction = bundle of His
what is the vagal maneuver?
aka carotid massage
it prolongs AV conduction and increases sub AVN conduction
what is heart block?
a block in conduction from the SA node to the AV node so the His/purkinje system never gets activated
patiens present with:
- dizziness
- syncope
- tachycardia
- fatigue
treat with pacemaker
what is 1st degree heart block?
constant prolonged PR interval
but all p waves are conducted, there’s no dropped QRS intervals
normal in athletes; improves with exercise
PR > 200 ms
block is usually in the AV node = favorable prognosis
what is 2nd degree heart block?
some p waves are conducted but others are not! there are two subtypes:
- Mobitz 1 (Wenkebach)
PR interval get progressively longer until a QRS is dropped and doesn’t happen –> this is because the SA node sends out a signal and it’s delayed, and each time it’s just a little more delayed until there isn’t a squeeze at all
usually due to AV dysfunction; improves with exercise
grouped beating and irregular RR intervals on EKG
“longer longer longer drop that is a Wenkebach!” or “Wenkebach gives you Warning”
- Mobitz 2
PR interval is lengthened consistently and then eventually a beat is dropped – so it’s like 1st degree HB of over 200 ms but there’s also a dropped QRS complex
usually due to block in the HIS-purkinje system; usually symptomatic due to numerous dropped beats= worse prognosis
what is 3rd degree heart block?
total block of conduction; some other slower pacemaker in the heart is depolarizing the ventricles –> the atria and ventricles contract independently of each other
constant R-R intervals because the atria and ventricles are consistent in and of themselves even though they’re not beating together
block usually in the HIS-purkinje system and patients are symptomatic
what are the 2 types of heart blocks?
- AV node disease
usually less dangerous; conduction improves with exertion (sympathetic activity)
1st degree and Mobitz I
- HIS-purkinje disease
more dangerous! usually does not improve with exertion; often progresses to complete heart block and requires a pacemaker
Mobitz II and 3rd degree
what commonly causes 1st degree heart block?
- B blockers
- Ca+2 channel blockers
- well-trained athletes because of increased parasympathetic tone when they’re at rest
- digoxin
all of these decrease conduction through the AV node
how long should a normal QRS complex be?
120 ms = 3 little boxes
which infectious disease is related to heart block?
lyme disease = spirochete infection with borrelia burgdorferi
stage 2 of the disease patients can develop lyme carditis which presents with varying degrees of AV block!
AV block will improve with antibiotics
which other structures can act as pacemakers if the SA node isn’t working?
AV node = 40-60 bmp
HIS, bundle branches, purkinje = 25-40
when a lower pacemaker depolarizes the ventricles this is called an escape rhythm
the rate of the lower pacemaker determines symptoms –> AV node will probably lead to fatigue and exercise intolerance while the others will cause dizziness, syncope and hypotension
what is bundle branch block? what will it look like on EKG?
if both bundle branches are blocked it will result in AV block (fibrosis of the HIS bundle)
if only one bundle branch is blocked you won’t get AV block, you’ll have a normal PR interval but the QRS will be prolonged because it takes longer for the one bundle to depolarize both ventricles (MI, cardiomyopathy, myocarditis)
you will see a classic R-S-R’ which is a little tiny extra peak before the QRS complex
on lead V1, prolonged QRS pointing up is a RBBB and downward pointing is LBBB
what is a normal PR interval?
< 200 ms
what is atrial flutter?
atrial rate = 240-300+
ventricular response can be regular or regularly irregular
what is atrial fibrillation?
atrial rate = 400+ bpm
ventricular response is irregularly irregular
what is an SVT?
SVT = super ventricular arrhythmia
160-250 bpm
circuit involving the AV node –> since the AV node is faster than the SA node, it takes over so the P wave happens at the same time as QRS
if the circuit is outside the AV node and involves an abnormal connection between the atria and ventricle that’s called a bypass track
what is ventricular tachycardia
the ventricular cardiomyocytes are the origin of the tachycardia; the ventricles are going really fast
QRS is wide because the contraction is starting in the cardiomyocytes and has to go cell to cell instead of being able to use the purkinje fibers and bundles so the depolarization process is much slower
usually the weird conduction doesn’t go retrograde all the way up to the AV node to the atria so the atria will beat on their own = AV dissociation
what is the normal axis of the heart?
-30 to +60
if you want to look at the anterior portion of the heart, which leads should you look at?
V2, V3, V4
if you want to look at the septum portion of the heart, which leads should you look at?
V1 and V2
if you want to look at the left lateral portion of the heart, which leads should you look at?
I, aVL, V5, V6
if you want to look at the left inferior portion of the heart, which leads should you look at?
II, III, aVF
if you want to look at the right ventricle of the heart, which leads should you look at?
aVR
what is left axis deviation?
axis of the heart is between -30 to -90
ex. when you have chronic HTN, the heart will get thicker and there will be an electrical shift because the LV has enlarged so the heart is slightly shifted
what is right axis deviation?
axis of the heart is between 90-180
what is extreme axis deviation?
axis of the heart is between 180 and -90
what is the direction of depolarization?
endocardium to epicardium
what is ST elevation?
if the supply of oxygen is less than the demand like during a severe coronary occlusion, then the hypoxia causes:
- loss of ATP and ATP dependent transport
- loss of Na/K ATPase pump that keeps cells hyperpolarized
- K+ATP channels open more widely with more loss of intracellular K+ which closes some fast Na+ channels –> this means that depolarization occurs more slowly with earlier repolarization
this can cause arrhythmias!
the T wave is a really high peak on the EKG in the lead that corresponds to which vessel is being blocked causing the MI
what are the EKG changes you see following an MI?
- minutes: peaked T wave
- minutes-hours: ST elevation (like the ST segment is sloped upwards)
- hours-days: loss of R wave with Q wave formation which signifies dead tissue because electricity has to go around dead tissue
- days: T wave inversion
- weeks to months: normal EKG but with a Q wave indicating the dead tissue
slide 81
what is the QT interval?
ventricular depolarization and depolarization!
duration depends on heart rate so you have to “correct” your QT interval to match it up with your heart rate –> QTc = QT/√RR interval
myocardium depolarization decreases with heart rate to allow next depolarization
what is an LAFB?
LAFB = left anterior fascicular block (of the bundles)
you will see:
1. left axis deviation
- prolonged QRS
- Q1S3 syndrome on EKG
what is an LPFB?
LPFB = left posterior fascicular block (of the bundles)
you will see:
1. right axis deviation
- prolonged QRS
- S1Q3 syndrome in EKG
what conditions could lead to a RBBB?
- normal variant
- damage to RBB
- chronic HTN
- MI
- cardiomyopathy
- congenital heart disease
- PE
- Cor Pulmonate
- Lev’s disease
what conditions could lead to a LAFB?
- chronic HTN
- dilated cardiomyopathy
- aging
- degenerative fibrotic disease
- aortic stenosis
- aortic root dilation
- acute MI
- electrical conduction abnormality
- lung disease
what conditions could lead to LBBB?
- chronic HTN
- ischemic heart disease
- anterior MI
- dilated cardiomyopathy
- fibrosis of LBB
- hyperkalemia
- digoxin toxicity
- aortic stenosis
what’s the criteria for left atrial hypertrophy?
- terminal negative P wave deflection in V1 >0.04 s and 0.1 mV = greater than 1 small box
- P-mitrale in lead II = notched P wave due to a longer and delayed depolarization of the LA which forms the second half of the P wave and therefore forms a dip in the P wave
- P wave duration > 120 ms because it’s taking a longer time to depolarize a thickened LA
- ratio of P wave duration to PR duration > 1:1.6
slide 94
what’s the criteria for right atrial hypertrophy?
- P wave amplitude > 2.5 mm in II and/or 1.5 mm in V1
so the P wave is going to look extra tall because extra electricity is being conducted through the RA which contributes to the first part of the P wave - QR, Qr, qR or qRs in V1
- QRS voltage is < 5 mm in V1 and V2/V1 voltage ratio is >6
slide 94
what is the criteria for biatrial enlargement?
- features of both RAE and LAE in the same EKG
- P wave in lead II >2.5 mm tall and > 120 ms in duration
- initial positive component of P wave in V1 > 1.5 mm tale and prominent P-terminal force
slide 94
what is the criteria for right ventricular hypertrophy?
- V1 R wave is greater than the S wave OR R in V1 greater than 7 mm
- right axis deviation
- in V1, T wave inversion
- S waves in V5 and V6
so normally the R wave is negative in V1 and positive in V6 since the resulting vector is towards the LV but with RV hypertrophy, the axis shifts towards V1 and you get a positive R wave in V1 and a smaller R wave with a big negative S wave in V6
what is the EKG criteria for left ventricular hypertrophy?
- largest R or S wave in limb leads >20 mm = huge voltage spike! can even start to overlap the leads below on the next line down
- S wave in V1 and V2 >30 mm
- R waves in leads V5 or V6 >30 mm because there’s more tissue to depolarize
- left axis deviation
- QRS duration of >0.09 sec
- S wave in V1 + R wave in V5 or V6 >35 mm
- R wave >11 mm in aVL
- R wave > 15 mm in lead I
- ST elevation in V1-V3
- prominent U waves in V1-V3
what is the Sokolow+Lyon and Cornell criteria for left ventricular hypertrophy?
Sokolow+Lyon criteria: S V1 + R V5 or V6 > 35 mm
Cornell critter: S V3 + R aVL > 28 mm in men and 20 mm in women
is the endocardium or epicardium more susceptible to ischemia? how does this effect EKGs?
endocardium is more susceptible
the coronary arteries are closer to the epicardium so the endocardium is more susceptible to ischemia since branching vessels are what supply it
so since it’s the most susceptible, when there’s ischemia it can’t sustain normal activation/depolarization which leads to depolarization occurring earlier in this section and force is opposite to ischemic area = t waves loose the upright orientation and become inverted in areas of ischemia
which leads correspond to the LAD?
V1-V4
V1 and V2 are kind of on the right side too but they still tell you info about the LAD
which leads correspond to the right coronary artery?
II, III and aVF
