EKG Flashcards
normal axis
I: up
aVF: up
left axis deviation
I: up
aVF: down
right axis deviation
I: down
aVF: up
extreme right axis deviation
I: down
aVF: down
Heart rate from EKG
300/ big boxes
duration of small box
40 msec
duration of big box
200 msec
inferior leads
II, III, aVF
right coronary artery
appearance: normal
(II: no S wave)
septal leads
V1, V2
left anterior descending artery
appearance: small P wave; upside down
(V2: upright T wave)
anterior leads
V3, V4
left anterior descending artery
appearance: small P wave, tall QRS and T
(V3: upside down QRS)
lateral leads
I, aVL, V5, V6
circumflex artery
appearance: small P waves
What is unique about lead aVR?
no Q wave
P wave
atrial depolarization/ contraction
QRS complex
ventricular depolarization/ contraction
atrial repolarization
less than 120ms
T wave
ventricular repolarization
QT interval
less than 1/2 R-R interval
beginning of Q to end of T wave
less than 440ms
ventricular depol and repol
ST segment
end of S wave to beginning of T wave
PR interval
beginning of P wave to R wave
less than 200ms
PR segment
end of P wave to beginning of Q wave
AV node conduction to Bundle of His
intraventricular conduction delay (IVCD)
widened QRS with no other abnormalities
RBBB
widened QRS with rabbit ears on V1 or V2 (big split)
LBBB
widened QRS with rabbit ears on lead V5 or V6
considered a STEMI if new
ventricular origin of beat
no P wave before widened QRS
ischemia
ST segment depression (2mm or 2 small boxes)
T wave inversion
injury
ST elevation (2mm or 2 small boxes) T wave hypertrophy (tombstone)
infarction
significant Q waves (at least 1/3 size of QRS)
STEMI
ST segment elevation
severe if there is a giant Q wave
Wolf-Parkinson-White syndrome
short PR interval
direct pathway from SA node to ventricles: high HR
due to re-entry
What does a prolonged QT interval put a patient at risk for?
ventricular tachyarrhythmias
ex: torsades de pointe and v. fib
type 1 AV block
prolonged PR interval
type 3 AV block (complete heart block)
P waves and QRS complexes are not related to each other
Tx: pacemaker
type 2 AV block: Mobitz type I
increasing length of PR intervals leading to a dropped QRS
going going gone
type 2 AV block: Mobitz type II
normal PR interval leading to a dropped beat
risk for type 3 AV block
type 3 AV block (complete heart block)
P waves and QRS complexes are not related to each other
ventricular hypertrophy
increase voltage, can have inverted T wave (increases CAD risk)
delayed depolarization/repolarization
pericarditis
diffuse ST elevation in all leads
altered automaticity
myocyte fires that is not stimulated by SA node
can alter slope of depolarization: phase 4 pushed to threshold
triggered automaticity
AP “triggers” a 2nd AP immediately after it
delayed after-depolarization
Re-entry
unidirectional block in normally contiguous pathway(ex: from fibrosis or MI = now noncontiguous)
impulse takes a slower alternative pathway: moves anterograde and retrograde (normal pathway has had time to repolarize enough to trigger)
retrograde pathway sets up loop leading to ventricular tachycardia
HR: >140 and sustained
junctional rhythm
no P waves, constant firing of atria
seen in digitalis intoxication
due to enhanced automaticity
multifocal atrial tachycardia
constant firing from multiple sites in the atria: lots of EKG morphologies
see in emphysema due to high CO levels
due to enhanced automaticity
V-tach
due to organized re-entry
Tx: DC cardioconversion then maintain with Class I (slow conduction and increse refractory period) or III (prolong repol. and increase effective refractory period)
SVT
due to re-entry
arrhythmias due to enhanced automaticity
sinus tachycardia
atrial premature beat
ventricular premature beat
What might make a latent pacemaker prone to acceleration?
beta stimulation hypokalemia fiber stretch hypoxemia acidosis injury
arrhythmias due to abnormal “triggered” automaticity
early after depolarization: interrupts phase 3 (can trigger long QT (torsades))
delayed after depolarization: interrupts phase 4 (occur as a result of Ca overload (digitalis))
ventricular bigeminy
due to digitalis (Ca overload)
exacerbated by: catecholamines, hypokalemia
torsades de pointes
polymorphic ventricular tachycardia triggered by EAD
occurs in QT prolongation (phase 2 and 3)
see in K channel blockers
exacerbated by: low HR, hypokalemia
re-entry
arrhythmias due to re-entry
atrium: a. fib/flutter
AV node: PSVT
ventricle: ventricular tachycardia/fibrillation
Drugs treat by interrupting re-entry: change conduction velocity, refractory period, convert unidirectional block to complete block
