ECG Flashcards
physiological Q wave
since heart is 3D the Q waves exists b some depolarisation current is moving away from the + electrode
S wave
movement away at eh end o depolarisation
-dereieves from the end of the base of the ventricles (terminal part of ventricular depolarisation)
T
ventricular repolarisation
- still ^ b moving away from the positive electrode in Lead 2
P
a d not the contraction
QRS
V d not the contraction b follows it
issues with lateral wall of LV
L1 avL
- coronary artery disease / accusation
inferior
avF
gets its supply from the right coronary artery
anterior wall conditon
- widow maker
- pericardial leads
e. g
widow maker
v3 v4
prolonged pq interval
use
prolonged interval of P Q
LONGER
2nd degree heart. block morbid type 2
p qrs p qrs p no qrs
- symptomatic ; risk of complete stop ; MI
- measure intervals and make sure qrs follows the p wave
third degree heart block
atrial and ventricles fire continuously but the ventricular pacemaker cells fire slowly,
- SAn and AVn slow not susceptible
- need pacemaker
bundle branch block
- problem in the bundle branch of either R or L so see a wider complex
- L branch damage sign of heart damage
arrhythmia
- supraventricualr; start in sinus node/ atrium cells/ AVN
- ventricular; start at the heart
S
- QRS normal
- narrow complex
- rate is super super high
- most common arrhythmia ; happens d atria firing quivering ,b is still delivered to LV and rV so okay pressure, not hypotensive
- irregularly irregular
VF
- ## they can go back to normal b thunking their own heart or shock them back to life
AVF
- SOW <60
- ABNORMLA
- fast
- tachybrady syndrome ;
- base line
- atria isn’t working. well, so b just stays the atria wc then clots wc can embolise to the brain c stroke
PBC
- ventricular
- wide complex
- premature before next qrs complex is predicted to happen
- can be asymptomatic
- if isolated no issue
- can progress to ventricular tachycardia (sustained )
- more than 3 ventricular tachycardia
apex of heart?
- 5th intercostal
what doe the bipolar allow
- communication since one is - and one is + so they can communicate
types of heart Block
- SAn to AVn singa defectos
- brachycardia, dizziness, syncope
1st degree
- 1st degree AV block
- prolonged PR intervals >0.2 seconds (<5 boxes)
2nd
- WENKEBACH (mobitz 1) ;PR- longer than drop no QRS (longer longer longer drop that is a wenkebach)
- mobitz tpye2 ; say longer then drop >0.2 seconds
3rd
- AV and SAN work independently so constant P and constant QRS
- overlap of P and QRS b they are independent
- ventricular pacemaker (myocytes) take over and they work at 20-40bpm wc is too slow to maintain bp so p urgently needs a pacemaker
bundle branch block
- obstruction on one of the bundle branches
- LBBBor RBBB
- unaffected branch depolarises first so you get two little R peaks and its broader QRS complex b of the delayed depolarisation
- > 3 squares
- look at leads V1 and see W look at lead V6 and see M
Arrhythmia
- abnormal rhythms
- can arise supraventrocular ie ATRIA (san avn atria)
difference bw supra ventricular and ventricular
SV = normal but narrow QRS V = wide and weird QRS
SV
- most comon
- foci in atria uncoordinated firing , only some impulses travel through the AVN so depending on how many can get through the AVN determines the symptoms; if lots = tachycardia, little; brachycardia, or sometimes tachybradycadia
- b is still being delivered,
- no P wave b san not firing
- only some electric
a fib types
- coarse
fine
what does fib c
- some b in the atria is static and so it clots c embolism ; going to brain, LA, coronary arteries
premature ventricular contration
- wide QRS complex
- happens before next QRS
- can be asympomiatic or can feel palpitates
- dont c issue if random b can lead to ventricular fib
- more than pvc = ventricular tachycardia
ventricular fibrillation
- random ventricles myocytes firing
- lethal b b is not being sent around therefor v in bp
- no cardiac output and leads to death
classification of arrhythmia
- hr<60 = Brady cardia can be heart block / simple bradycardia
- tachycardia >100 = tachycardia <120 = narrow complex af/flutter /SVT/sinus tachycardia if <120ms = broad complex VT/VF
ECG in ischameia
-look at leads at the side of the heart
ischaemia test
- look at troponin it will be negative since the tissues hasn’t died yet
mi tst
- troponin positive
types of inafarcrs
- full thickness STEMI ST segment elevation MI
- non-stemi = not full thickness of cardiac wall
stemi
d occulsion of the coronary artery
-look at leads
why do Myocardial necrosis andscar tissue lead to pathological Q wave
-no one knowns
whats a Q wave and types
negative defelciton
- pathological and non
- depnds on lead their sizes but leads 3 and avR has slightly bigger
- Q should never be bigger than 25% of r
are all q waves a sign of old infarcts?
no PE too
non scemi
- infarct only the endocardial so outside is infarcts b of coronary artery is half occluded and you can get b to the outside b closer to it but the endocardial part dies
- t wave normally upright in all leads except avR and V1 where they are negative inverstion
- pathological t wave >3mm deep
how to differentiate
tropinon release
hypokalaemia
- U wave post the
- T waves flip and get deeper
hyporkalemia
- fast hypekaelima b na+ channels being inactivated so you get
- tall peaked T waves , then you loose T waves b lose ventricular repolarisation
- wide QRS not normal conduction
