ECG conditions Flashcards
whats AV block and what are the types
failure of conduction of impulses from atria to ventricles via the AVnode and Bundle of His
- 3 types:
- first degree heart block
- second degree heart block : MOBITZ type 1 second degree heart block / mobits type 2 secon degree heart block
- third degree
whats the causes of AV block
- degeneration of electrical activity of conducting system with age - sclerosis (stiffening) and fibrosis (hardening)
- MI
- medication
- vavlular heart disease
first degree heart block
- failure of impulse conduction from atria to ventricules and bundle of his
- P wave is okay , in sinus rhythm
- PRinterval is >0.2 (more than 5 little squares)
just slow and normal p wave follows
second degree heart block mobitz type 1
failure of impulse conduction from atria to ventricles and bundle of his
- PR intervals progressively get longer than collapse, P wave with no QRS
- ok ok ok collapse, that wenkenbach
- theres a cut off of electrical activity to the AVN
second degree AV block mobitz type 2
pR intervals remain constantly long and then sudden drop of QRS
-P wave regular
third degree AVN block
atria and ventricules fire independently
ventricular pacemaker (ventricular myocytes) takes control= escape rhythm , so you get firing at rate of 20-40bpm
wc is too low to maintian nomrla bp
urgently need a pacemaker
wide QRS complex
bundle branch block and does left or right depolarise first
left than right
delayed conduction within the bundle branch
can be RBBB or LBBB
P wave and PR interval okay but really wide QRS >3 squares
W in V1 and M in V6 of LBBB
arrthymias
abnormal rhythm of heart arising from :
SUPRAVENTRICULAR
- atria
- SAN
- AVN
VENTRICULAR
- ventricules
What are the two catergories of arrythmias and their features
supraventicular
- narrow QRS complex
- can be ectopic atrial foci, SAN, atria
venticular
- wide and bizarre QRS complex
- ectopic sites of the ventricles (but the ventricular pathway so its just any place in the ventricles)
atrial arryhtmia
supraventricular arrythmia
arises from multiple atrial foci, rapid chaotic impulses
No P wave just wavy baseline ,
irregular R-R intervals
impulses reach AVN at rapid irregular rate but not all impulses pass through the AVN and it doesnt conduct all
but when it conducts it the ventricles work normally and theres a normal QRS complex
types of Afib
- slow where the ventricules respond <60 bpm
- fast where ventricular response >100 bpm
- normal rate = 60-100bpm
afib with coarse fibrillation (amplitute >0.5mm) or fine fibrillation (amplitude <0.5m)
consequences of atrial fibrillation
- atria just quiver and dont contract so b stasis
- irregular -regular HR b ventricles still working
- increased b stasis wc clots in atria and can cause isachemic stroke
premature ventricular ectopic beats
where random foci in the ventricles send off electrical acitivity
impulses not spread via the his-purkinje system
- much slower depolarisation so wide QRS
- premature = occurs earlier than would be expected for next sinus impulse
can be asympt. or cause palpitations without haemoldynamic consequences
why learn about premature ventricular ectopic beats
progresses to ventricular tachycardia then ventricular fib
ventricular tachycardia
sequence of >3 consequetive tachycardia
persistent VTACH is a dangerous rhythm requiring urgent treatment
high risk progression to ventricular fibrillation
ventricular fibrillation
abnormal chaotic fast ventricular depolarisation
impulses from numerous ectopic sites in ventricles
no coordinated contraction
ventricules quiver
no cardaic output so cardiac arrest
classfification of bradycardia and tachycardia
bradycardia
heart block / simple brachycardi
tachycardia
narrow complex? = afib, sinus tachycardia, svt
broad complex?= ventricular tachy / vfib
mi types on ecg
stemi and nstemi
stemi goes through full thickness of myocardium whilst nstemi is just sub-epicardial injury
necrosis vs ischaemia
necrosis is tissue death and so chemical markers are released
ischaemia no markers are released
what are ECG signs of MI
stemi = ST segment elevatoin
after the incident a patholgoical Q wave because no electrical activity because of dead tissue
deep q waves >2 is normal in L2 AVR but not in V1-3
- nstemi = ST wave depresion and T wave inversion
- stemi = ST wave elevation
what is the definition of a q wave
any negative deflectio that precedes a R WAVE
what other conditon do you get q waves and what are other ECG findings of that condition
PE
S wave in lead 1 (downward deflection od S wave)
Q wave in L3
inverted Twave in lead 3
pathological Q waves
if >1 small square its wide
if >2 small squares its deep - except L3 and AVR wc is kinda normal
depth more than 1/4 of subseuent R waves
stable vs unstable angina differences and ecg
stable = pain only when exerting activity
unstable = pain even at rest
stable angina no ECG changes on ST depression in exerion
unstbale ST depression and T wave inversion
what is the pattern at which the signs are seen in an ecg
1.
hypokalemia what is it and ECG changes
mild <3.5 mmol /moderate <3 / severe <2.5 mmol
palpitations, weakness, ascending paralysis, arryhtmia
ECG :
- U wave between ST
- T wave flattening and inversion
- peaked P wave
hyperkalaemia what is it and ECG finding
>5 mmol/L
- tall tented T wave
- loss of P wave
- widening QRS
where do you listen to heart murmur
All Prostitutes take money
- aortic 2nd intercostal space right boarder
- pulmonary 2nd intercostal space left sternal border
- tricupsid 4th intercostal space left sternal border
- mitral 5th intercostal space midclavicular line
where the apex of heart
5th intercostal space left sternal border
