pathology on an ECG Flashcards
what is an arrhythmia
- abnormal conduction in atria or ventricles
- narrow QRS = atrial arrhyhmia
- broad QRS = rhythm originates in the ventricles and not travelling down normal conduction path
ectopic beats
- 1 cause of an arrhythmia
- generated by an excited area of myocardium that spontaneously depolarise
3 types
- atrial ectopics = abnormal and early P wave
- atrioventricular junctional ectopics = activate ventricles travelling through the purkunji-his system = normal QRS. inverted p wave but can be masked by QRS complex
- ventricular ectopics =impulse spreads slowly so broad QRS eg ventricular tachycardia
re-entry loop
can cause an arrhytmia
- electrical impulse splits down 2 paths (normally fine as it meets again)
BUT if there is damage:
unidirectional conduction block => travels back on itself and takes alternative route = abnormal contraction of the heart
- AV node re - entry fast and slow can cause supra ventricular tachycardia
- atrioventricular - accessory pathway between atria and ventricles (wolff parkinson white syndrome)
- atrial flutter - re-entry loop in atria
atrial tachycardia
heart rate > 100bpm
P and t wave can merge
Av node re entry tachycardia
atrial flutter
re entry loop in atria
Av node cant keep up with rate of atrial depolarisation
sawtooth baseline due to consecutive P waves
atrial fibrillation
- generated by multiple ectopic foci
- atria quiver
- irregular R-R intervals due to ranom ventricle conduction
- irreglar pulse strength due to different length of filling time due to random contraction
- quivering = stasis of blood = thrombus formation (more likely in atria ) can cause ischemic stroke
ventricular tachycardia
due to ectopic focus in the ventricular myocardium
3+ ventricular beats
broad QRS
can turn into ventricular fibrillation
ventricular fibrillation
- chaotic ventricular fibrillation via numerous ecropic foci
- no coordination int he contraction of ventricles and atria
= cardiac arrest
torsades de pointes
polymorphic ventricular tachcardia
QRS all look different
can be because of ant-arrhytmic drugs
heart block
prolonged PR >5 small boxes
causes:
ischaemic heart disease and hypokalaemia
second degree AV block
mobitz type 1
- mobitz type 1 = PR interval becomes progressively longer until one o the RS interval is dropped
mobitz type 11
Pr interval is constant but ocasionaly no P wave condivted so QRS complex is dropped
-> 3rd degree heart block
2:1 block
second degree AV block
alternateP waves arent conducted
no consecutive PR intervals
3rd degree AV block
atria and ventricles work independently
= ventricular pacemaker cells take over as an escape rhythm but they are slow is broad QRS
=blood pressure cant be maintained
STEMI
- area of heart muscle is damaged all the way through due to full occlusion of coronoary artery via thrombus or embolism
NSTEMI
partial thickness mycardial infarction -> damange is mainly on inner part of myocardium
-depressed ST segment / inverted T wave
- within hours = raised troponin I and T
- after a few weeks it will go back to normal
hyperkalemia
resting membrane becomes more positive => slight depolarisation => inactivates voltage gated Na channels => slower uptake of ventricular A.P and slower heart rate
hypokalemia
K conc < 3.5mmol/L
delayed repolarisation => lengthened ventricular A.P => ventricular fibrillation
1) low t wave
2) high U wave
3) low ST segment
delayed afterdepolarisation
membrane depolarises without stimulation
eg , if there is a high intracellular Ca it can trigger contractions and AP
early afterdepolarisations
membrane depolarises without stimulation during repolarisation following a contraction
occurs if there is a long QT interval as longer AP
can lead to ventricular fibrillation
