Flashcards in CVS - ECG Abnormalities Deck (33)
Why do abnormal heart rhythms arise?
- abnormal impulse formation
- abnormal conduction
Where can rhythms arise from within the heart?
- sinus node (supraventricular)
- atrium (supraventricular)
- AV node (supraventricular)
What do the QRS complexes look like when the heart is in a supraventricular rhythym?
The ventricular depolarisation is normal, so the QRS complexes are also normal and narrow
What do the QRS complexes look like in ventricular rhythms?
They are wide (due to depolarisation taking longer) and vary in shape depending on where the rhythm originates from
What is the difference between sinus tachycardia and sinus bradycardia?
Sinus bradycardia is a sinus rhythm with a rate of less than 60 bpm. Sinus tachycardia is a sinus rhythm with a rate of over 100 bpm.
What is atrial fibrillation?
When impulses originate from multiple atrial foci, resulting in chaotic depolarisation. There are no P waves, just a 'wavy' unsteady baseline and a narrow irregular QRS complex.
True or false - the pulse and heart rate remain regular in atrial fibrillation?
False - they are irregularly irregular
What is a 'heart block'?
Delay/failure of impulses from atria to ventricles via the AV node and Bundle of His
Give two causes of AV conduction blocks
- acute myocardial infarction
- degenerative changes
What is first degree heart block?
Slow conduction in AV node and Bundle of His means that PR interval is prolonged (over 5 small squares). The QRS is normal, and P wave is normal.
What is the difference between the two types of 2nd degree heart block?
Mobitz type 1 involves progressive lengthening of PR interval until one P is not conducted and the QRS complex doesn't occur. The cycle then begins again.
Mobitz type 2 has a normal PR interval, but a sudden non-conduction of a beat occurs. This has a high risk of progression to complete heart block.
What is 3rd degree heart block?
Atrial depolarisation is normal but impulses not conducted to the ventricle, so the ventricular pacemaker must take over (ventricular escape rhythm). The HR is very slow and has wide QRS complexes, requires urgent pacemaker insertion.
What is the relationship between P waves and QRS complexes in third degree heart block?
There isn't one - PR interval is completely variable from beat to beat
Why do ventricular ectopic beats appear larger than a normal QRS complex on ECG traces?
The impulse is not spread via the fast His-Purkinje system, so there is a much slower depolarisation of the ventricle and a wide QRS complex
What must occur for a rhythm to be described as "ventricular tachycardia"?
Must be run of three consecutive ectopics
Why is persistent ventricular tachycardia dangerous?
There is a high risk of it becoming ventricular fibrillation
What is ventricular fibrillation?
Abnormal/chaotic/fast ventricular depolarisation which occurs due to impulses originating from numerous ectopic sites in ventricular muscle. There is no co-ordinated contraction and the ventricles appear to quiver. No cardiac output.
Why is ventricular fibrillation more dangerous than atrial fibrillation?
Ventricular fibrillation has no cardiac output as the ventricles are unable to contract, while atrial fibrillation still has cardiac output
Which leads should be checked if the lateral area of the heart is suspected to be damaged?
I, aVL, V5 and V6
Which leads should be checked if the inferior area of the heart is suspected to be damaged?
II, III and aVF
Which leads should be checked if the septal area of the heart is suspected to be damaged?
V1 and V2
Which leads should be checked if the anterior area of the heart is suspected to be damaged?
V3 and V4
Which muscle region in the heart is at most risk of reduced perfusion?
The sub endocardium muscle is furthest from the coronary arteries and therefore most vulnerable
How would sub-endocardial muscle damage be seen in an ECG?
ST segment depression and T wave inversion due to abnormal current during repolarisation.
What is "ST segment elevation myocardial infarction (STEMI)"?
Muscle injury which extends full thickness from endocardium to epicardium due to complete occlusion of lumen by thrombus. Can lead to muscle necrosis.
What do pathological Q waves indicate?
Muscle necrosis has occurred following a myocardial infarction
How does hyperkalaemia affect the resting membrane potential?
It becomes less negative (more depolarised)
How does hypokalaemia affect the resting membrane potential?
It becomes more negative (hyperpolarised)
How does hyperkalaemia affect an ECG?
At first, the T wave is elevated. As hyperkalaemia worsens, PR interval becomes prolonged, ST segment is depressed and there is a high T wave. Eventually, there is an atrial standstill and intraventricular block, progressing to ventricular fibrillation