CVS 13 - Interpreting ECG's (Part 2) Flashcards
What does the QT interval denote?
How long should the corrected QT interval (QTc) be?
What does a prolonged QTc suggest?
- QT interval is the time for depolarisation + repolarisation of the ventricles. Varies with HR so is corrected for HR (QTc)
- Upper limit of QTc is 0.44-0.45 seconds (11 small boxes)
- Prolonged ventricular repolarisation - associated risk for dangerous arrhythmia.
What are the ECG characteristics of a normal sinus rhythm? (5 characteristics)
- Regular HR of 60-100bpm
- Each QRS complex is preceded by a normal P-wave
- Normal P waves, should be upright in leads l, ll + inverted in aVR
- PR interval should remain constant
- QRS complexes are less than 100ms wide
What are AV conduction blocks? (heart block)
What are the 4 types of heart block?
What are the causes of heart block?
- Delay of conduction of impulses from atria to ventricles via AV node + bundle of His.
- 1st degree, 2nd degree (Mobitz type 1 + 2) + 3rd degree
- Degeneration of conducting system w/age, acute myocardial ischaemia, medications etc.
What are the ECG characteristics of all 4 types of heart block?
Type 1 = Normal P-waves followed by a QRS complex, but PR-interval is >0.2 seconds.
Mobitz type 1 = Successful lengthening of PR-interval until QRS complex is dropped
Mobitz type 2 = PR-intervals don’t lengthen, sudden QRS complex dropping. High risk of progression to complete heart block.
Type 3 = Atria + ventricles depolarising independently, complete failure of AV conduction. Rhythm down to 20-40bpm (ventricular pacemaker takes over) very wide QRS complex.
What is bundle branch block (BBB) and what are the ECG characteristics?
- Delayed conduction within bundle branches (right or left)
- P waves and PR-interval normal
- Widened QRS complex (over 0.12 seconds) - as ventricular depolarisation now takes longer.
What are the 2 broad categories of arrhythmias?
What kind of QRS complexes are seen on the ECG with these 2 categories?
1) Supraventricular (arising from above the ventricles) - normal or narrow QRS complexes (as they tend to be tachycardias)
2) Ventricular (arising from the ventricles) - wide + bizarre QRS complexes (as normal conduction pathways not being used).
What are the ECG characteristics associated with atrial fibrillation (Afib)?
- Arising from multiple atrial foci + rapid chaotic impulses.
- No P-waves (just wavy baseline) + irregular R-R intervals
- Not all impulses conducted at AV node, those that are DP ventricles normally do QRS complexes are normal.
- Can have a slow, fast or normal HR, with either fine or course fibrillation (don’t mistake for P-waves, they are absent)
What are the haemodynamic effects/biggest complication with Afib?
- Atrial contraction lost, atria just quiver. HR and pulse “irregularly irregular”.
- Loss of atrial contraction increases blood stasis, can get blood clots in LA therefore, Afib is a large risk factor for ischaemic stroke secondary to emboli.
- Most common arrhythmia in general population
What are premature ventricular contractions (PVC’s)?
What are the ECG characteristics associated w/PVC’s?
What can 3 or more successive PVC’s lead to?
- Ectopic focus in ventricular muscle, impulses don’t spread via His-Purkinje system, so DP much slower.
- Therefore wide QRS complexes.
- Ventricular tachycardia (VTACH) - a dangerous rhythm with high risk of progression to Vfib.
What is ventricular fibrillation (Vfib)?
- Abnormal, chaotic, fast ventricular depolarisation
- Impulses from multiple ectopic sites in ventricles, no coordinated contraction of ventricles, they just quiver.
- No CO, if sustained leads to cardiac arrest.
NB: See slide 27 for great flow chart to working out which arrhythmia is present.
What is the difference between myocardial ischaemia + myocardial infarction?
What are the 2 classifications of myocardial infarction?
Ischaemia = Lack of perfusion to muscle but no muscle necrosis. Blood tests therefore negative for troponins.
Infarction = Lack of perfusion to muscle and necrosis present. Blood tests therefore positive for troponins.
1) STEMI = ST elevation MI
2) NSTEMI - non-ST elevation MI
What is STEMI caused by?
What are the associated ECG changes?
- Complete occlusion of coronary artery (not just partial) + full thickness of myocardium undergoes necrosis.
- ST elevation most important sign, also get hyper-acute or inversed T-waves, and pathological Q-waves.
What are pathological Q-waves?
- A Q-wave preceding an R wave that is >0.04 seconds wide or > 2 small squares deep. Depth is more than 1/4 of the subsequent R-wave.
The ECG changes in NSTEMI + unstable angina (severe ischaemia) are the same. How would you differentiate between them?
- Differentiate by blood tests (presence of troponins). Present in NSTEMI not in unstable angina, as there is absence of myocardial cell death.
What are the ECG changes seen in NSTEMI and unstable angina (severe ischaemia)?
- ST depression + T-wave inversion (normally upright in all leads except aVR + V1).