ECGs + Conduction problems Flashcards
Describe what leads would show ST elevation for anterior, lateral, inferior MI + what artery would be implicated?
Anterior/Septal leads
- V1-4
- LAD
Lateral leads
- I, aVL, V5, V6
- LCX or LAD
Inferior leads
- II, III, aVF
- RCA [RMA] and/or LCX
Describe the difference between 1st, 2nd, 3rd degree heart blocks
(1.) 1st degree - indicated on an ECG by a prolonged PR interval. no missed beats.
(2. ) Mobitz I second degree AV block
- progressive prolongation of PR interval followed by a dropped QRS complex
(3. ) Mobitz type II second degree AV block
- normal PR interval with dropped QRS beat too
(4. ) 3rd degree heart block
- complete absence of AV conduction
- no relationship between P and QRS complex
What is a bundle branch block?
What would you seen in an ECG for a LBBB and RBBB?
(1. ) Condition where there is a delay or blockage in electrical impulses pathway.
(2. ) Damage/blockage to these pathways can arise from Myocardial infarction, ischaemia, SA node disease etc. This causes an alteration in the depolarisation of the ventricles.
(3. ) LBBB = W in V1 (WiLLiaM) + M in V6
(4. ) RBBB = M in V1, W in V6 (MaRRoW)
Note: it w and m notches aren’t clear look in other chest leads such as V3.
RF for LBBB and RBBB?
(1. ) LBBB: Dilated Cardiomyopathy, LVH, HTN
(2. ) RBBB: Thin tall young people, PE
(3. ) MI Myocarditis
What would you seen in an ECG for atrial flutter
- ‘Sawtooth pattern’ in lead II, III, aVF
Causes of AF?
(1. ) CAD
(2. ) HTN
(3. ) Valvular heart disease
(4. ) Hypothyroidism
Symptoms of AF? (4)
- Breathlessness/dyspnoea
- Palpitations
- Syncope/dizziness
- Chest discomfort
Mx of AF
(1. ) CHA2DS2-Vasc
- Stroke risk assessed for pts w/ nonvalvular AF
- if >2 give anticoag
(2. ) Rate Control: BB or CCB
- if fails consider digoxin, then amiodarone
(3. ) Rhythm control: Cardioversion
- this is 1st line if acute + pt is haemodynamically unstable (inc RR, chest pain, hypotension, oedema) +/- amiodarone
- if refractory consider ablation
(4. ) Investigate underlying cause
- usually due to an inferior MI (RCA occlusion) -> carry out Ix for MI: tropnins, PCI Mx.
Describe what you’d see on an ECG for AF?
AF is an example of a SVT
(1. ) Absence of P waves
(2. ) Fibrillation in V1
(3. ) R-R interval is irregularly irregular
(4. ) QRS complex is narrow and irregular
What is paroxysmal AF?
spontaneous termination within 7 days - although this commonly occurs within 48hrs.
Describe the lead placement in an ECG
- V1 = right sternal edge, 4th ICS
- V2 = left sternal edge, 4th ICS
- V3 = halfway between V2 and V4
- V4 = 5th ICS in midclavicular line.
- V5 = anterior axillary line
- V6 = mid-axillary line
What are the types of arrhythmias are there?
(1. ) Tachycardia >100bpm
- This can be further subdivided into SVT (above ventricles) or ventricular
- SVT e.g. AF, flutter, sinus tachy
- Ventricular e.g. ventricular tachycardia, ventricular fibrillation
(2. ) Bradycardia <60bpm
- e.g. heart blocks, sinus bradycardia)
What would you seen in an ECG for a SVT condition
(1. ) Narrow QRS complex tacchycardia
(2. ) Ddx = AF, atrial flutter, sinus tachycardia, SVT
How would you manage a Sinus tachycardia?
(1. ) Treat underlying cause
(2. ) Give fluids as hypovolaemia usually causes s.tacy
How would you manage a pt where they’ve had or been given too much BB, CCB, digoxin?
(1. ) Glucagon for BB
(2. ) Ca for CCB
(3. ) Digibond for digoxin
Management of heart block
This is for symptomatic HB such as mobitz type 2, third degree heart block
(1. ) Atropine (dec PNS) which helps inc HR
(2. ) Epinephrine (inc SNS)
(3. ) Pacing
What are the four groups of antiarrhythmics drugs?
- class I, Na-channel blockers;
- class II, beta-blockers
- class III, K-channel blockers
- class IV, Ca-channel blockers; and miscellaneous antiarrhythmics
How do Na channel blockers work as anti-arrhythmics?
slows HR by slowing depolarization, reducing cell excitability, and reducing conduction velocity.
How do beta-blockers work? When is it CI?
(1. ) They act on beta-adrenergic receptors found in the heart (B1) and smooth muscles of vessels (B2). Activation of beta-R (via NA or Epi) causes a Ca influx into cells via L-type channels.
(2. ) B-blockers prevent this from happening, thus dec HR.
(3. ) CI = in pts on CCB, asthma
How do K-channel blockers work as anti-arrhythmics?
(1. ) K channels blockers causes less K to leave the cells, this reduces the rate of repolarisation.
(2. ) This prolongs AP and thus prolongs the refractory periods (where cell is unexcitable by new stimulus). So less likely to generate an AP.
(3. ) Longer repolarization prevents the fast conduction of AP throughout the heart, which eventually leads to a slower HR.
(4. ) Amiodarone is an example
How do CCB work and what are the two types and their uses?
(1.) CCB inhibit L-type Ca channels.
(2. ) The two groups are:
- Dihydropyridines: these are not antiarrhythmics and are selective for vascular smooth muscle and are used for HTN (e.g. amlodipine)
- Non-dihydropyridines: these are used to target myocytes (e.g. verapamil)
How does digoxin work
(1. ) Mimics the effect of the vagal nerve i.e. dec HR
(2. ) H/E digoxin has a narrow therapeutic window and an overdose could cause arrhythmias
Effect of hi and low K on ECG
(1. ) Hyperkalaemia:
- Tall T waves
- flattening of P waves
- broadening of QRS eventually ‘sine wave pattern’
(2. ) Hypokalaemia:
- Flattening of T wave
- QT prolongation
Effect of hi and low Ca on ECG
- Hypercalcaemia: QT shortening
- Hypocalcaemia: QT prolongation
Steps to ECG interpreting?
(1. ) Rate
(2. ) Rhythm
(3. ) Axis
(4. ) P, PR, QRS, ST, QT
Mx of SVT
Stable pt (i.e. no shock, syncopes, HF, MI)
(1. ) Valsvular movement e.g. blowing into syringe
(2. ) If fails consider IV adenosine
- this is CI in asthma
- consider BB or CCB
Unstable
(1. ) Synchronised DC shock
(2. ) IV amiodarone
When would use ECG in your IX?
(1. ) Chest pain
- Acute MI, pericarditis, PE
(2. ) Palpitations
(3. ) Breathlessness
- HF, LBBB, previous MI
(4. ) Blackout
Describe which part of the ECG represents the following:
(1. ) Ventricular repolarisation
(2. ) Atrial depolarisation
(3. ) Ventricular depolarisation of <120ms
(4. ) Normal duration of 120-200ms
(5. ) Assesses activity within lateral myocardial territory
(6. ) Assesses activity within inferior myocardial territory
(7. ) Yields complexes that are normally inverted compared to the anterior and inferior leads
(1. ) T-wave
(2. ) P-wave
(3. ) QRS complex
(4. ) PR-interval
(5. ) Leads I, avL, V5, 6
(6. ) Leads II, III, aVF
(7. ) aVR
