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what is the normal PR interval?
3-5 small squares
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what is the width of a normal QRS complex?
less than 3 small squares
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what does one small square represent?
0.04sec
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what does one large square represent?
0.2sec
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if there is an irregular rhythm, how do you work out the rate?
count the number of QRS complexes in 30 large squares (i.e. 6 seconds) and times by 10
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what are the p and t waves like in VT?
there are no P or T waves in VT
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describe the rhythm of mobitz 1?
regularly irregular
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describe the PR interval of mobitz1
PR interval is progressively prolonged until an impulse fails to be conducted to the ventricles and the cycle then repeats
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which are the septal leads?
V1, V2
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which are the inferior leads?
II, III, aVF
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which are the lateral leads?
i, aVL, V5, V6
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which are the anterior leads?
V3, V4
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what are the 3 disease processes for acute coronary syndrome?
- rupture of atherosclerotic plaque
- smooth muscle constriction
- thrombus formation
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what is ST Segment Depression a sign of?
myocardial ischaemia
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what is T wave inversion a sign of
myocardial ischaemia, but very non specific
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what is acute ST elevation a sign of?
possible acute MI
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what is Resolving ST elevation with Q wave formation a sign of?
usually a subsequent sign of a full thickness infarction
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describe cardiac chest pain - symptoms
- central crushing
- radiating to left side, jaw
- associated with sweaty, nausea, vomiting, SOB
- vice like pain
- sudden and severe
- gradually gets worse
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what are the physical signs of a patient suffering from cardiac chest pain?
- collapse
- nausea
- vomit
- sweaty/clammy
- altered vital signs
- irreg. heart beats/palps
- SOB
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how does unstable angina present? 3 ways
- angina of effort with growing frequency over days, provoked by less exertion
- angina occurring recurrently and UNPREDICTABLY - not specific to exercise
- unprovoked and prolonged episode of chest pain
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what are the ECG findings of unstable angina?
- normal
- ST depression = high risk
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what are the chemical findings of unstable angina?
- cardiac enzymes: usually normal
- troponin: minor release suggests high risk
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what is the initial treatment for all ACS?
- Oxygen
- Aspirin 300 mg orally (crush/chew)
- Nitroglycerine (GTN spray or tablet)
- Morphine (or diamorphine)
- call expert help!
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what is the definitive treatment for unstable angina?
- MONA
- LMW heparin
- beta blocker
- if high risk: glycoprotein IIb/IIIa inhibitor
- clopidogrel
- iv/buccal nitrate for ongoing chest pain
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what are the ECG findings of NSTEMI?
- non specific
- ST depression
- T wave inversion
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what are the chemical findings of NSTEMI?
- raised troponin release
- and elevated CKMB
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what are the ECG findings of STEMI?
- acute ST elevation
- with Q waves likely to develop later
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what are the chemical findings of STEMI?
- raised troponin release
- and elevated CKMB
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what is the definitive treatment for NSTEMI?
- MONA
- LMW heparin
- beta blocker
- if high risk:
- glycoprotein IIb/IIIa inhibitor
- clopidogrel
- iv or buccal nitrates for ongoing chest pain
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what is the definitive treatment for STEMI?
- after MONA
- early repercussion therapy: PCI (percutaneous coronary intervention) or thrombolysis
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which blood tests need to be done if ACS is suspected?
- FBC
- U&E
- clotting screen
- troponin
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what is the differential diagnosis for narrow complex tachycardia?
- 1. sinus tachycardia: normal P wave followed by normal QRS
- 2. atrial tachyarrhythmias including:
- a) atrial fibrillation: absent P wave, irreg. QRS
- b) atrial flutter: atrial rate usually 300bpm giving flutter/sawtooth baseline and ventricular rate 150bpm so 2:1 block
- c) atrial tachy: ban shape P waves, may outnumber QRS
- d) multifocal atrial tacky: 3or more P wave morphologies, irreg QRS
- supraventricular tachycardia: P wave absent or inverted after QRS
- 3. junctional tachycardia: rate 150-250bpm, P wave either buried in QRS or occurring after QRS
- a) AV nodal re-entry tachycardia
- b) AV re-entry tachycardia, includes access path e.g. WPW
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what is the initial treatment for SVT?
- O2, iv access
- check if rhythm is regular or irregular
- if irregular treat as AF
- if regular: vagal manoeuvres e.g. carotid sinus massage or valsalva manoeuvre
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if vagal manoeuvres are unsuccessful what should be given, how much? why? what is half life and MOA?
- adenosine 6mg bolus first: causes transient AV block
- WARN PT BEFORE ABOUT SE
- half life: short 10s!
- MOA: 2 ways
- 1. transiently slowing ventricles to show underlying atrial rhythm
- 2. cardioverting junctional tachycardia to sinus rhythm
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why are CSM or valsalva used?
transiently INCREASE AV block to unmask underlying atrial rhythm
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what are the SE of adenosine?
- transient chest tightness
- dyspnoea
- headache
- flushing
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what are the 3 relative CI to adenosine?
- asthma
- 2nd/3rd degree AV block
- sinoatrial disease (unless pacemaker)
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what is adenosine potentiated by?
dipyradimole
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what is adenosine antagonised by?
theophylline
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if adenosine is not effective in SVT what can be used? what does it depend on?
- pt stable: amiodarone
- pt unstable: sedation and DC cardioversion
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how can it be checked if a patient is stable?
- BP < 90
- HR > 200
- impaired consciousness
- heart failure
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what are the features of Mobitz II?
- intermittent failure of AV conduction
- get occasional missed QRS complexes after normal atrial contraction
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what is motibz II caused by?
- anterior wall MI
- degenerative changes in conduction system
- severe coronary artery diseae
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in mobitz II where is the problem?
- bundle of His
- bundle branches
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if a patient is uncompromised with motibz II what should be given and why?
- up to max 3mg atropine
- because higher risk of developing complete AV block or systole
- may need cardiac pacing
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once initial treatment for ACS has happened, which other investigations need to be done?
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