Prescribed Drugs And ECGs Flashcards
Describe the normal ventricular action potential
Baseline - slow leaky Na channel Upstroke - voltage gated Na channel Down blip - voltage gated K leaving Plateau - K still leaving but Ca in through L type CC Downstroke - CC close so just K leaving
Describe the pacemaker cell action potential
Initial up - T type Ca open so Ca in
Upstroke - L type Ca open so Ca in
Downstroke - K channel open so K out
Baseline - slow leaky Na channel
What happens to the ECG when Na channels are blocked and why
Reduced rate and rise of ventricular cell action potential
Wide QRS
Elevated R in AVR
+/- RBBB
VT and VF can occur due to the slowed conduction resulting in re-entrant circuits
Which drugs inhibit fast Na channels
CVS: class 1a/c antiarrythmics, propranolol, verapamil
Psych: carbamezapine, amitriptyline, citalopram
Illicit: cocaine
Amantadine
Antihistamine
Antimalarials (chloroquine)
Describe the ECG in hyperkalaemia
Peaked T wave
Small, broad P
Wide QRS
Prolonged PR
Describe the ECG changes when calcium channels are blocked
Pacemaker cells slow/unable to initiate a cardiac impulse - sinus brady +/- av blocks
You may get ventricular escape rhythms - wide QRS
Name some calcium channel blockers
Nifedipine
Amlodipine
Verapamil
Diltiiazem
What can nifedipine do to an ECG
Reflex tachycardia
What does blocking the K channel do to an ECG
Prolongs the action potential (delayed repolarisation) = QT prolongation. This can lead to TdP
Delayed repolarisation minimises the difference of charge across the membrane = depolarisation can happen again early = early afterdepolarisation. This can lead to re-entry and polymorphic VT
U wave is often prominent in precordial leads
Why do you get VT with K channel blocking drugs
The delay in repolarisation leads to a reduced difference in charge across the membrane. This can lead to early afterdepolarisations which then lead to re-entry tachycardia
which drugs block the K channel
CVS: antiarrhythmics 1a/1c/3
Psych: tricyclics, citalopram, antipsychotics (chlorpromazine, haloperidol, olanzapine)
Antihistamine
Antimalarials
Antibiotics: ciprofloxacin, clarithromycin, erythromycin
What does digoxin do to an ECG
Digoxin toxicity: Atrial tachycardia with AV block (due to increased vagal tone causing AVN depression). Can lead to ventricular ectopics
Digoxin effect: Flat/inverted T and ST depression and Short QT
How does digoxin work (ions and channels)
Blocks NaKATPase
Intracellular Na rises
Intracellular Ca rises
Positive inotropic effect
Action of sympathetics on the heart (receptor and ions)
B1 receptor
Increase permeability to Na and Ca to increase excitability therefore increased conduction
What are the action of parasympathetics on the heart (receptor and effect)
Muscarinic receptors
Reduce atria exciteability
Slow the conduction to the ventricles
B blockers do what to an ECG
Bradycardia
+/- AV block (long PR often first sign)
+/- prolong QT - sotalol
+/- wide QRS - propranolol
Why would you end up with TdP, VT or VF in B blocker OD
Sotalol and propranolol prolong the QT interval due to blocking the K channel
If you block the sympathetic system what ECG changes might you see
Bradycardia
AV block
What do sympathomimetics do to an ECG
Sinus or atrial tachycardia
+/- ventricular dysarrhythmias in high dose
What do anticholinergics do to an ECG
Sinus and atrial tachycardia
Premature ventricular beats
Name some drugs with an anti cholinergic effect
Antihistamines
Atropine
TCAs
Antipsychotics eg clozapine
What do cholinomimetics do to an ECG
Bradycardia
AV block
What HR would you expect with the various escape rhythms
AVN: 40-60bpm
Ventricular: 20-40bpm
Which drugs prolong your QT interval
CVS: antiarrhythmics 1a/1c/3, sotalol
Psych: TCAs, citalopram, antipsychotics (haloperidol, chlorpromazine, olanzapine)
Antihistamines
Antimalarials
Antibiotics (clarythromycin, erythromycin, ciprofloxacin)
How is TdP treated immediately
IV MgSO4 2g over 10 minutes
Or
4ml 50% Mg
Compare PMVT and TdP
PMVT: multiple ventricular foci and therefore QRS morphology is constantly changing, it is a wide complex tachycardia, AV dissociation
TdP: PMVT + QT prolongation needed for diagnosis. QRS twists around the isoelectric point
What can often be the first sign of CCB or Bblocker toxicity
Prolonged PR interval (even in absence of bradycardia)
What ion channel does propranolol effect in OD and what is the result
Fast sodium channels
QRS widening with a positive R wave in AVR
What ion channel does sotalol block in toxicity and what is the result
Potassium channels
QT prolongation which can lead to TdP
What channels are effected in TCA OD and what is the result?
Muscarinic - sinus tachy
Fast Na - wide QRS (lead to VT) + Tall R in AVR
K - QT prolongation
Other than ECG changes how might someone with TCA toxicity present
Anticholinergic toxidrome
Hypotension
Seizures
How is TCA toxicity managed
IV sodium bicarb an hyperventilate
+ activated charcoal, benzo’s for seizures, fluids for hypotension
