Pharmacology: Arrhythmias Flashcards
two mechanisms behind cardiac arrhythmias
- alterations in impulse formation
2. abnormalities in impulse conduction
two alterations in impulse formation
- change in automaticity
- triggered activity
describe change in automaticity
latent pacemakers take over the rhythm (faster than SA node) and there is a loss of overdrive suppression
when does an escape beat happen in changing automaticity
slow AV node
when does an ectopic beat happen in changing automaticity
if latent pacemakers fire faster e.g. ischaemia, hypokalaemia
two forms of triggered activity
early afterdepolarisations
delayed afterdepolarisations
describe early afterdepolarisations
occur in phase 2 or 3 and when the HR is slow, often stems from purkinje fibres and can lead to torsades de pointes
what is torsades de pointes
polymorphic VT
describe delayed afterdepolarisations
caused by increased Ca2+ and occurs when the heart rate is fast (can be caused by drugs e.g. digoxin
three categories of abnormalities in impulse conduction
- re-entry
- conduction block
- accessory tract
describe re-entry
re-entrant circuit with unidirectional block with retrograde conduction
what does conduction block through the AV node cause?
heart block
accessory tract
bundle of Kent is faster than the AV node and can trigger tachyarrhythmias
anti-arrhythmic drug classification
Vaughn-Williams
class 1A
Na+ channels at a moderate rate, slowing rise of AP and increasing refractory period
examples of class 1A drugs
disopyramide
procainamide
when are class 1A drugs used?
ventricular arrhythmias
class 1B
Na+ channels at a rapid rate, preventing premature beats (ischaemic zone)
when are class 1B drugs used
ventricular arrhythmias following MI
class 1C
Na+ channels at a slow rate, depressing conduction
when are class 1C used?
paroxysmal AF
adverse of 1C
can trigger ventricular arrhythmias
class II
beta blockers that decrease rate of depolarisation through SA and AV nodes
when are class II drugs used?
SVT
adverse of class II
excess sympathetic drive can trigger VT
class III
K+ channel openers that prolong AP and increase refractory period suppressing re-entry
when is class III used
SVT and VT(everything when other drugs are contradicted)
adverse of class III, specifically amiodarone
pulmonary fibrosis
thyroid disorders
photosensitivity
peripheral neuropathy
examples of class III
amiodarone and sotolol
example of class 1B
lidocaine
example of 1C
flecainide
example of class II
metoprolol
class IV
Ca2+ blockers, slow conduction in SA and AV and decrease force of cardiac contraction
when is class IV used?
atrial flutter
AF
adverse of Ca2+ blockers
can cause heart block (largely replaced by adenosine)
example of a class IV drug
verapamil
mechanism of action of adenosine
activates A1-adenosine receptors (Gi/o) opening ACh-sensitive K+ channels causing hyperpolarisation, suppressing conduction
when is adenosine used?
paroxysmal SVT e.g. WPW
role of digoxin
stimulates vagal activity slowing conduction and prolonging refractory period
when is digoxin used?
AF
when is digoxin used?
slow fast AF
ECG in digoxin toxicity
reverse tick (downward sloping of ST wave with rapid upstroke back to isoelectric line with bradycardia)
when should digoxin, amiodarone and verapamil be avoided (slow AV conduction)?
aberrant pathways
SE of amiodarone
thyroid disease
liver disease
pulmonary fibrosis
peripheral neuropathy
monitoring in amiodarone
TFTs and LFTs every 6 months
