Rhythm Control Agents Flashcards
Amiodarone is a class ?antiarrhythmic agent
Amiodarone is a class III antiarrhythmic agent
Amiodarone mechanism
blocking potassium channels which inhibits repolarisation and hence prolongs the action potential.
Amiodarone also has other actions such as blocking sodium channels (a class I effect)
Amiodarone - loading doses are frequently used because
very long half-life (20-100 days)
Amiodarone causes thrombophlebitis because
it is usually/ideally administed via central veins
Amiodarone interacts with drugs commonly used because it is a
p450 inhibitor
Amiodarone has proarrhythmic effects due to lengthening of the QT interval
true
Monitoring of patients taking amiodarone
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months
Adverse effects of amiodarone use
thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval
Important drug interactions of amiodarone include:
decreased metabolism of warfarin, therefore increased INR
increased digoxin levels
decreased metabolism of warfarin leads to an increased/decreased INR
increased
Flecainide is a Vaughan Williams class ? antiarrhythmic.
Flecainide is a Vaughan Williams class 1c antiarrhythmic.
Flecainide mechanism
It slows conduction of the action potential by acting as a potent sodium channel blocker (specifically the Nav1.5 sodium channels).
Flecainide ECG changes
reflected by widening of the QRS complex and prolongation of the PR interval.
Flecainide was actually shown to increase mortality post-myocardial infarction and is, therefore, contraindicated in this situation.
true
Flecainide contraindications
post myocardial infarction
structural heart disease: e.g. heart failure
sinus node dysfunction; second-degree or greater AV block
atrial flutter
Flecainide Adverse effects
negatively inotropic bradycardia proarrhythmic oral paraesthesia visual disturbances
Adenosine is most commonly used to terminate
supraventricular tachycardias
Adenosine:
Mechanism of action
causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
Adenosine:
Half life
adenosine has a very short half-life of about 8-10 seconds
Adenosine: Adverse effects
chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
The effects of adenosine are enhanced by
dipyridamole (antiplatelet agent)
The effects of adenosine are blocked by
theophyllines
Adenosine should ideally be infused via a
large-calibre cannula due to it’s short half-life
Digoxin Mechanism of action
decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
Digoxin is sometimes used for improving symptoms and mortality in patients with heart failure.
false
is sometimes used for improving symptoms (but not mortality) in patients with heart failure.
digoxin has a narrow therapeutic index
true
digoxin is monitored routinely
digoxin level is not monitored routinely, except in suspected toxicity
digoxin if toxicity is suspected concentration should be measured within
8 to 12 hours of the last dose
Digoxin toxicity
Plasma concentration alone determines whether a patient has developed digoxin toxicity
false
Digoxin toxicity - Plasma concentration alone does not determine whether a patient has developed digoxin toxicity
Digoxin toxicity may occur even when the concentration is within the therapeutic range
true
Digoxin toxicity BNF advises that the likelihood of toxicity increases progressively from
1.5 to 3 mcg/l.
Digoxin toxicity features
generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia
Digoxin toxicity management
Digibind
correct arrhythmias
monitor potassium
Digoxin toxicity - Precipitating factors:
classically hypokalaemia
This is due to?
digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
Digoxin toxicity - Precipitating factors: drugs?
drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics
Digoxin toxicity - Precipitating factors: electolytes
hypernatraemia
acidosis
hypokalaemia hypomagnesaemia, hypercalcaemia, hypoalbuminaemia hypothermia hypothyroidism
Digoxin toxicity - Precipitating factors:
increasing age
renal failure
myocardial ischaemia
ECG: digoxin
down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
Statins mechanism
inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
Statins adverse effects
myopathy
liver impairment
Statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke
true
For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage
Statins contraindications
macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course
pregnancy
Who should receive a statin?
all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
anyone with a 10-year cardiovascular risk >= 10%
patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins
patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
Statins should be taken at night as
this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins.
NICE currently recommends the following for the prevention of cardiovascular disease::
atorvastatin 20mg for primary prevention
increase the dose if non-HDL has not reduced for >= 40%
atorvastatin 80mg for secondary prevention
Statins - risk factors for myopathy?
advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus
statins - Myopathy is more common in
lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
statins - myopathy: includes
myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase
statins - checking LFTs at
checking LFTs at baseline, 3 months and 12 months.
statins -treatment should be discontinued if
serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
Nicotinic acid (niacin) is used in the treatment of patients with hyperlipidaemia
true
Nicotinic acid (niacin) As well as lowering cholesterol and triglyceride concentrations it also raises
HDL levels.
Nicotinic acid (niacin) Adverse effects
flushing: mediated by prostaglandins
impaired glucose tolerance
myositis
