Rhythm Control Agents Flashcards by Dua Khan

Amiodarone is a class ?antiarrhythmic agent

Amiodarone is a class III antiarrhythmic agent

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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)

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Amiodarone - loading doses are frequently used because

very long half-life (20-100 days)

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Amiodarone causes thrombophlebitis because

it is usually/ideally administed via central veins

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Amiodarone interacts with drugs commonly used because it is a

p450 inhibitor

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Amiodarone has proarrhythmic effects due to lengthening of the QT interval

true

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Monitoring of patients taking amiodarone

TFT, LFT, U&E, CXR prior to treatment

TFT, LFT every 6 months

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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

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Important drug interactions of amiodarone include:

decreased metabolism of warfarin, therefore increased INR

increased digoxin levels

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decreased metabolism of warfarin leads to an increased/decreased INR

increased

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Flecainide is a Vaughan Williams class ? antiarrhythmic.

Flecainide is a Vaughan Williams class 1c antiarrhythmic.

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Flecainide mechanism

It slows conduction of the action potential by acting as a potent sodium channel blocker (specifically the Nav1.5 sodium channels).

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Flecainide ECG changes

reflected by widening of the QRS complex and prolongation of the PR interval.

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Flecainide was actually shown to increase mortality post-myocardial infarction and is, therefore, contraindicated in this situation.

true

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Flecainide contraindications

post myocardial infarction
structural heart disease: e.g. heart failure
sinus node dysfunction; second-degree or greater AV block
atrial flutter

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Flecainide Adverse effects

negatively inotropic
bradycardia
proarrhythmic
oral paraesthesia
visual disturbances

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Adenosine is most commonly used to terminate

supraventricular tachycardias

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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

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Adenosine:

Half life

adenosine has a very short half-life of about 8-10 seconds

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Adenosine: Adverse effects

chest pain
bronchospasm
transient flushing

can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

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The effects of adenosine are enhanced by

dipyridamole (antiplatelet agent)

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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