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4th year passmedicine by topic > Rhythm Control Agents > Flashcards

Rhythm Control Agents Flashcards

1
Q

Amiodarone is a class ?antiarrhythmic agent

A

Amiodarone is a class III antiarrhythmic agent

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2
Q

Amiodarone mechanism

A

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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3
Q

Amiodarone - loading doses are frequently used because

A

very long half-life (20-100 days)

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4
Q

Amiodarone causes thrombophlebitis because

A

it is usually/ideally administed via central veins

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5
Q

Amiodarone interacts with drugs commonly used because it is a

A

p450 inhibitor

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6
Q

Amiodarone has proarrhythmic effects due to lengthening of the QT interval

A

true

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7
Q

Monitoring of patients taking amiodarone

A

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

TFT, LFT every 6 months

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8
Q

Adverse effects of amiodarone use

A 
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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9
Q

Important drug interactions of amiodarone include:

A

decreased metabolism of warfarin, therefore increased INR

increased digoxin levels

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10
Q

decreased metabolism of warfarin leads to an increased/decreased INR

A

increased

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11
Q

Flecainide is a Vaughan Williams class ? antiarrhythmic.

A

Flecainide is a Vaughan Williams class 1c antiarrhythmic.

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12
Q

Flecainide mechanism

A

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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13
Q

Flecainide ECG changes

A

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

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14
Q

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

A

true

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15
Q

Flecainide contraindications

A

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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16
Q

Flecainide Adverse effects

A 
negatively inotropic
bradycardia
proarrhythmic
oral paraesthesia
visual disturbances
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17
Q

Adenosine is most commonly used to terminate

A

supraventricular tachycardias

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18
Q

Adenosine:

Mechanism of action

A

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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19
Q

Adenosine:

Half life

A

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

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20
Q

Adenosine: Adverse effects

A

chest pain
bronchospasm
transient flushing

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

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21
Q

The effects of adenosine are enhanced by

A

dipyridamole (antiplatelet agent)

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22
Q

The effects of adenosine are blocked by

A

theophyllines

23
Q

Adenosine should ideally be infused via a

A

large-calibre cannula due to it’s short half-life

24
Q

Digoxin Mechanism of action

A

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

25
Q

Digoxin is sometimes used for improving symptoms and mortality in patients with heart failure.

A

false

is sometimes used for improving symptoms (but not mortality) in patients with heart failure.

26
Q

digoxin has a narrow therapeutic index

A

true

27
Q

digoxin is monitored routinely

A

digoxin level is not monitored routinely, except in suspected toxicity

28
Q

digoxin if toxicity is suspected concentration should be measured within

A

8 to 12 hours of the last dose

29
Q

Digoxin toxicity

Plasma concentration alone determines whether a patient has developed digoxin toxicity

A

false

Digoxin toxicity - Plasma concentration alone does not determine whether a patient has developed digoxin toxicity

30
Q

Digoxin toxicity may occur even when the concentration is within the therapeutic range

A

true

31
Q

Digoxin toxicity BNF advises that the likelihood of toxicity increases progressively from

A

1.5 to 3 mcg/l.

32
Q

Digoxin toxicity features

A

generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia

33
Q

Digoxin toxicity management

A

Digibind
correct arrhythmias
monitor potassium

34
Q

Digoxin toxicity - Precipitating factors:
classically hypokalaemia
This is due to?

A

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

35
Q

Digoxin toxicity - Precipitating factors: drugs?

A

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

36
Q

Digoxin toxicity - Precipitating factors: electolytes

A

hypernatraemia
acidosis

hypokalaemia
hypomagnesaemia, hypercalcaemia, 
hypoalbuminaemia
hypothermia
hypothyroidism
37
Q

Digoxin toxicity - Precipitating factors:

A

increasing age
renal failure
myocardial ischaemia

38
Q

ECG: digoxin

A

down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

39
Q

Statins mechanism

A

inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.

40
Q

Statins adverse effects

A

myopathy

liver impairment

41
Q

Statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke

A

true
For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage

42
Q

Statins contraindications

A

macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course
pregnancy

43
Q

Who should receive a statin?

A

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

44
Q

Statins should be taken at night as

A

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.

45
Q

NICE currently recommends the following for the prevention of cardiovascular disease::

A

atorvastatin 20mg for primary prevention
increase the dose if non-HDL has not reduced for >= 40%
atorvastatin 80mg for secondary prevention

46
Q

Statins - risk factors for myopathy?

A

advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus

47
Q

statins - Myopathy is more common in

A

lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

48
Q

statins - myopathy: includes

A

myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase

49
Q

statins - checking LFTs at

A

checking LFTs at baseline, 3 months and 12 months.

50
Q

statins -treatment should be discontinued if

A

serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

51
Q

Nicotinic acid (niacin) is used in the treatment of patients with hyperlipidaemia

A

true

52
Q

Nicotinic acid (niacin) As well as lowering cholesterol and triglyceride concentrations it also raises

A

HDL levels.

53
Q

Nicotinic acid (niacin) Adverse effects

A

flushing: mediated by prostaglandins
impaired glucose tolerance
myositis

4th year passmedicine by topic (96 decks)

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