Arrhythmias Flashcards

1
Q

Define arrhythmia

A

An arrhythmia is a condition in which the heart beats with an irregular or abnormal rhythm.

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2
Q

What is Atrial fibrillation

A

In atrial fibrillation, electrical impulses do not originate in the sinoatrial node, but from a different part of the atrium or the nearby pulmonary veins. These abnormal electrical impulses become rapid and disorganised… radiating through the atrial walls in an uncoordinated manner. This can cause the walls of the atria to fibrillate (quiver rapidly) rather than contracting normally. During AF, because the Atria do not contract regularly, blood does not empty efficiently into the ventricles and begins to pool in the atria… which can cause clots to form. If blood clots become dislodged, they can travel to brain causing a stroke.

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3
Q

Treatment of AF

A
  • Treatment aims to prevent complications such as Stroke and VTE.
  • AF can be managed by controlling ventricular rate (‘rate control’) or attempting to restore and maintain sinus rhythm (‘rhythm control’).
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4
Q

Rate control

A
  1. Rate control is the preferred first line option using a BETA-BLOCKER (not sotalol) or rate-limiting CALCIUM-CHANNEL BLOCKER (e.g. Diltiazem or Verapamil) except in patients with new-onset AF, atrial flutter suitable for an ablation strategy, AF with a reversible cause, or if rhythm control more suitable. Digoxin is effective in predominantly sedentary patients with non-paroxysmal AF.
  2. When a single drug fails to control ventricular rate… a combination of two drugs (beta blocker, DIGOXIN or diltiazem) can be used.
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5
Q

Rhythm control

A
  1. Rhythm control is achieved using a BETA-BLOCKER. If a beta-blocker is ineffective or not tolerated, use an oral anti-arrhythmic drug such as SOTALOL, FLECAINIDE, PROPAFENONE OR AMIODARONE
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6
Q

Which anti-arrhythmic drugs can be classified into those that act on Supraventricular arrhythmias

A

Supraventricular arrhythmias (occur in the area above the ventricles) in the atria. An example of this is Verapamil.

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7
Q

Anti-arrhythmic drugs which act on both supraventricular and ventricular arrhythmias

A

Amiodarone

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8
Q

Drugs that act on only ventricular arrhythmias

A

Lidocaine

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9
Q

usually treatment of choice for terminating paroxysmal supraventricular tachycardia

A

• Adenosine is usually treatment of choice for terminating paroxysmal supraventricular tachycardia. As it has a very short half-life (8-10 secs, but prolonged if taking dipyridamole).

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10
Q

Can adenosine be used after a b-blocker

A

yes unlike verapamil

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11
Q

Most preferable in asthma - adenosine or verapamil

A

Verapamil

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12
Q

Vaughan Williams Classification (alternate classification but less clinical significance):

  • Class I:
  • Class II:
  • Class III:
  • Class IV:
A
  • Class I: membrane stabilising drug (e.g. Lidocaine, Flecainide)
  • Class II: Beta-blockers
  • Class III: Amiodarone, Sotalol (also Class II)
  • Class IV: CCB (includes Verapamil but not dihydropyridines).
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13
Q

Amiodarone: HIGH RISK MEDICINE

A

 This drug should only be initiated under specialist supervision, usually in a hospital setting
 It has a very long half-life (several weeks) and only needs to be given ONCE daily. But high doses can cause nausea, unless divided.
 It can take weeks or months to reach a steady state, but I.V. Amiodarone acts relatively rapidly.

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14
Q

Side effects of Amiodarone

A
  • Side effects: change in taste, constipation, corneal deposits, hypothyroidism, movement disorders, photosensitivity reaction, vomiting, hypotension (following rapid IV injection)
  • Other side effects: arrhythmias, hepatic disorders, hyperthyroidism, nausea, respiratory disorders and skin reactions

 Most patients will develop corneal microdeposits (reversible on withdrawal) … these rarely interfere with vision, but drivers may be dazzled by headlights at night. Amiodarone can cause phototoxicity … so, advise patients to shield skin from sunlight using wide-spectrum sunscreen
 It contains iodine which can cause both hyper/hypothyroidism, monitor Thyroid function every 6 months.
 Patients showing signs of weight loss, palpitations and insomnia may be suffering from Hypothyroidism associated with amiodarone use.
 This drug may cause slight grey skin discolouration as a side-effect, this is common
 Pneumonitis should be suspected if new/progressive shortness of breath or cough develops. Neurological symptoms suggest the patient is experiencing peripheral neuropathy (nerve dysfunction)

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15
Q

Monitoring with amiodarone

A

 LFTs are required before treatment + then every 6 months. Any signs of hepatoxicity mean the drug should be stopped.
 It contains iodine which can cause both hyper/hypothyroidism, monitor Thyroid function before treatment and then every 6 months.
o Serum potassium concentration should be measured before treatment.
o Chest x-ray required before treatment.
• IV: monitor ECG, liver transaminases and resuscitation facilities must be available.

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16
Q

Amiodarone interactions

A

 Amiodarone increases plasma concentration of warfarin, digoxin, diltiazem, verapamil and phenytoin (thus, half dose of digoxin).
 There is an increased risk of arrhythmias if given with amitriptyline, lithium, quinines, erythromycin and haloperidol.
 Avoid concomitant use of amiodarone with Sofosbuvir and daclatasvir, simeprevir and sofosbuvir, or sofosbuvir and ledipasvir, due to risk of bradycardia and heart block (signs include - SOB, light-headedness, palpitations, fainting, unusual tiredness or chest pain)
 Avoid in Pregnancy + Breastfeeding and increased risk of Myopathy If given with Simvastatin.

17
Q

B-blockers mode of action and uses

A
  • Reduce cardiac output by BLOCKING beta-receptors in the heart. They also act on beta-receptors in the liver, bronchi and pancreas.
     Beta-blockers are also of use in angina by reducing the work of the heart, and may prevent recurrence of MI
     They block sympathetic activity in HF. Bisoprolol and carvedilol can reduce the mortality of HF.
     Additionally, beta-blockers can be used for symptoms of anxiety (Propranolol) and in the prophylaxis of migraine.
     They reduce Blood pressure through various (not fully understood) mechanisms.
18
Q

B-blockers contra-indicated in

A
  • Contraindicated in patients with second- or third-degree heart block
  • Beta-blockers should not be suddenly stopped – advise patients to seek advice from their GP.
  • Due to their action on the bronchi they can cause bronchospasm and should usually be avoided in patients with asthma. Patients who suffer from COPD or Asthma would require a cardio selective beta blocker e.g. Atenolol, Bisoprolol, Metoprolol, Nebivolol, Acebutolol.
  • Due to their action on the liver and pancreas they can affect carbohydrate metabolism causing either hyper- or hypoglycæmia in patients with or without diabetes. They can still be used in diabetes with caution.
19
Q

Water-soluble B-blockers

A

Celiprolol, Atenolol, Nadolol and Sotalol (CANS) are water-soluble and can’t cross the BBB, causing less sleep disturbances and nightmares.

20
Q

Digoxin (Cardiac Glycoside): HIGH RISK MEDICINE - mode of action and half life

A
  • Digoxin increases force of myocardial contraction (positively inotropic) and reduces heart rate (negatively chronotopic). It can be used for Atrial fibrillation or flutter and heart failure.
  • It has a long half-life hence once daily dosing, but if patient is seeing no effect then dose can be increased to ONE tablet TWICE daily. Dose is determined by renal function. Can be taken with or without food. Try to take them at the same time each day.
  • In AF and atrial flutter, digoxin is used to reduce ventricular rate. However, a β-blocker or non-dihydropyridine CCB is usually more effective.
  • In severe HF, digoxin is used as a third-line treatment in patients who are already taking an ACE inhibitor, β-blocker and either an aldosterone antagonist or ARB. It is used at an earlier stage in patients with co-existing AF.
21
Q

Blood monitoring with digoxin

A

• If blood monitoring is required a sample should be taken at least 6 hours after a dose.

22
Q

Digoxin increases the risk of..

A

Digoxin increases the risk of hypokalaemia and ways to overcome this are to take potassium-sparing diuretics, potassium supplements or eating food with high potassium e.g. banana’s.

23
Q

• Signs + symptoms of Digoxin Toxicity:

A

• Nausea/vomiting, blurred/yellow vision, weight loss, anorexia, palpitations, hallucinations, abdominal pain. Patients suffering from digoxin toxicity will be treated with a digoxin specific antibody fragment a.k.a. Digifab

24
Q

Liquid and tablet formulations of digoxin

A

Liquid and tablet formulations have DIFFERENT BIOAVAILABILITIES, thus the patient’s dose will change.

25
Q

Side effects of digoxin

A

• Side effects - bradycardia, sickness, GI disturbance (diarrhoea), rash, headache, dizziness and visual disturbance (blurred or yellow vision).

26
Q

Digoxin interaction

A
  • Manufacturer advises reduce dose by half with concurrent use of amiodarone, dronedarone and quinine.
  • Digoxin may worsen conduction abnormalities, so is contraindicated in 2nd degree heart block and intermittent complete heart block. It shouldn’t be used in patients with or at risk of ventricular arrhythmias.
  • The dose should be reduced in renal failure, as digoxin is eliminated via kidneys.
  • Certain electrolyte abnormalities increase the risk of digoxin toxicity, including hypokalaemia, hypomagnesaemia and hypercalcaemia. Potassium disturbance is probably the most important of these, as digoxin competes with potassium to bind the Na+/K+ ATPase pump. When serum potassium levels are low, competition is reduced, and the effects of digoxin are enhanced.
  • Loop and thiazide diuretics increase risk of toxicity by causing hypokalaemia.
  • Amiodorone, CCB, spironolactone and quinine can all increase the plasma concentration of digoxin and risk of toxicity.
  • Avoid taking indigestion remedies for at least one hour before and after. They can reduce the amount of digoxin your body absorbs