Atrial Fibrillation Flashcards

1
Q

Describe in basic terms what AF is

A

The SA node is disregulated, sending multiple signals, resulting in fibrillation rather that contraction of the atria, resulting in a loss of atrial kick

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2
Q

What are some risk factors for AF

A

HTN, heart disease, valvular disease (pt heart in an ineffective state), obesity, diabetes, genetic predisposition

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3
Q

Stress on the atria causes……

A

Tissue heterogeneity, whereby the cells develop different electrical properties, causing unpredictable electrical signals

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4
Q

What dose paroxysmal AF refer too

A

Intermittent AF

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5
Q

Over time paroxysmal AF leads too…..

A

Over time these episodes lead to more stress on the atria more (calcium overload) leading to progressive fibrosis (scarring) leading to more persistent AF

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6
Q

Symptoms of AF

A

Fatigue, dizzy, SOB, weakness, Palpitations

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7
Q

Why are people in AF at an increased risk of stroke

A

Atria is quivering, not pumping blood effectively, thus blood in the atria can become stagnant.
When clots dislodge they can end up in the brain

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8
Q

What class of drug is metoprolol

A

Beta blocker

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9
Q

Beta blocks block…..

A

The affect of adrenaline or noradrenaline on the sympathetic nervous system

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10
Q

What is activated when the SNS is activated

A

Catecholamines, which stimulates adrenaline and noradrenaline to be thrown at organs leading to increase HR and other affects of adrenaline

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11
Q

What receptors are stimulated when fight or flight is activated

A

Adnergic receptors, alpha and beta

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12
Q

Beta blockers antagonise (block)…….

A

B adrenergic receptors

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13
Q

Beta blockers all end in the suffix…

A

Olol

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14
Q

How dose inhibiting B1 help AF

A

Decreases HR and cardiac output, helping the heart to fill slower and regain an atrial kick, becoming a more effective pump

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15
Q

Treatment If the patient is not compromised or is mildly compromised(rate over 120)

A

Administer 50 mg metoprolol tartrate PO.

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16
Q

Treatment if If the patient is moderately compromised

A

Administer 300 mg of amiodarone IV (over approximately 30 minutes).

Administer a further 150 mg of amiodarone IV over approximately 30 minutes if the ventricular rate remains predominantly greater than 120/minute.

Seek clinical advice if backup is not available for amiodarone, or amiodarone is contraindicated.

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17
Q

If the patient is severely compromised

A

Reconsider the diagnosis because it is very rare for atrial fibrillation or atrial flutter to cause severe compromise.
If the patient can obey commands:

Administer 0.5-1 mg/kg of ketamine IV (up to a maximum of 100 mg) to induce dissociation, and Cardiovert using maximum joules in synchronised mode. Repeat this once if the rhythm fails to revert.

If the patient cannot obey commands:
Cardiovert using maximum joules in synchronised mode. Repeat this once if the rhythm fails to revert.

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18
Q

Patients suitable for referral to primary care are

A

Those who are known to have paroxysmal atrial fibrillation and the rhythm reverts with metoprolol PO alone.

Those who have chronic atrial fibrillation, but the rate is now controlled with metoprolol PO alone and there are no active symptoms of myocardial ischaemia.

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19
Q

When do we see severe cardiac compromise in AF

A

It is rare for atrial fibrillation to be the primary cause of severe cardiovascular compromise. For this to occur it usually requires a combination of a very fast ventricular rate (160-200/minute) and severe heart disease.

If the patient is severely compromised, it is much more likely that there is another underlying condition such as septic shock and the diagnosis must be reconsidered prior to providing specific treatment for the dysrhythmia.

20
Q

Treatment of sepsis induced AF

A

Amiodarone should only be administered in the setting of sepsis if the patient is normotensive, the ventricular rate has failed to settle with 0.9% sodium chloride IV and cooling, and the patient has significant symptomatic myocardial ischaemia.

21
Q

Metoprolol mechanism of action

A

Metoprolol is an immediate release beta blocker. It antagonises (blocks) beta-1 receptors in the heart, causing a decrease in heart rate, cardiac output and blood pressure.

22
Q

Metoprolol indication

A

Adults with mild or no cardiovascular compromise as a result of fast atrial fibrillation or atrial flutter.
Adults with moderate cardiovascular compromise as a result of fast atrial fibrillation or atrial flutter, if amiodarone is not available or is contraindicated

23
Q

Metoprolol contraindications

A

Known severe allergy.

Hypotension. Metoprolol will further reduce the blood pressure

24
Q

Metoprolol cautions

A

First degree heart block. Metoprolol may cause bradycardia.

Known sick sinus syndrome without an internal pacemaker in place. Metoprolol may cause bradycardia.

Previous second or third degree heart block without an internal pacemaker in place. Metoprolol may cause worsening of heart block and bradycardia.

Asthma or COPD. Metoprolol may cause bronchospasm and should usually be withheld if the patient regularly takes bronchodilators.

Heart failure. Metoprolol will reduce cardiac output and may make heart failure worse. Pregnancy.

25
Q

Thoughts on metoprolol in pregnancy

A

Safety has not been demonstrated during pregnancy. The likelihood of administration being required in a woman who is pregnant is so low that personnel must seek clinical advice prior to administration.
May be administered if the patient is breastfeeding. Advise the patient to stop breastfeeding and seek further advice from their lead maternity carer or GP.

26
Q

Dosage of metoprolol

A

50 mg oral

27
Q

Adverse affects of metoprolol

A

Nil

28
Q

Onset of metoprolol

A

10-20 mins

29
Q

Duration of metoprolol

A

4-6 h

30
Q

Common interactions of metoprolol

A

The blood pressure effect will be potentiated by other medicines that lower blood pressure. For example, GTN, antihypertensive medicines and amiodarone.
The heart rate effects will be potentiated by other medicines that lower the heart rate. For example, amiodarone and centrally acting calcium channel blockers such as diltiazem.

31
Q

Use of metoprolol when patient is already beta blocked

A

Patients with chronic or paroxysmal atrial fibrillation/atrial flutter may be prescribed a beta blocker. Personnel should still administer metoprolol as indicated, even if the patient has taken their own beta blocker

32
Q

Mechanism of amiodarone

A

Amiodarone is an antidysrhythmic with a broad spectrum of activity.
Amiodarone has predominantly class III activity. It prolongs the action potential duration, reduces automaticity and prolongs the refractory period of atrial, nodal and ventricular tissues.
The electrophysiological effects result in a reduction in abnormal electrical activity (for example ectopy), a reduction in electrical conduction, a reduction in heart rate and a stabilisation of the SA and AV nodes.
Amiodarone also causes a small increase in coronary blood flow (although this is not usually clinically significant) and a reduction in myocardial oxygen consumption by reducing inotropy (the force of cardiac contraction).

33
Q

Indications of amiodarone

A

Cardiac arrest with VF or VT at any time after the first dose of adrenaline.
Adults with sustained VT in the absence of cardiac arrest.
Adults with moderate cardiovascular compromise as a result of fast atrial fibrillation or fast atrial flutter.

34
Q

Contrindactions of amiodarone

A

Known severe allergy.
Known severe allergy to iodine.
VT secondary to cyclic antidepressant poisoning. In this setting amiodarone administration can be associated with severe worsening of shock, without resolution of the rhythm.

35
Q

Cautions of amiodarone

A

None if the patient is in cardiac arrest.

Poor perfusion or signs of low cardiac output. Amiodarone reduces inotropy and may cause a significant fall in cardiac output, particularly when administered rapidly.

Hypotension. Amiodarone causes vasodilation and may worsen hypotension, particularly when administered rapidly.

Atrial fibrillation associated with sepsis. Amiodarone may cause a significant fall in cardiac output.

Known sick sinus syndrome without an internal pacemaker in place. Amiodarone slows the heart rate and severe bradycardia may occur following reversion of a tachydysrhythmia.

Previous 2nd or 3rd degree heart block without an internal pacemaker in place. Amiodarone slows the heart rate and severe bradycardia may occur following reversion of a tachydysrhythmia.

Pregnancy.

36
Q

Doseage of amiodarone in AF

A

Tachydysrhythmia in an adult:
300 mg IV over 30 minutes.
A further 150 mg IV over 30 minutes may be administered if the tachydysrhythmia persists.

37
Q

Admin of amiodarone

A

Tachydysrhythmia:
Place 300 mg of amiodarone in 100 ml of 5% glucose and label. 1 drop/second via a standard IV administration set will deliver 100 ml over approximately 30 minutes. Slow the rate of infusion if hypotension occurs.
The administration set will need to be flushed with 0.9% sodium chloride to ensure that all of the amiodarone has been administered.
An IV infusion over 30 minutes is the preferred method of administration. However, it is acceptable to dilute 300 mg of amiodarone to a total volume of 20-30 ml using 5% glucose or 0.9% sodium chloride. Administer this IV over 30 minutes and slow the rate of infusion if hypotension occurs.

38
Q

Adverse affects of amiodarone

A

Hypotension. Lightheadedness. Bradydysrhythmia.

39
Q

Adverse affects of amiodarone

A

Hypotension. Lightheadedness. Bradydysrhythmia.

40
Q

Amiodarone onset

A

5-10 mins

41
Q

Amiodarone duration

A

1-4 hours after a single dose.
Amiodarone is taken up into tissues and slowly released. This may result in a prolonged half-life, particularly when more than one dose has been administered. This is why many references quote a half- life of 10-60 days, but the clinical duration of effect is much shorter than this.

42
Q

Amiodarone preparation

A

Ampoule containing 150 mg in 3 ml.

43
Q

Common interactions of amiodarone

A

May potentiate the action of cyclic antidepressants in cyclic poisoning.
May cause bradycardia following reversion of dysrhythmia if the patient is taking a beta-blocker and/or a centrally acting calcium channel blocker (for example diltiazem).

44
Q

If the indication is atrial fibrillation causing moderate cardiovascular compromise, the goal of treatment is

A

to control the ventricular rate and not to revert the rhythm to sinus rhythm, although treatment with amiodarone may result in reversion of the rhythm to sinus rhythm. If a patient has been in atrial fibrillation for longer than a few days, there is a small risk that this may be associated with emboli leaving the left atrium. This is why amiodarone is reserved for patients with cardiovascular compromise that is clinically significant.

45
Q

Simple explination of amiodarone mechanism

A

Blocks channels and beta adrpergic receptors, stopping overactive signals thus stabilising heart rhythm