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PA20016 > Heart 2 need to finish > Flashcards

Heart 2 need to finish Flashcards

1
Q

What is one of the classifications for anti-arrhythmic drugs?

A

The Vaughan Williams Classification.

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2
Q

What are the 4 different classes of anti-arrhythmic drugs?

A

Sodium channel blockers, beta-blockers, drugs that prolong the action potential duration and calcium channel blockers.

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3
Q

What are examples of sodium channel blockers?

A

Disopyramide, lidocaine, flecainide.

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4
Q

What are some examples of beta blockers?

A

Propranolol, atenolol, esmolol.

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5
Q

What are some examples of drugs that prolong the action potential duration?

A

Amidorane, sotalol.

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6
Q

What are some examples of calcium channel blockers?

A

Verapamol, ditiazeam.

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7
Q

What is the mechanism for sodium channel blockers?

A

They block opened fast voltage-activated sodium channels and slow down the upstroke of the cardiac action potential and therefore slow down the action potential conduction. They act on the Bundle of His, Purkinje fibres and on ventricular and atrial myocytes.

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8
Q

What does it mean that sodium channel blockers are use dependent?

A

The block is increased with increased heart rate - reducing action potential frequency.

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9
Q

How does the dissociation rate for different sodium channel blockers vary?

A

(group 1) Disopyramide, procainamide and quinidine have an immediate dissociation rate, (group 2)lidocaine has a fast dissociation rate and flecainide and propafenone have a slow dissociation rate.

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10
Q

How are group 1 and 2 sodium channel blockers different to group 3 sodium channel blockers?

A

Group 1 and 2 also block K+ channels in phase 3, causing a prolonged QT phase.

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11
Q

What are the adverse effects of group 1 sodium channel blockers?

A

Atropine-like effects if given orally, myocardial dysfunction (negative inotropic effect).

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12
Q

What are the adverse effects of group 2 sodium channel blockers?

A

CNS effects - drowsiness, disorientation, convulsions, respiratory depression.

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13
Q

What are the adverse effects of group 3 sodium channel blockers?

A

They can cause sudden cardiac death in patients with myocadial infarction.

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14
Q

What is the mechanism of beta blockers?

A

They block cardiac beta1 adrenoceptors.

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15
Q

How do the examples of beta blockers vary?

A

Propranolol is a long acting non-selective beta blocker, atenolol is beta1 selective and is water soluble, esmolol is a short acting beta1 selective blocker.

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16
Q

What are some of the adverse reactions of beta blockers?

A

Bradycardia, myocardial depression, bronchoconstriction, increased risk of hypoglycaemia unawareness and sleep disturbances and nightmares.

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17
Q

What is the mechanism of drugs that prolong the action potential duration?

A

Block the voltage-activated potassium channels in repolarisation phase 3 of the action potential.

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18
Q

What is the effect of drugs that prolong the action potential duration?

A

Prolong the duration of the cardiac action potential and increase refractoriness.

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19
Q

What are some of the other actions of amidarone?

A

They block Na+ channels, block Ca2+ channels, decrease expression of beta1-adrenoceptors and are a modest alpha adrenergic receptor antagonist.

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20
Q

What are some of the other effects of sotalol?

A

A non-selective beta blocker.

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21
Q

What are some of the adverse effects of amiodarone?

A

It is highly lipophilic (high distribution in other tissues so has lots of side effects), it has a slow onset and a very long plasma half life, arrhythmias, thyroid adnormalities, corneal deposits, pulmonary disorders, skin pigmentation.

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22
Q

What is the mechanism of calcium channel blockers?

A

They block L-type voltage-activated calcium channels, and slow down conduction at the AV node.

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23
Q

What are some of the adverse effects of calcium channel blockers?

A

Bradycardia, reduced myocardial contractility, constipation, hypotension.

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24
Q

What are some anti-arrhythmic drugs that are outside the Vaughan Williams classification?

A

Adrenaline, atropine, isoprenaline, adenosine, digoxin, calcium chloride, magnesium chloride.

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25
Q

What are the most common tachyarrhythmias?

A

Paroxysmal SVT, atrial fibrillation and atrial flutter.

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26
Q

What are the most dangerous tachyarrhythmias?

A

Ventricular tachycardia, ventricular fibrillation.

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27
Q

What are the causes of tachyarrhythmias?

A

Pre-existing CV diseases, certain disease and conditions, electrolyte imbalances and drugs.

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28
Q

What drugs can cause tachyarrhythmias?

A

Asthma inhalers, anti-arrthymic drugs, anti-hypertensives, antifungal drugs, antibiotics, antihistamines.

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29
Q

What electrolyte imbalance can cause tachyarrhythmias?

A

Hypokalaemia.

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30
Q

What disease and conditions can cause tachyarrhythmias?

A

Congenital heart defects, hyperthyroidism, pheochromocytoma.

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31
Q

What are some non-medical causes of tachyarrhythmias?

A

Stress and anxiety, lack of sleep and sleep disorders, excess of alcohol, caffeine, recreational drug use and abuse (ecstasy, cocaine, amphetamine and heroin).

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32
Q

What are some genetic disorders that cause tachyarrhythmias?

A

Channelopathies, abnormal conduction pathways in the heart, storage and release of calcium from the SR.

33
Q

What are channelopathies?

A

Mutations in cardiac voltage-activated Na+, Ca2+ and K+ channels and associated proteins.

34
Q

What are some examples of channelopathies?

A

Long QT syndrome and brugada syndrome.

35
Q

What is an example of a condition in which patients have an abnormal conduction pathway in the heart?

A

Wolff-Parkinson-White syndrome.

36
Q

What is a condition that causes storage and release of calcium from the SR?

A

CPVT - catecholaminergic polymorphic ventricular tachycardia.

37
Q

What are the mechanisms behind tachyarrhythmias?

A

Automaticity (enhanced or abnormal) or triggered - re-entry, AVNRT, AVRT, early after-depolarisation and delayed-after depolarisation.

38
Q

What are the two types of automaticity that can cause tachyarrhythmias?

A

Enhanced due to sympathetic overactivity or abnormal due to ectopic pacemaker.

39
Q

What is AVNRT?

A

Atrioventricular nodal re-entrant tachycardia.

40
Q

What causes an additional action potential in AVNRT?

A

Due to premature atrial contraction.

41
Q

What are the two pathways of contraction in the AVN?

A

Slow conducting but with a faster recovery and fast conducting with a longer refractory period.

42
Q

What is the normal conduction in the AVN?

A

An AP enters both pathways but only the fast pathway will reach the ventricles, first initiating systolic contraction. This is unidirectional excitation as the wave of refractoriness following the AP will prevent any further reexcitation.

43
Q

How is AVNRT triggered?

A

There is an additional action potential that occurs between the two consecutive action potentials from the SAN.

44
Q

How is a high heart rate created in AVNRT?

A

The additional action potential reaches the bottom point of the AVN, refractoriness has recovered and the AP will excite the ventricles and go back to the atria via the fast pathway 2 - re exciting the atria. This is repeated and a circular movement of excitation is created, leading to a high HR.

45
Q

What is AVRT?

A

Atrioventricular reciprocating tachycardia.

46
Q

What are the significant features about ECGs of AVRT?

A

There are shorter PR intervals, delta waves preceding QRS (slow rise in QRS) and increased QRS duration.

47
Q

What tachyarrthymias can AVRT cause?

A

PVST via the AVN, VT via the accessory pathway and VF in patients with atrial fibrillation.

48
Q

What is required for AVRT to occur?

A

There needs to be the normal AV conduction system and the accessory pathway - this is an extra pathway that exists between the atrium and the ventricles.

49
Q

What is significant about the AV node?

A

It contains special tissue that slows down conduction.

50
Q

What is the pathological basis for micro-re-entry?

A

Focal ischaemia or infarction around the terminal branching Purkinje fibres.

51
Q

How can ischaemia cause micro-re-entry?

A

Ischaemic myocardium depolarises and slows down conduction along one branch of the Purkinje fibre, thus creating a slow conducting pathway in parallel with the normally fast conducting fibres.

52
Q

What are the causes of ventricular tachycardia?

A

AVRT and micr-re-entry.

53
Q

What are the acute treatments of long-lasting episodes of PVST?

A

Adenosine in hospital, and vagal maneuvers to restore sinus rhythm.

54
Q

What does supraventricular mean?

A

Rhythms caused by activity above the ventricles - mainly the atrioventricular node.

55
Q

What are the supraventricular tachycardias?

A

Paroxysmal supraventricular tachycardia (PVST), atrial fibrillation and atrial flutter.

56
Q

What are the two mechanisms of PVST?

A

Atrioventricular nodal re-entrant tachycardia (AVNRT) and atrioventricular reciprocating tachycardia (AVRT).

57
Q

What are the ventricular tachyarrthythmias?

A

Ventricular tachycardia and ventricular fibrillation.

58
Q

What are the main causes of tachyarrthymias?

A

Pre-existing diseases that lead to myocardia ischaemia and infarctions.

59
Q

What is myocardial ischaemia?

A

When blood flow to the heart is obstructed by partial or complete blockade of a coronary artery by a build up of plaques.

60
Q

What is a physical procedure that can be used to stop AVNRT and AVRT?

A

Catheter ablation - a thin tube is inserted to stop abnormal electrical pathways.

61
Q

What are some rate control drugs that can be used?

A

Verapamil on class IV and beta-blockers for class II, along with digoxin.

62
Q

What are some rhythm controlling drugs that can be used to treat PSVT?

A

Flecainide, sotalol and amidarone.

63
Q

What is enhanced automaticity?

A

Accelerated generation of action potentials by normal pacemaker tissue or by abnormal tissue within the myocardium.

64
Q

What are the three mechanisms of atrial fibrillation?

A

Enhanced automaticity, EADs and DADs.

65
Q

What does EAD stand for?

A

Early after depolarisation - the reactivation of L-type channels during a prolonged plateau.

66
Q

What are some of the causes of EAD?

A

Slow heart rate, drugs that prolong the QT interval, genetics.

67
Q

What does DAD stand for?

A

Delayed after depolarisation.

68
Q

What causes DAD?

A

Build up of cytosolic calcium.

69
Q

What factors can promote DAD?

A

Fast HR, drugs such as digoxin and genetics.

70
Q

What does the QT interval represent?

A

The time elapsed between the ventricular depolarisation and repolarisation.

71
Q

What can early after depolarisations result in?

A

Torsades de pointes, tachycardia and other arrthythmias.

72
Q

What is the difference between atrial fibrillation and atrial flutter?

A

Fibrillation is a fast irregular heartbeat, whereas flutter is a fast regular heartbeat.

73
Q

What are the most common causes of atrial fibrillation?

A

Random focal ectopic activity from the pulmonary vein in the left atrium.

74
Q

What is the most common cause of atrial flutters?

A

One or more foci of excitation in the atria (due to micro re-entry or EADs). The heart rate may be within the normal range due to decremental pulse conduction at the AVN.

75
Q

What is the main cause of stroke?

A

Atrial fibrillation.

76
Q

What treatment is only used for SVTs?

A

Adenosine, verapamil, diltiazem, digoxin.

77
Q

What treatment can be used for both SVTs and VTs?

A

Amiodarone, sotalol, beta-blockers, flecainide, disopyramide.

78
Q

What treatment can only be used for VTs?

A

Lidocaine.

PA20016 (10 decks)

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