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02. Cardiovascular System > Arrhythmias - Therapy > Flashcards

Arrhythmias - Therapy Flashcards

1
Q

<p>What is an arrhythmia?</p>

A

<p>–Any deviation from the normal rhythm of the heart</p>

<p>•<strong>Sinus arrhythmia</strong></p>

<p><strong>•Supraventricular arrhythmia</strong></p>

<p>–Atrial fibrillation</p>

<p>–SVT (junctional)</p>

<p><strong>•Ventricular arrhythmia</strong></p>

<p>–Ventricular tachycardia</p>

<p>–Ventricular fibrillation</p>

<p>•(<strong>Heart block)</strong></p>

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2
Q

<p>What is heart block?</p>

A

<p>Heart blockis an abnormalheartrhythm where theheartbeats too slowly (bradycardia). In this condition, the electrical signals that tell theheartto contract are partially or totally blocked between the upper chambers (atria) and the lower chambers (ventricles).</p>

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3
Q

<p>How are the electrical signals different in atrial fibrillatino?</p>

A

<p>Electrical signals are disorganised in atrial fibrillation</p>

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4
Q

<p>What is the pathology associated with this ECG?</p>

A

<p>Ventricular fibrillation</p>

<p>Note - P waves are absent</p>

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5
Q

<p>What is the pathology associated with this ECG?</p>

A

<p>Ventricular tachycardia</p>

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6
Q

<p>What is the pathology associated with this ECG?</p>

A

<p>Atrial fibrilaltion</p>

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7
Q

<p>What is responsible for the uneven distribution of ions which accounts for the uneven resting membrane potential?</p>

A

<p>•Sodium-potassium ATPase pump</p>

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8
Q

<p>What causes myocardial muscle to contract?</p>

A

<p>Movement of ions across the myocyte cell membrane - propagation of an electrical impulse - leads to myocardial muscle contraction</p>

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9
Q

What are the different phases of the action potential?

A
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10
Q

<p>What are the different classes of drugs that are used to treat arrhythmias?</p>

A

<p>•Class 1</p>

<p>–Class Ia</p>

<p>–Class Ib</p>

<p>–Class Ic</p>

<p>•Class II</p>

<p>•Class III</p>

<p>•Class IV</p>

<p>•Other</p>

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11
Q

What are class 1 anti arrhythmic drugs?

A
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12
Q

<p>What is the action of Class 1 a drugs?</p>

A

<p>Block sodium channels</p>

<p>Delay repolarisation</p>

<p>Increase action potential duration</p>

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13
Q

<p>What can class 1 a drugs be used for?</p>

A

<p>AF</p>

<p>Premature atrial/ventricular contractions</p>

<p>Ventricular tachycardia</p>

<p>Wolff-Parkinson-white syndrome</p>

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14
Q

<p>Name some class 1 a drugs</p>

A

<p>Disopyramide</p>

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15
Q

<p>What are the actions of 1 b drugs?</p>

A

<p>Block sodium channels</p>

<p>Accelerate repolarization</p>

<p>Decrease the action potential duration</p>

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16
Q

<p>What can class 1 b drugs be used for?</p>

A

<p>Used for ventricular dysrhythmias only (premature ventricular contractions, ventricular tachycardia, ventricular fibrillation)</p>

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17
Q

<p>What are the common type 1b drugs?</p>

A

<p>phenytoin, lidocaine</p>

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18
Q

<p>What is the effect of class 1c drugs?</p>

A

<p>•Block sodium channels (more pronounced effect)</p>

<p>•Little effect on action potential duration or repolarization</p>

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19
Q

What are class 1 c drugs used for?

A

Severe ventricular dysrhythmias

May be used in atrial fibrillation/flutter

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20
Q

<p>What are class 1 c drugs used for?</p>

A

<p>Severe ventricular dysrhythmias</p>

<p>May be used in atrial fibrillation/flutter</p>

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21
Q

<p>Give an example of a class 1 c drug</p>

A

<p>Flecainide</p>

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22
Q

<p>What are the Class 2 drugs?</p>

A

<p>Beta Blockers</p>

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23
Q

<p>What stage of the heart cycle do beta blockers act on?</p>

A

<p>Phase 4 depolarisation</p>

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24
Q

<p>What is the effect of beta blockers on the transmission of impulses in the heart?</p>

A

<p>Reduces thetransmission of impulses in the heart’s conduction system</p>

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25
Q

<p>What type of heart dysrhythmia are beta blocers used for?</p>

A

<p>•General myocardial depressants for both supraventricular and ventricular dysrhythmias</p>

<p>•Now first line for atrial fibrillation (Bisoprolol)</p>

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26
Q

<p>What are examples of beta blockers?</p>

A

<p>Atenolol and Bisoprolol</p>

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27
Q

<p>What are class 3 drugs?</p>

A

<p>Amiodarone and sotalol</p>

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28
Q

<p>What stage of the action potential do amiodarone and sotalol funciton in?</p>

A

<p>•Increase action potential duration</p>

<p>•Prolong repolarization in phase 3</p>

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29
Q

<p>What type of dysrhythmia is amiodarone and sotalol used for?</p>

A

<p>•Used for dysrhythmias that are difficult to treat</p>

<p>•Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs</p>

<p>Sustained ventricular tachycardia</p>

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30
Q

<p>What are type 4 drugs?</p>

A

<p>Calcium channel blockers</p>

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31
Q

<p>What stage of the actionpotential do calcium channels function in?</p>

A

<p>Depress phase 4 depolarisation</p>

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32
Q

<p>What type of dysrhythmia are CCB's used for?</p>

A

<p>•Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter</p>

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33
Q

<p>What drugs are Antidysrhythmics but don't fit into one particular class?</p>

A

<p>Digoxin, adenosine</p>

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34
Q

<p>How does digoxin function?</p>

A

<p>•Inhibits the sodium-potassium ATPase pump</p>

<p>•Positive inotrope—improves the strength of cardiac contraction</p>

<p>•Allows more calcium to be available for contraction</p>

35
Q

<p>What is digoxin used for?</p>

A

<p>•Used for heart failure (HFrEF) and atrial dysrhythmias (AF)</p>

36
Q

<p>What are the signs of digoxin toxicity?</p>

A

<p>Yellow glow</p>

<p>‘Reverse tick’ appearance of ST segment in lateral leads</p>

37
Q

<p>What are the effects of digoxin toxicity?</p>

A

<p>•Nausea and vomiting</p>

<p>•Xanthopsia</p>

<p>•Bradycardia</p>

<p>•Tachycardia</p>

<p>•Arrhythmias: VT and VF</p>

38
Q

<p>What is a common use of digoxin in old people?</p>

A

<p>Rate control</p>

39
Q

<p>What is the treatment of digoxin toxicity?</p>

A

<p>Stop Digoxin</p>

<p>Give digibind if there is a very high risk of significant arrhythmia</p>

<p>(Digoxin toxicity is more serious if potassium levels are low)</p>

40
Q

<p>What is amiodarone used for?</p>

A

<p>•Used for VT and occasionally in supraventricular tachycardia</p>

41
Q

<p>What does amiodarone have side effects with?</p>

A

<p>•Many interactions with other drugs: particularly digoxin</p>

42
Q

How do class 3 drugs work? Including amiodarone

A

Prolong refractoriness

43
Q

<p>What are the side effects of amiodarone?</p>

A

<p>–Thyroid (hypo or hyperthyroidism)</p>

<p>–Pulmonary fibrosis</p>

<p>–Slate – grey pigmentation</p>

<p>–Corneal deposits</p>

<p>–LFT abnormalities</p>

44
Q

<p>How do class 3 drugs work? Including amiodarone</p>

A

<p>Prolong refractoriness</p>

<p></p>

45
Q

<p>How does adenosine work?</p>

A

<p>Slows conduction through the AV node</p>

46
Q

<p>What is adenosine used to treat?</p>

A

<p>Used to convert paroxysmal supraventricular tachycardia to sinus rhythm</p>

47
Q
A
48
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Q
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50
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51
Q
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52
Q
A
53
Q

<p>What can adenosine cause?</p>

A

<p>Aysistole for a few seconds</p>

54
Q

<p>What is a common side effect amongst all antidysrhythmics?</p>

A

<p>Can cause arrhythmias</p>

55
Q

<p>What are indications for anticoagulation?</p>

A

<p>Atrial fibrillation - risk of stroke, peripheral emboli</p>

56
Q

<p>What is the differencebetween arterial and venous thrombosis?</p>

A

<p>Arterial thrombosis - platelets stick to artery walls - white in colour</p>

<p>(associated with MI, stroke and ischaemia)</p>

<p>Venous Thrombosis - Deveops in stagnant blood flow. Red in colour - associated with congestive heart failure, cancer and surgery</p>

57
Q

<p>What isWolff-Parkinson-White (WPW) syndrome?</p>

A

<p>Wolff-Parkinson-White (WPW) syndrome is a heart condition that causes the heart to beat abnormally fast for periods of time.</p>

58
Q

<p>What are the different types of heart block?</p>

A

<p>TYPE 1 -slowed conduction</p>

<p>TYPE 2 -intermittent conduction failure</p>

<p>TYPE 3 -complete conduction failure</p>

59
Q

<p>Where can heart block occur?</p>

A

<p>Anywhere in the specialized conduction system:</p>

<p><strong>Sino-atrial connections</strong></p>

<p><strong>AV junction</strong></p>

<p><strong>Bundle branches and their fascicles</strong></p>

<p><strong>Purkinje fibers</strong></p>

60
Q

<p>What is sinoatrial arrest?</p>

A

<p>Sinoatrial arrest(also known assinus arrestorsinus pause) is a medical condition wherein thesinoatrial nodeof thehearttransiently ceases to generate the electrical impulses that normally stimulate themyocardialtissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes</p>

61
Q

<p>What is an escape rhythm?</p>

A

<p>When a pacemaker other than the sinoatrial node is pacing the heart</p>

62
Q

<p>How can sinus arrest lead to cardiac arrest?</p>

A

<p>If no other pacemaker begins pacing during an episode of sinus arrest</p>

63
Q

<p>What is an ectopic rhythm?</p>

A

<p>An ectopic rhythm is an irregular heart rhythm due to a premature heartbeat. Ectopic rhythm is also known as premature atrial contraction, premature ventricular contraction, and extrasystole.</p>

64
Q

What are the causes of ectopic beats?

A
65
Q

<p>What is a premature atrial contraction?</p>

A

<p>An early heartbeat that originates in the heart’s upper chambers (atria) is a premature atrial contraction (PAC). In healthy children, irregular heartbeats are almost always PACs and are harmless.</p>

66
Q

<p>What is a ventricular premature contraction?</p>

A

<p>When the irregularity comes from the lower chambers of the heart (ventricles), it is called a premature ventricular contraction(PVC). The risk of PVC rises with age. You are at increased risk of PVC if you have a family history of PVC or if you have had a heart attack.</p>

67
Q

<p>What usually follows an ectopic beat?</p>

A

<p>When your heart experiences an early beat, a brief pause usually follows. You generally become aware of it on the next beat, which feels much stronger. It can feel like fluttering, or as though your heart skipped a beat.</p>

68
Q

What is the third commonest cause of death in the US?

A
69
Q

<p>What is the epidemiology of AF?</p>

A

<p>The prevalence of AF roughly doubles with each advancing decade of age, from 0.5% at age 50–59 years to almost 9% at age 80–89 years.3 Conversely, AF is very uncommon in infants and children, unless concomitant structural or congenital heart disease is present.</p>

70
Q

<p>What are the indications for anticoagulation?</p>

A

<div>•Atrial fibrillation - reduce stroke risk by 80%</div>

<div>•DVT/PE</div>

<div>•After surgery</div>

<div>•Immobilisation:those at high risk of DVT will get prophylactic dose of anticoagulation</div>

71
Q

<p>What is the effect of warfarin?</p>

A

<p>Inhibits the production of active clotting factors</p>

72
Q

<p>What is vitamin K needed for?</p>

A

<p>Blood clotting</p>

73
Q

<p>What drugs increase warfarin activity and why?</p>

A

<p>Aspirin - decrease binding to albumin</p>

<p>Cimetidine and Disulfuram - inhibit degradation</p>

<p>Antibiotics - decreases the synthesis of clotting factors</p>

74
Q

How do you monitor warfarin therapy?

A

INR (international normalised ratio)

75
Q

<p>What drugs react with warfarin to promote bleeding and why?</p>

A

<p>Aspirin - inhibition of platelets</p>

<p>Heparin antimetabolites - inhibition of clotting factors</p>

76
Q

What factors are used to assess bleeding risk when on warfarin?

A
77
Q

What are the characteristics of an ideal anticoagulant?

A
78
Q

<p>What drugs decrease warfarin activity and why?</p>

A

<p>Barbituates, phenytoin</p>

<p>Induction of metabolizing Barbiturate</p>

<p>Enzymes (cytochrome P450)</p>

<p>Vitamin K</p>

<p>Promotes clotting factor synthesis</p>

<p>cholestyramine</p>

<p>Reduces absorption</p>

79
Q

What is the benefiot of dabigatran over warfarin?

A

Reduces cumulative hazard rates

80
Q

<p>How do you monitor warfarin therapy?</p>

A

<p>INR (international normalised ratio)</p>

<p></p>

81
Q

<p>What are the adverse side effects of warfarin?</p>

A

<div>·Bleeding (dose related)</div>

<div>·Teratogenic (chondrodysplasia)</div>

<div>·Avoid in first and third trimesters</div>

<div>·(Retroplacental bleeding and fetal intracerebral bleeding).</div>

82
Q

<p>How do the drugs warfarin, rivaroxaban, apixaban and dabigatran reduce blood clot formation?</p>

A

<p>Reduces the production of thrombin from prothrombin - thrombin is the enzyme that converts fibrinogen into fibrin</p>

83
Q

<p>What is the benefiot of dabigatran over warfarin?</p>

A

<p>Reduces cumulative hazard rates</p>

02. Cardiovascular System (72 decks)

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