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Drugs > Elm 15 Antidysrhythmic Drugs > Flashcards

Elm 15 Antidysrhythmic Drugs Flashcards

1
Q

Q: What is a dysrhythmia (arrhythmia)?

A

A: An abnormal heart rhythm that can be too fast, too slow, or irregular.

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2
Q

Q: How can dysrhythmias affect health?

A

A: They can compromise the heart’s ability to supply blood to the body or increase the risk of other conditions, potentially causing the heart to stop pumping blood.

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3
Q

Q: How common are dysrhythmias in the UK?

A

A: They are very common, affecting over 2 million people each year.

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4
Q

Q: Name three risk factors for developing dysrhythmias.

A

A: Age, alcohol consumption, and smoking.

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5
Q

Q: What is the most common form of dysrhythmia in Europe?

A

A: Atrial fibrillation.

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6
Q

Q: What part of the heart initiates the heartbeat?

A

A: The sinoatrial node (SAN).

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7
Q

Q: What is the function of the atrioventricular node (AVN)?

A

A: It acts as a gatekeeper, causing a delay between atrial and ventricular contraction.

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8
Q

Q: Through which structures do the signals from the AVN propagate to the ventricles?

A

A: The Bundle of His and Purkinje fibers.

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9
Q

Q: What does an ECG/EKG measure?

A

A: It measures the electrical activity across the whole heart.

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10
Q

Q: Describe the P wave, QRS complex, and T wave on an ECG.

A

A: P wave represents atrial depolarization, QRS complex represents ventricular depolarization, and T wave represents ventricular repolarization.

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11
Q

Q: What is the difference between arrhythmia and dysrhythmia?

A

A: Arrhythmia is the absence of rhythm, while dysrhythmia is a disruption of normal rhythm.

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12
Q

Q: Name the four main classifications of dysrhythmias based on heart rate and rhythm.

A

A: Atrial, junctional, ventricular, fibrillation, tachycardias, and bradycardias.

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13
Q

Q: What is an ectopic pacemaker?

A

A: Cardiac tissue other than the SAN that initiates a heartbeat.

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14
Q

Q: What causes delayed after-depolarization?

A

A: A buildup of calcium in the cells that leads to a train of action potentials.

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15
Q

Q: What are re-entry circuits in the context of dysrhythmias?

A

A: Abnormalities where action potentials travel in circles due to tissue damage or abnormality.

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16
Q

Q: What is a heart block?

A

A: Damage to conducting paths that disrupts atrial-ventricular signaling.

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17
Q

Q: What are early after-depolarizations?

A

A: They occur when an action potential is prolonged, reactivating voltage-gated calcium and potassium channels.

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18
Q

Q: What causes delayed after-depolarizations?

A

A: Calcium overload and buildup in the cytoplasm, leading to depolarization through the Na/Ca exchanger.

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19
Q

Q: What is the mechanism of re-entry circuits involving damaged tissue?

A

A: Signal re-enters through damaged tissue due to differential conduction properties, potentially exciting the heart inappropriately.

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20
Q

Q: How does an AVN re-entry circuit cause dysrhythmia?

A

A: If the slow pathway is refractory while the fast pathway recovers, it can cause the signal to excite the fast path in a retrograde direction.

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21
Q

Q: What is the most common type of dysrhythmia, especially in those over 80?

A

A: Atrial fibrillation.

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22
Q

Q: What mechanisms cause atrial fibrillation?

A

A: Re-entry circuits and ectopic pacemakers.

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23
Q

Q: What is the atrial rate during atrial fibrillation, and how does it affect the ventricles?

A

A: The atrial rate can be up to 600 bpm locally, with occasional conduction to the ventricles causing an irregular rhythm.

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24
Q

Q: What are common symptoms and risks associated with atrial fibrillation?

A

A: Fatigue, palpitations, and an increased risk of stroke.

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25
Q

Q: What are the risk factors for atrial fibrillation?

A

A: Heart disease, high blood pressure, congenital heart disorders, and genetics.

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26
Q

Q: What is paroxysmal supraventricular tachycardia (PSVT) and its prevalence?

A

A: It is a dysrhythmia caused by a re-entry circuit through the AVN, affecting 0.2% of the population.

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27
Q

Q: What is the ventricular rate during PSVT and common symptoms?

A

A: The ventricular rate can be up to 250 bpm, causing palpitations, shortness of breath, and chest pain.

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28
Q

Q: How can attacks of PSVT be halted?

A

A: By performing the Valsalva maneuver.

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29
Q

Q: What triggers PSVT?

A

A: Anxiety, stress, caffeine, and smoking.

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30
Q

Q: What causes ventricular fibrillation, and what is its immediate consequence?

A

A: Ventricular re-entry circuits or ectopic foci cause the ventricles to cease coordinated beating, leading to a rapidly fatal outcome.

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31
Q

Q: How is ventricular fibrillation detected on an ECG?

A

A: There are no QRS waves.

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32
Q

Q: How can ventricular fibrillation be treated?

A

A: By using a DC shock to restore contraction.

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33
Q

Q: What is heart block and its primary symptom?

A

A: It is a condition characterized by bradycardia due to damage to the AVN, impairing atrial-ventricular conduction.

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34
Q

Q: Describe the three degrees of heart block.

A

1st degree: Slowed conduction with an increased PQ interval but a QRS complex for every P wave.
2nd degree: Missing QRS complexes.
3rd degree: No impulses get from the atria to the ventricles, but the ventricles or AVN may take over as a slower pacemaker.

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35
Q

Q: What is Wolff-Parkinson-White syndrome, and its mechanism?

A

A: It is a congenital abnormality with an accessory AV pathway called the Kent bundle, causing a global re-entry circuit and re-entry AV tachycardia.

36
Q

Q: How does Wolff-Parkinson-White syndrome affect ventricular rates during atrial fibrillation?

A

A: The Kent bundle lacks a rate-limiter, so atrial fibrillation can lead to a fast ventricular rate and potentially ventricular fibrillation.

37
Q

Q: What are the primary treatments for dysrhythmias?

A

A: Pharmacological, surgical, and electrical interventions.

38
Q

Q: What is the Vaughan Williams classification system?

A

A: It divides anti-dysrhythmic drugs into four classes based on their mechanisms of action.

39
Q

Q: What is the mechanism of action for Class 1(a, b, c) drugs in the Vaughan Williams system?

A

A: They block sodium channels, affecting depolarization.

40
Q

Q: How do Class 2 drugs in the Vaughan Williams system work?

A

A: They are beta-1 adrenoceptor blockers that affect the sympathetic nervous system at the pacemaker potential and plateau phase.

41
Q

Q: What is the mechanism of action for Class 3 drugs in the Vaughan Williams system?

A

A: They block potassium channels, prolonging the action potential.

42
Q

Q: What do Class 4 drugs in the Vaughan Williams system do?

A

A: They block calcium channels.

43
Q

Q: What are some weaknesses of the Vaughan Williams classification system?

A

A: Many drugs have multiple sites of action, actions may differ in disease states versus healthy tissue, and many useful drugs are not included.

44
Q

Q: What is the more modern classification system for anti-dysrhythmic drugs proposed by Lei et al.?

A

A: It has 7 classes with subclasses and prioritizes clinical utility over the mechanism.

45
Q

Q: What is the mechanism of action for Class 1a anti-dysrhythmic drugs?

A

A: Moderate Na channel block, increased ERP, and increased action potential duration.

46
Q

Q: Give an example of a Class 1a anti-dysrhythmic drug and its uses.

A

A: Disopyramide, used to prevent ventricular, supraventricular, and Wolff-Parkinson-White (WPW) syndrome dysrhythmias, especially after a heart attack and defibrillation.

47
Q

Q: What are the side effects and contraindications of Disopyramide?

A

A: Side effects include GI tract issues, arrhythmias, cognitive problems, visual and urinary disorders, hypotension, and depressed force of contraction. Contraindicated in heart block and heart failure.

48
Q

Q: What is the mechanism of action for Class 1b anti-dysrhythmic drugs?

A

A: Weak Na channel block, decreased ERP, and shorter action potential duration.

49
Q

Q: Describe the use and properties of a class 1b drug as an anti-dysrhythmic drug.

A

A: Lidocaine binds to inactivated Na channels and is use-dependent. It is used intravenously to suppress ventricular dysrhythmias, especially after defibrillation, and is also a local anesthetic.

50
Q

Q: What are the side effects and contraindications of Lidocaine?

A

A: Adverse side effects include CNS excitation and depression, bradycardia, hypotension, and dysrhythmias. Contraindicated in WPW syndrome and severe heart block.

51
Q

Q: What is the mechanism of action for Class 1c anti-dysrhythmic drugs?

A

A: Strong Na channel block with no change in ERP or action potential duration.

52
Q

Q: Provide details on the use of class 1c drug and its risks.

A

A: Flecainide is used for supraventricular and ventricular arrhythmias under specialist supervision. It has a narrow therapeutic window and is contraindicated after a heart attack due to increased risk of death.

53
Q

Q: How do Class 1a and 1b drugs affect K channels?

A

A: Class 1a drugs block K channels, while Class 1b drugs promote K channels.

54
Q

Q: What is the mechanism of action for Class 2 anti-dysrhythmic drugs?

A

A: They affect the slope of the pacemaker current and the plateau phase by reducing automaticity and slowing SAN and AVN conduction.

55
Q

Q: Give an example of a Class 2 anti-dysrhythmic drug and its uses.

A

A: Atenolol, used for dysrhythmias triggered by sympathetic activation, such as atrial fibrillation and supraventricular tachycardias, and to prevent dysrhythmias after a heart attack.

56
Q

Q: What are the side effects of beta-blockers like Atenolol?

A

A: Bronchoconstriction, heart failure, heart block, masked signs of hypoglycemia in type 1 diabetes, decreased glucose mobilization, decreased insulin sensitivity, cold extremities, and Raynaud’s phenomenon.

57
Q

Q: What is the mechanism of action for Class 3 anti-dysrhythmic drugs?

A

A: They block K channels, delaying repolarization, which prolongs the action potential and refractory period.

58
Q

Q: Describe the use and properties of Amiodarone.

A

A: Amiodarone is used for a wide range of dysrhythmias, including atrial fibrillation/flutter, ventricular and supraventricular tachycardias, and WPW syndrome. It is administered orally or intravenously.

59
Q

Q: What are the side effects of Amiodarone?

A

A: Bradycardia, AVN block, Torsades de Pointes (TDP), thyroid interference, lung fibrosis, vision problems, liver toxicity, blue-gray skin color, and many drug interactions due to metabolism by CYP3A4.

60
Q

Q: Why is Amiodarone’s use complicated by its pharmacokinetics?

A

A: It has a very long plasma half-life, takes a long time to reach a steady state, and binds to tissues extensively.

61
Q

Q: What is the preferred route of administration for Amiodarone in cardiovascular emergencies?

A

A: Intravenous administration into a central vein for refractory ventricular fibrillation.

62
Q

Q: What is the mechanism of action for Class 4 anti-dysrhythmic drugs?

A

A: They block L-type voltage-gated Ca channels, reducing automaticity, re-entry tendency, and AVN conduction velocity.

63
Q

Q: What are the subtypes of L-type Ca channels and the drugs that act on them?

A

A: CaV 1.1-1.4, found in heart, smooth, and skeletal muscle. Drugs include Verapamil, Diltiazem, and Dihydropyridines.

64
Q

Q: How do Dihydropyridines differ from Verapamil in their action?

A

A: Dihydropyridines bind to the inactivated state and act more on vascular smooth muscle, while Verapamil binds to the open state and acts more on the heart.

65
Q

Q: What are the uses and side effects of Verapamil?

A

A: Verapamil is used for PSVT, AF, angina, hypertension, and cluster headaches. Side effects include headache, constipation, flushing, hypotension, and various drug interactions.

66
Q

Q: Why should grapefruit be avoided when taking drugs like Verapamil?

A

A: Grapefruit contains furanocoumarins that inhibit CYP3A4, increasing drug concentration and adverse effects. It also contains naringin, which reduces drug transport from the GI tract.

67
Q

Q: What is the mechanism of action for Adenosine as an unclassified anti-dysrhythmic drug?

A

A: Adenosine activates A1 receptors coupled to Gi proteins, leading to Ca influx, hyperpolarization, and inhibition of voltage-gated Ca channels.

68
Q

Q: What are the indications and side effects of Adenosine?

A

A: Adenosine is used to suppress PSVT, ventricular tachycardia with WPW, and supraventricular tachycardias during surgery. Side effects include bradycardia, facial flushing, chest pain, bronchospasm, and dyspnea.

69
Q

Q: How does Digoxin work as an unclassified anti-dysrhythmic drug?

A

vA: Digoxin blocks the Na/K pump, indirectly blocking Na/Ca exchange, increasing intracellular Ca, stimulating the parasympathetic NS, and increasing AVN refractory period.

70
Q

Q: What are the uses and side effects of Digoxin?

A

A: Digoxin is used for heart failure and AF with heart failure. Side effects include nausea, vomiting, visual problems, ventricular tachyarrhythmias, and a narrow therapeutic window.

71
Q

Q: What increases the toxicity of Digoxin?

A

A: Hypokalemia increases Digoxin toxicity as it binds to the K site on the Na pump. It is contraindicated in ventricular dysrhythmias, WPW syndrome, and heart block.

72
Q

Q: What is the mechanism of action for Atropine in treating bradycardia?

A

A: Atropine is a competitive antagonist at M2 receptors, blocking their action and increasing heart rate.

73
Q

Q: What are the side effects and contraindications of Atropine?

A

A: Side effects include dizziness, drowsiness, photophobia, constipation, headache, nausea, palpitations, and tachycardia. It is contraindicated in glaucoma, GI tract disorders, and urinary retention.

74
Q

Q: What severe interaction should be avoided when using Atropine?

A

A: Atropine has a severe interaction with phenylephrine, which can cause hypotension. It also interacts with any drug with muscarinic actions.

75
Q

Q: What is ablation in the context of dysrhythmia treatment?

A

A: Ablation is a surgical procedure used to correct dysrhythmias by destroying the problematic heart tissue, commonly used for supraventricular tachycardias and WPW syndrome.

76
Q

Q: Why is ablation not usually the first-line treatment for dysrhythmias?

A

A: Ablation is risky and therefore reserved for cases where other treatments have failed or are not suitable.

77
Q

Q: What is cardioversion and how is it performed?

A

A: Cardioversion is a method to jolt the heart out of an abnormal rhythm, which can be done pharmacologically or with synchronized electrical shocks timed with the R wave to minimize risk.

78
Q

Q: How does synchronized electrical cardioversion work?

A

A: It delivers a shock synchronized with the cardiac cycle, specifically during the R wave, to minimize the risk of triggering a worse dysrhythmia.

79
Q

Flashcard 143
Q: What is defibrillation used for?

A

A: Defibrillation delivers a non-synchronized pulse of electricity to treat pulseless ventricular tachycardia or ventricular fibrillation, not for restarting the heart from a flat-line ECG.

80
Q

Q: What is the purpose of Automated External Defibrillators (AEDs)?

A

A: AEDs are designed for public use to provide shocks only when necessary, helping to save lives during sudden cardiac arrests.

81
Q

Q: What is an implantable cardioverter-defibrillator (ICD)?

A

A: An ICD is a device implanted in patients with life-threatening dysrhythmias, such as ventricular fibrillation, which constantly monitors heart activity and administers shocks when needed.

82
Q

Q: How are ICDs implanted?

A

A: The procedure for implanting an ICD is similar to that of implanting a cardiac pacemaker, with electrodes placed in the heart.

83
Q

Q: What is the hERG gene and its significance in drug development?

A

A: The hERG gene codes for a potassium channel important in cardiac action potentials, and mutations can lead to long QT syndrome, increasing the risk of dangerous dysrhythmias like torsades de pointes (TDP).

84
Q

Q: Why must new drugs be tested for effects on the hERG channel?

A

A: Drugs that interfere with hERG channel function can cause long QT syndrome and TDP, leading to withdrawal from the market, so early testing is essential in drug development.

85
Q

Q: Which anti-dysrhythmic drugs are known to prolong the QT interval and increase the risk of TDP?

A

A: Amiodarone and disopyramide are examples of anti-dysrhythmic drugs that can prolong the action potential and QT interval, increasing the risk of TDP.

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