the lecture about the conventional medications used to treat cardiac arrhythmias. the electrical conduction system of the heart can be affected in many different ways and there are several classes of drugs, each with a unique mechanism that targets different portions of the cardiac cycle [see questions 4-9]. quinidine is in class Ia, which works to slow the phase 0 depolarization, thereby prolonging action potential and slowing conduction. it is indicated in atrial fibrillation, atrial flutter, and some other arrhythmias, but tends to be avoided due to its high side effect profile; GI upset, cinchonism (a host of symptoms including nausea/vomiting, tinnitus, headache, disorientation), and torsade de pointes (an abnormal heart rhythm normally found in ventricular tachycardia where the peaks and troughs of the Q wave are equidistant from the baseline).
mexiletine is indicated in ventricular arrhythmias and recurrent ventricular tachycardia post-MI. it is class 1b; still a sodium channel blocker like quinidine but acts upon phase 3 repolarization instead of phase 0. side effect include drowsiness, confusion, and pro-arrhythmic potential. flecainide is used for supra-ventricular arrhythmias; arrhythmias that have an origin above the ventricles. the main side effect is its pro-arrhythmic potential; thus it is contraindicated in patients with a history of an MI or ventricular arrhythmia related to an acute ischemic event.
atenolol is a drug in class II anti-arrhythmics, drugs which diminish phase 4 repolarization by acting as beta-adrenergic blockers, thus decreasing sympathetic tone in the myocardium. it is indicated in tachyarrhythmias, a-flutter, a-fib, hypertension, angina, among other conditions, and stabilizes heart rate by the mechanism mentioned above; resulting in decreased automaticity in the various pacemaker cells in the heart. side effects might include drowsiness, bradycardia, dizziness, hypotension.
amiodarone is a typical class III anti-arrhythmic drug, causing a K+ channel blockade that results in prolonged phase 3 repolarization. it is indicated for arrhythmias with a ventricular origin and contains high amounts of iodine, which can cause blue-gray discoloration of the skin as a side effect. other side effects include dizziness / light headedness and pulmonary fibrosis.
the last class of anti arrhythmic, class IV, is represented by verapamil; these are drugs that block calcium channels, resulting in slowed phase 0 depolarization, which results in decreased AV conduction and a slower heart rate. side effects might include flushing, dizziness, hypotension.
there are other drugs that do not fall into the 6 major classes; one such drug is adenosine, which is produced endogenously from the breakdown of ATP. pharmacologically, adenosine has the effect of lengthening the refractory period and decreasing automaticity in the AV node by acting directly on the sinus pacemaker cells and vagal nerve terminals. it is administered by IV and can work as quickly as 15 seconds. it is the drug of choice for patients with PSVT (paroxysmal supraventricular tachycardias).
atropine is a drug derived from the nightshade belladonna which is used in cases of severe bradycardia with hypotension. it works by competitively inhibiting muscarinic acetylcholine receptors, thus blocking parasympathetic activity. thus it can also be used orally to treat diarrhea due to its effect of slowing peristalsis. it is also an effective antidote to organophosphate poisoning; these pesticides work by inhibiting acetylcholinesterase, leaving an abundance of acetylcholine-- while atropine works to block the effects of acetylchoine in the synapse.
digoxin is an anti-arrhythmic derived from the plant digitalis lanata and is classified as a cardiac glycoside. it both increases cardiac contractility as well as lowering conductivity, leading to a more stable, stronger heart beat. it works by inhibiting the Na/K ATPase and allowing for more intracellular influx of Na and Ca, as well as increasing the AV node's sensitivity to vagal stimulation. an overdose can cause "digitalis intoxication" which has a host of symptoms which might include bradycardia, fatigue, nausea, vomiting, blurred vision. digibind is used in such cases, an antibody formulated against digoxin (harvested IgG from sheep that are immunized with digoxin) which forms complexes that can be excreted via the kidneys.
questions
1. what are the five phases of the cardiac rhythm?
2. how does the origin of the arrhythmia correspond with prognosis?
3. common causes of arrhythmias?
4. describe the mechanism for the anti-arrhythmic drug class Ia.
5. describe the mechanism for the anti-arrhythmic drug class Ib.
6. describe the mechanism for the anti-arrhythmic drug class Ic.
7. describe the mechanism for the anti-arrhythmic drug class II.
8. describe the mechanism for the anti-arrhythmic drug class III.
9. describe the mechanism for the anti-arrhythmic drug class IV.
quinidine...
10. what class is quinidine?
11. indications?
12. mechanism of action?
13. side effects?
14. what is cinchonism?
15. what is torsade de pointes?
mexiletine...
16. what class is mexiletine? what is the mechanism?
17. indications?
18. side effects?
flecainide...
19. class? mechanism?
20. indications?
21. side effects?
22. contraindicated for which patients?
atenolol...
23. class?
24. indications?
25. mechanism of action?
26. side effects?
amiodarone...
27. indicated for...
28. mechanism of action?
29. contains high amounts of...
30. [29] results in what side effect?
31. other side effects?
verapamil...
32. which class? mechanism?
33. side effects?
adenosine...
34. drug of choice for which disorder?
35. breakdown product of...
36. mechanism of action?
37. acts directly on...
38. increases vagal tone by...
39. method of administration? onset of action?
atropine...
40. derived from...
41. cardiac use is for treatment of...
42. mechanism of action?
43. oral atropine can be used for...
44. can act as an antidote for...
45. symptoms of organophosphate poisoning?
46. specific antidote for atropine overdose? mechanism?
digoxin...
47. belongs to which family of drugs?
48. derived from which plant?
49. difference between digoxin and digitoxin?
50. mechanism of action?
51. effect on AV node?
52. effect on kidneys?
53. effect on EKG?
54. what is digitalis intoxication?
55. what is digibind?
answers
1. sodium channels open
sodium channels close, potassium channels begin to open
calcium and potassium channels open
calcium channels close
return to resting membrane potential
[Na, Na/K, Ca/K, Ca, return]
2. arrhythmias that originate in the atrias are generally more benign while ventricular arrhythmias are generally fatal within minutes.
3. ischemic damage
electrolyte disturbances
pH imbalance
4. sodium channel blockade: slow phase 0 depolarization-- prolong action potential and slow conduction.
5. sodium channel blockade: shorten phase 3 repolarization and decrease action potential duration by blocking sodium channels.
6. sodium channel blockade: markedly slow phase 0 depolarization.
7. diminish phase 4 repolarization, thus depressing automaticity.
8. prolong phase 3 repolarization without altering phase 0.
9. slow phase 4 depolarization and slow conduction, particularly at the AV node.
10. class Ia.
11. a-flutter, a-fib, AV and ventricular arrhythmias.
12. diminished inward flow of sodium at phase 0 results in decreased automaticity and a longer refractory period.
13. arrhythmias
GI symptoms: nausea, diarrhea, vomiting
cinchonism
torsade de pointes
14. nausea / vomiting
tinnitus
headache / disorientation
psychosis.
15. abnormal rhythm of ventricular tachycardia; peaks and troughs of Q wave are equidistant from baseline.
16. class 1b: blocks open sodium channels and shortens phase 3 repolarization.
17. ventricular arrhythmias, recurrent v-tach post MI.
18. drowsiness, confusion, pro-arrhythmias.
19. class Ic- sodium channel blocker.
20. supraventricular arrhythmias, WPW syndrome.
21. pro-arrhythmic.
22. patients with history of MI or ventricular arrhythmia due to acute ischemic event.
23. class II.
24. tachyarrhythmias
a-flutter, fib
PSVT
hypertension
angina
25. reduced sympathetic myocardial tone.
26. bradycardia, hypotension, fatigue, dizziness.
27. ventricular arrhythmias.
28. potassium channel blockade; prolong phase 3 repolarization.
29. iodine.
30. blue-gray skin discoloration.
31. dizziness, light headedness, pulmonary fibrosis.
32. class IV-- calcium channel blocker, slows phase 0 depolarization resulting in slowed AV conduction.
33. dizziness, flushing, hypotension, headaches.
34. PVST.
35. ATP.
36. prolongs refractory period and decreases automaticity in AV node.
37. sinus pacemaker cells and vagal nerve terminals
38. working between the SA and AV nodes.
39. IV, 15 seconds.
40. belladonna.
41. bradycardia and hypotension.
42. competitive inhibitor of muscarinic AcH receptors; blocks parasympathetic pathway.
43. diarrhea due its effect of slowing peristalsis.
44. pesticides that inhibit acetylcholinesterase.
45. SLUDGE:
salivation, lacrimation, urination, diarrhea, gastric distress, emesis
46. physostigmine; a reversible acetylcholinesterase inhibitor.
47. cardiac glycosides.
48. digoxin lanata.
49. digitoxoin has a longer half life and higher potential for toxicity.
50. inhibits Na/K ATPase, leads to more influx of Na and Ca intracellularly, allowing for higher contractility while decreasing conductivity and thereby stabilizing heart rate.
51. increases sensitivity to vagal stimulation.
52. increases renal perfusion.
53. flattening or inversion of t wave.
54. cardiac symptoms such as bradycardia, heart block
GI symptoms such as N/V, anorexia and diarrhea
eye symptoms such as blurred vision, double vision
55. antibodies specific to digoxin used to clear digoxin from the body after intoxication.
No comments:
Post a Comment