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Cardio Drugs > Anti-arrythmics > Flashcards

Anti-arrythmics Flashcards

1
Q

Class IA antiarrythmics (list them)

A
  1. QUinidine
  2. Procainamide
  3. DisoPYRAMIDE
    “the QUeen Proclaim’s Diso’s PYRAMID.”

Intermediate inhibtion of Phase 0

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2
Q

Quinidine

A

Class IA antiarrythmic

Toxicity: cinchonism (tinnitus, headache, GI disturbance) and thrombocytopenia

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3
Q

Disopyramide

A

Class IA antiarrythmic, longer duration of action, toxicity = antimuscarinic effects and heart failure

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4
Q

Procainamide

A

Class IA antiarrythmic
Toxicity: Increased arrythmias, Hypotension, SLE-like syndrome (auto-antibodies that form immune complexes cause kidney, eye, lung problems)

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5
Q

Class IA antiarrythmics Mechanism, Applications and Pharmacokinetics

A

Mechanism:
Inc. AP duration, Inc effective refractory period, Inc QT interval via I-NA channel block and some I-K block.

Application: Atrial and ventricular arrhythmias, especially reentrant, ectopic supraventricular and ventricular tachycardia.

Pharmacokinetics: Duration 2-3 Hrs, Oral and parenteral, oral slow-release forms available

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6
Q

Class IB Antiarrhthymics (List them)

A
  1. LIDocaine
  2. MEXIletine
  3. Tocainide

“I’d Buy LIDy’s MEXIcan Taco’s”

“IB is Best post-MI”

Weak inhibition of phase 0 (due to rpid binding and release) - bind less avidly to non-resting Na channels, thus most selective for frequently depolarizing scells (i.e. ectopic pacemakers)

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7
Q

Lidocaine

A

Class IB Antiarrhythmic, Local anesthetic, CNS stimulation/ depression, Cardiovascular depression

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8
Q

Mexiletine

A

Class IB Antiarrhythmic, oral activity and longer duration of action than lidocaine
Toxicities: Local anesthetic, CNS stimulation/ depression, Cardiovascular depression

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9
Q

Class IB Antiarrhythmics: Mechanism, Application, Pharmacokinetics

A

Mechanism: Dec. AP duration, Preferentially affect ischemic or depolarized purkinje and ventricular tissue.

Application: Acute ventricular arrhythmias (especially post MI), and in digitalis-induced arrhythmias

Pharmacokinetics: IV and IM, duration 1-2 Hr

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10
Q

Class IC Antiarrhythmics (list them)

A
  1. Flecainide
  2. Propafenone
  3. Moricizine

“1C is Contraindicated in structural heart disease and Post-MI”

“More Fries Please”

Strong inhibition of Phase 0, does not prolong QT, slow rate of dissociation during diastole (more effective at higher rates of depolarization - “use dependence”)

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11
Q

Flecainide

A

Class IC anti-arrhythmic, Toxicity is increased arrhythmias, CNS excitation

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12
Q

Class IC Antiarrhythmics Mechanism, application and pharamcokinetics

A

Selective us and state-dependent block of funny current leads to slowed conduction velocity and pacemaker velocity. No effect on AP duration.

Mechanism: Useful in ventricular tachycardias that progress to vfib and intractable SVT. Usually last-resort in refractory tachyarrhythmias. For pts without structure abnormalities

Pharmacokinetics: Taken Orally, duration 20h

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13
Q

Class 2 Antiarrhythmics (List them)

A

Beta-blockers (-olol’s)

  1. Metoprolol
  2. Propranolol
  3. Esmolol
  4. Atenolol
  5. Timolol
  6. Sotalol
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14
Q

Propanolol

A

Class II Antiarrythmic: beta blocker

Toxicity = bronchospasm, cardiac depression, AV block, hypotension

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15
Q

Sotalol

A 
Class II Antiarrythmic: beta blocker AND iK block (class III activity)
Toxicity: Dose-related torsades de points --> cardiac depression
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16
Q

Metoprolol

A

Class II Antiarrythmic: beta-blocker that’s B1 specific. Toxicities = bronchospasm, cardiac depression, AV block, hypotension

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17
Q

Class 2 Antiarrhythmics: Mechanism, Applications, Pharmacokinetics

A

Mechanism: Act on SA/AV nodes by decreasing cAMP, dec Ca currents, suppress abnormal pacemakers by decreasing the slope of phase 4

Applications: V-tach, SVT, slowing ventricular rate during A-fib and A-flutter

Pharmacokinetics: Oral, duration 4-7 hr

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18
Q

Class III Antiarrhythmics (List them)

A
  1. Amiodarone
  2. Ibutilide
  3. Dofetilide
  4. Sotalol
    “AIDS”
    Act on ventricular myocytes, K+ Channel blockers
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19
Q

Amiodarone

A

Class III antiarrythmic
Class II, II, III, and IV effects because it alters the lipid membranes: remember to check PFT’s (pulm), LFT’s (liver), and TFTs (thyroid) when using amiodarone.

  • deposits on skin, cornea, optic neuritis.
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20
Q

Dronedarone

A

Class III antiarrythmic
structural analog of amiodarone lacking iodine. half life of 24 hours, lacks major side effects of amiodarone. Toxicities include Diarrhea, nausea, vomiting, abdominal pain, photosensitivity, QT PROLONGATION

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21
Q

Sotalol

A

Class III antiarrythmic

toxicities: Dose-related torsades de points, excessive B-block - cardiac depression

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22
Q

Ibutilide

A

Class III antiarrythmic

toxicity = torsades de pointes

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23
Q

Dofetilide

A

Class III antiarrythmic

toxicity = Torsade de Pointes

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24
Q

Class III antiarrythmics: mechanism, applicaiton and Pharmacodynamics

A

Mechanism:
K+ channel blockers, act on ventricular myocytes. Inc AP duraiton, Inc ERP.

Applications: Used when other antiarrhythmics fail (last resort). Inc QT interval.

Pharmacodynamics: Oral 6-7 hr

25
Q

Class IV Antiarrythmics: list them

A

Ca channel blockers, most selective for rapidly depolarizing cells (use-dependent), act on AV/SA nodes

  1. Verapamil
  2. Diltiazam
26
Q

Verapamil

A

Class IV antiarrhythmic

Toxicity: Cardiac (CHF, AV block, Sinus node depression) constipation, flushing edema, gingival hyperplasia

27
Q

Diltiazem

A

Class IV anti arrhythmic

Toxicity: Cardiac (CHF, AV block, Sinus node depression) constipation, flushing edema, gingival hyperplasia

28
Q

Dihydropyridines

A

Ca channel blockers but not useful in arrhythmias, sometimes ppt arrhythmias

29
Q

Class IV antiarrhythmics: Mechanism, application and pharmacokinetics

A

Mechanism: Decrease conduction velocity, increase ERP, increase PR intervall.

Application: Use in prevention of nodal arrhythmias (i.e. SVT)
- use-dependent: selective for rapidly depolarizing cells

Pharmacokinetics: oral or parenteral, duration 6-7 hrs

30
Q

Adenosine

A

Antiarrhythmic:
- Increases K+ out of cells in AV node, which hyperpolarizes the cell causing a slower Phase 4.
- Decreases Calcium influx into cell, slowing phase zero.
Transiet AV block, and also used for coronary artery vasodilation.
- very short acting (15s)
- Toxicity includes flushing, hypotension, chest pain. Effects are blocked by theophylline and caffeine which mimic adenosine structure.

31
Q

Magnesium Ion

A

Effective in torsades de points and digoxin

  • IV
  • Toxicity is muscle weakness, respiratory paralysis
32
Q

Potassium ion

A

Increased in all K currents, decreased automaticity, decreased digitalis toxicity. Oral or IV. Both hypokalemia and hyperkalemia are associated with arrhythmogenesis. SEvere hyperkalemia causes cardiac arrest

33
Q

Nitroglycerin

A

Vasodilates by releasing nitric oxide in smooth muscle, causing an increase in cGMP and smooth muscle relaxation.
Dilates veins&raquo_space;» arteries. Decreases preload (decreased venous return due to venodilation)

Clinical use: Anginal, pulmonary edema

Toxicity: hypotension, flushing, headache, development of tolerance (nitrate-free interval at night prevents tolerance)

Do not use with Sildenafil: increases cGMP dramatically

34
Q

Isosorbide dinitrate

A

Vasodilates by releasing nitric oxide in smooth muscle, causing an increase in cGMP and smooth muscle relaxation.
Dilates veins&raquo_space;» arteries. Decreases preload (decreased venous return due to venodilation)

Clinical use: Anginal, pulmonary edema

Toxicity: hypotension, flushing, headache, development of tolerance (nitrate-free interval at night prevents tolerance)

Do not use with Sildenafil: increases cGMP dramatically

35
Q

Sildenafil

A

(Viagra)
Medaites normal erectile function by relaxing smooth muscle in corpora cavernosa

PDE5 mediates cGMP breakdown in tissue, Sildenafil inhibits PDE5, thus increasing cGMP –> enhances erections

Sildenafil potentiates actions of nitrates used for angina leading to severe hypotension and some heart attacks

36
Q

Vardenafil

A

Levitra - same mechanism as viagra:
Medaites normal erectile function by relaxing smooth muscle in corpora cavernosa

PDE5 mediates cGMP breakdown in tissue, Sildenafil inhibits PDE5, thus increasing cGMP –> enhances erections

Sildenafil potentiates actions of nitrates used for angina leading to severe hypotension and some heart attacks

37
Q

Tadalafil

A

Cialis - same mecahnism as sildenafil
Medaites normal erectile function by relaxing smooth muscle in corpora cavernosa

PDE5 mediates cGMP breakdown in tissue, Sildenafil inhibits PDE5, thus increasing cGMP –> enhances erections

Sildenafil potentiates actions of nitrates used for angina leading to severe hypotension and some heart attacks

38
Q

Verapamil

A

Vasodilator - Calcium channel blocker. Non-dihydropyridine (=BINDS OPEN CHANNELS - thus frequency of opening determines extent of blockade)
Mechanism: Blocks voltage-dependent L-type Ca channels of cardiac and smooth muscle, reducing contractility.

More effective on the HEART than vascular smooth muscle (Ventricle-Verapamil)

Applications: Hypertension, angina, arrhythmias, Prinzmetal’sangina, Raynauds

Toxicity: Cardiac depression (negative chronotropic effects), AV block, peripheral edema, flushing from vasodilation, dizziness and constipation

39
Q

Nifedipine

A

Vasodilator - Calcium channel blocker. Dihydropyridine (= EFFECTS CLOSED L-CHANNELS also bronchodilates, effects vsm>cardiac m.)

Mechanism: Blocks voltage-dependent L-type Ca channels of cardiac and smooth muscle, reducing contractility.
More effective on VASCULAR SMOOTH MUSCLE than THE HEART

Applications: Hypertension, angina, NOT ARRYTHMIAS, Prinzmetal’sangina, Raynauds

Toxicity: Cardiac depression (negative chronotropic effects), AV block, peripheral edema, flushing from vasodilation, dizziness and constipation

40
Q

Diltiazem

A

Vasodilator - Calcium channel blocker. Non-dihydropyridine.
Mechanism: Blocks voltage-dependent L-type Ca channels of cardiac and smooth muscle, reducing contractility.
More effective on heart muscle than vascular smooth muscle.

Applications: Hypertension, angina, arrhythmias, Prinzmetal’sangina, Raynauds

Toxicity: Cardiac depression (negative chronotropic effects), AV block, peripheral edema, flushing from vasodilation, dizziness and constipation

41
Q

Amlodipine

A

Vasodilator - Calcium channel blocker. Dihydropyridine (=effects vsm>cardiac m.)

Mechanism: Blocks voltage-dependent L-type Ca channels of cardiac and smooth muscle, reducing contractility.
More effective on VASCULAR SMOOTH MUSCLE than THE HEART

Applications: Hypertension, angina, NOT ARRYTHMIAS, Prinzmetal’sangina, Raynauds

Toxicity: Cardiac depression (negative chronotropic effects), AV block, peripheral edema, flushing from vasodilation, dizziness and constipation

42
Q

Immediate Treatment of an MI

A

“MONA”

  1. Morphine
  2. Oxygen
  3. Nitroglycerine
  4. ASA (Aspirin)
43
Q

Aspirin

A

ASA
Mechanism: Irreversibly inhibits cyclo-oxygenase (COX1 and COX2) enzyme by covalent acetylation. Platelets cannot synthesize new enzyme so effect lasts until new platelets are produced.
- Increased bleeding time, decreased TXA2 and PGAs. No effect on PT or PTT.

Low dose- inhibits COX1 mostly - less platelet aggregation, increased GI Bleeding
High dose - inhibits COX1 and COX2 - dec TXA, dec PGE2, dec PGI2, dec mucosal protection = more GI bleeding and dec platelet aggregation

Toxicity: Gastric ulceration, tinnitus (CNVIII). Chronic use –> acute renal falure, upper GI bleeding
Reye’s syndrome in children with viral infection.

Use clopidogrel if allergic to ASA (bronchoconstriction

44
Q

Clopidogrel

A

ADP receptor inhibitor
Inhibits platelet aggregation by irreversiby blocking ADP receptors, preventing expression of GPIIb/IIIa on platelets. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Application: Acute coronary syndrome, coronary stenting
Toxicity: fever, mouth ulcers

45
Q

Prasugrel

A

(same as clopidogrel)

ADP receptor inhibitor
Inhibits platelet aggregation by irreversiby blocking ADP receptors, preventing expression of GPIIb/IIIa on platelets. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Application: Acute coronary syndrome, coronary stenting
Toxicity: fever, mouth ulcers

46
Q

Abciximab

A

GP IIb/IIIa inhibitor
Mechanism: Bind to the glycoprotein receptor IIb/IIIa (direct inhibition) on activated platelets, preventing aggregation. Abciximab is made from monoclonal Ab Fab fragments.

Clinical Use: Acute coronary syndromes, percutaneous transluminal coronary angioplasty

Toxicity: Bleeding, thrombocytopenia w/in 24 hrs

47
Q

Eptifibatide

A

GP IIb/IIIa inhibitor - same as Abciximab and tirofibam
Mechanism: Bind to the glycoprotein receptor IIb/IIIa (direct inhibition) on activated platelets, preventing aggregation.

Clinical Use: Acute coronary syndromes, percutaneous transluminal coronary angioplasty

Toxicity: Bleeding, thrombocytopenia w/in 24 hrs

48
Q

tirofiban

A

GP IIb/IIIa inhibitor - same as tirofiban and eptifibatide
Mechanism: Bind to the glycoprotein receptor IIb/IIIa (direct inhibition) on activated platelets, preventing aggregation.

Clinical Use: Acute coronary syndromes, percutaneous transluminal coronary angioplasty

Toxicity: Bleeding, thrombocytopenia w/in 24 hrs

49
Q

Thrombolytics (List them)

A
  1. Alteplase
  2. reteplase
  3. tenecteplase
  4. urokinase
  5. streptokinase (Derived from streptococci, may induce hypersensitivity reaction
50
Q

Alteplase

A

Alteplase (tPA)

Mechanism: Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases both PT and PTT. NO change in platelet count (Platelets are not being used up any faster.)

Application: Early MI, Early ischemic stroke, direct thrombolysis of severe pulmonary embolism

Toxicity:
Bleeding. Contraindicated in bleeding patients.

51
Q

Reteplase

A

Reteplase (rPA)

Mechanism: Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases both PT and PTT. NO change in platelet count (Platelets are not being used up any faster.)

Application: Early MI, Early ischemic stroke, direct thrombolysis of severe pulmonary embolism

Toxicity:
Bleeding. Contraindicated in bleeding patients.

52
Q

tenecteplase

A

TNK-tPA

Mechanism: Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases both PT and PTT. NO change in platelet count (Platelets are not being used up any faster.)

Application: Early MI, Early ischemic stroke, direct thrombolysis of severe pulmonary embolism

Toxicity:
Bleeding. Contraindicated in bleeding patients.

53
Q

Direct Thrombin Inhibitors (List them)

A
  1. Desirudin
  2. Bivalirudin
  3. Argatroban
54
Q

Bivalirudin

A

Direct Thrombin Inhibitor
Derivatives of hirudin, the anticoagulant used by leeches. Inhibits thrombin. Used as an alternative to heparin for anticoagulating patients with Heparin-induced thrombocytopenia.

55
Q

Argatroban

A

Direct Thrombin Inhibitor
Derivatives of hirudin, the anticoagulant used by leeches. Inhibits thrombin. Used as an alternative to heparin for anticoagulating patients with Heparin-induced thrombocytopenia.
Hepatic clearance

56
Q

Heparin

A

Indirect Thrombin inhibitor
Mechanism: A highly sulfated GAG with a negative charge, Heparin is a cofactor for the activation of thrombin, which decreases thrombin and decreases factor Xa. It has a short half-life.

Application: Immediate anticoag. for PE, ACS, MI, DVT. Used during pregnancy. Increases PTT (dec. Xa)

Toxicity: Bleeding, thrombocytopenia, osteoporosis, drug-drug interactions. Antidote is protamine sulfate, a positively charged molecule that binds heparin. Treat HIT with argatroban.

57
Q

Warfarin

A

Oral Anticoagulant
Mechanism: inhibits vitamin K epoxide reductase, affecting the synthesis of new coagulant factors. Interferes with II, VII, IX, X, and proteins C and S. Affects extrinsic pathwya and increases PT. (Dec. factor VII)

Appplication: chronic anticoag., venous thromboembolism profylaxis… not used in pregnant women (use heparin instead)

Toxicity: Bleeding (esp w ASA), teratogenic, skin/tissue necrosis (due to relative dec. in PC/PS compared to 2,7,9,10 since PC and PS have shorter half life –> thrombosis and skin necrosis. Give heparin w warfarin to prevent WSN)

58
Q

New Oral Anticoagulants (List them)

A

Dabigatran

Rivaroboxan

Cardio Drugs (1 decks)

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