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Pharm - Cardiovascular > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

Anti-arrhythmic drugs general mechanisms:

A
  • suppress the initiating mechanism (or the initiator
  • ->promote re-entry)
  • altering the re-entrant circuit
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2
Q

4 ways to slow automatic rhythms via spontaneous pacemaker cells:

A

1) decrease phase 4 slope
2) increase threshold potential
3) increase maximum diastolic potential
4) increase Action potential duration (APD)

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3
Q

Abnormal stimuli can be decreased by increasing refractory peroid - what are the drug mechanisms here?

A

Messing with either:

  • blocking Na channels
  • prolonging the AP
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4
Q

Group Ia drugs

A

quinidine
procainamide
disopyramide

ERP/ARP ratio INCREASED! = less chance to be stimulated by abnormal impulse

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5
Q

Group Ib drugs

A

lidocaine

mexiletine

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6
Q

Group Ic drugs

A

propafenone

flecainide

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7
Q

Group II drugs

A

beta- adrenergic antagonists

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8
Q

Group III drugs

A 
dronedarone
amiodarone
sotalol
ibutilide
dofetilide
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9
Q

Group IV drugs

A

verpamil

diltiazem

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10
Q

Miscellaneous drugs

A

adenosine

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11
Q

Class I anti-arrhythmic drugs

  • general properties:
  • effects:
A

1) either local anesthetic or membrane stabilizing properties
2) a) predominant effect=block the fast inward Na cahnnel ==> result in decreased maximum depol rate (Vmax) of the action potential (phase 0) ==> slows intracardiac conduction
b) block K channels = delayed phase 3, prolonged QRS and QT durations
c) block Ca at high doses = depressed phase 2 in myocardial tissue and phase 0 in nodal tissue

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12
Q

Quinidine
1-Drug class?
2- primary mechs?
3-ancillary actions?

A

1) Class Ia
2) Primary mech = block rapid inward Na channels=
a) decreased Vmax of phase 0
b) slowed conduction (more in His-purkinje system than atria)
==> effects on Na channels are greatest at fast heart rate
3) ancillary:
a) block K channels = increased QT interval = inc APD
b) block muscarinic receptors = HR
c) competitive antagonist of alpha adrenergic receptors = decrease BP
d) block a-receptors = dec BP

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13
Q

Quinidine - Clinical applications:

A

only used in refractory patients:

a) convert symptomatic atrial fibrilation or flutter
b) prevent recurrences of atrial fib (AF)
c) treats documented life-threatening ventricular arrhythmias

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14
Q

Quinidine - adverse effects:

A
  • nausea
  • vomiting
  • diarrhea - most common?*
  • cinchonism (tinnitus, hearing loss, blurred vision)
  • -hypotension - alpha1 block = vasodilation (mild)
  • -proarrhythmic - torsade de pointes due to prolongation of QT interval

Class Ia

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15
Q

Quinidine - drug interactions:

A

1) of CYP3A4 - quinidines metabolism is a) inh by cimetidine & b) induces by phenytoin, phenopbarbital, rifampicin –> reduced plastma concentrations of quinidine to subtherapeutic range
2) potentn inhibitor of CYP2D6 - interferes with biotransformation and actions of CYP2D6 - metabolized rx= propafenone, mexiletine, flecainide, metoprolol, and timolol
3) increased digoxin toxicity if used concurrently with quinidine
4) worsens neuromuscular blockage in patients with myasthenia gravis

Class Ia

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16
Q

Two dangerous adverse effects of quinidine?

A
  • hypotension (due to alpha block)

- proarrhythmic (dorsade de pointes - increased QT interval = sets the stage for EAD)

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17
Q

Procainamide

  • MOA?
  • How different from quinidine?
A

1) block rapid inward Na channels = slows conduction, automaticity and excitability in the myocardium & purkinje fibers
2) block K channels = prolong APD and refractoriness

– difference: little or no effect on M receptors and no alpha block effects

Class Ia

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18
Q

procainamide

-Clinical application?

A

1) ventricular arrhythmias-
a) treat documented, life threatening ventricular arrhythmias
b) suppress ventricular arrhythmias that occur immediately post MI
c) convert sustained VT (IV loading takes up to 20min, therefore only used when there is time)
2) supraventricular arrhythmias: Use in the acute treatment of:
a) re-entrant SVT
b) atrial fib
c) atrial flutter associated with wolff-parkinson-white syndrome

class Ia

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19
Q

procainamide

-Adverse effects?

A

1) cardiac:
* a) aggravation of arrhythmia, torsade de pointes - (contraindicated in long QT syndrome, history of TdP or hypokalemia)
b) heart block, sinus node dysfunction
2) extracardiac:
* a) nausea & vomit = common!*
* b) drug induced lupus syndrome (SLE-like syndrome in slow acetylators): small joint arthralgia, pericarditis, fever, weakness, skin lesions, lymphadenopathy, anemia, and hepatomegaly. Presence of antinuclear antibodies. (ALL GOES AWAY AFTER STOP PROCAINAMIDE)
c) decreased kidney function

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20
Q

Class Ib

  • general properties:
  • effective against?
A
  • includes lidocaine, phenytoin, mexiletin, tocainide
    1) bind weakly to Na channels = weak effect on phase 0 depolarization
    2) accelerate phase 3 repolarization = shorten APR and QT
    3) little effect on PR, QRS, or QT at usual doses

-Effective in digitalis and MI induced arrhythmia

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21
Q

Wolff-Parkinson White syndome? What kind of arrhythmia is this?Which drug treats?

A
  • there is another fast path down to the ventricles beside the AV node
  • supraventricular arrhythmia
  • use procianamide
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22
Q

Lidocaine

-MOA?

A

1) blocks open and inactivated Na channels = reduced Vmax
2) shortens cardiac action potential due to blockade of slow inactivated Na channel and Ca channels
3) lowers the slope of phase 4 - altered threshold for excitability
4) in abnormal conduction system: slows ventricular rate and potentiates infranodal block

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23
Q

Drug that is most effecting in ischemic tissues?

Review MOAs.

A

LIDOCAINE

MOA:

1) blocks open and inactivated Na channels = reduced Vmax
2) shortens cardiac action potential due to blockade of slow inactivated Na channel and Ca channels
3) lowers the slope of phase 4 - altered threshold for excitability
4) in abnormal conduction system: slows ventricular rate and potentiates infranodal block

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24
Q

Patient comes in with acute MI with ventricular tachycardia… what drug to give? why?

A

Lidocain used to be best but now use amiodarone (classIII) - bc it shortens cardiac action potential

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25
Q

Lidocaine

- clinical applications

A

1) used to be the first line drug for ventricular arrhythmias - especially post MI ventricular arrhythmias
2) now we use amiodarone (class III) for immediately life threatening or symptomatic arrhythmias
3) ineffective in atrial tissues (atrial AP so short)
3) ineffective for prophylaxis of arrhythmias after MI

Class Ib

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26
Q

Lidocaine - clinical pharmacology:

A

class Ib

  • this drug undergoes significant first pass hepatic metabolism –> MUST USE IV
  • requires multiple loading doses and maintenance infusion (2 compartment drug so if you dont maintain the heart effects go away)
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27
Q

Lidocaine- Adverse effects?

A

Class Ib

1) CNS -
a) tinnitus or seizure upon rapid bolus.
b) high doses=drowsiness, confusion hallucinations, coma
2) Be careful with if taken in HF patients bc this decreased cardiac function with decreased clearance results in increased plasma concentrations

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28
Q

Class Ic agents -

-MOA?

A

1) potent Na channel inhibitors (strongest binders to Na channels among class I agents - SLOW ON-OFF PROPERTY)
2) lengthen PR, QRS and APD
3) Little effect on repolarization (QT unchanged)

(Propafenone, flecainide, morizicine)

29
Q

Propafenone

-MOA?

A

Class Ic

1) strong inh of Na channels
2) inh Beta1 adrenergic receptors due to marked structural similarity to proponolol

30
Q

Propafenone

-Clinical applications:

A

-Used primarily to treat arrhythmias, PSVT, and ventricular arrhythmias in patients with no or minimal heart disease and preserved ventricular function (beta inhibitory effects-not good to decrease HR action even more if ventricular function sucks already)

31
Q

Flecainide

-MOA?

A

Class Ic

  • potent Na channel block = prolonged phase 0 and widens QRS (SLOW ON-OFF EFFECT)
  • markedly slows intraventricular conduction
  • QT is unchanged bc K channels not affected
  • lengthened PR (depressed AV nodal conduction)
32
Q

flecainide

  • clinical applications:
  • Adverse effect?
A

class Ic

1) use only in the treatment of refractory & life threatening ectopic ventricular arrhythmias
2) Adverse effect: not a first line agent due to propensity for fatal pro-arrhythmic effects -caused a lot of deaths back in the day (CAST I Study)

33
Q

Class II anti-arrhythmics

  • MOA?
  • General properties?
A

1) Beta-adrenergic antagonists
2) General:
a) decrease SA nodal automaticity
b) decrease AV nodal conduction
c) decrease ventricular contractility
d) effective for supraventricular arrhyhtmias due to excessive sympathetic activity
e) NOT effective in severe arrhythmias such as VT
f) ONLY DRUG THAT IS CLEARLY EFFECTIVE IN PREVENTING SUDDEN CARDIAC DEATH IN PATIENTS WITH PRIOR MI

34
Q

Only drug thats effective in preventing sudden cardiac death in patients with prior MI or cardiac ischemia??

A

Class II - beta adrenergic antagonists

35
Q

Exercise induced tachycardia use what drug?

A

Class II agents - beta adrenergic antagonists bc youre treating the sympathetic cause to their inc HR by blocking B1 whcih increases HR when stimulated

36
Q

Class III agents:

  • MOA?
  • MAIN effect?
  • general uses?
A

(dronedarone, amiodarone, sotalol, ibutilide, dofetilide)

1) multiple effects at K, Ca, Na channels and Beta-receptors
2) prolong phase 3 repolarization = increase QT interval
3) useful for ventricular re-entry/fibrillatory arrhythmia (EFFECTIVE IN MANY TYPES OF ARRHYTHMIAS)

37
Q

Amiodarone

-MOA?

A

class III
1) blocks K channels - inc refractoriness and APD (QT interval increases)
2) blocks Na channels that are in the inactivated state
3) blocks Ca channels = slows SA node phase 4
4) slows conduction through the AV node
5) noncompetitive blockade of alpha, beta, and M receptors
ALL CONTRIBUTE TO WIDE ANTIARRHYTHMETIC EFFICACY

38
Q

Amiodarone is structurally similar to?

A

thyroxine and procainamide

39
Q

What does amiodarones major metabolite do? what does it cause?

A

-noncompetitive inhibition of thyroid hormone binding to nuclear receptors = cardiac hypothyroidism

40
Q

Amiodarone - clinical applications

A
  • VERY WIDELY USED TO TREAT RIDE RANGE OF ARRHYTHMIAS
  • conversion and slowing of AF maintaining sinus rhythm in AF
  • AV nodal re-entrant tachychardia
  • tachycardias associated with the WPW syndrome
  • PO for recurrent life threatening VT or VF resistant to other Rx
  • IV FOR ACUTE TERMINATION OF VT OR VF AND IS REPLACING LIDOCANE AS FIRST LINE THERAPY FOR OUT OF HOSPITAL CARDIAC ARREST
41
Q

Out of hospital cardiac arrest drug?

A

Amiodarone

42
Q

Amiodarone - clinical pharmacology?

A

1) highly lipid soluble
2) extremely variable and complex pharmacokinetics
* *3) extensively metabolized to desethyl amiodarone (DEA) which has more anatiarrhythmic potency that drug itself
4) rapidly concentrated win some tissues including the myocardium - accumulates more slowly in other tissues = good and very large Vd
5) if tissues are not saturated then rapid redistribution out of myocardium occurs = occurrence of arrhythmias after discontinuation or rapid dose reduction
6) T1/2 approx 5-68 hrs
7) as tissues become saturated T1/2 approx 13 to 103 days

43
Q

Amiodarone - adverse effects?

A
  • *1) IV > 5mg/kg decreases cardiac contractility & PVR = hypotension (due to polysorbate 80 or benzyl alcohol in IV formulation)
    2) usual dosages improves myocardial contractility
  • *3) MOST SERIOUS- lethal interstitial pneumonitis - frequent in patients with preexisting lung disease (REVERSIBLE CXR/3mo)
  • *4) hyper- or hypothyoridism - wide spectrum of effects
    5) accumulation of corneal microdeposits
    6) photosensitivity
    7) elevated serum hepatic enzyme levels
44
Q

Amiodarone effects on thyroid:

A

1) inh of 1,5’ deiodinase enzyme activity = dec peripheral conversion of T4 to T3 and dec clearance of T4 and reverse T3 (rT3) (hypo)
2) inhibition of entry of T4 and T3 into peripheral tissue
3) inhibition of type 2,5’-deiodinase enzyme activity in the pituitary due to feedback regulation
4) may have a direct cytotoxic effect on the thyroid fllicular cells ,which causes a destructive thyroiditis
5) amiodarone and its metabolite desethylamiodarone can act as a competitive antagonist of T3 at the cardiac cellular level

45
Q

T3 and T4 effects of amiodarone

A
  • within first month T4 serum levels rise 20-40% and then gradually fall toward high normal
  • T3 serum levels decrease up to 30% within first few weeks and then remain slightly low or low normal
  • serum rT3 levels increase 20% and remain increased
  • serum thryrotropin (TSH) rise initially but return to normal after 2-3 months
46
Q

Amiodarone induced thyrotoxicosis - two main types:

A
  • Type 1: usually affects patients with latent or pre-existing thyroid disorders and is more common in areas of low iodine intake - caused biodine induced excess thyroid hormone synthesis and release (JOD BASEDOW PHENOMENON)
  • Type 2: occurs in patients with a previously normal thyroid gland and is caused by a destructive thyroiditis leads to release of preformed thyroid hormones from damaged follicular cells
  • some mixed form toxicities do occur = iodine excess and destroying of follicles
47
Q

amiodarone induced hypothyroidism -

A
  • enhanced susceptibility to the inhibitory effect of iodine on thyroid hormone synthesis and the anability of the thyroid gland to escape from the wolff-chaikoff effect after an iodine load in patients with pre-existing Hashimoto thyroiditis
  • iodine induced damage to thyroid follicles may accelerate the natural trend of Hishi toward hypothyroidism.
48
Q

Class IV drugs

  • general:
  • MOA?
A

(verapamil, ditiazem)

1) calcium channel antagonists that preferentially act on cardiac tissue
2) MOA:
a) depress SA nodal automaticity and AV nodal conduction
b) decrease ventricular contractility
c) similiar to Class II, primary effects on nodal phase 0 depolarization (Ca channels)

49
Q

Ca channel blockers -

molecular targets and sites of action?

A

1) Ca Channel Blockers (CCBs) interfere with entry of Ca into cells through voltage dependent L and T type calcium channels - diminish the degree to which Ca can enter
2) No CCB bind to all pores- therefore blockade by CCB is incomplete
3) major sites of action:
a) vascular smooth muscle cells
b) cardiac myoctes
c) SA and AV nodal cells

50
Q

L-type channels structure and which unit is functionally relevant to CCB?

A

made up of alpha1 alpha2 beta and gamma units.

the alpha1 subunit contains the pores for Ca entry

CCBs bind to sites in the subunits and diminishes the degree to wihcih the Ca channel pores open in response to voltage depolarization

51
Q

2 main classes of CCB drugs:

A

1) dihydropyridine (DHP):
a) NIFEDIPINE and related compounds;
b) EFFECTS MAINLY IN VASCULATURE
c) NOT used as antiarrhythmics
2) Non-dihydropyridine (DHDP):
a) phenylalkylamine: VERAPAMIL & derivatives
b) Benzothiazepine: DILTIAZEM & derivatives
c) EFFECTS MAINLY IN THE HEART
d) USED AS ANTIARRHYHTMICS

52
Q

Major cardiovascular actions of CCBs? Ratio of vasodilation to negative inotropy

A

1) vasodilation: more marked in arterial and arteriolar vessels that on veins
2) NEGATIVE CHRONOTROPIC AND DROMOTROPIC effects seen on SA and AV nodal conducting tissue (DHDP agents only)
3) NEGATIVE INOTROPIC effects seen on myocardial cells; in the case of DHPs this effect may be offset by reflex adrenergic stimulation after peripheral vasodilation
4) Ratio of vasodilation to negative inotropy is 10:1 for nifedipine and 1:1 for diltiazem and verapamil

53
Q

Non-cardiovascular effects of CCBs:

A

1) CCBs have little or no effect on other smooth muscle
2) CCBs may relax uterine smooth muscle and have been used in therapy for pre-term contractions
3) skeletal muscle does not respond to conventional CCBs

54
Q

CCBs:

Main clinical application:

A

1) system hypertension (especially DHP group)
2) angina pectoris
3) supraventricular tachycardia
4) post-infarct protected - decrease workload, afterload and O2 demand

55
Q

Verapamil:

-MOA?

A

Class IV

1) “slow” inward Ca channels in nodal tissue are primarily affected
2) decreased SA automaticity = decreased HR
3) decreased conduction = increased PR interval
4) cardiac depression (dec ventricular contractility and dec HR)
5) no effect on ventricular Na conduction - ineffective on ventricular arrhythmia

56
Q

Verapamil -

-clinical applications:

A

1) supraventricular tachycardia (IV=conversion, PO=maintenance)
2) rate control in atrial fib
3) angina pectoris
4) hypertension

57
Q

Verapamil

-adverse effects:

A

1) headache, flushing, dizziness, ankle edema
* *2) constipation
* *3) exacerbate CHF
4) hypotension IV
5) AV heart block in combination with beta-blockers

58
Q

Verapamil

-contraindications:

A

1) sick sinus syndrome - sinus node doesnt discharge regularly
2) pre-existing AV nodal disease (already have AV block for example
* *3) WPW syndrome with atrial fib - blocks slow AV node path and so the other fast path that shouldnt be there gets all the signals
* *4) ventricular tachycardia

59
Q

Miscellaneous antiarrhythmics

drug names:

A

Adenosine and digoxin

60
Q

Adenosine MOA

A

1) activates A1 adenosine receptor in SA and AV nodes = increase cAMP-independent, Ach/adosensitive K channels, I_ACh,Ado=
a) hyperpolarization of SA node and slowing of firing rate
b) shortening of AP duration of atrial cells
c) depression of AV conduction velocity
2) activates A2 adenosine receptors in vasculature = activate K channels=
a) increases endothelial cell Ca concentration = increased nitric oxide production
b) hyperpolarization of vascular smooth muscle====> vasdilation
3) stimulaets pulmonary stretch receptors-tight in chest

61
Q

Adenosine - clinical applications:

A
  • *1) very effective for acute conversion of paroxysmal supraventricular tachycardia caused by re-entry involving accessory bypass pathways
    2) at 6mg dose = 60% patients respond and at 12mg 92% respond
    3) diagnostic too in narrow and wide complex tachycardia bc of selective action adenosine on the AV node
62
Q

Adenosine - clinical pharmacology

A

1) susceptibility to degredation and rapid plasma metabolism
* 2) must use as IV bolus to a central vein
* *3) t1/2 = 10-15sec
4) enzymatic metabolism in erythrocytes and vascular endothelium

63
Q

Adenosine adverse effects:

A

1) hypotension
2) flushing
3) complete heart block
4) CNS effects
5) dyspnea - tight chest

64
Q

Management of bradycardia:

A

1) atropine - not long term use - just symptomatic
2) isoproterenol - effective in bradycardia induced TdP - not long term
3) pacing - pace maker is used in symptomatic bradycardia that is more of a permanent nature

65
Q

Management sinus tachycardia, PSVT:

A
  • vagal stimulation through carotid sinus massage or Valsalva maneuver is sometimes used effectively in patients with sinus tachycardia or paroxysmal supraventricular tachycardia
66
Q

Drug of choice for life threatening ventricular tachycardia?

A

amiodarone

67
Q

supraventricular or ventricular tachycardia presents use?

A

amiodarone

68
Q

If not sure if supraventricular or ventricular tachycardia use what drug and why?

A

give adenosine bc its halflife is so quick if it works great if not itll be gone in 10-15 seconds

Pharm - Cardiovascular (6 decks)

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