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Pharm exam 2 > CV-antiarythmics > Flashcards

CV-antiarythmics Flashcards

1
Q

Class Ia antiarrhythmic agents:

A

QUINIDINE, PROCAINAMIDE, DISOPYRAMIDE

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2
Q

Class Ia antiarrhythmic agents:

A

‘Moderate’ binding to Na+ channels
moderate effects on phase 0 depolarization
K+ channel blockade
delayed phase 3 repolarization
prolonged QRS and QT
Ca2+ channel blocking effect at high doses
depressed phase 2 and nodal phase 0
‘Moderate’ binding to Na+ channels
moderate effects on phase 0 depolarization
K+ channel blockade
delayed phase 3 repolarization
prolonged QRS and QT
Ca2+ channel blocking effect at high doses
depressed phase 2 and nodal phase 0

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3
Q

Class I general characteristics

A

Block fast inward Na+ channels to varying degrees in conductive tissues of the heart
Decrease maximum depolarization rate (Vmax of phase 0)
reduce automaticity, delay conduction
Prolong ERP  ERP/APD increased
useful in varying degrees for ventricular dysrhythmia and/or digitalis or MI-induced arrhythmia

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4
Q

Quinidine MOA

A

Primary: Block rapid inward Na+ channel
Decreased Vmax of phase 0
Slowed conduction (His-Purkinje > atria)
Effects greatest at fast HR

Multiple actions – dose-dependent effects
Block K+ channels - APD
Block α receptors - BP
Block M receptors - HR in intact subjects

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5
Q

Clinical use quinidine

A

Risk/benefit ratio must be considered in each patient
Only used in refractory patients to
Convert symptomatic AF or flutter
Prevent recurrences of AF
Treat documented, life-threatening ventricular arrhythmias

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6
Q

Quinidine adverse effects

A

nausea, vomiting, diarrhea (most common)
cinchonism (tinnitus, hearing loss, blurred vision)
hypotension due to α-adrenergic blocking effect
proarrhythmic (torsades de pointes – increased QT interval)

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7
Q

MOA procainamide

A

Block rapid inward Na+ channel  slows
conduction
automaticity
excitability

Blocks K+ channels  prolongs APD & refractoriness

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8
Q

Diff tween Quinidine and Procainamide

A

Cf. Quinidine: Procainamide has very little vagolytic activity and does not prolong the QT interval to as great an extent, less likely to cause torsades de pointes

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9
Q

Ventricular Clinical use Procainamide*

A

life-threatening ventricular arrhythmias occurig post MI

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10
Q

Supra ventricular clinical use of Priocainamide*

A

Reentrant SVT
Atrial fibrillation
Atrial flutter associated with Wolff-Parkinson-White syndrome

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11
Q

Adverse effects Procainamide

A

40% stop use in 6 months
Cardiac:
arrhythmia aggravation, torsades de pointes (contraindicated in long QT syndrome, history of TdP, hypokalemia)**

heart block, sinus node dysfunction

Extracardiac:
*SLE-like syndrome: (15-20%, in slow acetylators) arthralgia, pericarditis, fever, weakness, skin lesions, lymphadenopathy, anemia and hepatomegaly

*GI nausea and vomiting: very common

Decrease kidney functions

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12
Q

Class Ib agents

A

Lidocaine, Phenytoin, Mexiletine, Tocainide

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13
Q

Class Ib general characterisitcs

A

‘Weak’ binding to Na+ channels
weak effect on phase 0 depolarization due to rapid ‘on-off’ receptor kinetics
Accelerated phase 3 repolarization
shortened APD and QT

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14
Q

clinical use for Ib agents*

A

digitalis and MI-induced arrhythmia

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15
Q

MOA Lidocaine

A

Blocks open and inactivated Na+ channels - reduces Vmax**

Shorten cardiac action potential

More effective in ischemic tissues

Lowers the slope of phase 4; altering threshold for excitability

produces variable effects in abnormal conduction system
Slows ventricular rate
Potentiates infranodal block

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16
Q

Clinical use Lidocaine

A

Used to be first-line rx for ventricular arrhythmias (post-MI)
Now (ECC/AHA 2005): second choice behind amiodarone for
immediately life-threatening or symptomatic arrhythmias
Ineffective for prophylaxis of arrhythmias after MI
Ineffective in atrial tissue

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17
Q

Pharmokinetics of interest

A

Extensive first-pass hepatic metabolism sobetter IV use.

need multiple loading doses and a maintenance infusion

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18
Q

Adverse effects lidcaine

A

rapid bolus: tinnitus, seizure
High doses: drowsiness, confusion, hallucinations, coma
Cardiac functions dec so dec clearance, inc concentrations

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19
Q

Class Ic agents

A

Moricizine, Flecainide, Propafenone

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20
Q

Class Ic general characteristics

A

Strongest binding to Na+ channels*
slow ‘on-off’ kinetics – strong effects on phase 0 depolarization
lengthened QRS and APD
Little effect on repolarization - QT unchanged
lengthened PR (depressed AV nodal conduction)

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21
Q

Propafenone MOA

A

Strong inhibitor of Na+ channel*

Can inhibits B-adrenergic R: marked structural similarity to propranolol

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22
Q

Propafenone Clinical use

A

used primarily to treat atrial arrhythmias, PSVT, and ventricular arrhythmias in patients with no or minimal heart disease and preserved ventricular function

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23
Q

Flecainide MOA

A

potent Na+ channel blockade  prolongs phase 0 and widens QRS
markedly slows intraventricular conduction

24
Q

Flecainide clinical usage

A

use only in the treatment of refractory life-threatening ectopic ventricular arrhythmia
not considered a first-line agent due to propensity for fatal proarrhythmic effects

25
Q

Class II general characterisitics

A

B-adrenergic antagonists
Decrease: SA nodal automaticity (phase 4)
AV nodal conduction
Ventricular contractility
Effective for supraventricular arrhythmias due to excessive sympathetic activity
Not very effective in severe arrhythmias such as recurrent VT
Are the only antiarrhythmic drugs found to be clearly effective in preventing sudden cardiac death in patients with prior MI

26
Q

Class II- B adreneergic antagonists general use etc

A

Multiple effects at K+, Ca2+, Na+ channels & β-receptors
Main effect: prolong phase 3 repolarization; inc QT
Useful for ventricular re-entry/fibrillatory arrhythmia
Effective in many types of arrhythmias

27
Q

Class II B adrenergic antagonists

A

Dronedarone, Amiodarone, Sotalol, Ibutilide, Dofetilide - DASID

28
Q

Amiodarone MOA

A

diverse pharmacologic actions

Blocks K+ channels  prolongs refractoriness and APD
Blocks Na+ channels that are in the inactivated state
Block Ca2+ channels  slows SA node phase 4
Slows conduction through the AV node
Noncompetitive blockade of α-, β-, and M receptors

Explains diverse antiarrhythmic actions

29
Q

Amiodarone Clinical usage

A

Effective in a wide range of arrhythmias, now very widely used**

Conversion and slowing of AF, maintaining sinus rhythm in AF
AV nodal reentrant tachycardia
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 lidocaineas first-line therapy for out-of-hospital cardiac arrest**

30
Q

pharmokinetics Amiodarone

A

highly lipid-soluble compound
extremely variable and complex pharmacokinetics
extensively metabolized to desethyl amiodarone (DEA)
DEA has antiarrhythmic potency greater than amiodarone*
rapidly concentrated in some tissues, including myocardium, but it accumulates more slowly in others  very large VD
Until all tissues are saturated, rapid redistribution out of the myocardium may be responsible for early recurrence of arrhythmias after discontinuation or rapid dose reduction**
After IV administration: T1/2  5 – 68 hrs
As tissues become saturated: T1/2  13 to 103 days

31
Q

Adverse effects Amiodarone

A

IV > 5mg/kg decreases cardiac contractility & PVR  hypotension***

Usual dosages improve myocardial contractility

  • Most serious: lethal interstitial pneumonitis, more frequent in patients with preexisting lung disease. Reversible with CXR/3 months
  • Hyperthyroidism or hypothyroidism: diverse effects on the thyroid

Accumulation of corneal microdeposits

Photosensitivity

Elevated serum hepatic enzyme levels

32
Q

Class IV agents

A

Verapamil, Diltiazem

33
Q

Class IV general characterisitcs

A

Ca2+ channel antagonists (cardiac)
similar in utility to Class II agents with primary effects on nodal phase 0 depolarization
depressed SA nodal automaticity, AV nodal conduction, decreased ventricular contractility

34
Q

Calcium blockers (class 4) major cardiovascular sites of action

A

vascular smooth muscle cells
cardiac myocytes
SA and AV nodal cells

35
Q

Calcium channel blocker characterisitcs and which 2 subtype of calcium channels are affected?

A

By binding to specific sites in Ca2+ channel subunits,CCBs diminish the degree to which the Ca2+ channel pores open in response to voltage depolarization

Ca2+ channel blockers (CCBs) interfere with the entry of Ca2+into cells through voltage-dependent L- and T-type Ca2+ channels.**

36
Q

L-type Ca2+ channel 1 subunit

A
  • No CCB binds to all pores  blockade is incomplete
    4 subunits a-1, a-2, B, y
    a-1 containspores
37
Q

CCB 2 classes

A

DHP (Dihydropyridine) and NDHP (Nondihydopyridine)

38
Q

Dihydropyridine (DHP) (1)

A

Nifedipine

Effects mainly in the vasculature

39
Q

NDHP

A

Phenylalkylamine - Verapamil & derivatives
Benzothiazepine - Diltiazem & derivatives

*both affect mainly in heart

40
Q

Cardiovascular effects CCB

A

Vasodilation
more marked in arterial and arteriolar vessels than on veins

Negative inotropic effectsare seen on myocardial cells; in the case of DHPs, this effect may be offset by reflex adrenergic stimulation after peripheral vasodilation.

Ratios of vasodilation to negative inotropy for the prototype CCBs were 10 : 1 for nifedipine, 1 : 1 for diltiazem and verapamil.

41
Q

Cardiovascular events occuring only with NDHP

A

Negative chronotropic and dromotropic effectsare seen on the SA and AV nodal conducting tissue (NDHP agents only).

42
Q

CCB non cardiovascular effects (or lack there of)

A

CCBs have little or no effect on other smooth muscle

CCBs may relax uterine smooth muscle and have been used in therapy for preterm contractions

Skeletal muscle does not respond to conventional CCBs

43
Q

Main clinicaluses of CCB

A

Systemic Hypertension

Angina Pectoris

Supraventricular Tachycardia

Post-infarct protection

44
Q

Veramapil MOA

A 
“slow” inward Ca2+ channels in nodal tissue are primarily affected 
↓SA automaticity  ↓HR
↓AV conduction  ↑PR interval
cardiac depression (↓ ventricular contractility and ↓HR)
no effect on ventricular Na+ conduction  ineffective on ventricular arrhythmia
45
Q

Veramapil clinical applications

A

supraventricular tachycardia (IV – conversion, PO – maintenance)
rate control in Afib
angina pectoris
hypertension

46
Q

Veramapil adverse effects

A

Headache, flushing, dizziness, ankle edema
Constipation
Exacerbate CHF
Hypotension (IV)
AV heart block in combination with β-blockers

47
Q

Contraindications

A

Sick sinus syndrome
Pre-existing AV nodal disease
WPW syndrome with Afib
Ventricular tachycardia

48
Q

Misc. antiarrythmia drugs

A

Adenosine, Digoxin

49
Q

Adenosine MOA A1 rec

A

Activates A1receptor in SA & AV nodes  activates cAMP–independent, Ach/Ado-sensitive K+ channels 
SA node hyperpolarization and dec firing rate
Shortening of AP duration of atrial cells
Depression of A-V conduction velocity

50
Q

Adenosine MOA A2 rec

A

Activates A2receptor in vasculature  K+ channels
inc endothelial Ca2+ - inc
NO
Smooth muscle hyperpolarization - vasodilation

Stimulates pulmonary stretch receptors

51
Q

Clin use adenosine

A

Very effective for acute conversion of paroxysmal supraventricular tachycardia caused by reentry involving accessory bypass pathways. At a dose of 6mg, 60% of patients respond, and an additional 32% respond when given a 12-mg dose.

52
Q

Pharmokinetics Adenosine

A

susceptibility to degradation and rapid plasma metabolism
Must use as IV bolus to a central vein (brachial, antecubital)
t½=10-15 sec
enzymatic metabolism in erythrocytes and vascular endothelium

53
Q

Adenosine adverse effects

A

hypotension, flushing, complete heart block, CNS effects, dyspnea

54
Q

Management of Bradycardia

A

atropine – produces a vagal block to increase HR
isoproterenol – β1-stimulated increase in HR
Pacemaker

55
Q

Management of Sinus tachcardia or PSVT

A

vagal stimulation through carotid sinus massage or Valsalva maneuver

Pharm exam 2 (8 decks)

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