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Cardiovascular > CV pharmacology > Flashcards

CV pharmacology Flashcards

1
Q

relationship between cardiac AP and ion channel currents

A
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2
Q

Arrhythmias are caused by ?

A

abnormal pacemaker activity
abnormal impulse propagation

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3
Q

The aim of therapy of the arrhythmias is to ?

A

reduce ectopic pacemaker activity
modify conduction or refractoriness in reentry circuits to disable circus movement

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4
Q

what do antiarrhythmic drugs do?

A
  • decrease automaticity of ectopic pacemakers more than that of SA node
  • reduce conduction and excitability and increase refractory period
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5
Q

3 subclasses are further defined by the effect of the agents on the Purkinje fiber AP:

class I

A
  • Class Ia: slow rate of rise of AP and prolong duration = slowing conduction and increasing refractoriness (moderate depression of phase 0 upstroke of the action potential)
  • Class Ib: shorten AP duration; do not affect conduction or refractoriness (minimal depression of phase 0 upstroke of AP)
  • Class Ic: Dissociates from channel with slow kinetics (no change in AP duration)
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6
Q

What is the drug classification for antiarrhythmics

A

Vaughan-Williams Classification system

  • Block fast Na channels (class I)
  • BB (class II)
  • block K channels (class III)
  • CCB (class IV)
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7
Q

what drugs are class Ia?

A

quinidine, procainamide, disopyramide

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8
Q

what drugs are class Ib?

A

lidocaine, mexiletine

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9
Q

what drugs are class Ic?

A

flecainide, propafenone

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10
Q

Quinidine MOA/effect

A
  1. potent anticholinergic properties that affect SA and AV nodes = increase SA nodal discharge rate and AV nodal conduction
    - may lead to increased ventricular rates with afib or aflutter
    - Addition of BB, non-dihydropyridine CCB, or digoxin protects against this
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11
Q

SE of Quinidine

A

GI-related - N/V/D
Proarrhythmic – torsades
Can interact with CYP3A4 inducers or inhibitors

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12
Q

difference between Quinidine vs Procainamide

A

Does not have the anticholinergic activity of quinidine

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13
Q

SE of procainamide

A
  • Prolongs QT interval = risk of torsades
  • SLE – MC adverse event
  • N/V/D and drug fever
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14
Q

disopyramide effect

A

Potent anticholinergic and negative inotropic effects limits uses clinically

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15
Q

SE/CI of disopyramide

A
  • Prolongs QT = torsades
  • CI: reduced LV EF (<40%)
  • Precipitation of CHF
  • Anticholinergic effects – dry mouth, urinary retention, constipation, blurred vision
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16
Q

lidocaine effect

A
  • Selective to ischemic tissue, and esp to active fast Na channels in bundle of HIS, Purkinje fibers, and ventricular myocardium
  • Primarily effective in treating ventricular dysrhythmias, especially those associated with acute MI
  • Little effect: non-ischemic tissue, atrial myocardium, and automaticity of the SA node
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17
Q

monitoring for lidocaine

A

Cleared by hepatic metabolism, therefore, monitor closely for signs of toxicity in patients with liver failure

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18
Q

SE of lidocaine

A

CNS effects of dizziness, paresthesia, disorientation, tremor, agitation, seizures and respiratory arrest

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19
Q

effect of mexiletine

A
  • Not used as a single agent - combo w/ class IA and III drugs for the tx of refractory ventricular dysrhythmias
  • Similar to lidocaine, but in oral form
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20
Q

SE mexiletine

A
  • GI – N/V, limits use
  • neurologic - dizziness, confusion, ataxia, and speech disturbances
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21
Q

MOA of Flecainide (Tambacor)

A
  • Slows conduction velocity in Purkinje fibers & AV node
  • lengthen PR interval & QRS duration
  • MC for afib/flutter
  • for VT but it sucks
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22
Q

SE of flecainide

A
  • Rapid VT, resistant to resuscitation, esp with CAD, LV dysfunction, LVH or valvular disease - AVOID in any heart dz
  • Blurred vision, dizziness, HA, tremor, N/V
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23
Q

MOA of propafenone

A
  • Class IC
  • Slows conduction velocity in Purkinje fibers and AV node; also has a mild nonselective BB effect
  • lengthen PR interval and QRS duration = conduction disturbances (bradycardia, blocks)
  • MC for afib/flutter
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24
Q

SE of propafenone

A
  • May cause VT similar to flecainide, so avoid in any form of heart dz
  • Blurred vision, dizziness, HA, N/V, bronchospasm, and taste disturbances (metallic taste)
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25
Q

MOA of BB

A
  • Decrease automaticity, prolong AV conduction, and prolong refractoriness - Negative chronotropic and inotropic effects
  • Suppresses ventricular dysrhythmias + supraventricular dysrhythmias
  • esp helpful when used in combination with other AAD
  • Metoprolol MC
26
Q

which BB can be used as a continuous IV infusion for rapid afib/flutter

A

esmolol

27
Q

MOA of class III AAD

A
  • Block K channels and prolong repolarization, widening QRS and prolonging QT interval.
  • Decrease automaticity and conduction and prolong refractoriness.
28
Q

Avoid concomitant use of class III AADs with ?

A

other drugs that can prolong QT interval to minimize the risk of torsades

29
Q

MOA of amiodarone

A
  1. Possesses characteristics of all 4 classes
    - Primarily K channel blocker, also blocks Na channels, has non-selective BB activity, weak CCB properties
    - Works on all cardiac cells (SA node, AV node, atria, ventricles and Purkinjes)
  2. Minimal/no negative inotropic effects - Can be used w/ LV dysfunction
30
Q

SE of amiodarone

A
  • Has potential to for its metabolite to accumulate and cause adverse effects in numerous organs, including the lungs, thyroid, eyes, heart, liver, skin, GI tract, and nervous system
  • GI common - N/V, anorexia, abd pain (take w/ food)
  • Neurologic toxicities occur frequently - Tremors, ataxia, peripheral neuropathy, fatigue and insomnia
  • Liver toxicity is rare, but screening LFTs Q6 mo
  • Derm - photosensitivity, blue/gray discoloration - Sunscreen + sun exposure avoidance to help
31
Q

amiodarone is a potent inhibitor of what enzyme?

A

CYP3A4

  • Many DDI
  • Potentiates the anticoagulation effects of warfarin; close monitoring is essential
  • Can double serum digoxin concentrations
32
Q

MOA of sotalol

A
  1. Class III that also has nonselective beta-adrenergic blocking properties
    - May decrease cardiac contractility and therefore should be avoided in patients with LV dysfunction
  2. Prolongs atrial and ventricular refractoriness
33
Q

SE of sotalol

A
  1. QT prolongation common - monitored for closely
    - DC if QT interval > 550 ms
    - Avoid combining with other QT prolonging drugs
  2. Most SE from BB properties
34
Q

MOA of dofetilide

A

Results in prolonged AP and an increased QT interval

  • Affects atria > ventricles
  • No negative inotropic effects = safe in LV dysfunction
35
Q

SE of dofetilide

A

torsades de pointes - Admit, telemetry Q12 hr EKG’s for first 3 days of loading to monitor QT interval and adjust dose

36
Q

CI with dofetilide

A
  • Cimetidine, ketoconazole, megestrol, prochlorperazine, Bactrim, or verapamil - Avoid inhibitors of the CYP3A4 isoenzyme
  • Renally cleared, avoid if CrCl < 20 mL/min
37
Q

MOA of dronedarone

A
  • Exact MOA unknown; exhibits AA properties of all 4 classes
  • Some considered it the “safe cousin of amiodarone”; but not nearly as effective, and side effects and toxicities are still common
38
Q

SE of dronedarone

A

CHF exacerbation
QT prolongation
bradycardia
hepatotoxicity
pulmonary toxicity
photosensitivity
N/D
pruritis
dyspepsia

39
Q

CI of dronedarone

A
  • Symptomatic CHF & recent decompensation requiring hospitalization
  • Permanent AF
  • Severe hepatic impairment
40
Q

monitoring for dronedarone

A

BUN/Cr; EKG q 3 mos; LFT’s during 1st 6 mos of Tx

41
Q

effect and indication for ibutilide

A

Ibutilide - Corvert

  • Structurally similar to sotalol, but no BBing activity
  • IV only, and indicated only for afib/flutter cardioversion
42
Q

SE of ibutilide

A

torsades

  • Monitored on telemetry following IV infusion
  • Avoid: LV dysfunction and electrolyte abnormalities (esp hypokalemia and hypomagnesemia)
43
Q

verapamil

A

CCB

44
Q

diltiazem

A

CCB

45
Q

MOA of CCB

A
  • Decrease automaticity and AV conduction
  • Potent negative inotropic effects - avoid LV dysfunction
46
Q

MOA of digoxin

A

Predominant AA effect is on AV node

  • Inhibits Ca currents in AV node and activates Ach-mediated K+ currents in atrium
  • Slows conduction thru AV node and prolongs AV nodal refractory period
  • Therefore, mainly used for slowing the ventricular rate in afib/flutter, as well as terminating reentrant arrhythmias involving AV node
47
Q

On EKG you see PR prolongation and ST segment depression, what is going on?

A

digoxin effect

48
Q

toxicity of digoxin is a risk if ____ are administered that destroy intestinal microflora

A

antibiotics

49
Q

PK of digoxin

A
  • Half-life - 36 hrs = once daily dosing
  • Renal elimination = reduced dose/dosing intervals with renal insufficiency
  • IV or oral - Tablets are incompletely bioavailable
  • intestinal microflora may metabolize digoxin = reduced bioavailability = need higher doses
  • Slow distribution to effector sites - Even w/ IV
  • Requires loading dose 0.6-1 mg x 24 hrs, then reduce to maintenance dose
50
Q

what drugs specific can decrease digoxin clearance?

A

Amiodarone
quinidine
verapamil
diltiazem
itraconazole
propafenone
flecainide

dose should be decreased if combining with these drugs

51
Q

signs of digoxin toxicity?

A
  • declining renal function, electrolyte abnormalities, hypoxia or DDI
  • Visual disturbances, dizziness, weakness, N/V/D, anorexia
  • Essentially ANY dysrhythmia can result from digoxin toxicity
52
Q

tx of digoxin toxicity

A
  • IV hydration and electrolyte correction
  • Digoxin immune Fab - an immunoglobulin fragment with specific and high affinity for digoxin molecules
53
Q

MOA of adenosine

A
  • Activates K channels and by increasing outward K current hyperpolarizes the membrane potential, decreasing spontaneous SA nodal depolarization
  • Inhibits automaticity and conduction in the SA and AV nodes
54
Q

adenosine is used for converting what abnormality to sinus rhythm?

A

SVT to sinus rhythm; essentially causing sinus arrest

55
Q

SE of adenosine

A

Chest discomfort, dyspnea, flushing, HA

56
Q

what is atropine

A
  • Parasympatholytic drug that enhances both sinus nodal automaticity & AV nodal conduction through direct vagolytic action
  • Blocks Ach at parasympathetic neuroeffector sites
57
Q

when is atropine used?

A

emergent setting of symptomatic bradycardia

58
Q

SE of atropine

A
  • tachycardia - may result in poor outcomes in pts with MI, so use cautiously
  • paradoxical slowing HR with Mobitz type II AVB and 3rd degree AVB - monitor
59
Q

which AADs are safe for LV dysfunction

A
  1. amiodarone
  2. dofetilide
60
Q

which AADs should be avoided in LV dysfunction

A
  1. Flecainide
  2. sotalol
  3. ibutilide
  4. CCB

Cardiovascular (24 decks)

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