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My Pharm II > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

___ comes in on phase zero, -60, -70mv

A

NA

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2
Q

Look at slide 4-7

A

.

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3
Q

Phase ____ mediated by _________ in SA node, ___ in Muscle cell

A

zero

calcium

NA

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4
Q

Factors that ______ automaticity at the higher pacemaker sites will passively favor the movement of the pacemaker to lower sites. Vagal influences?

A

reduce

Digitalis drugs
Parasympathomimetic drugs
Halothane

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5
Q

For re-entry to occur: ___________. examples?

A

NA mediated

-Unidirectional block of impulse conduction (area of injury).
-Slow conduction via an alternate pathway
Impulse finds the unidirectional block repolarized and able to conduct the impulse retrograde
-Impulse reactivates the alternate pathway and repeats the process.

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6
Q

Re-entry, Can occur at many sites:

A

SA Node: SA nodal re-entry
Atrium: Atrial tachycardia or flutter
AV Node: AV nodal re-entry and tachycardias mediated by accessory pathways
Ventricle: VT

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7
Q

Na+ Channels:

Ca+2 Channels:

A
  • Atria
  • Ventricles
  • SA Node
  • AV Node
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8
Q

Na+ channel blockers (Type I)

A

slow conduction and prolong the QRS complexes in the atria and ventricles.

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9
Q

Ca+2 channel blockers (Type IV)

A

slow the atrial rate (SA node effect) and slow conduction through the AV node (prolonging the PR interval)

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10
Q

K+ Channel Blockade (Type III)

A

Interrupts reentry by slowing conduction or increasing the refractory period.

Prolongs the QT interval and induces triggered activity in the ventricle causing polymorphic VT (Torsades de Pointes).

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11
Q

Class I:

A

Inhibits fast sodium channels

  • IA: Quinidine, Procainamide, Disopyramide, Moricizine
  • IB: Lidocaine, Mexilitine, Phenytoin
  • IC: Flecainide, Propafenone
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12
Q

Class II:

A

Decrease rate of depolarization

-Beta Blockers

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13
Q

Class III:

A

Inhibit potassium ion channels

  • Amiodarone, Dronedarone
  • Sotalol
  • Ibutilide
  • Dofetilide
  • Bretylium
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14
Q

Class IV:

A

Inhibit slow calcium channels

  • Diltiazem
  • Verapamil
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15
Q

Class II and IV have similar effects

A

.

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16
Q

Effects on the Action Potential:

A 
Type Ia: Slows phase 0, prolongs 3
Type Ib: Slows 0, shortens 3
Type Ic: Very slow 0, no 3 effects
Type II: Reduces slope of 4
Type III: Prolongs 3
Type IV: Reduces slope of 4
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17
Q

Class II: Beta Blockers

A

-Slow heart rate resulting in decreased myocardial oxygen requirements.

  • Slow conduction of cardiac impulses through atrial tissue.
  • Prolonged the P-R interval
  • Duration of action of the cardiac action potential in ventricular myocardium is unchanged.
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18
Q

Unclassified:

A

Adenosine and digoxin

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19
Q

Procainamide (IA) MOA:

A
  • Na+ and K+ channel blocker.
  • Depresses automaticity by decreasing the slope of phase -0 depolarization, increases refractoriness
  • Prevent reentry by converting unidirectional to bidirectional block.
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20
Q

Procainamide (IA) Indications:

A
  • Ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways
  • SVT, A. fib., PVCs, and VT
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21
Q

50-80% pts become ANA positive - lupus-like symptoms from what drug?

A

Procainamide

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22
Q

Procainamide (IA) metabolite

A

Metabolite- N-acetyl procainamide (NAPA)

  • half life 6-10 hours
  • renally eliminated- may accumulate
  • increased risk of s/e, QT prolongation
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23
Q

Quinidine (IA) Use:

A

A.flutter, A.fib, V.tach, V.fib

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24
Q

Quinidine (IA) Toxicity

A

QT prolongation, V.tach (high doses for a.fib conversion)
Loose stools
Thrombocytopenia
Cinchonism: includes headache and tinnitus

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25
Q

Quinidine (IA) Pharmacokinetics

A
  • Potent CYP2D6 inhibitor*
  • PGP inhibition
  • Half life 6-8H
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26
Q

In new med called Nudexta – for uncontrolled mood behaviors

A

Quinidine

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27
Q

Disopyramide (IA)

A
  • Similar to quinidine without alpha effects
  • Anticholinergic effects
  • Used for atrial and ventricular tachyarrhythmias
28
Q

Disopyramide (IA) Toxicity

A
  • Anticholinergic side effects
  • Heart failure exacerbation
  • QT prolongation
  • Thrombocytopenia
  • Renally eliminated
29
Q

Lidocaine (IB) Indications:

A
  • For ventricular arrhythmias, particularly reentry dysrhythmias.
  • Ineffective against supraventricular arrhythmias.
30
Q

Early sign of Lidocaine (IB) toxicity

A

Nystagmus

31
Q

Lidocaine (IB)

A

Reduce dose in CHF, liver disease

Almost no effect on QT interval

32
Q

Phenytoin (IB) Indications:

A
  • Useful in the suppression of ventricular dysrhythmias associated with digitalis toxicity.
  • Also, paradoxical v. tach or torsades de pointes that is associated with prolonged QTc interval.
33
Q

Phenytoin (IB) Toxicity:

A
  • Rapid administration associated with resp. arrest, severe hypotension, vent. ectopy, and death.
  • CNS: drowsiness, nystagmus, nausea, vertigo
34
Q

Class ___ are most pro-arrythmic of all antiarrythmics – So highest risk of arrythmias

A

IC

35
Q

Flecainide (IC) Mechanism of Action:

A
  • Blocks sodium, potassium, and calcium channels
  • Depresses action potential phase 0.
  • Prolongs QRS and to a lesser extent PR interval.
  • May suppress SA node like Beta blockers and Calcium Channel blockers.
  • Delays conduction in bypass tracts.
36
Q

Flecainide (IC) Indications:

A
  • Effective in suppressing PVCs
  • Atrial tachydysrhythmias including WPW
    - Delays conduction in bypass tracts
37
Q

Flecainide (IC) Side Effects:

A
  • Moderate negative inotropic effect
    - Do not administer with CAD, LV failures, V.tach
  • Vertigo
  • Difficulty in visual accommodation
38
Q

Atrial arrythmias only

A

B.Blockers

39
Q

Beta Blockers (II) Mechanism of Action:

A
  • Beta blockade leads to slowing of the S-A node (decreased slope of phase 4 depolarization)
  • Slow the rate depolarization of ectopic pacemakers
  • Prolonged A-V nodal conduction
  • Increased refractoriness of A-V node
40
Q

Beta Blockers (II) Toxicity

A
  • Profound bradycardia or asystole
  • LV failure
  • Acute bronchospasm
  • Decreased CO
41
Q

Amiodarone (III) Mechanism of Action

A

-Potent inhibitor of abnormal automaticity.

  • Prolongs the effective refractory period and action potential duration in all cardiac tissues including accessory bypass tracts.
    • Blocks inactivated Na+ channels and K+ movement.
    • Has an antiadrenergic effect (noncompetitive blockade of alpha and beta receptors).
    • Prolongs PR, QRS, and QT intervals.
  • May potentiate slowing of the SA Node and AV conduction.
    - May potentiate Beta Blockers and Ca+2 Channel blockers.
42
Q

Amiodarone (III) Indications:

A

-IV for the acute termination of ventricular and supraventricular arrhythmias

  • Recurrent V Fib. or recurrent unstable V. Tach in patients unresponsive to or unable to tolerate other agents
  • Effective in maintaining SR in patients with A. Fib.
  • Suppression of tachydysrhythmias associated with WPW.
43
Q

Long amio take, more it builds up, longer half-life is. Could have effects for years

A

.

44
Q

Amiodarone (III) Toxicity: Resp, CV, Heme, Hepatic, Endo, Other

A

Resp: ARDS, pulmonary fibrosis
CV: bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest
Heme: coagulation abnormalities
Hepatic: increased LFTs, liver failure
Endo: hypo- or hyperthyroidism
Other: Peripheral neuropathy, muscle weakness

45
Q

Dronedarone (III) indications

A

For atrial fibrillation to maintain NSR

46
Q

Dronedarone (III) Contraindications

A
  • Increased risk of death, stroke and heart failure for patients with decompensated heart failure or permanent afib
  • Second/third degree heart block, HR <50 bpm
  • Medications that inhibit CYP3A4, prolong QTc
  • Pregnancy
  • Significant liver disease
  • Doesn’t have iodine in it like amio does*
47
Q

Ibutilide/Dofetilide (III) uses/incidences

A
  • Used for conversion of atrial fibrillation to NSR

- High incidence of Torsades and ventricular tachyarrythmias

48
Q

Verapamil (IV) Mechanism of Action:

A
  • Selectively blocks slow channels by inhibiting the normal Ca+2 influx into the cell.
  • Slow channel activity is most important in S-A and A-V nodes.
  • prolongs A-V nodal conduction and refractoriness.
  • Depresses the rate of S-A node discharge.
49
Q

Verapamil (IV) Indications:

A
  • Treat SVT.
  • Slow ventricular rate in A. Fib. and Flutter.
  • No effect on accessory tracts.**
50
Q

Verapamil (IV) Toxicity:

A
  • Hypotension is a major side-effect
  • Bradycardia, asystole, and A-V Block have been seen
  • Myocardial depression is uncommon in pts. with reasonable LV function
51
Q

Diltiazem (IV) Mechanism of Action:

A

Slow channel blocking prolongs A-V nodal conduction and refractoriness.

52
Q

Diltiazem (IV) drug interactions

A

Potent CYP3A4 inhibitors

53
Q

Amiodarone (III) Drug Interactions

A
  • CYP3A4 substrate

- CYP3A4, CYP2C9, and PGP inhibitor

54
Q

Diltiazem (IV) Toxicity

A
  • Bradycardia, hypotension
  • Edema
  • Constipation
55
Q

Ventricular rates are easier to control in _____ than ______

A

A. Fib

A. Flutter.

56
Q

Digoxin Mechanism of Action:

A
  • Inhibits Na+/K+ ATPase.
  • Directly prolongs the effective refractory period in the A-V node.
  • Slows the ventricular response rate in a. fib.
  • But, enhances conduction through accessory pathways.***
  • Can increase ventricular response in WPW.
57
Q

Adenosine Mechanism of Action:

A
  • Effects A1 receptoirs
  • Activates K+ channels that hyperpolarize nodal tissue causing a transient 3rd degree AV block*
  • Less effect in the atrium (already hyperpolarized).
  • Depression of the action potential in the A-V and SA Node.
  • Inhibits effects of increased cAMP, reduces calcium currents to increase AV note refractoriness
  • Bolus dose may induce transient sympathetic acivation via carotid barorectpros
  • continuous infusion causes hypotension
58
Q

It is inactivated by cellular uptake.

A

Adenosine

59
Q

Adenosine Toxicity:

A
  • Facial flushing, dyspnea, and chest pressure most common, but subside in <60 seconds.
  • May exacerbate bronchoconstriction in asthmatic patients.**
60
Q

Class IA and class III drugs block potassium channels and prolong QTc interval. Highest risk of what?

A

Torsades

61
Q

Predisposing Factors to Torsades

A
  • Low K+, Mg++, slow heart rates, and pre-existing QT prolongation may predispose to drug induced arrhythmias
  • Torsades occurs in 1-8% of patients who receive QT prolonging drugs.
62
Q

_______ highest risk of QT-prolongation, then ______

A

Haldol

ABX

63
Q

Look at slide 66

A

.

64
Q

Usually associated with Class IC drugs in the setting of structural heart disease

A

Wide Complex Ventricular Rhythm

-Excessive plasma concentrations of drug or an abrupt change in the dose may result in this prodysrrhythmia

65
Q

which meds cause QT prolongation

A

Class IA and III

  • Amiodarone
  • Dronedarone
  • Quinidine
  • Procainamide
  • Disopyramide

My Pharm II (8 decks)

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