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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
Quinidine (IA) Pharmacokinetics
- Potent CYP2D6 inhibitor* - PGP inhibition - Half life 6-8H
26
In new med called Nudexta – for uncontrolled mood behaviors
Quinidine
27
Disopyramide (IA)
- Similar to quinidine without alpha effects - Anticholinergic effects - Used for atrial and ventricular tachyarrhythmias
28
Disopyramide (IA) Toxicity
- Anticholinergic side effects - Heart failure exacerbation - QT prolongation - Thrombocytopenia - Renally eliminated
29
Lidocaine (IB) Indications:
- For ventricular arrhythmias, particularly reentry dysrhythmias. - Ineffective against supraventricular arrhythmias.
30
Early sign of Lidocaine (IB) toxicity
Nystagmus
31
Lidocaine (IB)
Reduce dose in CHF, liver disease | Almost no effect on QT interval
32
Phenytoin (IB) Indications:
- 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
Phenytoin (IB) Toxicity:
- Rapid administration associated with resp. arrest, severe hypotension, vent. ectopy, and death. - CNS: drowsiness, nystagmus, nausea, vertigo
34
Class ___ are most pro-arrythmic of all antiarrythmics – So highest risk of arrythmias
IC
35
Flecainide (IC) Mechanism of Action:
- 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
Flecainide (IC) Indications:
- Effective in suppressing PVCs - Atrial tachydysrhythmias including WPW - Delays conduction in bypass tracts
37
Flecainide (IC) Side Effects:
- Moderate negative inotropic effect - Do not administer with CAD, LV failures, V.tach - Vertigo - Difficulty in visual accommodation
38
Atrial arrythmias only
B.Blockers
39
Beta Blockers (II) Mechanism of Action:
- 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
Beta Blockers (II) Toxicity
- Profound bradycardia or asystole - LV failure - Acute bronchospasm - Decreased CO
41
Amiodarone (III) Mechanism of Action
-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
Amiodarone (III) Indications:
-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
Long amio take, more it builds up, longer half-life is. Could have effects for years
.
44
Amiodarone (III) Toxicity: Resp, CV, Heme, Hepatic, Endo, Other
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
Dronedarone (III) indications
For atrial fibrillation to maintain NSR
46
Dronedarone (III) Contraindications
- 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
Ibutilide/Dofetilide (III) uses/incidences
- Used for conversion of atrial fibrillation to NSR | - High incidence of Torsades and ventricular tachyarrythmias
48
Verapamil (IV) Mechanism of Action:
- 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
Verapamil (IV) Indications:
- Treat SVT. - Slow ventricular rate in A. Fib. and Flutter. - No effect on accessory tracts.**
50
Verapamil (IV) Toxicity:
- 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
Diltiazem (IV) Mechanism of Action:
Slow channel blocking prolongs A-V nodal conduction and refractoriness.
52
Diltiazem (IV) drug interactions
Potent CYP3A4 inhibitors
53
Amiodarone (III) Drug Interactions
- CYP3A4 substrate | - CYP3A4, CYP2C9, and PGP inhibitor
54
Diltiazem (IV) Toxicity
- Bradycardia, hypotension - Edema - Constipation
55
Ventricular rates are easier to control in _____ than ______
A. Fib A. Flutter.
56
Digoxin Mechanism of Action:
- 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
Adenosine Mechanism of Action:
- 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
It is inactivated by cellular uptake.
Adenosine
59
Adenosine Toxicity:
- Facial flushing, dyspnea, and chest pressure most common, but subside in <60 seconds. - May exacerbate bronchoconstriction in asthmatic patients.**
60
Class IA and class III drugs block potassium channels and prolong QTc interval. Highest risk of what?
Torsades
61
Predisposing Factors to Torsades
- 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
_______ highest risk of QT-prolongation, then ______
Haldol ABX
63
Look at slide 66
.
64
Usually associated with Class IC drugs in the setting of structural heart disease
Wide Complex Ventricular Rhythm -Excessive plasma concentrations of drug or an abrupt change in the dose may result in this prodysrrhythmia
65
which meds cause QT prolongation
Class IA and III - Amiodarone - Dronedarone - Quinidine - Procainamide - Disopyramide

My Pharm II (8 decks)

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