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Cardio II Flashcards

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1
Q

What is the consequence of arrhythmias in terms of mechanical performance?

A

Ventricular stroke volume may be directly affected, leading to a decrease in cardiac output

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2
Q

What is the consequence of arrhythmias in terms of proarrhythmic/arrhythmogenic?

A

If not corrected, may lead to more severe forms of arrhythmias

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3
Q

What is the consequence of arrhythmias in terms of thrombogenesis?

A

Chronic arrhythmias may lead to the generation of thrombin in heart chambers

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4
Q

What are the four ways of decreasing spontaneous activity?

A
  1. Decreased phase 4 slope
  2. Increased threshold
  3. Increased maximum diastolic potential
  4. Increased AP duration
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5
Q

What are the two ways of increasing refractoriness?

A

Na channel blocker or AP prolonging

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6
Q

What is the MOA of Na channel blockers to increase refractoriness?

A

Shifts the voltage dependence of recovery

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7
Q

What is the MOA of AP prolonging drugs?

A

Blocks K channels, to slow the rate of K efflux

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8
Q

What is the general MOA of class I agents?

A

Block fast Na channels in the conductive tissues of the heart

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9
Q

What is the effect of class I drugs on the maximum depolarization rate?

A

Decreases

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10
Q

What is the effect of class I drugs on the automaticity and conduction?

A

Reduce automaticity

Delay conduction

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11
Q

What is the effect of class I drugs on ERP?

A

prolonged, leading to increased ERP/APD

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12
Q

What are the two major diseases that class I drugs are used in?

A

MI induce arrhythmias

Ventricular dysrhythmias

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13
Q

What type of drug is quinidine?

A

Class Ia

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14
Q

What type of drug is procainamide?

A

Class Ia

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15
Q

What type of drug is disopyramide?

A

Class Ia

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16
Q

What are the three class Ia drugs?

A

Quinidine
Procainamide
Disopyramide

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17
Q

What type of drug is lidocaine?

A

Class Ib

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18
Q

What type of drug is mexiletine?

A

Class Ib

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19
Q

What type of drug is propafenone?

A

Class Ic

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20
Q

What type of drug is flecainide?

A

Class Ic

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21
Q

What is the MOA of class Ia drugs? How does this affect the depolarization curve? (3)

A

Blocks both Na and K channels, and blocks Ca channels at high doses

Na block = prolonged phase 0
K blocked = delayed phase 3 repolarization
Ca blocked = depressed phase 2 and nodal phase 0

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22
Q

What is the primary MOA of quinidine?

A

Blocks rapid Na channel, lowering Vmax of phase 0

Causes slowed conduction

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23
Q

What are the three dose- dependent effects of quinidine?

A
  1. Blocks K channels (Increased APD)
  2. Blocks alpha receptors (lower BP)
  3. Blocks M receptors (higher HR)
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24
Q

What are the applications of quinidine?

A

only used in refractory cases of AF/ atrial flutter

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25
What are the adverse effects of Quinidine? (4)
n/v/d Cinchonism Hypotension Proarrhythmic
26
What is cinchonism, and what drug may cause it?
Tinnitus, hearing loss, blurred vision Quinidine
27
How can Quinidine decrease Bp?
blocking alpha receptors
28
How can Quinidine cause torsades de pointes?
Block K channels can lead to an increased QT via prolonged plateau
29
What is the MOA of Procainamide? (2)
Blocks rapid inward Na channel to slow conduction Blocks K channels to prolong APD and refractoriness
30
What are the clinical application of Procainamide? (4)
Suppress life threatening ventricular arrhythmias Reentrant SVT A-fib A-flutter d/t WPW
31
What is the effect of Procainamide on M and alpha receptors? Consequence of this?
None, thus no hypotension or tachycardia
32
What is wolf-parkinson white syndrome (WPW)?
two pathways of ventricular conduction (slow and fast)
33
What are the adverse cardiac effects of Procainamide?
Arrhythmia aggrevation | Torsades de pointes
34
What are the adverse extracardiac effects of Procainamide?
SLE like syndrome N/v
35
What are the drugs that should never be given to a pt with a h/o torsades de pointes?
Procainamide | Quinidine
36
What is the MOA of Lidocaine?
Blocks open and inactivated Na channels, causing a shortened repolarization, reduced Vmax, and lowered phase 4
37
What is the effect of Lidocaine on the cardiac AP?
Shortened
38
What are the two effects of lidocaine in abnormal conduction systems?
Slows ventricular rate | potentiates infranodal block
39
What is the clinical application of lidocaine?
treat ventricular arrhythmias (second choice after amiodarone)
40
Is lidocaine effective for prophylaxis of arrhythmias after an MI? How about in atrial tissue
No and no
41
Why must lidocaine be given IV, with multiple loading doses?
Has an extensive first pass effect
42
What are the adverse reactions of lidocaine?
tinnitus/Szs in rapid bolus
43
What is the MOA of class Ic drugs?
Strong binding to Na channels, causing strong effects on phase 0 depolarization
44
What is the effects of class Ic drugs on Qt interval? QRS complex? PR?
QT unchanged Longer QRS Longer PR
45
What type of drug is propafenone? MOA?
Class Ic | Strongly inhibits Na channels
46
What is the adverse effect of propafenone?
beta adrenergic inhibition =
47
Propafenone looks similar structurally to what drug? What is the consequence of this?
Propranolol | Lowers HR and ventricular output
48
Why should you avoid giving pts with heart failure propafenone?
beta blocking effects will decrease CO
49
What type of drug is Flecainide? MOA?
Class Ic | Blocks Na and prolonger 0, widens QRS, and markedly slows intraventricular conduction
50
What are the clinical application for Flecainide?
**Refractory** life-threatening ectopic ventricular arrhythmias
51
Why isn't Flecainide used as a first line treatment against ventricular arrhythmias?
Propensity for fatal proarrhythmic effects
52
What type of drugs are class II drugs? MOA?
beta blockers Slow SA node automaticity Lower AV node conduction Decrease ventricular contractility
53
When are class 2 drugs used?
Supraventricular arrhythmias due to excessive sympathetic activity
54
What is the only type of antiarrhythmic drugs found to be clearly effective in preventing sudden cardiac death in pts with prior MI?
Class ii (beta blockers)
55
What is the MOA of class III drugs?
Work on everything, except adenosine (Ca, Na, *K*, alpha, beta, ACh)
56
What is the main effect of class III drugs?
Prolong phase 3 repolarization (prolonged QT)
57
What is the clinical use of class III drugs?
Arrhythmias
58
What are the 5 class 3 drugs?
``` Dronedarone Amiodarone Sotalol Ibutilide Dofetilide ```
59
What class of drug is Amiodarone?
3
60
What is the effect and consequence of Amiodarone on K channels?
Blocks, prolongs refractoriness and APD
61
What is the effect and consequence of Amiodarone on Na channels?
Blocks Na channels that are in the inactivated state
62
What is the effect and consequence of Amiodarone on Ca channels?
Blocks to slow SA node phase 4
63
Does amiodarone have a competitive or noncompetitive block on alpha, beta, and M receptor?
Noncompetitive
64
What are the clinical applications of Amiodarone? (3)
Convert AF AV node tachycardia **Acute termination of VT or VF**
65
What are the main adverse effects of amiodarone?
DEA (metabolic product) has very high antiarrhythmic potency rapid redistribution out of heart may lead to early recurrence of arrhythmias
66
Why is the fact that amiodarone is lipid soluble problematic?
Difficult to determine the [plasma]
67
What are the side effects of using Amiodarone Iv?
Decreases cardiac contractility and PVR, causing hypotension
68
What is the most serious side effect of amiodarone?
Lethal interstitial pneumonitis
69
What are the effect of amiodarone on hyperthyroidism or hypothyroidism?
can cause either via destruction Inhibit Iodine conversion

Pharm (73 decks)

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