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Pharmacology COPY > EXAM #1: CV PHARM 2 > Flashcards

EXAM #1: CV PHARM 2 Flashcards

1
Q

What are the three consequences of arrhythmia?

A

1) Compromise of mechanical performance
2) Arrhythmogenesis/ evolution
3) Thrombogenesis

Note that decreased mechanical performance of the LV leads to a direct decrease in SV and CO.

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2
Q

What are the four general mechanisms that anti-arrhythmic drugs decrease spontaneous activity of the heart?

A

1) Decrease phase 4 slope
2) Increase threshold
3) Increase maximum diastolic potential
4) Increase action potential duration (ADP) i.e. effective refractory period

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3
Q

What is the maximum diastolic potential?

A

The absolute value of the repolarization–deepening (called increase) this will DECREASE spontaneous activity

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4
Q

What does increasing the action potential duration do to the ERP/ADP ratio?

A

Decreases the ERP/ADP ratio–>arrhythmothgenic

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5
Q

What are the two ways to increase refractoriness?

A

1) Na+ channel blockers, which increase the effective refractory period
2) Increase AP duration with K+ channel blockers

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6
Q

Why do Na+ channel blockers increase the ERP?

A

Blocking Na+ channels shifts the voltage dependence of recovery and delays the point to which 25% of the channels have recovered

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7
Q

Why do K+ channel blockers increase the action potential duration?

A

Decrease phase 3 re-polarization b/c of less K+ efflux

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8
Q

What is the general mechanism of action of the Class I antiarrhythmics?

A

Blockade of fast inward Na+ channels in conductive tissues of the heart

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9
Q

What are the physiologic effects of Class I antiarrhythmics?

A

Blockade of the fast inward Na+ channels:

1) Decreases the maximum depolarization rate of Phase 0
2) Slows intracardiac conduction

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10
Q

How does the channel specificity of Class Ia antiarrhythmics change with increasing dose?

A

1) Moderate binding to Na+ channels
2) K+ channel blockade
3) Ca++ channel blocking at high doses

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11
Q

What are the general physiologic effects of the Class Ia antiarrhythmics at increasing doses?

A

1) Na+ moderately slows Phase 0
2) K+ delays Phase 3 and prolongs the QRS/QT interval
3) Ca++ blockade depresses Phase 2 in myocardial tissue and Phase 0 in nodal tissue

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12
Q

What are the Class Ia antiarrhythmics?

A

Quinidine
Procainamide
Disopyramide

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13
Q

What is the primary mechanism of action of Quinidine and its associated effects? What are the ancillary mechanisms of action of Quinidine?

A

Primary MOA is to block rapid inward Na+ channel, which:

  • Decreases Vmax of Phase 0
  • Slows conduction

Secondarily, Quinidine

  • Block K+ channels–>increasing QT interval
  • Blocks M receptors–>increasing HR
  • Alpha antagonist–>decrease BP
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14
Q

What are the indications for Quinidine?

A

Only used in refractory patients to:

  • Conversion of symptomatic a-fib or a-flutter
  • Prevent recurrence of a-fib
  • Treat documented life-threatening ventricular arrhythmias
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15
Q

What are the adverse effects of Quinidine?

A

1) Cinchonism (tinnitus)
2) Thrombocytopenia
3) Torsades de Pointes
4) Nausea
5) Hypotension

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16
Q

What is cinchonism?

A

This is a triad of symptoms seen from quidine overdose or its natural source, cinchona bark, including:

  • Tinnitus
  • Hearing-loss
  • Blurred vision
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17
Q

What is the mechanism of action of Procainamide?

A

1) Blocks rapid inward Na+ channels, which decreases the Vmax of Phase 0
2) Blocks K+ channels, which will prolong the APD

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18
Q

What are the physiologic effects of Procainamide?

A

Decreased conduction, automaticity, and excitability

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19
Q

How does Procainamide compare to Quinidine?

A

Procainamide > Quinidine b/c it has:

  • No effect on muscarinic receptors
  • Does antagonize alpha receptors i.e. no hypotension
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20
Q

What are the clinical indications for Procainamide?

A

1) Life-threatening ventricular arrhythmias
2) Re-entrant SVT
3) A-fib
4) A-flutter with WPW

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21
Q

What is the pharmacokinetic pearl to remember about Procainamide?

A

IV loading takes 20 minutes i.e. this is NOT a good agent to treat ventricular arrhythmia acutely

22
Q

What are the cardiac adverse effects associated with Procainamide?

A

Arrhythmia aggravation b/c of prolonged APD and QT interval–> Torsades de Pointes

23
Q

When are Quinidine and Procanamide contraindicated?

A

Patients with a hx of:

  • Torsades De Pointes
  • Long QT
  • Hypokalemia
  • Heart block
  • Sinus node dysfunction
24
Q

What are the extra-cardiac adverse effects of Procainamide?

A

1) SLE-like syndrome
2) Nausea and vomiting
3) Decreased kidney function

25
Q

What are the Class Ib antiarrhythmics?

A

Lidocaine
Phenytoin
Mexiletin
Tocainide

26
Q

What is the general mechanism of action of the Class Ib antiarrhythmics?

A

1) Weak binding to Na+ channels–>small impact on Phase 0 depolarization
2) Acceleration of phase 3 repolarization with little effect on ADP or QT interval

27
Q

What is the mechanism of action of Lidocaine?

A

1) Blocks open and inactivated Na+ channels, reducing Vmax of Phase 0
2) Shortens cardiac action potential (in cases where the AP has been long) by binding to SLOW Na+ channels and Ca++ channels
3) Lower the slope of phase 4, increasing the threshold for excitation

28
Q

What can cause a prolonged cardiac action potential?

A
  • Ischemia
  • MI
  • Digitalis

This is caused by a slow inactivation of Na+ channels, which are blocked by Lidocaine.

29
Q

What are the clinical indications for Lidocaine?

A

Previously first line for ventricular tachycardia but now SECONDARY to amiodarone

30
Q

Is Lidocaine effective for prophylaxis of arrhythmias secondary to MI?

A

NO

31
Q

What are the key pharmacologic points to remember about Lidocaine?

A

1) Extensive 1st pass metabolism necessitates IV administration
2) Requires a multiple loading doses and maintenance infusions

32
Q

What are the adverse effects associated with Lidocaine administration?

A

1) Rapid bolus can cause tinnitus and seizure

2) High doses induce CNS depression

33
Q

Why should care be taken when giving Lidocaine to HF patients?

A

Decreased clearance and increased plasma concentrations could lead to adverse effects

34
Q

List the Class Ic antiarrhythmics?

A

Propafenone
Flecainide
Morizicine

35
Q

What is the general mechanism of action of the Class Ic antiarrhythmics?

A
  • Strong binding to Na+ channels (most potent), which will:

1) Increase APD, QRS, and PR interval

36
Q

What is the specific mechanism of action of Propafenone?

A

1) Strong inhibitor of Na+ channel

2) B-adrenergic antagonism

37
Q

Why does Propafenone have some Beta effects?

A

Similar structure to propranolol

38
Q

What are the clinical indications for Propafenone?

A

1) Atrial arrhythmia
2) PSVT
3) Ventricular arrhythmia in patients with NO HEART DISEASE

39
Q

What is the specific mechanism of action of Flecainide?

A

This is a potent Na+ channel blocker which,

  • Decreased Phase 0
  • Marked slowing of intraventricular conduction to increase the QRS duration
40
Q

What are clinical indications for Flecainide?

A

Refractory ectopic ventricular arrhythmias

41
Q

What is the general mechanism of action of the Class II antiarrhythmics?

A

Beta-adrenergic antagonists

42
Q

What are the physiologic effects of Class II antiarrhythmics?

A
  • Decreased SA nodal automaticity
  • Decreased conduction through the AV node
  • Decreased ventricular contractility
43
Q

What are Class II antiarrhythmics effective for treating?

A

1) SVT due to excessive sympathetic activity

2) ONLY drugs effective in preventing sudden cardiac death s/p MI

44
Q

What are Class II antiarrhythmics ineffective at treating?

A

Severe arrhythmias such as recurrent VT

45
Q

What is the general mechanism of action of the Class III antiarrhythmics?

A

1) Block K+, Ca++, Na+, and B-receptors

2) MAIN effect is K+, which prolongs phase 3 repolarization, increasing the QT interval

46
Q

What is the specific mechanism of action of Amiodarone?

A

Class III i.e. blocks:

1) K+ channels which prolongs refractriness and APD
2) Na+ channels in the inactivated state
3) Ca++ channels to slow phase 4 in nodal cells

47
Q

What are the indications for Amiodarone?

A

1) Acute termination of VT or VF (replacing lidocaine)
2) Conversion of a-fib
3) AVNRT
4) WPW

48
Q

Why is Amiodarone replacing Lidocaine out-of-hospital?

A

B/c of its multiple receptor effects and ability to prevent numerous types of arrhythmias

49
Q

Why are there multiple adverse effects associated with Amiodarone?

A

1) Highly lipophilic
2) Multiple receptor effects
3) Extremely long half-life

50
Q

What are the adverse effects associated with Amiodarone?

A

1) Until tissue/myocardium concentrations are equilibrated, redistribution OUT of the myocardium can cause early RECURRENCE of arrhythmia
2) Decreased contractility leading to hypotension (in high doses > 5mg)
3) LETHAL interstitial pneumonitis
4) Hyperthyroidism OR hypothyroidism

Pharmacology COPY (64 decks)

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