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Pharmacology > Deja review Cardio/Renal agents - Antiarrhythmics > Flashcards

Deja review Cardio/Renal agents - Antiarrhythmics Flashcards

1
Q

Describe what happens during phase 0

A

sodium ion channels open (inward) -> leads to depolerization

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2
Q

Describe what happens during phase 1

A

sodium ion channels are inactivated, potassium ion channels (outward) are activated; chloride ion channels (inward) are activated

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3
Q

Describe what happens during phase 2

A

Plateau phase; slow influx of calcium ion balanced by outward potassium ion current (delayed rectifier current Ik-funny sodium channel)

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4
Q

Describe what happens during phase 3

A

Repolarization phase; outward K+ current INC and inward calcium ion current DEC

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5
Q

Describe what happens during phase 4

A

Membrane returns to resting potential

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6
Q

What phase of cardiac action potential do amiodarone and sotalol work?

A

phase 0 and 3

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7
Q

What phase of cardiac action potential do lidocaine, flecainide, and quinidine work?

A

phase 0

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8
Q

What phase of cardiac action potential do ß blockers work?

A

phase 2 and 4

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9
Q

what is responsible for maintaining the electrochemical gradient at resting membrane potential?

A

Na+/K+ ATPase

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10
Q

What ion current is responsible for the depolarization of sinoatrial (SA) and atrioventricular (AV) nodal fibers?

A

Calcium ion (inward)

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11
Q

What ion current is responsible for the repolarization of SA and AV nodal fibers?

A

Potassium ion (outward)

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12
Q

How does phase 4 of the action potential in slow response fibers (SA and AV nodes) differ from that of fast response fibers?

A

slow response fibers displays automaticity (ability to depolarize spontaneously); rising phase 4 slope of the action potential = pacemaker potential

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13
Q

What ion current is responsible for the “pacemaker current” (rising slope of phase 4) in slow response fibers?

A

Sodium ion (inward); calcium ion (inward); potassium ion (outward)

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14
Q

The pacemaker of the heart has the fastest uprising phase 4 slope; where is this pacemaker in nondisease patients?

A

SA node

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15
Q

Where is the SA node located?

A

right atrium

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16
Q

How do the effective refractory period (ERP) and relative refractory period (RRP) differ from each other?

A

No stimulus, no matter the strength, can elicit a response with fibers in the ERP, whereas a strong enough stimulus will elicit a response.

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17
Q

What are the 3 states the voltage gated Na+ channel exists in?

A

1) Resting state
2) Open state
3) Inactivated state

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18
Q

What state(s) of the voltage gated Na+ channel is/are most susceptible to drugs?

A

Open state inactivated state

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19
Q

What 2 types of gates does the voltage gated Na+ channel have?

A

1) M (activating)

2) H (inactivating)

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20
Q

Why is the rate of recovery from an action potential slower in ischemic tissue?

A

The cells are already partly depolarized at rest

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21
Q

What class of antiarrhythmic agents has membrane-stabilizing effects?

A

ß-blockers

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22
Q

Antiarrhythmic agents are grouped into 4 classes according to what classification system?

A

Vaughn-Williams classification

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23
Q

Give the general mechanism of action for ech of the following antiarrythmic drugs classes:

  • Class I
  • Class II
  • Class III
  • Class IV
A
  • Class I: Na+ channel blockers
  • Class II: ß-blockers
  • Class III: K+ channel blockers
  • Class IV: Ca2+ Channel blockers
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24
Q

Class I antiarrhythmics are further subdivided into what casses?

A

1A; 1B; 1C

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25
Q

Give examples of antiarrhythmic drugs in class 1a

A

“ABBA Performed Dancing Queen”

Quinidine (antimalarial antiprotozoal agent); procainamide; disopyramide

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26
Q

Give examples of antiarrhythmic drugs in class 1b

A

“Backstreetboys Mainly Lack Talent (and phenytoin)”

-Mexiletine; lidocaine; tocainide; phenytoin

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27
Q

Give examples of antiarrhythmic drugs in class 1c

A

“Carly (rae jepsen) is Extremely Freaking Painful”

-Encainide; flecainide; propafenone; moricizine

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28
Q

Give examples of antiarrhythmic drugs in class 2

A

Propranolol; esmolol; metoprolol

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29
Q

Give examples of antiarrhythmic drugs in class 3

A

Amiodarone; sotalol; ibutilide; dofertilide

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30
Q

Give examples of antiarrhythmic drugs in class 4

A

Verapamil, diltiazem

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31
Q

Name 3 antiarrhythmic drugs that don’t fit in the Vaughn-Williams classification system

A

1) Digoxin
2) Adenosine
3) Magnesium

32
Q

Magnesium is used to treat what specific type of arrhythmia?

A

Torsades de pointes (polymorphic ventricular tachycardia)

33
Q

Adenosine is used to treat what types of arrhythmias?

A

Paroxysmal supraventricular tachycardia (PSVT), specifically narrow complex tachcardia or supraventricular tachycardia (SVT) with aberrancy; AV nodal arrhythmias (adenosine causes transitent AV block).
-Note: synchronized cardioversion and NOT adenosine should be used on symptomatic patients or unstable tachycardia with pulses

34
Q

Where anatomically should the IV be placed to administer adenosine?

A

As close to the heart as possible, that is, the antecubital fossa since adenosine has an extremely short half-life. Adenosine rapid IV push should be followed immediately by a 5-10 cc (mL) flush of saline to facilitate its delivery to the heart

35
Q

What is the mechanism of action of adenosine?

A

Stimulates α1 receptors which causes a DEC in cyclic adenosine monophosphate (cAMP) (via G2 coupled second messenger system); INC K+ efflux leading to INC hyperpolarizationl INC refractory period in AV node

36
Q

What are the adverse effects of adenosine?

A

Flushing, chest pain, dyspnea, hypotension

37
Q

What 2 drugs can antagonize the effects of adenosine?

A

Theophylline and caffiene

38
Q

How is adenosine dosed?

A

6mg initially by rapid IV push, if not effective within 1-2 minutes, give 12 mg repeat dose (follow each bolus of adenosine with normal saline flush). The 12 mg dose may be repeated once

39
Q

What is the most deadly ion that can be administered?

A

Potassium ion

40
Q

What EKG changes are seen in hyperkalemia?

A

Flattened P waves, widened QRS complex, peaked T waves, sine waves, ventricular fibrillation

41
Q

What EKG changes are seen in hypokalemia?

A

Flattened or inverted T waves, U waves, ST-segment depression

42
Q

What do class 1a antiarrhythmics do to each of the following?

  • Action potential duration:
  • ERP:
  • Conduction velocity
  • Phase 4 slope
A
  • Action potential duration: INC
  • ERP: INC
  • Conduction velocity: DEC
  • Phase 4 slope: DEC
43
Q

What do class Ib antiarrhythmics do to each of the following?

  • Action potential duration:
  • ERP:
  • Conduction velocity
  • Phase 4 slope
A
  • Action potential duration: DEC
  • ERP: Little or no change
  • Conduction velocity: DEC (primarily in ischemic tissue)
  • Phase 4 slope: DEC
44
Q

What do class 1c antiarrhythmics do to each of the following?

  • Action potential duration:
  • ERP:
  • Conduction velocity
  • Phase 4 slope
A
  • Action potential duration: Little or no change
  • ERP: Little or no change
  • Conduction velocity: DEC
  • Phase 4 slope: DEC
45
Q

Drugs that affect the strength of heart muscle contraction are referred to as what types of agents?

A

Inotropes (either positive or negative)

46
Q

Drugs that affect the heart rate are referred to as what types of agents?

A

Chronotropes (either positive or negative)

47
Q

Drugs that affect AV conduction velocity are referred to as what types of agents?

A

Dromotropes (either positive or negative)

48
Q

QT interval prolongation, and thus torsades de pointes, is more likely to occur with what two classes of antiarrhythmics?

A

1) class 1a

2) class 3

49
Q

Which class 1a antiarrhythmic also blocks α-adrenergic and muscarinic receptors, thus potentially leading to INC heart rate and AV conduction?

A

Quinidine

50
Q

What are the adverse effects of quinidine?

A

Tachycardia, proarrhythmic, INC digoxin levels via protein binding displacement, nausea, vomiting, diarrhea, cinchonism

51
Q

What is cinchonism?

A

Syndrome that may include tinnitus, high frequency hearing loss, deafness, vertigo, blurred vision, diplopia, photophobia, headache, confusion, delirium

52
Q

What are the adverse effects of procainamide?

A

Drug induced lupus (25-30% of patients), pro-arrhythmic, depression, psychosis, hallucination, nausea, vomiting, diarrhea, agranulocytosis, thrombocytopenia, hypotension

53
Q

What drugs can cause drug induced lupus?

A

Procainamide, isoniazid (INH), chlorpromazine, penicillamine, sulfasalazine, hydralazine, methyldopa, quinidine, phenytoin, minocycline, valproic acid, carbamazepine, chlorpromazine

54
Q

Which class 1a antiarrhythmic can cause peripheral vasoconstriction?

A

Disopyramide

55
Q

What are the adverse effects of disopyramide?

A

Anticholinergic adverse effects, such as urinary retention, dry mouth, dry eyes, blurred vision, constipation, sedation

56
Q

True or false? Lidocaine is useful in the treatment of atrial arrhythmias?

A

False

57
Q

True or false? Lidocaine is useful in the treatment of ventricular arrhythmias?

A

True

58
Q

True or false? Lidocainse is useful in the treatment of AV junctional arrhythmias?

A

False

59
Q

What are the adverse effects of lidocaine?

A

Proarrhythmic, sedation, agitation, confusion, paresthesias, seizures

60
Q

What class 1b antiarrhythmic can cause pulmonary fibrosis?

A

Tocainide

61
Q

Propafenone, even though a class 1c antiarrhythmic, exhibits what other type of antiarrhythmic activity?

A

ß-adrenergic receptor blockade

62
Q

Encainide and flecaininde INC _____ in postmyocardial infarction (MI) patients with arrhythmias?

A

sudden cardiac death

63
Q

Sotalol, even though a class III antiarrhythmic, exhibits what other type of antiarrhythmic activty?

A

ß-adrenergic receptor blockade

64
Q

Even though this agent is labeled as a class III antiarrhythmic, it displays class I, II, III, and IV antiarrhythmic activity

A

Amiodarone

65
Q

What is the 1/2 life of amiodarone?

A

40-60 days

66
Q

What are the adverse effects of amiodarone?

A

Pulmonary fibrosis, tremor, ataxia, dizziness, hyperthyroidism, hypothyroidism, hepatotoxicity, photosensitivity, blue skin discoloration, neuropathy, muscle weakness, proarrhythmic, corneal deposits, lipid abnormalities, hypotension, nausea, vomiting, congestive heart failure (CHF), optic neuritis, pneumonitis, abnormal taste, abnormal smell, syndrome of inappropriate secretion of antiduretic hormone (SIADH)

67
Q

How should patients on amiodarone therapy be monitored?

A

EKG thyroid function tests (TFTs), pulmonary function tests (PFTs), liver function tests (LFTs), electrolytes, ophthalmology exam

68
Q

Verapamil should not be given in what types of arrhythmias?

A

Wolff-Parkinson-White (WPW) syndrome, ventricular tachcardia

69
Q

What are the adverse effects of verapamil?

A

Drug interactions, constipation, hypotension, AV block, CHF, dizziness, flushing

70
Q

Digoxin is used to control ventricular rate in what types of arrhythmias?

A

Atrial fibrillation, atrial flutter

71
Q

Digoxin induced arrhythmias are treated by what drugs?

A

Lidocaine, phenytoin

72
Q

Digoxin does what to each of the follow?

  • Strength of heart muscle contraction:
  • Heart rate:
  • AV conduction velocity:
A
  • Strength of heart muscle contraction: INC (positive inotrope)
  • Heart rate: DEC (negative chronotrope)
  • AV conduction velocity: DEC (negative dromotrope)
73
Q

What does QTc stand for?

A

Corrected QT interval

74
Q

How is QTc calculated?

A

(QT)/(square root of R to R interval)

75
Q

Why must the QT interval be corrected?

A

The QT interval is dependent on heart rate, so higher heart rates will display shorter QT intervals on EKG. It is corrected to remove the variable of the heart rate

76
Q

What is the normal value for QTc?

A

Less than 440 milliseconds

77
Q

What does a long QT interval put a patient at risk for?

A

Torsades de pointes, a ventricular arrhythmia that can degenerate into ventricular fibrillation

Pharmacology (15 decks)

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