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CPR II Exam 1 > Drugs for Cardiac Arrhythmia > Flashcards

Drugs for Cardiac Arrhythmia Flashcards

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1
Q

What are the 3 class 1A antiarrhythmic drugs?

A
  • Quinidine
  • Procainamide
  • Disopyramide
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2
Q

What are the 2 class 1B antiarrhythmic drugs?

A
  • Lidocaine
  • Mexiletine
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3
Q

What are the 2 class 1C antiarrhythmic drugs?

A
  • Flecainide
  • Propafenone
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4
Q

What are the two class 2 antiarrhythmic drugs (beta-blockers)?

A
  • Esmolol
  • Propranolol
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5
Q

What are the four class 3 antiarrhythmic drugs?

A
  • Amiodarone
  • Sotalol
  • Dofetilide
  • Ibutilide
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6
Q

What are the two class 4 antiarrhythmic drugs?

A
  • Verapamil
  • Diltiazem
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7
Q

What is the one miscellaneous agents used as an antiarrhythmic drug?

A

Adenosine

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8
Q

What are the 3 cell types in the heart that exhibit fast AP?

A
  • Ventricular contractile cardiomyocytes
  • Atrial cardiomyocytes
  • Purkinje fibers
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9
Q

What are the 2 cell types in the heart that exhibit slow (pacemaker) AP’s?

A
  • SA node cells
  • AV node cells
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10
Q

Briefly describe the 5 phases of fast AP in cardiac muscle?

A
  • Phase 0: depolarization; inward Na+ flux
  • Phase 1: partial repolarization K+ efflux, while fast Na+ channels close
  • Phase 2: plateau, K+ exiting, offset by Ca<strong>2</strong>+ entering thru slow channels
  • Phase 3: Ca<strong>2</strong>+ channels close and K+ begins to exit rapidly = repolarization
  • Phase 4: stable RMP gradually restored by Na+/K+ ATPase and Na+/Ca2+ exchanger
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11
Q

Describe the ion currents involved in phase 4 of the slow (pacemarker) AP?

A
  • Poorly selective ionic influx (Na+, K+) known as pacemaker current (Funny current, If) - activated by hyperpolarization
  • Slow Ca2+ influx [via T-type (transient) channels]
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12
Q

What is responsible for the rapid upstroke of phase 0 and repolarization of phase 3 of the pacemaker AP?

A
  • Phase 0: influx of Ca2+ thru slow L-type (long-acting) Ca2+ channels
  • Phase 3: inactivation of Ca2+ channels w/ ↑ K+ efflux
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13
Q

How does a resting potential that is less negative affect the time needed for an AP to reach threshold and affect on firing rate?

A
  • Less time is needed to reach threshold
  • Firing rate ↑
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14
Q

What are the 3 states that the Na+ channel found on cardiac myocytes exists in and describe each?

A
  • Resting: the channel is closed but ready to generate AP
  • Activated state: depolarization to threshold opens m-gates greatly ↑ Na+ permeability
  • Inactivated state: h-gates are closed, inward Na+ flux is inhibited, the channl is not available for reactivation –> refractory period
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15
Q

Which channels are blocked by Class 1A antiarrhythmics?

A
  • Block Na+ channels
  • Block K+ channels
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16
Q

Class 1A antiarrhythmics block sodium channels in a state dependent manner, preferentially when in what state?

Cells with what characteristics will be preferentially targeted?

A
  • Preferentially bind to open (activated) Na+ channels
  • Ectopic pacemaker cells w/ faster rhythms will be preferentially targeted
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17
Q

What is the effect of Class 1A antiarrhythmics on the the different phases of the AP, QRS and QT intervals?

A
  • Decrease slope of phase 0 (blockade of Na+ channels)
  • Prolong AP duration (blockade of K+ channels)
  • Prolong QRS and QT intervals of the ECG
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18
Q

What is the clinical use of the class 1A antiarrhythmic, procainamide?

A
  • Tx sustained ventricular tachycardias, may be used in arrhythmias associated w/ MI
  • Paroxysmal supraventricular tachycardia (PSVT)
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19
Q

The class 1A antiarrhythmic, procainamide also has blocking effects where?

(which ganglion?)

A
  • Antimuscarinic
  • Ganglion blocking
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20
Q

What are 3 cardiac AE’s associated with the class 1A antiarrhythmics, Procainamide and Quinidine?

A
  • QT interval prolongation
  • Induction of torsade de pointes arrhythmias and syncope
  • Excessive inhibition of conduction
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21
Q

What are some rare extra-cardiac and common AE’s associated with the class 1A antiarrhythmic, Procainamide?

A
  • Drug-induced lupus syndrome w/ arthritis, pleuritis, pulmonary dz, hepatitis
  • Agranulocytosis
  • Common = N/V, diarrhea, rash, fever, or hypotension
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22
Q

What is the clinical use for the class 1A antiarrhythmic, Quinidine?

A
  • Restoring rhythm in Afib/flutter pt’s w/ normal (but arrhythmic) hearts
  • Sustained ventricular arrhythmia
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23
Q

The class 1A antiarrhythmic, Quinidine, also has what other blocking effects?

(anticholinergic or antimuscarinic)

A
  • Anticholinergic effects
  • Beta-blocking effects
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24
Q

What is the triad of Cinchonism and what class 1A antiarrhythmic may cause this as an AE?

A
  • HA, dizziness, and tinnitus
  • Quinidine
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25
What are some of the **extra**-cardiac AE's associated with the class 1A antiarrhythmic, Quinidine?
- **GI effects** --\> diarrhea + N/V - **Cinchonism** - **Thrombocytopenia** **- Hepatitis** and fever
26
What is the main clinical implication for the class 1A antiarrhythmic, Disopyramide?
Prevent **recurrence of ventricular tachycardia** or **ventricular fibrillation**
27
Other than antiarrhythmic activity, what other type of effect does Disopyramide have and what are the AE's associated with this effect?
- Potent **antimuscarinic effect** - Dry mouth + blurred vision + constipation + urinary retention + exacerbation of glaucoma
28
What are the cardiac AE's of the class 1A antiarrhythmic, Quinidine?
- QT interval prolongation --\> induction of torsade de pointes arrhythmia - Negative inotrope effect - may **precipitate** HF
29
Which ion channel(s) are blocked by the class 1B antiarrhythmic?
**Na+** channels **only**
30
Class 1B antiarrhythmic exhibit state-dependent blocking of Na+ channels in which state? Preferentially bind cells in what state of membrane potential?
- **Inactivated** Na+ channels - **Depolarized cells**
31
What is the kinetics of dissociation from the Na+ channel like for the class 1A, 1B, and 1C antiarrhythmics and how does this correlate with their strength of blockade?
- **Class 1A** = dissociate w/ **intermediate** kinetics = **medium** blockade - **Class 1B =** dissociate w/ **fast** kinetics = **weak** blockade - **Class 1C** = dissociate w/ **slow** kinetics = **strong** blockade
32
What is the effect of class 1B antiarrhythmics on AP and QT duration?
- May **shorten** AP - Since **do not block** K+ channels, do **not** prolong AP or QT duration on ECG
33
Why is the class 1B antiarrhythmic, Lidocaine useful in damaged tissue based on its MOA?
- Blocks **inactivated** Na+ channels (**use-dependence**) - **Selectively** blocks conduction in **depolarized tissue**, making **damaged** tissue **"electrically silent."**
34
Why does the class 1B antiarrhythmic, Lidocaine have no effect on cardiac conductivity in normal tissue?
**Rapid kinetics** results in recovery from block between AP, exerts **greater effects in depolarized (i.e., ischemic)** and/or **rapidly driven tissues**
35
What are the 2 clinical indications for the use of the class 1B antiarrhythmic, Lidocaine?
- In **mono-** and **polymorphic** ventricular tachycardias - **Very efficient** in **arrhythmias** assoc. w/ **acute MI**
36
What is the pharmacokinetics of the class 1B antiarrhythmic, Lidocaine like and needs to be given via which route?
**Extensive** **first-pass** metabolism; **must give IV**
37
What is the least toxic of all class 1 antiarrhythmics?
Lidocaine (class 1B)
38
What are some of the CV and neurological AE's associated with the class 1B antiarrhythmic, Lidocaine?
- **CV** = may cause **hypotension** in pt's w/ HF by inhibiting contractility - **Neuro** = paresthesias, tremor, slurred speech, and convulsions
39
Which class 1B antiarrhythmic is a lidocaine analog modified to reduce first-pass metabolism and permit **chronic oral therapy?**
Mexiletine
40
The electrophysiological and antiarrhythmic effects of the class 1B antiarrhythmic, Mexiletine are similar to what?
**Lidocaine** (since is a modified analog)
41
What are the 2 clinical uses for the class 1B antiarrhythmic, Mexiletine?
- Ventricular arrhythmias - Relieve **chronic pain**, especially pain due to **diabetic neuropathy** and **nerve injury**
42
What are 4 AE's associated with the class 1B antiarrhythmic, Mexiletine?
- Tremor - Blurred vision - Nausea - Lethargy
43
Which ion channel(s) are blocked by class 1C antiarrhythmics?
- Block **Na+** channels - Block **certain K+** channels
44
What is the strength of the Na+ channel block associated with class 1C antiarrhythmics and preferentially block channels in which state?
- **Strong/long-lasting** block due to **slow** dissociation from channel - Preferentially bind Na+ channel in **open (activated) state**
45
Which interval is prolonged by the class 1C antiarrhythmics due to blockage of certain K+ channels?
- Prolong **QRS** interval - **NO** effect on AP or QT duration
46
What is the clinical use of the class 1C antiarrhythmic, Flecainide? Patients with which cardiac status specifically?
- In pts with **normal hearts** - Tx of **supraventricular arrhythmias** including **atrial fibrillation**, **paroxysmal SVT** (**AV nodal reentrant tachy, AV reentrate tachy**) - **Life-threatening** ventricular arrhythmias, such as **sustained V-Tach**
47
The class 1C antiarrhythmic, Flecainide may be very effective in suppressing premature ventricular contractions, but pt's with what cardiac status are at risk for AE's and what are these effects?
- May cause **severe** exacerbation of **ventricular arrhythmias** if given to: - Pts w/ **preexisting** **ventricular tachyarrhythmias**, a **previous MI**, or those w/ **ventricular ectopic rhythms**
48
Which class 1C antiarrhythmic also possesses weak β-blocking activity?
**Propafenone** (kind of sounds like **propranolol**)
49
What are the 2 clinical uses of the class 1C antiarrhythmic, Propafenone? Specifically pt's with what cardiac status?
- Pt's **WITHOUT** structural disease - **Prevent** paroxysmal **atrial fibrillation** and **SVT** - Used in **sustained ventricular arrhythmias**
50
The class 1C antiarrhythmic, Propafenone, should not be combined with inhibitors of what 2 enzymes as the risk of proarrhythmia may be increased?
**CYP2D6** and **CYP3A4** inhibitors
51
What are 3 AE's associated with the class 1C antiarrhythmic, Propafenone?
- **Exacerbation** of **ventricular arrhytmias** - **Metallic taste** - **Constipation**
52
What is the effect of the sympathetic NS on the If, T-type and L-type Ca2+ channels involved in pacemaker action potentials?
- ↑ **slope** of **phase 4** due to effects on **If** and **T-type Ca2+ channels** - Effect on **L-type Ca2+ channels** = **lowers** the **threshold**
53
What is the effect of the class 2 antiarrhythmic (beta-blockers) at the SA and AV node? Effect on which 2 intervals?
- **SA** **node** = ↓ HR (**increase** RR interval) - **AV node** = ↓ AV conductance (**increase** PR interval)
54
What is the effect of the class 2 antiarrhythmic (beta-blockers) on the slop of phase 4 and the threshold of the pacemarker AP?
- **Decreased** slope due to effects on **If and T-type** Ca2+ channels - **Increased** threshold due to effect on **L-type** Ca2+ channels \*Net effect = **slow AP** + ↓ HR + ↓ AV conductance
55
What are the 4 clinical indications for the use of the class 2 antiarrhythmic, Propranolol for arrhythmias? Decrease mortaility from arrhythmias in which pt's?
- **Arrhythmias** associated w/ **STRESS** (i.e., **catecholamines**) - **Re-entrant** arrhythmias that involve **AV node** --\> AVNRT and AVRT - **Afib** and **flutter** - **Arrhythmias** associated w/ **MI** --\> ↓ mortality in pt's with acute MI
56
Which class of antiarrhythmics is reserved for use in pt's with a **structually normal heart?**
Class 1C = **Flecainide** and **Propafenone**
57
Which class 2 antiarrhythmic is a **short-acting (t1/2 5-10 min)** SELECTIVE β1-blocker?
Esmolol
58
Due to it's short half-life how is Esmolol administered clinically as an antiarrhythmic?
**Continous IV infusion** when rapid adrenergic blockade is desired
59
What are the 3 clinical uses for the class II antiarrhythmic, Esmolol?
- **Supraventricular arrhythmias** - Arrhythmias association with **thyrotoxicosis, myocardial ischemia/infarction** - As an **adjunct** drug in **general anesthesia** to control arrhythmias in **perioperative period**
60
List some of the AE's associated with the class 2 antiarrhythmic, beta-blockers.
- Bradycardia + Bronchoconstriction - Impaired liver glucose mobilization - Worsens blood lipid profile - Sedation + depression + fatigure - Rapid withdrawl --\> rebound HTN
61
What are 6 contraindications for the the class 2 antiarrhythmic, beta-blockers?
- Asthma - Peripheral vascular disease - Raynaud's - Type 1 DM on insulin - Bradyarrhythmias, AV conduction problems - Severe depression of cardiac function
62
Which K+ channels in the heart are **open** in the resting state?
**Inward rectifying K+ channels**
63
Class 3 antiarrhytmics block which ion channel and in which state?
Bind **K+ channels** in the **resting state** = **reverse use dependence**
64
What is the effect of class 3 antiarrhytmics on the AP, QT interval and refractory period?
- **Prolong** AP **duration** - **Prolong** QT interval - **Prolong refractory period**
65
K+ channels in the heart are responsible regulating which parts of the membrane potential?
- Regulation of **resting potential** via **inward rectifying K+** channels which are **open** in resting state - Regulation of **AP** via **voltage-gate K+** channels which **repolarize** and limit the frequence of AP's (regulate duration of the **refractory period**)
66
Which class 3 antiarrhytmic prolongs QT interval and APD **uniformly** over a **wide range** of heart rates and in **all cardiac tissues**?
Amiodarone
67
What are the 2 clinical uses for the class 3 antiarrhytmic, Amiodarone?
- Tx of **ventricular arrhythmias** - **Atrial fibrillation**
68
What is unique about the pharmacokinetics of the class 3 antiarrhytmic, Amiodarone, including t1/2, elimination, and interactions?
- **Major** metabolite has **t1/2 = ~ 50 days** - Effects maintainied for **1-3 months** after discontinuation and metabolites may be found in tissues **1 year** later (**highly lipophilic**) - **Inhibits** many CYP enzymes so can affect metabolism of other drugs
69
Which class 3 antiarrhythmic has a lower incidence of torsade de pointes as an AE compard to others in the class?
Amiodarone
70
What are 5 of the extra-cardiac AE's associated with the class 3 antiarrhytmic, Amiodarone?
- **Pulmonary fibrosis** (can be **fatal**) - **Hepatitis** - **Hyper**thyroidism or **hypo**thyroidism - **Corneal** micro-deposits - **Bluish** discoloration of the skin
71
What are the 2 MOA's of the class 3 antiarrythmic, Sotalol?
- **Non**-selective **β**-AR **antagonist** (class 2) - **Blocks** inward-rectifier K+ channels (class 3) = **prolongs ADP**
72
What are the 2 clinical uses of the class 3 antiarrhythmic, Sotalol?
- Tx of **life-threatening** ventricular tachyarrhythmias - Maintenance of sinus rhythm in pt's w/ **atrial fibrillation**
73
What are the 2 major AE's associated with the class 3 antiarrhytmic, Sotalol?
- Depression of cardiac function (same as β-blockers) - Provokes **torsade de pointes**
74
What is the specific MOA of the class 3 antiarrhythmic, Dofetilide? Effect of drug is most pronounced at which HR's?
- Potent and **"pure" IKr (inward K+ rectifier) blocker** - More **pronounced** effect at **lower HR's**
75
Why does the class 3 antiarrhythmic, Dofetilide have a narrow therapeutic window?
Majority is **excreted** by kidneys; must adjust dose based on **Cr** clearance
76
What are the major AE's of the class 3 antiarrhythmic, Dofetilide?
- **Torsades de pointe** **- QT interval** prolongation and ↑ risk of ventricular arrhythmias
77
What is the clinical use for the class 3 antiarrhytmic, Dofetilide?
Maintenance of **normal sinus rhythm** in pt's with **chronic atrial fibrillation/atrial flutter** AFTER **cardioconversion**
78
What is the specific MOA of the class 3 antiarrhytmic, Ibutilide?
Similar to **dofetilide**, slows cardiac repolarization as a **IKr blocker**
79
How is the the class 3 antiarrhytmic, Ibutilide adminstered and it's clinical use?
Via **rapid IV infusion** for **immediate** conversions of **acute atrial fibrillation** or **flutter** ---\> **sinus rhythm**
80
What are the AE's associated with the class 3 antiarrhytmic, Ibutilide? Due to AE's pt's require what?
- **Torsades de pointes**, requires immediate cardioconversion - **Must** monitor EKG continously unti **QTc** returns to baseline - **Incrased** risk of other **arrhytmias**
81
Which specific channels and in which state do the class 4 antiarrhytmics (verapamil and diltiazem) block?
Both **activated** and **inactivated** L-type Ca2+ channels
82
What is the effect of the class 4 antiarrhytmics on the slope of phase 0, threshold potential at the SA node, and refractory period?
- **Decrease** the slope of **phase 0** - ↑ **L-type Ca2+** threshold potential in **SA** node = **slows depolarization** --\> **bradycardia** - **Prolongs** refractory period in **AV** **node =** **prolongs APD** and **conduction time**
83
What are the 2 clinical uses for the class 4 antiarrhythmics?
- **Prevention** of **paroxysmal SVT** - **Rate control** in **atrial fibrillation** and **atrial flutter**
84
What are the cardiac and extracardiac AE's of the class 4 antiarrhythmics?
- CHF (**negative inotropy**) - **AV block** - **SA node** arrest - **Bradyarrhythmias** - **Hypo**tension - Constipation
85
What is the MOA of adenosine in the heart (ie., receptors and effect)?
- **Activates** **K+** current and **inhibits** **Ca2+** and **Funny current** - Causes marked **hyperpolarization** and **suppression** of **AP's** in **SLOW cells** - **Inhibits** AV conduction and **increases** nodal **refractory period**
86
What is the clinical use of Adenosine for arrhythmias?
Conversion to **sinus rhythm** in **paroxysmal SVT**
87
What are 5 AE's associated with Adenosine?
- **SOB** - **Bronchoconstriction** (both **A1** and **A2B** adenosine receptors) - **Chest burning/fullness** - **AV block** - **Hypo**tension
88
What drug classes treat supraventricular and ventricular arrhythmias? What drug classes treat ventricular arrhythymias only? What drug classes treat supraventricular arryhthmias only?
Classes IA, IC, III Class IB Class II, IV, V

CPR II Exam 1 (25 decks)

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