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2020 CPR II Cardio Exam 1 > Drugs for Cardiac Arrhythmia (Konorev) > Flashcards

Drugs for Cardiac Arrhythmia (Konorev) Flashcards

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?

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?

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

2020 CPR II Cardio Exam 1 (31 decks)

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