Lecture 19: CV Pharmacology Flashcards

(49 cards)

1
Q

How does a SA node action potential look like?

A
  1. Sodium influx via funny channels
  2. Calcium influx
  3. Potassium efflux
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2
Q

What are the 5 phases of a cardiac myocyte action potential?

A
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3
Q

What is the effect of hypercalcemia on the cardiac action potential?

A

Extends the plateau phase

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4
Q

What are the 2 general mechanisms behind arrhythmias?

A
  1. Abnormal pacemaker activity
  2. Abnormal impulse propagation
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5
Q

What do antiarrhythmic drugs tend to focus on?

A

Ectopic pacemakers, reducing their automaticity.

It does not affect the SA node itself as much.

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6
Q

What do antiarrhythmic drugs do to depolarized tissue primarily?

A
  • Reduce conduction and excitability
  • Increase refractory period

Effect is more pronounced in depolarized tissue rather than polarized.

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7
Q

What are the 4 classes of antiarrhythmic drugs?

A
  1. Class I: fast sodium channel blockers
  2. Class II: BBs
  3. Class III: Potassium channel blockers
  4. Class IV: CCBs
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8
Q

What are the 3 subclasses of class I antiarrhythmics based on and what are the 3 subclasses?

A

Defined by their effects on purkinje fiber AP

  1. Class 1a: slow the rate of rise of the AP and prolong its duration (moderate depression of the phase 0 upstroke) (Quinidine, procainamide, disopyramide)
  2. Class 1b: Shorten AP (minimal depression of the phase 0 upstroke) (lidocaine, mexiletine)
  3. Class 1c: Dissociates from channel with slow kinetics (no change in AP duration) (flecainide, propafenone)
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9
Q

What is the main purpose of quinidine and what is it often used with?

A
  • Class 1a drug that works as an anticholinergic on SA and AV nodes.
  • Often combined with BBs, non-DHP CCBs, or digoxin to prevent increased ventricular rate.

Proarrhythmic that can cause torsades

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10
Q

What does procainamide do?

A
  • Similar to quinidine but lacks anticholinergic activity.
  • Prolongs QT interval = torsades risk
  • MC ADE: Lupus
  • Main use: WPW

Class 1a

Treats Wolff, can cause wolf

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11
Q

What is the profile of disopyramide?

A
  1. Class 1a
  2. Potent anticholinergic and negative inotrope
  3. QT prolongation
  4. CI in pts with HFrEF
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12
Q

What is lidocaine selective for in the heart?

A

Ischemic tissue, primarily active fast sodium channels below the AV node

Class 1b

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13
Q

Class 1a antiarrhythmic mnemonic

A

Double Quarter Pounder

  • Disopyramide
  • Quinidine
  • Procainamide
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14
Q

When is lidocaine used?

A

Ventricular dysrhythmias, especially those associated with MI.

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15
Q

What kind of patients should we be cautious of injecting lidocaine into?

A

Hepatic impairment

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16
Q

What is the difference between lidocaine and mexiletine?

A

Mexiletine is oral

class 1b

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17
Q

What is mexiletine often used with combination with?

A

Class 1a and III for refractory ventricular dysrhythmias

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18
Q

What is the main SE of mexiletine?

A

GI use (limits the use of them)

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19
Q

What is the profile of flecainide?

A
  • Slows conduction velocity in the purkinje and AV node
  • MC use: afib/aflutter
  • May cause rapid VT in someone with structural abnormalities

Class 1c

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20
Q

Class 1b antiarrhythmic mnemonic

A

Lettuce Tomato Mayo

  • Lidocaine
  • phenyToin
  • Mexilitine

Liddy’s Mexican Pub

T is actually for tocainide, but we didn’t learn about it

21
Q

What is the profile of propafenone?

A
  • Slows conduction velocity in the purkinje fibers and AV node + mild non-selective BB effect
  • lengthens PR and QRS => bradycardia or heart block
  • MC use: Afib/Aflutter
  • Avoid in structural heart disease
  • Additional SE of metallic taste

Class 1c

Similar to flecainide

22
Q

What patients should never get class 1c antiarrhythmics?

A

Structural Heart Disease

23
Q

What are BBs mainly used for?

A
  • Decrease automaticity, prolong AV conduction, prolong refractory period
  • Suppressing ventricular dysrhythmias and SVTs
24
Q

Class 1c antiarrhythmic mnemonic

A

Fries Please

  • Flecainide
  • Propafenone
25
What BB is good for IV infusions?
Esmolol
26
What do class III antiarrhythmics do?
1. Block **potassium channels** and **prolong repolarization**, widening QRS and prolonging QT. ## Footnote Avoid combining with other QT prolongation drugs. May cause TORSADES
27
What is the profile of amiodarone?
* Characteristics of **all 4 antiarrhythmic classes**! (primarily Class III) * Works on all cardiac cells, but is primarily a **potassium channel blocker** * **OK to use in LV dysfunction** (mild negative inotrope effect) * Can **buildup in toxicity** | Amiodarine should be **avoided in bradycardic patients**
28
How do we screen for pulmonary toxicity in amiodarone?
1. Annual CXR 2. Stop Amiodarone ASAP
29
What mineral effect can amiodarone mimic?
* Iodine, so it can induce hypo or hyperthyroidism. * Q6months TSH checks
30
What are the toxicities that amiodarone can cause?
1. Pulmonary 2. Thyroid (iodine) 3. Ocular (deposits) 4. Neurologic (tremors, ataxia) 5. Dermatologic **(blue/gray discoloration & photosensitivity)** 6. Liver | Derm = smurf looking
31
What does amiodarone interact with?
CYP3A4 inhibitor: can **potentiate warfarin and digoxin** | Doubles digoxin levels
32
What is the profile of sotalol?
* Primarily a potassium channel blocker but **also has non-selective BB properties (negative inotrope)** * Prolongs atrial and ventricular refractoriness * ADE: **QT prolongation** (d/c if QT interval > 550ms) | Class III drug since it is primarily a potassium channel blocker.
33
What is the profile of dofetilide?
* Prolongs **AP and QT interval** (**OK to use in LV dysfunction**) * Mainly **atrial focused** * MC ADE: **Torsades**, gotta monitor IP. * 3 days, 6 doses inpatient, **EKG 2 hrs after every dose.**
34
What concomitant drug use CIs usage of dofetilide?
* Cimetidine * Ketoconazole * Megestrol * Prochlorperazine * Bactrim * Verapamil | Also Renal impairment
35
What is the profile of dronedarone?
* Similar to amiodarone with less efficacy but less SEs also * CI: Symptomatic CHF or recent decompensation, Permanent AF, Hepatic impairment | Class III antiarrhythmic
36
What is the profile of ibutilide/corvert?
* Similar to sotalol * IV only, used solely for **afib/aflutter cardioversion** * Can cause **torsades** * Avoid in **LV dysfunction and lyte abnormalities**
37
What are the two Class IV antiarrhythmics?
Verapamil and diltiazem
38
What do class IV antiarrhythmics do and their main weakness?
* Decrease automaticity and AV conduction * **negative inotrope** = avoid in pts with LV dysfunction.
39
What does digoxin do?
* **Inhibition of Ca channels in AV** node and **activates K+ channels.** * Slows conduction through AV node, prolonging refractoriness * **Slows ventricular rate in afib/aflutter and terminating AVNRTs**
40
What are the EKG changes associated with digoxin?
* PR prolongation * ST segment depression ## Footnote Pt in afib
41
What is the concern with oral digoxin?
* Poor bioavailability * Toxicity can occur if ABX are also administered. (microflora metabolize it)
42
What are the pharmacokinetics of digoxin?
* Half life of 36hrs * **Renal elimination** * Clearance is decreased by: **Amiodarone**, quinidine, verapamil, diltiazem, itraconazole, propafenone, and flecainide
43
What is the therapeutic range of digoxin?
0.5-2 NANOgrams/mL
44
What does digoxin toxicity cause?
* Visual disturbances, dizziness, weakness, N/V/D, anorexia * Any dysrhythmia can occur
45
How do you treat digoxin toxicity?
* IV hydration + lyte correction * Digoxin immune Fab can be used to bind
46
What does adenosine do?
* Activate potassium channel and hyperpolarizes membrane, decreasing SA node depolarization * **Short-term AV nodal blocker** * Use: **conversion of SVT to sinus rhythm**
47
What is the dosing for adenosine?
6, 6, 12 mg
48
What does atropine do?
* Parasympatholytic drug that **enhances sinus nodal automaticity and AV nodal conduction** * Use: **Emergent bradycardia** * Caution: MI pts that get converted into tachycardia will have a worse supply-demand mismatch.
49
What is the paradoxical effect of atropine?
Slows HR in pts with mobitz type II AVB and 3rd deg AVB.