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Cardiology (Fall 2023) > Lecture 19: CV Pharmacology > Flashcards

Lecture 19: CV Pharmacology Flashcards

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
Q

What BB is good for IV infusions?

A

Esmolol

26
Q

What do class III antiarrhythmics do?

A
  1. Block potassium channels and prolong repolarization, widening QRS and prolonging QT.

Avoid combining with other QT prolongation drugs. May cause TORSADES

27
Q

What is the profile of amiodarone?

A
  • 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
Q

How do we screen for pulmonary toxicity in amiodarone?

A
  1. Annual CXR
  2. Stop Amiodarone ASAP
29
Q

What mineral effect can amiodarone mimic?

A
  • Iodine, so it can induce hypo or hyperthyroidism.
  • Q6months TSH checks
30
Q

What are the toxicities that amiodarone can cause?

A
  1. Pulmonary
  2. Thyroid (iodine)
  3. Ocular (deposits)
  4. Neurologic (tremors, ataxia)
  5. Dermatologic (blue/gray discoloration & photosensitivity)
  6. Liver

Derm = smurf looking

31
Q

What does amiodarone interact with?

A

CYP3A4 inhibitor: can potentiate warfarin and digoxin

Doubles digoxin levels

32
Q

What is the profile of sotalol?

A
  • 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
Q

What is the profile of dofetilide?

A
  • 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
Q

What concomitant drug use CIs usage of dofetilide?

A
  • Cimetidine
  • Ketoconazole
  • Megestrol
  • Prochlorperazine
  • Bactrim
  • Verapamil

Also Renal impairment

35
Q

What is the profile of dronedarone?

A
  • Similar to amiodarone with less efficacy but less SEs also
  • CI: Symptomatic CHF or recent decompensation, Permanent AF, Hepatic impairment

Class III antiarrhythmic

36
Q

What is the profile of ibutilide/corvert?

A
  • Similar to sotalol
  • IV only, used solely for afib/aflutter cardioversion
  • Can cause torsades
  • Avoid in LV dysfunction and lyte abnormalities
37
Q

What are the two Class IV antiarrhythmics?

A

Verapamil and diltiazem

38
Q

What do class IV antiarrhythmics do and their main weakness?

A
  • Decrease automaticity and AV conduction
  • negative inotrope = avoid in pts with LV dysfunction.
39
Q

What does digoxin do?

A
  • 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
Q

What are the EKG changes associated with digoxin?

A
  • PR prolongation
  • ST segment depression

Pt in afib

41
Q

What is the concern with oral digoxin?

A
  • Poor bioavailability
  • Toxicity can occur if ABX are also administered. (microflora metabolize it)
42
Q

What are the pharmacokinetics of digoxin?

A
  • Half life of 36hrs
  • Renal elimination
  • Clearance is decreased by: Amiodarone, quinidine, verapamil, diltiazem, itraconazole, propafenone, and flecainide
43
Q

What is the therapeutic range of digoxin?

A

0.5-2 NANOgrams/mL

44
Q

What does digoxin toxicity cause?

A
  • Visual disturbances, dizziness, weakness, N/V/D, anorexia
  • Any dysrhythmia can occur
45
Q

How do you treat digoxin toxicity?

A
  • IV hydration + lyte correction
  • Digoxin immune Fab can be used to bind
46
Q

What does adenosine do?

A
  • Activate potassium channel and hyperpolarizes membrane, decreasing SA node depolarization
  • Short-term AV nodal blocker
  • Use: conversion of SVT to sinus rhythm
47
Q

What is the dosing for adenosine?

A

6, 6, 12 mg

48
Q

What does atropine do?

A
  • 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
Q

What is the paradoxical effect of atropine?

A

Slows HR in pts with mobitz type II AVB and 3rd deg AVB.

Cardiology (Fall 2023) (45 decks)

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