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My Notes > Cardio drugs > Flashcards

Cardio drugs Flashcards

1
Q

What are the effects of quinidine? What other drug do we often administer with it?

A
  1. Block open Na+ channel (↑ AP duration, ↑ ERP)
  2. Muscarinic receptor block (↑ HR)
  3. Alpha block (→ reflex tachy)

Due to muscarinic block we often give digitalis to slow AV conduction

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2
Q

What is the term for the condition caused by quinidine toxicity? What are main side effects?

A

Cinchonism:
- Antimuscarinic: constipation, cycloplegia, mydriasis, ↑QT interval → torsades de pointe

  • Anti-α: diarrhea (relaxed sphincters), miosis
  • Other: CNS excitation, tinnitus
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3
Q

Drug interactions of quinidine:

A
  1. Hyperkalemia → enhances effects; hypokalema → reduces

2. Displaces digoxin from tissue-binding sites → higher free conc. → potential toxicity

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4
Q

Toxicities of procainamide

A
  1. hapten → hypersensitivity rxn → SLE-like syndrome (also occurs with hydralazine and isoniazid; anti-histone is highly specific serum test)
  2. metab by N-acetyltransferase → [ ] varies w/ slow/fast metabolizers
  3. hematotoxicity → do routine CBC, watch for infxn/bleeding
  4. CV effects (torsades) - has some antimuscarinic activity
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5
Q

Name 3 Class IA antiarrhythmics

A
  1. Quinidine
  2. Procainamide
  3. Disopyramide

“The Queen Proclaims Diso’s pyramid”

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6
Q

How do Class IB drugs work?

A
  1. Block inactivated Na+ channels (so targets depolarized tissue s.a. MI tissue)→ keep channels refractory
  2. Block slow Na+ “window” current that normally prolongs plateau → ↓ AP duration

These effects allow for increased filling time (diastole) so the heart can function better post-MI

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7
Q

What is the most important Class IB antiarrhythmic and when is it used?

A

Lidocaine

  • post MI
  • Open-heart surgery (like MI, lots of depolarized tissue to act on)
  • Digoxin toxicity (digoxin depolarizes heart mm. by blocking Na+ pump)
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8
Q

What are the adverse effects of digoxin?

A

CNS toxicity - seizures

Least cardiotoxic of conventional anti-arrhythmics (this is why we prefer electrical cardioversion > chemical)

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9
Q

Why is lidocaine administered by IV for arrhythmia? What are the forms of lidocaine that can be taken orally?

A

IV only b/c first-pass metabolism;

Mexiletine and Tocainide

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10
Q

Why are class IC antiarrhthmics only a last resort? What conditions would warrant its use?

A

They are very proarrhthmogenic (esp. post-MI) and in multiple studies has led to sudden death.

Used in SVTs (including A fib.) and last resort in refractory VT.

IC is Contraindicated in structural and ischemic heart disease

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11
Q

What do class II antiarrhythmics do?

A

Beta blockade → ↓ cAMP, ↓ Ca 2+ currents → decrease slope of phase 4 depolarization in SA/AV node → suppress abnormal pacemakers

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12
Q

Give 6 examples of class II antiarrhythmics

A
  1. metoprolol
  2. propranolol
  3. esmolol
  4. atenolol
  5. timolol
  6. carvedilol
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13
Q

What are class II antiarrhythmics used for?

A
  1. Prophylaxis post-MI is most common use, not as antiarrhythmic (negative inotropic effect → ↓ O2 demand so angina does not → MI)
  2. SVT (β-blockers slow AV node conduction especially)
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14
Q

What are the side effects of β-blockers?

A

Sexual: impotence
Respiratory: exacerbation of COPD and asthma (bronchoconstriction)
CVS: bradycardia, AV block, CHF (depressive effects); exacerbation of vasospasm in Prinzmetal angina (propranolol)
CNS: sedation, sleep alterations
Metabolic: dyslipidemia (↓ lipolysis)

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15
Q

Who should not take β-blockers? How can overdose be treated?

A

Cocaine users: risk of unopposed α-adrenergic receptor agonist activity

Treat β-blocker overdose with glucagon

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16
Q

What is the mechanism of action of class III antiarrhythmics?

A

prolonged repolarization

17
Q

What are the clinical uses for class III antiarrhythmics?

A

a. fib., a. flutter.
v. tachy
(blocks repol. of all cells so wide use)

18
Q

Why does amiodarone suck?

A

T1/2 = 80 days (so it takes forever to get to steady state and to remove from body if toxic)
Why? because it acts as a strong hapten (via iodination) →
1. pulmonary fibrosis (binds to lung proteins → chronic inflamm → irreversible damage)
2. hepatotoxicity
3. hypo/hyperthyroidism (amiodarone is 40% iodine by wt)
4. Deposits anywhere, esp. cornea and skin (→ “smurf” skin b/c iodine + sugar = purple/blue color) → photodermatitis
5. Neurologic effects
6. Constipation
7. CVS effects (brady, heart block, CHF)

19
Q

What tests should you use to follow patients taking amiodarone?

A

PFTs, LFTs, TFTs

20
Q

Besides its effects as a class III antiarrhythmic, what other classes does amiodarone effect?

A

I, II, and IV (all classes) + alters lipid membrane

21
Q

List 4 class III antiarrhythmics

A 
Amiodarone
Ibutilide
Dofetilide
Sotalol
(AIDS)
22
Q

Describe the use of sotalol as an antiarrhthmic

A
  1. class II and III
  2. used only for life-threatening ventricular arrhthmias
  3. Causes torsades de pointes and excessive β-blockade
23
Q

Which is a more pressing issue: atrial or ventricular arrhythmias?

A

ventricular → can lead to death quickly vs. atrial which has a main risk of thrombosis

24
Q

What is the toxicity of ibutilide?

A

torsades de pointes

25
Q

What are the only two Ca2+ channel blockers that are approved for use as antiarrhythmics (class IV)?

A

Verapamil, diltiazem

these vs. dihydropyridine Ca+ channel blockers have high affinity for cardiac channels vs. vascular → no reflex tachy

26
Q

What is the mechanism of class IV antiarrhythmics?

A

block slow L-type Ca2+ channels → ↓ phase 0 & 4 slopes in SA and AV node → prevention of nodal arrhythmias (s.a. SVT) and rate control in a. fib.

27
Q

What are the risks associated with class IV antiarrhythmics?

A
  1. CV: AV block, CHF, sinus node depression
  2. vascular: flushing, edema (for DPH calcium channel blockers, not the cardiac ones verapamil, diltiazam)
  3. GI: constipation
28
Q

What drug interactions arise with class III antiarrhythmics?

A
  • Additive AV block w/ β-blockers, digoxin; (↑ PR interval)

- Verapamil displaces digoxin from tissue binding sites → ↑ serum [ ]

29
Q

Describe the cause of torsade de pointes

A

anything that prevents K+ efflux (class III antiarrhythmics, antimuscarinics [atropine, antipsychotics, TCAs, antihistamines, meperidine, amantadine, quinidine]) → cells maintained depolarized → ↑ QT interval → torsade

My Notes (23 decks)

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