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Crrab 1 > K+ and Ca2+ blockers > Flashcards

K+ and Ca2+ blockers Flashcards

1
Q

How do we achieve the goal of antiarrhythmics?

A
  1. decrease or increase conduction velocity
  2. Alter the excitability of cardiac cells by changing EFP
  3. Suppress abnormal automaticity
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2
Q

What are class III antiarrhythmics and what do they act on?

A

K channel blockers

  • block them slows repolarization
  • increases AP duration and ERP
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3
Q

What are Class III antiarrhythmics useful for?

A
  • suppressing reentry
  • prolong time cell is unexcitable
  • Prolongs QT
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4
Q

What is common a Class III AA drug? what other effects does it have on CV system?

A

Amiodarone

  • prolongs AP
  • also a potent to blocks Na+
  • Weak B-blocker
  • Weak Ca2+ blocker
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5
Q

What are some extra-cardiac effects and therapeutic uses of Amiodarone?

A

Vasodilation

V-Tach, V-fib and A flutter/fib

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6
Q

What are the pharmacokinetics of Amiodarone?

A

Hepatic and metabolite is bioactive

  • 1-3 month long 1/2 life
  • Substrate for CYP3A4 (Statins)
  • Inhibits several P450’s like Warfarin and Digoxin
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7
Q

What is the toxicity of Amiodarone?

A

Bradycardia and heart block in pts with preexistingSA and AV node dz.

  • Heart lung liver skin and tears accumulation
  • Blocks T4–>T3 conversion
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8
Q

What does increasing T3 lead to?

A

Increase in beta receptors in the heart

  • increase HR, Force and contraction
  • Leads to increase CO
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9
Q

What is the most important adverse effect of Amiodarone?

A

Pulmonary toxicity

- dose related

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10
Q

What are some other causes of amiodarone toxicity?

A
  1. hypersensitivity hepatits
  2. Photodermatitis, gray blue skin in sun exposed areas. Skin deposits
  3. Corneal micro-deposits- Halos develop in periph visual fields
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11
Q

What is Dofetilide?

A

Class III AA

  • Very selective K channel blockers
  • Prolongs AP
  • Increase QT
  • increase refractory in His-Purkinje system
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12
Q

What is the toxicity, pharmacokinetics and therapeutic use of Dofetilide?

A
  1. life threatening Ventricular arrhythmias
  2. CPY3A4 metabolism
  3. Maintenance and restoration of normal sinus rhythm in A-fib.
    - Contraindicated in Long QT, Bradycard and hypokalemia
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13
Q

What is the mnemonic for Class III AA?

A 
AIDS 
Amiodarone
Dofetilide
Ibutilide 
Sotalol
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14
Q

What is the cardiac effects of ibutilide?

A
  • Prolongs AP
  • Also slow inward Na ACTIVATOR (delays repole)
  • inhibits Na inactivation (increase ERP)
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15
Q

What is the toxicity, PK and therapeutic use?

A
  1. Excessive qt interval prolongation leading to Torsades and life threatening ventricular arrhythmias
  2. Hepatic metab
  3. Acute conversion of a-fib and fibrillation to NS rhythm
    - more effective for termination of flutter in 20 minutes
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16
Q

Why is amiodarone contraindicated in pts with heart block and SA node dysfunction?

A

Because of its Class IV effects causing bradycardia and atrioventricular block

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17
Q

What is the MOA of class IV AA?

A

bind to L-type Ca2+ channels located on VSM, cardiac myocytes and SA/AV nodes

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18
Q

What are the Class IV AA effects then?

A
  • Vasodilation

- Decreased myocardial contractility

19
Q

Which phase of the AP curve does Class IV affect?

A

Phase 2

  • blocking Ca thus shortens phase 2
  • shortens AP (increase ERP)
  • reduces force of contraction
  • less available for trop to bind to
20
Q

What does blocking Ca like Class IV AA do to the nodal cells?

A

Blocks pacemaker currents

  • slows HR
  • Decreased conduction velocity (mainly Av node)
  • prolong PR
21
Q

What are Class IV AA’s commonly used for?

A

HTN

-Resistance= x/r^4

22
Q

Why are Class IV AA indicated for angina?

A
  1. Vasodilation
  2. Leads to reduced art pressure decrease afterload and thus oxygen demand
  3. Decrease HR and contractility
  4. Reverse or prevent vasospasm
23
Q

What else are Class IV useful for?

A
  1. Ectopic foci causing aberrant AP firing

2. Helps block reentry which can cause SVT by prolonging repole

24
Q

What are the 2 subclasses of Class IV AA’s?

A
  1. Dihydropyridines
  2. Non-dihydropyridines
  • differ in specificity for cardiac vs vascular L type Ca2+ channels
25
Q

What are Diydropyridines mainly used for?

A

Smooth muscle selective class

  • Reduced systemic vascular resistance and art pressure to treat HTN
  • NOT ANGINA- leads to reflex tachycardia
26
Q

What are the two non-dihydropyridines?

A
  1. Verapamil
  2. Diltiazem
    - only two used clinically
27
Q

What is Verapamil mainly used for?

A

Selective in myocardium

  • less effective in vasodilator drug
  • good for angina, arrhythmias, reducing cardiac O2 demand and treating vasospasms
28
Q

What is diltiazem mainly used for?

A

Between Verpamil and Dihydropyridines for Vascular selectivity
- reduce arterial pressure without tanking it

29
Q

What is contraindicated with Class IV AA drugs?

A

B-blockers

30
Q

What are some side effects and contraindications of Class IV drugs?

A

Flushing, edema, constipation, HoTN, reflex tach, nervousness, lack of energy
- Preexsting bradycard, conduction defect or HF

31
Q

What is the therapeutic use of Varapamil?

A

SVT, a-fib and flutter

– Contraindicated in Wolff-Parkinson-White

32
Q

What is the MOA of Adenosine?

A

Activation of K channels and inhibition of L-type Ca channels

  • Hyperpolarization
  • suppression of Ca dependent AP’s ( Nodal tissue)
33
Q

What blunts the action of adenosine because they are adenosine receptor antagonists?

A

Caffeine

Theophylline

34
Q

What is adenosine used for?

A

SVT

- 15 sec 1/2 life

35
Q

What are some SE of adenosine?

A

-Flushing and HA
-AV block
-Rapid arterial HoTN and reversed shortly after infusion
-SENSE OF IMPENDING DOOM
- bronchospasm
-

36
Q

Who is adenosine contraindicated from?

A

2 and 3rd degree AV blocks pts

37
Q

What is the cardiac glycoside drug used in the US and for what?

A

Digitalis

  • HF mainly
  • a-fib/flutter
  • some reduction of Ventricular rate when driven from above
38
Q

What is the MOA of Digitalis?

A

Inhibits Na/K/ATPase pump

  • increase intracellular Na
  • shutting down Na/Ca pumpt
  • increase intracellular Ca
  • Increase contractibility
  • Increase SV but decreased HR to keep
39
Q

What happens to the membrane potential with someone on digoxin?

A

Depolarized

- decreased intracellular K and increase intracellular Na

40
Q

How does digitoxin affect conduction?

A

decreased it through the SA and AV–> increasing refractory period
- Increase intracellular Ca leads to decreased extracellular. Thus less to influx of the funny channels thus slowing the rate.

41
Q

What are some side effects of digitalis?

A

Extreme AV block

  • Hyperkalemia
  • cholinergic effects–> N, v, d, blurry yellow vision, arrhythmias
42
Q

When is digitalis contrindicated?

A
  1. AV block
  2. Hypokalemia
  3. WPW
  4. Renal failure
  5. Class I, II, III, IV,, NSAIDS and diuretics
43
Q

Arrhythmias cause by what from digitalis?

A

Increase automacity and decrease AV conduction

Crrab 1 (27 decks)

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