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Primaries > CV drugs, antiarrhythmics, inotropes > Flashcards

CV drugs, antiarrhythmics, inotropes Flashcards

1
Q

How are antiarrythmic drugs classified

A

Vaughn Williams:

Class I to Class IV

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2
Q

How do class I antiarrhythmic drugs work? (including subtypes)

A

Sodium channel blockade.

Subclasses of this action reflect effects on the action potential duration (APD) and the kinetics of sodium channel blockade.

Class 1A action prolong the APD and dissociate from the channel with intermediate kinetics
- ie. quinidine, procainamdie

Class 1B action shorten the APD in some tissues of the heart and dissociate from the channel with rapid kinetics
- ie. lignocaine, phenytoin

Class 1C action have minimal effects on the APD and dissociate from the channel with slow kinetics.
- ie. flecanide, encainide

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3
Q

How do class II antiarrhythmic drugs work?

A

Sympatholytic.

Drugs with this action reduce β-adrenergic activity in the heart.

  • increase effective refractory period of AV & decreased automaticity, decreased QT duration -> decrease HR & O2 consumption
    ie. metoprolol, esmolol, propanolol
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4
Q

How do class III antiarrhythmic drugs work?

A

Prolongation of the APD

Most drugs with this action block the rapid component of the delayed rectifier potassium current, IKr.
Eg Amiodarone, sotalol, bretylium
Amiodarone has Class I, II, III and IV effects

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5
Q

How do class IV antiarrhythmic drugs work?

A

Blockade of Cardiac channel current

This action slows conduction in regions where the action potential upstroke is calcium dependent, eg, the SA and AV nodes.
• inhibit inward slow calcium ion currents that may contribute to development of VT
• block L type Ca2+ channels -> impair SA node pacemaker activity.
• decrease duration of action potential but no effect on automaticity
• ie. verapamil, diltiazem, nifedipine

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6
Q

Procainamide

  • Class?
  • Metabolism?
  • Half life?
  • Elimination?
  • When to be wary?
  • Dosing
  • Therapeutic use
A
  • Class 1A + Class 3
  • Hepatic metabolism to N acetylprocainamide (NAPA) (Class 3)
  • Half life 3-4 hours
  • Renal elimination
  • Beware in renal and heart failure (decreased clearance and reduced volume of distribution)
  • > accumulation NAPA -> Torsades

12mg/kg loading
2-5mg/min maintenance

  • Use in most atrial and ventricular arrhythmias
  • Usually 2nd/3rd line after lidocaine or amiodarone for sustained VT/arrhythmias
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7
Q

Quinidine

- Class?

A

Class 1A + 3

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8
Q

Lidocaine

- Class?

A

Class 1B

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9
Q

Flecainide

- Class?

A

Class 1C

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10
Q

Propranolol

- Class?

A

Class 2

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11
Q

Esmolol

- Class?

A

Class 2

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12
Q

Amiodarone

- Class and mechanism of action?

A

Amiodarone is an antiarrhythmic agent with a complex mechanism of action and many effects.
“Class 3 but has effects from all classes”

K+ channel blockade in cardiac myocytes, inhibiting the slow outward current and slowing repolarisation (Class III)
β-blocker-like activity on SA and AV nodes, decreasing automaticity and slowing nodal conduction (Class II)
Ca2+ channel blocker-like activity on L-type Ca2+ channels, decreasing the slow inward Ca2+ current, increasing depolarisation time and decreasing nodal conduction (Class IV)
α-blocker-like activity, decreasing SVR

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13
Q

Amiodarone pharmacokinetics?

A

Absorption
- Poor PO absorption with bioavailability ~50%.

Distribution
- Highly protein bound with very high VD of ~70L.kg-1s due to accumulation in fat and muscle.

Metabolism
- Hepatic metabolism with inhibition of CYP3A4, to the active desmethylamiodarone

Elimination
- Very long t1/2 of up to ~55 days. Biliary, skin, and lacrimal elimination, with < 5% of drug eliminated renally. Not removed by dialysis.

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14
Q

Amiodarone dose?

A

DOSE

IV – bolus 5mg/kg in 250mL of 5% dextrose (60min) -> infusion 15mg/kg/day
PO – load -> 200mg tds reducing to od

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15
Q

Amiodarone indication and adverse effects?

A

INDICATIONS

stabilisation of supraventricular & ventricular dysrhythmias

ADVERSE EFFECTS

Cardiac

  • Hypotension, bradycardia
  • Prolong QT -> TdP

BITCH

  • Blue skin - from skin deposits esp sun effected areas
  • Interstitial lung disease
  • Thyroid effects
  • Corneal depostis
  • Hepatic

(Drug interactions
CYP3A4:
- Drugs that inhibit this enzyme increase levels of amiodarone (ie. H2 blocker cimetidine)
- Drugs that induce CYP3A4 decrease levels of amiodarone (ie. rifampin)
Cytochrome P450
- Inhibits this enzyme
- Can result in high levels of statins, digoxin, warfarin

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16
Q

Verapamil

  • Class?
  • Use?
A 
Calcium channel blocker, class IV
Also considered as treatment for SVT
17
Q

Diltiazem

- Class?

A

Calcium channel blocker, class IV

18
Q

Adenosine

  • what is it?
  • Mechanism of action?
A
  • short acting anti-arrhythmic
  • naturally occurring purine nucleoside
  • Forms from breakdown of ATP
Mechanism of action
Heart - acts at SA + AV pacemaker cells
- Binds to adenosine A1 receptor which is coupled to inhibitory G protein
-> inactived Adenylate cyclase
-> inhibits cAMP + PKA synthesis
-> Decreased Ca influx and increased K efflux
-> hyperpolarisation of cell membrane
-> AV nodal conduction is slowed
-> Delayed action potential in SA node
-> negative chronotropy &amp; dromotropy

Vascular smooth muscle relaxation -> vasodilation

19
Q

Adenosine pharmacokinetics?

A

PHARMACOKINETICS

Onset – 10 seconds
Duration – 10 seconds
Absorption – must be given IV
Distribution
Metabolism – absorbed by RBC’s and endothelium
Elimination – t ½ = 10 seconds
20
Q

Adenosine adverse effects?

A

Toxicity

  • Flushing
  • SOB
  • Chest burning
21
Q

Digoxin

Mechanism of action?

A

blocks Na-K-ATPase

  • > build up of Na intracellularly -> Na leaves cell via Na/Ca antiporter -> intracellular Ca increases -> positive inotropy
  • > decrease of K intracellularly -> Dromotromy (slows AV node)

Vagal stimulation -> slows AV node

22
Q

Adrenaline vs noradrenaline vs dopamine?

- Compare and contrast

A

Adrenaline

  • non selective direct acting adrenergic agonist
  • Targets alpha and beta receptors
  • Alpha response - (fight or flight -> vasoconstriction, midriasis, increased CO, urinary retention)
  • Beta response - bronchodilation

Noradrenaline

  • Alpha 1 -> vasoconstriction
  • No Beta 2 activity

Dopamine

  • Non selective direct acting adrenergic agonist
  • Dose dependent
  • Low dose -> dopamine only
  • Higher doses -> B1 then A1
  • Can be used in treatment of heart failure and hypotensive shock
23
Q

Alpha 1 receptor response?

A

“Fight or flight”

Vasoconstriction
Mydriasis
Urinary retention
Glycogenolysis
Inhibition of renin release

eg phenylephrine (blocked nose), oxymetazoline

24
Q

What happens when Alpha 2 receptor are activated?

A

Found on presynaptic cleft and activation results in decreased production of cAMP
-> Decreased release of noradrenaline

A2 on pancreatic islet -> Decreased insulin section

eg. clonidine - reduction in BP

25
Q

B1 receptor response?

A

Heart

  • Increased HR
  • Increased contractility
  • Increased AV conduction

Kidney
- Increased renin release (increases retention + BP)

Eg Dobutamine - used in heart failure

26
Q

B2 receptor response?

A

Heart

  • accelerates SA node
  • Increases contractility

vascular smooth muscle
- Relaxation -> increased perfusion

Lungs
-Bronchodilation

Smooth muscle of GIT + uterus

  • decreased motility
  • Inhibition of labour

Pancreas
- Increased insulin secretion
Liver
- Gluconeogenesis + glycogenolysis

eg. Short acting - salbutamol
Long acting - salmeterol

27
Q

B3 receptor response

A

Adipose tissue
- Lipolysis

Bladder
- relaxation of detrusor -> prevention of urination (eg mirabegron)

28
Q

Alpha 1 blocker response?

A

Vasodilation
Bladder neck and prostate gland smooth muscle relaxation

Eg prazosin -> acts more on vessels
- tamsulosin

SEs orthostatic hypotension, headaches

29
Q

Alpha 2 blocker response

A

Not really used clinically

30
Q

1st generation beta blocker

A

Non selective
- Eg propranolol, sotalol, timolol

Used in prophylaxis of migraines, decrease IOP for glaucoma
Avoid in COPD/Asthma due to B2 antagonism -> bronchoconstriction

31
Q

2nd generation beta blockers

A 
B1 selective (however at high doses become nonselective)
- Eg atenolol, bisoprolol, esmolol, metoprolol
32
Q

3rd generation beta blocker

A

Non selective (Beta + alpha 1 blockade)

  • beta and alpha blockade
  • eg. carvedilol (also has antioxidant effect, good for heart)

Selective

  • vasodilation by NO release
  • eg nebivolol
33
Q

Digoxin adverse effects?

A

ADVERSE EFFECTS

digoxin toxicity
ST depression (reverse tick appearance)
tachycardias (flutter with block, VT, VF)
bradycardia -> complete heart block
headache
GI symptoms
Drug interactions

increased digoxin levels (e.g. P glycoprotein inhibitors (efflux pump in distal renal tubules and intestine), and increased bioavailability)
-> amiodarone, verapamil, quinidine, spirinolactone, clarithromycin, itraconazole, captopril
decreased digoxin levels
-> cholestyramine, oral antacids, metoclopramide, neomycin, sulfasalazine, rifampicin

Primaries (5 decks)

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