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Pharmacology MBBS > Antiarrhythmic Drugs and CHF Rx > Flashcards

Antiarrhythmic Drugs and CHF Rx Flashcards

1
Q

Bradycardiac drug

A 
Ivabradine 
 Blocks funny channels ➡️  inhibits SAN ➡️ decreases heart rate ➡️ decreases oxygen demand
Uses:
1. Stable angina
2. Chronic CHF
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2
Q

Vaughan Williams classification of antiarrhythmic drugs

A 
Classes:
1. Na+ channel blockers
2. β blockers
3. K+ channel blockers
4. Ca+2 channel blockers
5. Miscellaneous
 • Adenosine
 • MgSO4
 • Atropine
 • Digoxin
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3
Q

Prophylaxis of SVT/PVST (Atrial arrhythmia)

A

AVN blockers used in order of decreasing preference:

  1. β blockers
  2. Verapamil: Ca+2 channel blocker
  3. Digoxin: parasympathomimetic effect
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4
Q

Treatment of acute attack of SVT/PVST

A

Short acting AVN blocker
DoC is IV adenosine
If not effective then AVN inhibiting agents like IV esmolol.
Edrophonium can also be used as it has parasympathomimetic effect on AVN ➡️ AVN inhibition

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5
Q

Treatment of acute attack of atrial fibrillation/ flutter

A

ToC: cardioversion
If not:
DoC IV Ibutelide followed by repeat cardioversion

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6
Q

Long term treatment of atrial fibrillation/ flutter

A 
1. Rate control:
 To maintain ventricular rates <100 
 Inhibit AVN, DoC is β blockers
2. Rhythm control:
 Atrial myocytes are made refractory
• Na+ channel blockers to block depolarisation
• K+ channel blockers to block repolarisation , preferred
 DoC Amiodarone
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7
Q

Class I of antiarrhythmic drugs and their basic properties

A 
Blocks Na+ channels
1. Ia
 1-10 sec 
 In open state
 Significant K+ channel blocker 
2. Ib 
 <1 sec
 In closed state
 K+ channel opener
3. Ic 
 >10 sec
 In open state
 Negligible K+ channel blocker
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8
Q 
Properties of subclass 
Ia of class-I
 of antiarrhythmic drugs
A
  1. Delay in depolarisation less than Ic
  2. Maximum delay of repolarisation
  3. QT prolongation ➡️ risk of Torsades de pointes
  4. Increase refractoriness of both normal cells and accessory pathway
  5. Anticholinergic effect ➡️ increases AVN condition instead ➡️ PR shortening
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9
Q 
Properties of subclass 
Ib of class I
 of antiarrhythmic drugs
A
  1. Negligible delay in depolarisation
  2. Early opening of K+ channels ➡️ early repolarisation
  3. QT shortening
  4. No effect on AVN ➡️ no effect on PR interval
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10
Q 
Properties of subclass
 Ic of class I 
of antiarrhythmic drugs
A
  1. Maximal delay in depolarisation
  2. Negligible effect in repolarisation
  3. No effect on QT interval
  4. Increase refractoriness in both normal cells and accessory pathway
  5. AVN inhibition ➡️ PR prolongation
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11
Q

Examples of Ic subclass of Class I antiarrhythmic drugs

A
  1. Flecainide
  2. Encainide
  3. Propafenone
  4. Moracizine
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12
Q

Uses of subclass Ic of Class I antiarrhythmic drugs

A

Most arrythmogenic. So used in:

  1. Refractory/ life threatening arrhythmias in SVT/PVST, ventricular tachycardia/ fibrillation
  2. Flecainide is also used in diagnosis of Brugada syndrome
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13
Q

Flecainide

A

Preferred Ic subclass antiarrhythmic drugs for general uses
Also used for diagnosis of Brugada syndrome
S/E:
1. Worsen CHF
2. Blurring vision
DoC for WPW syndrome

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14
Q

Propafenone and moracizine

A

Both are Ic subclass of antiarrhythmic drugs
Propafenone:
Inhibits both Na+ and Ca+2 channels
Weak β blocker
Moracizine: not used because of low efficacy

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15
Q

Uses of Ia subclass of antiarrhythmic drugs

A

Increase AVN so convert atrial arrhythmias into VT/ VF
So when used in SVT/ PVST, it is given with AVN blockers (β blockers, verapamil, digoxin)
Side effect:WT prolongation

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16
Q

Examples of Ia antiarrhythmic drugs

A
  1. Quinidine
  2. Procainamide
  3. Disopyramine
  4. Ajmaline: diagnosis of Brugada syndrome
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17
Q

Quinidine

A
  1. Ia subclass of antiarrhythmic
  2. Anti malarial
  3. Antipyretic
    S/E:
  4. Diarrhoea M/C
  5. Cinchonism (tinnitus, vertigo)
  6. α blocker ➡️ hypotension
  7. QT prolongation at normal doses
  8. Ventricular tachycardia (high doses)
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18
Q

Procainamide

A 
Ia subclass of antiarrhythmic
S/E:
1. Ganglion blocker ➡️ hypotension
2. SLE
DoC for atrial fibrillation associated with WPW syndrome
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19
Q

Disopyramide

A 
Ia subclass of antiarrhythmics
Maximum anticholinergic effect
S/E:
1. Mydriasis
2. Dry mouth
3. Urine retention
CI:
1. Glaucoma
2. BPH
3. CHF
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20
Q

Uses of antiarrhythmics based on effects on accessory pathway

A 
Wolff-Parkinson-White syndrome treatment
ToC: radiofrequency ablation, if not
DoC: oral flecainide 
Associated atrial fibrillation: DoC
 IV procainamide
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21
Q

Ib subclass of antiarrhythmics are not useful in atrial arrhythmia because

A

In atria the Na+ channels are closed (depolarised state) for a shorter time compared to ventricles

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22
Q

Drugs belonging to Ib subclass of antiarrhythmics

A
  1. Lidocaine
  2. Mexiletine
  3. Phenytoin
  4. Tocainide- clinically not used
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23
Q

Lidocaine

A

Ib subclass of antiarrhythmics
High 1st pass metabolism (oral)
For systemic uses- given IV
High volume of distribution ➡️ loading dose required
Uses:
DoC for induced VT/VF associated with MI and digitalis toxicity (Ca+2 accumulation)

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24
Q

Side effects of lidocaine

A 
•Neurological
 1. Paresthesia
 2. Tremor
 3. Nystagmus- earliest sign of toxicity
 4. Delirium
 5. Seizures (Phenytoin is CI here)
  Treatment is instead benzodiazepines 
•Malignant hyperthermia
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25
Q

Mexiletine

A 
Ib subclass of antiarrhythmics 
Oral derivative of lidocaine
Uses:
1. Ventricular tachycardia
2. Neuropathic pain (stopping action potentials)
3. Myotonia
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26
Q

Phenytoin

A 
Ib subclass of antiarrhythmics
Used for treatment of digoxin indices VT
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27
Q

Uses of class II anti-arrhythmic drugs

A 
β blockers
Inhibit both AVN and SAN
DoC for:
1. Idiopathic ventricular tachycardia
2. Ventricular premature beats
3. Congenital long QT syndrome (long term treatment)
4. Rate control: atrial fibrillation/ flutter
5. Catecholamine induced arrhythmia
6. Acute attack of SVT/PVST
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28
Q

DoC for rate control of atrial fibrillation/ flutter

A

β blockers
For stable patients: metaprolol
For unstable patients: esmolol shortest acting

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29
Q

Causes of catecholamine induced arrhythmia

A
  1. Pheochromocytoma
  2. Exercise
  3. Emotional
  4. Anaesthetic agents (halothane, cyclopropane)
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30
Q

QT prolongation is caused by

Delay in repolarisation is seen in

A

Classes Ia and III of antiarrhythmics

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31
Q

Class III antiarrhythmic drugs

A 
K+ channel blockers
Delay in repolarisation 
Increase QT interval
Causes torsades de pointes 
Maximum: Ibutilide
Minimum: Amiodarone
QT prolongation is not seen in Vernakant
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32
Q

Examples of Class III antiarrhythmics

A 
S. Sotalol
B. Bretylium 
D. Dofetilide 
I. Ibutilide
V. Vernakant
A. Amiodarone
33
Q

Amiodarone

A

Widest spectrum antiarrhythmic drugs
Blocks: K, Na, Ca, α and β receptor channels
Least risk of QT prolongation among Class III
High volume of distribution ➡️ loading dose is given
Longest acting drug-53 days
Most toxic side effects due to iodine present in it

34
Q

Uses of Amiodarone

A

DoC in:

  1. VT / VF except those caused by MI or digoxin toxicity (where lidocaine is used
  2. Rhythm control in Atrial fibrillation/ flutter (rate control-β blockers)
35
Q

Vernakant

A

Multi ion channel blocker of K, Na, Ca channel
No QT prolongation since it hardly affects the ventricles
Uses: Rx of atrial fibrillation
S/E: cardiogenic shock

36
Q

Ibutilide

A

Shortest acting K+ blocker
Given IV
Use: Rx of acute attack of atrial fibrillation/flutter

37
Q

Bretylium

A

K+ channel blocker- class III antiarrhythmic
Use: Rx of ventricular fibrillation
Known as medical defibrillator
S/E: hypotension (DoC: Norepinephrine)

38
Q

Sotalol

A 
K+ channel blocker
Use: Rx of
1. Atrial fibrillation/ flutter
2. Ventricular tachycardia
3. Ventricular fibrillation
39
Q

Dofetilide

A

K+ channel blocker
Uses of both Ibutelide and Amiodarone
Oral bioavailability: 100%

40
Q

Dronedarone

Uses

A 
Amiodarone-iodine = dronedarone
Less toxic but less efficacious
Do not preferred 
Uses:
1. Similar to Amiodarone
2. As a substitute to Amiodarone intolerance
41
Q

Dronedarone properties

A 
Amiodarone-iodine = dronedarone
CI:
1. Pregnancy (category X drug)
2. Lactation
3. CHF
t1/2: 12 hours
Food increases absorption so it is given along with food
42
Q

Side effects of amiodarone

A 
Potassium. Pulmonary fibrosis
Channel. Corneal deposits
Blocker. Blue/ grey skin / ceruloderma 
Makes. Myocarditis
Liver. Liver granulomas
And.  α-1 blockade ➡️ hypotension
Skin. Photosensitivity
Toxic. To thyroid
43
Q

Pulmonary fibrosis seen due to amiodarone

A

Type II pneumocyte damage

DoC: prednisolone

44
Q

Whorl like pattern of corneal deposits or
Vortex keratopathy or
Cornea vertecellata is seen in

A 
1. Fabry’s disease 
Drugs like:
2. Amiodarone (M/C)
3. Chloroquine 
4. Chlorpromazine 
5. Indomethacin (least common)
45
Q

Amiodarone and thyroid

A

In most areas (euthyroid):
Hypothyroidism since excess iodine is inhibitory

In iodine deficiency zones:
Hyperthyroidism since iodine is available

46
Q

Non DHP calcium channel blockers as antiarrhythmics

A

Cause mild vasodilation ➡️ reflex tachycardia
Delay in recovery of CC from block ➡️ SAN andAVN inhibition ➡️ decreases HR
• Near normal heart rate
• Inhibition of AVN
Uses:
1. SVT / PVST
2. Stable angina as monotherapy

47
Q

DHP calcium channel blockers as antiarrhythmics

A

Vasodilation ➡️ significant reflex tachycardia
So never used in arrhythmias
Use: stable angina along with β blockers

48
Q

Adenosine as an Class V antiarrhythmic drug

Mechanism of action

A 
Adenosine stimulates:
1. A1 receptor: Gi
 • Inhibits AVN
 • Bronchoconstriction
2. A2 receptor: Gs
 Vasodilation
49
Q

Adenosine as Class V antiarrhythmic

Pharmacokinetics

A

Adenosine
Rapid IV infusion
Rapidly taken up by cellular adenosine uptake protein ➡️ t1/2: 1-5 sec ➡️ shortest acting antiarrhythmic

50
Q

Uses of adenosine as a class V antiarrhythmic

A

Adenosine

  1. DoC: acute attack of SVT/ PVST
  2. To control hypotension in surgeries
  3. Diagnosis of coronary artery disease
51
Q

Side effects of adenosine

A
  1. Flushing (vasodilation)
  2. Dyspnea (bronchoconstriction)
    Above 2 are M/C
  3. Drug interactions with theophylline and dipyridamole
52
Q

Contraindications of adenosine

A
  1. Bronchial asthma
  2. COPD
    In cases of acute attack of SVT/ PVST with asthma/ COPD, DoC is IV verapamil (β blockers also can’t be used)
  3. In patients with transplanted heart ➡️ denervation hypersensitivity
53
Q

Drug interactions of adenosine

A
  1. Theophylline (bronchodilator)
    PDE inhibitor and adenosine receptor antagonism ➡️ adenosine failure
  2. Dipyridamole:
    Inhibits cellular adenosine uptake protein ➡️ adenosine toxicity ➡️ opening of K+ channels in atrium ➡️ action potential graph shortens ➡️ atrial fibrillation
54
Q

MgSO4 as class V antiarrhythmic

A

Blocks Ca2+ channels ➡️ early opening of K+ channels ➡️ shortening of QT
Use: treatment of long QT syndrome for acute attacks ➡️ torsades (both congenital and acquired)

55
Q

Long term treatment of QT syndrome

A 
1. Congenital:
 ToC: pacing using ICD (implantable cardioverter defibrillator), if not
 DoC: β blocker 
2. Acquired:
 Avoid drugs causing QT prolongation
56
Q

Atropine as class V antiarrhythmic

A

Stimulates both SAN (increases HR) and AVN (increases conduction)
Uses:
1. Treatment of bradyarrhythmia like:
• sinus arrest
• sinus bradycardia
• inferior wall MI
2. AVN block reversal like digoxin toxicity.

57
Q

Digoxin as class V antiarrhythmic

A 
Parasympathomimetic effect
Blocks AVN
Slow onset of action so not used on acute cases
Uses:
 Long term Rx of SVT/ PVST (chronic CHF)
58
Q

Most common pathophysiology of acute CHF

A

MI ➡️
acute insult to myocardium ➡️
decreased contraction ➡️
stasis of blood on left ventricle and atrium ➡️
contraction of blood in pulmonary veins ➡️
fluid leaks into interstitial ➡️
pulmonary oedema

59
Q

Treatment of acute CHF

A
  1. Pulmonary oedema of treated 1st:
    • DoC: Furosemide
    + morphine (decrease afterload and preload)
    • If not responding: IV NTG
    • If not responding: BNP analogues
  2. Then for decreased contractions:
    +ve inotropes are given
    • Dobutamine (except in CHF with oliguria- dopamine)
    • If not responding: phosphodiesterase-3 inhibitors
60
Q

Recent drugs for pulmonary oedema

A
  1. Cinaciguat:
    Activates guanylate cyclase ➡️ increases cGMP ➡️ vasodilation
  2. Serelaxin:
    Relaxin analogue ➡️ vasodilation
61
Q

Recent drugs for decreased cardiac contraction for acute CHF

A
  1. Omecamtiv mecarbil:
    Selective myosin stimulator which does not increase O2 demand
  2. Istaroxime:
    Mechanism: Na+/K+ ATPase inhibitor and Ca+2 ATPase stimulator
62
Q

Pathophysiology of decompensated CHF

A

Chronic CHF
➡️ gradual decrease in cardiac output
➡️ decreased O2 supply
➡️ body activated compensatory mechanism ➡️ fails
➡️ presentation and treatment same as acute CHF
Both of these together of called AHFS Acute Heart Failure Syndrome

63
Q

Pathophysiology of (compensated) chronic CHF

A 
Compensation succeeds 
➡️ increased catecholamines ➡️:
1. Heart: contraction and HR increases
2. Blood vessel: vasoconstriction
3. Liver: stimulates renin: RAAS
 vasoconstriction, Na+/ H2O retention
➡️ cardiac remodeling (myocardial cells increase in size)
➡️ increased O2 demand (proportional to decrease in O2 supply)
➡️ mortality
64
Q 
Treatment of (compensated) chronic CHF
SHIBA
A

To decrease mortality, block cardiac remodeling by blocking catecholamine actions
1. Heart:
β blockers decrease contraction
Ivabradine decreases HR
2. Blood vessels: isosorbide dinitrate + hydralazine for vasodilation
3. RAAS: ACEi/ARB, spironolactone decreases Na+/H2O retention
If symptomatic, digoxin (does not decrease mortality)

65
Q

Mechanism of natriuretic peptides

A

Increase in blood volume ➡️ increase stretch in renal blood vessel, atrium, ventricles ➡️ release of urodilatin, ANP and BNP respectively
Kidney: natriuresis and diuresis
Blood vessel: vasodilation
➡️ Increase blood flow to kidney, heart

66
Q

Examples of natriuretic peptide analogues

A

Urodilatin: ularitide
ANP: carperitide
BNP: nesiritide (FDA approved)
Decrease blood flow to kidney, heart ➡️ decreases pulmonary oedema

67
Q

Nesiritide

A 
BNP analogue
OV route
Use: acute CHF (decreases pulmonary oedema)
S/E: M/C hypotension
Metabolised by neutral endopeptidase
68
Q

Sacubitril

A 
Blocks neutral endopeptidase (metabolises nesiritide)
Use: chronic CHF
 Used along with Valsartan 
S/E: angioedema
CI: with ACEi
 Within 36 hrs of use of ACEi
69
Q

PDE-3 inhibitors

A

Blocks metabolism of cAMP in heart and blood vessels ➡️
Increased cardiac contraction and vasodilation ➡️ inodilators
Eg., inamrinone (not preferred because of thrombocytopenia), milrinone, enoximone, levosimendan

70
Q

Milrinone, enoximone

A 
PDE-3 inhibitors
Use:
1. Resistant left sided heart failure 
2. DoC for right heart failure
3. Patient of CHF in β blocker
71
Q

Levosimendan

A 
Mechanism:
1. PDE-3 inhibitor
2. Opens K+ channel ➡️ vasodilation
3. Sensitises myocardium to calcium ions
Uses:
In case of ineffectiveness of other drugs to acute CHF
72
Q

Drug regimen followed in chronic CHF for primary set of drugs

A 
1. ACEi/ARB:
• started at low doses
• doses increased weekly till max
If well tolerated ➡️
2. Switch to Sacubutril + Valsartan:
3. β blockers:
• at midway of ACEi/ARB dose increase
• started at low doses 
• doses increased every 2 weeks till max
73
Q

Drug regimen when primary set of drugs against chronic CHF is not effective

A 
4. Add spironolactone
 If not responding
5. Add Ivabradine 
 If not responding
6. Add Isosorbide dinitrate + hydralazine
If symptomatic add digoxin
74
Q

Why ACEi/ ARB and β blockers are started at low doses in chronic CHF

A

ACEi/ARB are started at low doses to decrease the risk of postural hypotension in patients already having high renin levels

β blockers are started at low doses and increased gradually to prevent decompensation

75
Q

Digoxin basic features

A 
Sources: Digitalis lanata (white foxglove)
• Good oral absorption
• High distribution so high loading dose
• t1/2 of 36-48 hrs
Digitalisation:
 Steady level of digitalis takes 7-10 days
• Renal elimination
Mechanism: cellular and organ level
76
Q

Extracellular mechanisms of digoxin action

A

Blocks Na+/K+ ATPase pump (reverse depolarisation) ➡️ decrease in:
1. Na+ efflux ➡️ increased intracellular Na+
2. K+ influx ➡️ increased extracellular K+ ➡️ hyperkalemia
Hyperkalemia inhibits digoxin (K+ binds to Na+/K+ ATPase)

77
Q

Why are patients on diuretics not preferred digoxin

A

For these patients, there is hypokalemia ➡️
inhibition of digoxin by K+ is reduced ➡️
Digoxin toxicity

78
Q

Intracellular mechanism of digoxin

A

Increased intracellular Na+ blocks Na+/Ca2+ exchanger pump ➡️ Ca2+ efflux reduced ➡️ Intracellular Ca increases ➡️ Increased contraction ➡️ extra depolarisation called DAD Delayed After Depolarisation ➡️ Further increase in Ca2+ ➡️ extra systole

Pharmacology MBBS (19 decks)

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