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Pharmacology MBBS > Antiarrhythmic Drugs and CHF Rx > Flashcards

Antiarrhythmic Drugs and CHF Rx Flashcards

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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
Mexiletine
``` Ib subclass of antiarrhythmics Oral derivative of lidocaine Uses: 1. Ventricular tachycardia 2. Neuropathic pain (stopping action potentials) 3. Myotonia ```
26
Phenytoin
``` Ib subclass of antiarrhythmics Used for treatment of digoxin indices VT ```
27
Uses of class II anti-arrhythmic drugs
``` 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 ```
28
DoC for rate control of atrial fibrillation/ flutter
β blockers For stable patients: metaprolol For unstable patients: esmolol shortest acting
29
Causes of catecholamine induced arrhythmia
1. Pheochromocytoma 2. Exercise 3. Emotional 4. Anaesthetic agents (halothane, cyclopropane)
30
QT prolongation is caused by | Delay in repolarisation is seen in
Classes Ia and III of antiarrhythmics
31
Class III antiarrhythmic drugs
``` K+ channel blockers Delay in repolarisation Increase QT interval Causes torsades de pointes Maximum: Ibutilide Minimum: Amiodarone QT prolongation is not seen in Vernakant ```
32
Examples of Class III antiarrhythmics
``` S. Sotalol B. Bretylium D. Dofetilide I. Ibutilide V. Vernakant A. Amiodarone ```
33
Amiodarone
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
Uses of Amiodarone
DoC in: 1. VT / VF except those caused by MI or digoxin toxicity (where lidocaine is used 3. Rhythm control in Atrial fibrillation/ flutter (rate control-β blockers)
35
Vernakant
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
Ibutilide
Shortest acting K+ blocker Given IV Use: Rx of acute attack of atrial fibrillation/flutter
37
Bretylium
K+ channel blocker- class III antiarrhythmic Use: Rx of ventricular fibrillation Known as medical defibrillator S/E: hypotension (DoC: Norepinephrine)
38
Sotalol
``` K+ channel blocker Use: Rx of 1. Atrial fibrillation/ flutter 2. Ventricular tachycardia 3. Ventricular fibrillation ```
39
Dofetilide
K+ channel blocker Uses of both Ibutelide and Amiodarone Oral bioavailability: 100%
40
Dronedarone | Uses
``` Amiodarone-iodine = dronedarone Less toxic but less efficacious Do not preferred Uses: 1. Similar to Amiodarone 2. As a substitute to Amiodarone intolerance ```
41
Dronedarone properties
``` 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
Side effects of amiodarone
``` 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
Pulmonary fibrosis seen due to amiodarone
Type II pneumocyte damage | DoC: prednisolone
44
Whorl like pattern of corneal deposits or Vortex keratopathy or Cornea vertecellata is seen in
``` 1. Fabry’s disease Drugs like: 2. Amiodarone (M/C) 3. Chloroquine 4. Chlorpromazine 5. Indomethacin (least common) ```
45
Amiodarone and thyroid
In most areas (euthyroid): Hypothyroidism since excess iodine is inhibitory In iodine deficiency zones: Hyperthyroidism since iodine is available
46
Non DHP calcium channel blockers as antiarrhythmics
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
DHP calcium channel blockers as antiarrhythmics
Vasodilation ➡️ significant reflex tachycardia So never used in arrhythmias Use: stable angina along with β blockers
48
Adenosine as an Class V antiarrhythmic drug | Mechanism of action
``` Adenosine stimulates: 1. A1 receptor: Gi • Inhibits AVN • Bronchoconstriction 2. A2 receptor: Gs Vasodilation ```
49
Adenosine as Class V antiarrhythmic | Pharmacokinetics
Adenosine Rapid IV infusion Rapidly taken up by cellular adenosine uptake protein ➡️ t1/2: 1-5 sec ➡️ shortest acting antiarrhythmic
50
Uses of adenosine as a class V antiarrhythmic
Adenosine 1. DoC: acute attack of SVT/ PVST 2. To control hypotension in surgeries 3. Diagnosis of coronary artery disease
51
Side effects of adenosine
1. Flushing (vasodilation) 2. Dyspnea (bronchoconstriction) Above 2 are M/C 3. Drug interactions with theophylline and dipyridamole
52
Contraindications of adenosine
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
Drug interactions of adenosine
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
MgSO4 as class V antiarrhythmic
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
Long term treatment of QT syndrome
``` 1. Congenital: ToC: pacing using ICD (implantable cardioverter defibrillator), if not DoC: β blocker 2. Acquired: Avoid drugs causing QT prolongation ```
56
Atropine as class V antiarrhythmic
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
Digoxin as class V antiarrhythmic
``` Parasympathomimetic effect Blocks AVN Slow onset of action so not used on acute cases Uses: Long term Rx of SVT/ PVST (chronic CHF) ```
58
Most common pathophysiology of acute CHF
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
Treatment of acute CHF
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
Recent drugs for pulmonary oedema
1. Cinaciguat: Activates guanylate cyclase ➡️ increases cGMP ➡️ vasodilation 2. Serelaxin: Relaxin analogue ➡️ vasodilation
61
Recent drugs for decreased cardiac contraction for acute CHF
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
Pathophysiology of decompensated CHF
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
Pathophysiology of (compensated) chronic CHF
``` 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
``` Treatment of (compensated) chronic CHF SHIBA ```
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
Mechanism of natriuretic peptides
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
Examples of natriuretic peptide analogues
Urodilatin: ularitide ANP: carperitide BNP: nesiritide (FDA approved) Decrease blood flow to kidney, heart ➡️ decreases pulmonary oedema
67
Nesiritide
``` BNP analogue OV route Use: acute CHF (decreases pulmonary oedema) S/E: M/C hypotension Metabolised by neutral endopeptidase ```
68
Sacubitril
``` 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
PDE-3 inhibitors
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
Milrinone, enoximone
``` PDE-3 inhibitors Use: 1. Resistant left sided heart failure 2. DoC for right heart failure 3. Patient of CHF in β blocker ```
71
Levosimendan
``` 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
Drug regimen followed in chronic CHF for primary set of drugs
``` 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
Drug regimen when primary set of drugs against chronic CHF is not effective
``` 4. Add spironolactone If not responding 5. Add Ivabradine If not responding 6. Add Isosorbide dinitrate + hydralazine If symptomatic add digoxin ```
74
Why ACEi/ ARB and β blockers are started at low doses in chronic CHF
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
Digoxin basic features
``` 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
Extracellular mechanisms of digoxin action
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
Why are patients on diuretics not preferred digoxin
For these patients, there is hypokalemia ➡️ inhibition of digoxin by K+ is reduced ➡️ Digoxin toxicity
78
Intracellular mechanism of digoxin
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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