# Antiarrhythmics and Lipid-Lowering Drugs for NEET PG Pharmacology: Atrial Fibrillation (ICMR 2026), Adenosine, Amiodarone, Statins

Source: https://tracknation.in/story/antiarrhythmics-and-lipid-lowering-drugs-for-neet-pg-pharmacology-atrial-fibrillation-icmr-2026-adenosine-amiodarone-statins (TrackNation — free UPSC notes with PYQs)

> NEET PG Pharmacology: atrial fibrillation under India's ICMR 2026 workflow (rate target, CHA2DS2-VASc, DOAC vs warfarin, rhythm-control choice), adenosine for PSVT, amiodarone toxicity, flecainide and the CAST trial, sotalol and QT, procainamide lupus, digoxin toxicity and interactions, statins, ezetimibe, fibrates and PCSK9 inhibitors, with a diagram, hooks, vignette MCQs and cards.

## Start Here

🎯 **Exam priority: High.** *Expect: a narrow-complex tachycardia given adenosine, amiodarone side effects, AF
anticoagulation, digoxin toxicity with hypokalaemia, and statin myopathy.*

CBME mapping: **PH 4.6–4.7**. Atrial fibrillation follows India's **ICMR workflow (January 2026)**.

## Atrial Fibrillation (ICMR 2026)

*Atrial fibrillation decisions per the ICMR Standard Treatment Workflow (January 2026). Drawn by TrackNation.*

- Signs: irregularly irregular pulse. Types: paroxysmal (< 7 days), persistent (7 days–1 year), long-standing persistent
(> 1 year), permanent.

- **Rate control** (target < 110/min): metoprolol, diltiazem or verapamil if no heart failure; beta-blocker + digoxin in heart
failure.

- **Stroke prevention**: anticoagulate if **CHA2DS2-VASc > 1** (age > 75 and prior stroke/TIA score 2 each).
Prefer a **DOAC**; warfarin (INR 2–3) only for severe mitral stenosis or a metallic valve. HAS-BLED > 3 = high bleeding risk.

- **Rhythm control**: unstable → immediate cardioversion after heparin. Long term: flecainide or propafenone with a normal
heart (flecainide also as a single "pill in the pocket" dose); amiodarone in heart failure; amiodarone or sotalol with CAD or LVH.

## Antiarrhythmic Drugs

| **Drug**

 | **Use (label / ICMR)**

 | **Key toxicity or rule (label)**

 |
| Adenosine

 | Converts PSVT (including WPW-related)

 | Rapid IV bolus; half-life < 10 s; blocked by caffeine and theophylline, potentiated by dipyridamole

 |
| Amiodarone

 | Life-threatening arrhythmias only; AF rhythm control in heart failure, CAD, LVH (ICMR)

 | Boxed: pulmonary, hepatic, cardiac toxicity; thyroid (hypo or hyper); corneal deposits, optic neuropathy; half-life 15–142 days

 |
| Flecainide

 | SVT prevention without structural heart disease; AF 'pill in the pocket' (ICMR)

 | CAST trial: excess mortality after MI

 |
| Sotalol

 | AF rhythm control (ICMR)

 | Boxed proarrhythmia; reduce or stop if QT ≥ 500 ms; dose by creatinine clearance

 |
| Procainamide

 | —

 | Lupus-like syndrome; positive ANA

 |
| Diltiazem IV

 | Rate control in AF or flutter; converts PSVT

 | —

 |
| Digoxin

 | Rate control with a beta-blocker in heart failure (ICMR)

 | Toxicity: nausea, vomiting, visual disturbance, arrhythmias; worse with low K or Mg, high Ca, renal failure, old age; antidote digoxin immune Fab

 |

**Children (ICMR paediatric tachyarrhythmia workflow)**: adenosine 100–200 mcg/kg by rapid IV push followed at once by a 5–10 mL
saline flush, recording the ECG.

Digoxin levels rise with quinidine and amiodarone (measure digoxin first; with amiodarone cut the digoxin dose by about 15–30%); digoxin is not recommended in acute MI.

## Lipid-Lowering Drugs

| **Drug**

 | **Action (label)**

 | **Key point**

 |
| Statins (atorvastatin, rosuvastatin)

 | HMG-CoA reductase inhibitors

 | Myopathy and rhabdomyolysis (age ≥ 65, hypothyroidism, renal impairment, interacting drugs, high dose); rosuvastatin starts at 5 mg in Asian patients; ICMR high-intensity: atorvastatin 40–80 or rosuvastatin 20–40 mg

 |
| Ezetimibe

 | Blocks intestinal cholesterol absorption via NPC1L1

 | Added to statins

 |
| Fenofibrate

 | Lowers triglycerides

 | Severe hypertriglyceridaemia (≥ 500 mg/dL)

 |
| Evolocumab

 | PCSK9 inhibitor (injection)

 | Reduces major cardiovascular events

 |

## Traps the Examiner Sets

- Adenosine needs a fast push and flush (half-life < 10 s); theophylline blocks it, dipyridamole boosts it.

- Amiodarone: lungs, liver, thyroid (both ways), eyes, skin — and it lasts for weeks after stopping.

- Flecainide is avoided after MI or with structural heart disease (CAST).

- AF rate target is < 110/min; DOAC first; warfarin only for severe MS or metallic valve.

- Digoxin toxicity is worse with hypokalaemia; antidote is digoxin immune Fab.

- Statin myopathy: stop if CK is markedly raised.

## Memory Hooks & Shortcuts

*Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.*

- 🧠 **Adenosine: Ten seconds, Theophylline stops it** — half-life < 10 s; methylxanthines antagonise

- 🧠 **Amiodarone's PFT-LET (Pulmonary, Function of Thyroid, Liver, Eyes, Toxicity lasts)** — lung, thyroid, liver, eye toxicity; very long half-life

- 🧠 **Flecainide Fails after infarction** — CAST: excess deaths after MI

- 🧠 **AF: 110, score 2, DOAC first** — rate < 110; anticoagulate if CHA2DS2-VASc > 1; DOAC preferred

- 🧠 **Low K, high toxicity** — hypokalaemia predisposes to digoxin toxicity

- 🧠 **Statins Strain the muscles** — myopathy and rhabdomyolysis

## Rapid-Revision Cards

- < 110/min.

- Metoprolol, diltiazem, verapamil (no HF); BB + digoxin in HF.

- CHA2DS2-VASc > 1; DOAC preferred.

- Only severe MS or metallic valve; INR 2–3.

- > 3 = high bleeding risk.

- Immediate cardioversion after heparin.

- Normal heart flecainide/propafenone; HF amiodarone.

- PSVT; rapid bolus; t½ < 10 s.

- Blocked by theophylline/caffeine; boosted by dipyridamole.

- 100–200 mcg/kg push + 5–10 mL flush.

- Pulmonary, hepatic, cardiac toxicity.

- Thyroid (both), corneal deposits, optic neuropathy; t½ 15–142 days.

- No structural heart disease; CAST excess deaths after MI.

- Proarrhythmia; act if QT ≥ 500 ms; dose by CrCl.

- Lupus-like; ANA.

- Nausea, vomiting, yellow-green vision, arrhythmias (bigeminy).

- Low K, low Mg, high Ca, renal failure, old age.

- Digoxin immune Fab.

- Amiodarone: cut digoxin 15–30%; quinidine: 30–50%.

- HMG-CoA reductase inhibitors; myopathy risk factors.

- Start 5 mg.

- Atorvastatin 40–80 or rosuvastatin 20–40.

- NPC1L1; blocks cholesterol absorption.

- TG ≥ 500 mg/dL.

- PCSK9 inhibitor.

## Sources

*Facts in this article were checked against these documents.*

- Standard Treatment Workflow: Atrial Fibrillation — Indian Council of Medical Research / Department of Health Research, MoHFW, January 2026

- Standard Treatment Workflow: Tachyarrhythmia (paediatric) — Indian Council of Medical Research, MoHFW, July 2024

- Prescribing labels: amiodarone, adenosine, flecainide, sotalol, procainamide, diltiazem injection, Lanoxin, Lipitor, Crestor, Zetia, fenofibrate, Repatha — DailyMed, US National Library of Medicine, current labels, accessed November 2026 (link)

- Competency Based Undergraduate Curriculum, Pharmacology (PH 4.6–4.7) — National Medical Commission, 2024

## Test Yourself: Practice Questions

Twenty-four questions in NEET PG style, most of them clinical vignettes.

## Practice Questions (NEET PG pattern)

*Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer
was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.*

**Q1.** A 28-year-old has a regular narrow-complex tachycardia at 190/min with stable BP; vagal manoeuvres fail. The drug of choice is

- (a) atropine

- (b) digoxin orally

- (c) amiodarone infusion

- (d) adenosine by rapid IV bolus

**Answer: (d)** — Adenosine converts PSVT (including WPW-related) to sinus rhythm; it must be given as a rapid bolus.

**Q2.** Adenosine must be pushed fast and flushed because

- (a) it binds plasma proteins

- (b) it is a prodrug

- (c) it is irritant to veins

- (d) its half-life in blood is less than 10 seconds

**Answer: (d)** — Cleared by cellular uptake with a half-life < 10 seconds.

**Q3.** A patient on theophylline for COPD gets usual-dose adenosine for PSVT without effect. The reason is

- (a) adenosine is renally cleared

- (b) COPD blocks adenosine receptors

- (c) theophylline competitively antagonises adenosine

- (d) theophylline induces adenosine metabolism

**Answer: (c)** — Methylxanthines (caffeine, theophylline) antagonise adenosine; dipyridamole potentiates it.

**Q4.** The ICMR paediatric dose of adenosine is

- (a) 0.01 mg/kg orally

- (b) 100–200 mcg/kg rapid IV push followed by a 5–10 mL saline flush

- (c) 1 mg/kg IM

- (d) 6 mg/kg slow infusion

**Answer: (b)** — ICMR tachyarrhythmia workflow.

**Q5.** A man on amiodarone for 2 years develops dry cough and breathlessness with bilateral infiltrates. Suspect

- (a) ACE-inhibitor cough

- (b) beta-blocker bronchospasm

- (c) amiodarone pulmonary toxicity

- (d) digoxin toxicity

**Answer: (c)** — Boxed warning: pulmonary toxicity (hypersensitivity or interstitial pneumonitis), fatal in about 10% of cases.

**Q6.** A woman on amiodarone becomes tired, cold-intolerant and gains weight. Check

- (a) CK

- (b) ANA

- (c) thyroid function: amiodarone causes hypo- or hyperthyroidism

- (d) serum digoxin

**Answer: (c)** — Thyroid abnormalities (hyper or hypo) are listed warnings.

**Q7.** Amiodarone adverse effects may persist for weeks after stopping because

- (a) it is a prodrug

- (b) its half-life is 15–142 days

- (c) it causes enzyme induction

- (d) it is renally excreted unchanged

**Answer: (b)** — Long half-life of amiodarone and its active metabolite.

**Q8.** A patient on amiodarone reports haloes; slit-lamp shows corneal deposits. These are

- (a) common and reversible

- (b) a sign of imminent blindness

- (c) an indication to start steroids

- (d) due to digoxin

**Answer: (a)** — Corneal microdeposits are common and reversible; optic neuropathy is rare but can cause blindness.

**Q9.** Flecainide is avoided in a man with a past myocardial infarction because

- (a) it is ineffective

- (b) it causes lupus

- (c) the CAST trial showed excess mortality or cardiac arrest

- (d) it causes thyroid disease

**Answer: (c)** — CAST: higher mortality or non-fatal cardiac arrest with flecainide after MI; it is used without structural heart disease.

**Q10.** On sotalol, a patient's QT interval reaches 520 ms. The label advises

- (a) reduce the dose, lengthen the interval or stop the drug

- (b) add amiodarone

- (c) double the dose

- (d) ignore unless symptomatic

**Answer: (a)** — If QT ≥ 500 ms: reduce dose, lengthen interval or discontinue; dose by creatinine clearance.

**Q11.** Long-term procainamide can produce

- (a) pulmonary fibrosis

- (b) a lupus-like syndrome with positive ANA

- (c) hypothyroidism

- (d) gingival hyperplasia

**Answer: (b)** — Positive ANA with or without lupus-like syndrome.

**Q12.** A 70-year-old with AF, hypertension and diabetes (CHA2DS2-VASc 3) and no valve disease needs stroke prevention. ICMR prefers

- (a) a direct oral anticoagulant

- (b) warfarin in all cases

- (c) no anticoagulation

- (d) aspirin alone

**Answer: (a)** — OAC if score > 1; DOAC preferred; VKA only for severe mitral stenosis or metallic valve.

**Q13.** In AF, the ICMR target heart rate for rate control is

- (a) exactly 80 per minute

- (b) below 60 per minute

- (c) below 150 per minute

- (d) below 110 per minute

**Answer: (d)** — Rate aim < 110/min with a beta-blocker, calcium blocker, or BB + digoxin in heart failure.

**Q14.** A woman with AF has a metallic mitral valve. Her anticoagulant is

- (a) warfarin with INR 2–3

- (b) a DOAC

- (c) aspirin

- (d) clopidogrel

**Answer: (a)** — VKA (warfarin) only if severe MS or metallic valve; aim INR 2–3.

**Q15.** A man with AF and heart failure needs rate control. ICMR suggests

- (a) verapamil

- (b) diltiazem alone

- (c) flecainide

- (d) a beta-blocker plus digoxin

**Answer: (d)** — BB + digoxin in HF; metoprolol, diltiazem or verapamil only if no evidence of CHF.

**Q16.** A patient with AF becomes hypotensive and confused at a rate of 170/min. The management is

- (a) start warfarin and wait

- (b) oral metoprolol and review next week

- (c) immediate cardioversion after heparin

- (d) digoxin orally

**Answer: (c)** — Haemodynamic instability: immediate cardioversion after heparinisation.

**Q17.** For long-term rhythm control in AF with heart failure, ICMR lists

- (a) amiodarone

- (b) digoxin

- (c) propafenone

- (d) flecainide

**Answer: (a)** — CHF: amiodarone; normal heart: flecainide or propafenone.

**Q18.** An elderly woman with heart failure on digoxin and high-dose furosemide develops nausea, yellow-green vision and bigeminy. A key precipitating factor is

- (a) hyperkalaemia

- (b) hypokalaemia

- (c) hypocalcaemia

- (d) hypernatraemia

**Answer: (b)** — Furosemide causes hypokalaemia; hypokalaemia (also hypercalcaemia, hypomagnesaemia, renal impairment, old age) predisposes to digoxin toxicity. Yellow-green vision and bigeminy are classic toxicity signs.

**Q19.** The specific antidote for life-threatening digoxin toxicity is

- (a) naloxone

- (b) digoxin immune Fab

- (c) atropine

- (d) calcium gluconate

**Answer: (b)** — Digoxin Immune Fab (Digibind, DigiFab).

**Q20.** A patient stable on digoxin is started on amiodarone. The label advises

- (a) checking digoxin levels and reducing the digoxin dose

- (b) doubling digoxin

- (c) no change

- (d) stopping amiodarone after 1 day

**Answer: (a)** — Amiodarone raises digoxin levels: measure digoxin first and reduce the dose by about 15–30% (30–50% with quinidine).

**Q21.** A 70-year-old with hypothyroidism on atorvastatin 80 mg develops muscle pain with a very high CK. The label advises

- (a) ignoring it

- (b) stopping the statin

- (c) adding a fibrate

- (d) doubling the dose

**Answer: (b)** — Risk factors include age ≥ 65 and uncontrolled hypothyroidism; discontinue if CK is markedly raised or myopathy suspected.

**Q22.** Rosuvastatin in Asian patients should start at

- (a) 5 mg once daily

- (b) 80 mg once daily

- (c) 40 mg once daily

- (d) 20 mg twice daily

**Answer: (a)** — Crestor label: initiate at 5 mg in Asian patients.

**Q23.** Ezetimibe lowers cholesterol by

- (a) activating PPAR-alpha

- (b) inhibiting HMG-CoA reductase

- (c) blocking intestinal cholesterol absorption via NPC1L1

- (d) inhibiting PCSK9

**Answer: (c)** — Zetia inhibits absorption of cholesterol by the small intestine; target NPC1L1.

**Q24.** A man has triglycerides of 900 mg/dL. A drug indicated specifically to lower such severe hypertriglyceridaemia is

- (a) colestyramine

- (b) fenofibrate

- (c) ezetimibe

- (d) evolocumab

**Answer: (b)** — Fenofibrate: severe hypertriglyceridaemia (TG ≥ 500 mg/dL).

### Active Recall

From memory: outline the ICMR approach to atrial fibrillation (rate target, anticoagulation rule, DOAC vs warfarin, rhythm drug by heart type); give the uses and toxicities of adenosine, amiodarone, flecainide, sotalol, procainamide and digoxin; and compare statins, ezetimibe, fibrates and PCSK9 inhibitors.