NEET PG Cardiovascular Pharmacology Glossary 2026: Antihypertensives, Antiarrhythmics, Anti-Anginals and Heart Failure Drugs

You are staring at 47 cardiovascular drugs. The NEET PG paper has 200 questions, and 8-10 of them will be pure CVS pharmacology — antihypertensives, antiarrhythmics, heart failure drugs, and anti-anginals. You need mechanisms, side effects, contraindications, and drug interactions memorized cold.

This isnt another textbook chapter. Its a high-yield reference glossary built specifically for NEET PG 2026 and INICET — every drug mechanism explained in 2-3 lines, every side effect pattern condensed into mnemonics, every MCQ trap highlighted upfront. Cardiology accounts for 15-18% of your NEET PG score. Get the pharmacology right, and you have scored 30-35 marks before touching pathology or medicine.

The four major CVS drug classes — antihypertensives (ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, diuretics), antiarrhythmics (Vaughan Williams Class I-IV), anti-anginals (nitrates, ranolazine, ivabradine), and heart failure drugs (digoxin, sacubitril-valsartan, aldosterone antagonists) — represent your highest-yield pharmacology topics. Master these 47 drugs and their 200+ testable facts, and cardiovascular pharmacology becomes your strength, not your weakness.

Antihypertensive Drugs: The Big Five Categories

ACE Inhibitors (The "-pril" Family)

Core Mechanism: Block angiotensin-converting enzyme → ↓ angiotensin II → ↓ aldosterone → vasodilation + ↓ sodium retention. Key Drugs: Lisinopril, enalapril, captopril, ramipril, perindopril High-Yield Facts:

• Captopril: First ACE inhibitor, shortest half-life (8 hours), contains sulfhydryl group

• Lisinopril: Longest half-life (24 hours), doesnt require hepatic activation

• Enalapril: Prodrug, requires conversion to enalaprilat

Side Effects Mnemonic - "ACE CHOP":

• Angioedema (0.1-0.5%, higher in blacks)

• Cough (dry, nonproductive, 10-15%)

• Elevated potassium (hyperkalemia)

• Creatinine rise (reversible azotemia)

• Hypotension (first-dose effect)

• Oliguria (in bilateral renal artery stenosis)

• Pregnancy contraindicated (teratogenic)

MCQ Traps:

• Angioedema is NOT dose-dependent and can occur years after starting therapy

• ACE inhibitors are protective in diabetic nephropathy even without hypertension

• Contraindicated in bilateral renal artery stenosis (causes acute kidney injury)

For deeper understanding of ACE inhibitor mechanisms and clinical applications, explore NEET PG cardiovascular pharmacology lessons.

Angiotensin Receptor Blockers (ARBs - The "-sartan" Family)

Core Mechanism: Block angiotensin II at AT1 receptors → same effects as ACE inhibitors but no bradykinin accumulation. Key Drugs: Losartan, valsartan, telmisartan, olmesartan, irbesartan High-Yield Facts:

• Losartan: Active metabolite E-3174, also blocks uric acid reabsorption

• Telmisartan: Longest half-life (24 hours), PPAR-γ agonist activity

• Valsartan: Component of sacubitril-valsartan (Entresto)

Side Effects: Similar to ACE inhibitors BUT NO COUGH, NO ANGIOEDEMA Clinical Pearl: ARBs are first choice when ACE inhibitors cause cough (10% of patients). When drilling cardiovascular pharmacology MCQs, Oncourse's adaptive question bank automatically increases ARB mechanism questions if you miss them repeatedly, closing gaps faster than random revision.

Beta-Blockers: Selective vs Non-Selective

Core Mechanism: Block β-adrenergic receptors → ↓ heart rate + ↓ contractility + ↓ renin release.

#### Non-Selective Beta-Blockers (β1 + β2)
Drugs: Propranolol, nadolol, timolol

• Propranolol: Prototype, lipophilic, crosses BBB, has membrane-stabilizing activity

• Nadolol: Hydrophilic, long half-life, no hepatic metabolism

#### Cardioselective Beta-Blockers (β1 > β2)
Drugs: Metoprolol, atenolol, bisoprolol, nebivolol

• Atenolol: Hydrophilic, renal elimination

• Metoprolol: Lipophilic, hepatic metabolism

• Nebivolol: Additional NO-mediated vasodilation

#### Beta-Blockers with α-Blocking Activity
Drugs: Labetalol (α1 + β), carvedilol (α1 + β + antioxidant)

Side Effects Mnemonic - "BETA BLOCK":

• Bronchospasm (avoid in asthma)

• Erectile dysfunction

• Tiredness/fatigue

• AV conduction blocks

• Bradycardia

• Lipid profile worsening (↑ TG, ↓ HDL)

• Overall mask hypoglycemia symptoms

• Cold extremities

• Kontraindicated in cocaine toxicity (unopposed α-stimulation)

MCQ Traps:

• ISA (Intrinsic Sympathomimetic Activity): Pindolol, acebutolol — less bradycardia, less lipid changes

• Beta-blockers without ISA preferred post-MI for mortality benefit

Calcium Channel Blockers: Three Distinct Classes

Core Mechanism: Block L-type calcium channels → vasodilation and/or ↓ cardiac contractility/conduction.

#### Dihydropyridines (The "-pine" Family)
Drugs: Nifedipine, amlodipine, felodipine, nicardipine

• Mechanism: Selective vascular calcium channel blockade

• Effects: Peripheral vasodilation, no cardiac depression

• Amlodipine: Longest half-life (30-50 hours), least negative inotropic effect

#### Non-Dihydropyridines
Verapamil (Phenylalkylamine):

• Negative inotrope + negative chronotrope + negative dromotrope

• Constipation (most common side effect)

• Strong CYP3A4 inhibitor

Diltiazem (Benzothiazepine):

• Intermediate between verapamil and dihydropyridines

• Less constipation than verapamil

• Less peripheral edema than dihydropyridines

Side Effects by Class:

• Dihydropyridines: Peripheral edema (not heart failure), flushing, reflex tachycardia

• Verapamil: Constipation (most common), AV block, negative inotropy

• Diltiazem: AV block, negative inotropy (less than verapamil)

The "ABCD" mnemonic for heart failure drugs (ACE inhibitors, Beta-blockers, CCBs avoided, Diuretics) has visual mnemonics available in Oncourse flashcard decks — students can move from reading this glossary to active recall in one tap.

Diuretics in Hypertension

#### Thiazide and Thiazide-Like Diuretics
Drugs: Hydrochlorothiazide (HCTZ), chlorthalidone, indapamide
Mechanism: Block Na-Cl cotransporter in distal convoluted tubule

Chlorthalidone vs HCTZ:

• Chlorthalidone: Longer half-life (24-72 hours), better cardiovascular outcomes in trials

• HCTZ: Shorter half-life (6-12 hours), more commonly used

Side Effects - "THIAZIDE HIT":

• Thrombocytopenia

• Hyponatremia

• Impotence

• Alkalosis (metabolic)

• Zinc deficiency (rare)

• Increased glucose

• Decreased potassium

• Elevated uric acid

• Hypercalcemia

• Increased cholesterol

• Tinnitus (high doses)

#### Loop Diuretics in HTN

Limited Role: Only in hypertension with fluid overload Drug: Furosemide Major Concern: Ototoxicity (especially with aminoglycosides)

Antiarrhythmic Drugs: Vaughan Williams Classification

Class I: Sodium Channel Blockers

Core Mechanism: Block fast Na+ channels → ↓ phase 0 depolarization → ↓ conduction velocity.

#### Class IA: Intermediate Kinetics
Drugs: Quinidine, procainamide, disopyramide

• Quinidine: Prototype, antimalarial activity, cinchonism

• Procainamide: Lupus-like syndrome (slow acetylators), NAPA metabolite

• Disopyramide: Strong negative inotrope, anticholinergic effects

Effects: ↓ conduction velocity, ↑ refractory period, ↓ contractility

#### Class IB: Fast Kinetics
Drugs: Lidocaine, mexiletine, phenytoin

• Lidocaine: IV only, hepatic metabolism, CNS toxicity

• Mexiletine: Oral lidocaine analog

• Phenytoin: Antiepileptic with antiarrhythmic properties

Effects: Minimal effect on normal tissue, preferentially blocks ischemic/depolarized cells

#### Class IC: Slow Kinetics
Drugs: Flecainide, propafenone

• Flecainide: Most potent Na+ channel blocker, avoid in structural heart disease

• Propafenone: Weak β-blocking activity

CAST Study Warning: Class IC drugs increase mortality in post-MI patients with structural heart disease.

Class II: Beta-Blockers

Mechanism: Block β1 receptors → ↓ SA node firing, ↓ AV conduction, ↓ contractility Key Drugs: Propranolol, metoprolol, esmolol Esmolol: Ultra-short acting (half-life 9 minutes), IV only, metabolized by RBC esterases

Class III: Potassium Channel Blockers

Core Mechanism: Block K+ channels → ↑ action potential duration → ↑ refractory period. Amiodarone:

• Unique Properties: Contains iodine (37% by weight), affects all four Vaughan Williams classes

• Tissue Accumulation: Half-life 20-100 days, takes months to reach steady state

• Side Effects: Pulmonary fibrosis (most serious), thyroid dysfunction, hepatotoxicity, corneal deposits, blue-gray skin

Dronedarone:

• "Safer Amiodarone": No iodine, shorter half-life

• Major Limitation: Contraindicated in permanent AF and heart failure

Sotalol:

• Dual Action: β-blocker + Class III activity

• Torsades Risk: Dose-related, worse in hypokalemia

Ibutilide & Dofetilide:

• Use: Acute AF/flutter conversion

• Risk: High torsades potential, requires inpatient monitoring

Class IV: Calcium Channel Blockers

Drugs: Verapamil, diltiazem Mechanism: Block L-type Ca2+ channels → ↓ SA node automaticity, ↓ AV conduction Use: Supraventricular arrhythmias (NOT ventricular) Drug-Drug Interaction Pearl: Verapamil + digoxin = doubled digoxin levels.

CVS pharmacology is flagged as a high-priority topic cluster in Oncourse's High-Yield Topic Tracker — it shows exactly how many CVS pharma questions you have attempted, your accuracy trend, and recommends your next study path (e.g., antiarrhythmics → ECG interpretation → related clinical scenarios).

Anti-Anginal Agents

Nitrates: NO Donors

Core Mechanism: Release nitric oxide → cGMP ↑ → smooth muscle relaxation → venous > arterial dilation. Nitroglycerin (GTN):

• Routes: Sublingual, IV, transdermal patches, oral sustained-release

• Onset: Sublingual 1-3 minutes, patch 30-60 minutes

• Duration: Sublingual 10-30 minutes, patch 8-12 hours

Isosorbide Dinitrate (ISDN):

• Bioavailability: 25% (extensive first-pass metabolism)

• Duration: 4-6 hours

• Active Metabolites: Isosorbide-2-mononitrate, isosorbide-5-mononitrate

Isosorbide Mononitrate (ISMN):

• Advantage: 100% bioavailability (no first-pass metabolism)

• Duration: 6-8 hours

• Dosing: Asymmetric (8 AM, 2 PM) to prevent tolerance

Side Effects:

• Headache: Most common, related to cerebral vasodilation

• Hypotension: Especially orthostatic

• Reflex Tachycardia: Compensatory response

• Methemoglobinemia: Rare, with high doses

Tolerance: Develops within 24-48 hours of continuous exposure Prevention: Nitrate-free interval (10-12 hours daily)

Ranolazine: Late Sodium Channel Blocker

Mechanism: Selective inhibition of late INa → ↓ intracellular Na+ → ↓ Ca2+ overload → ↓ diastolic tension. Clinical Use: Chronic stable angina when first-line therapy inadequate Unique Feature: Anti-anginal without affecting heart rate or blood pressure Major Drug Interaction: CYP3A4 substrate, levels doubled by ketoconazole QT Prolongation: Dose-related, but rarely causes torsades

Ivabradine: If Channel Blocker

Mechanism: Selective If channel blockade in SA node → ↓ heart rate WITHOUT affecting contractility. Clinical Uses:

• Chronic stable angina (when β-blockers contraindicated)

• Heart failure with reduced ejection fraction (EF ≤35%) + sinus rhythm + HR ≥70 bpm

Side Effects: Luminous phenomena (phosphenes) — 15% of patients report visual brightness Contraindications: Atrial fibrillation (no effect on irregularly irregular rhythm)

Heart Failure Drugs

ACE Inhibitors and ARBs in Heart Failure

Mortality Benefit: Both classes reduce mortality in heart failure with reduced ejection fraction (HFrEF). Target Doses:

• Lisinopril: 20-40 mg daily

• Enalapril: 10-20 mg twice daily

• Losartan: 50-150 mg daily

Beta-Blockers in Heart Failure

Evidence-Based Choices: Only three β-blockers have proven mortality benefit in HFrEF:

• Metoprolol Succinate: Extended-release only

• Carvedilol: α + β blocker

• Bisoprolol: Highly β1-selective

Contraindications in Acute HF: Never start β-blockers during acute decompensated heart failure.

Aldosterone Receptor Antagonists

Spironolactone:

• Mortality Benefit: RALES trial, severe heart failure

• Side Effects: Gynecomastia (dose-related), hyperkalemia

• Monitoring: Potassium and creatinine at 1 week, 1 month, 3 months

Eplerenone:

• Advantages: No gynecomastia, more selective for mineralocorticoid receptor

• Cost: Significantly more expensive than spironolactone

• Evidence: EMPHASIS-HF trial, mild-moderate heart failure

Digoxin: The Cardiac Glycoside

Mechanism:

• Positive Inotrope: Na+/K+-ATPase inhibition → ↑ intracellular Ca2+

• Negative Chronotrope: Enhanced vagal tone → ↓ SA node firing + ↓ AV conduction

Pharmacokinetics:

• Half-Life: 36 hours (normal kidney function)

• Elimination: 85% renal, 15% hepatic

• Loading Dose: 8-12 mcg/kg (lean body weight)

Therapeutic Range: 0.5-2.0 ng/mL (some prefer 0.5-1.0 ng/mL for heart failure) Digoxin Toxicity Signs:

• Early: Nausea, vomiting, anorexia, visual disturbances (yellow halos)

• Cardiac: Any arrhythmia except rapid AF, bidirectional VT (pathognomonic)

• Treatment: Digoxin-specific antibodies (Digibind), correct electrolytes

Drug Interactions:

• ↑ Digoxin Levels: Amiodarone, verapamil, quinidine, erythromycin

• ↓ Digoxin Levels: Cholestyramine, sucralfate, antacids

Sacubitril-Valsartan (ARNI)

Mechanism:

• Sacubitril: Neprilysin inhibitor → ↑ natriuretic peptides (ANP, BNP)

• Valsartan: ARB component

Evidence: PARADIGM-HF trial showed 20% reduction in cardiovascular death vs enalapril Washout Period: Stop ACE inhibitors 36 hours before starting (angioedema risk) Contraindications: History of angioedema with ACE inhibitors/ARBs

Newer Heart Failure Therapies

SGLT2 Inhibitors in Heart Failure:

• Mechanism: Sodium-glucose cotransporter 2 inhibition

• Benefits: Reduce heart failure hospitalizations even in non-diabetics

• Key Drugs: Dapagliflozin, empagliflozin

• Side Effects: Genital fungal infections, DKA risk

Ivabradine in Heart Failure:

• Indication: HFrEF with EF ≤35%, sinus rhythm, HR ≥70 bpm despite optimal β-blocker

• Benefit: Reduces heart failure hospitalizations

• Contraindications: Atrial fibrillation, severe hepatic impairment

Quick Reference Drug Tables

High-Yield MCQ Patterns and Traps

Antihypertensive MCQ Traps

1. "Best initial therapy for diabetic with hypertension" → ACE inhibitor (renal protection) 2. "Hypertension with asthma" → Avoid β-blockers (even cardioselective) 3. "Bilateral renal artery stenosis" → Avoid ACE inhibitors and ARBs 4. "African American with hypertension" → Thiazides or CCBs (ACE inhibitors less effective)

Antiarrhythmic MCQ Traps

1. "Post-MI patient with VT" → Avoid Class IC drugs (CAST study) 2. "Amiodarone + warfarin" → Monitor INR closely (amiodarone inhibits warfarin metabolism) 3. "WPW with AF" → Avoid digoxin, verapamil, diltiazem (can facilitate conduction down accessory pathway) 4. "Torsades de pointes treatment" → IV magnesium + correct electrolytes

Heart Failure MCQ Traps

1. "Acute decompensated heart failure" → Never start β-blockers 2. "Digoxin toxicity with normal levels" → Check potassium (hypokalemia increases toxicity) 3. "Best mortality benefit in heart failure" → ACE inhibitors (not digoxin) 4. "Spironolactone monitoring" → Potassium and creatinine (hyperkalemia risk)

Contraindications Quick Reference

Absolute Contraindications

ACE Inhibitors/ARBs:

• Bilateral renal artery stenosis

• Pregnancy

• History of angioedema

Beta-Blockers:

• Severe asthma/COPD

• 2nd/3rd degree AV block (without pacemaker)

• Cardiogenic shock

Calcium Channel Blockers:

• Verapamil/Diltiazem: Severe heart failure, 2nd/3rd degree AV block

• Dihydropyridines: Severe aortic stenosis

Digoxin:

• 2nd/3rd degree AV block

• Ventricular tachycardia/fibrillation

• Hypertrophic cardiomyopathy with outflow obstruction

Pharmacology mastery comes from pattern recognition. Use Synapses visual mnemonics to lock in drug mechanisms — the "ABCD" heart failure drugs, the "ACE CHOP" side effects, and Vaughan Williams classifications become automatic recall, not forced memorization.

Drug Interactions: High-Yield for NEET PG

CYP450 Interactions

Strong CYP3A4 Inhibitors: Amiodarone, verapamil, diltiazem

• Effect: Increase levels of: simvastatin, digoxin, warfarin

P-glycoprotein Interactions:

• Inhibitors: Amiodarone, verapamil, quinidine

• Substrate: Digoxin

• Result: Increased digoxin toxicity risk

Clinically Significant Combinations

1. Amiodarone + Warfarin → ↑ INR (inhibits warfarin metabolism) 2. Verapamil + Digoxin → ↑ digoxin levels (P-gp inhibition) 3. ACE Inhibitor + K+-sparing Diuretic → Hyperkalemia risk 4. β-blocker + Verapamil/Diltiazem → Severe bradycardia/AV block

Electrolyte-Drug Interactions

• Hypokalemia → ↑ digoxin toxicity, ↑ QT prolongation with Class III drugs

• Hypomagnesemia → ↑ torsades risk with any QT-prolonging drug

• Hypercalcemia → ↑ digoxin toxicity

Frequently Asked Questions

Which antihypertensive is best for diabetic nephropathy?

ACE inhibitors or ARBs provide renal protection independent of blood pressure lowering. They reduce proteinuria and slow progression to end-stage renal disease. Start with ACE inhibitor; switch to ARB if cough develops.

Why is amiodarone contraindicated in pregnancy?

Amiodarone contains 37% iodine by weight, which can cause fetal thyroid dysfunction, growth retardation, and developmental abnormalities. The drug accumulates in fetal tissues and has a very long elimination half-life.

When should you avoid beta-blockers in heart failure?

Never start β-blockers during acute decompensated heart failure. Only initiate when patient is stable and euvolemic. Start low (e.g., carvedilol 3.125 mg twice daily) and titrate slowly over weeks to months.

What makes Class IC antiarrhythmics dangerous post-MI?

The CAST study showed increased mortality with flecainide and encainide in post-MI patients. These drugs have slow dissociation kinetics from sodium channels, creating proarrhythmic effects especially in ischemic myocardium.

How do you differentiate digoxin toxicity from heart failure symptoms?

Digoxin toxicity presents with GI symptoms (nausea, vomiting, anorexia) and visual disturbances (yellow/green halos) before cardiac manifestations. Heart failure typically causes dyspnea and edema without GI or visual symptoms.

Why is there a washout period before starting sacubitril-valsartan?

Both ACE inhibitors and neprilysin inhibition can increase bradykinin levels. Concurrent use significantly increases angioedema risk. The 36-hour washout allows ACE inhibitor levels to decline before starting the combination therapy.

Master Your CVS Pharmacology

You now have 47 cardiovascular drugs mapped with mechanisms, side effects, contraindications, and MCQ traps. The NEET PG 2026 cardiovascular pharmacology questions are testing pattern recognition — can you spot the hypokalemic patient with digoxin toxicity, the asthmatic who needs CCBs instead of β-blockers, or the post-MI patient who shouldnt get Class IC drugs?

Focus your next 2-3 study sessions on drug interactions and contraindications. These account for 40% of cardiovascular pharmacology MCQs but are often overlooked during mechanism memorization.

Practice with targeted MCQs to drill these patterns. Convert your reading knowledge into exam performance through active recall and spaced repetition. The difference between knowing enalapril is an ACE inhibitor and recognizing why it shouldnt be given to a patient with bilateral renal artery stenosis is what separates average scores from top percentile ranks.

Prepare smarter with Oncourse AI — adaptive MCQs, spaced repetition, and AI explanations built for NEET PG. Download free on Android and iOS.