Cvs drugs their classification and moa in a single line

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I have enough from my textbook knowledge to give a comprehensive answer. Here is the complete CVS drug list with classification and MOA in a single line each:

Cardiovascular (CVS) Drugs - Classification & Mechanism of Action

1. ANTIHYPERTENSIVES

Drug	Class	MOA (Single Line)
Atenolol, Metoprolol, Carvedilol	Beta-1 blockers (cardioselective / non-selective)	Block beta-1 adrenergic receptors on the heart -> reduce heart rate, contractility, and renin release.
Amlodipine, Nifedipine, Diltiazem, Verapamil	Calcium channel blockers (dihydropyridines / non-DHP)	Block L-type voltage-gated Ca²⁺ channels in vascular smooth muscle/myocardium -> vasodilation and/or reduced cardiac output.
Enalapril, Ramipril, Lisinopril	ACE Inhibitors	Inhibit angiotensin-converting enzyme -> prevent conversion of Ang I to Ang II -> vasodilation + decreased aldosterone.
Losartan, Valsartan, Candesartan	ARBs (Angiotensin Receptor Blockers)	Selectively block AT1 receptors -> block vasoconstriction and aldosterone secretion caused by Ang II.
Hydralazine	Direct vasodilator	Directly relaxes arteriolar smooth muscle (opens K⁺ channels) -> reduces peripheral vascular resistance.
Minoxidil	Direct vasodilator (K⁺ channel opener)	Opens ATP-sensitive K⁺ channels in vascular smooth muscle -> hyperpolarization -> arteriolar vasodilation.
Sodium nitroprusside	Direct vasodilator	Releases nitric oxide (NO) -> activates guanylyl cyclase -> increases cGMP -> dilates arteries AND veins.
Prazosin, Doxazosin	Alpha-1 blockers	Block post-synaptic alpha-1 adrenergic receptors on arterioles and venules -> vasodilation.
Clonidine, Methyldopa	Central alpha-2 agonists	Stimulate pre-synaptic alpha-2 receptors in the brainstem (NTS) -> reduce sympathetic outflow -> lower BP and HR.
Eplerenone, Spironolactone	Aldosterone antagonists (K⁺-sparing diuretics)	Competitively block mineralocorticoid receptors -> reduce Na⁺ retention and K⁺ excretion -> mild BP lowering.
Hydrochlorothiazide, Chlorthalidone	Thiazide diuretics	Inhibit Na⁺/Cl⁻ co-transporter (NCC) in distal convoluted tubule -> reduce plasma volume -> lower BP.
Furosemide	Loop diuretic	Inhibit NKCC2 co-transporter in thick ascending limb of loop of Henle -> profound diuresis -> reduce preload/BP.
Sacubitril + Valsartan	ARB-Neprilysin inhibitor (ARNI)	Valsartan blocks AT1R; Sacubitril inhibits neprilysin -> raises natriuretic peptides -> promotes natriuresis and vasodilation.

2. ANTIARRHYTHMICS (Vaughan-Williams Classification)

Drug	Class	MOA (Single Line)
Quinidine, Procainamide, Disopyramide	Class IA - Na⁺ channel blockers (intermediate dissociation)	Block fast Na⁺ channels (use-dependent) + K⁺ channels -> slow conduction AND prolong refractory period.
Lidocaine, Mexiletine, Tocainide	Class IB - Na⁺ channel blockers (fast dissociation)	Preferentially block inactivated Na⁺ channels in ischemic tissue -> shorten action potential duration.
Flecainide, Propafenone	Class IC - Na⁺ channel blockers (slow dissociation)	Markedly slow conduction by blocking Na⁺ channels (no effect on repolarization).
Propranolol, Esmolol, Sotalol (partial)	Class II - Beta blockers	Block beta-1 receptors -> decrease SA node automaticity, slow AV conduction, reduce ectopic pacemaker activity.
Amiodarone, Sotalol, Dofetilide, Ibutilide	Class III - K⁺ channel blockers	Block outward K⁺ channels (IKr) -> prolong action potential duration and effective refractory period.
Verapamil, Diltiazem	Class IV - Ca²⁺ channel blockers	Block L-type Ca²⁺ channels in SA/AV node -> slow conduction and automaticity (useful in SVT).
Adenosine	Unclassified	Activates A1 receptors -> increases K⁺ conductance + decreases cAMP -> transient AV block (used in SVT).
Digoxin	Cardiac glycoside	Inhibits Na⁺/K⁺-ATPase -> raises intracellular Ca²⁺ -> positive inotropy + increased vagal tone -> slows AV conduction.
Atropine	Anticholinergic	Blocks muscarinic M2 receptors on the SA/AV node -> increases heart rate (used in bradycardia).

3. ANTI-ANGINAL DRUGS

Drug	Class	MOA (Single Line)
Nitroglycerin, Isosorbide dinitrate	Organic nitrates	Release NO -> activate guanylyl cyclase -> increase cGMP -> venodilation (reduces preload) + coronary vasodilation.
Atenolol, Metoprolol	Beta blockers	Reduce HR and contractility -> decrease myocardial O₂ demand.
Amlodipine	DHP calcium channel blocker	Vasodilate coronary and peripheral arteries -> reduce afterload and increase coronary perfusion.
Ranolazine	Late Na⁺ current inhibitor	Inhibits late inward Na⁺ current -> reduces Na⁺/Ca²⁺ overload in ischemic myocardium -> relieves angina without affecting HR or BP.
Ivabradine	HCN channel (If current) inhibitor	Blocks funny (If) current in SA node -> selectively reduces heart rate without affecting contractility.

4. HEART FAILURE DRUGS

Drug	Class	MOA (Single Line)
Digoxin	Cardiac glycoside	Inhibits Na⁺/K⁺-ATPase -> indirect increase in intracellular Ca²⁺ -> positive inotropy + controls ventricular rate in AF.
Dobutamine	Beta-1 agonist (inotrope)	Stimulates beta-1 receptors -> increases cAMP -> increases Ca²⁺ -> positive inotropic and mild chronotropic effect.
Dopamine	Dopaminergic/adrenergic agonist	Low dose: D1 stimulation -> renal vasodilation; Intermediate: beta-1 -> inotropy; High dose: alpha-1 -> vasoconstriction.
Milrinone	PDE-3 inhibitor (inodilator)	Inhibits phosphodiesterase-3 -> raises intracellular cAMP -> positive inotropy + vasodilation (inodilator).
Furosemide	Loop diuretic	Inhibit NKCC2 -> reduce fluid overload and pulmonary congestion.
Carvedilol, Bisoprolol, Metoprolol succinate	Beta blockers	Block beta-1/beta-2 receptors -> reduce catecholamine-mediated cardiac remodeling in chronic HF.
Spironolactone, Eplerenone	Aldosterone antagonists	Block aldosterone -> reduce cardiac fibrosis, Na⁺ retention, and K⁺ loss -> reduce mortality in HF.
Sacubitril/Valsartan	ARNI	Neprilysin inhibition raises BNP/ANP -> promotes natriuresis + venodilation; AT1 blockade reduces remodeling.
Dapagliflozin, Empagliflozin	SGLT2 inhibitors	Inhibit renal glucose-Na⁺ co-transporter -> osmotic diuresis + natriuresis + reduced cardiac preload/afterload (also HF mortality benefit independent of diabetes).
Levosimendan	Calcium sensitizer	Sensitizes troponin C to Ca²⁺ -> increases contractility without raising intracellular Ca²⁺ + opens K-ATP channels (vasodilation).

5. ANTICOAGULANTS & ANTITHROMBOTICS

Drug	Class	MOA (Single Line)
Heparin (UFH)	Indirect thrombin inhibitor	Binds antithrombin III -> potentiates inhibition of thrombin (IIa) and factor Xa.
Enoxaparin, Dalteparin	LMWH	Bind antithrombin III -> preferentially inhibit factor Xa over thrombin.
Warfarin	Vitamin K antagonist	Inhibit vitamin K epoxide reductase -> reduce synthesis of factors II, VII, IX, X, protein C & S.
Dabigatran	Direct thrombin inhibitor (DTI)	Directly and reversibly inhibit thrombin (factor IIa) -> prevent fibrin formation.
Rivaroxaban, Apixaban, Edoxaban	Direct factor Xa inhibitors	Directly inhibit factor Xa -> block conversion of prothrombin to thrombin.
Aspirin	Antiplatelet (COX inhibitor)	Irreversibly acetylates COX-1 -> blocks TXA₂ synthesis in platelets -> inhibits platelet aggregation.
Clopidogrel, Ticagrelor, Prasugrel	ADP receptor (P2Y12) antagonists	Block platelet P2Y12 ADP receptors -> prevent ADP-induced platelet aggregation (Ticagrelor: reversible; others: irreversible).
Abciximab, Eptifibatide, Tirofiban	GPIIb/IIIa inhibitors	Block the final common platelet aggregation pathway (GPIIb/IIIa receptor) -> prevent fibrinogen binding.
Streptokinase, Alteplase (tPA)	Thrombolytics	Activate plasminogen to plasmin -> plasmin cleaves fibrin clots -> thrombolysis.

6. LIPID-LOWERING DRUGS

Drug	Class	MOA (Single Line)
Atorvastatin, Rosuvastatin, Simvastatin	Statins (HMG-CoA reductase inhibitors)	Inhibit HMG-CoA reductase (rate-limiting step in cholesterol synthesis) -> upregulate LDL receptors -> lower LDL.
Ezetimibe	Cholesterol absorption inhibitor	Inhibits NPC1L1 transporter in small intestinal brush border -> reduces dietary and biliary cholesterol absorption.
Evolocumab, Alirocumab	PCSK9 inhibitors (monoclonal antibodies)	Bind and inhibit PCSK9 -> prevent LDL receptor degradation -> more LDL receptors on hepatocytes -> lower LDL.
Fenofibrate, Gemfibrozil	Fibrates (PPAR-alpha agonists)	Activate PPAR-alpha -> increase lipoprotein lipase expression + reduce VLDL synthesis -> primarily lower triglycerides.
Niacin (Nicotinic acid)	B-vitamin / HDL-raising agent	Inhibits adipose tissue lipolysis -> reduces FFA flux to liver -> decreases VLDL/LDL synthesis + raises HDL.
Cholestyramine, Colestipol	Bile acid sequestrants	Bind bile acids in gut -> interrupt enterohepatic circulation -> liver upregulates LDL receptors -> lowers LDL.
Inclisiran	siRNA (PCSK9-targeting)	Small interfering RNA silences PCSK9 mRNA in hepatocytes -> sustained reduction in PCSK9 -> lower LDL.
Icosapentaenoic acid (Vascepa)	Omega-3 fatty acid	Reduces hepatic VLDL synthesis and triglyceride levels; also has anti-inflammatory and anti-atherosclerotic effects.

7. DRUGS USED IN SHOCK / VASOACTIVES

Drug	Class	MOA (Single Line)
Norepinephrine	Alpha-1 + Beta-1 agonist (vasopressor)	Primarily stimulates alpha-1 -> vasoconstriction -> raises MAP; mild beta-1 -> maintains cardiac output.
Epinephrine	Alpha + Beta agonist	Low dose: beta-2 -> vasodilation; High dose: alpha-1 -> vasoconstriction; increases HR, contractility (anaphylaxis, cardiac arrest).
Vasopressin	V1 receptor agonist	Activates V1 receptors on vascular smooth muscle -> vasoconstriction (used as vasopressor in refractory septic shock).
Phenylephrine	Pure alpha-1 agonist	Selectively stimulates alpha-1 -> peripheral vasoconstriction -> raises BP (used in vasodilatory shock, spinal hypotension).
Isoproterenol	Non-selective beta agonist	Stimulate beta-1 and beta-2 -> increase HR, contractility, and bronchodilation (used in refractory bradycardia/heart block).

Source references: Katzung's Basic and Clinical Pharmacology, 16th Ed. | Goodman & Gilman's Pharmacological Basis of Therapeutics | Miller's Anesthesia, 10th Ed.

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