| Drugs | Mechanism | Indication | Side Effects/Management | |
|---|---|---|---|---|
| Class I-A | *🔹Quinidine | |||
| 🔹Procainamide | ||||
| 🔹Disopyramide* | 🔹 Na⁺ Channel Inhibitor | 🔹 Ventricular arrhythmias | ||
| 🔹 Atrial arrhythmias | ||||
| 🔹 WPW (Procainamide) | 🔹 ↑ QT → Torsades | |||
| 🔹 Ventricular arrhythmias | ||||
| 🔹 Anticholinergic effects | ||||
| 🔹 Quinidine ⇒ Cinchonism (tinnitus, confusion, psychosis) | ||||
| 🔹 Procainamide ⇒ Drug-induced SLE | ||||
| 🔹 Disopyramide ⇒ Myocardial depression | ||||
| Class I-B | *🔹Lidocaine | |||
| 🔹Mexiletine* | 🔹 Na⁺ Channel Inhibitor | 🔹 Ventricular arrhythmias | ||
| 🔹 Digitalis-induced cardiac arrhythmias | 🔹 Ventricular arrhythmias | |||
| 🔹 Cardiovascular depression | ||||
| 🔹 CNS effects (tremor, agitation) | ||||
| Class I-c | *🔹Flecainide | |||
| 🔹Propafenone* | 🔹 Na⁺ Channel Inhibitor | 🔹 Atrial arrhythmias | 🔹 Ventricular arrhythmias | |
| 🔹 Not used if structural heart disease is present | ||||
| Class II | *🔹 Atenolol | |||
| 🔹 Bisoprolol | ||||
| 🔹 Carvedilol | ||||
| 🔹 Esmolol | ||||
| 🔹 Labetalol | ||||
| 🔹 Metoprolol | ||||
| 🔹 Propranolol* | 🔹 β-adrenergic antagonist | |||
| 🔸 β1-Selective ⇒ "A-M" | ||||
| 🔸 Nonselective ⇒ "N-Z" | ||||
| 🔸 Carvedilol/Labetalol ⇒ α/β block | 🔹 Atrial fibrillation/flutter | |||
| 🔹 AVNRT | ||||
| 🔹 Angina/ACS | ||||
| 🔹 Hypertension | ||||
| 🔹 Heart Failure | ||||
| 🔹 Migraine PPX (Propranolol) | ||||
| 🔹 Thyrotoxicosis (Propranolol) | ||||
| 🔹 Variceal PPX (Nadolol) | ||||
| 🔹 Glaucoma (Timolol) | 🔹 Fatigue | |||
| 🔹 Erectile dysfunction | ||||
| 🔹 Depression | ||||
| 🔹 Mild HLD | ||||
| 🔹 Metoprolol ⇒ Bradyarrhythmias | ||||
| 🔹 Caution with acute exacerbation of HF, asthma, COPD | ||||
| 🔹 Beta Blocker Overdose ⇒ Bradycardia, AV block, shock; Tx ⇒ Fluids, Atropine, Glucagon | ||||
| Class III | *🔹 Amiodarone | |||
| 🔹 Ibutilide | ||||
| 🔹 Dofetilide | ||||
| 🔹 Sotalol* | 🔹 K⁺ Channel Blocker (Reverse Use-Dependence) |
💡 Reverse use dependency Enhanced effect at slower heart rates → seen with Class III drugs. | 🔹 Ventricular arrhythmias 🔹 Atrial arrhythmias | 🔹 ↑ QT → Torsades 🔹 Ventricular arrhythmias (Least with Amiodarone) 🔹 Amiodarone ⇒ Pulmonary fibrosis, hepatotoxicity, hypo or hyperthyroidism, bradyarrhythmias, corneal deposits, blue/gray skin
(see the table below for Thyroid effects of amiodarone) | | Class IV | 🔹 Diltiazem 🔹 Verapamil | 🔹 Ca²⁺ Channel Blocker (Non-Dihydropyridine) | 🔹 Atrial fibrillation/flutter 🔹 AVNRT 🔹 Angina 🔹 Hypertension | 🔹 Constipation 🔹 Edema 🔹 Bradyarrhythmias 🔹 Hyperprolactinemia (Verapamil) 🔹 Reflex tachycardia |
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| Disorder | Features | Treatment |
|---|---|---|
| Decreased T4-T3 conversion | ● ↑ T4 | |
| ● ↓ T3 | ||
| ● Normal/↑ TSH | None needed | |
| Inhibition of thyroid hormone synthesis | ● ↑ TSH | |
| ● ↓ T4 | Levothyroxine | |
| AIT type 1 (iodine-induced increase in thyroid hormone synthesis) | ● ↓ TSH | |
| ● ↑ T3 & T4 | ||
| ● ↓ RAIU | ||
| ● Increased vascularity on ultrasound | Antithyroid drugs | |
| AIT type 2 (destructive thyroiditis) | ● ↓ TSH | |
| ● ↑ T3 & T4 | ||
| ● Undetectable RAIU | ||
| ● Decreased vascularity on ultrasound | Glucocorticoids |
| Drug Class | Examples | Mechanism of Action | Adverse Effects/Toxicities |
|---|---|---|---|
| Osmotic Diuretics | 🔸Mannitol | ||
| 🔸Isosorbide | 🔹 Increases osmolarity of the blood, leading to increased urine output | 🔹 Dehydration | |
| 🔹 Pulmonary edema | |||
| Carbonic Anhydrase Inhibitors | 🔸Acetazolamide | ||
| 🔸Dorzolamide | 🔹 Inhibits carbonic anhydrase, leading to decreased reabsorption of bicarbonate in the proximal tubule | 🔹 Hyperammonemia with Paresthesias | |
| 🔹 Proximal renal tubular acidosis | |||
| 🔹 Hypokalemia | |||
| 🔹 Sulfa allergy reaction | |||
| Thiazide Diuretics | 🔸Hydrochlorothiazide | ||
| 🔸Amiloride | |||
| 🔸Chlorthalidone | |||
| 🔸Metolazone | 🔹 Inhibits Na⁺-Cl⁻ symporter in the distal convoluted tubule | 🔹 Hypokalemia | |
| 🔹 Hyponatremia | |||
| 🔹 Metabolic alkalosis | |||
| 🔹 Hyperglycemia | |||
| 🔹 Hyperlipidemia | |||
| 🔹 Hypercalcemia | |||
| 🔹 Hyperuricemia | |||
| Loop Diuretics (Potassium-Wasting) | 🔸Furosemide | ||
| 🔸Torsemide | |||
| 🔸Bumetanide | |||
| 🔸Ethacrynic Acid | 🔹 Inhibits Na⁺-K⁺-2Cl⁻ symporter in the thick ascending limb of the loop of Henle | 🔹 Hypokalemia | |
| 🔹 Dehydration/hypovolemia | |||
| 🔹 Hypocalcemia | |||
| 🔹 Hyperuricemia | |||
| 🔹 Ototoxicity | |||
| Potassium-Sparing Agents | 🅰️ Mineralocorticoid Receptor Antagonists | ||
| 🔸Spironolactone | |||
| 🔸Eplerenone |
🅱️ Na⁺ Channel Inhibitors 🔸Amiloride 🔸Triamterene | 🅰️ Antagonizes aldosterone at the mineralocorticoid receptor
🅱️ Blocks Na⁺ channels in the distal tubule and collecting duct | 🔹 Hyperkalemia 🔹 Metabolic acidosis 🔹 Sexual dysfunction 🔹 Gynecomastia (Spironolactone) |
| Class / Drug | Mechanism | Indication | Side Effects/Management |
|---|---|---|---|
| **Arteriolar/Venous Dilators |
🔹Hydralazine 🔹Nitroprusside** | 🔹 Arterial/venous dilator (NO release → ↑ cGMP) | 🔹 Hypertension (Hydralazine - Usually in pregnancy) 🔹 Hypertension emergency (Nitroprusside) | 🔹 Headache 🔹 Edema 🔹 Reflex tachycardia 🔹 Drug-induced SLE (Hydralazine) 🔹 Cyanide toxicity (Nitroprusside) 🔹 Methemoglobinemia (Nitroprusside) | | **Nitrovasodilators
🔹Nitroglycerine 🔹Isosorbide mono/di-nitrate** | 🔹 Vasodilatation (veins > arterial) | 🔹 AnginaAngina | 🔹 Flushing 🔹 Headache 🔹 Hypotension 🔹 Reflex tachycardia 🔹 Contraindicated if on PDE inhibitor 🔹 Methemoglobinemia | | **Glycosides
Digoxin** | 🔹 Inhibitor of Na⁺ ATPase → increased cardiac calcium and contractility 🔹 Increased vagal tone | 🔹 HFrEF 🔹 Atrial fibrillation | 🔹 GI (nausea, vomiting, abdominal pain) 🔹 Hyperkalemia (poor prognostic) 🔹 Neurologic (confusion, weakness) 🔹 Visual disturbances (scotomas, change in color vision) 🔹 Arrhythmias ⇒ Ventricular arrhythmias, heart block, bradycardia 🔹 ↑ Risk for toxicity with renal failure, hypokalemia 🔹 Reverse severe toxicity with digoxin Fab | | Adenosine | 🔹 Transient induction of heart block by activating K⁺ channels, increasing K⁺ efflux, hyperpolarizing cells | 🔹 Supraventricular tachycardia (Important!) | 🔹 Effects blunted by caffeine and theophylline 🔹 Flushing 🔹 Chest pain 🔹 Sense of impending doom 🔹 Bronchospasm | | Atropine | 🔹 Muscarinic receptor antagonist | 🔹 Bradycardia | 🔹 Dry mouth 🔹 Constipation 🔹 Urinary retention 🔹 Confusion | | Sacubitril | 🔹 Neprilysin inhibitor, ↑ levels of ANP/BNP | 🔹 Heart failure requiring rate control | 🔹 Hypotension 🔹 Hyperkalemia 🔹 AKI 🔹 Angioedema | | Ivabradine | 🔹 Inhibits funny channel, slowing heart rate | 🔹 HFrEF | 🔹 Bradycardia 🔹 Visual changes (phosphenes) (hyperluminousity) | | Ranolazine | 🔹 Inhibits late Na⁺ current, reducing diastolic wall tension / O₂ consumption | 🔹 Angina | 🔹 QT prolongation |
Digoxin Makes the heart slow and powerful
Electrolyte Imbalances
Hypokalemia → digoxin competes with K+ for binding to Na+/K+-ATPase
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Although it can increase serum potassium, spironolactone also predisposes to digoxin toxicity because it decreases renal clearance of digoxin (spironolactone - digoxin interaction is not related to potassium)
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Though hypokalemia is a major cause of digoxin toxicity, hyperkalemia is seen in digoxin toxicity and is associated with poor prognosis
Medical Conditions
Renal failure (reduced digoxin excretion)
Volume depletion (treatment with diuretics)
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Patients on furosemide and spironolactone are at increased risk of having digoxin toxicity
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Hypothyroidism
Drugs like amiodarone, verapamil, quinidine, and propafenone increase serum levels of digoxin by interfering with its metabolism.
Reduce digoxin dose by 25%–50% when starting amiodarone, with weekly monitoring of digoxin levels for several weeks.