Cardiovascular Drug Introduction Cardiovascular medications can be broken down into the following categories: antiarrhythmics antihypertensives inotropes vasodilators diuretics antihyperlipidemics anticoagulants thrombolytics Cardiovascular Drug Table Antiarrhythmics Class I (Na+ Channel Block) Name Mechanism of Action Key Indication Key Toxicity Lidocaine Na+ channel blockage preferentially binds to Na+ channels in the deactivated state Acute ventricular arrhythmia secondary to: myocardial infarction digitalis toxicity cardiac manipulation (i.e., catherization, surgery) Cardiotoxicity: arrhythmia bradycardia Neurotoxicity: excitation/depression Procainamide Na+ channel blockage preferentially binds to Na+ channels in the deactivated state Ventricular arrhythmia Supraventricular arrhythmia SLE-like syndrome: increased incidence in slow acetylators Quinidine Na+ channel blockage preferentially binds to Na+ channels in the activated state Ventricular arrhythmia/tachycardia Atrial fibrillation/flutter Cinchonism ↑ QT interval Class II (β-Block) See antihypertensives below Class III (K+ Channel Block) Name Mechanism of Action Key Indication Key Toxicity Amiodarone K+, Ca2+, and Na+ channel blocker: broad-spectrum anti-arrhythmic Most types of arrhythmias: secondary due to broad mechanism of action Pulmonary fibrosis Hyper- or hypothyroidism Blue pigment of the skin "smurf skin" Corneal deposits Hepatotoxic Photophobia Bretylium Unknown Ventricular arrhythmia resistant to typical antiarrhythmic therapy: considered last-resort Orthostatic hypotension Nausea Vomiting Sotalol β-blocker K+ channel blocker Ventricular arrhythmia Atrial fibrillation/flutter Torsades de pointes β-blockade Class IV (Ca2+ Channel Blockers) Name Mechanism of Action Key Indication Key Toxicity Amlodipine Nicardipine Nifedipine Ca2+ channel blocker preferentially in vasculature Angina Hypertension Peripheral edema Pulmonary edema Flushing/dizziness Reflex tachycardia Remember, they act on vascular smooth muscle Gingival hyperplasia Dilitiazem Verapamil Ca2+ channel blocker preferentially in vasculature Supraventricular tachycardia Angina Hypertension Cardiac depression Constipation Other Antiarrythmics Name Mechanism of Action Key Indication Key Toxicity Adenosine Adenosine receptor agonist: ↓ cAMP via Gi AV nodal arrhythmia Paroxysmal supraventricular tachycardias Impending doom Vasodilation Dyspnea secondary to bronchoconstriction Atropine Muscarinic antagonist Inhibit secretions Sinus bradycardia AV block Adjuvant with anticholinesterase Antimuscarinic/cholinergic effects Digoxin Cardiac Na+/K+ ATPase inhibitor Heart failure Atrial fibrillation Arrhythmia Nausea Vomiting Diarrhea Blurry yellow vision Epinephrine β- and α-agonist: β > α Anaphylactic reactions Hypotension Secondary to β- and α-adrenergic receptor effects β > α Ibutilide K+ channel blocker Atrial fibrillation/flutter Torsades de pointes Isoproterenol β-agonist Heart block Bradyarrhythmias Bronchospasm Arrhythmias Angina Flushing Magnesium sulfate Effect on Ca2+ and K+ fluxes Torsades de pointes Digitalis-induced arrhythmia Cardiac arrest ↓ Deep tendon reflexes Antihypertensives β-Blockers Name Mechanism of Action Key Indication Key Toxicity Atenolol β-blocker β1 > β2 Hypertension Angina Post-MI secondary prevention Bradycardia Heart failure AV block Esmolol β-blocker β1 > β2 Supraventricular tachycardia Cardiac arrest Bradycardia Hypotension Metoprolol β-blocker β1 > β2 Hypertension Angina Acute myocardial infarction in hemodynamically stable patients ↓ Morbidity and mortality in heart failure Hypotension Bradycardia AV block Dyslipidemia Carteolol β-blocker Open-angle glaucoma Intraocular hypertension Conjunctival hyperemia Propranolol β-blocker β1 = β2 Hypertension Angina Essential tremor Migraine prophylaxis Thyrotoxicosis Supraventricular arrhythmias: also ventricular tachycardias Bradycardia AV block COPD and asthma exacerbation Vasospasm exacerbation in Prinzmetal angina Sotalol β-blocker K+ channel blocker Ventricular arrhythmia Atrial fibrillation/flutter Torsades de pointes β-blockade Carvedilol α- and β-blocker Congestive heart failure Hypertension Antiarrhythmic Hypotension Cardiovascular effects: bradycardia, etc. Labetolol α- and β-blocker Hypertension Hypertensive emergencies: such as in pregnancy (i.e., gestational HTN, preeclampsia, eclampsia, etc.) Orthostatic hypotension ACE Inhibitors Name Mechanism of Action Key Indication Key Toxicity Benazepril Captopril Enalapril Lisinopril Angiotensin-converting enzyme (ACE) inhibitor Hypertension Heart failure Diabetic kidney disease Cough Hyperkalemia Teratogen Angioedema ↓ Glomerular filtration rate (GFR) Hypotensio Angiotensin II Antagonists Name Mechanism of Action Key Indication Key Toxicity Losartan Candesartan Valsartan Angiotensin receptor blockers (ARBs) Hypertension Heart failure Diabetic kidney disease Hyperkalemia Teratogen ↓ Glomerular filtration rate (GFR) Hypotension Antiadrenergics Name Mechanism of Action Key Indication Key Toxicity Clonidine α2-agonist Hypertension Attention deficit hyperactive disorder (ADHD) Tourette syndrome Opioid withdrawal Depression of the CNS Respiratory depression Bradycardia Hypotension Miosis Doxazosin Terazosin α1-blocker Hypertension Benign prostatic hyperplasia symptoms Orthostatic hypotension Urinary incontinence Inotropes Name Mechanism of Action Key Indication Key Toxicity Amrinone Milrinone Phosphodiesterase (PDE) inhibitor Heart failure Arrhythmia Dobutamine β- and α-agonist β1 > β2, α Heart failure Tachyarrhythmia Hypertension Dopamine Dopamine, β- and α-agonist D1 = D2 > β > α Low cardiac output/poor perfusion Hypotension At low doses, increases renal perfusion Arrhythmia Angina Epinephrine β- and α-agonist β > α Type I hypersensitivity reactions Hypotension secondary to septic shock Cardiac arrest Angina Arrhythmia Anxiety Respiratory difficulties Norepinephrine β- and α-agonist α > β Hypotension Cardiac arrest Septic shock Hypertension Bradycardia Arrhythmia Anxiety Dyspnea Phenylephrine α-agonist α1 > α2 Hypotension Decongestant Hypertension Reflex bradycardia Anxiety Pulmonary edema Vasodilators Name Mechanism of Action Key Indication Key Toxicity Hydralazine ↑ cGMP, leading to smooth muscle relaxation Severe hypertension Heart failure Tachycardia SLE Nitroprusside ↑ cGMP Severe hypertension Decompensated heart failure Hypotension Cyanide toxicity (potential) Minoxidil Arteriolar vasodilator Opens K+ channels Severe hypertension Androgenetic alopecia Tachycardia Salt and water retention Hirsutism Diazoxide Opens K+ channels in smooth muscle Severe hypertension Hypoglycemia in the setting of insulin-secreting tumors Hypotension Hyperglycemia Diuretics Carbonic Anhydrase Inhibitors Name Mechanism of Action Key Indication Key Toxicity Acetazolamide Carbonic anhydrase inhibitor Edema Mountain sickness Glaucoma Idiopathic intracranial hypertension (pseudotumor cerebri) Metabolic acidosis Hyperammonemia Paresthesias Sulfa allergy Loop Diuretics Name Mechanism of Action Key Indication Key Toxicity Bumetanide Furosemide Torsemide Inhibit Na+/K+/2Cl− transporter of thick ascending limb of loop of Henle Hypertension Edema: due to heart failure, liver failure, nephrotic syndrome Hypercalcemia Ototoxicity Metabolic hypokalemic alkalosis Hypovolemia Sulfa allergy Insterstitial nephritis Gout Efficacy is decreased when used with NSAIDs Thiazide Diuretics Name Mechanism of Action Key Indication Key Toxicity Chlorothiazide Hydrochlorothiazide (HCTZ) NaCl reabsorption inhibitor in distal convoluted tubule Heart failure Edema Nephrogenic diabetes insipidous Calcium nephrolithiasis Sulfa allergy Hypokalemia Hyper-uricemia, glycemia, calcemia, lipidemia Metabolic alkalosis K+ Sparing Diuretics Name Mechanism of Action Key Indication Key Toxicity Amiloride ENaC epithelial channel blocker in cortical collecting ducts Heart failure Hyperaldosteronism Nephrogenic diabetes insipidus States of K+ depletion (i.e., use of thiazides) Hyperkalemia Spirolactone Aldosterone receptor blocker in cortical collecting ducts (in their cytoplasm) Heart failure Hyperaldosteronism Hepatic ascites Hyperkalemia Gynecomastia Antihyperlipidemics HMG-CoA Reductase Inhibitors Name Mechanism of Action Key Indication Key Toxicity Atorvastatin Cerivastatin Fluvastatin Lovastatin Pravastatin Simvastatin HMG-CoA reducase inhibitor Vascular disease secondary to atherosclerosis Myopathy Hepatotoxicity Potential for teratogenicity contraindicated in pregnancy Other Antihyperlipidemics Name Mechanism of Action Key Indication Key Toxicity Fenofibrate Gemfibrozil PPAR-α agonists Upregulates lipoprotein lipase Hypertriglyceridemia, low HDL cholesterol Can ↑ HDL in most patients Myopathy Gallstones (cholesterol) Niacin ↑ HDL and ↓ LDL and triglycerides Dyslipidemia Flushing, pruritis NSAIDs can help Hepatotoxicity Hyperuricemia Hyperglycemia Anticoagulants Name Mechanism of Action Key Indication Key Toxicity Abciximab Tirofiban GpIIb/IIIa inhibitor Unstable angina Prevention of cardiac ischemia in percutaneous coronary intervention Bleeding Thrombocytopenia Anagrelide Phosphodiesterase III inhibitor Thrombocythemia can be seen in myeloproliferative disorders Palpitations Headache Thrombocytopenia Bleeding Cilostazol Phosphodiesterase III inhibitor Secondary ischemic stroke prevention Intermittent claudication Thromboembolic complication prevention i.e., cardiac valve replacement, percutaneous coronary intervention Headache Flushing Hypotension Aspirin Irreversible COX inhibitor Impairs TXA2 synthesis Treatment and prevention of arterial thrombosis Tinnitus Gastrointestinal toxicity Renal toxicity Reye syndrome: children with viral infection Metabolic acidosis-respiratory alkalosis: respiratory alkalosis early Platelet Aggregation Antagonists Name Mechanism of Action Key Indication Key Toxicity Ticlopidine Clopidogrel ADP-receptor antagonist thus impairs expression of GpIIb/IIIa receptors Acute coronary syndrome Prevention of cardiac ischemia in percutaneous coronary intervention Treatment and prevention of arterial thrombosis Leukopenia (ticlopidine) Thrombotic thrombocytopenic purpura Thrombolytics Thrombin Inhibitor Name Mechanism of Action Key Indication Key Toxicity Alteplase Streptokinase Urokinase Aids in conversion of plasminogen to plasmin Early myocardial infarction and ischemic stroke Pulmonary embolism Bleeding Other Name Mechanism of Action Key Indication Key Toxicity Digoxin-Immune Fab Binds excess digoxin or digitoxin Digoxin toxicity Heart failure exacerbation Albumin Blood volume expander: acts as an oncotic agent Antihyperbilirubinemic: Binds to various substances in the bloods (i.e., bilirubin, drugs, etc.) Hypovolemia Subacute bacterial peritonitis Cirrhosis Heart failure Edema