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First Aid-- Cardiovascular Pharmacology
Terms in this set (74)
Anti HTN-- Primary (essential)
Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.
Anti HTN with CHF
Diuretics, ACE inhibitors/ARBs, β-blockers (compensated CHF), aldosterone antagonists. NO BETA BLOCKERS FOR ACUTE DECOMPENSATED CHF-- Lower BP
Anti HTN with DM
ACE inhibitors/ARBs. Calcium channel blockers, diuretics, β-blockers, α-blockers.
ACEI/ARBs protect against nephropathy
Calcium channel blockers: Names
Dihydropyridine: Amlodipine, nimodipine, nifedipine; Non-dihydropyridine: diltiazem, verapamil.
Calcium channel blockers: Mechanism
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reduce muscle contractility.
Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.
Heart—verapamil > diltiazem > amlodipine = nifedipine.
Calcium channel blockers: Use
Dihydropyridine (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud phenomenon.
Non-dihydropyridine: hypertension, angina, atrial fibrillation/flutter.
Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).
Calcium channel blockers: Toxicity
Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation.
Increase cGMP--> smooth mm relaxation. Vasodilates arterioles > veins; afterload reduction.
Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with methyldopa.
Frequently coadministered with a β-blocker to prevent reflex tachycardia.
Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache,
angina. Lupus-like syndrome.
Hypertensive Emergency: Drugs used
Nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.
Hypertensive Emergency: Nitroprusside
Short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).
Hypertensive Emergency: Fenoldopam
Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. Decrease BP and increase natriuresis.
Nitroglycerine, Isosorbide dinitrate: MOA
Vasodilate by increasing NO in vascular smooth muscle, increase in cGMP and smooth muscle relaxation. Dilate veins >> arteries. DECREASE preload.
Nitroglycerine, Isosorbide dinitrate: Use
Angina, acute coronary syndrome, pulmonary edema
Nitroglycerine, Isosorbide dinitrate: Toxicity
Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache.
"Monday disease" in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure.
Goal of Anti-angina therapy
Reduction of myocardial O2 consumption, decrease determinants of MVO2--> contractility, preload (end diastolic volume), afterload (blood pressure), heart rate
Nitrates, Nifedipine (Affect preload)
Decrease: End diastolic volume, BP, Ejection time, MVO2, Increase (reflex): contractility, heart rate
Beta-blockers, Verapamil (Affect Afterload)
Decrease: BP, contractility, heart rate, MVO2
Increase: End diastolic volume, Ejection time
Nitrates + Beta blockers
Decrease: BP, Heart Rate, MVO2
No effect: End diastolic volume, contractility, ejection time
B-blockers contraindicated in angina
Pindolol and acebutolol
HMG-CoA reductase Inhibitors: Names, Prefix
Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin (-STATIN)
HMG-CoA reductase Inhibitors: Effect on LDL, HDL, Triglycerides
Decreases: LDL, Triglycerides
HMG-CoA reductase Inhibitors: MOA
Inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)
HMG-CoA reductase Inhibitors: SE
Hepatoxicity (LFT), rhabdomyolysis (esp with fibrates and niacin)
Niacin (B3): Effect on LDL, HDL, Triglycerides
Decrease: LDL, Triglycerides
Niacin (B3): MOA
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis
Niacin (B3): SE
Red, flushed face, which is increased by aspirin or long- term use
Hyperglycemia (acanthosis nigricans)
Hyperuricemia (exacerbates gout)
Cholesterol Absorption Blocker: Name
Cholesterol Absorption Blocker: Effect on LDL, HDL, Triglycerides
No change to Triglycerides nor HDL
Cholesterol Absorption Blocker: MOA
Prevent cholesterol absorption by small intestine brush boarder
Cholesterol Absorption Blocker: SE
Increase in LFTs (rare), diarrhea
Bile Acid Resins: Names
cholestyramine, colestipol, colesevelam
Bile Acid Resins: Effect on LDL, HDL, Triglycerides
Increase: HDL, Triglycerides
Bile Acid Resins: MOA
Prevent intestinal reabsorption
of bile acids; liver must use cholesterol to make more
Bile Acid Resins: SE
Tastes bad and causes GI discomfort, decrease absorption of fat-soluble vitamins
gemfibrozil, clofibrate, bezafibrate, fenofibrate
Fibrates: Effect on LDL, HDL, Triglycerides
Decrease in LDL, triglycerides
Increase in HDL
Upregulate LPL, increase TG clearance
Activates PPAR-α to induce HDL synthesis
Myositis (risk with concurrent statins), hepatotoxicity (increased LFTs), cholesterol gallstones (esp. with concurrent bile acid resins)
Cardiac Glycosides: Name and PK
Digoxin—75% bioavailability, 20-40% protein bound, t1/2 = 40 hours, urinary excretion.
Cardiac Glycosides (digoxin): MOA
Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. Increase
[Ca2+]intracellular--> positive inotropy.
Stimulates vagus nerve--> decrease HR.
Cardiac Glycosides (digoxin): Use
CHF (increased contractility)
Atrial fibrillation (decrease conduction at AV node and depression of SA node).
Cardiac Glycosides (digoxin): Toxicity
Cholinergic—nausea, vomiting, diarrhea, blurry yellow vision (Van Gogh).
ECG— increase PR, decrease QT, ST scooping, T-wave inversion, arrhythmia, AV block.
Can lead to hyperkalemia, indicates poor prognosis.
Factors predisposing to toxicity—renal failure (decreased excretion), hypokalemia (permissive for digoxin
binding at K+-binding site on Na+/K+ ATPase), verapamil, amiodarone, quinidine (decrease digoxin clearance; displaces digoxin from tissue-binding sites).
Cardiac Glycosides (digoxin): Antidote to toxicity
Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.
Antiarrhythmics-- Class I (Inhibits...)
Na++ channel blocker.
Slow or block conduction (especially in depolarized cells). Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells.
State dependent (selectively depress tissue
that is frequently depolarized [e.g., tachycardia]). Hyperkalemia causes toxicity for all class I drugs.
Antiarrhythmics Class IA: Names
Quinidine, Procainamide, Disopyramide
Antiarrhythmics Class IA: MOA
Increase AP duration, increase effective refractory period (ERP), increase QT interval.
Antiarrhythmics Class IA: Use
Atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
Antiarrhythmics Class IA: Toxicity
Cinchonism (headache, tinnitus with quinidine)
Reversible SLE-like syndrome (procainamide)
Heart failure (disopyramide)
Thrombocytopenia, torsades de pointes due to QT interval.
Antiarrhythmics Class IB: Names
Antiarrhythmics Class IB: MOA
Decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.
Phenytoin can also fall into the IB category.
Antiarrhythmics Class IB: Use
Acute ventricular arrhythmias (especially post- MI), digitalis-induced arrhythmias.
Antiarrhythmics Class IB: Toxicity
CNS stimulation/depression, cardiovascular depression.
Antiarrhythmics Class IC: Names
Antiarrhythmics Class IC: MOA
Significantly prolongs refractory period in AV node.
Minimal effect on AP duration.
Antiarrhythmics Class IC: Use
SVTs, including atrial fibrillation. Only as a last resort in refractory VT.
Antiarrhythmics Class IC: Toxicity
Proarrhythmic, especially post-MI (contraindicated).
Contraindicated in structural and ischemic heart disease.
Antiarrhythmics Class II: Names, Class
Metoprolol, propranolol, esmolol, atenolol, timolol, cavedilol
Antiarrhythmics Class II: MOA
Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents. Suppress abnormal pacemakers by decreasing slope of phase 4.
AV node particularly sensitive— increase PR interval. Esmolol very short acting.
Antiarrhythmics Class II: Use
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
Antiarrhythmics Class II: Toxicity
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
Metoprolol can cause dyslipidemia.
Propranolol can exacerbate vasospasm in Prinzmetal angina.
Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity). Treat overdose with glucagon.
Antiarrhythmics: Class III: Names and Class
Amiodarone, Ibutilide, Dofetilide, Sotalol
Antiarrhythmics: Class III: MOA
Increase AP duration, increase effective refractory period. Used when other antiarrhythmics fail. Increase QT interval.
Amiodarone has class I, II, III, IV effects, and alters lipid membrane
Antiarrhythmics: Class III: Use
Atrial fibrillation, atrial flutter
Ventricular tachycardia (amiodarone, sotalol).
Antiarrhythmics: Class III: Toxicity
Sotalol—torsades de pointes, excessive β blockade.
Ibutilide—torsades de pointes.
Amiodarone—pulmonary fibrosis, hepatotoxicity, hypothyroidism/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF). PFT, LFT, TFT needed
Antiarrhythmics: Class IV: Names and Class
Ca++ channel blockers
Antiarrhythmics: Class IV: MOA
Decrease conduction velocity, increase effective refractory period, increase PR interval.
Antiarrhythmics: Class IV: Use
Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.
Antiarrhythmics: Class IV: Toxicity
Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression).
Adenosine: MOA, SE
Increase K+ out of cells--> hyperpolarizing the cell and decrease I-Ca.
Drug of choice in diagnosing/abolishing supraventricular tachycardia.
Very short acting (~ 15 sec).
Adverse effects include flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.
Effective in torsades de pointes and digoxin toxicity.
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