Cardio Flashcards
Nifedipine
1) HTN, angina, Prinzmetal’s angina, Raynaud’s
2) Ca2+ Channel Blockers/Block voltage dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility -more vascular sm. muscle effects
3) Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
Verapamil
1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s, nodal arrhythmias (SVT)
2) Anti-arrhythmics: Ca2+ Channel Blockers(Class IV)/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility -more heart effects – decrease conduction velocity, increase ERP and PR interval
3) Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
Diltiazem
1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s, nodal arrhythmias (SVT)
2) Anti-arrhythmics: Ca2+ Channel Blockers (Class IV)/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility -more heart effects – decrease conduction velocity, increase ERP and PR interval
3) Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
Amlodipine
1) HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s
2) Ca2+ Channel Blockers/Block voltgae dependent L-type Ca2+ channel of cardiac and smooth muscle and thereby reduce muscle contractility -more vascular smooth muscle effects
3) Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
Hydralazine
1) Severe HTN (pregnancy), CHF, reflex tachycardia (w/ beta-blocker)
2) Increase cGMP to cause sm. muscle relaxation -vasodilates arterioles > veins -Afterload reduction
3) Compensatory tachycardia, fluid retention, nausea, headache, angina, lupus-like syndrome
4) Contraindicated in angina and CAD
Nitroprusside
1) Malignant HTN
2) Increases cGMP via direct release of NO; short acting
3) Cyanide toxicity
Fenoldopam
1) Malignant HTN
2) Dopamine (D1) receptor agonist -leads to coronary, peripheral, renal, and splanchnic vasodilation -decreases BP and increases naturesis
Nitroglycerin, isosorbide dinitrate
1) Angina, pulmonary edema
2) Vasodilator – release of NO in sm. muscle –> increases cGMP and sm muscle relaxation -dilates veins»_space; arteries (decreases preload)
3) reflex tachycardia, hypotension, flushing, headache
4) “Monday Disease” –> devleop tolerance during the week and loss of tolerance during weekend resulting in side effects
Lovastatin
1) Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2) HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3) Hepatotoxicity (increase LFTs), rhabdomyolysis
Pravastatin
1) Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2) HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3) Hepatotoxicity (increase LFTs), rhabdomyolysis
Simvastatin
1) Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2) HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3) Hepatotoxicity (increase LFTs), rhabdomyolysis
Atorvastatin
1) Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2) HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3) Hepatotoxicity (increase LFTs), rhabdomyolysis
Rosuvastatin
1) Lipid-lowering agent (sig. decrease of LDL and slight decrease of triglycerides, increase HDL)
2) HMG-CoA Reductase Inhibitors/ Inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
3) Hepatotoxicity (increase LFTs), rhabdomyolysis
Niacin (B3)
1) Lipid-lowering agent (decreases LDL and TG, sig increases HDL) *PRIMARILY TO INCREASE HDL.
2) Inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion into circulation
3) Red flushed face (Mediated by PGEs, reduced by aspirin or long term use), hyperglycemia (acanthosis nigrans), HYPERURICEMIA (excerbates gout), Hepatitis
Cholestyramine
1) Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2) Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more)
3) Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones
Colestipol
1) Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2) Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more)
3) Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones
Colesevelam
1) Lipid-lowering agents (decrease LDL, slightly increase TG and HDL
2) Bile Acid Resins/Prevent intestinal reabsorption of bile acids (liver has to make more)
3) Bad taste, GI discomfort, decreases absorption of fat-soluble vitamins, cholesterol gallstones
Ezetimibe
1) Lipid-loweing agents (decrease LDL
)2) Cholesterol Absorption Blockers/Prevent cholesterol reabsorption at small intestine brush border
3) Rare increase in LFTs, diarrhea , Myopathy
Gemfibrozil
1) Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL) . FIBRATES FOR INCREASED TG.
2) Fibrates/Upregulates LPL –> increases TG clearance
3) Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones. WATCH MYOSITIS WHEN USED WITH STATINS AND NIACIN.
Clofibrate
1) Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2) Fibrates/Upregulates LPL –> increases TG clearance
3) Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones
Bezafibrate
1) Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2) Fibrates/Upregulates LPL –> increases TG clearance
3) Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones
Fenofibrate
1) Lipid-lower agents (sig decrease TGs, slightly decrease LDL, increase HDL)
2) Fibrates/Upregulates LPL –> increases TG clearance
3) Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones
Digoxin
1) CHF (increase contractility), A.fib (decrease conduction at AV node, depression of SA node)
2) Cardiac Glycoside/Direct inhibition of Na+/K+ ATPase leads to indirect inhibtion of Na+/Ca2+ exchanger/antiport –> increases Ca2+ concentration(positive inotropy) -stimulates vagus nerve to decrease HR
3) Cholinergic –> N/V/D, blurry yellow vision, EKG changes (increased PR, decrased QT, ST scooping, T-wave inversion, arrhythmia, AV block), hyperkalemia -Factors predisposing to toxicity –> renal failure, hypokalemia, quinidine (decreases clearance)
4) Antidote –> slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg2+
Quinidine
1) Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2) Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3) Cinchonism – headache, tinnitus; thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity
Procainamide
1) Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2) Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3) Reversible SLE-like syndrome, thrombocytopenia, Torsades de Pointes (increased QT),hyperkalemia causes increased toxicity
Disopyramide
1) Atrial and ventricular arrhythmias – re-entrant and ectopic supraventricular, ventricular tachycardia
2) Anti-arrhythmics:Na+ Channel Blocker (Class IA)/ Slow or block conduction – increase AP duration, ERP and QT interval
3) Heart failure, thrombocytopenia, Torsades de Pointes (increased QT), hyperkalemia causes increased toxicity
Lidocaine
1) Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2) Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3) Local anesthetic, CNS stimulation/depression, cardiovascular depression
4) Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity
Mexiletine
1) Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2) Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3) Local anesthetic, CNS stimulation/depression, cardiovascular depression
4) Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity
Tocainide
1) Acute ventricular arrhythmias (esp post-MI), digitalis-induced arrhythmias
2) Anti-arrhythmics:Na+ Channel Blocker (Class IB)/ Slow or block conduction –decrease AP duration
3) Local anesthetic, CNS stimulation/depression, cardiovascular depression
4) Preferentially affects ischemic or depolarized Purkinje and ventricular tissue, hyperkalemia causes increased toxicity
Flecainide
1) V.tach that progress to V.fib, intractable SVT, last resort in refractory tachyarrhythmias
2) Anti-arrhythmias: Na+ Channel Blocker (Class IC)/ Slow or block conduction – no effect on AP duration
3) Pro-arrhythmic (esp post-MI), prolongs refractory period in AV node4)Contraindicated post-MI and in pts with structural abnormalities, hyperkalemia causes increased toxicity
Propafenone
1) V.tach that progress to V.fib, intractable SVT, last resort in refractory tachyarrhythmias
2) Anti-arrhythmias: Na+ Channel Blocker (Class IC)/ Slow or block conduction – no effect on AP duration
3) Pro-arrhythmic (esp post-MI), prolongs refractory period in AV node4)Contraindicated post-MI and in pts with structural abnormalities, hyperkalemia causes increased toxicity
Metoprolol
1) V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2) Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3) Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia, dyslipidemia4)Treat overdose with glucagon
Propranolol
1) V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2) Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3) Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia4)Exacerbate vasospasm in Prinzmetal’s angina
Esmolol
1) V.tach, SVT, slowing ventricular rate during a.fib and a.flutter
2) Anti-arrhythmics: Beta-Blockers (Class II)/ Decrease cAMP and Ca2+ currents to decrease SA and AV nodal activity – suppress abnormal pacemakers by decreasing slope of phase 4
3) Impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), mask signs of hypoglycemia4)Very short-acting
Amiodarone
1) When other anti-arrhythmics fail
2) Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3) Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits (blue/grey) – cause photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) – check PFTs, LFTs, TFTs4) Has Class I, II, III and IV effects – alters the lipid membrane
Ibutilide
1) When other anti-arrhythmics fail
2) Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3) Torsades de Pointes
Dofetilide
1) When other anti-arrhythmics fail
2) Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
Sotalol
1) When other anti-arrhythmics fail
2) Anti-arrhythmics: K+ Channel Blockers (Class III)/ Decrease cAMP and Ca2+ currents to decrase SA and AV nodal activity –increase AP, ERP, and QT interval
3)Torsades de Pointes, excessive beta-block
Adenosine
1) Diagnosing/abolishing SVT
2) Increase K+ removal from cell –> hyperpolarize the cell and decrease I(Ca), very short-acting
3) Flushing, hypotension, chest pain
4) Effects blocked by theophylline and caffeine
Mg2+
1)Torsades de Pointes, Digoxin toxicity
meds for an MI
MONAB: morphine, oxygen, nitrates, aspirin, Beta blockers
