Cardio Flashcards
Hydralazine
MOA: increase cGMP leading to smooth muscle relaxation
Vasodilates ARTERIOLES
Reduces afterload
Clinical: severe hypertension, CHF
Hypertension in Pregnancy (1st line with methyldopa)
Co-administered with B-blocker to prevent reflex tachycardia
Sympatholytics and diuretics to prevent edema and reflex tachycardia
Toxicity: compensatory tachycardia, fluid retention, nausea, headache, angina, lupus-like syndrome (develop antihistone Abs)
Use with diuretics and sympatholytics to decrease edema and reflex tachycardia
CI: angina and CAD
Fenoldopam
Dopamine D2 receptor agonist
Coronary, peripheral, renal and splanchnic vasodilation
Decrease BP and increase natriuresis
Class IA antiarrhythmics
Quinidine, Procainamide, Disopyramide
General MOA: Na+ Channel blockers
Slow or block conduction
Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells
Specific MOA: Increase AP duration, Increase refractory period, increase QT interval (some K+ blocking effect–>increase repolarization and QT prolong)
Clinical: atrial and ventricular arrythmias, especially re-entrant and ectopic SVT and VT
Toxicity: enhanced by hyperkalemia
Cinchonism-headache, tinnitus (quinidine)
Reversible SLE like syndrome (Procainamide)
heart failure (disopyramide), thromobcytopenia
TORSADES DE POINTES
Statins
MOA: Inhibit HMG-CoA reductase (inhbitiing the conversion of HMG-CoA to mevalonate-cholesterol precursor)
Decrease hepatic cholesterol synthesis increasing LDL receptors which increases uptake of LDL from circulation
Decrease cholesterol and stabilize atheromatous plaques
Main effect: decrease LDL
Other effects: slight increase in HDL and slight decrease in triglycerides
SE: hepatotoxicity (Increased LFTs), (myopathy), rhabdomyoloysis (can lead to acute renal failure-especiall with fibrates and niacin)
Adenosine
Antiarrhythmic
Increases K+ out of cells hyperpolarizing the cell and decreasing intracellular Calcium
Drug of choice in diagnosing/abolishing supraventricular tachycardia
Very short acting
SE: flushing, hypotension, chest pain
Effects blocked by theophylline and caffeine
Milirone
MOA: phosphodiesterase isoenzyme 3 inhibitor
PDE I3 metabolizes cAMP
cAMP increases conductance of calcium channel in SR leading to more calcium entering the cell therefore inhibition of PDE increases contractility
increase in cAMP in vascular smooth muscle leads to vasodilation
Dihydropyridine Calcium Channel Blockers
Amlodipine, nimodipine, nifedipine
MOA: Block voltage dependent L-type calcium channels of cardiac and smooth muscle reducing muscle contractility
Work better on vascular smooth muscle
Clinical: (not nimodipine) hypertension, angina (including Prinzmetal) Raynaud phenomenon
Nimodipine: subarachonoid hemorrhage (prevents cerebral vasospasm)
Amlodipine: isolated systolic hypertension (with thiazide diuretics)
Toxicity: cardiac depression, AV block, peripheral edema-add ace or arb, flushing, dizziness, hyperprolactinemia, and constipation
Niacin (vitamin B3)
MOA: inhibits lipolysis in adipose tissue
Reduces hepatic VLDL synthesis
Decrease HDL clearance
Main effect: Increase HDL
Other effects: decrease LDL and slightly decrease triglycerides
SE: red, flushed face which is mediated by prostglandins (prevent with use of aspirin)
Hyperglycemia, hyperuricemia (exacerbates gout)
Class II antiarrhythmics
Beta Blockers
MOA: decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents
Suppress abnormal pacemakers by decreasing slope of phase 4
Decreased contracitlity, bradycardia and AV block lead to decreased CO
AV node particular sensitive-increase PR interval
Clinical: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
Toxicity: impotence, exacrabtion of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), sedation, sleep alterations,
may mask hypoglycemia
Metoprolol can cause dyslipidemia
Propanolol can exacerbate vasospasm in Prinzmetal angina
CI in cocaine users
Treat overdose with glucagon (increases cAMP in cardiac myocytes leading to increased HR and contractility)
Cholesterol absorption blockers
Ezetimibe
MOA: prevent cholesterol absorption at small intestine brush border
Main effect: decrease LDL
No other effects
SE: rear increase in LFTs
diarrhea
Class III antiarrhythmics
Amiodarone, Ibutilide, Deofetilide, Sotalol
MOA: K+ channel blockers
Increase AP duration, Increased ERP, prolong refractory period,
Used when other antiarrhymics fail, Increase QT interval (not amiaridone), increase PR interval
Clincal: atrial fibrillation, atrial flutter, ventricular tachycardia (amiodarone, sotalol)
Toxicity:
Sotalol: torsades de pointes, excessive B blockade, only one that causes mild bradycardia
Ibutilide: torsades de pointes
Amiodarone: pulmonary fibrosis, hepatotoxicty, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits (blue/gray), resulting in photdermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF), little risk to torsades de pointes!
Omega 3 Fatty Acids
MOA: decrease triglyceride synthesis
Main effect: decrease triglycerides
SE: nausea
Cardiac Glycosides (Digoxin)
MOA: direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport
Leads to increased Ca2+ positive inotropy
Stimulates vagus nerve decreasing HR
Clinical: Systolic dysfunction, CHF (increased contractility), atrial fibrillation (vagal nerve decreased conduction at AV node and depression of SA node)
Toxicity:
Cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, confusion, delirium, fatigue
ECG-Increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia (ventricular tachycardia or fibrillation leads to mortality), AV block
Can lead to hyperkalemia which indicates poor prognosis
Factors predisposing to toxicity: renal failure (decreased excretion), hypokalemia, verapamil, amirodarone, quinidine
Antidote: slowly normalize K+ cardiac pacer (insulin, karyexalate, hemodialysis, oral activated charcoal) anti-digoxin Fab fragments, Mg2+
Class IB antiarrhythmics
Lidocaine, Mexiletine
General MOA: Na+ Channel blockers
Slow or block conduction
Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells
Specific MOA: Decrease AP duration
Clinical: Preferentially affects ischemic of depolarized Purkinje and ventricular tissue
Acute ventricular arrhytmias (especially POST MI), digitalis induced arrhythmias
Toxicity: CNS stimulation/depression, cardiovascular depression
Class IC antiarrhythmics
Flecainide, Propafenone
General MOA: Na+ Channel blockers
Slow or block conduction
Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells
Specific MOA: prolongs refractory period in AV node
minimal effect on AP duration
Clinical: SVTs, including atrial fibrillation, last resort in refractory ventricular tachycardia
Toxicity: proarrhythmic (especially post MI-CI),
Class IV antiarrhythmics
Verapamil, diltiazem
MOA: Calcium Channel blockers
Decrease conduction velocity, Increase ERP, Increase PR interval
Blocks SA and AV node conduction by slowing diastolic depolarization
Clinical: prevention of nodal arrhythmias, rate control in atrial fibrillation
Prophylaxis for cluster headache (V)
Toxicity: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
Nondihydropyridine calcium channel blockers
Verapamil and diltiazem
MOA: Block voltage dependent L-type calcium channels of cardiac and smooth muscle reducing muscle contractility
Used more on heart (verampil the best)
Clinical: hypertension, angina, atrial fibrillation/flutter
Toxicity: cardiac depression, SEVERE AV BLOCK, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation (verapamil). gingival hyperplasia (verapamil)
Verapamil contraindicated in CHF
Bile acid resins
Cholestyramine, colestipol, colesvelam
MOA: prevent intestinal reabsoprtion of bile acids
liver must use cholesterol to make more
Main effect: decrease LDL
Other effect: slighlty increas HDL and slighlty increase triglycerides
SE: patients hate it, tastes bad and causes GI discomfort, decreased absorption of fat-soluble vitamins
Cholesterol gallstones
Nitroprusside
Decrease preload and afterload
venous and arterial dilation
Short acting
Increase cGMP via direct release of NO
Can cause Cyanide toxicity
Cyanide toxicity: normally cyanide metabolized by liver to thiocyanate
Clinical: altered mental status and lactic acidosis
Toxicity give sodium thiosulfate works by donating additional sulfur to enhance metabolism and detoxification
Nitroglycerin, isosorbide dinitrate
MOA: vasodilate by increase NO in vascular smooth muscle leading to increased cGMP and smooth muscle relaxation
Dilate veins over arteries
Decrease preload leading to decreased LV volume during diastole (decreases wall stress and cardiac oxygen demand)
Clinical: angina, acute coronary syndrome, pulmonary edema
Toxicity: Reflex tachycardia (treat with B-blockers), hypotension, flushing, headache,
Development of tolerance over the weekend rewsults in tachycardia, dizziness, and headache upon reexposure
Fibrates
Gemfibrozil, clofibrate, bezafibrate, fenofibrate
MOA: Upregulate lipoprotein lipase leading to increased triglyceride clearance
Activates PPAR-a to induce HDL synthesis
increase hepatic cholesterol synthesis, decrease triglyceride synthesis
Main effect: lower triglycerides
Other effects: decrease LDL, increase HDL
SE: myositis (increase risk with concurrent statins), hepatotoxicity (increase LFTs), cholesterol gallstones
Mg2+
Antiarrhythmic
Effective in tosades de pointes and digoxin toxicity
Nesiritide
Recombinant BNP used for heart failure
Ergonovine
Constricts vascular smooth muscle by stimulating both alpha adrenergic and serotonergic receptors
In prinzmetals angina can induce coronary spasm, chest pain and ST segment elevation
