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Cardio drugs

Terms in this set (88)

Essential hypertension Rx
Diuretics, ACE I, ARBs, CCB
CHF Rx
diuretics, ACE I / ARBs, B blockers (compensated CHF, contraindicated if decompensated), K+ sparing diuretics
Diabetes mellitus + HTN rx
ACE I/ ARBs, CCB, diuretics, Beta-blockers, alpha-blockers. ACE I are protective against diabetic nephropathy
Hydralazine mechanism
increase in cGMP --> smooth muscle relaxation. vasodilates arterioles > veins. Afterload reduction
Hydralazine clinical use
severe hypertension, CHF. 1st line therapy for HTN in pregnancy with methyldopa. co admin with B-blocker to prevent reflex tachycardia
Hydralazine toxicity
compensatory tachycardia (contraindicated in angina/CAD, fluid retention, nausea, headache, angina. lupus like syndrome
minoxidil mechanism
K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle
minoxidil clinical use
severe HTN
minoxidil toxicity
hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention
CCBs
nifedipine, verapamil, diltiazem
CCB mechanism
block V-gated L-type Ca2+ channels of cardiac and smooth muscle --> reduction in muscle contractility. effect on Vascular SM-N> D> V effect on heart V (Ventricle) > D> N
CCB clinical use
hypertension, angina, arrhythmias (not N), Prinzmetal's angina, Raynaud's
CCB toxicity
cardiac depression, AV block, peripheral edema, flushing, dizziness and constipation
nitroglycerin, isosorbide dinitrate mechanism
vasodilate by releasing NO in smooth muscle --> increase in cGMP and smooth muscle relaxation dilates veins >>>arteries (venodilation). decrease in preload
nitroglycerin, isosorbide dinitrate clinical use
angina, pulmonary edema. (also used as aphrodesiac and erection enhancer )
nitroglycerin, isosorbide dinitrate toxicity
reflex tachycardia, hypotension, flushing, headache, "monday disease" in industrial exposure (development of tolerance for vasodilating action during the work week and loss of tolerance over the weekend --> tachycardia, dizziness and headache on reexposure)
malignant HTN RX
Nitroprusside, fenoldopam, diazoxide
nitroprusside mechanism
short acting; increase in cGMP via direct release of NO
nitroprusside toxicity
cyanide toxicity
fenoldopam mechanism
dopamine D1 R agonist-- relaxes renal vascular smooth muscle
diazoxide mechanism
K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle
diazoxide toxicity
hyperglycemia (reduces insulin release)
Antianginal therapy
nitrates (decrease preload), B-blockers (decrease afterload), CCB - Nifedipine (similar to Nitrates) and verapamil (similar to B-blockers) (NB: pindolol and acebutolol are partial B agonists - contraindicated in angina)
lipid lowering agents
HMG- CoA reductase inhibitors (-"statin"), Niacin, Bile acid resins, cholesterol absorption blockers, Fibrates
HMG-CoA reductase inhibitors
lovastatin, pravastatin, simvastatin, atovastatin, rosuvastatin
HMG-CoA reductase mechanism
inhibits cholesterol precursor mevalonate
HMG-CoA reductase effect
large decrease in LDL, small increase in HDL and small decrease in TG
HMG-CoA reductase SE/problems
hepatoxicity (increase LFTs), rhabdomyolysis
Niacin mechanism
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
Niacin effect
medium decrease in LDL, medium increase in HDL, small decrease in TG
Niacin SE
red, flushed face (decreased by aspirin or long term use); hyperglycemia (acanthosis nigricans); hyperuricemia (exacerbates gout)
Bile acid resins
cholestyramine, colestipol, colesevelam
cholestyramine, colestipol, colesevelam mechanism
prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
cholestyramine, colestipol, colesevelam effect
medium decrease in LDL, slight increase in HDL and TG
cholestyramine, colestipol, colesevelam SE
patients hate it- tastes bad and causes GI discomfort; decrease absorption of fat-soluble vitamins; cholesterol gallstones
cholesterol absorption blockers
ezetimibe
ezetimibe mechanism
prevent cholesterol reabsorption at small intestine brush border
ezetimibe effect
medium decrease in LDL, no effect on HDL and TG
ezetimibe SE
rare increase in LFTs
Fibrates
gemfibrozil, clofibrate, bezafibrate, fenofibrate
Fibrate mechanism
upregulate LDL --> increase TG clearance
fibrate effect
small decrease in LDL, small increase in HDL, large decrease in TG
Fibrate SE
myositis, hepatoxicity (increase LFTs), cholesterol gallstones
Cardiac glycosides
digoxin
Digoxin bioavailability, protein bound, half life, excretion
75% bioavailability, 20-40% protein bound, half life = 40 hours, urinary excretion
Digoxin mechanism
direct inhibition of Na+/K+ ATPase --> inhibition of Na+/Ca2+ exchanger. increase in [ca2+]i --> positive ionotropy. stimulates vagus nerve
Digoxin clinical use
CHF (increase contractility); atrial fibrillation (decrease conduction at AV node and depression of SA node)
Digoxin toxicity
cholinergic - nausea, vomiting, diarrhea, blurry yellow, vision (think Van Gogh); ECG -- increase PR, decrease QT, scooping, T wave inversion, arrhythmia, hyperkalemia; worsened by renal failure (decrease excretion), hypokalemia, quindine
Digoxin antidote
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+
Antiarrhythmics - Class I (properties)
Na+ channel blockers (slow or block conduction esp in depolarized cells)--> decr in slow of phase 4 depolarization and incr threshold for firing in abnormal pacemaker cells. State dependent (selectively depresses depolarized tissue). local anesthetics. hyperkalemia causes inc toxicity.
Class IA (drugs)
Quindine, procainamide, disopyramide (the Queen Proclaims Diso's pyramide)
Class IA mechanism
increase AP duration, increase effective refractory period, increase QT interval
Class IA use
affects both atrial and ventricular arrhthymias, esp reentrant and ectopic supraventricular and ventricular tachycardia
quinidine toxicity (specific)
(cinchonism) headache, tinnitus; thrombocytopenia; torsades (de pointes due to increase in QT interval)
procainamide toxicity (specific)
reversible SLE like syndrome
Class IB (drugs)
lidocaine, Mexiletine, Tocainide (phenytoin)
Class IB action
decrease AP duration, preferentially affects ischemic or depolarized purkinje and ventricular tissue.
Class IB clinical uses
POST MI (Acute ventricular arrhthymias) and digitalis induced arrhthymias
Class IB toxicity
local anesthetic. CNS stimulation/depression, CV depression
Class IC (drugs)
Flecainide, Encainide, Propafenone
Class IC mechanism
no effect on AP duration. For pts without structural abnormalities
Class IC uses
V-tachs (thats progress to VF) and in intractable SVT (last resort in refractory tachyarrthymias)
Class IC toxicity
proarrhythmic, esp in post-MI (CONTRAINDICATED). prolongs AV node refractory period
Antiarrhythmics class II
Beta blockers
Beta blockers (drugs)
propranolol, esmolol (very short acting), metoprolol, atenolol, timolol
Beta blockers mechanism (as anti-arrhthymic)
decrease cAMP--> decrease in ca2+ currents, Suppress abnormal pacemakers by decr slope of phase 4. AV node particularly sensitive-- incr PR interval.
Beta blockers clinical use (as anti-arrhthymic)
V-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
Beta Blocker toxicity
impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. (treat overdose with glucagon)
metoprolol toxicity (specfic)
dyslipidemia
Antiarrhythmics-class III
K+ channel blockers
K+ channel blockers (drugs)
Sotalol, ibutilide, bretylium, dofetilide, amiodarone
K+ channel blockers mechanism
increase AP duration, increase ERP, used when others fail. increase QT interval
sotalol toxicity (specific)
torsades de pointes, excessive B block
Ibutilide toxicity (specific)
torsades
bretylium toxicity (specific)
new arrthymias, hypotension
amiodarone toxicity
pulmonary fibrosis (PFTs), hepatotoxicity (LFTs), hypothyroidism/hyperthryoidism (TFTs) (amiodarone -40% I by weight) ( + others -corneal deposits, skin depositis - photodermititis, neurologic effects, constipation, CV effects)
amiodarone mechanism
Class III -K+ blocker; but has effects of Class I, II, III, and IV because it alters the lipid membrane
Antiarrthymics Class IV
calcium channel blockers (CCBs)
CCBs (as anti-arrhthymic)
Verapamil, diltiazem
CCB mechanism (as anti-arrhthymic)
primarily affect AV nodal cells. decrease conduction velocity, increase ERP, increase PR interval
CCB uses (as anti-arrhthymic)
prevention of nodal arrhythmias (SVT)
CCB toxicity
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
adenosine mechanism
increase K+ out of cells --> hyperpolarization of cell and decrease of ca2+ influx. very short acting (15 secs)
Adenosine uses
DOC in dxing/abolishing supraventricular tachycardia
adenosine toxicity
flushing, hypotension, chest pain
Adeosine (blocked by?)
theophylline (blocks?)
K+
depresses ectopic pacemakers in hypokalemia (dig toxicity)
Mg2+
effective in torsades de pointes and digoxin toxicity
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