Cardiovascular Pharmacology from First Aid 2013
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| show | Diuretics, ACE-I's, ARB's, Ca-channel blockers
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| Drug categories for treating CHF? | show 🗑
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| show | ACE inhibitors
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| show | Nifedipine, verapamil, diltiazem, amlodipine
MOA: reduce muscular contractility
Use: HTN, angina, Prinzmetal's, Raynaud's, arrhythmias (Not Nifedipine)
Tox: A/V block, peripheral edema, flushing, dizziness, constipation
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| show | Nifedipine ("Not Nif")
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| Which calcium channel blockers should be used preferentially for vascular smooth muscle? | show 🗑
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| show | Verapamil ("Verapamil =Whic Ventricle")
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| show | Verapamil, diltiazem
MOA: decrease conduction velocity and increase PR-interval
Use for SVT.
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| show | Increase cGMP -> smooth muscle relaxation
Vasodilates ARTERIES > VEINS, so reduces afterload.
Use: severe HTN
Tox: reflex tachycardia (co-administer beta-blockers), fluid retention, nausea, headache, angina, Lupus-like syndrome.
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| What should be given with hydralazine and why? | show 🗑
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| What should be given in the case of malignant hypertension? | show 🗑
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| show | Short acting release of NO -> cGMP
Use: Malignant HTN
Tox: releases CN-
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| Fenoldopam: MOA, Use, SFX | show 🗑
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| Nitrates: MOA, Use, Tox | show 🗑
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| show | Tolerance to nitrates is built up by industrial exposure during the work week. This tolerance is lost on Monday, causing tachycardia, dizziness, and headache.
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| show | Beta blockers, to prevent reflex tachycardia.
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| Cardiac glycosides: MOA, Use | show 🗑
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| show | Cholinergic effects: GI, nausea, blurry vision
Increased PR, decreased QT, AV block
Hyperkalemia
Rx: normalize K, give lidocaine, anti-digoxin Ig, Mg2+
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| show | Stains, niacin (B3), bile acid resins, cholesterol absorption blockers, and Fibrates
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| show | HMG-CoA reductase inhibitors, "-statin"
Decrease LDL, Trig; increase HDL
Tox: hepatotoxicity and rhabdomyolysis
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| show | Inhibit lipolysis in adipose tissue, reduce hepatic VLDL secretion.
Decrease LDL and Trig; increase HDL
Tox: flushed face, hyperglycemia, hyperuricemia (gout)
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| show | Prevent intestinal reabsorption of bile acids.
Begin with "chol-", e.g. cholestyramine.
Decrease LDL; increase Trig and HDL
Tox: nasty taste, GI upset, decreased absorption of ADEK, cholesterol gallstones
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| show | Ezetimibe: acts on brush border.
Decrease LDL.
Tox: diarrhea
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| show | Upregulates LPL -> increase triglyceride clearance.
Contain "-fibr-", e.g. gemfibrozil.
Tox: Myositis, hepatotoxicity, cholesterol gallstones
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| What is the mnemonic for anti-arrhythmics? | show 🗑
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| show | Slow or block Na+ conduction, decreasing the slope of Phase 0, and increasing the threshold for firing.
Hyperkalemia increases the toxicity of all Class I anti-arrhythmics.
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| Class IA anti-arrhythmics: Names, Use, Tox | show 🗑
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| Toxic side effect of Quinidine? | show 🗑
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| show | SLE-like syndrome
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| Toxic side effects of Disopyramide? | show 🗑
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| show | Lidocaine, Mexiletene, Tocainide
"I'd Buy Lido's Mexican Tacos"
Use: Decrease AP duration in ischemic, ventricular Purkinje cells. Use post-MI or post-digitalis-induced toxicity.
Tox: local anesthetic, CNS/CV depression
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| show | Class IB: Lidocaine
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| Class 1C anti-arrhythmics: Names, Use, Tox | show 🗑
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| show | Beta blockers: decrease SA and AV nodal activity, lengthening PR. End in "-olol".
Use: VTach, SVT, slowing down ventricles during Afib or Aflutter
Tox: Impotence, asthma, bradycardia, sedation, masking of hypoglycemia
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| show | Dyslipidemia, give glucagon to correct
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| Toxic side effect of Propanolol? | show 🗑
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| show | Potassium-channel blockers: increase AP duration, ERP, and QT interval (-> Torsades)
Use when other anti-arrhythmics fail
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| show | "AIDS":
Amiodarone
Ibutilide
Dofetilide
Sotalol
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| Toxic side effects of amiodarone? | show 🗑
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| show | Torsades
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| How do Class IV anti-arrhythmics work? What is their toxicity? | show 🗑
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| Which Calcium channel blockers should be used for arrhythmias? | show 🗑
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| show | Adenosine
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| How does adenosine work? | show 🗑
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| show | Theophylline and caffeine
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| show | Mg2+
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