Cardio Flashcards
(32 cards)
How to treat essential HTN?
ACD: ACEI/ARB, CCB, Diuretics
How to treat HTN from CHF?
AAB: ACEI/ARB, aldos-inhib’s (spironolactone), b-blockers (compensated CHF only, C/I’d in cardiogenic shock) + diuretics
How to treat HTN from DM?
ACEI/ARB, CCB, diuretics, b-blockers, a-blockers (ACEI are protective against DM nephropathy)
CCBs =
Mech, clin use, toxicity
Nifedipine, verapamil, diltiazem, amlodipine
- block V-dep L-type Ca ch in cardiac/SmM, to reduce m. contractility
- HTN, angina, arrhythmias (not nifedipine), Prinzmetal’s angina (#1 drug), Raynaud’s
- cardiac depression, AV block, periph edema, flushing, dizziness, constipation
Ca ch blockers to use in:
- vascular SmM
- heart
- amloDIPINE=nifeDIPINE > diltiazem > verapamil
- verapamil > diltiazem > amlodipine=nifedipine (Verapamil=Ventricle)
Hydralazine
mech, clin use, toxicity
- incr’s cGMP -> SmM relaxation; vasodil’s a>v; reduces afterload
- severe HTN, CHF; 1st line tx for HTN in preg w/ methyldopa; often given w/ b-blocker to prevent reflex tachy
- compensatory tachy (C/I’d in angina/CAD), fluid retention, N, HA, angina, lupus-like synd
Nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam…use for?
Malignant HTN
Nitroprusside =
- used for?
Short acting; incr’d cGMP via direct release of NO (can cause cyanide tox bc releases it)
- malig HTN
Nitroglycerin & isosorbide dinitrate
Mech, clin use, toxicity
- vasodil by releasing NO in SmM -> incr’d cGMP and SmM relaxation, dilates v>a, decr’d preload
- angina, pulm edema
- reflex tachy, hypotension, flushing, HA, “Monday dz” in industrial re-exposure
-statins
MoA, effect on LDL/HDL/TG, SEs
- inhibit HMG-CoA to mevalonate (choles precursor)
- VERY low, incr’d, decr’d
- hepatotox, rhabdymyolysis (myopathy), cog impairments
Niacin (B3)
MoA, effect on LDL/HDL/TG, SEs
- inhib lipolysis in adipose, reduces hepatic VLDL secretion into circ
- decr’d, incr’d, slightly decr’d
- red flushed face (give aspirin), hyperglc (acanthosis nigricans), hyperuricemia (gout), hypotension (vasodilatory -> decr anti-HTN meds), hepatitis
Cholestyramine, colestipol, colesevelam
MoA, effect on LDL/HDL/TG, SEs
- bile acid resins; prevents GI reab’n of bile acids, liver must use choles to make more
- decr’d, slightly incr’d, INCR’d TGs
- pt’s hate it, tastes bad, GI discomfort, decr’d ab’n of fat-soluble vitamins, CHOLES GALLSTONES
Ezetimibe
MoA, effect on LDL/HDL/TG, SEs
- prevents choles reab’n at SmI brush border
- decr’d LDL, nothing else
- rare incr’d LFTs (esp w/ statins), D
Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)
MoA, effect on LDL/HDL/TG, SEs
- upreg LPL -> incr’d TG clearance (from chylo’s and VLDL)
- decr’d LDL, incr’d HDL (incr’d apoA1), very decr’d TG
- myositis (esp w/ statins), hepatotox (incr’d LFTs), choles gallstones
Digoxin
Mech, clin use, SEs
- factors -> more tox
- antidote
- cardiac glycoside; inhib’s Na/K pump -> incr’d IC Ca -> (+) inotropy; also stim’s vagus -> decr’d HR
- CHF (incr’d contractility), Afib (decr’d SA/AV node conduc)
- cholinergic (NVD, VanGogh vision), ECG shows incr’d PR, decr’d QT, ST scooping, T inversion, arrhythmia, AV block; hyperK
- renal failure bc less out, hypoK (competes w/ K to bind pump), quinidine bc displaces digoxin from tissue binding sites
- KLAM: slowly nl’ize K, lidocaine, anti-digoxin Fab, Mg…also pacemaker
Class IA antiarrhythmics
Drugs
MoA
Used for
“the Queen Proclaim’s Diso’s pyramid”
- Quinidine, procainamide, disopyramide
- Na ch blocker: interm inhib of phase 0 depol, incr AcP length (QT int)
- A and V arrhy’s, esp reentrant and ectopic SVT and VT
Toxicities of:
- Quinidine
- Procainamide
- Disopyramide
- All Class IA antiarrhythmics
- cinchonism, HA, tinnitus
- SLE-like synd
- HF
- thrombocytopenia, TdP
Class IB antiarrhythmics Drugs MoA Used for Toxicities
“Lettuce, Tomato, Mayo”
- Lidocaine, Tocainide, Mexiletine
- Na ch blockers: wk inhib of phase 0 depol, decr’d AcP length
- ischemic or depol’d Purk/ventric tissues; acute ventric arrhy’s (esp post-MI), digitalis-induced arrhy’s…anything due to long QT bc here shortens QT
- local anesthetic, CNS stim’n/depression, CV depression
Class IC antiarrhythmics Drugs MoA Used for Toxicities C/I'd in?
“More Fries Please”
(Moricizine), Flecainide, Propafenone
- Na ch blocker: strong inhib of phase 0 depol; no change in AcP length
- VT->VF, retractable SVT, for nl struc hearts
- proarrhythmic, esp post-MI (C/I’d), prolongs refractory period in AV node
- struc heart dz and post-MI
Class II antiarrhythmics
Ex’s
Mech, clin use, toxicity
Metoprolol, propranolol, esmolol, atenolol, timolol (-olol)
- b-blocker: decr’s SA/AV node act by decr’ing cAMP, decr’ing Ca currents -> suppress abnl pacemakers by decr’ing slope of phase 4
- VT, SVT, slowing ventric rate during Afib/flutter
- impotence, more asthma, CV effect (bradycardia, AV block, CHF), CNS effects (sedation, sleep alt’s), may mask signs of hypoglc
SEs of:
- metoprolol; trt overdose w/?
- propranolol
- dyslipidemia, trt overdose w/ glucagon (incr’s cAMP)
- Prinzmetal’s angina vasospasm
Class III antiarrhythmics
Ex’s
Mech
“AIDS”
- Amiodarone, Ibutilide, Dofetilide, Sotalol
- K ch blocker: incr AcP length/QT; use when other antiarrhythmics fail
Toxicities of:
- Sotalol
- Ibutilide
- Amiodarone
- Remember to check ? when using amiodarone
- TdP, big b-block
- TdP
- Pulm fibrosis, hepatotox, hypo/hyperthyroidism (bc is 40% iodine), corneal deposits, skin deposits (blue/gray) -> photodermatitis, neuro effects, constipation, CV effects (bradycardia, heart block, CHF); has class I, II, III, IV effects bc alters lipid membrane
- check PFTs, LFTs, and TFTs
Class IV antiarrhythmics
Ex’s
Mech
Toxicity
- Verapamil, diltiazem
- CCBs: decr conduc vel, incr’d ERP/PR int, used to prevent nodal arrhythmias (SVT)
- constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
