Cardio Drugs Flashcards
Calcium Channel Blockers - names
amlodipine, nimodipine, nifedipine (dihydropyridine), diltiazem, verapamil (non-dihydropyridine)
CCB mechanism of action
block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility
- vascular smooth muscle – amlodipine = nifedipine > dilt > verapamil
- heart – verapamil > dilt > amlodipine = nifedipine
- verapamil likes the ventricle
CCB clinical use
dihydropyridine (except nimodipine): HTN, angina, Raynaud
non-dyhydropyridine: HTN, angina, afib/flutter
Nimodipine: SAH (prevents cerebral vasospasm)
CCB toxicity
cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia and constipation
hydralazine mechanism
increases cGMP –> smooth muscle relaxation. vasodilates arterioles > veins; afterload reduction
hydralazine clinical use
severe HTN, CHF. first line therapy for HTN in preggos, with methyldopa. frequently co-administered with a beta blocker to prevent reflex tachycardia
hydralazine toxicity
compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. **Lupus like syndrome (due to liver acetylation of the drug)
Drugs to treat hypertensive emergency
nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam
- Neil likes Neil’s fun clonipine
nitroprusside
short acting, increases cGMP via direct release of NO. can cause cyanide toxicity (releases cyanide)
fenoldopam
dopamin D1 receptor agonist - coronary, peripheral, renal and sphlanchnic vasodilation. Decreases B and natriuresis
nitroglycerin, isosorbide mononitrate mechanism
vasodilate by increasing NO in smooth muscle –> increases cGMP and smooth muscle reladation. dilates veins»_space; arteries, decreases preload
clinical use of nitro/isosorbide mononitrate
angina, ACS, pulmonary edema
toxicity of nitro/isosorbide mononitrate
reflex tachycardia (treat with beta blockers), hypotension, flushing, headache "Monday disease" - lack of use over the weekend causes lack of tolerance, more side effects on reexposure
niacin effects on LDL, HDL and TG
significantly decreases LDL, significantly increases HDL, decreases TG
**best for increasing HDL
bile acid resins effects on LDL, HDL and TG
significantly decrease LDL, slightly increases HDL and TG
HMG CoA reductase inhibitors effects on LDL, HDL and TG
significantly decreases LDL, increases HDL and decreases TG
** best for decreasing LDL
cholesterol absorption blockers effects on LDL, HDL and TG
significantly decreases LDL, no effect on HDL/TG
fibrates effects on LDL, HDL and TG
significantly decreases TG, decreases LDL and increases HDL
** best at decreasing TG
niacin mechanism of action and SE
- inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis
- SE: flushing (dec by aspirin, long term use), hyperglycemia, hyperuricemia
HMG CoA reductase mechanism of action and SE
inhibits conversion of HMG CoA –> mevalonate, a cholesterol precursor
- increase LDL receptor density
- hepatotoxic, rhabdo
bile acid resins mechanism of action and SE
- prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more
- tastes bad, GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gallstones
cholesterol blockers mechanism/SE
- blocks absorption at the small intestine brush border
- rare inc in LFTs, diarrhea, hepatotox when given with statins
fibrates mech of action/SE
- upregulate lipoprotein lipase, increase TG clearance
- activates PPARalpha to induce HDL synthesis
- suppresses 7alpha hydroxylase
- myositis, hepatotoxicity, cholesterol gallstones (esp with bile acid resins)
Digoxin pharmacokinetics
- 75% bioavailability
- 20-40% protein bound
- t 1/2 = 40 hours
- urinary excretion
digoxin mechanism and clinical use
- direct inhibition of Na/K ATPase leads to indirect inhibition of the Na/Ca exchanger/antiport
- more Ca means positive intropy
- stimulates vagus nerve –> decreased HR
- used in CHF, afib
dig toxicity
- cholinergic - n/v/d, blurry yellow vision
- ECG - increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block
- can lead to hyperK
- precipitators of tox: renal failure, hypoK, verapamil, amiodarone, quinidine
- antidote: normalize K, cardiac pacer, anti-dig Fab fragments, Mg
Class 1 antiarrythmics - Na blockers
slow or block conduction, decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Hyperkalemia causes increased toxicity for all class I drugs
Class 1A antiarrhythmics (names)
Quinidine, Procainamide, Disopyramide
- “Quarter PounDer”
Class 1A mechanism/clinical use
increase AP duration, increase effective refractory period, increase QT
- used for both atrial and ventricular arrhythmias, esp re-entrant and ectopic SVT and VT
Class 1A toxicity
cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades
Class 1B meds
lidocaine, mexiletine, also phenytoin?
“Lettuce and mayo”
Class 1B mechanism/use
- decreased AP duration, preferentially affect ischemic or depolarized purkinje/ventricle tissue
- acute ventricular arrhythmias (esp post MI)
Class 1B tox
CNS stimulation/depression, CV depression
Class 1C meds
flecainide, propafenone
“Can i have Fries Please?”
Class 1C mech/use
- significantly prolongs refractory period in AV node
- minimal effect on AP duration
- used in SVTs, including afib. only as a last resort in refractory VT
Class 1C toxicity
proarrhythmic, esp post-MI (contraindicated)
- fries are contraindicated post-MI
Class 2: beta blockers (names) and mechanism and use
metoprolol, propranolol, esmolol (short-acting), atenolol, timolol, carvedilol
- decrease SA and AV node activity by decreaseing cAMP and Ca currents. supress abnormal pacemakers by decreasing the slope of phase 4
- AV node particularly sensitive - inc PR
- used in SVT, afib and aflut
beta blocker toxicity
impotence, exacerbation of COPD and asthma, bradycardia, AV block, CHF, sedation, sleep alterations
- may mask the signs of hypoglycemia
- metop can cause dyslipidemia
- prop can exacerbate vasospasm of P. angina
- contraindicated in cocaine users
- treat overdoses with glucagon
Class III antiarrhythmics - K channel blockers mech and use
amiodarone, ibutilide, dofetilide, sotalol (AIDS)
- increase AP duration, inc ERP, used when other antiarrhythmics fail. increase QT!
- used in afib, aflut, Vtach (amiodarone, sotalol)
K channel blockers tox
- sotalol - torsades, excessive B blockade
- ibutilide - torsades
- amiodarone - LOW risk torsades, pulm fibrosis, hepatotoxic, thyroid up or down, corneal deposits, photodermatitis, neuro, constipation, CHF, bradycardia, heart block
Class IV antiarrhythmics - Ca channel blockers
verapamil, diltiazem (non-dihydropyridine)
- decrease conduction velocity, increased ERP, inc PR
- prevent nodal arrhythmias (SVT), rate control of afib
Ca channel blocker tox
constipation, flushing, edema, AV nodal block, CHF
adenosine
increases K out of cells, hyperpolarizes cell and decreases ICa
- drug of choice for diagnosing/abolishing SVT
- lasts 15 sec
- SE: flushing, hypotension, chest pain
- effects blocked by thephylline and caffeine
Mg2+
effective in torsades and dig tox
