cardio drugs Flashcards

Terms Definitions
phosphodiesterase inhibitors
htn, CHF
prototype for anticholinergic
class III anti-arrhythmics
class Ib anti-arrhythmics
- htn
- pheochromocytoma
MOA: Antianginal vasodilator prototype: releases nitric oxide (NO) in smooth muscle of veins, less in arteries, and causes relaxation through cGMP pathway.
Use: Standard of therapy in angina (both atherosclerotic and variant). CHF. HTN control
competitive aldosterone receptor antagonisturinary K excretion is decreasedtreat hyperaldosteronism, HTN, female hirsutisms.e. hyperkalemia, gynecomastia
class I-IV anti-arrhythmic actionstreatment of life threatening atrial and ventricular tachycardiasS.E. pulmonary fibrosis, hepatotoxicity, thyroid dysfxn
low molecular weight heparin
- vasoconstriction
- increases peripheral resistance, increases bp
- increased bp causes reflex bradycardia (blocked by atropine)
- Used to maintain bp in hypotensive states and to slow paroxysmal atrial tachycardia.
- nonselective beta blcoker
Flecainide Tox
Tox: arrhythmogenic, CNS excitation.
Note: Propafenone is similar. Side effect = metallic taste & constipation.
MOA: Membrane hyperpolarization and suppression of Ca2+ dependent action potentials causing decreased rate of conduction through AV node.
Use: Block nodal reentry arrhythmias. No effect on ventricular arrhythmia.
Prazosin Tox
Tox: first-dose orthostatic hypotension but less reflex tachycardia than nonselective a blockers. Syncope.
Captopril (PT)
MOA: Reversible Angiotensin-converting enzyme (ACE) inhibitor. Net effect = arterial & venous dilation & natriuresis
Use: HTN, diabetic nephropathy (dec. proteinuria and progression of renal dz), CHF (dec afterload, LV remodeling, and increased survival).
non-cardioselective B blockers:
propranolol, timolol, nadolol
prazosin is a prototype for
losartan is a prototype of...
angiotensin receptor blockertreat HTN and CHFS.E. proteinuria, renal failure, hypotension, teratogen, rash, hyperkalemia
cardiac glycosideinhibits Na/K ATPase pump -->increase intracell Na -->decreases Na/Ca exchange -->less Ca exits, conc. increases -->increased contractility of myocytesincreases parasymp. outflow a SA and AV node -->decreases HRuse - increases contractility in pt. w. left heart failureS.E. GI upset, blurry yellow vision, EKG changesS.E. exaccerbated by hypoK, renal failure, and quinidine use
osmotic diureticacts at proximal tubule and descending limb of loopincrease tubular osmolarity drawing water outdecreases intracranial or intraocular pressurecontraindicated in pts. w. CHF - can lead to pulmonary edema w. initial volume increase
HMG-CoA reductase inhibitor (statin)
- processed more by the kidneys than liver, so good for patients with liver issues.
HMG-CoA reductase inhibitor (statin)
- prodrug that must be converted (hydrolyzed) in GI tract to active compounds
- nonenzymatic activator of plasminogen
- serious hemorrhage is potential SE.
MOA: Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation.
Use: 2nd line treatment for high TGs after Fibrates. 1st line to increase HDL.
MOA: Selective dopamine 1 agonist resulting in vasodilation of vessels (especially renal, mesenteric, and coronary beds). Also leads to sodium and water excretion
Use: HTN emergency (IV) +/- concomitant renal insufficiency
Digoxin (PT)
MOA: Cardiac glycoside; Inhibits Na+/K+ ATPase (Inc intracellular Na+ disrupts Na+/Ca2+ exchanger thus Inc intracellular Ca2+ leading to positive inotropy), also a cardiac parasympathomimetic (Inc vagal tone).
Use: CHF, A-fib, A-flutter
MOA: Beta1 selective blocker: low lipid solubility, less CNS effect;
used for HTN.
Flecainide (PT)
MOA: Class IC antiarrhythmic prototype: marked Na+ channel blockade
Use: ventricular tachycardia and rapid atrial arrhythmias with Wolff-Parkinson-White syndrome.
Reserpine Tox
Tox: severe depression, suicide, ulcers, diarrhea.
prototype of calcium channel blcokers (DHP)
Indications for ACEi's
1. HTN2. CHF3. post-MI
do b-blockers have direct inhibitory effects on the SNS?
which of teh inotrope/pressors is/are inotrope(s) but not pressors?
metabolized to NO --> stimulates guanylate cyclase --> increases cGMPvasodilation of peripheral veins and arteriesacute management of hypertensive crisisS.E. cyanide toxicityonly given IVbalanced venous and arterial vasodilator -->decreases preload and afterloadchanges balanced - stroke volume maintained
Na channel blocker of cardiac myocytesphase 3 of repolarization and the entire duration of the AP is shortenedtreate acute ventricular arrhythmias, esp. from MI or surg.may cause cardiac arrhythmiasuse-dependent - more active at ion channels depolarizing more often
dilates arterial smooth muscleopens K channels in membrane, hyperpolarizing, inhibiting contractionpromotes hair growth
- shorter, genetically engineered form of tPA.
- diffuses more freely into clot the tPA
- shorter 1/2 life than tPA
which statin has the highest potency?
What are statins best at lowering?
- used in angioplasties
- inhibits platelet aggregation and is a weak vasodilator.
Hyralzine Tox
Tox: reflex tachycardia, salt and water retention (in response to vasodilation), lupus-like syndrome (hydralazine).
Niacin Tox
RED FLUSHED FACE (⇓ by aspirin)
HYPERGLYCEMIA (acanthosis nig)
Diazoxide Tox
Tox: Can cause hyperglycemia (reduces insulin release).
MOA: Alpha2 agonist: acts centrally to reduce SANS (NE) outflow, lowers BP.
Use: in HTN and in drug dependency states.
Methyldopa tox
Tox: sedation, drug induced positive Coombs hemolytic anemia,
GemFIBrozil, CloFIBrate, FenoFIBrate
MOA: Fibrate. Upregulates lipoprotein lipase which ⇑ TG clearance
Use: 1st treatment for High Triglycerides
Minoxidil Tox
Tox: Hypertrichosis (lots of hair growth), pericardial effusion, reflex tachycardia, angina, salt retention.
Procainamide (PT)
MOA: Class IA antiarrhythmic: moderate Na+ channel blockade. Use dependent-Class IA selectively block channels that are being used more frequently.
Use: AF, AFL, PSVT, Emergent VT
Mannitol Tox
Tox: expansion of extracellular fluid volume (pulls water out of cells) with resulting hyponatremia, headache, nausea. With excessive use, dehydration and hypernatremia.
Spironolactione (PT)
MOA: K+ sparing diuretic; comptetive antagonist of aldosterone at the aldosterone receptor in the DCT. Decreased Na+ absorption, K+ excretion, and BP.
Use: HTN, Edema, CHF, Primary hyperaldosteronism, Female Hirsutism (Androgen receptor blocking activity)
Digoxin Tox
Tox: calcium overload, arrhythmias, GI upset, Dig delirium = nausea, blurred vision, hallucinations.
Acetazolamide Tox
Tox: Metabolic acidosis, Renal stones (b/c of alkalinized urine), encephalopathy
digoxin is classified as a cardiac ________
this drug can provoke an systemic lupus erythromatosus effect (immunological effect)- causing glomerulonerphritis
captopril is a prototype of what class?
what is the MAJOR concern with digoxin
mixed alpha and beta receptor B-blockers
carvedilol, labetolol
potassium for arrhythmias
increase extracell conc., threshold for cardiac AP raised, making it more difficult to generate one -->rate of excitation reducedsuppresses ectopic pacemakers, esp. assoc. w. digoxin toxicityS.E. hyperkalemia, cardiac arrhythmia, paralysis, shock
what side effects to verapamil produce?
- constipation
what are the nonselective beta blockers?
- propranolol
What are the fibrates most effective on?
- inhibits formation of TXA2 by platelets and inhibits aggregation
- used in prophylaxis and tx of MI and stroke
CHOLEstyramine, COLEstipol, COLEsevelam Tox
⇓ absorption of fat vitamins
Ibutilide Tox/Variants
Tox: increased QT interval = torsades de pointes
Note: Dofetilide & Solatol are similar
Clonidine Tox
Tox: mild sedation, rebound HTN if stopped suddenly.
which of the inotrope/pressors is/are both inotrop(s) AND pressor(s)?
dopamine and epi
Low Molecular weight heparins
- Enoxaparin, Delteparin, Tinzaparin
- prophylaxis of DVT and PE
- binds antithrombin III and inhibist Xa
- administered SC
what are the thrombolytic drugs?
- tPA
- reteplase
- streptokinase
What is a cholesterol absorption inhibitor?
- Ezetimibe (Zetia)
Lovastatin, Pravastatin, Simvastatin, Atorvastatin, Rosuvastatin
MOA: HMG-CoA reductase inhibitor which blocks formation of cholesterol precursor Mevalonate.
Use: 1st line to lower LDLs
Captopril Tox
Tox: fetal renal damage, cough (due to block of bradykinin clearance), 1st Dose Hypotension, Acute renal failure, Hyperkalemia (blockade of ATII production may lead to decompensation & renal insufficiency).
MOA of anticholinergic
blocks activity of Ach at M receptors
What are the breakdown products of SNP
cyanide and NO
quinidinetype of drug and side effects
class Ia anti-arrhythmiccinchonism (vertigo, HA, tinnitus)GI upset
disopyramidetype of drug and side effects
class Ia anti-arrhythmicurinary retentiondouble visionconstipation
What happens in bypyridine toxicity?
- Inamrinone: nausea, vomiting, arrhythmias, thrombocytopenia, liver toxicity
- Milrinone: arrhythmias, less bone marrow depression and liver toxicity than Inamrinone.
All statins undergo....
extensive 1st pass metabolism by the liver.
what are the alpha one selective blockers?
- prazosin
- tamsulosin
indications for digoxin
CHF (3rd line for adults, 1st line for kids)atrial flutter - decreases AV node conduction, and therefore regulated ventricular contractions
MOA of ca-channel blockers
L type receptor blockers - inhibit contraction of smooth muscle
procainamidetype of drug and side effects
class Ia anti-arrhythmicdrug induced lupuspsychosis
verapamil and diltiazem
- Ca channel blocker
- block the channel and delay the recovery
- decrease rate of SA node depolarization and slow AV nodal conduction (useful in supraventricular tachyarrhythmias)
Beta adrenergic (dopaminergic) agonists
- stimulate SNS which leads to positive inotropic action
- MOA: stimulation of cardiac myocyte via beta 1 receptor and D1 receptor through the cAMP protein kinase A pathway
What are contraindications of fibrates?
- potentiate the actions of anticoagulants
- avoid in pts with hepatic or renal dysfxn
- safety not established in pregnant of lactating women
- increase risk of gallstones
- avoid concurrent use with statins
- t1/2 = 3 min
- IV bolus followed by IV infusion
- adverse effects are serious hemorrhage
- expensive
clinical uses of beta blockers
- hypertnesion
- angina, MI, acute coronary syndromes
- arrhythmias
- thyrotoxicosis
- adjunctive tx for panic (anxiety) attacks
- migraine headache
- pheochromocytome
What do fibrates do?
- derivatives of fibric acid that can reduce plasma levels of TG and cholesterol.
how do you tx a heparin overdose?
- stop administration
- protamine sulfate given slowly via IV
- fresh frozen plasma
2 mechs by which ACEi's works
1. blocks production of AII (and therefore aldosterone2. blocks breakdown of bradykinin
main diff b/w DHP and non-DHP?
DHP is more selective for vasculature (less cardio effects)
what do beta 2 adrenergic effects do?
- "2 lungs"
- relaxes bronchioles.
what is a medium dose of heparin for?
prevent propagation of a thrombus
why shouldn't you suddenly take a patient off a beta blocker?
rebound htn is possible, anginal attack and possibly MI due to receptor upregulation and supersensitivity.
what are common side effects of beta blockers?
- dizziness, fatigue, diarrhea, constipation, nausea, depression, sexual dysfxn, bizarre dreams.
What is the MOA of niacin?
inhibits the lipolysis of TG in adipose tissues - thereby making less free FAs available for production of LDLs and VLDLs.
what is the MOA of beta blockers?
- blocks existing sympathetic tone
- decreases heart rate and CO
- decreases exercise tolerance
- decreases O2 demand!!!!!
- decreased AV nodal conduction and increases the refractory period of AV node.
- also block increase in renin due to catecholamine release - somehow helps lower bp.
What are possible drug combinations for hyperlipidemia?
- niacin and bile acid sequestrants
- niacin and statins
- statins and ezetimibe (vytorin)
- statins and fibrates
What happens with too high levels of digoxin?
- marked shortening of AP
- Arrhythmias.
what does alpha 2 adrenergic effects do?
- CNS effects (ie: clonidine decreased symp tone)
what is the use of LMWH?
- SQ injection for prophylaxis of DVT associated with hip, knee and abdominal surgery
why are b-blockers risky to use in diabetics?
b/c they mask the tachycardia that usually signals to diabetics that they are hypoglycemic
why are Ca-channel blockers not used as a first line Tx in pts with hypertension
b/c it has been found dto have increased incidence of heart failure c.f. thiazides or ACEi's
What makes up a "red clot" ?
- occurs with slow blood flow and pressure
- lots of protein gets laid down and traps RBCs, making it "red".
- usually long and go far up a vessle
** Venous thrombosis**
what is the advantage of low molecular weight heparin in comparison to UFH?
- smaller, active pieces of regular heparin, so they have greaty anti Xa activity, and less platelet activity
- has a longer duration, simpler kinetics and clotting tests are not usually required.
- also less likely to cause HIT syndrome
where are the effects of anticholinergics most pronounced?
at the SA and AV nodes - result in increased pacemaker rates of the SA node and increased conduction through AV
what is a contraindication in using verapamil and diltiazem?
- use of a beta blocker bc it can cause AV block
class IA anti-arrhythmics
calcium channel blockers
class IV anti-arrhthymics
cardiac glycosides
- digoxin
- Inamrinone
- Milrinone
Spironolactone Tox
Tox: hyperkalemia, gynecomastia.
Statin Toxicity
Antihypertensive (rarely used): selective inhibitor of vesicle catecholamine-H+ antiporter whichcauses depletion of catecholamines and 5-HT from their stores.
Use: HTN
loop diurecticinhibits Na/K/2Cl transport system in thick ascending limbresults in NaCl, K and water retention in tubular lumenincreased water and electrolyte losstreat heart failure w. assoc. pulmonary edema, liver failure and renal failureHTN and hypercalcemias.e. hypokalemia, ototoxicity, hyperuricemia, allergic rxn to sulfa
treat erectile dysfunctioninhibits cGMP PDE type 5 found in corpus cavernosumrelaxes smooth m. of penisincreases blood flowcontraindicated in pt. on nitrates
HMG-CoA reductase inhibitor (statin)
HMG-CoA reductase inhibitor (statin)
MOA: Antihypertensive: prodrug of methylnorepinephrine, a CNS active a2 agonist. Reduces SANS (NE) outflow from vasomotor center.
Use: HTN
Prazosin (PT)
MOAS: Reversible Alpha1-selective blocker on vascular smooth smooth mucle = arteriolar and vasodilation.
Use: HTN and benign prostatic hyperplasia.
MOA: Prevents cholesterol reabsorption at small intestine brush border
Use: 2nd line treatment for high LDL after Statins
Nitroglycerin Tox/Variants
Tox: tachycardia, orthostatic hypotension, headache. Tolerance development (space out doses)
Variants: long acting oral nitrates = isosorbide dinitrate, isosorbide mononitrate (100% BIOAVALIABILITY).
MOA: Diuretic inhibits carbonic anhydrase in the proximal tubule; results in decreased reabsorption of bicarbonate leading to bicarbonate diuresis and potentially a hypercholerimic metabolic acidosis.
Use: glaucoma, mountain sickness, alkalosis
MOA: arteriolar vasodilator,
Use: severe HTN, 1st line for pregnacy HTN, CHF ( dec. afterload).
MOA: K+ channel opener-hyperpolarizes and relaxes vascular smooth muscle
Use: Severe HTN
indications for SNP and hydralazine
indications of B blockers
hypertensionheart failurearrhythmiaanginapost-MInon-cardio (migrain, stage fright, anxiety, flaucoma)
class III anti-arrhythmicsK channel blockers on cardiac myocytesprolong phase 3 repolarizationprolong entire APprolong QTmay cause cardiac arrhythmias
inhibit phosphodiesterase isozyme III -->increases cAMP -->opening of Ca channels -->increased contractilitytreatment of acute heart failureS.E. nausea/vomiting
class IV anti-arrhythmicsblock voltage gated Ca channelsslow phase 4 spontaneous depol.prolong PR intervaltreat SVT, rate reduction in a. fibS.E. hypotension, heart block
- monoclonal antibody
- prevents fibrinogen binding to glycoprotein and inhibits platelet aggregation
- greater antithrombotic activity than aspirin or heparin
HMG-CoA reductase inhibitor (statin)
- prodrug that must be converted (hydrolyzed) in GI to active compounds.
- slow, sustained oral anticoagulation
- inhibits vitamin K dependent modification of clotting factors prothrombin, VII, IX, X, protein C and S.
- oral administration only
- slow onset, metabolized by liver and kidneys
- PT test, INR
- LONG elimination t1/2 (2-5 days)
- LOTS of drug-drug interactions
MOA: Decreases the activity of platelet phosphodiesterase (which breaks down cAMP). Increase cAMP = decrease platelet aggregation. Also a direct arterial vasodilator.
Use: Intermittent claudication
Nifedipine Tox
Tox: constipation, headache, gingival overgrowths, tachycardia, arrhythmias (avoid rapid-onset forms in CAD), peripheral edema.
Nifedipine (PT)
MOA: Dihydropyridine calcium channel blocker. vasoselective for Calcium receptor (less cardiac depression than verapamil, diltiazem). Net effect = peripheral vasodilation
Use: Vasospastic Angina, HTN, Raynaud's phenomenon
Lidocaine Tox
Tox: CNS excitation (paresthesias, tremor, nausea, slurred speech, agitation, seizures).
Contra: WPW syndrome
Note: Mexilitine is like lidocain, given PO
GemFIBrozil, CloFIBrate, FenoFIBrate Tox
side effects of ACEi's
dry coughrenal failurehyperkalemiahypotensionangioedema - due to effects of increased bradykinin
vasodilator (moderate venodilator properties)
how are Ca-channel blockers metabolized?
direct relaxation of arteriolar smooth muscletreat hypertension and heart failureS.E. HA, tachy that may provoke angina in CAD pt., drug induced lupusgiven w. beta blocker to prevent reflex tachy
block Na channels on cardiac myoctyesprolong phase 0 of cardiac APdon't effect duration of APtreat severe refractory ventricular arrhythmiascan exacerbate or induce life threatening arrhythmiasuse dependent
ACE inhibitortreat HTN and CHFS.E. cough
Na channel blockers on cardiac myocytesprolong phase 0 depolarization - slowing conductiondelay phase 3 repolarizationincrease AP duration, ERP, and QT intervaltreat a. fib, a. flutter, v. tachmay cause arrhythmias
- vasodilates renal, coronary and mesenteric vascular beds
- increases blood flow to kidney
- used in shock to increase CO and enhance perfusion to kidney.
which statin has the lowest potency?
- blocks platelet aggregation by blocking ADP receptor
- prophylaxis of stroke, MI, PAD and acute coronary syndrome
What is Niacin best at raising?
Nitroprusside Tox
Tox: Same as nitroglycerin. Cyanide toxicity = lactic acidosis, arrhythmias, hypotension, cytotoxic hypoxia. Rx = Sulfur & Nitrites
Losartan (PT)
MOA Angiotensin II receptor blocker (AT1) prototype:
Use: HTN, diabetic nephropathy (dec. proteinuria and progression of renal dz), CHF (dec afterload, LV remodeling, and increased survival).
Atenolol Tox
Tox: asthma, bradycardia, AV block, heart failure.
Propanolol Tox
Tox: asthma (bronchospasm), AV block, sinus bradycardia, hypotension CHF.
Losartan Tox
Tox: Hypotension, NO COUGH, Acute renal failure, Hyperkalemia (blockade of ATII production may lead to decompensation & renal insufficiency).
Lidocaine, Mexiletine, Tocainide
MOA: Amide local anesthetic, medium-duration amide prototype: highly selective use-dependent class IB antiarrhythmic (mild Na+ block)
Use: for nerve block and post-MI ischemic ventricular arrhythmias.
Sildefanil Tox
Tox: severe hypotension when combined with nitrates, impaired blue-green color vision, Priapism.
Furosemide (PT)
MOA: Loop diuretic prototype; blocks Na+/K+/2Cl- transporter in thick ascending limb; Increased urinary excretion of K+, Mg2+, Ca2+ and volume depletion. High efficacy. Stimulates prostaglandin release (vasodilation of renal arterioles = ⇑ diuresis)
Use: acute pulmonary edema, refractory edematous states, hypercalcemia, hyperkalemia.
what drug initially results in compensatory SNS response such as renin release and tachycardia? (later these subside, and you get the vasodilatory effect you aimed for)
alpha antagonists
indications for ARBs
hypertensionCHFfor pts that cna't tolerate ACEi's b/c of the cough
which of the inotropes and pressors are synthetic compounds?
what is one factor that increases digoxin sensitivity
SE's of ARBs
m/c = dizziness, hypotension-renal failure-hyperkalemia
in addition to being an inotrope, digoxin is loosely classified as a(n) ______
main SE's of B blockers
-fatigue-bradycardia-lipid profile changes - increased triglycerides, and increasesd HDl, without a change in total cholesterol-carb metabolism - reduced carb metabolism and glu mobilization-raynaud's phenom.
nifedipine, etc.
block voltage gated Ca channelstreat HTN and Prinzmental's anginaS.E. bradycardia, heart block, GI upset
class II anti-arrhythmics
beta blockersdecrease cAMPdecrease Ca currentsdecrease slope of phase 4AV node particularly sensitive - increase PR interval
Which way of administering heparin is the slow prophylatic manner?
- effective in acute HF
- reduce preload or afterload, or both.
- MOA: causes sm mm relaxation by supplying NO
Propanolol (PT)
MOA: Nonselective beta blocker (B1 & B2 competitive antagonist). Class II antiarrhythmic. Decreases inotropy & HR, phase 4 slope; local anesthetic action but no partial agonist effect.
Used: HTN, angina, arrhythmias, migraine, hyperthyroidism, tremor, stage fright.
Hydrochlorothiazide (PT)
MOA: Thiazide diuretic; acts in distal convoluted tubule to block Na+/Cl- transporter. Ca2+ reabsorption is enhanced b/c Ca2+ and Na+ compete for ATP dependent reabsorption in DCT.
Use: 1st line in uncomplicated HTN, Edema, Diabetes Insipidus, Hypocalcemia, Recurrent renal calcium stone formation
SE's of digoxin (toxicity) (4)
increased automaticiy (PAC/PVC) by:-increasing P4 slope-decreasing phase 0 slope-afterdepolarizationsLong PR or AV blockv.fibST "scooping"
contraindications for ACEi's
1. pregnancy - hypotension2. renal failure
- Ca channel blocker
- block channel but do not effect recovery of channel & are not “frequency (use) dependent”
- long t1/2
- decrease PVR, venous return, and preload.
- can cause postural hypotension and syncope, orthostatic hypotension, esp with initial doses.
what does alpha 1 adrenergic effects do?
- vasoconstriction
- selective for beta 1
- increases SV and CO
- major SE: excessive tachycardia and arrhythmias
- beta agonist of choice in tx of systolic dysfxn and HF
- MOA: relax vascular sm mm and decrease preload and afterload
- short t1/2
- decrease PVR, venous return, and preload.
- can cause postural hypotension and syncope, orthostatic hypotension, esp with initial doses.
what are the nonselective alpha blockers?
- phenoxybenzamine
- phentolamine
what is a drug that is dangerous to stop abruptly due b/c of receptor upregulation?
indications for ca-channel blockers (DHP)
hypertension (not as first line)stable angina (not as first line)variant (Printzmetal's) - to control spasms
SE of alpha antagonist that stands out?
first dose hypotension
what is one of the main consequences of DHPs having a greater effect on vasculature than the heart?
reflex tachycardia
magnesium for arrhythmias
believed to effect ion flow through Na, K, Ca channelstreat torsades & digoxin toxicityS.E. hypermag, hypotension, delayed deep tendon reflexes, paralysis, shock
What is a small dose of heparin for?
prevent thromboembolism
Unfractionated Heparin (UFH) administration and MOA
Drug of choice for parenteral anticoagulant therapy
- combines with antithrombin III binds and inactivates clotting factors IIa, Xa, IXa, XIa, XIIa
- fast onset
- rapid parenteral anticoagulation
what are teh 2 vasodilators we talk about in the handout?
hydralazinesodium nitroprusside (SNP)
do ARB's work upstream or downstream from teh ACEi's?
downstream - step after!
2 MOAs of digoxin
1. blocks Na/K ATPase --> increases intracellular concentration of Na --> blocks the gradient for outflow of Ca from teh myoctye --> Ca stays in myocyte --> increased contractility, SV, CO2. direct effect on parasympathetic system - incresases sensivity of baroreceptors - fire more readily to vagal nuclei - decreases HR, causes vasodilation
how do you monitor heparin therapy?
- aPTT prior to starting
what are toxicities for warfarin use?
- hemorrhage
- anorexia, vomiting, nausea, diarrhea
- skin necrosis
What are adverse effects of fibrates?
- GI disturbances
- lithiasis, gallstones
- myositis, myopathy, rhabdymyolysis
what is one inappopriate use of inotropes/pressors?
using them to correct hypotension/shock, when the underlying problem is a preload problem (i.e. hypovolemia) - MUST CORRECT PRELOAD FIRST before afterload is manipulated
What is the MOA for fibrates?
ligand for PPARalpha agonist on nuclear receptors. they induce expression of lipoprotien lipase which leads to lipolysis of TG and decreases plasma concentrations.
what is a large dose of heparin for?
inhibit established pulmonary embolus
what is ACEi's effect on preload? afterload? SVR?
decrease afterload and SVR thru vasodilatory effectsdecrease preload b/c block aldosterone and therefore reabsorption of water
B1 antagonism due to b-blockers will cause waht?
reduction in renin secretion --> causes vasodilation
will hydralizine have an effect on preload?
no b/c its not a venodilator
what are side effects of heparin?
- hemorrhage
- hematoma at site of injection
- platelet aggregation, thrombocytopenia (heparin induced thrombocytopenia = HIT), acute hypersensitivity, alopecia, osteoporosis, priapism.
what are contraindications of heparin?
- any site of active or potential bleeding
- severe hypertension or known vascular aneurysm
- recent head, eye or spinal cord surgery
- head trauma
- LP or regional spinal anesthetic block
- TB, visceral carcinoma, GI ulcers
What are direct thrombin inhibitors?
- bind directly to thrombin and are smaller proteins.
- $$$$
- approved for use in pts with thrombosis related to HIT and during coronary angioplasty.
- Hirudin, lepirudin, bivalirudin, argatroban
beta 2 selective agonists
are about 10 fold more potent for beta 2 than beta 1. primarily greater selectivity for lung > hearts
What is the MOA of a cholesterol absorption inhibitor?
- selectively inhibits intestinal absorption of cholesterol and phytosterols
- effective even in the absence of dietary cholesterol bc it inhibits reabsorption of cholesterol excreted in the bile.
- can be used alone or in combination with statins or fibrates.
what is the main problem with propranolol
low bioavailability due to first pass effects
what is the most common side of toxicity outside of the heart for digoxin?
GI system - anorexia, nausea, vomiting, diarrhea.
What are the 2 main fibrate drugs?
1. gemfibrozil (1.5 hrs t1/2)
2. fenofibrate (20 hrs t1/2)
what do beta 1 effects do?
- work on heart
- stimulate heart rate and force of contraction
what is the objective of thrombolytic therapy?
- dissolve pathological blood clots by injecting a fibrinolytic enzyme or an activator of endogenous fibrinolysis without causing uncontrolled bleeding.
does ARB have an effect of cough?
nope. probably due to the fact that it doesn't affect bradykinin
What is the MOA of bile acid sequenstrants?
- bind to negatively charged bile acids and increase their excretion up to 10 fold.
- not absorbed or metabolized - totally excreted in the feces.
- increased excretion of the bile acids enhances the conversion of cholesterol into bile acids in the liver, and decline in hepatic cholesterol stimulates expression of LDL surface receptors and thereby lowers plasms LDL concentrations.
What are adverse effects of bile acid sequestrants?
- GI are the most common
- impaired absorption of fat soluble vitamins (A, D, E, K) and drugs such as digoxin, warfarin, fluvastatin, aspirin, thiazides.
- use with caution in pts with diverticulitis, preexisiting bowel disease.
Class II
Nodal Tissue
Class IB
Ventricular Aryths
Mech: synthetic, sulfated pentasaccharide -> binds antithrombin -> selective inhib of Factor Xa
Bile Acid Binding Resins
Fibrinolytic (TPA)
Fibrinolytic in MI
Class III
Broad spectrum anti-arryth
Other: Expensive and new/unproven
Mech: Binds PPARalpha (nuclear receptor that normally turns on fatty acid synth to make TGs in liver and brown adipose tissue) -> decrease TGs via stim of FA oxidation, increased liporpotein lipase synthesis and decreased apoC-III
Class IA
Tachyarrhythmias (Supraventricular and Ventricular)
B agonists
Acute Decomp HF
Dopamine, Dobutamine
Class IC
Response: decrease CONDUCTION, automaticity, increase QRS (VERY marked)
Aldosterone Antagonists
SE: hyperkalemia, gynecomastia, impotence (spironolactone) and menstrual irregularities(spironolactone)
B-adrenergic Blockers
Mech: competitively block B-ad receptors
Phosphodiesterase Inhibs
Mech: inhib phosphodiesterase type IIIa (SR of cardiac myocytes and vasc smooth M, not ED ones) -> increase cAMP in SR -> increase Ca in cells (similar to digoxin)
Class IV
Mech: block L-type Ca channel
Mech: Inhib hepatic HMG-CoA reductase (needed for chol synth) -> more LDL receptors expressed -> more LDL removed from blood
Direct Arterial Vasodilators
Response: decrease arteriolar contraction -> decrease afterload -> decrease O2 demand (work)
Cholesterol Absorption Blockers
Use: Adjuvant to statins
Other: efficacy and tolerability NOT change elderly and comorbid (preexisting) conditions (diabetes, heart fail)
ALMOST ALL PTS CAN TAKE SAFELY!!! (b-block have issues in diabetes and heart fail)
GP IIb/IIIa Receptor Inhibitor
Unstable Angina Thrombosis (percutaneous coronary interventions)
K+ Sparing Diuretics
Chronic Heart Failure (?), Hypertension
Block up pore
Oral X-Coags
Response: decrease growth of existing thrombi, prevent new thrombi formation
Use: restricted to acute decomp HF, decrease Sx, maintain circulatory stability, NO survival
Ca Channel Blockers
SE: headache, dizzy, flushing, hypotension, leg edema, V = constipation and nausea
Loop Diuretics
Other: resistance to diuretic effect happens lots in HF pts, overcome w/higher dose or adding thiazide.  Combo w/K-sparing diuretic (prevent K loss), action potentiated (increased) by renin-angiotensin inhibs (ACEI or ARB), also put on low sodium, high potassium diets, ONLY diuretic used for acute decomp, less effective than thiazide in hypertension, use in chronic renal failure w/high BP
Renin Angiotensin Inhib
Response: decrease venous and arterial contraction, SNS, and ventricular remodeling (for 2nd prevention), TPR (HT), increase renal Na/H2O excretion
Thiazide Diuretics
Use: No survival, only chronic stable heart failure (oral), combo w/loop diuretics, wide use as 1st line monotherapy for hypertension (esp blacks and old), low Na diet
Direct Thrombin Inhib
SE: bleeding, unlikely to cause thrombocytopenia (low platelet #)
Niacin (Nicotinic Acid)
Mech: Inhib lypolysis of TG via hormone sensitive lipase in fatty tissue -> less FFA transport to liver and hepatic TG synth -> less TG synth via inhibition of esterification of FA in liver
Renin Angiotensin Inhibitors (HF) 
Response: decrease venous and arterial contraction, VENTRICULAR REMODELING, SNS, preload and afterload, increase excretion of Na and H2O
Newer Drugs for Chronic Stable Angina
Ivabradine: block pacemaker current -> decrease HR
Nicorandil: open ATP-sensitive K channels -> coronary dilation
Trimetazidine: inhibit mitochondrial 3-ketoAcyl CoA thiolase -> FA use to carb use for E (more efficient)
Perhexilene: inhib mitochondrial carnitine-palmitoyl-transferase -> FA use to carb use for E
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