MOA: metabolized by CYP34A

↑ hepatic LDL receptor expression

↑ in HMG CoA reductase limits the fall of LDL because it ↑ hepatic cholesterol synthesis

↓ synthesis of ApoB-100 (which ↓ VLDL synthesis

Uses:

, ↑ stability of cholesterol plaques,

↑ ability to synthesize NO

↓plasma C-reactive protein 

S/E:

Hepatic damage (↑AST, ALT), myopathy (muscle pain and weakness), fatal rhabdomyalysis, fetal toxicity (category X teratogens)

Moa:  Not metabolized by CYP3A4 Same fxn as Simvastatin

      Uses: used to ↓ LDL by 25-35%

(whereas the 3 others can ↓ >30-35%) 

MOA: inc LDL reuptake causes

overall decreased LDL and TG, n.c. in VLDL, increased HDL

Uses: hyperlipidemia (added to tx w/ statin w/o

S/E: much risk)

although pregnancy is a risk (category C) 

MOA: increases LDL receptors and HMG CoA reductase

Uses: dec LDL, additive effect w/ statins

S/E: GI, (constipation, bloating), 

↓ bioavailability (of  Warfarin, propanolol, 4cyclines, furosemidem HCTZ, prava/fluvastatin, thyroxine). Pregnancy category C

same as Cholestyramine

[image]

Gemfibrozil

Fenofibrate 

MOA: binds PPARa (in liver, brown adipose, skeletal msk, heart, kidney)

fibrate binding PPARa -> activate apoA1 & II -> ↑ HDL

inc release of hepatic SREBP-1 -> inc LDL receptors

↓ VLDL, LDL, and TG. ↑ HDL

Uses: Tx Hypertriglyceridemia

S/E: Category C, GI, Myopathy, gallstones

Antianginal effect:

↓ HR, ↓ myocardial contractility, ↓ cardiac afterload (↓ DBP), ↑ diastolic perfusion time due to ↓ HR

in order to ↑ endocardial Blood Flow

S/E: sudden withdrawal may precipitate MI, bronchoconstriction

antianginal 

MOA: vasodilator and inhibition of platelet aggregation, preferential to veins

↓ preload, ↓ wall tension during systole and

diastole, ↓ O2 demand and ↑ endocardial BF.

There is no change seen in DBP, HR, and contractility 

(sublingual does give ↓DBP and ↑HR)

S/E: headache, orthostatic hypotension

antianginal 

MOA: Nitrate vasodilator, same as NTG

Uses: give PO at 7 am and 2pm to decrease tolerance

antianginal

MOA: Nitrate vasodilator

Uses: give PO at 7am and 2pm to decrease tolerance

S/E: usually no orthostatic HTN

antianginal drug

MOA: L-type calcium channel blocker in vascular SM of arterioles, myocardial cells and SA and AV nodes, increase endocardial blood flow

- blocks Vasc smooth msk of resistance arterioles causes ↓ TPR and DBP

↓HR, ↓AV conduction, and ↓ myocardial dp/dt (all ↓ O2 demand).  decrease SV and CO

S/E: bradycardia, HF in pts w/ systolic dysfunction, hypotension, pedal edema, paradoxical anginas, GE reflux 

MOA: PO reversibly inhibits COX-1 and COX-2 (hence the synthesize of thromboxane A2); hepatic aspirin irreversibly inhibits COX1 -> hence can never again synthesize TXA2

↑ Bleeding Time, no effect on aPTT or PT

Uses:   ↓ incidence of MI and secondary MI by 50% in pts w/ unstable angina

antiplatelet

MOA: antagonist of the IIb/IIIa receptor (glycoprotein integrin receptor)

Irreversibly binds IIb/IIIA receptor which makes fibrinogen unable to bind platelets together by any factor

Uses: PCI (stenting or angioplasty), acute MI, angina, inc cardiac enzymes

S/E: bleeding

antiplatelet drugs

MOA: competitive inhibitor of IIb/IIIa

Uses: IV

S/E: bleeding 

Tirofiban

antiplatelet drug

MOA:

[1]blocks P2Y(1) blocks PLC -> blocks IPS -> no release of Ca from SR

[2] blocks P2Y(12) -> no inhibition of adenylate cyclase -> inc cAMP ->inhibits platelet aggregation and activation by lowering IC Ca concentration

Uses: P.O. decr incidence of stroke and MI in pts w/ atherosclerosis, prvt thrombosis, given to pts who failed aspirin therapy 

S/E: neutropenia, thrombocytopenia, agranulocytosis

antiplatelet

MOA: antagonist of purinergic (ADP) receptors. Irreversible P2Y(12)

Uses: P.O. reduces secondary MI another 9% when used in addition to aspirin.

S/E: much lower incidence of neutropenia and agranulocytosis 

antiplatelet adhesion:

blocks adhesion to platelets by maintaining the electronegativity of the damaged vascular wall -? blocks adhesion, aggregation, and the "release" reaction

Anticoag

inhibit activation of prothrombin (II) to thrombin (IIa)

MOA: binds ATIII, the terrorist of clotting factors, is enhanced by irreversible binding of HELParin

main targets = Clotting factors 2, 9, 10, 11 

↑ aPTT, no affect on PTT

 Interference: Protamine sulfate prevents Heparin + ATIII combination

Does not cross placental barrier

S/E: Heparin-induced thrombocytopenia (HIT) due to IgG binding PF4-heparin

TX: HIT pts with FLAg (fondaparinux, lepirudin, or agatroban)

MOA: LMWH

binds ATIII and primarily inhibit Factor X

- partially inhibited by protamine sulfate 

- give s.c. q12h or qd, they produce a predictable and reproducible anticoagulant effect w/o the need for lab monitoring of hemostasis

Uses:  tx of ischemic stroke, acute coronary syndrome, anticoagulant during hemodialysis

S/E: lower incidence of HIT, osteoporosis

anticoagulant 

MOA: synthetic sugar that mimics heparin binding ATIII, indirect Factor Xa inhibitor 

no affect on aPTT, Bleeding Time or PT

NO ANTIDOTE

S/E: superior to LMWH in tx of ACS

Anticoagulant

MOA: Direct inhibitor of free and clot bound thrombin (IIa)

No affect on platelets

NO ANTIDOTE

Uses: aPTT to 1.5-2.5 nl level

anticoag

MOA: Direct, competitive, reversible inhibitor of thrombin

- inhibits thrombin (wherever its found); inhibits platelet aggregation and TXA2 release

in aPTT. ↑ PT slightly when given alone, but greater when given w/  warfarin

Uses: tx DVT and HIT

anticoag

MOA: binds to Heparin and prevents binding w/ ATIII

Uses: paritally reverse LMWH effects

anticoag

MOA: inhibits Vitamin K epoxide reductase, stops post translational modification of Factors 2, 7, 9, 10

effect measured by PT time (factor 7 - extrinsic pathway), INR should be > 2-3X (INR >4 is bad = bleeding)

- usually does not ↑ aPTT

- biotransformed by CYP2C9 crosses placental barrier

Uses: prophylaxis of DVTs, A fib, prosthetic valves, rheumatic mitral disease, unstable angina

S/E: Teratogenic, cutaneous necrosis

anticoag

MOA: Reverses anticoagulant of warfarin after several hours

TX for warfarin overdose

fibrinolytic drugs

MOA: converts plasminogen to plasmin, degrades the fibrin and lyses thrombus

Uses: Reperfusion of coronary vessels after MI, PE, DVT, Ischemic stroke

S/E: bleeding 

think "Alternative T-PAse"

fibrinolytic drugs

MOA: unmodified t-PA produced by recombinant technology

Uses: IV degrades clotting factors 5 & 8

reperfusion of coronary vessels after MI, PE, DVT, Ischemic stroke

S/E: Bleeding

fibrinolytic

Strep = 5 letters, -tokinase = 8 letters

MOA: binds near carboxy terminus of plasminogen, convert plasminogen to plasmin

plasmin attacks fibrin or Factors 5, 8, and fibrinogen

Uses: reperfusion of coronary vessels after MI, PE, DVT, Ischemic stroke

S/E: bleeding

fibrinolytic

"I Mean No Caps" -- like fibrin caps

MOA: prevents binding to fibrin

lysine analog is the target (plasmin, plasminogen, t-PA, altelase, reteplase)

Uses: prevent bleeding caused by fibrinolytic therapy and the extracorporeal circulation of blood

Antidysrhythmic

- two i's stand for 2 way conduction block

- D is for depression of automaticity due to digoxin

- N is for Sodium channel blocker

MOA: Blocks Na channels -> ↓ ERP and ADP of fast fibers, depresses automaticity in partially depolarized tissues (ischemic or digoxin toxicity) w/ little effect on normally polarized tissues. Stops re-entry tachycardias by causing 2-way block of conduction areas. There is also  ↑ Threshold

 potential. No effect on AV conduction and no effect on EKG

Uses: TX pts w/ ventricular tachycardia after MI and digoxin induced PVCs

S/E: lCNS depression (nausea, tremor, paresthesia, slurred speech) and seizures (tx w/diazepam)

dysrhythmic drug

So Lame B

So Darn Lame

with my long QT

Ain't a Fib young mane'

MOA: 

L-isomer causes non-selective Beta-blockade in slow (SA and AV nodes) and fast fibers = ↓ HR, ↓ conduction velocity and ↓ automaticity (due to catecholamines)

D&L Isomers - blockade of outward repolarizing K current causing addition increase in ADP and ERP in fast fibers and AV node

- delayed V-repolarization increases the QT interval

Uses: cardioversion of Afib/flutter to sinus rhythm

DOC control (↓) v-rate in pts w/ persistent Afib. Chronic therapy to prevent life threatening V tach and V fib. ↓ number of shocks that pt experiences from ICD 9and does not effect energy required for defib

S/E: delay in repolarization can cause torsade de pointes. B-block can exacerbate HF due to decrease V contractility. AV block via b-blockade.

Antidysrhythmic drug

"We call her Ami-OOOOO. Cause' she prolongs everything."

MOA: blocks inward Na and outward K channels. Non-competitive blockade of a and beta-adrenoreceptors. Block of Na channels ↓ decreases automaticity. Block K delays repolarization

prolongs APD and ERP in atria and ventricles

Prolongs the PR, QRS and QT intervals. Reduced rate of firing of the SA node

Uses: tx Afib/flutter to sinus, recurrent vtach/vfib (DOC sotalol)

S/E: increase the energy required for defib w/ICD by as much as 50%, torsade, HF, pneumonitis, purple skin, peripheral neuropathy, thyroid dysfunction

dysrhythmic

MOA: blockade of Ca channels in slow fibers (AV node) 

↓ HR, ↓ conduction velocity in the AV node  

↑ PR in interval. ↑ ERP in AV node.

↓ Contractility.

                  Uses: ↓ V-rate in pts w/ Afib/flutter. Converts AVNRT to sinus rhythm by blocking re-entry

S/E: hypotension, sinus bradycardia, heart block

Antidysrhythmic drug

Moa: acts centrally to increase efferent vagal nerve activity, ↓ sympathetic outflow at serum concentrations within the therapeutic window,

( ↓ HR, ↓ conduction velocity in the AV node, ↑ ERP in the AV node).

Also partial inhibition of Na/K ATPase, ↑ SV via ↑ contractility. Effects are unrelated.

Uses: control V-rate in pts w/ Afib/flutter in the presence of HF caused by systolic dysfunction. ↑ contractility in pts w/ HF from systolic dysfunction.

S/E: at above therapeutic window the inhibition of Na/K ATPase causes ↑ Ca which can lead to automaticity (PACs and PVCs), sympathetic activity is ↑, ADP and ERP ↓ in response to ↑ Ca (which leads to after depolarizations), sinus bradycardia, AV block (↑ vagal tone and depressant effect).

Atenolol

Antidysrhythmic

Moa: B-blocker. Cardioselective. ↓ rate of discharge at the SA node. Suppress catecholamine-induced automaticity, ↓ conduction velocity and ↑ ERP of AV node (PR interval increases), ↑ ERP of fast fibers when the ERP has been shortened by b-agonists.

Uses: prevent V-dysrhythmias post MI, prevents PVCs triggered by stress, suppress tachy of hyperthyroid, controls V rate in pts w/ afib/flutter, suppress AVNRT, tx V-tach in patients w/ long QT  because b-blockers do no affect repolarization.

antidysrhythmic 

Moa: non-selective b-blocker

antidysrhythmic

Moa: cardioselective b-blocker. Same as Atenolol.

Uses: used to control V rate in pts w/ Afib/flutter or sinus tachy during cardiac cath because the T1/2 is short (9min).

                                                    S/E:

antidysrhythmic

"A den of Kittens" ... which means alot

- A is AV node and AVNRT

- K in Kitten is increased K conductance

Moa: ↑ K conductance to hyperpolarize AV node. Blocks symp stimulation from increasing Ca conductance in AV node. ↓ conduction velocity and ↑ ERP in AV node. AV conduction momentarily ceases (HEART STOPS!!).

Uses: very short T1/2. Used to dx AVNRT (paroxysmal Supraventricular tachy), converts AVNRT to normal sinus rhythm, produces coronary vasodilation during technetium scan in pts who cannot exercise.

S/E: transient asystole, intense burning in chest, flushing, Dyspnea. 

Drugs that decrease Cardiac Output:

Very few Drugs Stop Quick Blood

Verapamil

Diltiazem

Sotalol

Quinidine

Beta-blockers

amiOdarone

"0 as in no change"

Digoxin

- imagine a hand (your digits) squeezing the aortic pipes

antihypertensive

HydrochloroTHY-AZide

thy - you're or uri-cemia

az - azucar = sugar

Moa: Saluresis → lowers ECF volume →

↓ CO → ↓BP. This may cause a secondary rise in RAAS → 2ndary Hyperaldosteronism → hypokalemia. No effect of BP if GFR <30ml/min (use metolazone).

Uses: used as monotherapy to prevent/reverse the salt and water retention caused by other antihypertensive drugs. Prolonged therapy ↓ LVH. 

S/E: hyperuricemia, hyperglycemia (directly inhibit insulin secretion), Hypokalemia (muscle weakness, digoxin induced dysrhythmias)-can be prevented by Na restriction, K sparing diuretic, co-treatment w/ ACEi, ARB, B-blocker, oral K supplement. 

G U

Captopril

Enalapril

Lisinopril

anti-hypertensive

Moa: ACE Inhibitor. ↓ MAP due to ↓ TPR. Dilation of resistance arterioles (balanced vasodilation), ↑ compliance of larger arteries -> ↓ SBP, DBP, and MAP. HR is unchanged. RBF is ↑ by dilation of both efferent/afferent arterioles but GFR is unchanged. FF Is ↓ (constant GRF w/ ↑ RBF) so salt/water retention does not occur. Also, prevent/reverse cardiac remodeling caused by AT II. Plasma aldosterone is maintained by ACTH and plasma K concentration. CO unchanged

Uses: lower BP in about 50% of hypertensive pts (80% w/ Thiazide addition). DOC for pts w/ HF, LVH, DM (prevent glomerular damage) and pts w/ systolic dysfunction after MI. used to tx malignant HTN, renovascular HTN, and scleroderma HTN. Tend to work better in younger, Caucasian pts (combine w/ thiazide if other).

S/E: No hypokalemia, hyperuricemia, hyperglycemia, or hyperlipidemia. Hyperkalemia, Angioedema, skin rash, Dry cough (b/c ↓ breakdown of bradykinin > ↑ in PG synthesis > cough reflex)-dose related (one aspirin a day prevents the cough) (discontinue ACEi and start ARB). Fetotoxic (category X)-If pt becomes pregnant switch to methyldopa, atenolol, and nefidipine. 

Losartan

Valsartan

antihypertensives

Moa: ARBs (competitive blockade of the AT1 receptors) which blocks the effects of At-II. There is balanced vasodilation (CO unchanged). They have Hemodynamic and renal effects similar to ACE inhibitors. NOT inhibit bradykinin or ↑ synthesis of PGs like the ACE inhibitors. 

Uses: tx of HTN. Use w/ HCTZ if additional ↓ in BP is desired. Appropriate for tx of HF.

S/E: contraindicated in pregnancy or breast feeding mothers (category X), NO dry cough (so safe to use in pts who have cough on ACEIs), angioedema, hypotension, hyperkalemia. 

DOC for diabetes (?)

Nifedipine

Amlodipine

Felodipine

antihypertensives

Moa: Block L type Ca channels in VSM and cardiac muscle. BP falls as TPR is ↓ (dilate arterioles but not venules). SBP, DBP, and MAP are ↓. CO may be ↑ slightly. Slight Tachycardia may be present. RBF and GFR may ↑, ↓, or be unchanged, but there is no Na/water retention because there is a direct natriuretic effect. PRA, AT II, and Aldosterone are unchanged. 

Uses: First line in mild to moderate tx of HTN. Effective in tx of systolic HTN because they cause greater fall in SBP than DBP. Used to ↓ proteinuria in pts w/ type 2 DM but ACEI and ARBS remain DOC in DM pts. More effective in pts w/ low PRA (black and elderly). Can use in pts w/ COPD, asthma, LVH, dyssrhythmic, or PVD.

S/E: excessive vasodilation, pedal edema-due to dilation of precapillary sphincters à excess filtration of fluid into interstitial space, GERD, paradoxical angina from “coronary steal”. 

Labetalol

Atenolol

Metoprolol

Timolol

antihypertensive

Moa: Combines alpha and Beta blockade. MAP ↓ as TPR ↓. CO unchanged (balanced vasodilation-a-block)-cerebral, coronary, and renal BF are maintained. ↓ in basal HR (b-block). HR unchanged or ↓ slightly. ↓ in renal perfusion pressure can lead to ↑ FF and a slow retention of salt/water. This retention limits the antihypertensive effectà “pseudotolerance” (ECF volume may increase)

Uses: tx of hypertensive emergency –given IV- (onset 2-4 minutes). After control of BP w/ IV is obtained, p.o. therapy w/ Labetalol can be started. Often used w/ thiazide to further ↓ BP and prevent Na/water retention. Well suited for young pts w/ history of angina, MI, dysrhythmias, or mitral valve prolapse. Avoid in pts w/ DMII, PVD, asthma, COPD, and CHF. Given to mothers w/ preeclampsia to control BP. 

S/E: orthostatic hypotension, headaches, fatigue, and reduced sexual function. Poor lipid solubility so little effect on the fetus in preeclampsia.

antihypertensives

Moa: b-blocker.  ↓ in renal perfusion pressure can lead to ↑ FF and a slow retention of salt/water. This retention limits the antihypertensive effect

-> “pseudotolerance”. 

α-methlydopa

antihypertensive

"alpha- the safest -bet for little ones"

Moa: balanced vasodilation-CO unchanged. ↓ VR and ↓ DBP.

Uses: can be used in pediatric HT and HT during pregnancy. In hypertensive emergency the slow fall in BP prevents MI/CVA

S/E: sedation, dry mouth, rebound HTN, fatigue, flu-like symptoms, + coombs test, hepatitis. 

antihypertensive

"Clone - idine"

Cloning requires making to (a2) an androids. Change their brain and impairs their sympathy. 

Moa: a2-adrenoreceptor agonist > enters brain and ↓ sympathetic outflow by stimulation of post-synaptic a2-receptors in the rostral ventrolateral medulla > sympathetic reflexes are attenuated (not blocked). ↓ in renal perfusion pressure can lead to ↑ FF and a slow retention of salt/water (ECF can be increased). Plasma renin and AT-II are suppressed. CO unchanged.

Uses: usually used w/ a diuretic drug in the tx of mild to moderate HTN, but progressive Na/h2o retention limits fall in BP.

S/E: sedation, dry mouth, CNS-(dreams, restlessness, depression), CV (orthostatic hypotension, bradycardia, slow AV conduction), Withdrawl syndrome (rebound ↑ in sympathetic activity when drug is stopped). 

antihypertensive

Moa: relaxation of the VSM of arterioles >lowers TPR >↓ BP. ↓ BP causes baro-reflexly mediated ↑ in sympathetic discharge in the heart (↑ rate and dp/dt), vasculature (↓ venous capacitance), and kidney (b-1 stimulation > ↑ renin releaseà↑ Aldosterone). ↑ sympathetic activity cannot constrict arterioles b/c of the overwhelming effect of the drug. ↓TPR causes a ↑ in CO (MAP=CO x TPR).

Uses: rapid onset. Reserved for pts w/ severe HT resistant to combined therapy w/ first line drugs. Cannot be used as single agent due to tachy and ECF volume expansion (combo w/ b-blocker prevents tachy and ↑ in CO and myocardial O2 demand, as well as the sympathetically mediated Renin release-prevents secondary hyper-aldo).

S/E: tachy, palpitations, headache, edema, angina, SLE like syndrome (b/c slow acetylator), pyridoxine-responsive polyneuropathy.

antihypertensive

Moa: relaxation of the VSM of arterioles ->lowers TPR > ↓ BP. ↓ BP causes baro-reflexly mediated ↑ in sympathetic discharge in the heart (↑ rate and dp/dt), vasculature(↓ venous capacitance), and kidney (b-1 stimulation > ↑ renin release > ↑ Aldosterone). ↑ sympathetic activity cannot constrict arterioles b/c of the overwhelming effect of the drug. ↓TPR causes a ↑ in CO (MAP=CO x TPR).

Uses: rapid onset. Reserved for pts w/ severe HT resistant to combined therapy w/ first line drugs. Cannot be used as single agent due to tachy and ECF volume expansion (combo w/ b-blocker prevents tachy and ↑ in CO and myocardial O2 demand, as well as the sympathetically mediated Renin release-prevents secondary hyper-aldo). 

S/E: tachy, edema, angina pectoris, global hypertrichosis. 

antihypertensive

 Moa: relaxation of the VSM of arterioles > lowers TPRà↓ BP. ↓ BP causes baro-reflexly mediated ↑ in sympathetic discharge in the heart (↑ rate and dp/dt), vasculature(↓ venous capacitance), and kidney (b-1 stimulationà ↑ renin releaseà↑ Aldosterone). ↑ sympathetic activity cannot constrict arterioles b/c of the overwhelming effect of the drug. ↓TPR causes a ↑ in CO (MAP=CO x TPR).

Uses: rapid onset. Reserved for pts w/ severe HT resistant to combined therapy w/ first line drugs. Cannot be used as single agent due to tachy and ECF volume expansion (combo w/ b-blocker prevents tachy and ↑ in CO and myocardial O2 demand, as well as the sympathetically mediated Renin release-prevents secondary hyper-aldo). 

S/E: tachy, edema, angina pectoris, hyperglycemia (directly inhibits insulin release), relax uterine SM and may arrest labor if used to tx eclampsia. 

antihypertensive

Moa: rapid conversion to NO (and thiocyanate)à balanced vasodilation. ↑ CGMP relaxes vascular SM. ↑ venous capacitance (↓ filling pressures). ↓ afterload (DBP) due to ↓ TPR, ↑ myocardial energetics due to ↓ filling pressures (↓ wall stress) as SV is ↑, dilation of pulmonary arterioles causes ↓ RV afterload. Venodilation causes ↓ VRà↓CO.

Uses: only given to supine patients. Slow IV infusion in HTN emergencies in hospital (hypertensive encephalopathy, pulmonary edema). Controlled hypotension during surgery and to halt acute dissecting aortic aneurysm. ↑ CO in CHF and ↓ oxygen demand after MI.

S/E: tachy, headache, palpitations. Thiocyanate intoxication –associated w/ ↑ dose requirement-↓ renal function- (mental disorientation, metabolic acidosis, nausea, anorexia, hallucinations). May cause fetal cyanide poisoning in preeclamsia. 

tx for heart failure

Moa: loop diuretic that causes a saluresis (block NaCL symport) that ↓ ECF volume >↓ VR (preload) > ↓ventricular filling pressures. ↓ preload ↓ congestive symptoms of backward failure. Relieve congestive symptoms but do not improve survival.

Uses: 2/3 times/day b/c short action and ↑ reab of salt/water. Use smallest dose possible to prevent CHF. Give with K sparing diuretic.

S/E: hypokalemia.

Captopril

Enalapril

Lisinopril

HF tx

Moa: ACE inhibitor. Balanced vasodilation-dilation of both arterioles and venules. ↓ TPR and PVR. ↓ Venous return via ↑ venous capacitance. ↑ SV and EFà↓ LV-EDV, ↓LV-EDP, and ↓ wall stress and pulmonary congestion. ↑ in both RBF and GFR (RBF ↑ more leading to diuresis). No change in MAP or HR. Reverse cardiac remodeling cased by ATII. Improve functional status. ↓ mortality.

Uses: All patients w/ HF. Treat w/ ace inhibitor after MI to ↓ incidence of systolic HF and death. (T1/2 of only 2Hr - Captopril)

S/E: the blocking of ATII response to ↑ GFR can cause an impaired renal function (↓ GFR) (more likely in the others b/c of ↑ T1/2) 

hypertensive

Moa: given PO selectively dilates venules à ↓ cardiac preload. Nitrate (venodilator)- ↓ preload. Hydralazine (arterial+ hydralazine                             vasodilator)-↑SV and EF. ↓ LVEDV, LVEDP, vent wall stress, pulmonary congestion.

Uses: ↓ mortality (especially in african Americans) when added to standard therapy for HF.

S/E: prolonged hydralazine frequently causes SLE-like syndrome (Slow acetylator)

tx heart failure

Moa: aldosterone receptor antagonist.

Uses: prevents/reverses cardiac remodeling caused by aldosterone by ↓the turnover of collagen in the EC matrix of the ventricles. Reverses the cardiac remodeling. ↓ backward failure

S/E: Hyperkalemia (less chance if taking with captopril compared to other ACE inhibitors since its T1/2 is only 2Hr). partial agonist at androgen, estrogen, and aldosterone receptors so may cause gynecomastia, azoospermia, hirsutism, menstrual irregularities.

tx for HF

Moa: Aldosterone receptor antagonist. NOT a partial agonist at androgen, estrogen, and aldosterone receptors.

Uses: same as spironolactone

S/E: hyperkalemia. 

tx for HF

Moa: Beta receptor antagonist. Blocks B1, B2, A1. Start at low dose and go slow. B-blockà EF falls (pt feels bad). In several months EF will ↑ above pre-treatment value and pt feels better (can ↑ exercise). ↓ LV failure by 50%.

Uses: Prevent/reverse remodeling of the myocardium caused by excessive sympathetic stimulation and ↓ sudden death by preventing cardiac dysrythmias. Also have an antianginal effect. Used to TX pts already taking ACE inhibitor and diuretics.

S/E:

tx for HF

Moa: do not reverse cardiac remodeling. Positive inotropic effect. Inhibition of the Na/K/ATPase by binding to a phosphorylated aspartate of the enzyme > ↑ intracellular Na > the ↓ Na gradient slows extrusion of Ca by the Na/Ca exchanger. Ca is sequestered in the SR (so total Ca in the SR ↑). Now the “trigger” Ca causes greater amount of Ca releaseà ↑ cardiac contractility. Indirect effects (↑ vagal activity (slow HR, ↓ automaticity, ↑ ERP) and ↓ symp activity). Direct effects: inhibition of Na/K ATPase ↓ phase 4 membrane potential difference > closer to threshold > can produce spontaneous depolarizations (PACs and PVCs). ↑ Intracellular Ca ↑ probability of phase 4 automaticity and delayed after depolarizations which trigger dysrhythmias.

Uses: TX HF associated w/ systolic dysfunction. TX pts w/ Afib b/c ↑ vagal tone controls ventricular rate in presence of ↑ atrial rate and it ↑ ventricular contractility.

S/E: ↑ vagal tone can cause sinus bradycardia and AV block. PACs. PVCs. Late after-deprolarizations. Hypokalemia favors the phosphorylated state of the Na/K ATPase enzyme thus ↑ binding of Digoxin to it. Also anorexia, Nausea, and yellow-green vision

Tx of HF after MI

Moa: ↓ sympathetic tone (because it ↓ pain which is a stimulus of symp act and it also inhibits the carotid baroreflex). ↓ cardiac preload and afterload (↑ SV), ↓ HR and automaticity, ↓ cardiac oxygen demand

Tx of HF after MI

Moa: dose dependent receptor stimulation. Low dose: “renal” dose. Stim Dopamine receptorsàrenal arteriole vasodilation. Dilate renal afferent arterioles > ↑RBF > ↑ GFR and Na excretion. Intermediate: D1 and β1 stimulationà ↑ dp/dt, small ↑ in HR, ↑ SV and CO lead to ↑ GFR. Large dose: stim vascular α1 receptors >↑ TRp, DBP, arterial impedence-afterload (↓ SV and CO). venoconstriction ↑ VR and filling pressure > ↑ wall stress (negative effect).

Uses: Tx HF after MI to ↑ CO. 

S/E: large doses can cause Tachycardia due to β stimulation. 

tx for HF post MI

Moa: mixture of + and – enantiomers. Both stimulate β1 and β2 receptors. One is antagonist at α1 and the other an agonist (cancel out α). β1 stimulation ↑ SV via inotropic effect. Β2 stimulation causes ↓ VR and cardiac filling pressure. Does not ↑ DBP. Less tachycardia than dopamine

Uses:

                      S/E: little effect on HR but excessive doses can cause tachycardia. 

tx of HF post MI

Moa: inhibitor of type III phosphodiesteraseà↑ CAMP in cardiac myocytes and vascular SM. This ↑ dp/dt, faster myocardial relaxation during diastole, balanced vasodillation (↓ preload and afterload), ↓ PVR, ↑SV as result of ↑ dp/dt and ↓ preload and afterload. 

tx of HF post MI

Moa: IV. Small doses ↑ venous capacitance by dilating veinsà ↓ cardiac filling pressure. ↓ preload >↓ wall stress and ↑ subendocardial perfusion during diastole. Larger doses also dilate arterioles >↓ afterload

MONA

Morphine

Oxygen

Nitroglycerin

Aspirin