MOA: Balanced Vasodilation

-Decreases LVH > Prolongs Life

-Increases renal blood flow > Diuresis > decr. pulmonary congestion > incr. quality of life

DOC- HF, LVH, DM, post MI systolic dysfunction

Toxicity- CART HH

Cough  Angioedema  Renal Insufficiency  Teratogen  Hypotension with first dose  HypERkalemia

ACE inhibitors

-opril

Use the smallest dose to prevent hypotension

treats systolic dysfunction

A 3 of these drugs:

treat heart failure

decrease pulmonary congestion by decreasing preload

diuretics

Furosemide

Spironolactone

Epleronone

causes hypERkalemia

take with captopril since it has short half life

Spironolactone

Epleronone

HCTZ

Spiro

Epleronone

GFR must be >30 to work

treats hypertension

causes decr. insulin sensitivity

causes muscle weakness

Both of these drugs:

cause hypOkalemia

-which worsens Digoxin AEs

To prevent hypOkalemia give with:

ARBs, ACE inhibitors, spironolactone, B blockers, amiloride

or resistrict salt and take potassium supplements

HCTZ

Furosemide

MOA: decrease SNS by blocking a1, b1, b2 receptors

decreases contractility > reverses LVH > prolongs life

Balanced Vasodilation > decr. afterload & incr. SV >

incr. EF -- can use in pt's with EF < 35%

decr. HR > incr. filling time> shunts blood to endocardium

salt/water retention > leads to pseudotolerance

decreases automaticity > incr. ERP (most in AV only, sotalol in vent. and atrium also) --> slow conduction

B blockers

propranolol

atenolol

esmol

sotalol

blocks K+ channels> incr. ERP & APD in atria, ventricle, AV node --> TORSADES

DOC for recurrent V. tach

also use to cardiovert people with A. fib

treats heart failure

"Start low, go slow"

EF falls initially but then increases

use IV

Dysrrhythmia during cardiac catheterization

Propranolol

Other B blockers will work also

MOA: decr. contractility & decr. HR > blocks slow fibers in AV node> incr. ERP in AV node

also decr. SBP, SV, CO, wall tension

incr arterial compliance and blood flow to heart

Treats: Angina, chronic AVNRT

Toxicity- AV block

Verapamil

Dilt.

Causes constipation & AV block

Do NOT give with B blocker or Digoxin

Causes AV block

Do NOT give with cimetidine or digoxin

MOA: dilate arterioles > decr. afterload = decr. DBP > decr. wall tension and incr. BF to heart and incr. large artery compliance

Treats angina and hypertension

Toxicity- Pedal edema, paradoxical angina

do NOT give with grapefruit juice

DHP's

Amlodipine

Nefedipine

Fenlodipine

Apatient comes in with sudden chest pain and a ventricular rate of 200 and you think it might be AVNRT. You give them a drug and the dysrrhythmia goes away-- what drug did you give them?

What drugs should you send them home with?

Adenosine

Send home with B blocker or verapamil

decr. phase 4 automaticity in fast fibers

causes 2 way block to prevent reentry dysrrhythmia

prevents automaticity in ischemic tissue

Treats V. tach, digoxin induced PVCs

Toxicity- seizures

MOA- blocks Nain and Kout, noncompetitive a and b blocker, incr. ERP & ADP in atrium, ventricle, AV node

Prolongs PR, QRS, QT

use- cardiovert A. fib, turn Vtach to sinus rhythm, prophylaxis for Vtach

Class III- K channel blocker

toxicity- FATAL pulmonary fibrosis, purple man, thyroid problems

decr. preload and afterload and mortality

especially in blacks

Isosorbide dinitrate + hydralazine (arterial dilator)

causes SLE-like symptoms

treat heart failure in blacks

MOA: NO donor which decreases preload and wall tension

selective venodilation, decr. oxygen demand

slight incr. in myocardial blood flow to reverse ischemia

NO effect on afterload

Nitrates:

Nitroglycerin

Dinitrate

Mononitrate

Causes headaches and orthostatic hypertension

PO form has a potential for tolerance

SL acutely causes incr HR, incr. contractility, decr DBP

sit down while dosing

MOA- blocks GI transporter so cholesterol can't be absorbed

does NOT need LDL receptors to lower LDL

2nd choice anti-lipemic drug

MOA: stimulates GPR109A receptor

-decr. TG via lipolysis

-decr. LDL due to decr. VLDL & making bigger LDL particles

-decr. VLDL via ApoB100 degradation

-incr. HDL by preventing the liver from destroying HDL-ApoA> incr. direct pathway to reverse chol. transport

used to treat people with mixed hyperlipidemias (incr. LDL & TG)

Toxicities- flushing and pruritis at start. aspirin laropiprant helps by blocking PGD2

DON'T give with statin- worsens myopathy

MOA: ion exchange resins. causes bile acids to be lost in feces> more chol is used to make bile thus decr. pool

Effect- decr. LDL ONLY

Toxicities- constipation

decreases bioavailability of warfarin & pravastatin

Bile Acid Binders:

Cholestyramine

Colestipol

Colesevelam

used to lower LDL in pt w/ CV risk

does not affect bioavailability of other drugs

safe in preg. women

take 6 pills/day

MOA: binds to PPARa

-decr. TG by stimulating PPARa > incr. VLDL clearance & decr. VLDL synthesis

-decr. VLDL by reducing ApoCIII expression and incr. lipase synthesis

-decr. LDL by incr. SREBP synth > incr. LDL rec's

-incr. HDL by incr. ApoA1 synth.

Use in diabetics- esp. for VLDL and HDL

Fibrates:

Fenofibrate

Gemfibrozil

MOA: HMG CoA reductase inhibitor > can't make cholesterol > incr. LD rec's

Increases cholesterol plaque stability

Toxicities- myositis, teratogen, fatal rhabdomyolysis

Statins:

Simvastatin

Pravastatin

Atorvastatin

Rosuvastatin

Pravastatin

Rosuvastatin

MOA: cleaves plasminogen to form plasmin

degrades everything in site, including factors 5, 8, fibrinogen

use- MI, PE, DVT, stroke

Antidote- Aminocaproic Acid

Fibrinolytics:

TPA

Alteplase

Streptokinase

MOA: prevents vitamin K from being reduced > factors 2, 5, 7, 9, 10 can't get made

Treat- DVT, prevent thromboembolism in A. fib and prosthetic valves

Toxicities- teratogenic, metab. by P450

Antibiotics increase its activity due to destroying gut flora

increases INR

Antidote- phytonadione

MOA1- anti-platelets- makes wall neg. so platelets can't bind> incr. bleeding time

MOA2- anti-coagulant- binds to ATIII to inhibit clotting factors 2, 9-12

Use: DVT prophylaxis, treat DVT & PE, history of thrombosis, during pregnancy

half life increases as dose is increased

use PTT to measure activity

Antidote- protamine sulfate

1. PE increases heparin clearance

2. Congenital ATIII deficiency

3. Acquired ATIII deficiency- cirrhosis, nephrotic syndrome, DIC

4. Acute phase proteins

MOA: binds ATIII to inhibit factor 10

Use: DVT prophylaxis, stroke, ACS, dialysis

LMW heparins:

Ardeparin

Dalteparin

Enoxaparin

MOA- binds to ATIII to inhibit factors 2, 9-12

Use: DVT, PE, HIT

Direct inhibitor of factor 10

Use- DVT

Toxicity- BLEEDING

Metabolized by P450

MOA- direct, irreversible inhibitor of 2a

Use- HIT

take IV

MOA- Direct, reversible inhibitor of 2

Use- HIT, DVT

Increases INR when given with warfarin

MOA- direct reversible inhibitor of 2

Use- prevents thrombosis in A. fib

Toxicity- gastritis & dyspepsia

Dabigatran

Eating da big mac can give you dyspepsia

irreversible COX1 inhibitor

prevents TXA2 production

increases bleeding time

MOA- blocks II/III receptor so nothing can bind to platelet including fibrinogen

Use- PCI, ACS- MI or unstable angina

incr. bleeding time

TEA

Tirofiban

Eptifibatide

Abciximib

Eptifibatide

Tirofiban

MOA- blocks the P2Y(12) receptor that ADP binds to> platelets can't aggregate

Use- with aspirin to prevent MI or stroke

-if you have an aspirin hypersensitivity

-secondary prevention of stroke

incr. bleeding time

Ticlopidine

Clopidogrel

Anti-platelet med

causes neutropenia

give 10 days to get full effect

Ticlopidine

Same MOA as ACE inhibitors

Balanced Vasodilators

Angiotensin II receptor blockers

Increases compliance of small and larger arteries

Use- hypertension and heart failure

Toxicity- teratogenic, angioedema, hyperkalemia, hypotension

ARBs

Valsartan

Losartan

What do you treat hypertensive kids and pregnant women with?

Toxicity- sedation, dry mouth, rebound hypertension

a2 adrenocceptor agonist in brain> reduces sympathetic outflow

balanced vasodilation

incr. FF > salt/water retention> pseudotolerance

decreases rening and angII

Use- Hypertension

Toxicity- vivid dreams, orthostatic intolerance

withdrawal syndrome- incr. BP, tremor

MOA: NO dilates arteries and inhibits platelet aggregation

Balanced vasodilator

Use: hypertensive emergencies in SUPINE patients

stops dissecting aortic aneurysm

Super short half-life (30s)

Only use if other drugs haven't been able to decrease their hypertension

MOA: vasodilates resistance arterioles>

incr. HR, incr CO> take with B blocker

causes salt/water retention

Hydralazine

Minoxidil

Diazoxide

causes hairiness= hypertrichosis

also causes edema, angina

Which hemodynamic values get changed:

MOA:

Antidote:

Aspirin

incr. BT

TXA2 via irreversible COX1 inhibitor

none

Which hemodynamic values get changed:

MOA:

Antidote:

abciximab

eptifibatide

tirofiban

incr. BT

IIb/IIIa

none

Which hemodynamic values get changed:

MOA:

Antidote:

clopidogrel

ticlopidine

incr. BT

P2Y(12)

none

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Heparin

incr. BT, incr. PTT

2, 9-12

ATIII

Protamine sulfate

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Ardeparin

Dalteparin

Enoxaparin

no changes

10

ATIII

Protamine sulfate- partial

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Fondaparinux sc

NO change

10

ATIII

none

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Rivaroxaban

No change

10

Direct

None

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Lepirudin IV

incr. PTT

2a

Direct and IRREVERSIBLE

None

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Argatroban

incr. PTT

2

Direct

none

may incr. INR when given with warfarin

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Dabigatran

incr. PTT

2

direct

none

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

warfarin po- normal dose

incr. INR (PT)

2, 7, 9, 10

Decr. Vit KH2

Phytonadione

Which hemodynamic values get changed:

Clotting factors:

MOA:

Antidote:

Side effects:

warfarin po- overdose

incr PTT and INR (PT)

2, 7, 9, 10

decr. vitKH2

phytonadione

causes PACs, PVCs, AV block, affects green-yellow vision

Anti-platelets:

Aspirin

II/III inhibitors- tiro, epti, abc

P2y(12) inhibitors- ticlopidine, clopidogrel

Heparin

Factor 2 inhibitors:

LAD + warfarin overdose

Lepirudin

Argatroban

Dabigatran

Warfarin

--increased further by argatroban

FADE With Hot Rain

Fondaparinux

Ardeparin

Dalteparin

Enoxaparin

Warfarin

Heparin

Rivaroxaban

FADE

Fondaparinux + LMW heparins

Ardeparin

Dalteparin

Enoxaparin

Slow: Which drugs decrease conduction throught the AV node?

Fast: Which drugs decrease ventricular conduction?

Which decrease automaticity in both?

1. Verapamil, Digoxin, Adenosine

2. Lidocaine

3. B blockers incl. Sotalol, Amiodarone

B blockers

Clonidine

Hydralazine, Minoxidil, Diazoxide

1. Cytochrome P450

2. Hypoalbuminemia- nephrotic syndrome

3. Anion exchange resins like cholestyramine, colestipol

4. Increased K intake

B blockers

Digoxin

Verapamil, Dilt

SL NTG

Hydralazine, Minoxidil, Diazoxide

1. Drugs that cause hypOkalemia

2. Drugs that cause hypERkalemia

1. HCTZ, Furosemide

2. Spiro/Epleronone, ACEinhibitors/ARBs

low K, hyperaldosteronism

low Mg, HIGH Ca

Slow conductors: B blockers, Verapamil

Spironolactone- decreases renal clearance

"stuns" the heart so it can't react to other drugs (ie digoxin)

1. suppresses ventricular automaticity > decreases spontaneous phase 4 depolarization in ischemic/digoxin tissue > decr. PVCs in ischemic tissue

2. causes 2 way block to stop reentry v. tach

3. increases threshold potential to further suppress automaticity

--no effect on AV conduction and no effect on EKG

Verapamil- directly

Digoxin- via vagal stimulation

Adenosine

Lidocaine

Amiodarone

B blockers

Amiodarone

B blockers

Clonidine

Hydralazine, Minoxidil, Diazoxide

B blockers

Verapamil

Digoxin

SL Nitro- acutely

Hydralazine, Minoxidil, Diazoxide

Slight- Sodium Nitroprusside, Nifedipine, Amlodipine, Felodipine

HCTZ

Furosemide

Spiro/Epleronone

ACE inhibitors/ARBs

I'll pay CASH just for some balanced vasodilation

Clonidine

ACE inhibitors/ARBs

Sodium Nitroprusside

Hydralazine + Dinitrate

ACEinhibitors/ARBs

Dihydropyridines