528 Unit 3 CV Part 2 S12 - MARKY - npcourses.com Handout Samples/Advanced... · Unit 3 ©2014 Barkley & Associates ... Agents: carvedilol (Coreg), metoprolol (Toprol, Lopressor)

1

Unit 3 ©2014 Barkley & Associates

Advanced PharmacologyCardiovascular Agents Part 2

Thomas W. Barkley, Jr., PhD, ACNP‐BC, FAANPPresident, Barkley & Associates

www.NPcourses.comand

Professor of NursingDirector of Nurse Practitioner ProgramsCalifornia State University, Los Angeles

Robert Fellin, PharmD, BCPSFaculty, Barkley & Associates

Pharmacist, Cedars‐Sinai Medical CenterLos Angeles, CA


Heart Failure Affects approximately 6 million Americans

6-10% of individuals aged > 65 years have heart failure

500,000 new cases diagnosed each year

Direct and indirect health care costs of HF in 2010 were estimated to be $39.2 billion

300,000 deaths per year in the United States

$500 million annually is spent on pharmacologic therapy

2


Clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic demands of the body

Can result from reduced ventricular filling (diastolic dysfunction) and/or reduced myocardial contractility (systolic dysfunction)

Heart Failure


Compensatory Mechanisms in HF Cardiac “remodeling”

ventricular dilation

cardiac hypertrophy

SNS activation:

vasoconstriction

tachycardia

increased contractility

RAAS activation

Na & H2O retention

3


Neurohormonal Model:Heart Failure

Renin-Angiotensin SympatheticAldosterone System Nervous System

Sodium and water reabsorption Positive inotropicVasoconstriction Positive chronotropicPositive inotropic VasoconstrictionPositive chronotropic Arrhythmogenic effectsArrhythmogenic effects Ventricular dysfunction

Ventricular remodeling

RAAS SNS


Heart Failure – Key Concepts Cardiac output (CO): amount of blood pumped by each ventricle

per minute

Factors affecting cardiac output:1. Preload (Frank-Starling Law)2. Afterload

Amount of pressure in the aorta that must be overcome to eject blood

3. ContractilityStrength of contraction

Therapy is employed to maintain adequate preload, decreaseafterload or increase contractility to improve CO

4


New York Heart Association (NYHA) Functional Classification of Heart

FailureNYHA Class Manifestations

I No limitations of physical activity (i.e., normal activity causing no signs/symptoms)

II Slight limitations of physical activity but comfortable at rest (i.e., physical activity results in fatigue, palpitations, dyspnea or angina

III Marked limitations of physical activity but comfortable at rest

IV Severe; inability to carry out any physical activity without discomfort (signs/symptoms while at rest)


DiureticsIndications: Reduce signs/symptoms of volume overloadOutcomes: ↓ signs/symptoms, ↑ functional statusAgents: Loop diuretics: furosemide (Lasix), torsemide

(Demadex), bumetanide (Bumex)

Thiazide diuretics: HCTZ, metolazoneMOA: increase excretion of sodium and water

Adverse

Effects:

hypotension, ↓ K, ↓ Mg, ↓ Na, rash, azotemia

Rare: ototoxicity, pancreatitis, SLEComments: Utilize loop diuretics in severe volume overload or

renal impairment (CrCl < 30 ml/min)

Thiazides are less effective than loop diuretics when CrCl < 30 ml/min

5


ACE-inhibitorsIndications: Symptomatic left-ventricular systolic HF

Asymptomatic mod-severe HF (EF < 35-40%)Outcomes: ↓ mortality, ↓ symptoms, ↑ functional statusAgents: Captopril (Capoten), enalapril (Vasotec), fosinopril

(Monopril), lisinopril (Prinivil, Zestril), quinapril (Accupril), ramipril (Altace)

MOA: Cause vasodilation and block sodium and water retention

AdverseEffects:

Hypotension, ↑ K, cough, rash, renal impairment, angioedema, neutropenia

Contra-indications:

History of intolerance or adverse reactions, serum potassium > 5.5 mEq/L that cannot be reduced, symptomatic hypotension


First-line in all patients with LV systolic dysfunction

Add in patients already on diuretic for clinical volume overload and confirmed LV dysfunction

Monitor BP, renal function and potassium

Titrate to target dose over 1-2 weeks; full effect on functional status may take several months

ACE-inhibitors

6


Management of Side Effects:

Creat > 3 mg/dl: Use ACE-I with caution; titrate dosewith caution to 1/2 of maximum dose

Hyperkalemia: DO NOT use unless K can bereduced; use K-sparing diuretics with caution

Low BP: SBP < 90 mmHg acceptable in absence of orthostasis

ACE-I cough: R/O cough from pulmonary congestion; D/C only if intolerable

ACE-I intolerance: Angiotensin II receptor blocker (ARB)

long-term efficacy under evaluation

or HYD/ISDN


Angiotensin II - Receptor BlockersIndications: Symptomatic left-ventricular systolic HF

Asymptomatic mod-severe HF (EF < 35-40%)Outcomes: ↓ mortality, ↓ symptoms, ↑ functional statusAgents: Losartan (Cozaar), candesartan (Atacand), valsartan

(Diovan), irbesartan (Avapro), olmesartan (Benicar), telmisartan (Micardis), eprosartan (Teveten), azilsartan(Edarbi)

MOA: Same as ACE inhibitorsAdverseEffects:

Hypotension, ↑ K, cough (less than ACE inhibitor), HA, renal impairment, angioedema, neutropenia

Comments: Do not start if K > 5.5 mEq/LReserved for patients intolerant to ACE inhibitorsCombination therapy with ACE inhibitor: limited data to validate benefit on morbidity/mortality

7


Indications: All patients with NYHA II-III should receive a beta-blocker unless there are contra-indications or intolerances

Outcomes: ↓ mortality, ↓ hospitalizations, ↓ symptoms

Agents: carvedilol (Coreg), metoprolol (Toprol, Lopressor)

MOA: directly relaxes the heartAdverseEffects:

hypotension, dizziness, bradycardia, 2nd or 3rd degree heart block, fatigue, insomnia, nausea

Contra-indications:

Heart block, bradycardia (HR < 60), SBP < 90, asthma, patients requiring inotropes, severe hepatic disease, renal disease, PVD, severe hypoglycemia

Beta-blocking Agents


Aldosterone AntagonistsIndications: Adjunctive to standard therapy in NYHA III-IV; EF <

35%

Outcomes: ↓ morbidity & mortality, ↑ functional status,↓ hospitalizations

Agents: Spironolactone (Aldactone),eplerenone (Inspra)

MOA: Inhibits aldosterone

AdverseEffects:

↑ K, ↓ Na, gynecomastia (less with eplerenone), renal dysfunction

Contra-indications:

Sustained Creat > 2.5 mg/dl, K > 5.0 mEq/L that cannot be reduced

8


Vasodilators (HYD/Nitrate)Indications: Patients intolerant or with contraindications to ACE-

I/ARB; persistent dyspnea after ACE-I/ARB, diuretic, digoxin

Outcomes: ↓ mortality, ↓ symptoms

Agents: Hydralazine (HYD)isosorbide dinitrate, isosorbide mononitrate

MOA: Arterial (hydralazine) and venous (nitrate) vasodilation

AdverseEffects:

HYD: HA, nausea, dizziness, ↑ HR, SLEnitrate: HA, hypotension, flushing

Comments: May use nitrates alone in pts w/ concomitant angina; HYD alone in pts w/ concomitant HTNHYD: reduce frequency in renal dysfunction


Cardiac GlycosidesIndications: Patients with A fib + symptomatic HF

Symptomatic HF on ACE-I + diureticOutcomes: ↓ hospitalizations, ↓ symptoms, ↑ functional status, no

affect on mortalityAgents: digoxin (Lanoxin)

MOA: ↓ sympathetic tone, ↑ parasympathetic response, mayimprove contractility, slows conduction velocity, AV node blocker

AdverseEffects:

Confusion, A/N/V, visual disturbances, bradycardia, arrhythmia

Comments: Monitor renal function, monitor drug levels (goal: 0.5-1 ng/ml), higher incidence of adverse effects in elderly

9


Digoxin (Lanoxin)Interactions:

Many drug/drug interactions…

Dig + diuretics = hypokalemia & increased risk of dysrhythmias

Dig + ACEIs, spironolactone or K+ supplements = hyperkalemia

Dig + beta blockers = additive bradycardia

Dig + Ca intravenously = ↑ of dysrhythmias

Dig may ↓ the absorption of antacids and anti-lipid meds

Dig + quinidine, verapamil, amiodarone or alprazolam will decrease distribution and excretion of digoxin resulting in toxicity

Erythromycin and tetracyclines may ↑ plasma digoxin concentrations

Dig + ginseng = increased risk for digoxin toxicity


Dihydropyridine CCB

Indications: HTN in the setting of CHF

Outcomes: ↓ symptoms, mortalityAgents: Amlodipine, felodipine

Dosage: Amlodipine: 2.5-5 dailyfelodipine: 5 mg daily

AdverseEffects:

Hypotension, peripheral edema, HA, dizziness, nausea, abdominal, pain palpitations

Comments: Do not appear to increase mortalityFew studies of CCB in HF show either no difference or an increase in mortality (non-dihydropyridines)

10


Inotropic Agents MOA: increase intracellular cAMP thereby increasing the rate and

extent of calcium influx during systole and enhancing contractility

Dobutamine and milrinone have emerged as the two most commonly administered inotropes

Dopamine should generally be avoided except in instances of severe hypotension and cardiogenic shock

“Renal dose” dopamine (1-3 mcg/kg/min) may not be safe or effective


Dobutamine b1, b2 and a1 activity

Initial dose: 2.5-5 mcg/kg/min

Higher doses may be required for patients on b-blockers

Adverse effects: arrhythmogenic, may potentiate hypokalemia, myocardial ischemia

Tolerance to hemodynamic effects has been reported after 72 hours of continuous infusion

Increased mortality

11


Milrinone Potent inotropic and vasodilating effects

Loading dose: 50 mcg/kg over 10 minutes f/b a continuous infusion of 0.125-0.75 mcg/kg/min

Adverse effects: arrhythmogenic, thrombocytopenia, myocardial ischemia

Reduce dose for significant renal impairment

Physiologic effects not antagonized by

b-blockade

Increased mortality


Intravenous Vasodilators Hydralazine

arterial vasodilator that acts as an impedance reducing agent and typically increases cardiac output

Nitroglycerin venodilator that acts as preload reducer by increasing venous

capacitance

Nitroprusside mixed vasodilators act on both resistance and capacitance

vessels

12


Nitroglycerin

Preferred agent for pre-load reduction

Little or no effect on after-load (SVR)

Initial dose: 5-10 mcg/min

Tolerance to hemodynamic effects may develop over 12-72 hours

Adverse effects: hypotension, tachycardia

Used in combination with inotropic agent

Agent of choice for heart failure patients with ischemic component


Nitroprusside Primarily utilized in patients with significantly elevated SVR

Initial dose: 0.1-0.25 mcg/kg/min

Tolerance to hemodynamic effects may develop

Adverse effects: hypotension, reflex tachycardia

Rebound phenomenon occurs if discontinued abruptly; taper slowly

Can cause cyanide/thiocyanate toxicity with doses > 3 mcg/kg/min for > 3 days and in patients with renal impairment

13


Nesiritide Restricted to patients with acute, symptomatic, decompensated

heart failure (NYHA Stage IV) with evidence of fluid overload

Dose: 2 mcg/kg f/b continuous infusion of 0.01mcg/kg/min

Adverse effects: hypotension

Use with caution when SBP < 90 mm Hg

No dosage adjustment necessary for renal dysfunction

Limited data on outcomes and use > 48 hours


Mechanical Circulatory Support Intra-aortic balloon pump (IABP)

Impella

Tandem Heart

Ventricular assist device (VAD)

LVAD

BiVAD

Total Artificial Heart (TAH)

14


Anginal Syndromes Although difficult to fully assess, the AHA estimated the prevalence

of angina is

9.8 million annually

CHD is the leading cause of death in the US

Direct and indirect costs associated with CHD are estimated to be $286 billion per year

Outcome (survival) is determined by the number of vessels obstructed


Anginal Syndromes

Presentation is variable

Physical Exam Findings

Elevated BP

Levine’s sign = “clinched fist” sign

Transient S4 and apical systolic murmur not uncommon

Classifications:

Chronic stable angina

Unstable angina

Vasospastic angina (Prinzmetal’s angina)

15


Angina: Labs/Diagnostics ECG may be normal

Down sloping ST segment

T wave peak or inversion

Exercise ECG

Pharmacologic stress

test

Serum lipid levels

Cardiac catheterization

Coronary angiography –definitive but not necessary to make the diagnosis


Angina: Management Risk factor modification

Pharmacologic Therapy

Nitrates

Beta-blockers

Calcium channel blockers

Adjunct therapy

ACE Inhibitors

Antiplatelet therapy

Anticoagulant therapy

16


Major Goals in Treating Angina

1. Slow heart rate

2. Dilate veins (decrease preload)

3. Decrease contractility

4. Decrease BP = Decrease afterload


NitratesAgents: Isosorbide dinitrate, isosorbide mononitrate,

nitroglycerinMOA: Reduces myocardial oxygen demand due to

venodilation of coronary vasculatureIndications: Acute attacks, unstable and chronic angina

Dosage: Isosorbide mononitrate: 30 mg PO dailySL NTG 0.4 mg q5minutes prn chest pain x3

AdverseEffects:

Postural hypotension, headache, flushing, tachycardia, nausea

Comments: Utilize intermittent dosing that allows a drug-free interval to avoid toleranceVarious formulations (IV, PO, SL, topical)

17


Beta-blocking AgentsAgents: Atenolol, metoprolol, propranololMOA: Decreases cardiac contractility resulting in reduced

myocardial oxygen demandIndications: DOC for chronic stable angina; can be used in

unstable anginaDosage: Metoprolol 25 mg PO BID

atenolol 25 mg PO dailyAdverseEffects:

Dizziness, fatigue, bradycardia, decreased exercise tolerance, impotence

Comments: Monitor: HR, BPDo not discontinue abruptly!


Calcium Channel Blocking AgentsAgents: Amlodipine, felodipine, verapamil, diltiazemMOA: Reduces oxygen demand; may improve oxygen supply

Indications: Considered second line treatment; DOC for vasospastic angina

Dosage: Amlodipine 5 mg PO dailyfelodipine 2.5 mg PO daily

AdverseEffects:

Verapamil - constipation, bradycardiadiltiazem - HA, nauseaamlodipine - HA, flushing, peripheral edema

Comments: Monitor: HR, BPStable angina: may be used as monotherapy when unable to tolerate beta-blockersAvoid verapamil/diltiazem in patients w/ bradycardia

18


Ranolazine (Ranexa)MOA: unknownIndications: Chronic angina,

adjunct therapy for refractory angina with inadequate response to other antianginal (amlodipine, beta-blockers, and/or nitrates) drugs

Dosage: 500 mg PO BID (max: 1000 mg PO BID)

AdverseEffects:

Constipation, nausea, dizziness, headache,syncope, prolonged QT interval

Comments: Drug interactions: CYP3A InhibitorsMonitoring: baseline and follow-up EKGDoes NOT affect hemodynamics (BP, HR)


Adjunct Pharmacologic Therapy ACE inhibitors: lisinopril, captopril

decreases the incidence of death, MI, CVA, need for revascularization and worsening angina

Antiplatelet Therapy: aspirin, clopidogrel

reduces the incidence of acute MI and death

Anticoagulant Therapy: heparin, LMWH

acute coronary syndromes (ACS)

19


Drugs for Dysrhythmias


Drugs for Dysrhythmias Act by altering specific electrophysiological properties of the heart

Two basic mechanisms: Blocking flow through ion channels (conduction) Altering autonomic activity (automaticity)

Use has declined in recent years: use for prophylaxis may actually increase mortality Narrow therapeutic index May also worsen or create new dysrhythmias Less use of Class I agents, more use of classes II and III

(amiodarone) More use of catheter ablation and implantable defibrillators

20


Class IA: Sodium Channel Blockers

Disopyramide phosphate (Norpace)

Procainamide HCI (Pronestyl)

Quinidine gluconate (Quinaglute)

Comments:

Class I: Largest class of dysrhythmics

Subdivided into 3 groups: IA, IB, IC based on MOA

Blocking Na channels will prevent depolarization

Spread of the action potential across the myocardium will slow, and areas of ectopic pacemaker activity will be suppressed

All may cause new or worsen dysrhythmias

↓ HR hypotension, dizziness, syncope

Anticholinergic side effects

Class IA indications: A-fib, PACs, PVCs, VT



Class IB: Sodium Channel Blockers

Lidocaine (Xylocaine)

Mexiletine (Mexitil)

Indications: Severe ventricular dysrhythmias

Lidocaine only available as IV

Mexiletine only available as PO

Many CNS toxicities

Class IC: Sodium Channel Blockers

Flecainide (Tambocor)

Propafenone (Rythmol)

Indications: ventricular and atrial arrhythmias

Do not use in patients with structural heart disease

Class II: Beta-Adrenergic Blockers

Acebutolol (Sectral)

Esmolol (Brevibloc)

Propranolol (Inderal)

Indications: a-flutter and fib., tachydysrhythmias, ventricular dysrhythmias

Post-MI: decrease likelihood of sudden death


21


Class III: Potassium Channel Blockers

Comments:

Amiodarone (Cordarone, Pacerone)

Dofetilide (Tikosyn)*

Ibutilide (Corvert)

Sotalol (Betapace)

Dronedarone (Multaq)

*MD must be registered by manufacturer to prescribe

Block K+ ion channels in myocardial cells

Repolarization depends on replacement of K inside the cell

By blocking K channels, repolarization is delayed and the refractory period is lengthened, thereby stabilizing dysrhythmias

Effective for atrial and ventricular dysrhythmias

Serious SE: ↓ HR bradycardia and hypotension, worsen dysrhythmias, pulmonary toxicity (amiodarone), Torsades de pointes (sotalol, ibutilide)



Class IV: Calcium Channel Blockers

Diltiazem (Cardizem, others)

Verapamil (Calan, others)

Comments:

Only non-dihydropyridines are effective for dysrhythmias

Block Ca channels in both the heart and arterioles; the remainder are specific to only vascular smooth muscle

Similar effects of BBs

↓ automaticity and HR: hypotension

Effective only against supraventricular dysrhythmias


22


Miscellaneous Antidysrhythmics

Digoxin (Lanoxin)

Adenosine (Adenocard, Adenoscan)

Digoxin: Primarily used for HF; also prescribed for some atrial dysrhythmias

Monitor for toxicity

Drug-drug interactions: diuretics, ACEIs, K supplements, BBs, antacids, anti-lipids meds., Ca, quinidine, verapamil, amiodarone, alprazolam, ginseng

Digibind for overdose

Adenosine: naturally occurring nucleoside

Terminates PSVT (↓ conduction through the AV node and ↓ automaticity)



Drugs for Coagulation Problems VTE-related deaths in the United States are estimated at 300,000

annually

The incidence of VTE nearly doubles in each decade of life over the age of 50

Individuals considered at high risk for VTE include: trauma patients, surgical patients, stroke patients, s/p MI patients, spinal cord injury patients and metastatic cancer patients

23


Category of Medications

Anticoagulant Agents Heparin Low-Molecular-Weight Heparin

(LMWH) Factor Xa inhibitor Direct Thrombin Inhibitors Warfarin

Antiplatelet Agents Aspirin, dipyridamole, ticlopidine,

clopidogrel, prasugrel, ticagrelor Glycoprotein IIb/IIIa inhibitors

Thrombolytic Agents Alteplase, reteplase,

tenecteplase


HeparinIndications: Prophylaxis and treatment of thromboembolic disorders

Dosage: Prophylaxis: 5000 units SQ q8h or q12hTreatment: individualized, dependent on weight and adjusted to goal aPTT

AdverseEffects:

Bruising, bleedingHeparin Induced Thrombocytopenia (HIT)

Comments: Rapid-acting; short actingAdministered as a continuous infusion or SQMonitoring: aPTT, plateletsAntidote: protamine sulfate

24


Low-Molecular-Weight Heparin (LMWH)Agents: Enoxaparin, dalteparin, tinzaparinMOA: Inactivates factor Xa and IIa

Dosage: Dependent on indicationDose adjustment is necessary in renal impairment

AdverseEffects:

Bruising, bleedingHeparin Induced Thrombocytopenia (HIT)

Comments: Long actingAdministered as a SQ injection onlyMonitoring: platelets, factor Xa levels (??)Antidote: protamine sulfate (60-75% effective)NO epidural/spinal anesthesia or punctureESRD: use heparin


Fondaparinux (Arixtra®)MOA: Selectively binds to antithrombin III (ATIII); thus, potentiating

the neutralization of Factor Xa

Indications: Prophylaxis and treatment of VTE

Dosage: Prophylaxis: 2.5 mg SQ dailyVTE: 5 to 10 mg SQ daily (based on weight)

AdverseEffects:

Bruising, bleeding

Comments: Monitoring: noneContraindications: severe renal impairment or weight less than 50 kgDiscontinue if the platelet count < 100,000No antidote available

25


Factor Xa InhibitorsAgents: Rivaroxaban (Xarelto), apixaban (Eliquis)

MOA: Selectively inhibits factor Xa

Indications: Prophylaxis and treatment of VTE, non-valvular atrial fibrillation

Dosage: Dependent on indicationAdjust dose in hepatic/renal impairment

AdverseEffects:

Bleeding, syncope

Comments: Monitoring: noneContraindications: severe renal impairment or hepatic impairmentREMS program: rivaroxabanNo antidote available


Direct Thrombin InhibitorsAgents: Lepirudin, argatroban, bivalirudin (Angiomax),

dabigatran (Pradaxa)MOA: Inhibits thrombinIndications: VTE; alternative to heparin or LMWH; treatment of VTE in

patients w/ HIT; PCI (bivalirudin)Dosage: Individualized, dependent on weight

AdverseEffects:

Bruising, bleeding, postural hypotension, headache, flushing, tachycardia, nausea

Comments: Adjust dose in renal impairment (lepirudin, bivalirudin, dabigatran) and hepatic impairment (argatroban, dabigatran)Monitoring: aPTT (lepirudin, bivalirudin, argatroban)Causes elevations in INR (argatroban, lepirudin)No antidote available

26


Warfarin (Coumadin®) MOA: vitamin K antagonist

Dose is individualized, titrated to goal INR(2-3 for most indications)

Adverse effects: bruising, bleeding

Monitoring: INR

Antidote: vitamin K, blood products, factor VII

Many drug-drug and drug-food interactions

Contraindicated in pregnancy and when the risk clearly outweigh the benefits


Oral Antiplatelet AgentsAgents: Aspirin, dipyridamole, ticlopidine, clopidogrel,

prasugrel, ticagrelor, anagrelide*MOA: Inhibits platelet aggregationIndications: ACS, s/p PCI with or without stenting;

dipyridamole (therapeutic use??)Dosage: Aspirin: 81-325 mg daily; dipyridamole: 75-150 mg QID;

ticlopidine: 250 mg BID; clopidogrel: 75 mg daily; prasugrel: 10 mg daily; ticagrelor 90 mg BID

AdverseEffects:

Bruising, bleeding HA, hypotensionagranulocytosis, aplastic anemia

Comments: Contraindications: active bleeding, severebleeding riskDo not use prasugrel: h/o TIA/CVA, age > 75Discontinue prior to surgeryAnagrelide: treatment of thrombocytosis

27


Parenteral Antiplatelet AgentsAgents: Abciximab, eptifibatide, tirofibanMOA: Inhibit glycoprotein IIb/IIIa receptors causing an

inhibition of platelet aggregationIndications: PCI, ACS or both

Dosage: Individualized, dependent on weight

AdverseEffects:

Bleeding, thrombocytopeniaantichimeric antibody formation (abciximab)

Comments: Adjust dose in renal impairment (tirofiban, eptifibatide)Increased bleeding complications whencombined with heparin and/or thrombolyticsUnder investigation for “bridge therapy”No antidote available


Thrombolytic AgentsAgents: Alteplase, reteplase, tenecteplase, streptokinase

MOA: Directly dissolves the thrombusIndications: DVT, acute MI, massive PE, non-hemorrhagic

stroke, catheter clearanceDosage: Dependent on indication as well as weight

AdverseEffects:

Bleeding, hypotensionantibody formation (streptokinase)

Comments: Many absolute and relative contraindicationsALL patients must be evaluated for contraindications prior to administrationNo antidote available

28


Peripheral Arterial DiseaseAgent: Pentoxifylline (Trental) Cilostazol (Pletal)

MOA: Reduces blood viscosity, improves erythrocyte flexibility, inhibits platelet aggregation

Inhibits platelet aggregation, causes vasodilation

Dose: 400 mg TID 100 mg BID

Adverse effects:

Nausea, vomiting, thrombocytopenia

Palpitations, peripheral edema, dizziness, indigestion, diarrhea, headache

Comments: Should not replace surgical bypass or removal of arterial obstructions

Contraindications: CHFOther indications: PCI, CVA


Hemostatic AgentsAgents: Aminocaproic acid (Amicar) Tranexamic acid (Cyklokapron)MOA: Prevent fibrin from dissolving, thus enhancing the stability

of the clotIndications: Excessive bleeding resulting from systemic

hyperfibrinolysis (surgery, hemophilia, aplastic anemia)Dosage: Dependent on indication Dependent on indication;

weight based dosingAdverseEffects:

Bradyarrhythmia,hypotension, thrombosis,rash

Visual disturbances,retinal vascular occlusion,Immune hypersensitivity reaction

Contra-indications:

Disseminated intravascular coagulation (DIC)

Adjust dose in hepatic or renal insufficiencyAvoid concurrent use of clotting factors

Acquired defective color vision, subarachnoid hemorrhage

Avoid concurrent use of clotting factors

29


The End

Documents

528 Unit 3 CV Part 2 S12 - MARKY - npcourses.com Handout Samples/Advanced... · Unit 3 ©2014 Barkley & Associates ... Agents: carvedilol (Coreg), metoprolol (Toprol, Lopressor)