Cardiovascular Pharm

Pregunta	Respuesta
WHAT ARE THE 5 ADRENERGIC RECEPTORS?	Alpha 1 & Alpha 2 Beta 1 & Beta 2 Dopamine
ACTIVATION OF ALPHA 1 RECEPTORS	Alpha 1 Activation= Vasoconstriction: 1. Delay absorption of local anesthetics 2. Control superficial bleeding 3. Elevate blood pressure Adverse effects: hypertension, tissue necrosis with intravenous (IV) extravasation, and bradycardia.
ACTIVATION OF ALPHA 2 RECEPTORS	Activation of peripheral alpha2 receptors: no therapeutic applications.
ACTIVATION OF BETA 1 RECEPTORS	Heart- positive inotropic effect (+) heart rate and force of contraction, (+) cardiac output = (+) tissue perfusion. Enhancing impulse conduction through the atrioventricular (AV) node Restore cardiac function in cardiac arrest Adverse effects of beta1 activation: altered heart rate or rhythm and angina pectoris.
ACTIVATION OF BETA 2 RECEPTORS	Beta 2 Activation Bronchodilation FOR: asthma and delay of preterm labor adverse effect: hyperglycemia (mainly in diabetic patients) and tremor
EPINEPHRINE Uses & MOA	For: Management of cardiac arrest , control superficial bleeding, delay anesthetic absorption *Treatment of choice for anaphylactic shock MOA: Activation of all four adrenergic receptors: alpha 1, alpha 2, Beta 1, Beta 2 receptors
EPINEPHERINE Adverse Effects	Hypertension (severe) Cardiovascular effects: Anginal pain, tachycardia, Dysrhythmia Angina- increased cardiac work and oxygen deman Necrosis, Hyperglycemia
EPINEPHERINE Nursing Considerations	Use with caution in pt with hyperthyroidism, cardiac dysrhthmias, heart disease, or hypertension, angina pectoris, diabetes
NOREPINEPHERINE Uses & MOA	For: Hypotensive states and Cardiac arrest MOA: Activation of 3 adrenergic receptors: alpha 1, alpha 2, Beta 1 receptors ***Similar to epinephrine BUT, does NOT activate B2 receptors
NORPEPINEPHERINE Adverse Effects	Hypertension (severe) Cardiovascualr effects: anginal pain, tachycardia, dysrhythmias Angina- increased cardiac work and demand Necrosis
NOREPINEPHERINE Nursing Consideraions	Use with caution in pt with hyperthyroidism, cardiac dysrhthmias, heart disease, or hypertension, angina pectoris.
DOPAMINE Uses	Shock- B1 in heart receptors increase cardiac output, improve tissue perfusion. Dope Kidney receptors dilate renal blood vessels, improve renal perfusion. Alpha1 receptors- vasoconstriction may decrease renal perfusion, overriding dopamine activation. Thus monitoring urine output essential Heart Failure- B1 alleviate symptoms of reduced perfusion and reduced CO. increases myocardial contractility.
DOPAMINE MOA	Dose Dependent Receptor specificity: Dopamine, Beta1 and at high doses Alpha1 Low dose= dopamine only Mod dose= dopamine + Beta1 High dose= dopamine + Beta1 + alpha 1
DOPAMINE Adverse EffectsTS	AE: tachycardia, dysrhythmias, anginal pain (from B1 activation)
DOBUTAMINE Use and MOA	BETA 1 AGONIST For: improvement of hemodynamic status in patients with heart failure MOA: selective activation of Beta 1 adrenergic receptors
DOBUTAMINE AE & Contraindications	AE: Tachycardia & dysrhythmias. GREAT caution in patients with heart disease, hyperthyroidism, tachydysrhythmias, hypertension. Caution w/ angina pectoris, tricyclic antidepressants, general anesthetics.
PHENYLEPHRINE	NON-CATECHOLMINE MOA: selective ALPHA 1 AGONIST Use: Elevate blood pressure
NAME THE ANTI-DYSRHYTHMIC DRUGS	1) AMIODARONE Class III: - potassium channel blocker 2) ADENOSINE Class IV: - calcium channel blocker
AMIODARONE Therapeutic Uses Image: Smooth Smurf (binary/octet-stream)	ANTIDYSRHYTMIC For: Atrial & Ventricular Dysrhythmias Class III: - Prolong action potential duration and delays repolarization
AMIODARONE Adverse Effects Image: Smooth Smurf (binary/octet-stream)	ANTIDYSRHYTHMIC Cardiac: sinus bradycardia, dcereased contractility; Ophthalmic, smurf skin, photosensitivity TOXICITIES: thyroid, pulmonary, cardiac, liver, dermatologic
ADENOSINE Use & MOA Image: Calcium2 (binary/octet-stream)	ANTIDYSRHYTHMIC For: Supraventricular Tachycardia - decreases automaticity in the SA Node and slows conduction through the AV node Prolongs PR Interval MOA: Inhibits cAMP induced calcium influx= suppresses calcium- dependent action potentials in the SA & AV Nodes
ADENOSINE Adverse Effects Image: Calcium2 (binary/octet-stream)	ANTIDYSRHYTHMIC Minimal b/c rapidly cleared from blood. AE last less than 1 min. * must be given IV Sinus bradycardia, dyspnea (from bronchoconstriction), hypotension, facial flushing (from vasodilation)
ATROPINE Use & MOA	MUSCARINIC ANTAGONIST 1) Heart: Increase HR ; Treats symptomatic bradycardia 2) Exocrine Glands: Decrease secretions of exocrine glands 3) Smooth muscle relaxation myadriasis (pupil dilation) MOA: competitive blockade at muscarinic receptors. All responses are from preventing receptor activity by endogenous Acetylcholine
ATROPINE Adverse Effects	MUSCARINIC ANTAGONIST- ANTICHOLINERGIC AE: Dry mouth, blurred vision, photophobia, intraocular pressure, urinary retention, constipation, antihydrosis, tachycardia, asthma.
ATROPINE Drug-Drug Interactions	Drug-Drug Interactions: Antihistamines other muscarinic antagonists High risk patients: glaucoma, UT obstruction, tachycardia
MUSCARINIC RECEPTORS: Locations	Heart, Arterioles GI Tract, Gallbladder Lungs, Liver Urinary Bladder, Penis Lacrimal Glands, Eye
WHAT TYPES OF DYSRHTHMIAS MIGHT PHARMACEUTICALS TREAT?	SUPRAVENTRICULAR - Atrial fibrillation/ flutter Sustained SVT VENTRICULAR - sustained VT - ventricular fibrillation PVC Torsde de Pointes
NIACIN Use & MOA	ANTILIPIDEMIA Prophylaxis for Atherosclerotic Cardiovascular Disease MOA: Reduces LDL & TG levels and increases HDLs. Acts in liver and adipose tissue to inhibit synthesis of TGs , thus decreasing LDLs.
NIACIN Adverse Effects	HEPATOTOXICITY (severe liver damage) hyperglycemia, hyperuricemia= (+) uric acid GI distress Skin: intense flushing and itching. (take aspirin 30 min before dose) * slow titration up on dose due to adverse effects NEVER use w/ chronic liver disease, gout Caution w/ diabetes, peptic ulcer disease
ATORVASTATIN Therapeutic Use	Treat Hyperlipidemia/ Dyslipidemia, Hypercholesterolemia, Prevention of CV events, MI & stroke prevention in DM2, Increase HDLs
ATORVASTATIN MOA	MOA: Inhibition of HMG-CoA Reductase - enzyme pivitol to cholesterol synthesis Outcome= reduction of LDL & TG, Increase in HDL
ATORVASTATIN Adverse Effects	Pregnancy Category X Hepatotoxicity Myopathy/Rhabdomolysis
ATORVASTATIN Patient Education	Most effective when given at night. If meds stopped serum levels will return to pretreatment levels within weeks. - Life long treatment. Diet modification and exercise enhance therapeutic effects.
CLOPIDOGREL Therapeutic Indications	ANTIPLATELET prevention of atherothrombotic events in patients with ACS , unstable angina or MI. prevent blockage of coronary artery stents, reduce thrombotic events (MI, stroke, vascular death).
CLOPIDOGREL MOA	P2Y12 ADP RECEPTOR ANTAGONIST Prevents ADP stimulated platelet aggregation - irreversible antiplatelet effect platelet function and bleeding time return after 7-10 days after last dose
CLOPIDOGREL Adverse Effects	Bleeding Thrombotic thrombocytopenic purpura (TTP) neurologic renal dysfunction fever
ASPIRIN MOA	Blocks Thromboxane A2 which normally stimulates activation of new platelets and platelet aggregation. - Causes irreversible inhibition
ASPIRIN Therapeutic Indications	Ischemic stroke, transient ischemic attacks, acute MI, previous, MI, Chronic stable angina, unstable angina.
ASPIRIN Adverse Effects	bleeding risks, GI bleeds, Renal impairment, tinnitis, salicylate toxicity
DESCRIBE SALICYLATE TOXICITY	salicylate toxicity --> respiratory acidosis, metabolic acidosis, renal failure, altered mental status
ASPIRIN Contraindications	NO Pediatrics patients!!!! d/t risk for Reyes syndrome, Encephalopathy, and fatty liver degeneration

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	Creado por Kate Parvey hace más de 7 años