Class 1 Adrenergic Receptors (CV) Flashcards
Adrenergic receptors
-Alpha 1&2
-Beta 1&2
Alpha-1 effects
-Vasoconstriction
-Increases PVR, BP & closure of bladder sphincters
-Mydriasis (dilates pupils)
-NE>E
Alpha-2 effects
-Inhibits NE, Ach, & insulin release
-E>NE
Beta 1 effect on CV
-Increase HR, heart contractility, lipolysis, & renin
-E=NE
Beta 2 effects
-Vasodilation, decreases PVR
-Relaxes uterine smooth muscle
-Increases glycogenolysis & glucagon release
-E»NE
Management of HTN: Diuretics & anti-hypertensive therapy drugs
-Thiazide/thiazide-like diuretic
-ACE I
-ARBs
-Long-acting CCB
-Beta-blockers
-Single pill combination
-LATABS
Diuretics: general overview
▪ First line treatment for HTN
▪ MOA: Decrease volumes of plasma and extracellular fluid; reduces preload, CO and SVR (afterload)
▪ Reduces the workload of the heart
Angiotensin converting enzyme inhibitors (ACE I): General overview
▪ First-line treatment of HTN, HF & diabetes (renal protection)
▪ Typically given in combination with diuretics or Ca+ channel blockers to increase adherence
▪ Contraindicated in 2nd & 3rd trimester
ACE I: MOA
-Inhibit ACE which converts angiotensin I to angiotensin II (reduces vasoconstriction/BP)
-Reduces SVR (afterload)
-Prevents Na+ & H2O resorption by inhibiting aldosterone which is an anti-diuretic (decreases preload; ideal for HF patients)
ACE inhibitors “pril”
-“prils”
-Captopril
-Ramipril*
-Enalapril sodium*
-Fosinopril sodium
-Lisiopril*
-Perindopril erbumine
-Denotes ACE can be in combination with
hydrochlorothiazide (ERL)
ACE I: Indications for use
-HTN; decrease afterload (SVR)
-HF; prevents Na+ & H2O resorption and causes diuresis, decreases preload, stops the progression of LV hypertrophy post heart attack
-Diabetes; reduces Glomerular filtration pressure
ACE I contraindications
-K+> 5mmol/L
-Impaired kidney function
-Pregnant or lactating women
ACE I: Adverse events
-Fatigue, dizziness, mood changes, headaches, hypotension
-Non productive cough
-Hyperkalemia
-Angioedema
-Loss of taste, proteinuria, rash, pruritis, anemia, neutropenia, thrombocytosis and agranulocytosis
ACE I drug-drug interactions
-NSAIDS; reduce antihypertensive effects and may lead to nephrotoxicity
-Potassium supplements or Potassium sparing diuretics; hyperkalemia
-Lithium; lithium toxicity
Angiotensin receptor blockers (ARBs): MOA
-Block binding of angiotensin II to type 1 angiotensin II receptors; block vasoconstriction
-Vasopressor effects and blocks aldosterone secretion
-ARBs do not cause cough
-Contraindicated in 2nd & 3rd trimester of pregnancy
ARBs (TICLV)
-“Sartans”
▪ Losartan
▪ Valsartan
▪ Irbesartan
▪ Candesartan cilexetil
▪ Telmisartan
ARBs indications
-Heart Failure; decrease preload and afterload
-HTN
ARBs contraindications
-Pregnant or lactating women
-Older adults
-MI
ARBs: Adverse events
-Respiratory infections, dyspnea, nasal congestion, sinusitis, cough
-Headache, heartburn, dizziness, diarrhea & anxiety
-Inability to sleep, fatigue
-Back & muscle pain
ARBs toxicity & OD
-Hypotension
-Tachycardia
-Bradycardia occurs less often
ARBs: Drug to drug interactions
-NSAIDs; decreased antihypertensive effect; potential for kidney failure
-Lithium; inhibits Li+ elimination
-Phenobarbital; increases metabolism; decreases ARB effectiveness
-K+ sparing diuretics & K+ supplements; hyperkalemia
ACE I considerations & pt teaching
-Weaned off medication
-Na+ & K+ levels should be monitored during therapy
-May take several weeks to see therapeutic effects
ARBs considerations & pt teaching
-Reduced dosage with hypovolemia & liver dysfunction
-Report unusual dyspnea, dizziness, or excessive fatigue
Adrenergic blocking agents (beta blockers): General overview
-Block SNS stimulation of Beta 1 by competing with E & NE
-Cause the release of free fatty acids from adipose tissue; elevated triglycerides and reduced levels of (HDL)
Beta blockers: MOA (cardio-selective)
-Specific to Beta 1 receptors in the heart
-Reduces myocardial stimulation & oxygen demand by decreasing force of contraction
Beta blockers MOA (Non-selective)
-Block both Beta 1&2 receptors
-Reduces myocardial stimulation & myocardial oxygen demand by decreasing force of contraction
-Block Beta 2 receptors on the smooth muscle of the bronchioles and blood vessels
Beta blockers (cardio selective): BEAaNeM
“olol”
Metoprolol
Bisoprolol fumerate
Atenolol
Acebutalol
Esmolol
Nebivolol
Beta blockers (non-selective)
“olol”
Carvedilol
Labeltalol
Nadolol
Pindolol
Sotalol
Timolol
Propranolol
Beta blockers inidications for use
-Angina, AMI, HTN, HF, dysrhythmias
-Migraines & glaucoma