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119 Cards in this Set
- Front
- Back
Hypertension |
Generally refers to persistent elevation of blood pressure > or = 140/90 |
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Essential HTN |
Unknown direct cause |
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Secondary HTN |
Linked to another problem or a result of another disease process. |
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Modifiable risk factors for HTN |
Smoking, obesity, diabetes, dyslipidemia, physical inactivity, diet |
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Non-modifiable risk factors for HTN |
Age, gender (male >females), genetics |
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Nursing actions for HTN |
Primary prevention are assessing risk factors and compliance with meds, smoking cessation, physical activity, stress management, control diabetes, alcohol moderation, dietary management. Facilitate treatment of underlying causes Patient education-sometimes treatment can cause impotence meds will or can make you better so keep taking them |
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Target organ disease (TOD) from prolonged HTN |
1. Heart- left ventricular hypertrophy, angina, MI, CHF 2. Brain- transient ischemic attack (TIA) less severe and it can resolve, CVA 3. Kidneys- nephropathy 4. Eyes-retinopathy (impaired vision) 5. Circulation- peripheral vascular disease. Plaque and fatty deposits and calcium buildup on walls of artery |
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Pharmacological treatment options for HTN |
ABCDEs A. ACE A. ARBs B. Beta blockers C. Calcium channel blockers D. Diuretics E. Extras - alpha 1 antagonists -alpha beta receptor blockers -alpha2 adrenergic agonists -direct vasodilators -renin inhibitor |
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ACE-I |
Angiotensin converting enzyme inhibitor. "Prils". First line of treatment |
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ACE-I MOA |
Blocks the angiotensin converting enzyme (ACE) from converting angiotensin 1 to angiotensin 2. Leads to decreased vasoconstriction, decreased aldosterone,decreased water and na reabsorption and decreased BP. Allows for k+ uptake |
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ACE-I therapeutic effects |
Drop in BP- drop in constriction, decreased resistance, decreased afterload Renal vascular protective effects |
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Indications for ACE-I |
HTN CHF and MI for afterload reduction Renal protection in diabetic patients |
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Precautions of ACE-I |
Concurrent use of multiple drugs affecting BP. Impaired renal function African Americans increased risk of angioedema |
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Contrindications of ACE-I |
Baseline hyperkalemia Children, pregnant and lactating women |
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Side or adverse effects of ACE-I |
Most common is dry, unproductive cough, hacking Fatigue, dizziness, hyperkalemia Angioedema |
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Nursing actions for ACE-I |
Assess BP, I and OS, daily wts, side effects Cardiac and pulmonary Lab work- k levels, renal function Patient education to assess drug side effects, home BP, hypotension symptoms. |
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Examples of ACE-I |
Captopril, enalapril, lisinopril |
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ARBs |
Angiotensin II receptor blockers. "Sartans" |
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MOA ARBs |
Block binding of angiotensin II to receptors |
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Therapeutic effects of ARBs |
Decreased Bp- decreased constriction, decreased resistance and decreased afterload Renal vascular protective effects Use this for african Americans or when ACE-I isnt working |
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Indications for ARBs |
HTN- Intolerance of ACE-I Major use of this class is afterload reduction in CHF and MI Renal protection in diabetic patients |
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Precautions for ARBs |
Concurrent use of multiple drugs affecting BP increasing hypertensive effects Impaired renal function |
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Contraindications for ARBs |
Baseline hyperkalemia Pregnant and lactating women Pediatrics under 1 yr |
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Side or adverse effects of ARBs |
Headache, URI, sinusitis, muscle weakness Angioedema, cough, fatigue, dizziness, hyperkalemia |
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Nursing actions for ARBs |
Assess BP, I and O, daily wt, side effects Focus on cardiac and pulmonary Lab work serum K, renal function Patient education- side effects, home BP monitoring, other drugs interacting, hypotension symptoms, renal function, labs |
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Examples of ARBs |
Losartan, olmesartan |
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MOA of Beta blockers |
"Olols" Bind to and block beta 1 (heart) and beta 2 (smooth muscle in lung) receptors |
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Cardioselective beta blockers |
Bind to and block beta 1 receptors in the hearts electrical conduction system decreasing the heart rate |
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Non-selective Beta blockers |
Bind to and block beta 1 and beta 2 receptors decreasing the secretion of renin |
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Therapeutic effects of beta blockers |
Decrease BP- decreased constriction, decrease resistance, and decreased afterload Decrease in heart rate- decrease in SA node firing, negative chronotrope Decrease in myocardial contractility- decrease o2 requirements of heart cells. negative inotrope |
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Indications for beta blockers |
HTN Angina Dysrhythmias Left ventricular systolic dysfunction |
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Precautions for beta blockers |
Concurrent use of multiple drugs Pulmonary disease or illness affecting the beta 2 cells Heart failure- some dysrhythmias, bradycardia Can mask the evidence of hypoglycemia |
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Contraindications for beta blockers |
Pulmonary diseases |
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Side and adverse effects of beta blockers |
CHF Bronchospasm or bronchoconstriction causing dyspnea or wheezing Fatigue, depression, impotence |
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Nursing actions for beta blockers |
Assess bp, HR, pulmonary status, I and O, daily wts, side effects Physical assessment of cardiac and pulmonary Patient education- drug side effects, home HR and BP, hypotension symptoms, effects seen with stress testing, renal function, glucose |
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Examples of beta blockers |
Propranolol Atenolol Metroprolol |
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MOA of Calcium channel blockers (CCBs) |
Inhibits the transport of calcium into the myocardial and smooth muscle cells Decreased HR and force of myocardial contraction |
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Therapeutic effects of CCBs |
Decrease BP- decrease constriction, decreased resistance, decreased afterload HR-decrease in SA node firing, negative chronotrope Decreased myocardial contractility- decreases O2 requirements of myocardial cells, negative inotrope Decreases coronary artery spasms |
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Indications for CCBs |
HTN angina especially if coronary artery spasm Raynauds- migraine headaches. (Decreases cerebral artery spasms) -poor perfusion or circulation of hande can cause raynauds |
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Precautions for CCBs |
Concurrent use of other medications affecting BP Some cardiac dysrhythmias like bradycardia or heart block Heart failure Fluid overload |
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Contraindications for CCBs |
Acute MI Some cardiac dysrhythmias like bradycardia |
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Side or adverse effects of CCBs |
Some cardiac dysrhythmia- bradycardia or tachycardia Fluid overload, peripheral edema, heart failure Nausea, constipation |
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Nursimg actions for CCBs |
Asses BP, HR, I & O, peripheral edema, daily wt, side effects Physically assess- cardiac pulmonary Patient education- side effects of drugs, home HR & BP, hypotension symptoms and renal function |
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Examples of CCBs |
Verapamil Diltiazem Amlodipine Nifedipine |
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Diuretics |
Accelerate urine formation, excrete na and h2o Site of action is the kidneys, specifically the nephron Goal- increase urine formation or output resulting in net water loss from the body decreasing BP |
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Indications for diuretics |
Excess fluid volume, decreased renal function and HTN |
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Patient education for diuretics |
Drug side effects, daily weights, lab work, timing the doses such as taking in the am so you dont have to get up a lot at night or in the PM so it does not interfere with daily activities. Home BP monitoring Interactions with other drugs Also at risk for reaction with digoxin causing digoxin toxicity. |
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MOA for loop diuretics |
These cause the most diaresis Inhibits na and claims reabsorption in the loop of Henley and therefore h20 is released Dilates blood vessels decreasing systemic vascular resistance |
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Therapeutic effects of loop diuretics |
Potent diuresis resulting in substantial fluid loss Decreases BP |
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Indications for loop diuretics |
HTN fluid overload, edema associated with CHF, hepatic or renal disease |
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Precautions of loop diuretics |
Impaired renal function Pre-existing dehydration because it dehydrates more Pre-existing lyte imbalance like hypokalemia. |
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Contraindications for loop diuretics |
Chronic renal failure or anuria (no urine production) Untreated dehydration or electrolyte disturbances Sulfa allergy (chemically related sulfanamides) |
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Side or adverse effects of loop diuretics |
Lyte disturbances most common is hypokalemia Dehydration, hypotension, dizziness (from lower blood volume) |
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Nursing actions for loop diuretics |
Asses BP M, I & O, BUN, CREA, K & Mg There can be an elevated bun if there is protein breakdown from dehydration |
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Examples of loop diuretics |
Furosemide |
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MOA of Potassium sparing/aldosterone inhibiting diuretics |
Acts on distal tubules blocking Na and K exchange, blocks aldosterone receptors. This increases Na and H2O excretion while retaining K and H |
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Therapeutic effects of Potassium sparing/aldosterone inhibiting diuretics |
Diuresis with less K excretion Blocks the effects of aldosterone leads to potassium retention |
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Indications for Potassium sparing/aldosterone inhibiting diuretics |
HTN Fluid overload, edema Hyperaldosteronism |
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Precautions of Potassium sparing/aldosterone inhibiting diuretics |
Impaired renal function Pre-existing dehydration Pre existing lyte disturbance like hyperkalemia |
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Contraindications for Potassium sparing/aldosterone inhibiting diuretics |
Chronic renal failure Untreated dehydration or lyte disturbance. (An already elevated K before meds can increase after meds are given) |
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Side or adverse effects of Potassium sparing/aldosterone inhibiting diuretics |
Electrolyte disturbance= hyperkalemia Weakness and dizziness |
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Nursing actions for Potassium sparing/aldosterone inhibiting diuretics |
Concerned when given with ACE-I because they also inhibit aldosterone which results in retained k Assess BP, I and O, BUN and crea, K and Mg |
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Examples of Potassium sparing/aldosterone inhibiting diuretics |
Spironolactone |
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MOA of Thiazide and thiazide-like diuretics |
Inhibit Na, K and Cl reabsorption in distal tubules in kidneys resulting in water loss. Causes direct vasodilation of peripheral artierioles |
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Therapeutic effects of Thiazide and thiazide-like diuretics |
Excretion of water, na, k, and cl without altering pH. Also excrete bicarbonate. Peripheral artieriole dilation which results in decreased resistance and decreased afterload |
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Indications for Thiazide and thiazide-like diuretics |
HTN fluid overload or edema |
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Precautions of Thiazide and thiazide-like diuretics |
Impaired renal function Preexisiting dehydration Preexisiting lyte disturbance (hypokalemia) |
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Contraindications for Thiazide and thiazide-like diuretics |
Chronic renal failure Untreated dehydration or lyte disturbance |
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Side and adverse effects of Thiazide and thiazide-like diuretics |
Lyte disturbances low K and high Ca Headache and dizziness Thrombocytopenia, pancreatitis Increase lipids, glucose and uric acid Hyperglycemia from the inhibition of glucose uptake |
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Nursing actions for Thiazide and thiazide-like diuretics |
Assess BP, I & O, BUN, CREA, K, Mg, Ca |
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Examples of Thiazide and thiazide-like diuretics |
Thiazide- hydrochlorothiazide Thiazide-like: metolazone (these are similar to thiazide chemical properties are different but they act like a thiazide) |
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MOA of Osmotic diuretics |
Increase the Osmotic pressure in glomerular filtrate Fluid pulled into tension tubules, especially proximal and descending loop of Henle Inhibits tubular reabsorption of water and solute Produces rapid diuresis decreases cerebral edema and intracranial pressure |
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Therapeutic effects of Osmotic diuretics |
Osmotic diuresis with minimal effect on electrolytes Shifts fluid- decreasing cerebral edema= decrease intracranial pressure Rapid excretion of fluid from kidneys in early acute renal failure |
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Indications of Osmotic diuretics |
Considered the osmotic diuretic of choice Increased ICP Early acute renal failure |
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Precautions of Osmotic diuretics |
IV solution must be filtered Should be stopped if cardiac, pulmonary, or renal impairment occurs |
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Contraindications of Osmotic diuretics |
Severe renal disease Pulmonary edema |
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Side and adverse effects of Osmotic diuretics |
Convulsions from low Na Pulmonary congestion |
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Nursing actions of Osmotic diuretics |
Assess BP, I and O, BUN, CREA physical assessment- neuro, pulmonary, renal |
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Example of Osmotic diuretics |
Mannitol |
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MOA of Carbonic Anhydrase inhibitors (CAI) |
Decreases hydrogen availability for Na exchange in the proximal tubules resulting in h2O and na excretion. Inhibits carbonic anhydrase activity at multiple sites Decrease in aqueous humor production, decreased pressure in the eye |
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Therapeutic effects of CAIs |
Decreased circulating sodium bicarbonate alter acid base balance Decrease aqueous humor production which then decreases intraocular pressure Renal na and h2o excretion in the primary proximal tubules |
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Indications of CAIs |
Altitude sickness or metabolic alkalosis Glaucoma-increased IOP Edema resistant to other treatment |
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Precautions for CAIs |
Electrolyte and fluid volume disturbances |
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Contraindications for CAIs |
Severe renal or hepatic dysfunction Preexisiting electrolyte imbalance-hyponatremia or hypokalemia |
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Side or adverse effects of CAIs |
Acidosis Hypokalemia Drowsiness and parasthesias |
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Nursing actions for CAIs |
Assess BP, I & O, BUN, CREA, K, Mg, Na, acid base balance |
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Examples of CAIs |
Acetazolamide |
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MOA of alpha 1 antagonists |
Blocks alpha 1 receptors. Prevents norepinephrine from attaching causing smooth muscle relaxation |
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Therapeutic effects of Alpha 1 antagonists |
Decrease BP- decreased constriction, decreased resistance, decreased afterload Relaxes smooth muscle of prostatic capsule and bladder neck |
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Indications of Alpha 1 antagonists |
HTN benign prostatic hypertrophy- helps smooth muscle in prostate to relax so men can urinate |
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Precautions of Alpha 1 antagonists |
Concurrent use of multiple drugs effecting BP Hepatic or renal disease |
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Contraindications of Alpha 1 antagonists |
Acute heart failure |
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Side and adverse effects of Alpha 1 antagonists |
Orthostatic hypotension Dizziness and headache |
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Nursing actions of Alpha 1 antagonists |
Assessment of HR, BP, I&O, urinary symptoms Patient education- drug side effects, home BP monitoring, urinary function, hypotension symptoms |
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Examples of Alpha 1 antagonists |
Doxazosin Prazosin |
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MOA of alpha 1 and beta receptor blocker |
Act in periphery of heart and vessels Nonselective receptor blocker alpha one, beta 1 and beta 2 leads to smooth muscle relaxation Myocardial contractility- decreases oxygen demand of myocardial cells. Negative inotrope. |
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Therapeutic effects of alpha 1 and beta receptor blocker |
Decreased progression of heart failure Decreased BP- decreased constriction, decreased resistance, and decreased afterload Decreased heart rate- negative chronotrope Decreased myocardial contractility- negative inotrope |
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Indications of alpha 1 and beta receptor blocker |
Heart failure HTN angina |
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Precautions of alpha 1 and beta receptor blocker |
Concurrent use of multiple drugs affecting BP Pulmonary disease or illness Heart failure some cardiac dysrhythmias May mask evidence of hypoglycemia |
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Contraindications of alpha 1 and beta receptor blocker |
Some pulmonary diseases, some cardiac dysrhythmias |
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Side and adverse effects of alpha 1 and beta receptor blocker |
HF, bradycardia Bronchospasm, bronchoconstriction Fatigue, depression, impotence |
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Nursing actions of alpha 1 and beta receptor blocker |
Assessment HR and BP physical assessment: evidence of worsening HF patient education- drug side effects, home HR and BP, hypotension, renal function, glucose levels |
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Examples of alpha 1 and beta receptor blocker |
Carvedilol |
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MOA of alpha 2 adrenergic receptor stimulators (agonists) centrally acting |
Act in the brain Stimulates alpha 2 receptors in brain decreasing sympathetic outflow (decreased fight response) Decreased production of norepinephrine and decreased renin activity |
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Therapeutic effects of alpha 2 adrenergic receptor stimulators (agonists) |
Decreased BP- decreased constriction, decreased resistance, and decreased afterload Pain control, and alcohol/opiod/tobacco withdrawal management |
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Indications of alpha 2 adrenergic receptor stimulators (agonists) |
HTN off label uses- migraine headaches, pain, withdrawal symptoms |
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Precautions of alpha 2 adrenergic receptor stimulators (agonists) |
Concurrent use of multiple BP drugs Recent MI Chronic renal failure, liver dysfunction |
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Contraindications of alpha 2 adrenergic receptor stimulators (agonists) |
Acute heart failure Concurrent use of monoamine oxidase inhibitors (MAO-I) |
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Side and adverse effects of alpha 2 adrenergic receptor stimulators (agonists) |
Orthostatic hypotension, fatigue Dizziness, syncope |
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Nursing actions of alpha 2 adrenergic receptor stimulators (agonists) |
Monitor HR and BP Available as oral, topical, and epidural routes Patient education- drug side effects, BP monitoring, hypotension |
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Example of alpha 2 adrenergic receptor stimulators (agonists) |
Clonidine |
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MOA of direct vasodilators |
Direct arterial smooth muscle relaxation |
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Therapeutic effects of direct vasodilators |
Decreased BP- decreased constriction, decreased resistance, and decreased afterload |
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Indications of direct vasodilators |
HTN and malignant HTN (uncontrolled) |
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Precautions of direct vasodilators |
Concurrent use of multiple drugs affecting BP Renal disease Stroke |
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Contraindications of direct vasodilators |
Cerebral edema- vasodilation causes leaky capillaries Acute MI |
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Side and adverse effects of direct vasodilators |
Headache, dizziness Tachycardia |
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Nursimg implications of direct vasodilators |
Assessment of HR and BP patient education- drug side effects, BP monitoring, hypotension symptoms |
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Examples of direct vasodilators |
Hydralazine |