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119 Cards in this Set

  • Front
  • Back

Hypertension

Generally refers to persistent elevation of blood pressure > or = 140/90

Essential HTN

Unknown direct cause

Secondary HTN

Linked to another problem or a result of another disease process.

Modifiable risk factors for HTN

Smoking, obesity, diabetes, dyslipidemia, physical inactivity, diet

Non-modifiable risk factors for HTN

Age, gender (male >females), genetics

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

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

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


ACE-I

Angiotensin converting enzyme inhibitor.


"Prils".


First line of treatment

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

ACE-I therapeutic effects

Drop in BP- drop in constriction, decreased resistance, decreased afterload


Renal vascular protective effects

Indications for ACE-I

HTN


CHF and MI for afterload reduction


Renal protection in diabetic patients

Precautions of ACE-I

Concurrent use of multiple drugs affecting BP.


Impaired renal function


African Americans increased risk of angioedema

Contrindications of ACE-I

Baseline hyperkalemia


Children, pregnant and lactating women

Side or adverse effects of ACE-I

Most common is dry, unproductive cough, hacking


Fatigue, dizziness, hyperkalemia


Angioedema

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.

Examples of ACE-I

Captopril, enalapril, lisinopril

ARBs

Angiotensin II receptor blockers.


"Sartans"

MOA ARBs

Block binding of angiotensin II to receptors

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

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

Precautions for ARBs

Concurrent use of multiple drugs affecting BP increasing hypertensive effects


Impaired renal function

Contraindications for ARBs

Baseline hyperkalemia


Pregnant and lactating women


Pediatrics under 1 yr

Side or adverse effects of ARBs

Headache, URI, sinusitis, muscle weakness


Angioedema, cough, fatigue, dizziness, hyperkalemia

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

Examples of ARBs

Losartan, olmesartan

MOA of Beta blockers

"Olols"


Bind to and block beta 1 (heart) and beta 2 (smooth muscle in lung) receptors

Cardioselective beta blockers

Bind to and block beta 1 receptors in the hearts electrical conduction system decreasing the heart rate

Non-selective Beta blockers

Bind to and block beta 1 and beta 2 receptors decreasing the secretion of renin

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

Indications for beta blockers

HTN


Angina


Dysrhythmias


Left ventricular systolic dysfunction

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

Contraindications for beta blockers

Pulmonary diseases

Side and adverse effects of beta blockers

CHF


Bronchospasm or bronchoconstriction causing dyspnea or wheezing


Fatigue, depression, impotence

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

Examples of beta blockers

Propranolol


Atenolol


Metroprolol

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

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


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

Precautions for CCBs

Concurrent use of other medications affecting BP


Some cardiac dysrhythmias like bradycardia or heart block


Heart failure


Fluid overload

Contraindications for CCBs

Acute MI


Some cardiac dysrhythmias like bradycardia

Side or adverse effects of CCBs

Some cardiac dysrhythmia- bradycardia or tachycardia


Fluid overload, peripheral edema, heart failure


Nausea, constipation

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

Examples of CCBs

Verapamil


Diltiazem


Amlodipine


Nifedipine

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


Indications for diuretics

Excess fluid volume, decreased renal function and HTN

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.

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

Therapeutic effects of loop diuretics

Potent diuresis resulting in substantial fluid loss


Decreases BP

Indications for loop diuretics

HTN


fluid overload, edema associated with CHF, hepatic or renal disease

Precautions of loop diuretics

Impaired renal function


Pre-existing dehydration because it dehydrates more


Pre-existing lyte imbalance like hypokalemia.

Contraindications for loop diuretics

Chronic renal failure or anuria (no urine production)


Untreated dehydration or electrolyte disturbances


Sulfa allergy (chemically related sulfanamides)

Side or adverse effects of loop diuretics

Lyte disturbances most common is hypokalemia


Dehydration, hypotension, dizziness (from lower blood volume)

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

Examples of loop diuretics

Furosemide

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

Therapeutic effects of Potassium sparing/aldosterone inhibiting diuretics

Diuresis with less K excretion


Blocks the effects of aldosterone leads to potassium retention

Indications for Potassium sparing/aldosterone inhibiting diuretics

HTN


Fluid overload, edema


Hyperaldosteronism

Precautions of Potassium sparing/aldosterone inhibiting diuretics

Impaired renal function


Pre-existing dehydration


Pre existing lyte disturbance like hyperkalemia

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)

Side or adverse effects of Potassium sparing/aldosterone inhibiting diuretics

Electrolyte disturbance= hyperkalemia


Weakness and dizziness

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

Examples of Potassium sparing/aldosterone inhibiting diuretics

Spironolactone

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

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

Indications for Thiazide and thiazide-like diuretics

HTN


fluid overload or edema

Precautions of Thiazide and thiazide-like diuretics

Impaired renal function


Preexisiting dehydration


Preexisiting lyte disturbance (hypokalemia)

Contraindications for Thiazide and thiazide-like diuretics

Chronic renal failure


Untreated dehydration or lyte disturbance

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

Nursing actions for Thiazide and thiazide-like diuretics

Assess BP, I & O, BUN, CREA, K, Mg, Ca

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)

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

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

Indications of Osmotic diuretics

Considered the osmotic diuretic of choice


Increased ICP


Early acute renal failure

Precautions of Osmotic diuretics

IV solution must be filtered


Should be stopped if cardiac, pulmonary, or renal impairment occurs

Contraindications of Osmotic diuretics

Severe renal disease


Pulmonary edema

Side and adverse effects of Osmotic diuretics

Convulsions from low Na


Pulmonary congestion

Nursing actions of Osmotic diuretics

Assess BP, I and O, BUN, CREA


physical assessment- neuro, pulmonary, renal

Example of Osmotic diuretics

Mannitol

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

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

Indications of CAIs

Altitude sickness or metabolic alkalosis


Glaucoma-increased IOP


Edema resistant to other treatment

Precautions for CAIs

Electrolyte and fluid volume disturbances

Contraindications for CAIs

Severe renal or hepatic dysfunction


Preexisiting electrolyte imbalance-hyponatremia or hypokalemia

Side or adverse effects of CAIs

Acidosis


Hypokalemia


Drowsiness and parasthesias

Nursing actions for CAIs

Assess BP, I & O, BUN, CREA, K, Mg, Na, acid base balance

Examples of CAIs

Acetazolamide

MOA of alpha 1 antagonists

Blocks alpha 1 receptors. Prevents norepinephrine from attaching causing smooth muscle relaxation

Therapeutic effects of Alpha 1 antagonists

Decrease BP- decreased constriction, decreased resistance, decreased afterload


Relaxes smooth muscle of prostatic capsule and bladder neck

Indications of Alpha 1 antagonists

HTN


benign prostatic hypertrophy- helps smooth muscle in prostate to relax so men can urinate

Precautions of Alpha 1 antagonists

Concurrent use of multiple drugs effecting BP


Hepatic or renal disease

Contraindications of Alpha 1 antagonists

Acute heart failure

Side and adverse effects of Alpha 1 antagonists

Orthostatic hypotension


Dizziness and headache

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

Examples of Alpha 1 antagonists

Doxazosin


Prazosin

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.

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

Indications of alpha 1 and beta receptor blocker

Heart failure


HTN


angina

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

Contraindications of alpha 1 and beta receptor blocker

Some pulmonary diseases, some cardiac dysrhythmias

Side and adverse effects of alpha 1 and beta receptor blocker

HF, bradycardia


Bronchospasm, bronchoconstriction


Fatigue, depression, impotence

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

Examples of alpha 1 and beta receptor blocker

Carvedilol

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

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

Indications of alpha 2 adrenergic receptor stimulators (agonists)

HTN


off label uses- migraine headaches, pain, withdrawal symptoms

Precautions of alpha 2 adrenergic receptor stimulators (agonists)

Concurrent use of multiple BP drugs


Recent MI


Chronic renal failure, liver dysfunction

Contraindications of alpha 2 adrenergic receptor stimulators (agonists)

Acute heart failure


Concurrent use of monoamine oxidase inhibitors (MAO-I)

Side and adverse effects of alpha 2 adrenergic receptor stimulators (agonists)

Orthostatic hypotension, fatigue


Dizziness, syncope

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

Example of alpha 2 adrenergic receptor stimulators (agonists)

Clonidine

MOA of direct vasodilators

Direct arterial smooth muscle relaxation

Therapeutic effects of direct vasodilators

Decreased BP- decreased constriction, decreased resistance, and decreased afterload

Indications of direct vasodilators

HTN and malignant HTN (uncontrolled)

Precautions of direct vasodilators

Concurrent use of multiple drugs affecting BP


Renal disease


Stroke

Contraindications of direct vasodilators

Cerebral edema- vasodilation causes leaky capillaries


Acute MI

Side and adverse effects of direct vasodilators

Headache, dizziness


Tachycardia

Nursimg implications of direct vasodilators

Assessment of HR and BP


patient education- drug side effects, BP monitoring, hypotension symptoms

Examples of direct vasodilators

Hydralazine