Pharm: HTN

What are the 4 major medication categories used to treat hypertension?

Adrenergic drugs (SNS), RAAS drugs, vasodilators, and diuretics.

What determines arterial blood pressure?

Cardiac output × peripheral vascular resistance.

What factors determine cardiac output?

Heart rate, contractility, blood volume, and venous return.

What primarily determines peripheral vascular resistance?

Arteriolar constriction.

What is normal blood pressure?

Less than 120 systolic AND less than 80 diastolic.

What is elevated blood pressure?

120–129 systolic AND less than 80 diastolic.

What is Stage 1 hypertension?

130–139 systolic OR 80–89 diastolic.

What is Stage 2 hypertension?

140 or higher systolic OR 90 or higher diastolic.

What is a hypertensive crisis?

Systolic >180 and/or diastolic >120 mmHg.

What lifestyle changes can help lower blood pressure?

Reduce salt, eat a balanced diet, maintain healthy weight, exercise, limit alcohol, and do not smoke.

Which beta blockers are reviewed in this lecture?

Metoprolol and propranolol.

What is the MOA of beta blockers?

Block beta receptors.

What are therapeutic uses of beta blockers?

HTN, HF, post-MI, migraine, angina, and dysrhythmias.

What cardiovascular adverse effects can beta blockers cause?

Bradycardia and low blood pressure.

What respiratory adverse effect can beta blockers cause?

Bronchospasm.

How can beta blockers affect recognition of hypoglycemia?

They can mask blood sugar-related symptoms.

What CNS effects can beta blockers cause?

Depression, insomnia, and vivid dreams.

What sexual adverse effect can beta blockers cause?

Sexual dysfunction.

What drug class can interact with beta blockers?

Calcium channel blockers (CCBs).

What should the nurse check before administering a beta blocker?

Heart rate.

Should beta blockers be stopped abruptly?

No. Avoid abrupt discontinuation.

What alpha blocker is reviewed in this lecture?

Prazosin.

What is the MOA of prazosin?

Blocks alpha receptors.

What are therapeutic uses of prazosin?

HTN (rarely used) and BPH.

What is a major adverse effect of alpha blockers?

Orthostatic hypotension.

What is the first-dose effect of alpha blockers?

Significant orthostatic hypotension can occur with the first dose.

What cardiovascular response can occur with alpha blockers?

Reflex tachycardia.

What should patients taking alpha blockers be taught?

Monitor for and take precautions against orthostatic hypotension.

What central alpha-2 agonist is reviewed in this lecture?

Clonidine.

What is the MOA of clonidine?

Activates alpha-2 receptors, decreasing sympathetic outflow.

What are therapeutic uses of clonidine?

Resistant HTN and CNS indications.

What are adverse effects of clonidine?

Dry mouth, sedation, rebound hypertension, and minimal orthostatic hypotension.

What happens if clonidine is abruptly discontinued?

Rebound hypertension can occur.

What important teaching applies to clonidine?

Do not abruptly discontinue it; patch issues are common.

What does RAAS stand for?

Renin-angiotensin-aldosterone system.

What ACE inhibitor is the prototype?

Lisinopril (Zestril).

What is the MOA of lisinopril?

Blocks ACE, decreasing angiotensin II production and aldosterone release.

What are the indications for lisinopril?

HTN, HF, post-MI, nephropathy, and diabetic retinopathy.

What are major adverse effects of lisinopril?

Angioedema, cough, hyperkalemia, hyponatremia, rash, loss of taste, and increased serum creatinine.

What electrolyte changes can ACE inhibitors cause?

High potassium and low sodium.

What renal laboratory value may increase with ACE inhibitors?

Serum creatinine.

When are ACE inhibitors contraindicated in pregnancy?

Second and third trimesters.

What renal condition contraindicates ACE inhibitor use?

Bilateral renal artery stenosis.

What previous reaction contraindicates ACE inhibitor use?

History of angioedema.

What should a patient do if angioedema occurs while taking an ACE inhibitor?

Seek treatment immediately and never take the medication again.

What should be closely monitored with ACE inhibitors?

Renal function, especially in patients with HF.

What ARB is the prototype?

Losartan (Cozaar).

What is the MOA of losartan?

Directly blocks angiotensin II receptors.

What are the therapeutic uses of ARBs?

Same as ACE inhibitors.

How do ARB adverse effects compare with ACE inhibitors?

Similar, but ARBs cause less cough and hyperkalemia; angioedema risk is the same.

What are the nursing implications for ARBs?

Same as ACE inhibitors.

How do ACE inhibitors and ARBs affect glomerular filtration pressure?

They decrease glomerular filtration pressure.

What are the prototype aldosterone antagonists?

Eplerenone (Inspra) and spironolactone.

What other drug class are aldosterone antagonists considered?

Potassium-sparing diuretics.

What is the MOA of aldosterone antagonists?

Block aldosterone effects at the collecting tubule.

What does aldosterone normally do in the collecting tubule?

Increases Na+ and H2O reabsorption and increases K+ excretion.

What are therapeutic uses of aldosterone antagonists?

HTN and HF.

What is the major electrolyte adverse effect of aldosterone antagonists?

Hyperkalemia.

What renal laboratory value can increase with aldosterone antagonists?

Serum creatinine.

When should serum creatinine and potassium be checked after starting an aldosterone antagonist?

Within the first week.

What steroid receptor-mediated adverse effects can aldosterone antagonists cause?

Hirsutism, gynecomastia, impotence, and menstrual irregularities.

What should patients taking aldosterone antagonists avoid?

Potassium supplements and potassium-containing foods.

Why should potassium supplements be avoided with aldosterone antagonists?

They increase the risk of hyperkalemia.

What direct renin inhibitor is the prototype?

Aliskiren (Tekturna).

What is the MOA of aliskiren?

Directly blocks renin, decreasing angiotensin II production.

What is the therapeutic use of aliskiren?

Hypertension.

What are adverse effects of aliskiren?

Hyperkalemia, low-risk angioedema/cough, and dose-dependent diarrhea.

What should patients taking aliskiren avoid?

Potassium sources such as supplements and salt substitutes.

What adverse effects are shared by many RAAS drugs?

Kidney effects, hyperkalemia, angioedema, and possible cough.

What pregnancy concern is associated with RAAS drugs?

They are potentially teratogenic and should be avoided in the 2nd and 3rd trimesters.

What electrolyte abnormality is especially important with RAAS drugs?

Hyperkalemia.

What two types of calcium channel blockers are discussed?

Non-dihydropyridines and dihydropyridines.

What is the prototype non-dihydropyridine CCB?

Verapamil (Calan).

What is the MOA of verapamil?

Blocks calcium channels in both blood vessels and the heart.

What are the therapeutic uses of verapamil?

HTN, angina, and dysrhythmias.

What are adverse effects of verapamil?

Constipation, dizziness, flushing, headache, and partial or complete AV block.

What is the serious cardiac adverse effect of verapamil?

Partial or complete AV block.

When should verapamil never be used?

Sick sinus syndrome or 2nd- or 3rd-degree heart block.

What substances/drugs interact with verapamil?

Grapefruit juice, beta blockers, and digoxin.

What should patients taking verapamil avoid?

Grapefruit juice.

What medication safety issue exists with verapamil?

Immediate-release and extended-release products can be mixed up.

What pharmacokinetic issue occurs with verapamil?

High first-pass effect.

What is the prototype dihydropyridine CCB?

Nifedipine (Adalat).

What is the MOA of nifedipine?

Blocks calcium channels in blood vessels with little to no effect on the heart.

What are the therapeutic uses of nifedipine?

HTN and angina.

What are adverse effects of nifedipine?

Reflex tachycardia, flushing, headache, dizziness, peripheral edema, and gingival hyperplasia.

What important adverse effect should patients taking nifedipine be warned about?

Peripheral edema.

Should immediate-release nifedipine be used for hypertension?

No. Never administer immediate-release nifedipine for HTN.

Can extended-release nifedipine be crushed?

No. Crushing it could be deadly.

What is the main difference between verapamil and nifedipine?

Verapamil affects blood vessels AND the heart; nifedipine mainly affects blood vessels.

What direct vasodilator has hydralazine as its prototype?

Direct arteriolar vasodilator.

What is the MOA of hydralazine?

Directly dilates arterioles.

What are the therapeutic uses of hydralazine?

HTN, HF with a nitrate, and hypertensive crisis with the IV form.

What are adverse effects of hydralazine?

Reflex tachycardia, fluid retention, SLE-like syndrome, and hypotension.

What symptoms of hypotension should hydralazine patients recognize?

Dizziness and lightheadedness.

How can hydralazine patients reduce symptoms of hypotension?

Avoid abruptly changing from a seated to an upright position.

What look-alike/sound-alike medication can be confused with hydralazine?

Hydroxyzine.

What direct vasodilator is used for hypertensive emergencies?

Sodium nitroprusside.

What is the MOA of sodium nitroprusside?

Directly dilates veins and arterioles.

What is the therapeutic use of sodium nitroprusside?

Hypertensive emergency.