Alterations in Cardiac: Hypertension, Dyslipidemia and Angina

Unit Prototype: Clonidine

Class: Antihypertensive, central alpha-2 agonist

MOA: Stimulates central alpha-2 receptors in the vasomotor center of the brainstem, reducing

sympathetic outflow to the peripheral vasculature and heart. This decreases peripheral vascular

resistance and blood pressure.

Use: Hypertension (often resistant types), off-label for ADHD, withdrawal syndromes, and severe

pain management.

Adverse/Side Effects: Dry mouth, marked sedation/drowsiness, dizziness, constipation, rebound

hypertensive crisis if stopped abruptly.

Nursing Implications: Never stop abruptly; taper gradually over several days to avoid severe,

life-threatening rebound hypertension with tachycardic surges. Suggest chewable ice or sugar-free

gum for dry mouth.

Patient Education: Never stop this medication suddenly, even if you feel fine. Manage dry

mouth with ice chips or sugar-free gum. Change positions slowly. Report severe drowsiness.

Unit Prototype: Carvedilol

Class: Antihypertensive, alpha/beta-adrenergic blocker (non-selective alpha-1 blocker)

MOA: Non-selectively blocks beta-1 and beta-2 receptors (reducing cardiac output and heart

rate) and selectively blocks peripheral postsynaptic alpha-1 receptors, promoting arterial

vasodilation and decreasing systemic vascular resistance.

Use: Hypertension, heart failure (with LVEF preservation/improvement), post-MI left ventricular

dysfunction.

Adverse/Side Effects: Dizziness, profound orthostatic hypotension, bradycardia, fatigue,

bronchospasm (from non-selective beta-2 blockade), weight gain, hyperkalemia.

Nursing Implications: Administer with food to slow absorption and lower the risk of orthostatic

hypotension. Monitor for worsening heart failure symptoms (fluid retention, dyspnea) during

titration. Contraindicated in severe bradycardia, AV block, asthma/severe COPD, cardiogenic

shock.

Patient Education: Take with food. Change positions slowly. Report sudden weight gain or

worsening shortness of breath; this can mean worsening heart failure. Don't stop abruptly.

Unit Prototypes: Lisinopril

Class: Antihypertensive, ACE inhibitor

MOA: Competitively inhibits ACE, preventing conversion of Angiotensin I to Angiotensin II (a

potent vasoconstrictor). Reduces SVR and suppresses aldosterone production (reducing sodium

and water retention). Also prevents breakdown of bradykinin, which enhances vasodilatory

prostaglandins but is responsible for its signature cough.

Use: First-line hypertension management, heart failure, post-MI left ventricular dysfunction,

diabetic nephropathy (slows progression).

Adverse/Side Effects: Dry, persistent, non-productive cough (from bradykinin accumulation),

hyperkalemia, orthostatic hypotension, angioedema (life-threatening swelling of

face/lips/airway), acute kidney injury, dysgeusia (altered taste).

Nursing Implications: Monitor blood pressure, baseline serum creatinine/BUN, and potassium.

Discontinue immediately and secure the airway if angioedema occurs. Contraindicated in

pregnancy (Black Box Warning), history of ACE inhibitor-induced angioedema, bilateral renal

artery stenosis, and concurrent use with sacubitril/valsartan. Watch for hyperkalemia risk with

potassium supplements or potassium-sparing diuretics, and blunted effect/renal toxicity with

NSAIDs.

Patient Education: Report a dry cough; though it's not dangerous, it may warrant a switch to an

ARB. Seek emergency care immediately for facial/lip/airway swelling. If of childbearing age, use

reliable contraception and stop the drug immediately if pregnant.

Unit Prototype: Losartan

Class: Antihypertensive, angiotensin II receptor blocker (ARB)

MOA: Selectively blocks the binding of Angiotensin II to receptor sites in vascular smooth

muscle and the adrenal glands, blocking vasoconstriction and aldosterone release. Does not

inhibit ACE and does not prevent bradykinin breakdown, which is why it doesn't cause the cough

that ACE inhibitors do.

Use: Hypertension, heart failure, diabetic nephropathy. Often the go-to alternative for patients

who develop an ACE inhibitor-induced cough.

Adverse/Side Effects: Hyperkalemia, dizziness, hypotension, renal impairment. Lower incidence

of cough and angioedema compared to ACE inhibitors.

Nursing Implications: Monitor blood pressure, baseline renal function, and electrolytes.

Contraindicated in pregnancy (Black Box Warning), bilateral renal artery stenosis, and concurrent

use with aliskiren in diabetic patients. Same interaction risks as lisinopril with potassium-sparing

drugs (hyperkalemia) and NSAIDs (renal injury).

Patient Education: If of childbearing age, use reliable contraception and stop immediately if

pregnant. Report signs of dizziness or hyperkalemia (muscle weakness, irregular heartbeat). Don't

need to worry about the cough that comes with ACE inhibitors.

Prototype: Hydrochlorothiazide

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Therapeutic Classification: Antihypertensives, Diuretics

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Pharmacologic Classification: Thiazide diuretics

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Indication for Use: First-line management of primary hypertension; management of edema

associated with heart failure, hepatic impairment, or renal disease.

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Mechanism of Action: Inhibits sodium and chloride reabsorption in the distal convoluted tubule,

increasing excretion of sodium, water, chloride, and potassium. This reduces intravascular plasma

volume and decreases SVR over time → dec. plasma and extracellular fluid volumes, which

results in decreased preload, decreased peripheral resistance, and CO

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Adverse Effects: Hypokalemia, hyponatremia, hyperuricemia (may trigger gout attacks),

hyperglycemia, orthostatic hypotension, dehydration.

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Contraindications: Anuria, known hypersensitivity to sulfonamides (cross-reactivity risk),

severe electrolyte depletion, hepatic coma.

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Significant Drug Interactions:

a. Digoxin: Hypokalemia increases the risk of digoxin toxicity and fatal arrhythmias.

b. NSAIDs: Decrease diuretic and antihypertensive efficacy by inhibiting renal

prostaglandin synthesis.

c. Lithium: Reduced renal clearance leads to lithium toxicity.

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Nursing Implications: Monitor baseline and serum electrolytes, renal function, and uric acid.

a. Assess blood pressure, daily weights, strict intake/output ($I\&O$), and peripheral

edema.

b. Instruct patients to change positions slowly to prevent orthostatic falls and to take doses

in the morning to avoid nocturia.

c. Encourage potassium-rich foods unless contraindicated.

Unit Prototype: Metoprolol

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Therapeutic Classification: Antihypertensives, Antianginals

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Pharmacologic Classification: Beta-adrenergic receptor antagonists (Cardioselective)

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Indication for Use: Hypertension, angina pectoris, post-myocardial infarction, heart failure, rate

control in atrial fibrillation.

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Mechanism of Action: Selectively blocks β1-adrenergic receptors in cardiac tissue, decreasing

heart rate, myocardial contractility, and cardiac output; inhibits renin release from renal

juxtaglomerular cells.

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Adverse Effects: Bradycardia, hypotension, fatigue, erectile dysfunction, cold extremities,

masking of hypoglycemic tachycardia in diabetic patients.

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Contraindications: Severe bradycardia, high-degree AV block or cardiogenic shock, overt heart

failure.

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Significant Drug Interactions:-

a. Non-dihydropyridine CCBs (Verapamil/Diltiazem): Increased risk of severe bradycardia

and heart block.

b. Insulin/Oral Antidiabetics: Masks early signs of hypoglycemia (except diaphoresis).

Nursing Implications:

a. Always check apical pulse and blood pressure prior to administration; hold medication

and notify provider if pulse is below 60 bpm or systolic BP is under 90–100 mmHg.

b. Warn patients never to discontinue abruptly due to the risk of rebound hypertension,

severe angina, or myocardial infarction.

Prototype: Carvedilol (Non-selective beta blocker, A1 blocker)

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Therapeutic Classification: Antihypertensives

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Pharmacologic Classification: Alpha- and beta-adrenergic receptor antagonist

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Indication for Use: Hypertension, heart failure (with LVEF preservation/improvement), post-MI

left ventricular dysfunction.

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Mechanism of Action: Non-selectively blocks β1- and β2-adrenergic receptors (reducing CO and

heart rate, allowing bronchoconstriction to take place) and selectively blocks peripheral

postsynaptic α1-adrenergic receptors, promoting arterial vasodilation and decreasing SVR.

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Adverse Effects: Dizziness, profound orthostatic hypotension, bradycardia, fatigue,

bronchospasm (due to non-selective B2 blockade), weight gain, hyperkalemia.

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Contraindications: Severe bradycardia, AV block, bronchial asthma or severe COPD,

cardiogenic shock, severe hepatic impairment.

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Nursing Implications: Administer with food to slow absorption and lower the risk of orthostatic

hypotension. Monitor for worsening heart failure symptoms (fluid retention, dyspnea) during

titration

Unit Prototype: Prazosin

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Therapeutic Classification: Antihypertensives

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Pharmacologic Classification: Alpha-1 adrenergic blocker

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Indication for Use: Primary hypertension, benign prostatic hyperplasia (BPH) off-label symptom

management.

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Mechanism of Action: Selectively blocks vascular postsynaptic α1-adrenergic receptors,

preventing norepinephrine-induced vasoconstriction, leading to direct arterial and venous

vasodilation and reduced SVR.

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Adverse Effects: "First-dose syncope" (severe orthostatic collapse within 30–90 min of initial

dose), fluid retention, reflex tachycardia, nasal congestion, dizziness.

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Nursing Implications: Give the first dose (or any increased dose) at bedtime to minimize the

impact of first-dose syncope and orthostasis. Warn patients to change positions slowly and avoid

driving for 24 hours after the initial dose.

Unit Prototype: Clonidine

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Therapeutic Classification: Antihypertensives

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Pharmacologic Classification: Central alpha-2-adrenergic agonist

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Indication for Use: Management of hypertension (often resistant types); off-label use for ADHD,

withdrawal syndromes, and severe pain management.

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Mechanism of Action: Stimulates central A2-adrenergic receptors in the vasomotor center of the

brainstem, reducing sympathetic outflow to the peripheral vasculature and heart, decreasing

peripheral vascular resistance and blood pressure.

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Adverse Effects: Dry mouth, marked sedation/drowsiness, dizziness, constipation, rebound

hypertensive crisis if stopped abruptly.

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Nursing Implications: Never stop abruptly → taper off gradually over several days to avoid

severe, life-threatening rebound hypertension with tachycardic surges. Advise chewable ice or

sugar-free gum for dry mouth.

Unit Prototype: Lisinopril

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Therapeutic Classification: Antihypertensives

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Pharmacologic Classification: ACE inhibitor

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Indication for Use: First-line hypertension management, heart failure, post-MI LV dysfunction,

diabetic nephropathy (slows progression)

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Mechanism of Action: Competitively inhibits ACE, preventing the conversion of Angiotensin I

to Angiotensin II (a potent vasoconstrictor). Reduces SVR and suppresses aldosterone production

(reducing NaCl and water retention) → prevents the breakdown of bradykinin, enhancing

vasodilatory prostaglandins

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Adverse Effects: Dry, persistent, non-productive cough (bradykinin accumulation),

hyperkalemia, orthostatic hypotension, angioedema (life-threatening swelling of

face/lips/airway), acute kidney injury, dysgeusia.

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Contraindications: Pregnancy (Black Box Warning: fetal toxicity/death), history of ACE

inhibitor-induced angioedema, bilateral renal artery stenosis, concurrent use with

sacubitril/valsartan.

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Significant Drug Interactions:

a. Potassium Supplements/Potassium-Sparing Diuretics: Increased risk of life-threatening

hyperkalemia.

b. NSAIDs: Blunts antihypertensive effects and increases renal toxicity risk.

c. Lithium: Increased risk of lithium toxicity.

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Nursing Implications:

a. Monitor blood pressure, baseline serum creatinine/BUN, and potassium levels.

b. Discontinue immediately and secure the airway if angioedema occurs.

c. Educate female patients of childbearing age regarding strict pregnancy avoidance.

Unit Prototype: Losartan

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Therapeutic Classification: Antihypertensives

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Pharmacologic Classification: Angiotensin II receptor blocker (ARB)

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Indication for Use: Hypertension, heart failure, diabetic nephropathy (ideal alternative for

patients who develop Lisinopril-induced cough)

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Mechanism of Action: Selectively blocks the binding of Angiotensin II to the receptor sites in

vascular smooth muscle and the adrenal glands, blocking vasoconstriction and aldosterone

release. Does not inhibit ACE or prevent bradykinin breakdown

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Adverse Effects: Hyperkalemia, dizziness, hypotension, renal impairment; lower incidence of

cough and angioedema compared to ACE inhibitors

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Contraindications: Pregnancy (Black Box Warning: fetal toxicity), bilateral renal artery stenosis,

concurrent use with aliskiren in diabetic patients

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Significant Drug Interactions: Same as Lisinopril (potassium-sparing drugs increase

hyperkalemia risk; NSAIDs increase renal injury risk)

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Nursing Implications: Monitor blood pressure, baseline renal function, and electrolytes. Counsel

on pregnancy risks

Unit Prototype: Atorvastatin

Class: HMG-CoA reductase inhibitor (statin)

MOA: Blocks HMG-CoA reductase, the enzyme that controls the rate-limiting step in cholesterol

synthesis in the liver. This lowers LDL and triglycerides and raises HDL slightly. The liver also

upregulates LDL receptors to pull more LDL out of the blood.

Use: Hyperlipidemia, primary prevention of cardiovascular disease, secondary prevention after

MI/stroke.

Adverse/Side Effects: Myopathy/rhabdomyolysis (muscle pain, weakness, dark urine),

hepatotoxicity (elevated liver enzymes), GI upset, headache. Rare but serious: rhabdomyolysis

leading to acute kidney injury.

Nursing Implications: Check baseline liver function tests (LFTs) and lipid panel before starting;

monitor periodically. Assess for muscle pain/weakness. Give in the evening (older statins

matched cholesterol synthesis peak at night, though atorvastatin's long half-life makes timing less

critical). Avoid grapefruit juice (inhibits metabolism, raises drug levels).

Patient Education: Report unexplained muscle pain, tenderness, or weakness immediately.

Avoid grapefruit juice. Continue diet/exercise changes. Don't stop abruptly without talking to

provider. Contraindicated in pregnancy.

Unit Prototype: Cholestyramine

Class: Bile acid sequestrant (resin)

MOA: Binds bile acids in the intestine, forming an insoluble complex excreted in feces. Liver

pulls cholesterol from the blood to make more bile acids, lowering LDL.

Use: Hyperlipidemia (usually adjunct or for patients who can't tolerate statins), pruritus from bile

acid buildup in liver disease.

Adverse/Side Effects: GI effects are the big one: constipation, bloating, nausea, abdominal pain.

Can impair absorption of fat-soluble vitamins (A, D, E, K) and other oral drugs.

Nursing Implications: Give other oral medications 1 hour before or 4-6 hours after this drug,

since it binds them too. Monitor bowel function and lipid panel. Monitor for signs of fat-soluble

vitamin deficiency with long-term use.

Patient Education: Mix powder with water or juice; don't take dry. Increase fluid and fiber

intake to offset constipation. Take other medications at spaced-out times, not together with this

drug. Report severe constipation or new bleeding/bruising (could signal vitamin K deficiency).

Unit Prototype: Gemfibrozil

Class: Fibric acid derivative (fibrate)

MOA: Activates PPAR-alpha, which increases lipoprotein lipase activity. This accelerates

breakdown of VLDL and triglycerides, and increases HDL.

Use: Primarily for high triglycerides; can also raise HDL.

Adverse/Side Effects: GI upset (most common), gallstones (increased cholesterol excretion into

bile), myopathy (risk increases significantly if combined with a statin), hepatotoxicity.

Nursing Implications: Monitor lipid panel, LFTs, and CBC periodically. Ask about muscle pain,

especially if the patient is also on a statin (this combo raises rhabdomyolysis risk a lot). Monitor

for signs of gallbladder disease (RUQ pain).

Patient Education: Take 30 minutes before meals (morning and evening) for best effect. Report

muscle pain/weakness or dark urine. Report RUQ pain, which could mean gallstones. Avoid

alcohol.

Unit Prototype: Amlodipine

Class: Calcium channel blocker, dihydropyridine

MOA: Blocks calcium influx into vascular smooth muscle cells, causing arterial vasodilation.

Has minimal effect on the heart's conduction system or contractility compared to

non-dihydropyridines, so it mainly lowers blood pressure through decreased systemic vascular

resistance.

Use: Hypertension, chronic stable angina, vasospastic (Prinzmetal's) angina.-

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Adverse/Side Effects: Peripheral edema (classic side effect, from arteriolar dilation), reflex

tachycardia, flushing, headache, dizziness, gingival hyperplasia.

Nursing Implications: Monitor blood pressure and heart rate. Assess for peripheral edema.

Because it's a dihydropyridine, it doesn't need the same heart-rate caution as verapamil/diltiazem.

Patient Education: Change positions slowly to avoid orthostatic dizziness. Report swelling in

the legs/ankles. Maintain good oral hygiene and see the dentist regularly (gingival hyperplasia

risk). Don't stop abruptly.

Unit Prototype: Verapamil

Class: Calcium channel blocker, non-dihydropyridine (phenylalkylamine)

MOA: Blocks calcium channels in both vascular smooth muscle and cardiac tissue. Slows AV

node conduction and decreases heart rate and contractility, in addition to causing vasodilation.

Because it acts directly on the heart, it's more cardiac-selective than amlodipine.

Use: Hypertension, angina, supraventricular tachyarrhythmias (like a-fib/a-flutter, since it slows

AV conduction).

Adverse/Side Effects: Bradycardia, AV block, hypotension, constipation (notably common with

verapamil specifically), heart failure exacerbation (negative inotropic effect).

Nursing Implications: Check apical pulse and blood pressure before giving; hold and notify

provider for bradycardia or significant hypotension. Do not give with beta blockers without close

monitoring (additive risk of severe bradycardia/heart block). Monitor for signs of worsening heart

failure.

Patient Education: Report a resting pulse under 60, dizziness, or swelling. Increase fluids and

fiber for constipation. Avoid grapefruit juice. Don't stop abruptly.

Unit Prototype: Nitroglycerin

Class: Organic nitrate, vasodilator (antianginal)

MOA: Converted to nitric oxide in vascular smooth muscle, which activates guanylate cyclase

and increases cGMP, causing smooth muscle relaxation. At low doses, mainly dilates veins →

decreases preload and myocardial oxygen demand. At higher doses, also dilates arteries →

decreases afterload and can dilate coronary arteries to improve blood flow.

Use: Acute angina attacks (sublingual/spray), angina prophylaxis (extended-release oral,

transdermal patch), IV for unstable angina, acute MI, or hypertensive emergencies.

Adverse/Side Effects: Headache (very common, from cerebral vasodilation), hypotension, reflex

tachycardia, flushing, dizziness. Tolerance develops with continuous use.

Nursing Implications: Monitor blood pressure and heart rate closely, especially with IV use.

Provide a nitrate-free interval (usually overnight, 10-12 hours) with long-acting forms to prevent

tolerance. Never give with PDE5 inhibitors (sildenafil, etc.) — risk of severe, life-threatening hypotension

Patient Education: For sublingual tablets: sit or lie down before taking (risk of syncope), let it

dissolve under the tongue, can repeat every 5 minutes up to 3 doses, call 911 if pain isn't relieved

after the first dose. Store in original dark glass container away from light/heat. Report headache to

provider rather than stopping the drug (tolerable headache is expected; can be treated with mild

analgesics). Avoid alcohol. Never combine with erectile dysfunction drugs.

Unit Prototype: Isosorbide Dinitrate

Class: Organic nitrate, vasodilator (antianginal)

MOA: Same as nitroglycerin — converted to nitric oxide, activates guanylate cyclase, raises

cGMP, causing venous (and at higher doses, arterial) vasodilation, reducing preload and

myocardial oxygen demand.

Use: Prevention of angina (not for acute attacks — onset is slower than nitroglycerin), sometimes

combined with hydralazine for heart failure in specific populations.

Adverse/Side Effects: Headache, orthostatic hypotension, reflex tachycardia, dizziness, flushing.

Tolerance with continuous dosing.

Nursing Implications: Give on an empty stomach for better absorption when possible. Build in a

nitrate-free interval to prevent tolerance. Monitor BP and HR. Same caution with PDE5 inhibitors

as nitroglycerin.

Patient Education: Take on a scheduled basis for prevention, not for an acute attack in progress.

Change positions slowly. Report persistent or severe headache, but don't stop the drug on your

own. Avoid alcohol and PDE5 inhibitors (like sildenafil).

Unit Prototype: Isosorbide Mononitrate

Class: Organic nitrate, vasodilator (antianginal)

MOA: Same mechanism as the other nitrates — nitric oxide-mediated vasodilation via cGMP,

reducing preload and myocardial oxygen demand. It's actually the active metabolite of isosorbide

dinitrate, so it has better and more predictable oral bioavailability.

Use: Prevention of angina, long-term maintenance therapy (not for acute attacks, due to slow

onset).

Adverse/Side Effects: Headache, hypotension, reflex tachycardia, dizziness, flushing, tolerance

with continuous use.

Nursing Implications: Because of its longer, more predictable half-life, it's often dosed once or

twice daily with a built-in nitrate-free period. Monitor BP/HR. Same PDE5 inhibitor precaution.

Patient Education: Take at the same time(s) each day for prevention. Don't use for an acute

angina attack — it won't work fast enough. Report severe or persistent headaches without

stopping the medication. Avoid alcohol and PDE5 inhibitors.