Nursing Field Notes / Pharmacology · NCLEX Drug Review Series

💊 NCLEX DRUG REVIEW 1 · CNS 2 · Fluids & clots 3 · Blood pressure 4 · Heart & sugar 5 · GI & lipids 6 · Mixed 7 · Antibiotics 8 · Insulins

NCLEX Drugs 3 🫀

ACE Inhibitors · Beta Blockers · Calcium Channel Blockers · Alpha-1 Blockers · Alpha+Beta Blockers · Central Alpha-2 Agonists

NG-157 PHARM · CARDIOVASCULAR Series: NCLEX Drug Review 3 of 8 ADHD-friendly visual edition

The whole antihypertensive installment fits on one equation: BP = cardiac output × systemic vascular resistance. Every drug on this page lowers blood pressure by attacking one side of that multiplication — or both. Learn which side each class pulls on and the side effects stop being random: pull on the heart and you get bradycardia and fatigue; pull on the vessels and you get dizziness, flushing and ankle swelling.

📄 Simple Nursing original — opens in Drive →

💊 "-pril" = ACEBlocks angiotensin I → II. Dry nagging cough & ↑K⁺ are the giveaways.

🫀 "-olol" = beta blocker↓HR, ↓contractility, ↓conduction. Never stop abruptly — rebound.

🧱 CCB = Ca²⁺ door shutVessel dilation ± AV-node slowing. Ankle edema & no grapefruit.

🛏️ "-zosin" first doseAlpha-1 blockers drop BP hard on dose one — give it at bedtime.

🗺️

LINEUP

STEP 1 · WHAT'S IN THIS SET

Cora's 3-part study map for every drug on this page: CLASS → ACTION → WATCH. Six classes, all of them pressure-lowering.

🧭 This installment covers 6 classes

💊ACE Inhibitors
"-pril"

🫀Beta Blockers
"-olol"

🧱Calcium Channel Blockers

🚪Alpha-1 Blockers
"-zosin"

🔀Alpha + Beta Blockers
"-lol"

🧠Central Alpha-2 Agonists

🧠 Suffix triage first. "-pril" → ACE. "-olol" → beta. "-dipine" → calcium (vessel type). "-zosin" → alpha-1. If it ends in "-lol" but is carvedilol or labetalol, it is the dual alpha+beta blocker.

⚖️ The one equation this whole page hangs on

acts on the pump acts on the pipes acts on both

🧠 Pump or pipes? Ask it for every antihypertensive you meet. Pump drugs give you bradycardia, fatigue and heart block. Pipe drugs give you dizziness, flushing, headache and ankle edema.

📇 Brand ↔ generic — the pairs NCLEX actually asks

Class	Brand	Generic
ACE inhibitors "-pril"	Altace	ramipril
	Capoten	captopril
	Prinivil, Zestril	lisinopril
	Vasotec	enalapril
Beta blockers "-olol"	Inderal	propranolol non-selective
	Lopressor	metoprolol tartrate immediate release
	Toprol-XL	metoprolol succinate extended release
	Tenormin	atenolol beta-1 selective
Calcium channel blockers	Cardizem	diltiazem non-DHP
	Verelan, Isoptin, Calan	verapamil non-DHP
	Norvasc	amlodipine DHP
	Procardia	nifedipine DHP
Alpha-1 blockers "-zosin"	Minipress	prazosin
Alpha-1 blockers "-zosin"	Hytrin	terazosin
Alpha + beta blockers	Coreg	carvedilol
Alpha + beta blockers	Trandate, Normodyne	labetalol
Central alpha-2 agonist	Catapres	clonidine

⚠️ Tartrate vs succinate. Both are "metoprolol." Tartrate (Lopressor) is immediate-release; succinate (Toprol-XL) is extended-release and must never be crushed, split or chewed unless the specific product is scored and labeled as splittable.

🚨 The suffix trap that costs points

Alpha-1 blockers end in "-zosin" — prazosin, terazosin, doxazosin. They are not the same as Zosyn, which is an antibiotic (piperacillin–tazobactam) and has nothing to do with blood pressure.

🧠 "Zosin lowers, Zosyn kills." One relaxes vessels; one kills bacteria.

⭐ Two "-lol" drugs that are not plain beta blockers

Carvedilol and labetalol block alpha-1 and beta receptors. They lower BP two ways at once, so orthostatic hypotension is more prominent than with a pure beta blocker.

🧠 "CarLa does both." Carvedilol + Labetalol = alpha AND beta.

🧠 Source correction worth knowing

Some review sheets file clonidine (Catapres) under "alpha-2 antagonists." Clonidine is a central alpha-2 agonist — it stimulates the presynaptic autoreceptor, which turns sympathetic outflow down. The mechanism the sheet describes (less norepinephrine released, less sympathetic activity) is the agonist mechanism.

🧠 Agonist that acts like a brake. Stimulating an inhibitory autoreceptor reduces output — that is why an agonist lowers BP here.

🔎 One-line identity card for all six

💊 ACE inhibitors · ramipril, captopril, lisinopril, enalapril

DoesBlocks angiotensin I → angiotensin II ⇒ vasodilation, ↓ aldosteroneWatchDry cough, angiedema, ↑ K⁺, ↑ creatinine, first-dose hypotension

🫀 Beta blockers · propranolol, metoprolol, atenolol

DoesBlocks beta-1 ⇒ ↓ HR, ↓ contractility, ↓ AV conduction, ↓ reninWatchBradycardia, fatigue, masked hypoglycemia, bronchospasm (non-selective), rebound if stopped

🧱 Calcium channel blockers · diltiazem, verapamil, amlodipine, nifedipine

DoesBlocks Ca²⁺ entry ⇒ vessel + coronary dilation; non-DHPs also slow the AV nodeWatchAnkle edema, headache, flushing, constipation (verapamil), grapefruit

🚪 Alpha-1 blockers · prazosin, terazosin

DoesBlocks alpha-1 on vessel + bladder-neck/prostate smooth muscle ⇒ dilationWatchFirst-dose syncope, orthostatic hypotension, dizziness, nasal stuffiness

🔀 Alpha + beta blockers · carvedilol, labetalol

DoesAlpha-1 blockade (dilation) + beta blockade (↓ HR/contractility)WatchOrthostatic hypotension, bradycardia, bronchospasm, masked hypoglycemia

🧠 Central alpha-2 agonist · clonidine

DoesStimulates brainstem alpha-2 ⇒ less norepinephrine released ⇒ ↓ HR, ↓ SVRWatchSedation, dry mouth, bradycardia, severe rebound hypertension if stopped abruptly

⚙️

ACTION — WHERE EACH ONE ACTS

STEP 2 · MECHANISM

Six classes, four physical addresses: the RAAS cascade, the adrenergic synapse, the calcium channel, and the heart's own wiring.

🔗 Address 1 — the RAAS cascade, and where "-pril" cuts it

🧠 "PRIL puts the cough on the pillow." The cough is dry, nagging, non-productive and does not respond to cough syrup — the fix is switching to an ARB (see installment 4).

🔌 Address 2 — the adrenergic synapse: alpha-1, alpha-2, beta-1, beta-2

🧠 "1 heart, 2 lungs." Beta-1 = one heart. Beta-2 = two lungs. Alpha-1 = arteries squeeze. Alpha-2 = the auto-brake on the nerve itself.

💊 ACE inhibitors — "-pril"

Action: block conversion of angiotensin I to angiotensin II (a potent vasoconstrictor) ⇒ vasodilation and ↓ peripheral vascular resistance without directly increasing cardiac output, rate or contractility. Aldosterone falls too, so sodium and water are retained less.

🧪 Check the potassium. Less aldosterone = potassium held in = ↑ K⁺.
📈 Monitor BUN and creatinine — renal function can fall, especially with volume depletion.
⭐ Also protective in heart failure and diabetic kidney disease, not just hypertension.

⚠️ Angiedema is an airway emergency. Swelling of the lips, tongue, face or throat after any dose — stop the drug, get help, protect the airway. It can happen after months of uneventful use.

🫀 Beta blockers — "-olol"

Action: prevent sympathetic stimulation of the heart ⇒ ↓ heart rate, ↓ force of contraction, ↓ myocardial irritability, depressed SA-node automaticity, slower AV and intraventricular conduction — and suppressed renin release from the kidney.

💓 Net effect: ↓ myocardial oxygen demand — which is why they help angina and post-MI.
🫁 Non-selective agents (propranolol) also hit beta-2 ⇒ may cause bronchoconstriction.
🩺 Take an apical pulse for a full minute before giving.

🧠 "Beta blockers take the ABCDEs down": ↓Automaticity, ↓Blood pressure, ↓Contractility, ↓Dromotropy (conduction), ↓ Excitability.

🧱 Address 3 — the calcium channel, and the two CCB personalities

🧠 "DIP into the vessels; VERy DILigent about the heart." "-dipine" = vessel-selective. Verapamil and diltiazem also work on the heart's rate and conduction.

🚪 Alpha-1 blockers — "-zosin"

Action: block alpha-1 receptors on vascular smooth muscle ⇒ arteries and veins dilate ⇒ ↓ peripheral vascular resistance ⇒ ↓ BP. The same receptors sit in the bladder neck and prostate, which is why this class also treats BPH urinary symptoms.

⚠️ First-dose phenomenon. The very first dose (and every dose increase) can drop BP hard enough to cause syncope. Standard teaching: give the first dose at bedtime, and get up slowly afterwards.

🧠 Central alpha-2 agonist — clonidine

Action: stimulates alpha-2 receptors in the brainstem ⇒ less norepinephrine released ⇒ ↓ sympathetic outflow ⇒ ↓ HR, ↓ SVR, ↓ BP. It works "upstream," in the brain, rather than at the vessel itself.

⚠️ Rebound hypertension is severe. Stopping clonidine abruptly can cause a rapid, dangerous BP surge with tachycardia, sweating and agitation. It must be tapered. Transdermal patches are applied to a clean, dry, hairless site and rotated.

⚡ Address 4 — the heart's wiring, and what a beta blocker does to it

🧠 Bradycardia is not a side effect — it is the mechanism. The nursing job is deciding how much slowing is acceptable, using the prescriber's hold parameters.

🚨

WATCH — SAFETY & ADVERSE EFFECTS

STEP 3 · ASSESS

Almost every adverse effect on this page is the drug's own mechanism, taken one step too far.

🧍 Body map — where the side effects show up

🚨 Angiedema — stop and escalate

Swelling of the lips, tongue, periorbital tissue, face or larynx in a patient on any "-pril." Airway comes first.

❌ Hold the drug and notify the prescriber immediately.
🫁 Assess airway, voice change, stridor, difficulty swallowing.
⏱️ It is not dose-related and can appear after long uneventful use.

⚠️ Once a patient has ACE-inhibitor angiedema, that class is generally avoided for life.

🍬 Beta blockers mask hypoglycemia

The early warning signs of low blood sugar — tachycardia, tremor, palpitations — are sympathetic signs. Block beta receptors and the patient loses them.

💦 Diaphoresis usually still happens (cholinergic), so sweating becomes the key clue.
🧪 Teach diabetic patients to check glucose more often, not to rely on how they feel.

🧠 "Beta blockers steal the alarm bell but leave the sweat."

❌ Never stop these abruptly

Beta blockers and clonidine must never be discontinued abruptly. The receptors have up-regulated; removing the block unmasks a surge of sympathetic activity.

🫀 Beta blocker withdrawal → rebound tachycardia, hypertension, angina, risk of MI or dysrhythmia.
🧠 Clonidine withdrawal → severe rebound hypertension, agitation, sweating, headache.
📉 Both must be tapered over days to weeks per prescriber direction.

⚠️ The dangerous combination on this page

Verapamil or diltiazem + a beta blocker. Both slow the SA node and the AV node. Stacked together they can cause profound bradycardia, heart block or hypotension.

⚠️ If you see a non-dihydropyridine CCB and a beta blocker ordered together, that is a legitimate reason to call the prescriber and to monitor rate and rhythm closely.

🍊 Grapefruit juice + calcium channel blockers

Grapefruit inhibits intestinal CYP3A4, so more drug reaches the bloodstream. With CCBs that means exaggerated hypotension, flushing and headache.

🧠 "Grapefruit makes the dose bigger without changing the pill." Teach avoidance rather than timing tricks.

✅ Before you give it — the pre-dose check

🩺 Apical pulse for one full minute before any beta blocker, verapamil, diltiazem or digoxin-type drug.
🩸 Blood pressure — including a standing reading if orthostatic symptoms are a concern.
🧪 Potassium and creatinine before and during ACE-inhibitor therapy.
📋 Compare to the prescriber's written hold parameters; if none exist, ask for them.

⚠️ Commonly written parameters are "hold and notify if apical HR is below 60/min or systolic BP is below about 90–100 mmHg," but the exact numbers are prescriber- and facility-specific. Follow the order, not a remembered number.

🫁 Why a non-selective beta blocker is risky in asthma

🧠 Selectivity is dose-dependent. "Cardioselective" agents like metoprolol and atenolol lose their beta-1 selectivity as the dose climbs — asthma caution never fully disappears.

📋

TEACH — WHAT THE PATIENT MUST HEAR

STEP 4 · EDUCATE

Antihypertensives are taken by people who feel fine. Adherence teaching is the intervention.

✅ Orthostatic hypotension — the universal teaching point

🛏️ Dangle at the side of the bed before standing; rise in stages.
🚿 Warn about hot showers, hot tubs, alcohol and standing still — all worsen it.
💧 Report dizziness, lightheadedness or near-fainting rather than "pushing through."
🧍 Fall precautions for older adults, especially at night.

🧠 "Sit, dangle, stand, wait." Four beats before walking away from the bed.

📈 Self-monitoring is part of the prescription

🩸 Home BP and pulse log — pulse matters as much as pressure on this page.
⚖️ Daily weight at the same time, same scale, same clothing; report a sudden gain.
📞 Report a resting pulse under about 60/min, new swelling, or fainting.
💊 Bring the log to every visit — dose changes are made from trends, not single readings.

🧂 Salt substitutes and ACE inhibitors

Most "salt substitutes" are potassium chloride. On an ACE inhibitor, potassium is already being retained.

⚠️ Teach patients to avoid potassium-based salt substitutes and to check with the prescriber before any potassium supplement — including combination products and some sports drinks.

🍽️ Timing details worth memorizing

💊 Captopril is classically taught to be taken on an empty stomach — about an hour before meals — because food reduces its absorption.
🍲 Carvedilol is taken with food to slow absorption and reduce orthostatic hypotension.
🛏️ First "-zosin" dose at bedtime.
⏰ Extended-release products (Toprol-XL, Verelan, Procardia XL) are taken whole, once daily.

🤰 Pregnancy matters here

ACE inhibitors are contraindicated in pregnancy — they cause fetal injury. Any patient of childbearing potential needs that conversation and a plan.

Labetalol is one of the agents commonly used to treat hypertension in pregnancy.

🧠 "PRILs are not for pregnancy." Both start with P.

💊 NSAIDs quietly undo this whole page

NSAIDs promote sodium and water retention and blunt the antihypertensive effect of ACE inhibitors, beta blockers and diuretics — and add kidney risk on top of an ACE inhibitor.

🧠 Ask about over-the-counter drugs. Patients rarely list ibuprofen as "a medication."

📊 Pick-the-drug table — the distinguishing feature for each class

If the question mentions…	Think	Because
New dry, nagging, non-productive cough	ACE inhibitor	Bradykinin accumulation
Rising serum potassium	ACE inhibitor	Aldosterone suppressed
Swollen lips/tongue after a first dose or after months	ACE inhibitor (angiedema)	Airway emergency
Apical pulse 52, patient fatigued	Beta blocker or non-DHP CCB	Negative chronotropic effect
Asthma history + wheezing after a new BP pill	Non-selective beta blocker	Beta-2 blockade in the airway
Diabetic who "no longer feels" lows	Beta blocker	Adrenergic warning signs masked
Bilateral ankle swelling, clear lungs	Dihydropyridine CCB	Arteriolar dilation, not fluid overload
Constipation on a rate-control drug	Verapamil	Smooth-muscle relaxation in the gut
Fainted after the very first dose	"-zosin" alpha-1 blocker	First-dose phenomenon
Stopped the pill, BP shot up with sweating and agitation	Clonidine (or beta blocker)	Rebound sympathetic surge
Man with hypertension and BPH symptoms	"-zosin" alpha-1 blocker	Relaxes bladder neck and prostate too

⚡

QUICK RECALL

SAY IT OUT LOUD

💊 "-pril"Cough · ↑K⁺ · angiedema · not in pregnancy

🫀 "-olol"Apical pulse first · never stop abruptly · masks lows

🧱 CCB"-dipine" = vessels & edema · verapamil/diltiazem = heart & constipation

🚪 "-zosin" · 🧠 clonidineFirst dose at bedtime · taper clonidine or BP rebounds

🎯 Cover & check — 8 rapid-fire questions

Q1: A patient on lisinopril develops a persistent dry cough. What is the cause and the usual fix?

Bradykinin accumulation from ACE inhibition. It does not respond to cough medicine; the prescriber usually switches the patient to an ARB.

Q2: Which lab must be monitored on an ACE inhibitor, and which way does it move?

Potassium — it goes UP, because aldosterone is suppressed. Creatinine and BUN are watched too.

Q3: What assessment is done immediately before giving metoprolol?

Apical pulse for one full minute plus blood pressure, compared against the prescriber's hold parameters.

Q4: Why is propranolol a concern in asthma but amlodipine is not?

Propranolol is non-selective and blocks beta-2 receptors in the airway, which can cause bronchoconstriction. Amlodipine acts on vascular calcium channels and does not touch beta-2 receptors.

Q5: A patient on amlodipine reports new bilateral ankle swelling with clear lungs and no weight jump. What is happening?

Dose-related peripheral edema from arteriolar dilation — a known dihydropyridine effect, not fluid overload. Report it; diuretics do not treat it well.

Q6: Why must clonidine never be stopped abruptly?

Severe rebound hypertension with tachycardia, sweating, headache and agitation from an unopposed sympathetic surge. It must be tapered.

Q7: What is the first-dose phenomenon and how do you prevent harm from it?

A sharp BP drop with dizziness or syncope after the first dose of an alpha-1 blocker such as prazosin or terazosin. Give the first dose at bedtime and teach the patient to rise slowly.

Q8: Which two drug groups on this page should raise a flag when ordered together, and why?

A beta blocker plus verapamil or diltiazem — both depress SA-node automaticity and AV conduction, so together they can cause severe bradycardia or heart block.

🧠 The four mnemonics to walk into the exam with

"PRIL puts the cough on the pillow" — ACE inhibitor cough, plus ↑K⁺.
"1 heart, 2 lungs" — beta-1 cardiac, beta-2 pulmonary.
"DIP into the vessels; VERy DILigent about the heart" — CCB families.
"CarLa does both" — carvedilol and labetalol block alpha and beta.

🧠 Say each one out loud twice, then close the page and rebuild the six-class list from the suffixes alone.