Cardio Medication

Cardio Medication

DRUG THERAPY FOR HYPERLIPIDEMIA

Statins

Examples

•Rosuvastatin (Crestor)

•Simvastatin (Zocor)

•Fluvastatin

•Atorvastatin (Lipitor)

•Lovastatin (Mevacor)

Pravastatin (Pravacor)

Statins Indications

Primary hyperlipidemia

• Hyperlipidemia = too much fat/lipid in the blood, especially high cholesterol or LDL.

• So statins are given to help lower LDL cholesterol.

Prevention of cardiovascular disease
This means statins help reduce the chance of problems like heart attack and stroke.

• Primary prevention = the person has risk factors, but has not had heart disease yet.

  • Example: high LDL, diabetes, hypertension, smoking.

• Secondary prevention = the person already has cardiovascular disease.

  • Example: previous MI, CAD, or stroke.

  • Statins help prevent another event.

Mechanism of Action

“Statins inhibit HMG-CoA reductase.”

HMG-CoA reductase is an enzyme in the liver that helps the liver make cholesterol.

Think of the enzyme like a cholesterol-making machine.

Statin blocks HMG-CoA reductase

→ liver makes less cholesterol

→ blood cholesterol decreases.

Your slide describes this enzyme as important for cholesterol synthesis in the liver.

“Increased uptake of LDL from the bloodstream”

This part is very important.

When the liver makes less cholesterol, it responds by pulling more LDL out of the blood.

So:

Statin
→ liver cholesterol production ↓
→ liver removes more LDL from blood
→ LDL level ↓

That's why statins are especially good at lowering LDL.

“Can also raise HDL”

Remember:

• LDL = too much can contribute to plaque in arteries

• HDL = helps carry extra cholesterol back toward the liver

So statins mainly:

↓ LDL

and they can also:

↑ HDL somewhat

•Rosuvastatin has the greatest LDL reduction and HDL raising of the HMG-CoA reductase inhibitors.

•There is evidence that pravastatin may be the safest HMG-CoA reductase inhibitor in the setting of liver disease.

Statin side/adverse effects

Myalgia

Myalgia means muscle pain or aching.

A patient may say:

• “My muscles hurt.”

• “My legs feel sore.”

• “I feel weak.”

This is a common statin side effect. Cardio meds

Rhabdomyolysis

This is much more serious.

It means severe muscle breakdown.

When muscle cells break apart:

muscle damage
→ muscle contents enter the blood
→ kidneys have to filter them
→ kidneys can become injured

So if a patient taking a statin has severe muscle pain or weakness, that is more concerning than mild soreness.

NCLEX clue

Severe muscle pain + weakness + statin

Hepatotoxicity

This means liver damage.

Statins can cause liver enzymes to rise.

The important labs are:

• AST

• ALT

If they are elevated, it can mean the liver is being irritated or injured. Your slide specifically lists elevated liver enzymes as the concern. Cardio meds

NCLEX clue

If the patient develops signs of liver injury such as:

• jaundice

• dark urine

• unusual fatigue

• right upper abdominal discomfort

the provider should be notified.

GI symptoms

These are stomach/bowel side effects:

• nausea

• diarrhea

• constipation

These are usually less dangerous than rhabdomyolysis or liver injury. Cardio meds

---

Headache

Can happen, but this is not usually the main safety issue.

Contraindication:

Active liver disease:

If a patient already has active liver disease:

liver is already damaged
+
statin can stress the liver more

higher risk for worsening liver injury

That is why your slide lists active liver disease as a contraindication. Cardio meds

What to focus on for the quiz

The two biggest danger words are:

Muscle pain → think rhabdomyolysis

Elevated AST/ALT → think hepatotoxicity

Using coenzyme Q10 and replacing vitamin D in those deficient has been thought to potentially help reduce statin-induced myalgias.

Mild statin muscle aches → CoQ10/Vit D may be considered

Severe muscle pain/weakness → think rhabdomyolysis, report it

Drug Interactions

Grapefruit juice
can increase the amount of some statins in the blood, especially simvastatin, lovastatin, and atorvastatin.

Why this matters:

statin level ↑
→ side effects ↑
→ especially muscle injury/rhabdomyolysis risk

So for the quiz:

Statin + grapefruit = higher statin level

Your slide specifically lists this interaction. Cardio meds

Warfarin
Statins can increase the effect of warfarin.

That means:

warfarin effect ↑
→ blood takes longer to clot
→ bleeding risk ↑

So if the patient takes both, watch for bleeding and anticoagulation changes. Cardio meds

Clarithromycin / itraconazole
can also increase statin levels.

Same concern:

higher statin level = more adverse-effect risk

Monitoring

Lipid panel
checks whether the medication is actually lowering lipids.

Main things you may see:

• LDL

• HDL

• triglycerides

• total cholesterol

Think:

Lipid panel = Is the statin working?

Liver function tests
mainly include AST and ALT.

Think:

AST/ALT = Is the liver being injured?

CK = creatine kinase
This is especially important if the patient reports muscle pain or weakness.

Why?

Damaged muscle releases CK.

So:

muscle injury
→ CK ↑

If a patient on a statin has muscle symptoms, CK can help evaluate for rhabdomyolysis. Cardio meds

---

Evening dosing

Your slide says evening dosing is preferred because more cholesterol synthesis occurs during the night. Cardio meds

For your quiz, remember:

Statin → often evening

The main purpose is to have the drug active when the liver is producing more cholesterol.

ATI/NCLEX focus

ATI/NCLEX focus

The strongest scenario clues here are:

Statin + grapefruit → toxicity risk

Statin + warfarin → bleeding risk

Muscle pain → check CK

Possible liver injury → check AST/ALT

Lipid panel → checks effectiveness

Cholesterol absorption inhibitor:  Ezetimibe

Mechanism

Ezetimibe works mainly in the small intestine.

It blocks cholesterol from being absorbed into the body.

Less cholesterol absorbed from intestine
→ less cholesterol reaches the liver
→ blood cholesterol decreases
→ LDL decreases

So remember:

Ezetimibe = blocks cholesterol absorption in the intestine.

Primary hypercholesterolemia

This means the patient has high cholesterol, especially high LDL.

Ezetimibe can decrease:

• Total cholesterol

• LDL

• Triglycerides

It has only a small effect on increasing HDL. Cardio meds

Can be combined with statins

This is important because they work in different places:

Statin → liver → decreases cholesterol production

Ezetimibe → intestine → decreases cholesterol absorption

So together they can lower LDL more than either mechanism alone.

Important difference from bile acid sequestrants

Your slide says ezetimibe does not have the triglyceride-raising effect that can occur with bile acid-binding resins. Cardio meds

That is a useful comparison:

Ezetimibe → LDL ↓ without raising TG

Common side effects

These can happen, but they are usually not dangerous:

• Abdominal pain

• Diarrhea

• Headache

• Fatigue

• Sinusitis / upper respiratory infection

• Joint pain

Your slide says abdominal pain and diarrhea may be mild and do not necessarily require stopping the medication. Cardio meds

Serious side effects

Hepatotoxicity = liver injury.

This is especially important when ezetimibe is taken with a statin.

So:

Ezetimibe + statin
→ liver injury risk can increase
→ monitor liver enzymes

Myopathy / rhabdomyolysis

This means muscle injury.

• Myopathy = muscle disease/pain/weakness

• Rhabdomyolysis = severe muscle breakdown

Again, your slide says the risk is particularly important when used with statins. Cardio meds

Hypersensitivity reaction

This means an allergic reaction.

Possible findings:

• Angioedema = swelling, especially face/lips/tongue

• Rash

Angioedema is the dangerous one because swelling of the tongue/throat can affect the airway.

ATI/NCLEX focus

For ezetimibe, remember these red flags:

Muscle pain/weakness → think myopathy/rhabdomyolysis

Abnormal liver enzymes → hepatotoxicity

Face/lip/tongue swelling → angioedema → airway concern

And the combination that needs extra attention is:

Ezetimibe + statin = more concern for liver and muscle tox

Drug Interactions

• With statins: can increase the risk of liver enzyme elevation and muscle injury/myopathy.

• With bile acid sequestrants such as cholestyramine: they can reduce ezetimibe absorption, so give them 2–4 hours apart.

• With fibrates: can increase risk of gallstones and muscle problems, including myalgia, myopathy, and rhabdomyolysis.

ATI/NCLEX focus

If you see:

Ezetimibe + statin
→ think liver + muscle toxicity

Ezetimibe + cholestyramine
→ think separate doses by 2–4 hours

Ezetimibe + fibrate
→ think gallstones + muscle injury

The most testable point here is usually the 2–4 hour separation from bile acid sequestrants.

Bile acid resins
(Bile acid binding sequestrants)

Bile acid sequestrants — important new ideas

Examples:

• Colesevelam

• Colestipol

• Cholestyramine Cardio meds

Mechanism

These drugs work in the intestine.

They bind bile acids so the bile acids cannot be reabsorbed.

Then:

Bile acids are lost in stool
→ liver needs to make more bile acids
→ liver uses cholesterol to make them
→ blood cholesterol goes down

So the key idea is:

Bile acid sequestrants make the liver use up cholesterol.

Indication

They are used for primary hyperlipidemia.

They can be:

• used alone

• used with statins

• used when a patient cannot tolerate statins Cardio meds

Important warning

These drugs can increase triglycerides. Cardio meds

Common side effects

Because these drugs stay mostly in the intestine, many side effects are gastrointestinal:

• Constipation

• Bloating

• Nausea

• Flatulence = gas

• Abdominal pain

So for a quiz:

Bile acid sequestrants = GI problems, especially constipation

Increased triglycerides

These medications can make triglycerides go up.

So:

Already high TG
→ bile acid sequestrant can raise TG more
→ not a good choice

Your slide says they are generally not recommended when baseline triglycerides are already high. Cardio meds

Vitamin deficiency

Long-term use can reduce absorption of the fat-soluble vitamins:

• A

• D

• E

• K

Easy memory:

ADEK = fat-soluble vitamins

Why?

These drugs bind bile acids, and bile is important for absorbing fats and fat-soluble vitamins.

So:

Less bile available
→ less fat absorption
→ less absorption of A, D, E, K

Contraindications

Contraindication: complete biliary obstruction

This means bile cannot flow normally from the liver/gallbladder into the intestine.

If bile flow is completely blocked, these drugs are not appropriate. Cardio meds

Contraindication: hypertriglyceridemia

Your slide says avoid/contraindicated when triglycerides are around 300–400 mg/dL or higher, because the medication can raise them further. Cardio meds

ATI/NCLEX focus

The biggest things to remember are:

Constipation

Can raise triglycerides

Can decrease A, D, E, K absorption

Avoid with very high triglycerides

Bile acid resins
(Bile acid binding sequestrants)

The important new idea here is that bile acid sequestrants can trap other medications in the intestine.

So:

Bile acid sequestrant binds another drug
→ that drug is not absorbed well
→ less drug gets into the blood
→ the medication may not work as well

Timing rule

To reduce this problem, take the other medication:

• 1 hour BEFORE the bile acid sequestrant
  or

• 4–6 hours AFTER

That timing is very testable.

Drugs that can be affected

Your slide lists:

• Warfarin

• Thiazide diuretics

• Digoxin

• Levothyroxine

• Statins

• Glipizide

• Phenytoin

• Oral contraceptives

• Fat-soluble vitamins A, D, E, K

ATI/NCLEX focus

If the question says:

“Patient takes cholestyramine and levothyroxine”

Think:

Separate the medications

And the memory trick is:

1 before, 4–6 after

That is the main point to remember from this slide.

ATI/ NCLEX

High LDL + normal TG → bile acid sequestrant may be useful

Already very high triglycerides → be cautious, because TG can rise more

Easy memory

Bind bile → lose bile → liver uses cholesterol → LDL falls

The most important new point compared with ezetimibe is:

Bile acid sequestrants can raise triglycerides, but ezetimibe does not have that same effect

Fibric acids (fibrates)

Examples

• Gemfibrozil

• Fenofibrate

Main purpose

Fibrates are especially good for high triglycerides.

Think:

Fibrates = lower triglycerides

They can also:

• increase HDL

• have only a mild to moderate effect on lowering LDL

Mechanism

our slide says they increase lipid metabolism.

Simple meaning:

Triglyceride-rich particles
→ broken down faster
→ removed from the blood
→ triglycerides decrease

Lipolysis = breakdown of fat.

So:

More lipolysis = more fat breakdown

When to take

Your slide says:

Take 30 minutes before meals for best effect. Cardio meds

ATI/NCLEX focus

If the question says:

“Which medication is especially useful for very high triglycerides?”

Think:

Gemfibrozil or fenofibrate

Easy memory:

FIBRATE = fights fat, especially triglycerides.

Side Effects

For fibrates, the most important new points are:

• GI effects: nausea, indigestion (dyspepsia), diarrhea.

• Hepatotoxicity: can raise AST/ALT, so think liver injury.

• Myopathy: muscle pain/weakness can happen, especially when fibrates are combined with a statin.

• Gallstones: fibrates can increase cholesterol in bile, which can promote stone formation.

• Renal dysfunction: use extra caution in patients who already have kidney impairment. Cardio meds

The two major interactions are:

Fibrate + statin
→ much higher risk of myopathy/rhabdomyolysis

Fibrate + warfarin
→ warfarin effect can increase
→ bleeding risk increases Cardio meds

ATI/NCLEX focus

If a patient taking gemfibrozil + a statin reports severe muscle pain or weakness, think:

rhabdomyolysis risk

If taking gemfibrozil + warfarin, think:

bleeding risk / anticoagulation effect increased

PCSK9 inhibitors

PCSK9 inhibitors — important new points

Examples:

• Alirocumab

• Evolocumab Cardio meds

Mechanism — simple way

Your liver has LDL receptors.

Think of LDL receptors as little hands that grab LDL from the blood.

Normally, PCSK9 causes some of these LDL receptors to be destroyed.

PCSK9 inhibitor:

blocks PCSK9
→ more LDL receptors stay available on liver cells
→ liver grabs more LDL from blood
→ LDL level drops

So remember:

More LDL receptors = less LDL in the blood.

Who gets these medications?

They are useful when a patient:

• needs much more LDL lowering

• cannot tolerate statins

• is not reaching the LDL goal with other therapy Cardio meds

Administration

These are monoclonal antibodies, so they are not regular oral pills.

They are given:

Subcutaneous (SC) injection

SC = under the skin.

They are also stored in the refrigerator. Cardio meds

ATI/NCLEX memory

If you see:

Alirocumab / evolocumab

Think:

PCSK9 blocked → LDL receptors ↑ → LDL ↓

And:

PCSK9 inhibitors = SC injection + refrigerator

ide and Adverse Effects

• Injection-site reaction = redness, pain, or swelling where the medication was injected. This makes sense because these drugs are given subcutaneously.

• Allergic reaction = rash or hypersensitivity. Rare, but watch for more serious swelling or breathing difficulty.

• Flu-like symptoms can include fatigue, back pain, and muscle aches.

• Neurocognitive effects are rare and can mean confusion or memory problems.

• A small number of patients can have increased liver enzymes. Cardio meds

Drug interactions

Your slide says:

No known drug interactions. Cardio meds

ATI/NCLEX focus

For alirocumab/evolocumab, think:

Injection-site reaction is common

and if you compare them with statins:

PCSK9 inhibitors have fewer medication interactions according to your sli

Adenosine Triphosphate–Citrate Lyase (Acly) Inhibitor: Bempedoic acid

Bempedoic acid — important new points

This drug is mainly for lowering LDL cholesterol, especially when:

• statins do not lower LDL enough

• the patient cannot tolerate high-dose statins

• the patient is statin-intolerant

• more LDL lowering is needed even after statin or ezetimibe therapy

Mechanism

Bempedoic acid blocks the enzyme ACL.

That causes:

cholesterol synthesis in the liver ↓
→ liver cholesterol ↓
→ liver increases LDL receptors
→ more LDL is removed from blood
→ LDL decreases

So the key idea is:

Bempedoic acid lowers cholesterol production and increases LDL removal.

Very important difference from statins

Your slide says bempedoic acid is a prodrug activated mainly in the liver, not in muscle tissue. Cardio meds

That means:

it may have a lower risk of muscle-related side effects compared with statins.

ATI/NCLEX focus

If the question says:

“Patient cannot tolerate statins because of muscle problems”

Think:

Bempedoic acid may be another LDL-lowering option.

Easy memory:

Bempedoic acid = blocks cholesterol production in the liver, with less direct muscle exposure.

Side Effects

For bempedoic acid, these are the important safety points:

• Hyperuricemia = too much uric acid in the blood.

  • This can trigger gout.

  • So if the patient develops a red, hot, swollen, very painful joint, especially the big toe, think gout.

• Hepatotoxicity = liver injury.

  • Monitor liver function tests, especially AST/ALT.

• Other common effects:

  • muscle pain

  • back pain

  • abdominal pain

Serious but rare: tendon injury/rupture

This is a key test point.

A tendon connects muscle to bone.

The Achilles tendon is behind the ankle.

If the patient reports:

• sudden heel/ankle pain

• swelling

• difficulty walking

• feeling or hearing a “snap”

think:

possible tendon rupture

Your slide says this is more likely in patients older than 60 years. Cardio meds

ATI/NCLEX focus

For bempedoic acid, remember:

Uric acid ↑ → gout

Tendon pain/injury → possible tendon rupture

Those are the two most distinctive adverse effects compared with the other lipid drugs.

Niacin (B₃, Nicotinic acid)

For niacin, the most important new points are:

• Flushing, itching, rash happen because niacin causes histamine release and vasodilation. Your slide says these are common. Cardio meds

• The slide says aspirin or an NSAID can help reduce flushing.

• Tingling and headache can also occur.

Because niacin is a vasodilator, blood vessels widen:

vasodilation
→ blood pressure can drop
→ hypotension, especially if the patient already takes antihypertensive medications.

Another important point:

Niacin can raise blood glucose.

So in a patient with diabetes, monitor glucose carefully.

ATI/NCLEX focus

Think:

Niacin = flushing + hypotension + glucose can go up

If the question says a diabetic patient starts niacin, one important thing to monitor is:

blood glucose

Niacin (B₃, Nicotinic acid)

Niacin (Vitamin B3 / Nicotinic acid) — important new points

Niacin is a vitamin B3 medication that can lower blood fats.

Its main lipid effects are:

• Triglycerides ↓

• LDL ↓ a little

• It can also help raise HDL

Your slide says it works by limiting production of blood fats in the liver. Cardio meds

The important comparison is:

Niacin is not as effective as fibrates for lowering triglycerides. Cardio meds

Prescription niacin vs supplement niacin

This is important.

The niacin sold as a dietary supplement is not the same as prescription-dose niacin for treating lipid problems.

Your slide gives:

• dietary supplement: about 20 mg/day

• prescription: about 1–6 g/day Cardio meds

So a patient should not replace prescription niacin with an over-the-counter supplement.

Statin connection

Your slide says niacin is typically not used much in patients already being aggressively treated with statins. Cardio meds

ATI/NCLEX focus

Think:

Niacin = TG ↓, LDL ↓ mildly, HDL ↑

and remember:

Prescription dose is much higher than ordinary vitamin-supplement dose.

Omega-3 fatty acids

For omega-3 fatty acids, the most important new points are:

• Main use: lower triglycerides

• They work by helping decrease triglyceride secretion and improve triglyceride clearance. Cardio meds

There are prescription forms such as:

• Lovaza

• Vascepa

• Epanova

• Omtryg

Your slide also separates prescription omega-3 products from regular fish oil/omega-3 supplements. Cardio meds

Precaution

If the patient has an allergy to fish or shellfish, use caution. Cardio meds

Drug interaction

Omega-3s can increase bleeding risk when taken with:

• aspirin

• NSAIDs

• clopidogrel

• warfarin

So:

Omega-3 + antiplatelet/anticoagulant
→ bleeding risk ↑ Cardio meds

ATI/NCLEX focus

Omega-3 = triglycerides ↓

Fish/shellfish allergy = caution

Warfarin/aspirin/clopidogrel + omega-3 = watch for bleeding

1. Cardiac output

Cardiac output = how much blood the heart pumps each minute.

Cardiac output depends on:

• Heart rate

• Stroke volume

Heart rate

Heart rate = how fast the heart beats.

Drugs that lower heart rate:

• Beta blockers

• some calcium channel blockers

So:

Heart rate ↓
→ cardiac output ↓
→ blood pressure ↓

2. Stroke volume

Stroke volume = how much blood the heart pushes out with each beat.

Stroke volume is affected by:

• Contractility

• Preload

Contractility

Contractility = how strongly the heart squeezes.

Drugs that reduce contractility:

• Beta blockers

• some calcium channel blockers

So:

Contractility ↓
→ stroke volume ↓
→ cardiac output ↓
→ BP ↓

3. Preload

Preload = amount of blood returning to/filling the heart before it contracts.

More blood volume returning to the heart = more preload.

Preload depends on:

• Venous tone

• Vascular volume

Vascular volume

This means how much fluid/blood is circulating.

If body holds sodium and water:

Na⁺/water retention
→ blood volume ↑
→ preload ↑
→ stroke volume ↑
→ BP ↑

Drugs such as:

• Diuretics

• ACE inhibitors

• ARBs

• renin inhibitors

help reduce this pathway.

Especially:

Diuretics
→ urine output ↑
→ sodium/water ↓
→ blood volume ↓
→ preload ↓
→ BP ↓

4. Peripheral vascular resistance

This means:

How tight or narrow the arteries are.

If vessels constrict:

Resistance ↑
→ BP ↑

If vessels dilate:

Resistance ↓
→ BP ↓

Many antihypertensive drugs lower BP by causing vasodilation.

Examples:

• ACE inhibitors

• ARBs

• alpha-1 blockers

• calcium channel blockers

• hydralazine

• nitroprusside

Very important NCLEX connection

Think of high blood pressure in two simple ways:

Too much pump

Heart beating too fast/strong:

Beta blockers / some CCBs

Pipes too tight

Blood vessels constricted:

ACE inhibitors, ARBs, CCBs, vasodilators

Too much fluid

Too much sodium/water:

Diuretics

---

Easy memory

BP = Pump × Pipes

• Pump = cardiac output

• Pipes = vascular resistance

To lower BP, medications can:

• slow the pump

• weaken the pump

• remove fluid

• open the blood vessels

That is the main meaning of this entire diagram.

1. Brain / sympathetic nervous system

The brain can send sympathetic signals that increase:

• heart rate

• vessel constriction

• blood pressure

Central alpha-2 agonists

Example:

• Clonidine

They reduce sympathetic signals from the brain.

So:

sympathetic activity ↓
→ heart rate/BP ↓
→ vasoconstriction ↓

Peripheral alpha-1 blockers

Example:

• Prazosin

They block alpha-1 receptors on blood vessels.

Alpha-1 blocked
→ vessels relax
→ resistance ↓
→ BP ↓

2. Heart

Beta blockers

Examples:

• Propranolol

• Metoprolol

They reduce the heart's response to sympathetic stimulation.

So:

heart rate ↓
+
contractility ↓
→ cardiac output ↓
→ BP ↓

They also reduce renin release from the kidney.

Alpha + beta blockers

Example:

• Labetalol

These block:

• alpha receptors → vasodilation

• beta receptors → lower HR/contractility

So they lower BP in two ways.

3. Blood vessels

Calcium channel blockers

Examples:

• Amlodipine

• Nifedipine

They relax vascular smooth muscle.

So:

vasodilation
→ vascular resistance ↓
→ BP ↓

Direct vasodilator

Example:

• Hydralazine

This directly relaxes arteries.

So:

arteries widen
→ resistance ↓
→ BP ↓

4. Kidney + RAAS system

This is one of the most important parts of the picture.

RAAS means:

Renin-Angiotensin-Aldosterone System

It normally raises BP.

Think:

Renin
→ angiotensin I
→ angiotensin II
→ vasoconstriction + aldosterone
→ sodium/water retention
→ BP ↑

Different medications block different steps.

Renin inhibitor

Example:

• Aliskiren

Blocks renin activity early in the pathway.

So:

RAAS activity ↓
→ vasoconstriction ↓
→ fluid retention ↓
→ BP ↓

ACE inhibitors

Examples:

• Enalapril

• Ramipril

• Lisinopril

ACE normally changes:

Angiotensin I → Angiotensin II

ACE inhibitors block that conversion.

So:

Angiotensin II ↓
→ less vasoconstriction
→ less aldosterone
→ BP ↓

ARBs

Examples:

• Candesartan

• Irbesartan

• Valsartan

Angiotensin II may still be produced, but ARBs block its receptor.

So:

Angiotensin II cannot work effectively
→ less vasoconstriction
→ less aldosterone effect
→ BP ↓

Aldosterone antagonist

Example:

• Eplerenone

Blocks aldosterone.

So:

less sodium/water retention
→ blood volume ↓
→ BP ↓

5. Diuretics

Example:

• Hydrochlorothiazide

They make the kidney excrete more:

• sodium

• water

So:

sodium/water ↓
→ blood volume ↓
→ BP ↓

Anti-htn agents

First-line agents

These are the classes your slide says are initially used to treat hypertension:

• ACE inhibitors

• ARBs

• Calcium channel blockers

• Thiazide-type diuretics Cardio meds

For your quiz, think:

ACE/ARB + CCB + thiazide = main first-line groups

Second-line agents

These may be used when first-line drugs are not enough, are not tolerated, or another condition makes them useful:

• beta blockers

• alpha-1 blockers

• central alpha-2 agonists

• combined alpha/beta blockers

• direct vasodilators

• aldosterone receptor antagonists

• direct renin inhibitors Cardio meds

What does “RAAS suppressants” mean?

The dagger symbol † marks drugs that suppress the renin-angiotensin-aldosterone system.

These include:

• ACE inhibitors

• ARBs

• aldosterone receptor antagonists

• direct renin inhibitors

They lower BP by reducing effects such as:

vasoconstriction + sodium/water retention

What does “sympatholytic” mean?

The * marks drugs that reduce sympathetic nervous system activity.

These include:

• alpha-1 blockers

• central alpha-2 agonists

• combined alpha/beta blockers

Sympatholytic = anti-adrenergic = reduces fight-or-flight effects

So:

sympathetic activity ↓
→ HR and/or vessel constriction ↓
→ BP ↓

Quiz memory

First line: ACE/ARB, CCB, thiazide

RAAS drugs = block the hormone system that raises BP

Sympatholytics = reduce sympathetic “fight-or-flight” BP effects

• Adult patients with a 10-year cardiovascular risk of 10% or greater treatment should be initiated with one of the four classes of medications recommended: an ACE inhibitor or ARB, a calcium channel blocker, and/or a diuretic.

Anti-htn agents

This slide is telling you how many first-line blood-pressure medicines to start based on the stage of hypertension.

Stage 1 hypertension

Your slide defines it as:

• SBP 130–139
  or

• DBP 80–89

Usually:

Start with ONE first-line medication

Example:

• thiazide-like diuretic

• ACE inhibitor

Stage 2 hypertension

Your slide defines it as:

• SBP ≥ 140
  or

• DBP ≥ 90

Usually:

Start with TWO first-line medications from different classes

Examples:

• ACE inhibitor + thiazide-like diuretic

• calcium channel blocker + thiazide-like diuretic

Your slide summarizes this approach directly. Cardio meds

Important NCLEX idea

If either number is in the higher category, classify based on the higher stage.

Example:

BP = 136/92

• systolic 136 = Stage 1

• diastolic 92 = Stage 2

So overall:

Stage 2 hypertension

Easy memory

Stage 1 = 1 drug
Stage 2 = 2 drugs

That is the main testable point from this slide.

Considerations for Concurrent Conditions

The important new idea is:

Do not choose an antihypertensive only by the BP number. Look at the patient’s other conditions too.

Heart failure and/or chronic kidney disease

Your slide says:

ACE inhibitor or ARB

Why this makes sense:

RAAS blocked
→ less vasoconstriction
→ less sodium/water retention
→ less workload on the heart
→ BP decreases

For kidney disease, these drugs can also help reduce pressure inside the kidneys.

---

Coronary artery disease

Your slide says:

Calcium channel blockers may be added

Why?

They can:

• relax arteries

• decrease BP

• help relieve chest pain/angina

So think:

CAD + chest pain → CCB can help

---

History of myocardial infarction

Your slide says:

Beta blocker + usually an ACE inhibitor

Why beta blocker?

Heart rate ↓

• contractility ↓
  → heart needs less oxygen
  → less stress on the heart after MI

Why ACE inhibitor?

It reduces BP and workload on the heart.

---

Heart failure

Your slide says these may be beneficial together:

• Diuretic

• ACE inhibitor

• Aldosterone receptor antagonist

Think of what each one does:

Diuretic
→ fluid ↓

ACE inhibitor
→ vasoconstriction + aldosterone effects ↓

Aldosterone antagonist
→ sodium/water retention ↓

Together:

Less fluid + less pressure + less heart workload

---

Very important safety rule

Your slide says:

Do NOT use ACE inhibitor + ARB + direct renin inhibitor together in the same patient.

Why?

They all suppress the same RAAS pathway too much.

That can increase risk for:

• hypotension

• hyperkalemia

• kidney problems

ATI/NCLEX memory

Think:

• HF/CKD → ACE-I or ARB

• CAD/angina → CCB may help

• After MI → beta blocker + ACE-I

• HF → diuretic + ACE-I + aldosterone antagonist

• Never stack ACE-I + ARB + renin inhibitor together

Diuretics

Diuretics are called “water pills” because they help the kidneys remove more water and electrolytes through urine. Your slide lists them as useful for hypertension, heart failure, kidney disease, and edema. Cardio meds

The four types on your slide are:

• Thiazide diuretics

• Loop diuretics

• Potassium-sparing diuretics

• Carbonic anhydrase inhibitors Cardio meds

The most important thing for your quiz is that these classes do not all affect potassium the same way.

• Thiazide → can cause low potassium

• Loop → can cause low potassium

• Potassium-sparing → can cause high potassium

Easy memory:

Thiazide and Loop lose K
Potassium-sparing saves K

Thiazide diuretics

Examples:

• Hydrochlorothiazide (HCTZ)

• Chlorothiazide

• Chlorthalidone

• Indapamide

Mechanism

They work in the distal convoluted tubule of the kidney.

They block reabsorption of:

• sodium

• chloride

So more sodium stays in the urine, and water follows sodium.

That means:

Na⁺ excretion ↑
→ water excretion ↑
→ blood volume ↓
→ blood pressure ↓

They also increase potassium loss, so watch for:

Hypokalemia = low potassium

Uses

Your slide lists:

• Hypertension

• Mild heart failure

• Edema

ATI/NCLEX focus

The big test connection is:

Thiazide → potassium goes DOWN

So if a patient taking HCTZ develops:

• weakness

• muscle cramps

• irregular heartbeat

think:

possible hypokalemia

thiazide diuretics ;- Side Effects:

Dehydration + postural hypotension

Because thiazides make the patient lose water and sodium:

fluid volume ↓
→ BP can drop
→ dizziness when standing

Postural/orthostatic hypotension = BP drops when the patient stands up.

NCLEX clue:

Thiazide + dizziness when standing = think volume loss/hypotension

---

Hypokalemia

K⁺ < 3.5 mEq/L

Symptoms:

• muscle weakness

• cramps

• fatigue

• palpitations

• tingling/numbness

Most dangerous complication:

Dysrhythmias

So:

Thiazide → K lost in urine → hypokalemia → dysrhythmia risk

---

Hyponatremia

Low sodium

Mild:

• headache

• fatigue

• nausea

More serious:

• confusion

• seizures

• muscle cramps

• weakness

• vomiting

The key clue is:

Low sodium affects the brain

So confusion or seizures are more serious findings.

---

Hypomagnesemia

Low magnesium

Can cause:

• weakness

• muscle twitching

• tremors

Magnesium is important for normal muscle and cardiac function.

---

Hypercalcemia

Thiazides can cause calcium to increase in the blood.

Symptoms:

• increased thirst

• nausea/vomiting

• constipation

• fatigue

• muscle weakness

Can increase risk for:

Kidney stones

Easy memory:

Thiazide saves calcium

---

Hyperuricemia

Uric acid ↑

This can trigger:

Gout

So if the patient on HCTZ develops a red, hot, painful swollen joint, think gout.

---

Hyperglycemia

Thiazides can increase blood glucose.

So be careful in patients with:

Diabetes

Increased lipids

They can also increase lipid levels.

---

Most important ATI/NCLEX points

For thiazides, remember this pattern:

Na ↓
K ↓
Mg ↓
Ca ↑
Uric acid ↑
Glucose ↑

The biggest danger signs are:

• K low → dysrhythmias

• Na low → confusion/seizures

• Uric acid high → gout

• fluid loss → orthostatic hypotension

Considerations

For thiazide diuretics, these are the important teaching points:

• Take with food if it causes stomach upset.

• Eat potassium-rich foods because thiazides can lower potassium.

  • Examples: bananas, oranges, potatoes, spinach.

• Drink enough fluid unless the provider gives a fluid restriction.

• Do not take at bedtime because it increases urination and can cause nocturia = waking up at night to urinate. Your slide specifically lists these considerations. Cardio meds

ATI/NCLEX focus

If the patient asks when to take HCTZ:

Take it in the morning

If prescribed more than once daily:

take the later dose early enough to avoid nighttime urination.

Easy memory:

Diuretic in the morning = less bathroom trips at night

Diuretics:  loop

Loop diuretics — important points

Loop diuretics are the most potent/strongest diuretics in your slide. Cardio meds

Examples:

• Furosemide (Lasix)

• Bumetanide

• Torsemide

• Ethacrynic acid

How they work

They work in the ascending loop of Henle in the kidney.

They block the sodium-potassium-chloride transporter.

So:

Na⁺, K⁺, Cl⁻ reabsorption ↓
→ more electrolytes stay in urine
→ water follows them
→ large amount of urine
→ blood/fluid volume ↓

That is why they are much stronger than thiazides.

Main uses

Your slide lists:

• hypertension

• heart failure

• acute pulmonary edema

• chronic kidney disease

• acute renal failure Cardio meds

The biggest new idea is:

Loop diuretics are used when fluid needs to be removed quickly.

Example NCLEX scenario

Patient has heart failure with:

• severe shortness of breath

• crackles

• pulmonary edema

• excess fluid

Think:

Furosemide (Lasix)

Because:

Lasix → rapid fluid removal → lung congestion decreases → breathing improves

Important comparison

Thiazide
→ milder diuresis

Loop
→ powerful, rapid diuresis

Easy memory:

LOOP = Lose Lots Of Water + Potassium

And remember: loop diuretics can cause significant potassium loss, which becomes very important in the next side-effects section.

Side Effects:

For loop diuretics, the most important side effects are connected to how strongly they remove fluid and electrolytes.

Ototoxicity

Ototoxicity = damage to hearing.

Watch for:

• tinnitus = ringing in the ears

• difficulty hearing

This is a distinctive loop-diuretic adverse effect. Cardio meds

Dehydration + postural hypotension

Because loop diuretics remove a lot of fluid:

fluid volume ↓
→ BP can fall
→ dizziness when standing

That is why the slide says to monitor:

• blood pressure

• urine output Cardio meds

Metabolic alkalosis

Loop diuretics can contribute to metabolic alkalosis.

Possible symptoms from your slide:

• nausea

• vomiting

• diarrhea

• weakness

• fatigue

• confusion

• tremors

• tingling/numbness

For your quiz, just remember:

Loop diuretics can cause metabolic alkalosis.

Electrolyte losses

Loop diuretics can cause:

• Hypokalemia = low K

• Hyponatremia = low Na

• Hypomagnesemia = low Mg

• Hypocalcemia = low Ca

The calcium difference is very important:

Thiazide → calcium goes UP

Loop → calcium goes DOWN

That is a strong comparison question. Cardio meds

Hyperuricemia

Uric acid ↑
→ can trigger gout

ATI/NCLEX focus

For loop diuretics, remember:

K ↓, Na ↓, Mg ↓, Ca ↓

and the special side effect:

Ototoxicity

Easy memory:

Loops lose almost everything — including calcium.

Diuretics:  potassium-sparing

Potassium-sparing diuretics — important points

These drugs are weak diuretics, so they are often not used alone.

They are commonly combined with:

• thiazide diuretics

• loop diuretics

Why?

Because thiazides and loops can cause potassium loss, while potassium-sparing drugs help keep potassium in the body.

So:

Loop/thiazide lose K
Potassium-sparing saves K

Examples:

• Spironolactone

• Eplerenone

• Amiloride

• Triamterene Cardio meds

Mechanism

Spironolactone and eplerenone
block aldosterone receptors.

Aldosterone normally makes the kidney:

• keep sodium/water

• get rid of potassium

So when aldosterone is blocked:

Na/water reabsorption ↓
→ more fluid leaves in urine

and

K excretion ↓
→ potassium stays in the body

That means:

Potassium can go UP

Amiloride and triamterene

These block sodium channels in the distal tubule/collecting duct.

Result:

less sodium reabsorbed
→ less potassium lost

Again:

K stays in the body

Uses

Your slide lists:

• resistant hypertension

• primary hyperaldosteronism

• conditions causing hypokalemia

ATI/NCLEX focus

The biggest danger is:

Hyperkalemia

So if the patient takes spironolactone, be careful with:

• potassium supplements

• potassium-rich salt substitutes

• other drugs that also raise potassium

The main memory:

Spironolactone = saves potassium

•Side Effects:For potassium-sparing diuretics, the main side effect is:

Hyperkalemia

This means potassium is too high.

Your slide gives:

K⁺ > 5 mEq/L

Possible symptoms:

• weakness

• arrhythmias

• shortness of breath

• numbness/tingling

The most dangerous part is:

High potassium can cause dangerous cardiac dysrhythmias.

So ATI/NCLEX:

Potassium-sparing diuretic + high K
→ think cardiac risk

Spironolactone endocrine effects

Spironolactone can also affect hormones.

In men:

• gynecomastia = breast enlargement

In women:

• menstrual irregularities

So a good memory is:

Spironolactone = saves potassium + can cause hormone-related side effects

And yes, your slide is telling you there is more detail later in the aldosterone receptor antagonist slides 65–68, especially for spironolactone and eplerenone.

General Side Effects of All Diurectics

What all diuretics can do

Because they remove fluid:

• Dehydration

• Orthostatic hypotension

• Hyponatremia

So if a patient is dizzy when standing after a diuretic, think:

Too much fluid loss → BP drops

Potassium pattern

• Thiazide → K⁺ goes down

• Loop → K⁺ goes down

• Potassium-sparing → K⁺ goes up

This is one of the most important comparisons.

Calcium pattern

• Thiazide → calcium goes UP

• Loop → calcium goes DOWN

Easy memory:

Thiazide saves Ca
Loop loses Ca

Metabolic effects

Thiazides

• can increase blood glucose

• can increase lipids

So in diabetes, monitor glucose.

Loop diuretics

• can cause metabolic alkalosis

ATI/NCLEX memory

Think of the 3 main classes like this:

Thiazide: K↓, Ca↑, glucose↑

Loop: K↓, Ca↓, strong diuresis, alkalosis

Potassium-sparing: K↑

That comparison is more important than memorizing every side effect separatel

Contraindications

These are the important contraindications and drug interactions for diuretics.

Contraindications / major cautions

Renal impairment
Diuretics act through the kidneys, so kidney problems can make fluid and electrolyte changes harder to control.

Pre-existing electrolyte imbalance
Especially:

Potassium-sparing diuretic + already high K⁺ = dangerous hyperkalemia risk

Gout
Thiazide and loop diuretics can increase uric acid.

So:

uric acid ↑
→ gout can worsen

---

Drug interactions

ACE inhibitor / ARB + potassium-sparing diuretic
Both can increase potassium.

So:

K⁺ ↑ + K⁺ ↑
→ hyperkalemia risk

This is a very important ATI/NCLEX combination.

---

NSAIDs + diuretics
NSAIDs can reduce kidney blood flow.

That can:

• make the diuretic work less effectively

• increase kidney injury risk

Think:

NSAID can weaken the diuretic effect

---

Digoxin + loop/thiazide
This is very important.

Loop and thiazide diuretics can cause:

hypokalemia

Low potassium makes the heart more sensitive to digoxin.

So:

K⁺ ↓
→ digoxin toxicity risk ↑

This is one of the strongest medication connections to remember.

---

Lithium + diuretics
Diuretics can cause:

• dehydration

• hyponatremia

That can increase lithium levels and cause:

lithium toxicity

ATI/NCLEX memory

Remember these 4 combinations:

• Potassium-sparing + ACE/ARB → K⁺ too high

• Thiazide/loop + digoxin → toxicity risk if K⁺ low

• Diuretic + NSAID → weaker diuretic effect / kidney concern

• Diuretic + lithium → lithium toxicity risk

Ace inhibitors

ACE inhibitors — important new points

Examples end in -pril:

• captopril

• enalapril

• lisinopril

• ramipril

• benazepril

• fosinopril

Mechanism

ACE inhibitors block:

Angiotensin I → Angiotensin II

Because angiotensin II normally causes vasoconstriction and stimulates aldosterone, blocking it causes:

less vasoconstriction
→ blood vessels relax

and

less aldosterone
→ less sodium/water retention

So overall:

BP ↓ and heart workload ↓

Indications

Hypertension
They are commonly used to lower BP.

Your slide notes they may be less effective as single therapy in Black patients unless combined with another agent such as a diuretic. For your quiz, keep this as course-slide wording rather than a universal rule.

Heart failure
Why helpful:

less vasoconstriction + less fluid retention
→ less work for the heart

After MI
They help reduce cardiac workload and are commonly used after myocardial infarction. Cardio meds

Chronic kidney disease / diabetic nephropathy
This is an important point:

ACE inhibitors can help slow progression of diabetic kidney disease

So in a patient with diabetes + kidney disease, ACE inhibitors are often important unless contraindicated.

ATI/NCLEX memory

ACE inhibitor = -pril

and think:

less Ang II → vasodilation + less aldosterone

Side and Adverse Effects

For ACE inhibitors, focus on these safety points.

Common side effects

Dry cough
This happens because ACE inhibitors increase bradykinin.

So if a patient on lisinopril develops a persistent dry cough, think:

ACE inhibitor side effect

Hyperkalemia
ACE inhibitors reduce aldosterone.

Less aldosterone means:

less potassium excreted
→ K⁺ can increase

So avoid combining carelessly with:

• potassium supplements

• potassium-sparing diuretics

• other drugs that raise K⁺

First-dose hypotension
The BP can drop a lot after the first dose.

Symptoms:

• lightheadedness

• dizziness

• fatigue

Your slide says the first dose can be started in the evening to reduce problems from dizziness. Cardio meds

Serious side effects

Angioedema
This is swelling of:

• face

• lips

• tongue

• airway

This is an emergency because it can block breathing.

Think:

ACE inhibitor + facial/tongue swelling = airway priority

Renal impairment / acute kidney injury
ACE inhibitors can reduce GFR in some patients, especially with:

• preexisting kidney disease

• renal artery stenosis

Your slide says to stop if:

• creatinine > 2.5

• and/or K⁺ > 5.5

For your quiz, memorize those as your instructor’s course values. Cardio meds

Captopril-specific effects

Altered taste
= food may taste different.

Neutropenia
= low neutrophils, which increases infection risk.

ATI/NCLEX focus

The highest-yield pattern is:

ACE inhibitor = cough + hyperkalemia + hypotension + angioedema

And the dangerous findings are:

Tongue/face swelling → airway emergency

K⁺ very high → dysrhythmia risk

Creatinine rising → kidney concern

Angiotensin II receptor blockers (Arbs)

This is describing ARBs — Angiotensin II Receptor Blockers.

Examples:

• Losartan

• Valsartan

Easy clue:

ARBs end in “-sartan”

Mechanism

Normally, angiotensin II does 2 important things:

• causes vasoconstriction

• stimulates aldosterone

ARBs block angiotensin II from binding to its receptors.

So:

Angiotensin II blocked
→ blood vessels relax
→ arteriolar vasodilation

and

aldosterone effect decreases
→ kidneys excrete more sodium and water
→ blood volume decreases
→ BP decreases

Your slide describes these effects in the vascular smooth muscle, brain, heart, kidneys, and adrenal glands. Cardio meds

Important difference from ACE inhibitors

ACE inhibitors block the formation of angiotensin II.

ARBs allow angiotensin II to exist but:

block its receptor

Easy memory:

ACE-I = blocks making Ang II

ARB = blocks Ang II from working

ATI/NCLEX clue:

“-sartan” = ARB

Indication

For ARBs, the important new points are the indications and why they may be chosen instead of ACE inhibitors.

Main indications

Hypertension
ARBs lower BP and help reduce long-term risk of:

• stroke

• MI

• kidney damage

Your slide says they may be less effective as monotherapy in African-American patients. For your quiz, keep that as course-slide wording.

Heart failure
They can be used as part of combination therapy to improve symptoms and outcomes.

After MI
They can help:

• improve survival

• reduce harmful cardiac remodeling

Remodeling means the heart changes size/shape after injury, especially after an MI.

Chronic kidney disease, especially diabetes
ARBs can:

• reduce proteinuria

• slow kidney damage

• help protect renal function

Big comparison: ACE inhibitor vs ARB

The slide’s main message is:

ACE inhibitors and ARBs both lower BP

But:

ARBs are often better tolerated when ACE inhibitors cause problems such as cough

For your course, the slide also says ACE inhibitors may have some advantages in certain settings such as heart failure and CKD.

ATI/NCLEX memory

If a patient on an ACE inhibitor develops a persistent dry cough:

Think ARB as an alternative

And remember:

ARB = “-sartan” = hypertension, HF, post-MI, CKD/diabetic kidney protection

Side Effects

Common side effects

• Dizziness / lightheadedness from BP dropping, especially after the first dose

• Headache

• Fatigue

• Hyperkalemia = potassium goes too high

Why hyperkalemia?

ARB blocks angiotensin II
→ aldosterone effect decreases
→ kidneys excrete less potassium
→ K⁺ can rise

Less common

• Renal impairment

• Cough, but less often than with ACE inhibitors

• Angioedema, rare but serious

ATI/NCLEX focus

Remember this comparison:

ACE inhibitor = cough more common

ARB = cough less common

But both can cause:

Hyperkalemia + hypotension + kidney problems

And even though angioedema is rarer with ARBs, if the patient has face/lip/tongue swelling, treat it as an airway emergency.

Angiotensin II receptor blockers (Arbs)
Interactions

For ARBs, these interactions are very important because several can affect potassium, kidneys, or blood pressure.

Potassium-sparing diuretics / potassium supplements: ARBs can already increase potassium. If combined with spironolactone, eplerenone, or potassium supplements, the patient can develop hyperkalemia.

NSAIDs: can make ARBs work less effectively for blood pressure and can also increase the risk of kidney impairment.

ACE inhibitors: generally avoid using an ACE inhibitor and ARB together because it increases the risk of:

• hyperkalemia

• hypotension

• renal impairment

Aliskiren: avoid combining with an ARB in patients with diabetes or renal impairment because of increased kidney and potassium-related risk.

Lithium: ARBs can increase lithium levels, so watch for lithium toxicity and monitor levels when applicable.

ATI/NCLEX memory

ARB + K-sparing/K supplement → K⁺ too high

ARB + NSAID → kidney risk + BP medication may work less

ARB + ACE-I → avoid

ARB + lithium → lithium level can rise