Mr. Jennings’ team wants to break the vicious cycle. Learn exactly where ACE inhibitors and ARBs step in, why they work, and what that means for the patient in front of you.
Two days later. His fluid is coming off, and the cardiologist has just finished rounds.
They changed my blood pressure pill. Something about a “sartan” instead of a “pril.” Are they not the same thing? What does it actually do to me?
Kidney releases renin → angiotensinogen becomes angiotensin I → ACE in the lungs makes angiotensin II → angiotensin II binds its receptors and causes vasoconstriction, sodium and water reabsorption, aldosterone, ADH and sympathetic boost.
Angiotensin II has to be made, and then it has to land on a receptor. That gives us two places to interrupt.
Use the buttons to see what changes in the cascade with each type of drug.
Examples: lisinopril, enalapril, ramipril, benazepril, captopril.
They block ACE, so angiotensin I is not converted into angiotensin II. Less angiotensin II means all five effects are reduced: less vasoconstriction, less salt and water retention, less aldosterone, less ADH and less sympathetic boost.
Why they help in heart failure: less resistance to pump against (lower afterload) and less fluid returning to the heart (lower preload). The heart works easier, and over time these drugs help slow damaging changes to the heart.
Also used for: hypertension, after a heart attack, and to protect the kidneys in some patients with diabetes.
ACE also has a second job. It breaks down a substance called bradykinin. When ACE is blocked, bradykinin builds up. That is the reason ACE inhibitors cause two special side effects that ARBs mostly do not:
Examples: losartan, valsartan, irbesartan, olmesartan, candesartan.
ARB stands for angiotensin II receptor blocker. The receptor blocked is called AT1. Angiotensin II is still created, but it cannot bind, so it cannot do its five jobs. Think of a key that is made correctly but no longer fits the lock.
ARBs are used for the same conditions as ACE inhibitors. They are commonly chosen when a patient cannot tolerate the ACE inhibitor cough.
| ACE inhibitors | ARBs | |
|---|---|---|
| Name ending | –pril | –sartan |
| Where it blocks | Stops ACE from making angiotensin II | Blocks angiotensin II from binding its receptor |
| Angiotensin II | Much lower | Still made, but cannot work |
| Bradykinin | Builds up | Not affected |
| Dry cough | Common | Rare |
| Angioedema | Possible, an emergency | Much less common, but still report any swelling |
| Low BP, high potassium, kidney changes | Yes | Yes |
| Pregnancy | Avoid | Avoid |
Taking an ACE inhibitor and an ARB together is generally avoided because it raises the risk of high potassium and kidney injury. If you see both on a medication list, verify with the RN or pharmacist.
An ACE inhibitor cough is not usually dangerous. But it can be irritating enough that patients skip doses or stop taking the medication on their own, which puts their blood pressure and heart failure control at risk. Encourage your patients to tell you if a cough develops, so the provider can decide whether to switch to an ARB.
You do not need to memorize a list of side effects. If you know what angiotensin II normally does, you can predict what happens when it is missing.
| Angiotensin II normally… | With the drug, you may see… | What you would check |
|---|---|---|
| Constricts vessels | Low BP, dizziness, especially with first dose | BP, pulse, fall risk, rise slowly |
| Triggers aldosterone (dumps potassium) | High potassium: weakness, slow or irregular pulse | Potassium lab, pulse, muscle weakness |
| Keeps sodium and water | Less fluid retention (desired benefit), possible low volume if the patient is dehydrated | Daily weight, I&O, signs of dehydration |
| Raises filtration pressure in the kidney | Creatinine may rise, urine output may drop | Creatinine, BUN, urine output |
| (ACE inhibitors only) ACE breaks down bradykinin | Dry cough, angioedema | New cough, swelling of lips, tongue or face |
ACE inhibitors and ARBs can seriously harm a developing fetus and are avoided in pregnancy. Report any possibility of pregnancy to the RN or provider.
Open each section. All of it follows from the cause-and-effect map you just built.
Swelling of the lips, tongue, face or throat, or trouble breathing: possible angioedema. Stay with the patient, get help and activate the emergency response per your facility policy. Do not give the next dose.
Symptomatic low blood pressure, fainting, or high potassium signs: report right away to the RN or provider.
Two situations. Use the cause-and-effect map, not memorization.
I’ve had this dry, tickly cough for about three weeks, ever since they started the new pill. It keeps me awake. No swelling or trouble breathing, and my blood pressure has been fine.
“My lips and tongue feel puffy and my throat feels tight.”
You can now answer Mr. Jennings’ original question and explain what his medicine does.
Mr. Jennings asks, “What does my new pill do?” Explain it in plain language without using drug-class jargon.
“When your heart is weak, your body makes a hormone that squeezes your blood vessels and makes you hold on to salt and water. Your pill blocks that hormone from working. That takes the strain off your heart and helps your body let go of extra fluid. It can make you dizzy when you stand up, and it can change your potassium, so we’ll check your blood work. If your lips or tongue swell, get help right away.”
Review either module any time. Bring your questions to class or clinical.
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