The Med List: ACE Inhibitors

Today I’m starting a new series called The Med List. Once or twice a month, I’d like take a closer look at a single class of home medications and explore the medical implications for our patients who take these meds.

The patient’s medications list holds a wealth of information. Prescribed medications tell us about the patient’s medical history. They also give us clues to the patient’s possible current condition and presentation. Some medicines can better explain the clinical picture in front of us and others can be red flags regarding treatment options and the patients likely response.

Let’s kick off by looking a little closer at a class of medicines called Angiotensin Converting Enzyme Inhibitors. These meds are more commonly called ACE Inhibitors. Everyone calls ACE inhibitors ACE inhibitors in much the same way that  everyone calls International Business Machines IBM and everyone calls American Telephone and Telegraph AT&T.

ACE Inhibitors are primarily used to treat high blood pressure but they have other uses outside of the hypertensive patient population. They may be taken by congestive heart failure patients to reduce the workload on the left ventricle. They are also prescribed to some renal failure patients and they may be useful in managing a percentage of scleroderma patients.

ACE inhibitors impair the body’s ability to constrict peripheral blood vessels by inhibiting the action of an enzyme essential to vasoconstriction. To understand how it works, we need to take a brief look at the renin-angiotensin system. (Don’t worry, this won’t be as painful as it sounds.)

Renin is an enzyme produced by the kidneys in response to low blood pressure, low blood volume, low sodium levels or renal stimulation. Once renin is excreted into circulation it goes immediately to the liver and asks if the protien angiotensin can come out and play. Angiotensin always does – angiotensin is just an easy going protien that way.

Angiotensin, fresh from the liver, may play a minor role in vasoconstriction, but it isn’t very potent. It’s called Angiotensin I and it’s like a boyscout without a vasoconstriction badge. It just isn’t up to the task. So what it really needs to do is go looking for a scout leader and get it’s, “I know how to constrict blood vessels” badge.

You’ve probably already guessed who plays the scout leader in this over-stretched analogy. None other than Angiotensin Converting Enzyme. That’s right. Once angiotensin I pairs up with an angiotensin converting enzyme (An ACE if you will.) it gets its badge and becomes angiotensin II, a powerful vasoconstrictor. Blood vessels beware.

As a clever way to prevent vasoconstriction, ACE inhibitors slow the action of the scout leaders, angiotensin converting enzymes, so far fewer angiotensin I’s are able to become angiotensin II’s. Make sense? If you find all this scout talk insulting, you can also read this much more technical and intelectual sounding version of the story.

So that’s what ACE inhibitors do, but what does that mean to us?

1) It means that they most likely have a history of high blood pressure or heart failure. In either case we should be cautious about excessive fluid administration, be extra careful when giving drugs that can lower the blood pressure. (Like nitro for instance.) And recognize that drugs that typically elevate the blood pressure (Like Epinephrine) may have a somewhat blunted effect.

2) It means that they have a significantly decreased capacity to elevate their blood pressure in the presence of sympathetic stimulation, compensated shock states and head injury. We should expect to see them transition from compensated to decompensated shock much more rapidly that a patient with fully functioning angiotensin converting enzymes.

3.) It means that if the patient (or anyone else) takes too many of this medication (accidentally or on purpose) we should expect to see a precipitous drop in blood pressure.

4) It means that the patient on ACE inhibitors may be at risk for hyperkalemia. The renal action of angiotensinII retains sodium and excretes potassium. Therefore we should consider the possibility of hyperkalemia and potentially dangerous heart arrhythmias in our assessment.

Clearly there are some compelling reasons to be able to spot  an ACE inhibitor in the patients med list. The bad news is that there are a bunch of them being prescribed out there. The good news is that the generic names for all the varieties end with the letter combination pril. Here they are:

Benazepril (AKA Lotensin)

Captopril (AKA Capoten)

Enalapril (AKA Vasotec / Renitec)

Fosinopril (AKA Monopril)

Lisinopril (AKA Lisodur / Lopril / Novatec / Prinivil / Zestril)

Perindopril (AKA Coversy / Aceon)

Quinapril (AKA Accupril)

Ramipril (AKA Altace / Tritace / Ramace  / Ramiwin)

Zofenopril

If you’re paying attention to your patients medication lists, you’ve seen a bunch of these meds already. Fortunately, prescription pill bottles usually list both the generic and the trade name for the drug on the label. That gives us two chances to jog our memory.

But that’s not how med lists always come to us right? They come on wrinkled pieces of paper (Don’t lose that!) and printed computer sheets and patient charts and all other sorts of ways. It helps to be able to pick out an ACE inhibitor by either variety of names.

Comments

  1. Excellent rundown, Steve, I especially like the scouting analogy. 😉

    I used a similar one on my blog to describe heart blocks, called “Sex, Relationships and the Myocardial Conduction System.”

    I’m really curious to know how many EMS systems are starting to use ACE inhibitors as part of their field management of APE and CHF exacerbation.

  2. Steve,

    It might be worth noting that some patients can develop angioedema from this class of drug. The same has been suggested of the angiotensin II blockers (ARBs), albeit with lesser frequency. Angioedema can be severe enough to cause the soft tissues of the tongue and throat to swell and, if severe enough, cause airway obstruction. I have seen a patient experience angioedema for the first time 10 months after starting the medication.

    I never had need to treat a severe case, but for mild cases I have had patients take Benadryl and occasionally I prescribed a P.O. steroid. Stopping the ACE-I is of course most important. Some docs switch the patient to an ARB after the patient has experienced angioedema from the ACE-I since it is less likely to cause it.

    There are other acute therapies for the more life-threatening situations.

  3. I will be linking the hell out of TheEMTSpot in a new project that I’m working on, so if you see a sudden spur in Canadian hits, you’ll know why.

    … it’s quality (simple!) explanations like this that are needed in today’s EMS education. Too many people I know think “that stuff’s too complicated, can’t I just know that it’s a blood pressure pill?”

    *pushes the button* “That was easy.”

  4. EngineMedic says:

    This was absolutely amazing… if only all of Pharmacology had been taught like this. Thanks Steve… this was an awesome post

  5. Hi Steve. Thanks for the reminder. Its awesome to have a person like you put out the effort and always have something for everyone. I love it. : )

  6. Jaymazing says:

    “The Med List” is such a fantastic idea! What a wonderfully written article, too (not that I’m surprised, being a regular on this site). I’m excited to see what meds the next installment will be about!

    Thanks for being awesome, Steve

  7. Bruce Saunders says:

    Excellent post as ever,Steve. Pharmacology is one of those things that gets skipped over…even by MD’s! Looking forward to more in the series.

  8. Steve Whitehead says:

    @Ambulance_Driver I haven’t heard of anyone using these in the field. But it’s an interesting idea. It would help with the management of a very challenging patient group. Dig your blog too. Thanks for the comment.

    @Anthony Thanks for bringing this up because it is a significant issue for EMS folks to know about. Angioedema reactions didn’t fit well with the flow of the post but I secretly hoped someone would comment about them. Thanks Anthony.

    @Scott. Blogs live on links brother. Thanks for the juice. I’m glad you’re finding useful stuff.

    @Em, Grogg, JayMazing, Bruce, Thanks guys really. It’s always nice to work hard on a post and have people come by and say they like it. Definitely makes it worth coming back tomorrow and doing it again. I appreciate that.

  9. Scott Cook says:

    Thanks for the simple analogy. Always makes a dry drab topic easier to understand. Much better than getting a drug sheet and the instructor or supv. saying “here, read this. If you have any questions…”

  10. That’s what I call “breaking it down Sesame Street style.” Very nice.

  11. Steve,

    Awesome job! Thank you for tackling this topic, and making it both fun and easy to understand. I’d had the beta-blockers tip (typically end in ‘lol’) and the calcium channel blockers tip (typically end in ‘dipine’ with the exceptions of verapamil and diltiazem). Now I’ve got an easy way to remember those ACE inhibitors.

    Keep up the fantastic work!

  12. Steve, I took the time to read the much more technical and intelectual sounding version of the story. and im still confused about the whole thing. your version makes sense in a way that everyone can understand. especially those of us who have been boy scouts :). Thanks Steve

  13. I curious why ACE inhibitors would blunt the vasoconstrictive effect of catecholamines. Doesn’t epi have a direct (ie, unmediated) alpha effect?

  14. Steve Whitehead says:

    @Scott I agree, thanks for leaving the comment

    @Ben. Nice, I like it. I’m going to steal that now.

    @Jenn, Yup. And there’s two other goos ideas for future meds to add to “the list.”

    @Julio Great question. And the answer is a firm …maybe. The jury is still out on ACE inhibitor effect on epi.

    There are some animal studies that don’t do much to answer the question definitively, http://cat.inist.fr/?aModele=afficheN&cpsidt=1951999 and there are some reports of patients needing large doses of Epi to relieve Angioedema in the presence of ACE Inhibitors, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2683457/ but none of these give us a really firm answer.

    For now I’ll be keeping my language on the topic noncommittal.

  15. I currently have an outbreak of angioedema of my lips as well as inside my mouth. I have recently stopped taking lisinopril and Indapamide. So I’ve ruled these out as the cause so far.
    This swelling is very uncomfortable and annoying. I’ve been on Benadryl for 3 days now with no effect.
    I will be calling my MD tomorrow to be seen. I imagine that a week of Prednisone will help. Let’s just hope I can convince my MD to prescribe this. He’s not always with the program.

  16. I love ACEI drugs. ARBs will compete once good generics are available. Currently there is only one generic ARB
    on the market, losartan. It’s just not a very effective drug for the treatment of hypertension, and isn’t even on the preferred med list of many insurers despite its lower cost.

  17. Hey Steve, GREAT job on the article. I am an EMT-B going into my last month of practicum on car next week. I thought I knew lots about ACE inhibitors but this really drove it home. Honestly, KISS (keep it simple stupid) is what you did and that’s what works for people. I’ve read other articles and my textbooks over and over and over again and still was a little bit lost on what enzymes did what and which reacted with which but you cleared this right up. YOU should be teaching the teachers of EMS. This doesn’t even compare or come close to the education I got in school (although they did pretty good) but you do it so much better through a blog. A blog vs. in person class time, and you do it better…. that says a lot right there. Thanks so much.

    – Eric

  18. Cookie Walker says:

    Dear Steve,
    I am a nurse and used to be a paramedic/nurse but let it go after I left the ER settings. This was an excellent story that I will always remember…..How drugs work is a difficult thing to remember but now I will remember about ACE INHIBITORS.

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