Learning pharmacology can be difficult, with most classes teaching you drugs by their classification. I find it much more useful to teach pharmacology from the standpoint of USAGE…as in, what is the medication typically used for? This gives you the ability to apply what you are learning to clinical situations much more readily and allows you to have a more holistic view of your patient’s treatment regimen. Just my opinion, of course…but let’s take a look at antihypertensives and see if you agree.
Blood pressure lowering medications span several different drug classes:
- calcium channel blockers
- ACE inhibitors
- adrenergic blockers (beta and alpha receptor blockers)
Let’s take a quick look at each of these so you’ll have a basic understanding of how they work and why they work. But first…let’s review the physiologic factors that affect blood pressure.
Blood pressure physiology
Cardiac output: When cardiac output is low, blood pressure tends to be low…when cardiac output is high, blood pressure also tends to be high. Think about when you exercise. Your cardiac output increases drastically, and if you were to take your blood pressure at that moment, you’d likely see that it’s higher than usual.
Blood/fluid volume: Simply put, when volume states are higher, then blood pressure is higher. For example, your patient who missed dialysis and is fluid-volume overloaded will very likely have high blood pressure until they are dialyzed. This is also why you’ll see patients with hypertension prescribed a low-salt diet…the sodium causes water retention, which increases volume and, thereby, increases blood pressure. Think about how bloated you feel after a sushi binge…am I right or am I right?
Peripheral vascular resistance (PVR): Arteries are lined with smooth muscle that can constrict and relax as a way to control blood-pressure on an ongoing basis. When those muscles are constricted, we have higher peripheral vascular resistance, and therefore, higher blood pressure. A great analogy of this is the garden hose….when you put your thumb over the opening, you narrow it and greatly INCREASE the pressure of the water coming out of that hose.
As you will see, the medications used to treat blood pressure target each of these three control mechanisms. Ready to see how it all fits together?
Calcium channel blockers
One of the most commonly used medications, calcium channel blockers, inhibit muscle contraction. If you recall from physiology, muscle contraction relies on the influx of calcium…these medications block that inflow of calcium. Most CCBs affect just the arterioles, but some also affect the myocardium as well. Here are some examples of common CCBs:
- Amlodipine (Norvasc): affects vascular muscle
- Nicardipine (Cardene): affects vascular muscle
- Nifedipine (Procardia): affects vascular muscle
- Diltiazem (Cardizem): affects vascular muscle AND heart muscle
- Verapamil (Calan): affects vascular muscle AND heart muscle
If your drug ends in the suffix -pine, it’s likely to be a CCB. Note that not all CCBs end in -pine, but many of them do (amlodipine, nicardipine, felodipine, isradipine, nifedipine, nisoldipine, etc.)
Nursing Considerations for CCBs: Be watchful for dizziness and headache, both of which are pretty common side effects. Because CCBs can reduce cardiac contractility, be especially watchful for signs of heart failure (SOB, frothy sputum, edema and fatigue). Patients may also get a little constipated when taking CCBs…fiber and/or laxatives can help!
Angiotensin-converting enzyme inhibitors & angiotensin-receptor blockers
To understand how ACE-inhibitors work, you need to think back to your physiology course and the wonderful renin-angiotensin pathway. You probably remember that this pathway is a key player in fluid volume status and blood pressure control in the body. To review…when blood pressure falls or the body senses lower-than-normal Na levels, the kidneys excrete an enzyme called renin. Renin, in turn, converts another enzyme called angiotensin into angiotensin I. Next, angiotensin converting enzymes (ACE) convert angiotensin I into angiotensin II and that’s where the trouble starts. Ok, not really trouble…but angiotensin II does a LOT of things in the body to increase blood pressure:
- causes arteriole constriction
- stimulates the release of aldosterone, which stimulates the body to hang on to Na and water (increasing fluid volume)
- stimulates resorption of Na (leading to more water retention)
- stimulates the release of vasopressin, which also increases fluid retention by the kidneys.
So, when we INHIBIT this pathway, we inhibit the affects of that angiotensin II. ACE-inhibitors do just that! So, in effect, ACE-inhibitors are going to tackle hypertension in two ways: decreasing volume AND dilating the arteries. Win-win!
Some examples of common ACE-inhibitors:
- Get it? They end in -pril!
Another closely related classification are medications that block the angiotensin receptors…angiotensin receptor blockers (ARBs). They essentially have the same affect as those that inhibit the converting enzyme but just attack the process at another point in the pathway. Some examples of these are:
- Losartan (Cozaar)
- Olmesartan (Benicar)
- Check it out….these end in -sartan!
Nursing Considerations for ACE-inhibitors: The biggest thing to watch for with ACE-inhibitors is angioedema. This can be a life-threatenening emergency because of the intense swelling of the airway. If your patient is taking an ACEi (especially if it’s a new drug for them), pay close attention to ANY complaints of difficulty swallowing, hoarse voice or signs of swelling in the face, tongue or neck. It can come on FAST and can be terrifying for the patient (and the nurse!). Studies show it has been determined to be a result of impaired bradykinin metabolism in the body, which leads to bradykinin building up to dangerous levels.
There is evidence that the standard treatment for allergy-induced angioedema (corticosteroids, benadryl and epi) is not actually effective against angioedema due to ACEi. However, you may still see corticosteroids, benadryl and epi given, but there have been some studies that indicate superior treatments. One is a peptide called Icatibant, which is prohibitively expensive and not readily available, and the other is fresh-frozen plasma, which contains enzymes that break down bradykinin (read more about it here).
In some cases, the patient may need to be intubated until the swelling goes down, and, not to freak you out even more, but emergency tracheostomies have been done at the bedside when the swelling is so severe that an ET tube cannot be placed.
Note that angioedema can occur with ARBs as well, but it’s typically more likely to occur with ACEi (and MUCH more likely in African Americans and women). Also, be aware that the medication does not have to be new for the patient…angioedema can still occur after years of taking the medication.
A couple more things to watch for with ACEi:
- Persistent dry cough (many patients stop therapy because of this)
- Hyperkalemia secondary to reduced aldosterone levels (patient may need to monitor K intake, so knowing which foods are high in K is helpful for exams!)
- Report any signs of unusual bleeding or bruising…could be something called blood dyscrasia, which can occur….it’s very rare but very serious.
While we’ve seen that some of the meds we’ve already covered cause vasodilation indirectly, there are some that focus directly on vasodilation as a way to reduce blood pressure. The vasodilators act specifically on the smooth muscle, but aren’t used as often because they do cause a transient and reflexive tachycardia that can be unwelcome in your hypertensive patient. However, one such medication, hydrazine, is used pretty commonly in the clinical setting.
One you might see pretty commonly is nitroglycerin, which can be given as a continuous IV infusion in the ICU or topically as an ointment (Nitrobid and Nitropaste are common brands). Another vasodilator that is used for hypertensive crisis is nitroprusside (Nipride). This medication will be given via a continuous infusion and will require ICU-level monitoring.
Nursing Considerations for Vasodilators: Lots of side effects, so rarely are first-line choice. Watch for reflex tachycardia, meaning the heart beats faster to compensate for the fast drop in BP. You also want to watch for fluid retention as this is an unwelcome side effect as well. And, if your patient is on an MAO inhibitor, the effects of a vasodilator could be even MORE pronounced….be watchful!
When administering nitroglycerin ointment, make sure you WIPE OFF the previous dose before applying the new one (to prevent severe hypotension), and you absolutely DO NOT want to get this on your hands…it causes some pretty wicked headaches and more than one nurse has “gone down” with a nitro headache and hypotension just from simply not wearing gloves.
Though patients typically don’t enjoy taking diuretics (I mean, who wants to go to the bathroom that frequently? ), they do a pretty excellent job of controlling mild to moderate hypertension. Diuretics tend to have fewer side effects than the other antihypertensives, so you’ll often see them prescribed as first-line therapy in patients whose blood pressure isn’t terribly elevated (and some patients will likely have a diuretic + another antihypertensive). Common diuretics used to treat blood pressure include:
- hydrochlorothiazide (Hydrodiuril, HCTZ): inhibits sodium reabsorption at distal tubule
- furosemide (Lasix): inhibits sodium and chloride reabsorption at the loop of Henle
- spironolactone (Aldactone): potassium-sparing, works by inhibiting aldosterone at the distal tubule
- chlorothiazide (Diuruk): inhibits sodium reabsorption at distal tubule
These diuretics all essentially work by causing the loss of water AND the loss of electrolytes. So you’ve got to keep a close eye on those electrolytes if your patient is being diuresed….namely Na and K (though Cl and Ca are affected, too). Note that spironolactone is a potassium-sparing diuretic…meaning it’s going to “do its thang” at a different part of the renal tubule than its buddies, Lasix and HCTZ.
Nursing Considerations for Diuretics: Two important things to keep an eye on:
- If your patient is on a potassium-depleting diuretic…watch K levels and anticipate replacement.
- If your patient is on a potassium-sparing diuretic…watch those K levels as they may get too high!
Adrenergic blockers (beta blockers and alpha blockers)
Adrenergic blockers can inhibit beta receptors, alpha receptors or both. To understand how these drugs work, you need to remember what the beta and alpha receptors DO and where they are located.
- Beta1 receptors: primarily located in the heart to mimic the actions of the sympathetic nervous system…fight or flight (increased heart rate and blood pressure!)
- Beta2 receptors: some located in the heart but primarily located in vascular smooth muscle…also mimics that sympathetic nervous system response; these receptors induce vasoconstriction of the smooth muscle of the vessel wall
- Alpha receptors: located in vascular smooth muscle and induces vasoconstriction via muscle contraction
So, if we BLOCK these receptors…we BLOCK these actions. In other words, we BLOCK the fight-or-flight response of increased heart rate and increased blood pressure…we BLOCK the vasoconstriction of vessels…the result? We BLOCK hypertension. Go us! The most common adrenergic blocker used is metoprolol (Lopressor). And, good news….all the other beta-blockers end in -olol as well. Easy, right? Here are some common adrenergic blockers you’ll see in the clinical setting:
- metoprolol (Lopressor): beta1 blocker
- atenolol (Tenormin): also a beta1 blocker
- propanolol (Inderal): yep…it’s a beta blocker (beta1 and beta2…meaning it’s “non-selective”)
- carvedilol (Coreg): alpha AND beta blocker (notice it doesn’t end in -OLOL, but -ILOL…close but different!)
- clonidine (Catapres): alpha blocker (also does NOT end in -olol…you got this!)
Nursing Considerations for Adrenergic Blockers: watch for orthostatic hypotension, bradycardia, dizziness and dry mouth. Can also cause impotence in your male patients, so non-compliance can be an issue. Also, let the doc know if your patient has asthma and s/he has prescribed a non-selective beta blocker such as Inderal. If you recall, there are beta2 receptors in the lungs as well, and you wouldn’t want to cause any problems there (namely bronchoconstriction). In fact, many docs steer clear of ANY beta blocker in a patient with asthma…it is definitely not a disease you want to mess around with!
So, now that you’ve been introduced to antihypertensives, are you feeling more confident taking care of these patients in clinical? Go forth and be awesome!
WHEW! That was a lot of information! How would you like the highlights in one EASY TO USE reference sheet? We got your back!
Holland, L. N., & Adams, M. (2007). Core concepts in pharmacology (2nd ed.). Upper Saddle River,
NJ: Pearson Prentice Hall.
Farkas, J. (2017, June 03). Treatment of ACEi-induced angioedema. Retrieved January 25, 2018,