Chapter 23: Antianginal Drugs

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Welcome to the Deep Dive.

We are going straight to the heart of pharmacology today.

We're focusing on the body's, well, it's most demanding muscle, really, and what happens when oxygen supply line starts to fail.

Yeah, today we're tackling anti -engine drugs.

These are the complex tool kits that pharmacologists and clinicians use to try and fix the heart's oxygen crisis.

Our mission here is to give you a clear, structured look at the main drug classes,

how they work, their mechanisms, and importantly, the critical clinical safety rules you absolutely need to know.

Think of it as a shortcut through a whole chapter of cardiovascular pharmacology.

That's a good way to put it because the problem really at its root, it's a severe imbalance, the heart muscle, the myocardium, it just has enormous oxygen requirements.

And when the supply of oxygen dips below what the heart demands, the tissue gets damaged.

That state, we call it ischemia.

And when that imbalance gets bad enough that it actually causes chest pain, that's angina pectoris, right?

Precisely.

And that's often the main symptom, the warning sign for ischemic heart disease, which, you know, is still the number one killer in the US.

Wow, still number one.

Yeah.

And it's usually caused by the coronary arteries narrowing because of fatty plaques.

That's atherosclerosis, which leads straight to coronary artery disease or CAD.

Okay, so atherosclerosis leads to CAD, which causes the ischemia and the angina pain.

You got it.

And if that narrowing of that blockage becomes complete and stays that way for long enough, well, the tissue downstream dies.

That's a myocardial infarction or MI, a heart attack.

Right.

So these anti -anginal drugs we're discussing, they're trying to prevent that MI.

They are.

They work in two main ways.

Either they try to boost the oxygen supply getting to the heart or maybe more politely, they work to reduce the oxygen demand.

So the heart simply doesn't need as much oxygen in the first place, fixing that supplied man ratio.

Okay, let's talk about the pain itself first.

When someone feels that, you know, crushing chest pain, what's actually happening chemically?

What's triggering that sensation?

It's essentially metabolic distress.

When the heart muscle is starved for oxygen, it can't use its normal, efficient energy process aerobic metabolism.

So it switches to anaerobic metabolism.

Like running on fumes.

Kind of, yeah.

And the main waste product from that process is lactic acid.

Our source material highlights this.

The lactic acid, along with some other metabolic junk, builds up and irritates the pain receptors right there in the heart muscle.

Ah, so it's a chemical signal, not like a physical stretching or something.

Exactly.

It's a chemical alarm bell screaming, metabolic crisis, not enough oxygen.

That's a key distinction.

Okay, so clinically, angina isn't just one thing.

We usually talk about three main types, right?

How does knowing the specific type help choose the cause?

Oh, it's crucial because the underlying cause is different and that dictates the best treatment strategy.

So first you have chronic stable angina.

This is sometimes called classic or effort angina.

It's the most common type, usually caused by that fixed narrowing from atherosclerosis we mentioned.

The pain is predictable.

It comes on with exertion like running, climbing stairs, or sometimes stress, maybe cold weather, strong emotions.

Then it goes away.

Yes, that's key.

It typically subsides pretty quickly, usually within about 15 minutes, if the person rests or takes their medication like nitroglycerin.

Okay, predictable exertion related resolves with rest.

That's stable.

Now it sounds like the next type, unstable angina, is less stable.

That's putting it mildly.

Unstable angina is a sign that the underlying cat is getting worse, progressing.

It's sometimes called pre -infarction angina or crescendo angina because the pain tends to increase in severity, happen more often.

Crescendo, like building up.

Exactly.

And critically, it can happen even when the patient is completely at rest.

That's a major warning sign.

The risk of it progressing to a full -blown MI is very high.

Okay, that sounds much more serious.

And then there's a third type that seems different altogether, vasospastic angina.

Yeah, vasospastic angina or sometimes Prince metals or variant angina, it's kind of the wild card.

It's not caused by a fixed blockage from

Instead, it's caused by a sudden intense spasm in the smooth muscle layer of a coronary artery.

A spasm, like a muscle cramp, but in the heart's artery.

Pretty much, yeah.

And because it's a spasm, it often happens at rest, sometimes even during sleep.

It might follow a pattern like happening around the same time each day, but there's often no obvious trigger -like exertion.

And knowing it's a spasm is really important for treatment, you said.

Absolutely, because it points directly towards a specific class of drugs that are really good at relaxing that spasm.

Okay, let's dive into the drugs, then.

First up, the real mainstay, especially for acute attacks,

nitrates.

And the classic example is nitroglycerin, right?

NTG.

The goal seems simple, stop the pain, hopefully prevent an MI.

That's the immediate goal, yes.

Nitrates are powerful

vasodilators, meaning they relax and widen blood vessels.

All blood vessels.

Pretty much all of them, yes.

But their main therapeutic effect, the reason they work so well for angina, comes from their dilation of the veins.

Okay, hang on.

Dilating veins.

How does that help the heart, which is being fed by arteries?

Walk me through that.

Right.

It seems a bit indirect, but it's key.

When the veins dilate, they can hold more blood, so less blood rushes back to the heart from the body.

We call that a reduction in venous return.

Less blood coming back into the pump?

Exactly.

And that means the heart's main pumping chamber, the left ventricle, doesn't fill up as much or under as much pressure before it contracts.

This reduced volume and pressure is called reducing the preload.

Preload, okay.

So lower preload means the heart muscle doesn't have to stretch as much or work as hard to pump that blood out.

Its workload decreases and therefore its oxygen demand drops almost immediately.

Ah, I see.

So it primarily decreases demand by making the heart's job easier.

But nitrates also dilate arteries a bit too, right?

Does that help supply?

They do dilate arteries, especially the coronary arteries, particularly at higher doses.

This can help redistribute blood flow to ischemic areas, so there is some supply benefit too.

But the preload reduction is really the dominant effect for angina relief.

Okay.

Now, nitroglycerin.

You see it given in so many ways.

Tiny pills under the tongue, sprays, patches,

IV.

Why not just a regular pill you swallow?

Ah, well, that's because of something called the first pass effect.

If you swallow nitroglycerin, it goes straight from your gut to your liver.

And the liver is really good at breaking it down.

Almost all of it gets metabolized before it even gets a chance to reach the rest of your body and have an effect.

So swallowed NTG is basically useless for an acute angina attack?

Pretty much, yeah.

That's why for rapid relief, we need routes that bypass the liver and get the drugs straight into the bloodstream.

That's where sublingual tablets come in under the tongue.

Because it's very vascular under there.

Exactly.

Or a translingual spray sprayed onto or under the tongue.

Absorption is super fast.

You get relief within like two to three minutes, usually.

And there's a really important point about storing those little sublingual tablets, isn't there?

Oh, absolutely critical.

They lose their potency very quickly, especially once the bottle is opened and they're exposed to air, light and moisture.

They must be kept in their original amber glass container, tightly sealed.

They often only last about three to six months after opening.

Patients need to know this and get fresh supplies regularly.

That's a huge clinical pearl.

Okay, so that's for acute attacks.

What about preventing angina from happening in the first place?

For that, we use long -acting formulations.

These are designed for prophylaxis or prevention.

You might have long -acting oral capsules or tablets, topical ointments that are measured and applied to the skin, or transdermal patches that deliver the drug slowly over many hours.

These take longer to start working, maybe 30 to 60 minutes, but provide continuous coverage.

Got it.

Now safety, what are the main side effects or risks with nitrates?

The number one most common side effect, almost expected, is headache.

It's caused by that visa dilation, especially in the head.

Patients should be warned about it, told it's usually temporary, and often it gets better as they get used to the drug.

Sometimes acetaminophen can help.

Okay, headache.

What else?

You can sometimes see reflex tachycardia.

Reflex tachycardia, meaning the heart speeds up in response.

Why?

When the blood vessels dilate quickly,

blood pressure can drop.

The body has sensors,

baroreceptors that detect this drop.

They basically think, whoa, we're losing pressure, maybe bleeding,

and send a signal to the heart to speed up to compensate.

It's usually temporary.

Makes sense.

And there's something about tolerance, right?

Especially with the long acting forms.

Yes, this is really important for maintenance therapy.

If the body is exposed to nitrates continuously, 204 .7, the effect can wear off.

The drug stops working as well.

Tolerance develops.

Right.

So to prevent this, patients using long acting forms, especially patches or ointments, need a regular nitrate -free period.

Typically, this means taking the patch off for about eight to 12 hours, usually overnight, to allow the body's enzyme systems to kind of reset.

So a daily drug holiday, essentially.

You could call it that.

It's crucial for maintaining effectiveness long term.

Okay.

And finally, there's one interaction that is an absolute critical, life -threatening do -not -mix.

Yes.

Nitrates must never be taken concurrently with drugs used for erectile dysfunction.

Things like sildenafil, Viagra, Tadalafil, Cialis, Vardenafil, Levitra.

Why not?

Both classes of drugs are potent vasodilators.

Taken together, they can cause a sudden, profound, and potentially fatal drap in blood pressure.

It's an absolute contraindication.

Extremely dangerous.

Okay, let's shift gears.

If nitrates are often for the immediate crisis or involve preload, what about preventing that predictable exertion -related angina?

This sounds like where beta blockers come in, like Atenolol or Metaprol.

Exactly.

Beta blockers are workhorses for stable angina, especially exertional angina.

Their whole strategy is different from nitrates.

They work almost entirely by decreasing the heart's oxygen demand.

How do they do that?

Well, they block specific receptors on the heart muscle, the beta -1 receptors.

Blocking these has two main effects.

First, it slows down the heart rate.

It slows the signal from the heart's natural pacemaker, the SA node.

We call this a negative chronotropic effect.

Negative chrono.

So, slowing time, slowing rate.

Right.

And second, they reduce the force with which the heart muscle contracts.

Less forceful squeeze.

That's a negative endotropic effect.

Okay, slower rate, less forceful contraction.

Both obviously mean the heart is doing less work and needs less oxygen.

Precisely.

But there's a bonus benefit from slowing the heart rate, something we touched on earlier regarding oxygen supply.

Ah, right.

The filling time.

Exactly.

The heart muscle gets most of its own blood supply through the coronary arteries during diastole, the resting phase between beats.

When you slow the heart rate down with a beta blocker, you lengthen that diastolic period.

More time for the coronary arteries to fill up with oxygen -rich blood.

You got it.

So, even though their main job is decreasing demand, they indirectly improve supply too, just by giving the heart more time to refuel.

Which makes them really good for that exertional angina, where the problem starts when the heart rate climbs.

Perfect for it.

And their benefits go way beyond just angina control.

They are incredibly important after someone has had a myocardial infarction.

Why is that?

After an MI, the body releases a surge of stress hormones, catecholamines, like adrenaline.

These hormones can actually be harmful to the already damaged heart.

They increase its workload, can cause dangerous arrhythmias.

Beta blockers block the effects of these catecholamines on the heart.

So they protect the heart when it's vulnerable.

Yes.

Giving a beta blocker post -MI, unless there's a strong reason not to, is proven to improve survival rates.

It's standard practice.

Okay.

Very important.

Now, safety.

Beta blockers aren't for everyone.

What are the big cautions?

Well, remember, they block beta receptors.

While some are more selective for beta -1 in the heart, many also have some effect on beta -2 receptors, which are found in the lungs.

And blocking beta -2 in the lungs?

That's bad for asthma.

It can be very bad.

It can cause the airways to constrict bronchoconstriction.

So we have to be extremely cautious using beta blockers in patients with bronchial asthma or severe COPD.

Sometimes specific, highly selective beta -1 blockers are used carefully, but it's a major consideration.

Okay.

Caution in lung disease.

What else?

Another big one is diabetes mellitus.

Diabetes.

How do they interfere there?

Patients with diabetes rely on recognizing the symptoms of low blood sugar, hypoglycemia.

One of the earliest, most common warning signs is tachycardia, a fast racing heartbeat.

Beta blockers, by their very nature, prevent tachycardia, so they can mask that critical warning sign of hypoglycemia.

The patient might still get sweaty, but they won't feel their heart racing, potentially delaying treatments for dangerously low blood sugar.

Wow.

That's subtle, but really dangerous.

They hide the warning signal.

They do.

Patients need to be educated about this, and perhaps rely more on other signs or regular blood sugar monitoring.

Just like with nitrates having that one absolute don't, beta blockers have a critical don't regarding stopping them, right?

Absolutely.

You never stop a beta blocker abruptly, especially if the patient has been on it for a while.

There's the black box warning about this.

Why is stopping suddenly so bad?

The body gets used to the beta blockade.

If you suddenly remove it, the heart can become hypersensitive to catecholamines, leading to a dangerous rebound effect, severe high blood pressure, worsening angina, even triggering an MI or dangerous rhythms.

So they must always be tapered off slowly, under supervision?

Always.

Gradual dose reduction over a week or two is standard.

Never just stop cold turkey.

All right.

Moving on to our third major class, calcium channel blockers, or CCBs.

We're talking drugs like Filtiasum, Amlodipine, Verapamil.

How do these fit into the angina picture?

They seem to target something fundamental.

Calcium.

They do.

Calcium ions are absolutely essential for muscle contraction.

That includes the smooth muscle and blood vessel walls and the cardiac muscle in the heart itself.

So CCBs block calcium from getting into those muscle cells?

Essentially, yes.

They block specific calcium channels,

preventing or reducing the influx of calcium.

Less calcium inside the cell means less muscle contraction, leading to muscle relaxation.

Okay, so muscle relaxation.

How does that help with angina?

It sounds like it could affect both supply and demand.

It absolutely does.

It's a real two -pronged attack.

First, by relaxing the smooth muscle in the walls of the coronary arteries, they cause vasodilation.

Opening up the heart's own supply lines, so increasing oxygen supply.

Exactly.

And second, they also relax the smooth muscle and arteries throughout the body, the systemic circulation.

This lowers the overall resistance that the heart has to pump against.

Ah, less resistance for the heart to push against.

Right.

We call that reducing the afterload.

When afterload is lower, the heart doesn't have to

eject blood, which significantly reduces oxygen demand.

So, CCBs are versatile.

Boost supply by dilating coronaries, cut demand by reducing afterload.

That sounds useful.

Very useful.

They're first -line drugs, not just for angina, but also for hypertension because of that afterload reduction.

But they have a really specific, important role in one type of angina we talked about earlier.

Let me guess.

The spasm kind.

Vasospastic angina.

You got it.

Because vasospastic, Prince Metal angina, is caused by that intense coronary artery spasm, CCBs are the ideal treatment.

They directly relax that spasming smooth muscle, reversing the cause of the pain.

So they're the go -to for Prince Metals.

Definitely.

Beta blockers, for instance, don't really help with spasm and might even theoretically worsen it in some cases, so CCBs are preferred there.

Okay.

Now, safety and interactions.

Is there anything major patients need to know when taking CCBs?

Yes.

There's a significant food interaction to be aware of.

Grapefruit juice.

Grapefruit juice?

Really?

Yes.

It contains compounds that inhibit certain enzymes in the gut and liver, enzymes that are responsible for metabolizing many CCBs, especially drugs like nifatine.

So drinking grapefruit juice means the drug doesn't get broken down properly.

Right.

Which can lead to much higher levels of the CCB accumulating in the blood than expected, potentially causing toxicity like excessive vasodilation and severe hypotension.

So patients on many CCBs need to avoid grapefruit and grapefruit juice.

Good to know.

And wasn't there some historical issue with how certain CCBs were given?

Something about immediate release forms.

Ah, yes.

That's an important cautionary tale.

Years ago, there was practice, particularly with immediate release nifedipine capsules, of puncturing the capsule and having the patient bite and swallow it, or squirting the liquid under the tongue for rapid effect.

Trying to get it to work faster, like sublingual NTG?

Exactly.

But it turned out to be dangerous.

It caused a very rapid, often unpredictable, and sometimes profound drop in blood pressure, leading to bad outcomes, including potential harm in acute MI situations.

So we don't do that anymore?

No.

That practice is strongly discouraged.

For angina and hypertension management now, we primarily use extended release formulations of CCBs like nifedipine, which provide smoother, more controlled blood pressure lowering.

The immediate release forms are generally reserved for other specific situations, like sometimes managing premature labor, but not typically for angina.

Okay.

Before we get into the prashical nursing side, there's one more drug mentioned in the source material, a newer one, relatively speaking, renolazine or renexa.

Ah, renolazine, yes.

Approved back in 2006, specifically for chronic angina.

It's interesting because it's kind of different.

Different how?

Well, for starters, its exact mechanism of action isn't fully understood, which is unusual for a modern drug.

We know it has anti -anginal effects, but somehow it achieves this without significantly lowering the patient's heart rate or blood pressure.

Wait, really?

All the others work by reducing demand via HRBP or boosting supply via dilation?

This one stops the pain some other way.

It seems so.

It's thought to affect sodium channels in heart cells, which indirectly impacts calcium levels, but it doesn't have those direct hemodynamic effects like the other classes.

It's a bit of a mystery box.

So a drug we've been using for years, and we're still not entirely sure how it works.

That's intriguing.

Are there risks associated with it, given the uncertainty?

The main known risk is that it can prolong the QT interval on an electrocardiogram, ECG.

Ah, QT prolongation.

That's always a red flag for potential heart rhythm problems or arrhythmias.

Exactly.

Because of that risk, Ranilese isn't a first -line therapy.

It's generally reserved for patients with chronic angina who haven't gotten adequate relief from or can't tolerate the other standard anti -anginal drugs.

And it's definitely contraindicated in patients who already have a prolonged QT interval or who have significant liver impairment.

Okay, so a niche player used later on with a specific rhythm risk to watch out for.

Now maybe we can quickly synthesize the three main classes.

If we think about that supply versus demand balance, how does each class primarily tip the scales?

Okay, quick summary.

One, nitrates.

Their main action is decreasing demand by reducing preload, less volume returning to the heart.

They have some effect on supply via coronary dilation too, but preload reduction is key.

Two, beta blockers.

These are almost purely demand -focused.

They decrease heart rate and contractility, directly lowering the heart's workload and oxygen needs.

Plus that indirect supply benefit from longer diastolic filling time.

Okay, demand side.

Three, calcium channel blockers, CCBs.

These are the most balanced, really hitting both sides.

They increase supply by dilating coronary arteries.

They decrease demand by reducing afterload, systemic vasodilation, and to some extent contractility.

So thinking about the type of angina helps choose the class.

Like if it's classic stable angina, triggered by exertion.

Beta blockers are often a great choice because they directly tackle that heart rate increase.

If it's vasospastic angina.

CCBs definitely because they relax the spasm.

Exactly, and nitrates are crucial for acute relief regardless of the type and for long -term use often combined with the others.

All right, let's bring this home for the learner.

How do we apply all this knowledge and practice?

Let's talk about the nursing process, starting with assessment.

What do you need to check before giving any of these anti -anginal meds, especially vasodilators?

Assessment is absolutely key.

Because these drugs affect blood pressure off significantly, you have to watch out for orthostatic hypotension dizziness or fainting when standing up.

So check lying, sitting, and standing blood pressures before giving the dose.

Ideally, yes, especially when starting therapy or changing doses.

Get a baseline.

And you need clear parameters.

Generally, if the systolic blood pressure is low, say less than 90 millimeter Hg, or if the pulse is too slow, maybe under 60 or too fast, over 100, you need to hold the dose and check with the prescriber.

Don't just give it blindly.

Makes sense.

And obviously assess the chest pain itself thoroughly.

Absolutely.

Full pain assessment.

When did it start?

What does it feel like?

Crushing, sharp, burning?

How bad is it on a 0 -10 scale?

Where is it?

Does it radiate?

What brought it on?

What makes it better or worse?

You need all that detail.

Okay.

Moving to implementation, actually giving the meds.

Is there a general safety rule for administering any anti -anginal?

Yes.

A simple but vital one.

Whenever possible, have the patient sit down before you give them an anti -anginal, especially rapid acting ones like sublingual NTG.

To prevent falls if their pressure drops suddenly.

Exactly.

Orthostatic hypotension can happen fast and a fall can cause serious injury.

Having them seated minimizes that risk.

The hypotensive effect of NTG can last up to 30 minutes sometimes.

Good point.

Now let's revisit that sublingual NTG protocol.

This seems like one of the most critical pieces of patient education we can give.

What are the exact steps?

It needs to be crystal clear, almost memorized by the patient.

Step one.

At the very first sign of chest pain, sit down and place one tablet under your tongue.

Let it dissolve.

Don't swallow it whole.

Okay.

First sign.

Sit down.

One tablet.

Then what?

Wait five minutes.

If the pain is not completely gone after five minutes.

Still there after five minutes.

Then the patient or their family must call 911 immediately.

This is not negotiable.

Chest pain not relieved by one NTG could be an MI happening.

Call 911.

Can they take more while waiting?

Yes.

While waiting for emergency services to arrive, they can take a second tablet.

If still no relief after another five minutes, they can take a third tablet.

But that's the absolute maximum.

Three tablets total.

Space five minutes apart over 15 minutes.

And 911 should already be on the way after that first dose didn't work.

Okay.

One tab.

Wait five minutes.

Still pain.

Call 911.

Tick tab hashtag two.

Wait five minutes.

Still pain.

Tick tab hashtag three.

Maximum three doses.

Super clear.

Very clear.

Potentially life -saving.

What about other routes?

Topical ointments or patches?

Key things there are.

Rotate application sites to prevent skin irritation.

With ointments, use the special dose measuring paper they come with.

Don't just eyeball it and don't rub it in.

That increases absorption too quickly.

Just spread it lightly and cover it as directed.

For patches, remove the old one before applying the new one and remember that nitrate -free period we discussed.

And a specific safety note for patches during emergencies.

Yes.

If a patient needs defibrillation or cardioversion,

any transdermal patches, especially those with foil backing like NTG patches, must be removed first.

The electricity can arc through the patch, causing nasty skin burns.

Wow.

I hadn't thought of that.

Okay.

What about 5e nitroglycerin?

That sounds like serious business.

It is.

Usually for unstable angina or acute heart failure situations in the hospital, the big safety point there, besides needing an infusion pump for precise dosing, is the tubing.

5e nitroglycerin can be absorbed by standard PDC plastic tubing or it can decompose.

So you lose drug potency.

Exactly.

You end up underdosing the patient without realizing it.

So you must use the specific non -PDC infusion sets, special tubing and bags that are designed for NTG administration.

Hospitals have protocols for this and nurses need to be absolutely clear on the dosing is typically micrograms per minute and how that relates to the pump setting in milliliters per hour MLHR to avoid critical errors.

Right.

Unit conversion errors are always a risk.

Okay.

One more check.

With CCBs and beta blockers potentially affecting fluid balance, what monitoring is needed there?

Good point.

Both can sometimes worsen heart failure or cause edema.

So monitoring daily weights is important, especially in patients at risk.

Teach patients to weigh themselves at the same time each day, wearing similar clothing.

And they need to report any sudden weight gain immediately, like gaining two pounds or more in 24 hours or five pounds or more in a week.

That could signal fluid retention and worsening heart failure.

Okay.

Daily weights.

Finally, lifestyle advice.

What general warnings do patients on these vasodilators need?

Because these drugs lower blood pressure and cause vasodilation, patients need to be careful about anything else that could worsen that effect and increase their risk of dizziness, fainting or falls.

Like what?

Big ones include alcohol consumption, also a vasodilator, spending time in saunas or hot tubs, taking very hot showers or baths, or even just being out in very hot weather and getting dehydrated or overheated.

All these things can compound the vasodilation and orthostatic hypotension.

Caution is key.

Hashtag will be a outro.

Okay.

This has been quite a deep dive.

We've really unpacked the core anti -anginal drug classes, how nitrates tackle preload, how beta blockers slow the engine down and improve filling time, and how versatile CCBs are, hitting both supply and demand, especially for those coronary spasms.

And hopefully it's clear how crucial it is to match the drug's properties like rapid onset versus long duration to the actual goal, whether it's stopping an acute attack right now or preventing attacks over the long term.

Absolutely.

So here's a final thought for you, the learner, to take away something that really connects the pharmacology back to the bedside.

You know, the most advanced, newest anti -anginal drug isn't necessarily the most effective one in a crisis.

Hmm.

Interesting point.

The most effective one is the one the patient actually understands and knows how to use correctly when that chest pain hits.

Your ability to clearly teach that five -minute sublingual NTG rule to explain why they need that nitrate -free period, why they can't just stop their beta blocker, that's where your understanding of these drug properties directly translates into keeping your patients safe, maybe even saving their life.

Couldn't agree more.

That knowledge transfer, their patient education piece is absolutely paramount for safety and for the drugs to actually work as intended.

Well, thank you for joining us for this deep dive into anti -anginal pharmacology.

We hope it was helpful.

Hope so too.

We look forward to the next one.