Help with pharmacology: cardiac

missk88 · Nov 8, 2012

Anyone? Anything? :confused: Any little bit helps!!!

Esme12, ASN, BSN, RN · Nov 8, 2012

Med Tips
Hemodynamics: Controlling the Rate and Blood Pressure
Many of the treatment goals in the MICU have to do with controlling one or the other of these, because too much of either one increases cardiac work, either from the effort of a rapid rhythm or the work of pumping into a really tight arterial system. This is described in typically roundabout fashion as "myocardial oxygen consumption" - which is like measuring a car's horsepower by measuring gasoline consumption. Makes sense I guess...anyhow, the point is that a heart that's hurting doesn't want to beat too quickly, or work too hard at pumping blood into the arterial system. A rate nearer that of NSR is generally better, and a relatively dilated (rather than constricted) arterial bed is easier to pump into. (This last is what "afterload" is all about. "Preload" has to do with the amount of volume arriving in the LV - it's all supposed to get pumped out, right? If not, then things begin to back up - CHF ensues.)
Heart Rate
Digoxin: Dig is one of the real oldies - apparently doctors have been using digitalis leaf to control heart rate for at least a couple of hundred years. I can still just about remember the days before dig levels - the joke was "Load 'em till they start vomiting, then back off." We do it a little better now. Know your patient's BUN and creatinine. Dig is also just about the only oral inotrope around - there used to be a little blue pill in trials called enoxamone, which I thought worked very well - at least some of the time. Any new ones coming along?
Calcium Channel Blockers: Diltiazem, Nifedipine, Verapamil - these were the original three, and they formed a range of effect: Verapamil slows rate the most, nifedipine drops blood pressure the most, and diltiazem is in the middle somewhere. I know that most places use a lot of dilt drips - for whatever reason, I've only seen it done once or twice.
Beta Blockers: inderal, metoprolol, esmolol, nadolol, etc.
These are the meds most commonly used for controlling heart rate. A basic concept to grasp is the adrenergic receptor thing - there's lots about this in the "Pressors and Vasoactives" file, but basically there are three receptor groups (this is with a lot of lies thrown in - I understand that there are more, but keeping it simple will help here.) Alpha receptors live in the arteries. You have 1 heart, so that's where the beta-1s live. You have 2 lungs, that's where the beta-2s live
If you agonize a receptor, then it does more of what it's supposed to. If you antagonize it, then it does less of what it's supposed to. So if you give a beta-agonist, like albuterol, then the beta-2s in the lungs do their thing, and the bronchi open up. (And the heart rate goes up). Beta agonist. So then giving the opposite of albuterol, namely a beta-antagonist, or beta-blocker (everybody says "aha!" at this point), will block the betas, lowering the heart rate and, if you're unlucky, provoking an asthma attack in your patient. Which is why asthmatics don't get beta-blockers, they get something like verapamil instead.
We use a lot of lopressor and verapamil for rate control in our unit. Once in a while we'll see an esmolol drip, but I have to say that I think it doesn't really work very well.
Of course, there's always the heart rate that's too slow, but that's a whole other article...
And the Pressure
Diuretics: Everybody remembers that the three parts of a blood pressure are "pump", "volume", and "arterial squeeze"? Strategies for lowering blood pressure center around picking one of these. The pump component is treated by lowering the heart rate, with one or the other or even a cocktail of the meds we were talking about above.
The volume aspect is what diuretics are all about. There are a couple of kinds - the most commonly used are the loop diuretics: lasix, diuril, and I think bumex, which I understand were invented by the famous medical rock star Don ("Loopy") Henley. Something like that. I think I'm right when I remember being told that Lasix and Bumex work on one part of the loop, and that Diuril works on another part, and that the combination effect makes the drugs work together more powerfully - "synergistic diuresis" - wasn't that on the flip side of "Hotel California"...?
One recent development in the diuretic world is the idea of giving a big wallop of diuretic to patients who are acutely sliding down the slope into renal failure - the patients who have taken a recent kidney hit because of a prolonged hypotensive episode for example. The theory is that doing this will push the failing kidneys into making good amounts of urine, so that the patient will be able to get rid of fluids, if nothing else. At least that way they won't get into CHF. Obviously this doesn't solve the whole problem though.
Edecrine is a diuretic that can be given to patients with a lasix allergy. Turns out that patients with a sulfa allergy can be allergic to lasix as well...
The two last ones are mannitol and diamox. Mannitol we use in neuro situations when the worry is increasing ICP - rapid diuresis literally shrinks the brain. (Wouldn't work for me - too small already.) Mannitol easily forms crystals, so it gets filtered.
Diamox is interesting - it causes the kidneys to dump bicarb, so it's useful in alkalosis. Something I heard, which may or may not be true: you go climbing up Mount Everest. The air gets thin, and you start breathing rapidly - producing a respiratory alkalosis, right? Breathing rapidly blows off C02, which leaves you with a carbonic acid deficit, and a relative bicarb excess. (An absolute excess would be if you drank both bottles of Maalox you'd brought along.) Now your fingers and toes start tingling, you get shivery - what to do? Take your diamox pills - you'll dump bicarb, and your ph will come back down. Is this really true - is this really what altitude sickness is all about?
The third part of a blood pressure is "arterial squeeze". This is what SVR means: systemic vascular resistance, one of the numbers that comes up when you "shoot numbers" with a PA line. High is tight, low is loose. Another word for this resistance faced by the LV - which determines how hard it has to work to empty itself into the arterial bed - is "afterload". High afterload can be a good thing sometimes, usually in some form of hypovolemic or cardiogenic shock state where getting tight is the only thing keeping your patient's pressure up. But a nicotine addict will walk around in a tight state - which puts lots more work onto his heart. Also bad for anyone with any degree of pump failure - CHF, in other words. Loosening up a tight afterload really helps a failing heart. Flowers and nice dogs work too, maybe through the same mechanism.
Most commonly used in blood pressure situations are nitrates, which in the unit usually come in the form of IV nitroglycerine. Nitrates open up the arterial bed - and sure, they do do that - I mean we've all seen patients with angina respond to sublingual nitrate pills. But honestly, IV nitro just doesn't live up to its reputation as an antihypertensive.
For really serious hypertension situations, the drug to use is nipride (nitroprusside). This drug is da bomb. It really is like a bomb, too. This is a really serious, powerful drug, sort of the opposite of norepinephrine. Nipride must run in a line all by itself. Anything put to run through a nipride line may kill your patient. (It also isn't compatible with anything.) Don't even think about flushing a heplock with nipride in it - aspirate it instead, then flush with saline. Very serious medicine.
A useful nipride tip: if you use a very concentrated mix, like 250mg in 250cc, then if you decide to doulbe your rate, your rate change may only be a cc or two per hour. This is a bad idea - a much better idea is to use a dilute mix. I like 50mg in 250cc - that way if I want to change the dose, the change in rate will be something like 20 up to 35 cc per hour. The drip is much more titratable that way, and you'll be able to "fine-tune" the drip much more closely.
There are lots of oral antihypertensives: oral nitrates like isordil, oral ace inhibitors like captopril, alpha blockers like prazosin - (remember about antagonizing the alphas? - makes the arteries dilate.) The thing about oral meds is that they're not particularly titratable, which is something that you really want in the ICU.
The nice thing about IV nitro and nipride is that their effects go away really fast - turn the drips off, and their effects are gone within a minute or two. For the same reason, changing the drip rates produces quick responses in the patient. Titratable. It's a lot harder to go down and suck out an oral med that's halfway through the small intestine than it is to turn down the nipride... I have to say that it seems like the best oral BP med is sustained-release nifedipine. Excellent drug, but too powerful in it's regular form.
Ischemia We all know about this one, right? Tight coronary artery lesions, not enough oxygen is getting to the cardiac muscle tissue, and pain ensues. What to do? Anything that increases oxygen delivery, or that decreases the workload of the heart will help. So: first drug is what? Oxygen!
Next: probably nitrates. Sublingual, IV nitro, etc. Then, or maybe even at the same time, rate control. Ask the patient if he has asthma...
Antiarrhythmics
Obviously dating myself here (nobody else will date me), but of course the first thing I think of is lidocaine. There have been big changes in antiarrhythmic treatments lately though - now amiodarone comes first. Great drug - does all sorts of neat things like converting a-fib into sinus rhythm, controls ventricular arrhythmias - in fact, it comes first in the VT/ VF code algorithms now. Two percent of people on amiodarone get nasty fibrotic lung effects. Very unpleasant. Amiodarone gets loaded, usually 150mg over ten minutes (fast!), then dripped at 1 mg per minute for something like 6 hours, then half a milligram for another 18 hours and then changed to oral.
We really don't see anything like the numbers of VT/ VF codes that we used to back in the Ice Age - the difference is that now we clot-bust most MI patients - it's the MI's that mostly make for the really awful arrhythmic codes.
Lidocaine - yup, once in a while we still use lido. 50 to 100mg load, followed by a drip at 1-2 mg per minute. Lido can make people acutely bonkers, which usually goes away if it's stopped.
Procainamide - second antiarrythmic up until the rise of amiodarone - is it third now? Proc ("Proke") also gets loaded, and then run in mgs per minute. Been a long time since I saw this up and running. Be careful - a proc load can really drop your patient's pressure.
Adenosine - I love and hate adenosine. Very powerful drug, used to break rapid supraventricular rhythms - the problem is, it creates about ten seconds of asystole in both the patient and the nurse giving the drug...
Pressors/ Vasoactives
These meds have a FAQ file all to themselves, so that's where to go for the detailed stuff. The idea behind vasoactive drips is that they either raise ("Up" meds), or lower heart rate and/or blood pressure ("Down" meds).
"Up" Meds
Simple concept - raising blood pressure, which is what the word "pressor" is all about.
This stuff calls for a little memorization. The thing to figure out is: which set of receptors do you want to work on, and why? The answer depends on which of the three parts of the blood pressure is being affected. If it's pump (heart), then it's the beta-1s you want to go after. If it's volume - then you may not want to give a pressor at all if you can avoid it. If it's arterial squeeze (sepsis), then it's the alphas out in the arteries that you want to hit. There's more than you probably ever wanted to know on this subject in the "PA-lines" FAQ, which is where we go into this stuff in more detail. The main point is that "shooting the numbers" with your PA line gives you indices for all three parts: cardiac output/ index tells you about your patient's pump status, the SVR tells you about the arterial squeeze, and the CVP, wedge pressure, and stroke volume tell you about the, uh, volume.
Neosynephrine - (phenylephrine): "Neo" is pure alpha. This is what you want to use in sepsis, when the arteries are dilated. It doesn't have any direct effect on heart rate, but some people worry that it can constrict the coronary arteries too, producing angina, etc. I can't say that I've ever noticed that to happen, although these patients can certainly get angina from the tachycardic reflex to sepsis - "rate-related angina".
Levophed (norepinephrine) - this is sort of a "kitchen sink" pressor - it kicks both alphas and betas, but much more the first than the second. It gets used in sepsis a lot, and it works well, but if you notice that your septic patient is getting even more tachycardic than before, and maybe having some ectopy too, it might be a good idea to change to neo.
Dopamine - dopa is the only pressor that can be started on the floors, so no matter why the patient is having pressure problems, this is the one that they put up. It helps, too, but it's not always the drug you want to go up on - if your septic patient is tachycardic, using a lot of dopamine can only worsen that problem, and sometimes it can provoke VT or VF. Then again, for a patient with an inferior MI (the kind that makes brady-arrhythmias), it might be just the thing. A wire might be better though.
Vasopressin: I just don't understand this drug at all. We use it in two ranges, one for sepsis, one for GI bleeding, in both cases to tighten up arteries. But the dose for GI bleeding is ten times the rate of the dose for sepsis? How come it doesn't produce ten times the blood pressure? We used to use vasopressin together with IV nitroglycerine for GI bleeds before octreotide came along - what I do remember is that it causes bradycardia, or some slowing anyhow, often to heart rates in the 50's - that I would never have believed in septic patients who usually run in the 130's for days at a time. But what the heck - it works, I run it.
Dobutamine - This is the pure beta pressor (the only one with a "b" in it.) This is what you want to use when the pump isn't pumping - cardiogenic shock. Two problems with that: first, it "whips" a heart that's already failing - a balloon pump is much better. Second: it very easily causes lots of arrhythmias - something your cardiac patient doesn't need. Make sure their electrolyes are ok.
Sometimes used(Zebras): Epi, Isuprel, Amrinone, Milrinone. We'll use these drips sometimes in special situations - like maybe at the end of a code. Epinephrine - very powerful, very arrhythmogenic. Isuprel - "Prel": a powerful beta drug, also causes lots of arrhythmias, can be hard to control. I haven't seen a Prel drip in many moons. (Jayne: "Isuprel is completely gone - nobody even makes it any more." ) Amrinone - "the yellow stuff", and it's cousin milrinone - sort of the same as dobutamine, except different - maybe we see these once a year. Anybody know if they're used more in the CCU?
For extravasations: Regitine. This is a good one to know about, even if you never have to use it. A patient who has to get pressors through a peripheral line is at a real risk for injury around the site if the drip infiltrates into the tissue. Regitine is an alpha blocker, and gets injected ("infiltrated") into the tissues around the IV site to relax the vasoconstriction. Never seen it done, but I saw a dopamine infiltration wound once. Ugly.

"Down" Meds
Nitrates: nitrates are vasodilators - they open up coronary artery flow, and they lower SVR, so the heart gets 1: a better muscular blood supply and 2: less arterial resistance to push against. Nice.
Nipride - the ultimate down med. This is what you want to use if your patient has malignant hypertension, or something very acutely dangerous, like a leaky aortic aneurysm. Very powerful. Be especially careful with this one. The nice thing is that it both works and wears off so quickly, so that you can titrate it very easily - it doesn't take ten minutes for a change to show up.
Labetolol - this is a neat idea: it's both an alpha and a beta blocker. So it produces arterial dilation, and slower heart rate.

https://allnurses.com/nursing-educators-faculty/teaching-cardiac-medications-112149.html

http://www.heart.org/HEARTORG/Conditions/HeartAttack/PreventionTreatmentofHeartAttack/Cardiac-Medications_UCM_303937_Article.jsp

Pressors and Vasoactives

I think you will find this site helpful!

icufaq's.org

hodgieRN · Nov 9, 2012

I am heading of to bed after a long day at work. But I am really interested in answering this question! I will give you some tips in the morning. Deal?

hodgieRN · Nov 9, 2012

I won't be be able to provide the info posted by Esme12, but hopefully I can give some pointers.

As mentioned before, hemodynamics extend beyond the cardiac portion. The kidneys play a huge part in regulating the body...especially when discussing hypertension. Know the meds involved with aldosterone, which causes retention of sodium and excretion of potassium and hydrogen. Understand the system of Renin, Angiotensin, Angiotensin II, Angiotensin-converting enzymes, vasoconstriction, vasodilation. ACE inhibitors affect this system (all the -prils). Angiotensin II receptor Blockers (ARB) are all the -sartans.) Also, sodium levels, sodium excretion, sodium retention can have a wide effect on B/P.

Most calcium channel blockers (CCB) end in -pine except verapamil, diltiazem.

Know the diuretics. Differences between Thiazides, Loop, and Potassium-sparing. There are many Thaizide combo drugs with beta-blockers, ACE inhibitors, etc.

Heart failure medications play a big role since heart disease is the number one killer. HF pts are known have hospital re-admissions and increased mortality rates if not treated properly. Some meds have many different indications. ACE inhibitors are taken for blood pressure, but they are also taken by HF pts b/c it addresses cardiac remodeling. So know the different indications for a medication.

Know why a med is indicated and how it affects the body. A CCB lowers B/P and slows heart rate. But, CBB meds are given to HF pt's b/c it decreases the contractility of the heart.

Know the meds for arrythmias. A-fib, A-flutter, tackycardia, bradycardia all have specific meds for treatment. Some of these meds can have toxic effects on the body.

Know the meds that treat cholesterol, mainly -statins and niacin. Understand how they affect the liver.

Understand treatment for angina and the need for anticoagulants, anti-platelet, thrombolytic therapy.

kansasredneckwomen · Nov 10, 2012

Great question and even greater answers! Thank you for making the cardiac meds so much clearer! We just finished the unit prior to the post and I never understood how to keep the drugs separated as well as I do now that I have read your posts!

hodgieRN · Nov 11, 2012

No problem! Happy to help!

nurseprnRN, BSN, RN · Nov 12, 2012

You'll also find it very helpful before your pharm exam to take out your physiology book, lay it on the table next to the pharm text, and look up the physiological actions in the myocardium and vascular system as mentioned in the meds. Sorta puts it all together. Think "critical thinking."