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Captain Quinn
08-13-2006, 10:31 AM
Ok folks, I take my CCRN in the morning and I am reviewing some questions. I know some folks have mentioned they have found some of the information from the questions is wrong. Here is a question I am having trouble with.

"A 32 year old woman has SLE and Chronic Renal Failure. Over the past two weeks she has complained of feeling very fatigued and SOB after minimal exertion. She is also complaining of tightness in her chest while resting. She is on hemodialysis. Her Hgb is 4.5. Which of the following is indicated:

1. Epogen
2. Two Units of PRBCs
3. Nitro sublingual
4. Imuran


What do you smart folks think?

andy

gobucks1013
08-13-2006, 11:28 AM
Hey Capt. That is an interesting question. I may be missing some key element here, but I'd say get that woman some PRBCs! Hgb is critcally low (beyond normal CRF associated anemia) and she is exhibiting symptoms of myocardial ischemia.

I don't know if the lupus really plays a big role here outside of being the probable cause of her CRF. The bottom line is she needs red cells. I'd say for someone who is symptomatic with critical anemia, PRBCs is the quickest fix. Then you can talk about implementing more long term therapy such as Epogen.

Hope that helps. It's my best shot! :)

Sue

TranMan
08-13-2006, 11:31 AM
Nice post Andy. I guess I'll go out on a limb here. Letme preface this with "it's been a long time since I've study as hard as I did for the boards".

Well this patient definately needs blood, this is probably why she's having chest pain. lack of perfusion. However she is currently having Chest Pain. Would be nice to know her VS, but I don't think that would sway my decision too much. My vote is to give her NTG SL 1st, then give her blood.

Actually, give her O2 1st, the NTG, then blood. Or those things while you're waiting for the blood.

MmacFN
08-13-2006, 11:33 AM
HGB is very low

This is common in chronic renal failure but lets review the choices and narrow them down:

Choice # 1 - Epogen
- often used in CRF pts on or off dialysis. Helps to maintain RBC level

Choice # 2 - Two Units of PRBCs
- PRBC are often used to increase the RBC's (ergo oxygen carrying capacity) of pts.

Choice # 3 - Nitro sublingual
- Used as a smooth muscle relaxor in angina (sm muscle spasm) and chest pain as a precursor to NO3 for dilation and decrease in preload.

Choice # 4 - Imuran
- immunosuppressant medication for kidney transplants

Quickly, #3 & 4 are rules out for me as they are not what is causing the problem. #3 b/c it is clear the patient has SOB and activity intolerance due to anemia, not chest pain.

Normal hgb is 12-18. She is ~ 30% of normal.

Epogen takes weeks to increase a patients hgb and hct. This patients is displaying signs and symptoms of acute anemia now. Shes needs the PRBCs in my opinion.

I would say the answer is #2.

- 2 weeks of fatigue and SOB with exertion
- chest tightness
- Renal failure & Hemodialysis
- critical HGB level

All these point to acute anemia as the cause. All they sympotoms are most likely caused by anemia

MmacFN
08-13-2006, 11:37 AM
Hey Tran

I would suggest that nitro is contrindicated in this patient here is why:

pt already has low circulating volume of hgb. She is, more than likely, tachycardic in an attempt to compensate. Even in her hyperdynamic state, she is showing signs and symptoms. Add nitro and you will decrease BP and therefore CO. Do this and her symptoms will get signifigantly worse based on a decrease in delivery of oxygenated hgb.

This question doesnt give you enough information to point at cardiac issues, but it gives all the clues for anemia as the cause. Lets not forget she is 32 years old and has no mentioned cardiac hx, it is highly unlikely that she is having a cardiac event.

mike


Nice post Andy. I guess I'll go out on a limb here. Letme preface this with "it's been a long time since I've study as hard as I did for the boards".

Well this patient definately needs blood, this is probably why she's having chest pain. lack of perfusion. However she is currently having Chest Pain. Would be nice to know her VS, but I don't think that would sway my decision too much. My vote is to give her NTG SL 1st, then give her blood.

Actually, give her O2 1st, the NTG, then blood. Or those things while you're waiting for the blood.

gobucks1013
08-13-2006, 12:25 PM
Hey Mike,

I think she is having a cardiac event secondary to severe anemia. Not the same type of MI as a 55y/o 300+lb male 2ppd smoker with CAD. In this case, her body simply does not have the O2 carrying capacity to meets its own demands. She's having an anemia-induced MI or she sure is showing signs she's about to.

I actually had a healthy 35y/o man in the ICU once who was a trauma patient. He had both a spleen lac and a liver lac secondary to an MVA. The catch was, he was a Jehova's Witness and absolutely refuse blood products. His Hbg just continued to drop until he had an anemia-induced MI and sadly died. Talk about a helpless feeling.

I agree with your bottom line here: Fix the anemia, fix the CP, SOB etc.

MmacFN
08-13-2006, 12:34 PM
Exactly!

Its not a primary cardiac event but a secondary of the primary anemia. In this case, ngt wont help.



Hey Mike,

I think she is having a cardiac event secondary to severe anemia. Not the same type of MI as a 55y/o 300+lb male 2ppd smoker with CAD. In this case, her body simply does not have the O2 carrying capacity to meets its own demands. She's having an anemia-induced MI or she sure is showing signs she's about to.

I actually had a healthy 35y/o man in the ICU once who was a trauma patient. He had both a spleen lac and a liver lac secondary to an MVA. The catch was, he was a Jehova's Witness and absolutely refuse blood products. His Hbg just continued to drop until he had an anemia-induced MI and sadly died. Talk about a helpless feeling.

I agree with your bottom line here: Fix the anemia, fix the CP, SOB etc.

Captain Quinn
08-13-2006, 12:45 PM
Well guys, I went with giving the PRBC's. Here is what Pass CCRN said the answer was:

" RESPONSE: This patient is having symptoms of decreased tissue oxygenation. In acute situations, this reaction would be an indication for blood. In this patient, Epogen is a more appropriate treatment. It is used to treat anemia secondary to reduced renal production of erythropoeitin.

Test Taking Strategy: Connect the treatment with the cause. The cause of the symptoms is the decreased amount of Hgb to carry oxygen. The treatment is to increase the amount of Hgb by addressing the cause. The cause of anemia in the patient with chronic renal failure is decreased renal production of erythropoetin. Choose option A."

I think this is one of the questions they have wrong. Chest tightness when at rest sounds acute to me. Pretty weak answer justification in my book.

gobucks1013
08-13-2006, 01:28 PM
Epogen for an HGB of 4.5 and she is severly symptomatic?!

Yikes, I don't want whomever came up with that answer taking care of me of anyone I know! :eek5:

MmacFN
08-13-2006, 01:52 PM
:yikes:

Yah thats wrong.

Epogen is the long term tx not the acute one.

TranMan
08-13-2006, 04:28 PM
I would agree with everyone here that the answer to the question is wrong. Many of the board questions are like this. Ambiguous with several right answers and you have to pick the "best" answer. After looking over the question again, I would go with blood over the SL NTG 1st. Only b/c they didn't give us any indication of her VS. If the question did give her VS and they are w/i normal limits, then I would pick the SL NTG over blood (explanation below). Or if O2 was an option, I would pick that b/c it's immediate Tx that can't harm her even if she obviously needs blood.

I'm sure were all on the same page here. NTG would not neccesarily be contraindicated here nor harmful. I'll explain what I'm thinking here in a bit. Her Chest pain is obviously 2nd to anemia and poor perfusion and She obviously needs blood, no doubt about it.

It's hard to say whether "sublingual NTG" is inappropriate here b/c we don't know what her VS's are. If her BP is indeed low as suspected and she is indeed tachycardic, then I would NOT give her the SL NTG. In this state, NTG would be CI and could be harmful b/c it would drop her pressure and aggravate the situation. "IF" her VS are within normal limits (and that's possible), then Sublingual NTG may be beneficial. In this situation, with holding the NTG could actually be harmful to her. Blood takes time to get, usually 20-40 mins. if a patient is not already typed and cross and SL NTG can help relieve the pain within several minutes. If you don't do anything to relieve her CP right away, it could potentially turn into an MI by the time blood arrives.

Of course we're all familiar with the "MONA" Tx of chest pain. So appropriate initial Tx would consist of O2 (mask), small dose of Fentanyl (or MS), sm dose of versed for her anxiety, and "SL" NTG if VS's permit, 12 lead EKG. And I would still give Fent, versed, & the SL NTG gingerly. 1-2 tabs should help with the CP and not drop her pressure very much if at all. Too much of either Fent, Versed, or the SL NTG can drop her HD and worsen the situation fast. Keep in mind that she has CRF and probably just went through a hemodialysis tx. If this is the case we can assume she is bone dry. Hypovolemic patients do not tolerated sedation, pain meds, and SL NTG like they normally would.

Another question I have here is fluids. Would fluids help this young patient (assuming she doesn't have a cardiac Hx and IVFs are not normally contraindicated)? Would giving her fluids help perfuse her heart or would it further dilute her Hgb making her situation worse?
Again, remember that she has CRF and probably has probably just finish a Hemodialysis Tx and is dry.

What about Beta Blockers (BBs)? If she was compensating for her low perfusion state by increasing her HR, then would BBs be helpful or harmful? Obviously the tachycardia is helping to compensate for a low BP, but remember the heart gets perfused during diastole and not systole. Tachy = more time in systole = less perfusion for the heart. Tachycardia also uses up more O2 and can worsen the situation quickly. You guys/gals post up your thoughts and I'll share mine later.

Great Post Captain, and good discussion all. But for the sake of keeping it simple and to answer the question, blood would be the best answer of the bunch.

MmacFN
08-13-2006, 05:42 PM
Ok well here is what I think.

I would not give ntg to a 32 y/o with chest pain based on this scenario even without the vital signs. Here is how i justify that:

First lets all agree that the etiology here is chest pain secondary to hypoxia caused directly by anemia. We dont need anymore information than is given to know this because the HGB is a clincher and is backup by age & given hx. That rules out a primary cardiac cause.

Now, she is in a general oxygen supply vs demand mismatch which is due to a perfusion (not ventilation) problem. This being the case, her compensation can only be hemodynamically. Ergo tachycardia and increased SVR to increase circulation with the primary goal of getting the remaining hgb from lungs to end organs and back as fast as possible to avoid failure. She will have endrogenous catechalomines firing off everywhere to accomplish this goal (epi & norepi). She is in pain and SOB, shes guarenteed to be tachy and hypertensive here is why:

BP = CO & SVR
CO = Stroke Volume X HR
SV= contractility & Preload & Afterload (EDV - ESV)

(this is a simplistic explanation but gets accross the point without me getting into the chem)

There is only one way for her body to respond to hypoxia, increase the HR and the SVR as well as the contractility. All done with release of epi and norepi.

So here is why ntg is contraindicated in this patient.

NTG acts as an vasodilator because it converts to nitric oxide in the body. The endothelium (inner lining) of blood vessels use nitric oxide to signal the surrounding smooth muscle to relax, thus dilating the artery and increasing blood flow.

So here is the problem. The body is trying to increase SVR in order to speed return of blood to the lungs/heart in order to compensate for low circulating amount of hgb. If you give NTG you will decrease SVR and decrease the speed at which the patient can circulate the amount of hgb. This will absolutely result in increased hypoxia and chest pain.

It is easy to get caught up in the protocol driven world of AHA ACLS. NTG is really only indicated in angina (coronary spasm) and nothing else. Regardless of the etiology of the spasm, clot irritating the coronary (ACS) or just general angina, all ntg does is help to eleviate the pain by relaxing the smooth muscle.

NTG has not proven to have any effect on mortality rates due to ACS. The reason is that it doesnt fix the ACS problem which is a clot. It may have a minor decrease in MVO2 demand due to decreasing preload, but this has not been shown to change mortality.

Beta blockers in this patient would be 100% absolutely contraindicated. Decreasing her contracitility and HR would probably end in her arresting secondary to myocardial hypoxia.

Fluids would also be detrimental. By adding fluids to a patient who is not dehydrated or in need of preload only serves to increase the myocardial oxygen demand by increasing workload. This would make the patients c/p worse.

Anywho, thats how i see it.

NursePink
08-13-2006, 05:48 PM
I got in on this discussion late. My first inclination was as the rest of you guys... TRANSFUSE. Because I know we ALL love documentation, I dug this up off the epogen website. :)


Amgen started the first clinical trial of Epoetin alfa in late 1985 under the aegis of Drs. Joseph Eschbach and John Adamson at the Northwest Kidney Center in Seattle. Over the next year, the small phase 1/2 clinical trial confirmed that therapeutic doses of recombinant human erythropoietin stimulated consistent increases in patients' hematocrit levels. Furthermore, the requirement for maintenance blood transfusions for the dialysis patients treated was eliminated.

Reports of EPOGENŽ's ability to improve anemia associated with kidney failure first appeared in the January 8, 1987, issue of the New England Journal of Medicine. Included was a review of the phase 1/2 trial and an editorial that pointed to "convincing evidence for the therapeutic effectiveness of recombinant erythropoietin in anemic patients on long-term dialysis." The author, Dr. Allan Erslev, said these clinical trials "fully confirm our expectation that erythropoietin can increase not only the hemoglobin concentration, but also the well-being of patients on dialysis."

EPOGENŽ is indicated for the treatment of anemia in patients with chronic renal failure on dialysis. EPOGENŽ is contraindicated in patients with uncontrolled hypertension. Erythropoietic therapies may increase the risk of seizures, thrombotic events, and other serious events. The target hemoglobin (Hb) should not exceed 12 g/dL. If the Hb increase exceeds 1.0 g/dL in any 2-week period, dose reductions are recommended. In a study with hemodialysis patients with clinically evident cardiac disease, where the target hematocrit (Hct) was 42% (Hb = 14 g/dL), an increased incidence of thrombotic events and mortality was seen. The reason for increased mortality observed in this study is unknown.

Cases of pure red cell aplasia (PRCA) and of severe anemia, with or without other cytopenias associated with neutralizing antibodies to erythropoietin, have been reported in patients treated with EPOGENŽ. A sudden loss of response to EPOGENŽ, accompanied by severe anemia and low reticulocyte count, should be evaluated. If anti-erythropoietin antibody-associated anemia is suspected, withhold EPOGENŽ and other erythropoietic proteins. EPOGENŽ should be permanently discontinued in patients with antibody-mediated anemia. Patients should not be switched to other erythropoietic proteins.

The most commonly reported side effects in clinical trials were hypertension, headache, arthralgias, and nausea.



Starting doses of EPOGENŽ over the range of 50-100 units/kg of patient body weight administered three times per week have been shown to be safe and effective in patients with chronic renal failure. Because of the length of time required for the body to begin to utilize EPOGENŽ, a clinically significant increase in hematocrit is usually not observed in less than two weeks and may require up to six weeks in some patients.

MmacFN
08-13-2006, 05:54 PM
Here is the info on lupus, i think in this case, its a distractor from the problem which is the low hgb. The Lupus is most likely the cause of her renal failure especially if it was caught late.

Systemic lupus erythematosus (SLE or lupus) is a chronic, potentially debilitating or fatal autoimmune disease in which the immune system attacks the body’s cells and tissue, resulting in inflammation and tissue damage. SLE can affect any part of the body, but often harms the heart, joints (rheumatological), skin, lungs, blood vessels and brain/nervous system. Lupus is treatable, mainly with immunosuppression, though there is currently no cure for it.

Signs and symptoms

Common initial and chronic complaints are fever, malaise, joint pains, myalgias and fatigue. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms, however, they are considered suggestive.
Dermatological manifestationsAs many as 30% of patients present with some dermatological symptoms (and 65% suffer such symptoms at some point), with 30% to 50% suffering from the classic malar rash (or butterfly) rash associated with the disease. Patients may present with discoid lupus (thick, red scaly patches on the skin). Alopecia, mouth, nasal, and vaginal ulcers, and lesions on the skin are also possible manifestations. Musculoskeletal manifestationsPatients most often seek medical attention for joint pain, with small joints of the hand and wrist usually affected, although any joint is at risk. Unlike rheumatoid arthritis, SLE arthropathy is not usually destructive of bone, however, deformities caused by the disease may become irreversible in as many as 20% of patients. Hematological manifestationsAnemia and iron deficiency may develop in as many as half of patients. Low platelet and white blood cell counts may be due to the disease or a side-effect of pharmacological treatment. Patients may have an association with antiphospholipid antibody syndrome (a thrombotic disorder) where autoantibodies to phospholipids are present in the patient's serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged PTT (which usually occurs in hemorrhagic disorders) and a positive test for antiphospholipid antibodies, the combination of such findings have earned the term "lupus anticoagulant positive". Another autoantibody finding in lupus is the anticardiolipin antibody which can cause a false positive test for syphillis. Cardiac manifestationsPatients may present with inflammation of various parts of the heart: pericarditis, myocarditis and endocarditis. The endocarditis of SLE is characteristically non-infective (Libman-Sacks endocarditis), and involves either the mitral valve or the tricuspid valve. Atherosclerosis also tends to occur more often and advance more rapidly in SLE patients than in the general population. (Asanuma et al 2003, Bevra 2003, Roman et al 2003). Pulmonary manifestationsLung and plura inflammation can cause pleuritis, pleural effusion, lupus pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, pulmonary hemorrhage. Renal involvementPainless hematuria or proteinuria may often be the only presenting renal symptom. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end stage renal failure. Because of early recognition and management of SLE, end stage renal failure occurs in less than 5% of patients. Histologically, a hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities. This finding is due to immune complex deposition along the glomerular basement membrane leading to a typical granular appearance in immunofluorescence testing. Neurological manifestationsAbout 10% of patients may present with seizures or psychosis. A third may test positive for abnormalities in the cerebrospinal fluid. Other rarer manifestationsLupus gastroenteritis, lupus pancreatitis, lupus cystitis, autoimmune inner ear disease, parasympathetic dysfunction, retinal vasculitis, and systemic vasculitis. T-cell abnormalitiesAbnormalities in T cell signaling are associated with SLE, including deficiency in CD45 {phosphatase, increased expression of CD40 ligand. Also associated with SLE is increased expression of FcεRIγ, which replaces the TCR ζ chain, which is deficient in some SLE patients.Other abnormalities include:
increased and sustained calcium levels in T cells
moderate increase of inositol triphosphate
reduction in PKC phosphorylation
reduction in Ras-MAP kinase signalling

gobucks1013
08-13-2006, 06:45 PM
Okay. This is turning into a really good dicussion. You guys are very resourceful!

To answer some of tran's questions. If I used any fluids it would be minimal. One of the reasons being we don't know enough about this patient from the info given in the question. She might be non-compliant and maybe hasn't been dialyzed in a while. Our usual approach is to use fluids sparingly in CRF anyway. Besides, why give fluid when you can give blood? That is what she needs. If she is dry and we proceed with fluids, we could further hemo-dilute her and we may now be dealing with a Hgb in the 3's. :eek5:

I would also avoid beta blockers. If we are giving them just for the sake of slowing down her HR, again why don't we just give the blood? She needs red cell volume. And furthermore, the blood won't drop her BP like a BB might.

I'm sticking to my guns on this one. PRBCs all the way. That will fix all the symptoms.

TranMan
08-13-2006, 09:49 PM
OK you guys are right on the blood, I can't argue that. But I would agree that we don't have enough info on this patient. These scenarios that I'm talking about may seem to complicate the picture, but I just want you guys thinking of the bigger picture.

Noncompliant with HD = death. Most CRF patients are compliant with HD. It is very likely that she just had dialysis and is dry. I don't know for sure, but I have seen this scenario often. Patient comes to surgery day of dialysis dry and hypovolemic. IF this is the case, fluids would help her immediate problem until blood is available. Many young & healthy people if not hypovolemic will tolerate a Hgb of 7 no problem. She's young but not healthy. Without knowing if she's hypovolemic or not, you can't state fluids would harm her. If this is the case, I know fluids would help. But then again, we are not given that info. Just setting up a different scenario to get us thinking.

Other info I'd like to know is when did her CP start. If she's been having them for the last 4 hours, waiting another 20-40mins for blood to arrive won't kill her. If she just started having them, waiting for blood could kill her. See what I'm saying? What if...she just started having the CP 2 mins ago and she told you she had dialysis earlier today. Would you wait for the blood to come in 30mins and withhold fluid? If this was the situation, I would give fluids right away. Many a CRNA and Doc live by the creed that most problems can be solved with more fluid or tape. This is a bit of humor that holds some truth.
I agree with both that BBs are not a good idea since she is likely dry and it will make her worse. With the fluids and blood, her HR would likely come down.
Now you take a patient who is not hypovolemic (CVP ~10) and tachying away at 130-140 bpm because of her CP, I wouldn't say that I'm not gonna give her a 1-2mg of metoprolol or 10mg of Esmolol. They are B1 specific and would not VD her via B2 receptors. Her CO would also come down slightly b/c of the decrease HR.

Don't forget that not only is Hypotension bad for this situation, but so is Hypertension. In the face of CP, a Heart tachying away against tight pipes increases workload and oxygen demand with less supply. This too is a dangerous situation. Either extremes is bad for the heart. Depending on where she's at, we may have to temporarily treat her HD while waiting for the blood.

Mike, I have the 1997-1999 ACLS book. Waiting for the new one to come out this August. Under Indications for NTG, I see (paraphrased) SL NTG is the DOC for Tx of anginal episode. Effective for exertion as well as rest angina. It doesn't mention that it is only indicated/effective for coronary vasopasm.

My ACLS book also goes onto say "NTG should be used cautiously in patients with acute MI b/c it may induce hypotension, which can comprimise coronary artery perfusion and aggravate myocardial ischemia. A reduction in blood pressure of 10% or less has been deemed safe in patients with CAD."

Again, I would only try a SL NTG pill if her VS were stable (ie good BP) But I understand where your coming from. Let me clearly say I would not give her IV NTG regardless of her BP, good or bad. I was only thinking SL pill b/c I know it works quick (a couple of mins.) and only if her BP was stable. This will allow me to address her CP issue now. Again, Blood is the correct answer here, but waiting for blood could be the death of her as well. NTG also predominately VDs veins over Arteries, so a SL tablet would not likely drop a stable BP more than 10% anyway. Also I am thinking any more than 10% BP drop can also be easily reversed using a bit of Neosynephrine. Sure I don't want to Treat my overcorrection, but it's not the 1st or last time I've had to do that. Not saying this is the way to treat such a patient, but it's something I would try without fearing that I would be doing more harm. Also SL NTG is not the priority here and is rarely available around the OR anyway. Oxygen, possible fluids and/or BBs, 12 Lead EKG, labs (CKMB, total CK, Trop I), notify Cardiologist. Don't be too suprise if the Cardiologist orders you to give this patient a B1 specific BB like metoprolol. They love this protocol for CP.
A lot of these situations we all run into in the OR are rarely black and white. All to often they are grey and more grey. You always won't be able to definitely know or treat a problem. There are often many variables involved and you're are force to choose with limited knowledge the lesser of 2 evils. Which will give the patient maximal benefit with minimal harm.
I have been in many of these situations and have had to change gears back and forth after discussing the situation with other colleagues. Sometimes I'm right and sometimes I'm wrong. No shame in that. I just want to do what's best for the patient.

Again, this is good discussion and I am thrilled to see you guys posting quality info. I hope more people take a jab at this thread.

MmacFN
08-13-2006, 11:34 PM
Hey Tran well written

Well, you had mentioned this"

Mike, I have the 1997-1999 ACLS book. Waiting for the new one to come out this August. Under Indications for NTG, I see (paraphrased) SL NTG is the DOC for Tx of anginal episode. Effective for exertion as well as rest angina. It doesn't mention that it is only indicated/effective for coronary vasopasm.

I am regional faculty for AHA ACLS and PALS. Ive been teaching the new guidelines in my classes for about 3 months now. All three types of angina stable, unstable, and variant (Prinzmetal's) origionate from the same cause, myocardial ischemia. This ischemia is oft caused by coronary spasm, transient clot or increased demand with a clot decreasing ability to supply oxygenated blood to myocardium. The mechanism of action for ntg is exactly the same in all 3, smooth muscle relaxation supposedly dilating the coronaries allowing blood to flow past the clot or relax the spasm. In anycase, the research on ntg shows it has no effect on patient outcomes but also dosent harm (mostly, more on that in a sec).

My ACLS book also goes onto say "NTG should be used cautiously in patients with acute MI b/c it may induce hypotension, which can comprimise coronary artery perfusion and aggravate myocardial ischemia. A reduction in blood pressure of 10% or less has been deemed safe in patients with CAD."

The reason for this is IWMI with RVI. In approx. 40% of inferior wall MIs the right ventricle is involved and this is called a cocurrent Right Ventricle MI. Due to the small size and realtive easy work of the right ventricle, it is weak and relies on filling in order to push blood to the lungs via the pulmonary artery. This makes sense as there is no afterload against which the RV has to work like there is for the LV in the absence of pathology (pulmonary hypertension). This being the case, if you do anything which decreases preload you can have a signifigant drop in pressure due to the infarcted RV. No preload to lungs = no CO from LV.

Secondly, there is the risk of dropping the MAP such that it would cause an essential coronary steal. In some patients, microvascular vasodilation during exercise or pharmacological stimulation leads to a decrease of blood flow to the collateral-dependent myocardium, an observation described as coronary steal. This can cause a severe worsening of chest pain. There are no "magic numbers" for BP but it has been documented that coronary steal probably occurs with systolic BPs < 90 and MAPs < 75-80.

Dropping BP in anycase greater than 10% is typically contraindicated due to the incidence or arterio- and vasospasm. There is also a concurrent reflex HTN that occurs due to this. The only time this isnt an issue is probably when patients are under anesthesia as the reflex spasm is blunted.

In regards to to S/L vs IV nitro there is a signifigant difference. The s/l ntg tab is absorbed as fast as IV ntg is and provides 400 mcgs per pill within a 3-5 min period. IV ntg is typically started at 10 mcg/min for 60 mcg an hour with a 10 mcg increase every 5 minutes. In general, IV ntg is considerablly safer in the patient with a BP that is marginal to begin with because it can be stopped at anypoint where the s/l ntg cannot be taken back. The tx is, of course, fluid bolus to increase preload but once the BP drops and ischemia increases the damage may well be done by the time BP is back to norm with the fluids.

Without knowing if she's hypovolemic or not, you can't state fluids would harm her.

Sure, in a different scenario I would agree. However, in this one I would say fluids are contrindicated based on the information provided. I dont need to know her vitals to make that determination because the hx confirms the problem "days of SOB" lupus (which often causes anemia), critically low hgb and the c/p now.

I also agree the average person who is a chronic anemic can tolerate a hgb of 7.0. In this case, its 4.5. this is acute anemia with a patient in distress. If you were to give her fluids, hypotension or not, this hgb will be hemodiluted and you would have done her no favors. Increasing the pressure does absolutely nothing if the hgb isnt increased. The fact is, the BP numbers are irrelevant when you know the hgb is 4.5. Adding fluid will only increase the workload and MVO2 demand yet the concurrent increase in BP will not change the Supply of O2 as the hgb is now 3.0. I would withhold the fluid regardless of when the c/p started knowing her hgb. This patient could not tolerate a fluid bolus and would likely have a negative outcome from it.

Now you take a patient who is not hypovolemic (CVP ~10) and tachying away at 130-140 bpm because of her CP, I wouldn't say that I'm not gonna give her a 1-2mg of metoprolol or 10mg of Esmolol. They are B1 specific and would not VD her via B2 receptors. Her CO would also come down slightly b/c of the decrease HR.

Hmm. Here is what i would wonder then. If you had a patient who was dehyrated but SVR was up so her BP was within low normal range and her HR was 140 with c/p would you give beta blockers because of her HR? Of course you wouldnt ;) To me, this particular case is representative of the same situation. Just as in the dehydrated pt who is compensating, if you knock out the compensatory mechanism the patient may well suffer. In this case, the compensation IS the SVR and HR. With such a low hgb slowing the HR would probably cause for c/p than allowing it to be tachy. We are often guilty as health care providers of not giving the body credit for its self-correction. If her hgb was normal i would give her beta blockers assuming the HR increase was due to endrogenous catecholamines caused by a fight or flight response.

This is an excellent discussion! Fun Fun!



OK you guys are right on the blood, I can't argue that. But I would agree that we don't have enough info on this patient. These scenarios that I'm talking about may seem to complicate the picture, but I just want you guys thinking of the bigger picture.

Noncompliant with HD = death. Most CRF patients are compliant with HD. It is very likely that she just had dialysis and is dry. I don't know for sure, but I have seen this scenario often. Patient comes to surgery day of dialysis dry and hypovolemic. IF this is the case, fluids would help her immediate problem until blood is available. Many young & healthy people if not hypovolemic will tolerate a Hgb of 7 no problem. She's young but not healthy. Without knowing if she's hypovolemic or not, you can't state fluids would harm her. If this is the case, I know fluids would help. But then again, we are not given that info. Just setting up a different scenario to get us thinking.

Other info I'd like to know is when did her CP start. If she's been having them for the last 4 hours, waiting another 20-40mins for blood to arrive won't kill her. If she just started having them, waiting for blood could kill her. See what I'm saying? What if...she just started having the CP 2 mins ago and she told you she had dialysis earlier today. Would you wait for the blood to come in 30mins and withhold fluid? If this was the situation, I would give fluids right away. Many a CRNA and Doc live by the creed that most problems can be solved with more fluid or tape. This is a bit of humor that holds some truth.
I agree with both that BBs are not a good idea since she is likely dry and it will make her worse. With the fluids and blood, her HR would likely come down.
Now you take a patient who is not hypovolemic (CVP ~10) and tachying away at 130-140 bpm because of her CP, I wouldn't say that I'm not gonna give her a 1-2mg of metoprolol or 10mg of Esmolol. They are B1 specific and would not VD her via B2 receptors. Her CO would also come down slightly b/c of the decrease HR.

Don't forget that not only is Hypotension bad for this situation, but so is Hypertension. In the face of CP, a Heart tachying away against tight pipes increases workload and oxygen demand with less supply. This too is a dangerous situation. Either extremes is bad for the heart. Depending on where she's at, we may have to temporarily treat her HD while waiting for the blood.

Mike, I have the 1997-1999 ACLS book. Waiting for the new one to come out this August. Under Indications for NTG, I see (paraphrased) SL NTG is the DOC for Tx of anginal episode. Effective for exertion as well as rest angina. It doesn't mention that it is only indicated/effective for coronary vasopasm.

My ACLS book also goes onto say "NTG should be used cautiously in patients with acute MI b/c it may induce hypotension, which can comprimise coronary artery perfusion and aggravate myocardial ischemia. A reduction in blood pressure of 10% or less has been deemed safe in patients with CAD."

Again, I would only try a SL NTG pill if her VS were stable (ie good BP) But I understand where your coming from. Let me clearly say I would not give her IV NTG regardless of her BP, good or bad. I was only thinking SL pill b/c I know it works quick (a couple of mins.) and only if her BP was stable. This will allow me to address her CP issue now. Again, Blood is the correct answer here, but waiting for blood could be the death of her as well. NTG also predominately VDs veins over Arteries, so a SL tablet would not likely drop a stable BP more than 10% anyway. Also I am thinking any more than 10% BP drop can also be easily reversed using a bit of Neosynephrine. Sure I don't want to Treat my overcorrection, but it's not the 1st or last time I've had to do that. Not saying this is the way to treat such a patient, but it's something I would try without fearing that I would be doing more harm. Also SL NTG is not the priority here and is rarely available around the OR anyway. Oxygen, possible fluids and/or BBs, 12 Lead EKG, labs (CKMB, total CK, Trop I), notify Cardiologist. Don't be too suprise if the Cardiologist orders you to give this patient a B1 specific BB like metoprolol. They love this protocol for CP.
A lot of these situations we all run into in the OR are rarely black and white. All to often they are grey and more grey. You always won't be able to definitely know or treat a problem. There are often many variables involved and you're are force to choose with limited knowledge the lesser of 2 evils. Which will give the patient maximal benefit with minimal harm.
I have been in many of these situations and have had to change gears back and forth after discussing the situation with other colleagues. Sometimes I'm right and sometimes I'm wrong. No shame in that. I just want to do what's best for the patient.

Again, this is good discussion and I am thrilled to see you guys posting quality info. I hope more people take a jab at this thread.

TranMan
08-14-2006, 10:30 PM
Mike, great info on NTG.

I thought the SL NTG would help, but should have looked up the dose. At 400ug I take back my suggestion. I'm glad they don't stock the OR with the stuff, otherwise I may have tried it. Seriously, I would look up a dose prior to giving it though. For the record, I have never given anyone SL NTG for chest pain regardless of the cause. I was thinking of a little relief for her CP if BP allowed it while waiting for the blood. Like I said, I would avoid IV NTG. Had no idea he SL NTG was worse. My inexperience with it lead me to believe it wasn't as potent, but it is actually more!

I also agree the average person who is a chronic anemic can tolerate a hgb of 7.0. In this case, its 4.5. this is acute anemia with a patient in distress.
Whoa my bad. I'm not sure what I was reading, but this whole time was thinking the original post said hgb of 7.5. I just looked at the post again of 4.5. Yes at 4.5 hemodiluting her would worsen her not help. I couldn't figure out why you were so concerned about diluting a hgb of 7.5. I'm gonna blame tiredness on my part.
I agree with you in not giving fluids with a hgb of 4.5. I was suggesting fluids cuz I thought she was 7.5. Sorry for the confusion. BTW, I nevered disagreed with the blood. I just know it takes up to 40mins to get and was thinking of things you could do in the mean time that would help and not harm. For this patient, there's little to do. Maybe in another scenario.

I think you misunderstood me on the BBs. You are right about not giving it to this patient b/c she needs the blood and not BBs. I was saying that BBs (B1 specific) wouldn't be harmful IF the patient was NOT hypovolemic ( a different case) and was tachy d/t the CP rather than compensating. Of course we wouldn't want to block the body's efforts at compensating. Again, only if I was sure she wasn't dry and that the tachycardia was worsening the CP/MI then I would give a small dose of a B1Bs.

OK I need to slow down and read these carefully. Sorry for the misadvice all. In a totally different case, where the patient's hgb is 7.5 then I could consider things like BBs, fluids.

MmacFN
08-14-2006, 10:38 PM
hehe

n/p Tran everyone has been there done that when it comes to misreading! It can be easy to do. :)

We are on the same page ;)

RN29306
08-15-2006, 02:34 PM
I know I'll get fried for this and I totally believe she needs PRBCs in this instance and that it really doesn't matter if you give her Epogen or not if during the time for Epogen to work she dies of an anemic MI, but I found this to be an interesting read in perhaps why the CCRN question bank is hesitant to give PRBCs.....

From the "Anesthesia and Co-Existing Disease":
Treatment of the anemia of chronic renal disease is with recombinant human erythropoietin eliminating the need for blood transfusions and avoiding the symptoms of anemia in most patients. Blood transfusions are avoided if possible, as the resultant sensitization to HLA anitgens makes kidney transplant less successful. The goal of erythropoietin therapy is to maintain the hemtocrit between 36-40%.

I'll say it again before anyone points it out, I think the above out of the book is fine for someone say that comes in asymptomatic and simply finds out he or she is anemic. But the instance given describes someone having anemic chest pain and needs PRBCs in an emergent fashion. I didn't realize the bolded sentence and that giving PRBCs had an impact on down-the-road kidney transplatation. Perhaps this is what the CCRN is concerned with, but I think they are missing the big picture here and is a totally bad example.

gobucks1013
08-15-2006, 02:51 PM
That is really good info. I didn't realize that problem existed either.

I hate to sound like a skeptic or as though I'm dissing the CCRN folks that developed this question, but I'm inclined to believe the Epogen answer is a mistake in this case. I doubt they deemed erythropoietin therapy appropriate for the reason you found in Co-Existing (which by the way has been one of my fave books during school;)).

Thanks for sharing the info. It's something we should all keep in mind throughout our practice!

Sue

Captain Quinn
08-15-2006, 05:03 PM
heya folks. Just wanted to let you know I passed and now am Captain Quinn CCRN. I did think I would've done better, I only got 100 out of 125. But passing is passing right?

I've learned a ton from this discussion. Thanks everyone!


Captain

gobucks1013
08-15-2006, 05:38 PM
Congrats Capt! :)

RN29306
08-15-2006, 07:02 PM
Hey man, congratulations on your passing the CCRN. Hopefully you got some financial incentive from your employer by achieving this...

MmacFN
08-15-2006, 08:34 PM
congratz!!

RAYMAN
08-17-2006, 01:56 PM
Congrats on the CCRN!

Don't forget, guys, there is also now darboepoetin. It is a pegylated version that is given once every two weeks. :yumyum:

FutrCRNA
09-10-2006, 09:55 PM
My roomie and I both say give PRBCs then epogen. We agree with the consensus - treat the acute issues first.