What is a “MIBI scan” and who should get one?

“MIBI” is short for sestamibi, a mildly radioactive compound that is used to perform nuclear scans. Sestamibi = technetium-99 = methoxy-isobutyl-isonitrile.

Thallium = TI 201 is another radioactive agent that is used in myocardial perfusions scans.

Either of these agents can be used to perform a nuclear myocardial perfusion rest-stress test, which may also be referred to as single photon emission computed tomography (SPECT). They are equally sensitive in detecting areas of ischemia or scarring. Thallium may be more sensitive for detecting viable myocardium because it is lower energy and redistributes in tissue; it does not remain fixed in myocytes. However, it also has a much longer half-life (73 hours opposed to 6 hours for sestamibi).

These radioactive agents that are used to image the heart are different from the pharmacological agents that are used to stress the heart. Pharmacological agents include adenosine, dobutamine, persantine.

Stress modalities: exercise, pharmacological (*note the terminology is different than in the borrowed image below)

Imaging modalities: EKG, ECHO, nuclear, CT

Imaging modality
Stress modality EKG ECHO Nuclear
Exercise      
Pharmacological (adenosine, dobutamine, persantine)    

You can mix and match any of these to create a stress test that fits your patient’s condition/contraindications best!

Reference 

 

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How should I interpret pulse pressure?

How do pulse pressure and mean arterial pressure differ, and how are they related? 

Mean arterial pressure (MAP)
= 1/3*(systolic blood pressure) + 2/3*(diastolic blood pressure) 
= cardiac output [heart rate*stroke volume] * systemic vascular resistance 
= ¼ diastolic blood pressure + 0.4*(pulse pressure). 

MAP is an important way to measure blood pressure; MAP is what we use to titrate pressors and measure perfusion. However, consider the case of person #1 with a BP 130/80 and person #2 with a BP 160/60. Both of them have a MAP of 100 mm Hg by the first calculation, but clearly, the blood pressures are different–what is different is the originating pressure from the left ventricle, and pulse pressure correlates better with this. This chapter explains the factors that contribute to pulse pressure elegantly, but the simple equation is:

Pulse pressure (PP) = systolic blood pressure – diastolic blood pressure

What is a “high” PP and what is a “low” PP, and what do they signify?

There is no specific cut-off that I could find. However, if you think about 120/80 as a “normal” blood pressure, that indicates that a “normal” PP=40. The study cited below uses a cutoff of <30 mm Hg as a “low” PP. Therefore, it’s reasonable to think that a “high” PP is >50 and a “low” PP is <30.

Traditionally, we have been warned against high pulse pressure. Why? High PP is associated with increased cardiovascular death, as well as CAD, MI, and heart failure, because it signifies either/and a high systolic blood pressure and low diastolic blood pressure. In addition to heart failure, other conditions associated with a high PP include severe anemia, sepsis, thyrotoxicosis, aortic dissection, aortic regurgitation, neurological conditions (i.e. hemorrhage) or AVMs (things that might cause a high output heart failure state).

However, low PP can also be dangerous. If you think about it, someone with a systolic and diastolic blood pressure that are almost the same is in a “low flow” state; their blood pressure demonstrates they can’t push blood forward effectively. This study is one report about an association between low PP and cardiovascular death in patients with heart failure, specifically, advanced heart failure (NYHA Class III-IV). In addition to advanced heart failure, other conditions associated with a low PP include cardiogenic shock, tamponade, and severe aortic stenosis. 

Bonus question: what is “true MAP” and how is it calculated? “True MAP” is direct measurement of pulsatile flow…think about that…it’s measured through tonometry, usually of the brachial artery, which involves placement of an arterial line.

How much sliding scale insulin should I give?

The American Diabetes Association goals for inpatient management of diabetes can be found here. The goal fingerstick for non-critically ill patients is 140-180 mg/dL. Even though we don’t always do it (read: rarely do it), it is ideal to calculate a patient’s inpatient insulin regimen based on body weight. Sliding scales should not be the sole form of insulin administration as there is actually no evidence to support their use!

Sliding scale insulin is extra coverage and usually consists of short-acting insulin like lispro (Humalog) or insulin aspart (Novolog). These forms of insulin start working in 15-60 minues and peak in 1-3 hours.

Short-acting insulin vs. regular insulin for a sliding scale? Studies have found that there is no significant difference in outcomes, but generally regular insulin should be used for patients who are NPO, on TPN or continuous tube feeds.

To create an insulin sliding scale, calculate your patient’s “insulin sensitivity factor.”

ISF = 1700/total daily dose of insulin

For example: if someone takes 20 U insulin glargine (Lantus) and 2 U insulin lispro (Humalog) with meals, their total daily dose of insulin is 20 + 2*3= 26. 1700/26=65, so 1 U Humalog for sliding scale would be expected to lower their fingerstick glucose by 65.

The University of Pittsburgh put out a patient safety study with a preset protocol for low, moderate, and high-risk patient sliding scales that can be found here.

Important note: bedtime or “QHS” sliding scales should, generally speaking, be more gentle than mealtime sliding scales, as there is a risk for overnight hypoglycemia.

Help with mixing studies

You have a patient who presents with persistent bleeding, and heme/onc recommends a workup for bleeding disorders. One of the tests is a “mixing study.” This literally consists of mixing a patient’s plasma with normal plasma to see if there is a factor deficiency (aPTT corrects) or factor inhibitor (aPTT does not correct).

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Tatineni, Machenda

This is a good overview of a general approach to an abnormal PT or aPTT. (The whole PDF is a good review of workup for hypercoagulable disorders.)

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My patient has a penicillin allergy…what antibiotic do I choose?

Something like 10% of the US population reports an allergy to penicillin. However, as this CDC info sheet makes clear, <1% are truly allergic. That being said, if someone has ever had a reported reaction to a penicillin, think carefully before prescribing!

  1. Remind me what the penicillins are again? Obviously, anything with “penicillin” in the name (like penicillin G, benzathine penicillin), and derivatives like nafcillin, oxacillin, ampicillin, amoxicillin, and extended-spectrum forms like piperacillin and ticaricillin. The latter are important because they are found in medications like Zosyn and Unasyn which we typically think of as “big gun” antibiotics.
  2. Is it a true drug allergy? The difference between anaphylaxis and drug side effect can be life-saving. Allergy is an IgE-mediated reaction characterized by vasodilation (drop in blood pressure, flushing, tachycardia) and edema (wheezing, abdominal pain/gut edema) and in its most severe form, may cause anaphylactic shock. Hives are characteristic. On the other hand, side effects may be described as a “red rash,” nausea/diarrhea, dizziness, yeast infection. A family history of penicillin allergy doesn’t matter. Not discussed here are delayed allergic reactions, like SJS/TEN, serum sickness, DRESS, or other forms of organ damage. If someone has had a delayed reaction, they should never be given penicillins.
    • Questions to ask:
      • How quickly did your reaction happen? (Minutes, hours, days)
      • Did you have shortness of breath or swelling?
      • If there was a rash, was there blistering or peeling?
      • Did your doctors tell you there was organ damage? (liver, kidney dysfunction, changes in the blood counts, etc?)
  3. How long has it been since they took a penicillin? The data shows that over 80% of people who had a penicillin allergy 10 years ago won’t be allergic if they are given a penicillin drug again. Allergies change over the course of a person’s life, and sometimes what you were allergic to as a kid is no longer a problem.
  4. What are the risks of cross-sensitivity with cephalosporins and carbapenems? There is a reported 10% incidence of cross-sensitivity among penicillins, cephalosporins, and carbapenems (beta-lactam antibiotics). I found this review helpful in preparing this post, and one of the key takeaways is: “Persons who make IgE in response to cephalosporins seem to produce it only in response to a particular cephalosporin, whereas persons who make clinically significant IgE in response to penicillin tend to react to core penicillin break-down products.”
  5. What’s the deal with skin testing? Penicillin skin sensitivity testing is a critical tool for determining if someone is still at risk for an allergic reaction. It can be ordered for inpatients or outpatients, and can be done in conjunction with a pharmacist or allergist. If you are skeptical about the allergy (and brave) you can order a “test dose” or graded challenge of the medication, and if the patient tolerates it, put them on regular doses.
  6. I don’t have the time/energy to do skin testing, what can I use instead? People who are allergic to penicillin are more likely to have a reaction to a lower generation cephalosporin than higher generation. Cephalosporins to avoid: cephalexin, ceftriaxone, and cefpodoxime. Cefazolin and cefuroxime, because of their side chains, are less likely to react.  This review describes people who can be trialed on alternative beta-lactams and people who should continue to have complete avoidance. Going outside the beta-lactams, the world is your oyster: quinolones, vancomycin (or daptomycin), sulfa drugs (Bactrim), and aminoglycosides (gentamicin).

 

Treating ESBL

Let’s say you get a septic patient who has a history of “ESBL.” What does this mean, and what can you empirically treat with?

ESBL, or extended spectrum beta lactamases, refers to a group of bacteria that have developed resistance against beta-lactam antibiotics: penicillins, cephalosporins, and aztreonam. Common suspects include fecal and urinary organisms like E. coli and Klebsiella

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If you can’t use penicillins (piperacillin-tazobactam or Zosyn) or cephalosporins (which include heavy hitters like cefepime and ceftazidime), what are you left with? Carbapenems: meropenem is used more frequently, although imipenem and ertapenem are also options. It is sometimes possible to “power through” with high-dose cefepime (2 g q8h) but it’s best to have bacterial sensitivities before plowing down this path.

You also have the option of adding on fosfomycin and/or tigecycline sensitivities if you are stuck treating a difficult UTI.

Can you run a pressor through a peripheral IV?

We’ve all heard horror stories of patients getting digital necrosis from peripheral pressors:

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theangiologist.com

However, the data shows that you CAN run pressors safely through peripheral IVs with close monitoring and proper selection of an IV site. How?

The Journal of Critical Care from 2015 reviewed the available literature of the use of peripheral pressors in adults.This review concluded that there are very rare side effects in the first 6 hours of use, and that best practice is to place IVs in veins >4 mm in diameter (use an ultrasound to confirm!) and monitor at least every 2 hours for extravasation. There was poor quality data reporting adverse outcomes from site of administration of pressors–out of 85 studies included, there was only one randomized study. Furthermore, as this study notes, the rate of adverse effects is low when a good-sized vein in the forearm is used, and pressors can be restarted at another peripheral site when extravasation does occur.