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
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!



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.

What’s the difference between dobutamine and dopamine?

These two medications SOUND similar, but are in different categories.

  Dobutamine Dopamine
Class Inotrope Vasopressor
Receptors affected B1 agonist A1 agonist (dose dependent)
Effect Increased cardiac contractility Vasoconstriction, increased systemic vascular resistance
Common uses “Tailored therapy” for heart failure, ?septic shock Septic shock (>8), cardiogenic shock (4-7), promoting urine flow (0.5-3)
Side effects Tachycardia, may even cause hypotension (mild vasodilation), do not use in patients with HOCM Tachycardia/VT, tachyphylaxis, ischemic limb necrosis (do not give through a peripheral IV)



Which QTc is the right one?


This post is for the psychiatry resident who asked me about a patient who had a Bazett’s QTc in the 510’s, but a Hodges QTc of 470:

Generally, we are concerned about QTc because torsades=bad.Practically speaking, a QTc >500 is something to be worried about.

A really shocking number of medications prolong the QTc, and just as a reminder, include things like antiarrhythmics, ondansetron, and haloperidol, but also Benadryl, erythromycin, tacrolimus, and TCAs.

What are the different formulas for QTc?

  • Bazett’s formula: QTC = QT / √ RR
  • Fredericia’s formula: QTC = QT / RR 1/3
  • Framingham formula: QTC = QT + 0.154 (1 – RR)
  • Hodges formula: QTC = QT + 1.75 (heart rate – 60)

Based on my expert Internet search, it is unclear which is the “best.” I also asked a couple of our attending cardiologists and cards enthusiasts, who didn’t have strong opinions.

The current clinical standard is the most widely used Bazett formula, but with this formula, there is a known overcorrection at high heart rates and undercorrection at lower heart rates. The Fridericia and Framingham correction formulae showed the best rate correction and significantly improved prediction of 30‐day and 1‐year mortality. With current clinical standards, Bazett overestimated the number of patients with potential dangerous QTc prolongation, which could lead to unnecessary safety measurements as withholding the patient of first‐choice medication.

That all being said: use the QTc that will give your patient the safest plan. And if you remain skeptical of a prolonged QTc in a clinically stable patient, get repeat EKGs until it’s…less prolonged…and your problem is solved.

Should I give this patient with unstable angina heparin?

One of the tenets of treatment of ACS (unstable angina, NSTEMI, STEMI) is treatment with an anticoagulant like heparin or enoxaparin. The “heparin vs. enoxaparin” issue is a totally different discussion. What this post addresses is a gray area: does every patient with unstable angina need to be started on a heparin drip?

Heparin is a medication that has potential side effects (bleeding, immune reaction) and takes time and resources (maintaining a patient on a drip, PTT draws).

I think that if a patient has had chest pain within the past 24 hours, then it would be prudent to start a heparin drip, as unstable angina can escalate into an NSTEMI on short notice. There are several high-risk features that should prompt a heparin drip (reference):

  • history of MI
  • EKG changes
  • abnormal stress test
  • a strong history suggestive of UA

What about aspirin? EVERY patient with suspected unstable angina should get 324 mg of aspirin. There is virtually no harm to giving a single dose of aspirin, so you might as well give it.

What’s the difference between a pacemaker and an ICD?

Pacemaker (PPM)


Cardiac resynchronization therapy (CRT) Implantable cardiac defibrillator (ICD)
Function Generate a new pacing node Bi-ventricular pacing Defibrillate in case of VT/VF
Associated with… Sick sinus syndrome, afib CHF, conduction disease (ventricular dysynchrony) CHF
Indications Chronic afib with symptomatic bradycardia CHF with EF <35% and NYHA class III-VI symptoms, new LBBB with QRS >150 msec CHF with EF <35%
Where are the leads? Subcutaneous or internal

-single chamber: 1 lead in the RA or RV
-dual chamber: 2 leads, in the RA and RV (thought to resemble natural rhythm more, there are pros/cons)
– triple pacemaker: less common, 3 leads in RA/RV/LV

Lead in the RV, LV 1 lead that may extend into the RA and RV