What is the diagnostic accuracy of pulsus paradoxus for cardiac tamponade?

A classic Step 1 associations is: increased pulsus paradoxus=cardiac tamponade. But like everything in medicine, it’s not that simple. An abnormal pulsus paradoxus is not really sensitive or specific for cardiac tamponade. Pulsus paradoxus may also be present in patients with labored breathing, asthma attacks, pulmonary hypertension, constrictive pericarditis, PE, etc. This summary cites one report that “15% pulsus paradoxus in the face of relative hypotension was found in 97% of patients with moderate or severe tamponade and only 6% of patients with absent or mild tamponade.”

This review in Clinical Cardiology describes pulsus paradoxus as the “end of a spectrum” in cardiac tamponade, which frames it as what it is: an exam finding that if present, means that it’s more likely the patient is ALREADY in tamponade and you should act quickly…but just because it’s absent doesn’t mean the patient does NOT have tamponade.  This study reports that NHYA Class III symptoms (comfortable at rest but significant symptoms impairing function) were significantly associated the development of cardiac tamponade, which seems like it would be obvious, but can help in ambiguous cases. In my anecdotal experience, this is true, and relative hypotension, a narrow pulse pressure, and distended neck veins have been more sensitive for predicting tamponade.

NB: when trying to figure out if a pulsus paradoxus is abnormal, 20-30 mm Hg is considered high. But remember to take the pulse pressure into account! If the pulse pressure is narrow (like 110/90), then a pulsus of even 10 mm Hg might be abnormal and warrants immediate ultrasound.

What are the PCSK9 inhibitors?

There are two that are FDA approved: alirocumab (Praluent) and evolocumab (Repatha).

What is the biological basis of PCSK9 inhibitors?

LDL-R (for receptor) is found on the surface of hepatocytes. These receptors pick out LDL-c from the circulation, lowering the LDL level in the bloodstream. That’s a good thing!

PCSK9 is a protein that balances out the effect of LDL-R by binding to LDL-R and getting it degraded, thereby not allowing LDL-c to get reabsorbed. This means LDL levels may go up. (See this illustration and explanation) The PCSK9 inhibitors (mAbs) bind to PCSK9, which allows LDL-R to keep doing it’s job, and keep LDL-c levels low.

Are PCSK9 inhibitors effective? 

Yes. They are especially effective at reducing LDL levels when combined with statins. This review goes into exhaustive detail about trial data. However, no one knows for sure if they, like statins, reduce mortality from cardiovascular disease.

What caveats do I need to know about these drugs? 

  • Injected, not in pill form. This may be a barrier for some patients who either can’t (or won’t) inject themselves
  • These drugs are expensive! A year’s supply of evolocucamb is estimated to cost about $14,500. It’s unclear how much of that may be covered by insurance
  • The most common side effects are nasopharyngitis, congestion, and myalgia, but there are concerns about allergic reactions (it’s a monoclonal antibody) and cognitive impairment (subjective, but was reported in the phase III trials).
  • Patients with severe kidney and liver disease were excluded from studies, so if, for example, you have a patient with cirrhosis who wants to start one of these medications, talk with their hepatologist
  • Long-term studies on these drugs are lacking; there is a Cochrane review that reports that overall, follow up times for PCSK9 inhibitor studies have been short (26 months at the longest) and there have been few reported events.

Is is safe to give tPA/thrombolytics to someone who just underwent cardiac catheterization?

At my institution, we recently discussed a case of a patient with acute stroke in the setting of cardiac catheterization (right femoral access). The decision to push tPA was a tricky one, because he had just been cathed. When is it ok? When is it NOT ok?

Here are relative and absolute contraindications (respectively) for giving tPA:


As you can see, arterial puncture at a noncompressible site is a relative contraindication for tPA. So depending on where the puncture site was…the typical site for an arterial stick in a catheterization is between the bifurcation of the SFA and PFA and the branching point of the inferior epigastric artery. Typical site=compressible, “high stick”=noncompressible. If there is a “high stick,” tPA will confer a much higher risk of RP bleed and hemorrhage, and should be avoided.

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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.