How to assimilate information accurately and why aortic dissections and PEs get missed- the pretest probability

Medical school and medical training teaches us that we do tests to confirm the presence or absence of disease. This is the wrong way to think about things. A better concept is to realise that we start with a certain pre-test probability of a disease, which is determined by the base rates of that disease in the population and the patient’s clinical history. Tests can only ever modify this pre-test probability into becoming more or less likely. At a certain point the disease may become so unlikely that testing for it causes more harm than good. This greater harm may come from radiation, reactions to things such as contrast dyes, harmful therapy that might be initiated as a result of a false positive result e.g. antibiotics for a blood culture result that is a contaminant, or simply the fact that time is wasted not pursuing the most likely diagnosis. Other times the disease remains so likely that you may have to pursue repeat testing (take for example the high false-negative rate of COVID swabs).

Consider this scenario. You are the on call house officer. You get paged to the ward to review a 35 year old patient who is having abdominal pain. He was admitted 6 hours ago with severe central chest pain that came on over a matter of seconds and lasted 2 hours. His troponins and ECG have been normal. He has now developed abdominal pain of the same severity and also reaching its peak over a matter of seconds. Concerned about the possibility of aortic dissection you look for mediastinal widening on the chest Xray, pulse defecits, or any neurological symptoms as you know these are the things to look for in a dissection. None of these things are present. Satisfied, you order further ECGs and troponins. The next day you find out he died overnight of an aortic dissection. The next day your consultant tells you “it just shows you how useless clinical exam findings are for aortic dissection- you can’t rely on them. Most dissections have a normal Xray!”

Is this correct? Are these clinical exam findings useless? Is the chest Xray normal in most dissections, as commonly quoted? Well, not quite. They are actually reasonably good tests, including the chest Xray (1,2). The problem is not taking into account the pre-test probability of an aortic dissection, which in this case is high based on the clinical history. Continue reading

The test is not the disease

When I was a trainee intern we had a patient on my general medical placement present with 2 days of right arm swelling and tenderness, with dilated superficial veins over her arm and upper chest. Her d-dimer was normal. She had an ultrasound of the upper limbs looking for a DVT. This was negative. With a negative d-dimer and USS we were all ready to discharge the patient home (who was otherwise well), however the consultant, a mentor of mine, insisted on a CT venogram. We all rolled our eyes. Eye rolling turned into eye widening as the scan showed the subclavian vein thrombosis we had all been missing. Continue reading

Why shock is not all about the blood pressure


When calling the surgical or gastro registrar on the phone, one of the surefire questions you will be asked is ‘is the patient hemodynamically stable?’ This is no doubt an important question but unfortunately hemodynamic stability means different things to different people. There is generally a lack of willingness to look beyond a ‘normal’ vs ‘low’ blood pressure.

It should be made clear that hypotension is a sign of ‘decompensated’ shock. The idea that hypotension is a late sign of shock has been long recognized in the trauma literature where 18% of penetrating abdominal trauma can have over 750ml of blood in the abdomen despite normal vital signs (including 7% who had over 1500ml). In the majority of patients evidence of tissue hypoperfusion precedes the development of hypotension (1).

Why is this? Well, it is all about the concept that pressure does not equal flow. The body is quite adept at trying to maintain a normal blood pressure through various compensatory mechanism, chief amongst which is the sympathetic response. But this does not tell us whether perfusion at the tissue level is adequate- inadequacy of this is after all the definition of shock. This is especially true in young patients where the compensatory mechanisms are quite strong and blood pressure may be preserved till late in the piece, as illustrated by the graph at the top, of my creation (credit to MS paint).

This phenomenon is true in all situations- not just trauma- so it is relevant to the patients you will be seeing on ward calls. For example ‘normotensive shock’ is recognized in sepsis (2), cardiogenic shock (3), and just generally (4). What then are the signs of ‘normotensive shock’ you should look out for? Well, these are simply the signs of inadequate tissue perfusion- cool and clammy skin, oliguria, mental state changes and elevated lactate. Other signs which may accompany this that are not necessarily indicative of hypoperfusion but that do indicate a compensatory response are tachycardia and tachypnea.

It is also important to note two slightly related things. Firstly, a systolic blood pressure of 110 may be normal for a 20 year old but grossly hypotensive for a 70 year old with chronic hypertension. Secondly, it is sometimes difficult to tell whether a ‘soft’ blood pressure in a young person is just normal for them or whether they are actually hypotensive- a normal heart rate cannot be used to reassure you in this instance because not uncommonly shocked patients may have paradoxically increased parasympathetic tone (1) the exact mechanism for which is unclear. Older patients may also be on Beta Blockers.

The conclusion in all of this- next time you call the gastro reg with a patient who has vomited blood and is clammy with a lactate of 4 but has a normal blood pressure, the answer to the question ‘is the patient hemodynamically stable?’ is a ‘HELL NAH”.

Today’s post may sound basic but it is all about fundamentals- a fundamental which is often simply not done. Rather than spending 10 minutes documenting dual heart sounds, look and feel for the signs of shock!

Till next time.



  1. Identification and Resuscitation of the Trauma Patient in Shock Michael N. Cocchi, MDa , Edward Kimlin, MDa , Mark Walsh, MDb , Michael W. Donnino, MD. Emerg Med Clin N Am 25 (2007) 623–642
  2. Septic Shock. Advances in Diagnosis and Treatment. Christopher W. Seymour, MD, MSc and Matthew R. Rosengart, MD, MPH. JAMA. 2015 Aug 18; 314(7): 708–717.
  3. Menon V et al. Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: Report of the SHOCK trial registry. Am J Med 2000 Apr 1 108 374380
  4. Approach to Hemodynamic Shock and Vasopressors. Stefan Herget-Rosenthal, Fuat Saner and Lakhmir S. Chawla. CJASN March 2008, 3 (2) 546-553; DOI:

Jugular Venous PRESSURE- so why do we use it to assess volume?

There is perhaps no physical exam sign more enthused about by consultants and more bluffed by students than the jugular venous pressure (JVP). While initially I was not a believer, I have come recently to appreciate its usefulness. This epiphany did not occur without significant time spent perusing the literature and finally coming to understand what the JVP does and does not tell you.

The first point to make abundantly clear is that JVP is simply a surrogate for central venous pressure (CVP). This roughly estimates the right atrial pressure. The obvious first question a sceptic would ask is how good a job it does at this?

Well, if we refer to the JAMA rational clinical exam series from 2009 (1), a systematic review of sorts on different examination findings, we see that the JVP, and hepatojugular reflux, correlates reasonably well with invasively measured CVP. The table of likelihood ratios below combines findings from the three studies addressing this question, including one where hilariously medical students were better at estimating CVP than staff physicians.

Credit: Reference (1)

Continue reading

What does atypical chest pain mean? Part 1

“I just had my dinner, this hospital food is terrible by the way, look at this, what is this?….anyway  a couple minutes later the pain just grabbed me here”, he says rubbing the back of four fat, tobacco stained fingers up and down from his throat to his epigastrium.

“And you were just sitting down in your chair, right?” – “Yeah. I get this all the time though at home though”.

You sit down to wearily write your note; ‘Impression: Atypical chest pain, probably GORD. Plan: Serial troponins to exclude cardiac’.

Of course, the pain only lasted 10 minutes, so your troponins will probably be negative. So is the pain atypical?

Atypical is another in a series of medical terms that we use all the time which don’t really mean anything- or rather mean different things for different people and should probably be abandoned (1). Some clinicians even use it in order to facilitate admitting the patient to hospital (1).

The question of what exactly is ‘typical’ for angina, or how frequent something needs to be in order to be considered typical, is an interesting one, which provides fodder for many future blog posts. Surely though, positional pain or pain related to food can’t be angina? At least this is kind of what I have been given to understand. Not so easy apparently.

We will run through 3 examples of chest pain presentations well described in the literature which are associated with severe CAD, which many people might consider to be atypical. They go to show that few patients read the medical school textbook. Or maybe the medical school textbook is incomplete.

Post-prandial angina

8.6% of patients with ischemic heart disease experience post prandial angina (angina after meals), with higher incidence of three vessel disease and left main disease, and lower ejection fractions on average. Such angina is more likely to occur after the dinner meal (2). The mechanism is unclear but is thought to be related to either redistribution of blood flow to the gut or increases in cardiac output following meals. Increases in heart rate, blood pressure and systemic vascular resistance are all observed at the onset of angina, which usually occurs within 25 minutes of the meal (2,3). Continue reading

STEMI equivalents

It is another weary on call night, where annoyingly everyone has decided to have chest pain. As you sit down to scrutinise probably your tenth ECG, some ST elevation in lead AVR catches your eye. This jolts you from your torpor. Real pathology? You get your registrar to swing by and have a look. He furrows his brow as he looks down his nose at you, saying;

“ Remember, young padawan, one lead is no lead.” He reminds you of the STEMI criteria (1), which must be present in at least 2 anatomically contiguous leads:

  1. ≥1 mm (0.1 mV) of ST segment elevation in the limb leads
  2. ≥ 2 mm elevation in the precordial leads
  3. New LBBB

It turns out this teaching is not quite complete and will eventually cause you to miss some significant coronary occlusions. For you see, the classification of MIs into STEMI and NSTEMI is not some random division based on the aesthetic s of the ECG waveform. STEMI represents total occlusion of a coronary artery, therefore high risk of cardiogenic shock and death, and therefore benefit of immediate revascularisation. NSTEMI, on the other hand, an incomplete blockage, has failed to show benefit from immediate angiography (2).

The key point is that there are other ECG patterns that are also indicative of coronary occlusion which are simply not taught, mostly because they have only been described in the last decade or two, and unfortunately medicine can be slow to catch up. These “STEMI equivalents” cannot just be sat on, waiting for the troponin.


To start with, new LBBB is not even considered a STEMI criterion anymore (3). You can however interpret ST segments in a LBBB, despite what you might have been told, by utilising the ‘Scarbossi Criteria’. These will be covered in a separate post.

De Winter’s Waves

de winter
[Image Credit:]
ST depression indicating NSTEMI? Think again.

A decade ago, De Winter et al described the above ECG pattern consisting of  “1-to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. In most patients there was a 1- to 2-mm ST-elevation in lead aVR” (4). Continue reading