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In a previous blog we looked at the following patient who presented to the emergency department:

62 year old male presents to the Emergency Department with what he calls a flare-up of his congestive cardiac failure.

He states he is short of breath. He is a frequent presenter to the department with this complaint. He has not taken his frusemide for the past 48hours. He states that he feels very tired.

He is a well looking man with normal vitals. Heart sounds dual, no murmur. Normal JVP, bilateral pitting oedema to mid calves. Chest clear. Abdomen soft. His ECG and CXR are normal. Bloods including a troponin are normal.

I’m unsure of the diagnosis, but given he hasn’t taken his frusemide, I treat him with that. I am going to discharge him, however it is late at night and he lives alone, so we decide to keep him in the department overnight. In the morning, he looks well and feels better, but still lethargic, ECG is unchanged, but for some reason someone does a follow-up troponin and it is 4.

He is diagnosed with a NSTEMI and sent to cardiology.

I now ask the question, could it have been a pulmonary embolism and not a NSTEMI?

Certainly if we look at this case, we see that the patient had dyspnoea with a normal chest on auscultation and on chest X-ray. Hmmm.

What are the risk factors for pulmonary embolism? Well, we know of the classic ones of anything affecting Virchow’s triad. There are the hereditary factors of Protein C and S deficiency as well as others and the acquired factors such as immobility, recent surgery, cancer and others.

This patient had congestive cardiac failure (CCF). Is that a risk factor? As it turns out it is. In a population based study by Helt et al (Arch Intern med. 2002;162:1245-1248), the attributable risk associated with venous thromboembolism was 9.5%. So there is an increased risk in CCF.

What about symptoms and signs? Surely they would help.

Stein et al (Chest 1991;100:598-603) looked at patients with a suspected pulmonary embolism (PE) and with no previous evidence of cardiac or respiratory disease.

He then looked at the symptoms in patients with PE(n=117) and those without PE(n=248) as follows:

Dyspnoea – 73% with PE had it, but 72% of those with no PE also had dyspnoea.

Pleuritic Pain – 66% with a PE had it, and 59% without a PE also had it.

Leg Swelling – 28% with PE had it and 22% without PE had it.

None statistically significant.

Well how about signs, surely they must help?

Tachypnoea – 70% with PE had it as did 68% of those without PE.

Tachycardia – 30% with PE had it as did 24% of those without PE.

Deep venous Thrombosis – 11% had it in both groups.

Nothing was statistically significant.

What is interesting is that 97% of patients with a PE had.






So be on the lookout for those.

How about the TROPONIN rise – surely a pulmonary embolism can’t cause that?

Well, as it turns out it can. Although we are unsure of the pathophysiology, it is postulated that it is due to increase in right ventricular afterload and irreversible ischaemia. It is also a predictor of in-hospital death (Giannitsis et al Circulation;2000;102:211-217). It’s important to say that the troponin rose in a group of patients that had suffered at least a moderate if not a large PE.

Those with a small PE may not have a troponin rise.

So the level of troponin rise is important as a rise of >0.1 is a potential predictor of mortality, however in the above study, none of the troponins rose above 1.0.

One other important characteristic was that the troponins rose earlier, ie., within 3-5 hours, in PE.

Therefore it is important to note that although troponin can rise, it usually does not do so, to as high a level as when true cardiac ischaemia occurs.

So, how about my 62 year old gentleman – could it have been a PE? The answer is yes it could. What is against it, is the level of rise of troponin was probably too high for someone looking so well.

Could it have been a thoracic dissection?

We’ll look at that next time.


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