I came across this article in the Canadian Journal of Cardiology (doesn't everyone read it? No? I was directed there by a quick podcast from Amal Mattu), which provides a great approach to the common presentation of syncope.
Until now, I was following the wisdom of Dr Kylie Brown, who imparted this strategic mnemonic to remember the San Francisco syncope rule:
Congestive cardiac failure
ECG changes (long QTc, heart block, WPW, Brugada, LVH)
Systolic BP low
Short of breath
This, and many other, risk stratification devices have been developed, with ALiEM providing a good summary of these. Life in the Fast Lane, as always, has a great summary of syncope, with the helpful HEAD HEART VESSELS mnemonic of causes (originally from Syncope, Vertigo and Dizziness chapter by William F Young Jr in Emergency Medicine Secrets; see comments below).
What this article brings to the table is a stepwise approach to risk stratification, with the vast majority of presentations requiring only an ECG and able to be discharged. The majority of diagnoses for causes of syncope are made in the ED, and admission may only have limited additional value.
Syncope is caused by cerebral hypoperfusion. Most fainting is simply vasovagal syncope and the challenge lies in identifying the few patients who have potentially life-threatening causes of syncope. Syncope patients constitute 1%-2% of emergency department visits and approximately 30%-50% are admitted to hospital. The known causes are vasovagal syncope (50%), and orthostatic hypotension and cardiac syncope (7% each). Structural heart disease is noted in 3%. The 30-day mortality is only 0.7%, and the 30-day adverse outcome is 4.5%. Risk stratification and diagnosis are important. High-risk patients might have a fatal cause, and low-risk patients do not. Risk markers include syncope while supine or with marked exertion, without a prodrome, with structural heart disease or heart failure, with a family history of sudden death, and with an abnormal electrocardiographic findings. Ischemic heart disease and hypotension are also risk factors. The history captures the preceding situation or activity, prodromal symptoms, and symptoms after syncope. Very simple diagnostic scores exist to help. Investigations beyond an electrocardiogram are not usually needed, and aim to: (1) assess whether a structural substrate exists; (2) capture risk factor data, assuming it is related to the syncope; (3) capture data during clinical syncope; and (4) induce syncope under controlled conditions. The most commonly used tests are implantable loop recorders, which establish a diagnosis in 30%-40% of patients over 2-3 years; and tilt table testing. Neither are needed most of the time. A good history provides more useful and more accurate information in most patients.
They present an algorithm for management that steps through the risk factors and suggested disposition based on these.
The questions to consider when approaching a presentation of syncope are:
- Is it really syncope?
- Does the patient have high risk markers? The absence of any of these suggests a very low risk of a significant cardiac cause for their syncope.
- Is the history suggestive of vasovagal or orthostatic syncope?
If the patient did not have true syncope, does not have any high risk markers, or has a presentation consistent with vasovagal or orthostatic syncope, they have a very low risk for cardiac cause for their syncope, and admission can be avoided.
A good history provides more useful and more accurate information in most patients.