Syncope- The Podcast
You are working in the Emergency Department when a usually fit and well 28 year old footballer presents saying he has had a fainting episode whilst playing football. The triage nurse asks you if he can wait to be seen in the waiting room, or if he needs seeing more urgently
- Consider the physiology of syncope and how this may guide our investigations.
- Understand how to approach the patient with chest pain.
- Think about the main causes of syncope.
A transient loss of consciousness caused by global cerebral hypoperfusion
There are two very important words in this statement:
- Transient – a syncopal episode is short lived – usually less than a minute – and accompanied by a quick and complete recovery
- Global – it is all of the brain that is affected.
Cerebral Perfusion Pressure (CPP) = Mean Arterial Blood Pressure – Intracranial Pressure
As there are very few things that cause a transient and significant change in intracranial pressure we can discount it to some extent. So…
Cerebral Perfusion Pressure ∝ Mean Arterial Blood Pressure
Remembering back to the shock podcast we also know that
Mean Arterial Blood Pressure = Heart Rate x Stroke Volume x Systemic Vascular Resistance
Cerebral Perfusion Pressure ∝ Heart Rate x Stroke Volume x Systemic Vascular Resistance
Therefore any cause of syncope must be due to a reduction in heart rate and/or stroke volume and/or total peripheral resistance.
We can now use all of this information to consider about the causes of syncope and therefore how we got about treating them.
Remember that one or more of these conditions could be present and it is simply the addition of another that ‘tips the patient over the edge’. For example, the patient who is slowly bleeding for a leaking aortic aneurysm, (dropping their SV) who then strains to go to the toilet.
Let’s think about what could cause a temporary drop in heart rate, sufficient to cause a drop in blood pressure.
The heart is dependant on electrical activity to initiate contraction and relaxation of the ventricles. When this electrical activity is disrupted the heart simply won’t beat, or beat as much as we need.
Bifasicular, Trifasicular and Complete Heart Block – refers to the presence of conduction delay in all three fascicles below the AV node manifesting as bifascicular block and 3rd degree AV block. The electrical system is trying to fail and at any time this could result in complete heart block or even asystolic pauses (causing a drop in CPP and syncope).
Broadly speaking any time you see a slow heart rate, with any disruption of the electrical conduction (broad QRS, bundle branch block, AV block, A-V dissociation) in a patient with syncope the cause is cardiac until proven otherwise. There are excellent resources at Life in the Fast Lane to help you recognise these ECGs.
This is perhaps the most benign cause of syncope and very much a diagnosis of exclusion. Although the pathophysiology is complex, it is perhaps easiest to think of it as due to a reduced heart rate (although the lack of vagal tine affects SVR and SV (via a decrease in venous return) too.
There is almost always an identifiable trigger – these are an exaggerated vagal response to normal events, such a coughing, micturition, defaecation and vomiting, It can also happen after a large meal.
Should you explore the events the patient (and any witnesses) remember happening in the moments before the collapse.
The stroke volume can be reduced transiently by the heart beating too fast and the ventricles not having time to fill, or there being something stopping the ventricle emptying completely.
Tacharrythmias – VF and VT
We spend a lot of time thinking about these as part of the ‘shockable’ algorithm in Advanced Life Support, but there are times when this may not progress to full cardiac arrest. A patient may just have a short loved episode – enough to stop there being enough cerebral poerfusion – but with the heart starting again soon after. The patient may recall feeling palpitations or chest pain before their syncope
In younger patients these tachyarrythmias may be precipitated by a genetic condition such a Hypertrophic Cardiomyopathy, Arrythmogenic Right Ventricular Dysplasia or Long QT syndrome, so it is important to ask anyone who has a syncopal episode about any family history of sudden cardiac death.
Outflow tract obstruction – Aortic Stenosis
Although there are several disorders that can cause this (including Hypertrophic Obstructive Cardiomyopathy), the most common is Aortic Stenosis. Here there is a fixed stroke volume, which is unable to increase if the boy demands (for example if there is arterial vasodilatation during exercise).
The body is very good at adjusting the contraction of our blood vessels, so that when we change posture there isn’t immediately a sudden drop in the blood flow to our vital organs. This is dependant on the baroreceptor reflex.
A inadequate response to a change in posture can result in syncope. THere are two main reasons we see this:
- Medication – lots of, particularly older, patients are on medications that reduce their blood pressure.
- Older patients – here the baroreceptor reflex simply doesn’t work as well as it should
Remember that some of these three things can be present in the background and it is the addition of another that finally causes the syncope.
For example a patient that is insidiously bleeding from an aortic aneurysm or ruptured ectopic pregnancy, where their stroke volume is dropping slowly and then they do something else to decrease theur cerebral perfusion pressure like coughing, vomiting, going to the toilet or even standing up.
The other special case is pulmonary embolism. The mechanism for this is less clear, but is likely to be due to a drop in stroke volume, following right ventricular failure affecting the filling of the left ventricle or induce arrthymias from the right ventricular strain.
We have talked throughout about global cerebral hypoperfusion causing syncope. Thus, it is highly unlikely (if not impossible) for a stroke to cause syncope as this is due to focal cerebral hypoperfusion.
A myocardial infarction in itself also doesn’t casue syncope, but rather the knock on effects of this such as myocardial instability and tachyarrthymias.
Outflow tract obstruction
Now that we can understand he physiology it is much easier to think about the approach to the patient who has had a syncope.
As always this is vital. You need to spend time on this to discover exactly what the patient was doing just before they blacked out. Was there anything to suggest a vasovagal? Did they change posture? Did they have chest pain of feel palpitations? Do they take any medications? Is there any family history of sudden cardiac death?
This can be very focussed and is really centred on the cardiovascular system, particularly the structure of the heart. Is the apex beat in the correct place? Is there a murmur of aortic stenosis?
- ECG – this is the key investigation and you need to be an expert in looking for all of the conditions we have discussed above, such as heart block and HCM
- Urine BHCG – Any presong who is able to bear children should have a pregnancy test
- Ultrasound – This might be to look for either a AAA or free fluid from an ectopic.
You are working in the Emergency Department when a usually fit and well 28 year old footballer presents saying he has had a fainting episode whilst playing football. The triage nurse asks you if he can wait to be seen in the waiting room, or if he needs seeing more urgently..
You are certainly very concerned about this patient. He should not black out whilst exercising. You ask the triage nurse to bring him straight through to a monitored bed and get an ECG. You ask him a little bit more and he tell you his Dad died when he was young, but he’s not sure what of.
You recognise the large complexes in his ECG and are concerned this patient has had a syncopal episode caused by Hypertrophic Cardiomyopathy. You call the on call cardiologist who admits him for further investigations.