Blackout Flashcards
What is syncope
Syncope is a form of loss of consciousness in which hypoperfusion of the brain is the cause
Divisions of syncopal causes of loss of consciousness
Reflex
Cardiac
Orthostatic
Cerebrovascular
Explain orthostatic syncope
When we stand up there is a sudden drop in blood pressure that we compensate for by vasoconstriction, par- ticularly of the ‘capacitance’ veins in the legs. This reduces the intravascular space, enabling us to maintain the pressure. However, this vasoconstriction takes a few seconds, so to prevent a transient fall in blood pressure every time we stand, there is a temporary increase in heart rate. Patients with reduced intravascular volume (e.g. from dehydration) and/or in whom the normal autonomic response (transient tachycardia and peripheral vasoconstriction) to standing is blunted (e.g. due to drugs or autonomic neuropathy) are vulnerable to blackouts.
Which patients are vulnerable to orthostatic syncope (3)
Patients with reduced intravascular volume (e.g. from dehydration) and/or in whom the normal autonomic response (transient tachycardia and peripheral vasoconstriction) to standing is blunted (e.g. due to drugs or autonomic neuropathy) are vulner- able to blackouts.
Define cerebrovascular syncope
these are non-cardiac structural causes of reduced cerebral perfusion, i.e. obstructions to the blood flow between the heart and the brain. They are relatively uncommon.
Explain reflex syncope
This is believed to involve activation of a primitive reflex that leads mammals to ‘play dead’ when faced with danger. Their heart rate slows and their blood pressure drops temporarily, reducing cerebral perfusion and lead- ing to syncope
DDx of reflex syncope (3)
Vasovagal syncope
Carotid sinus hypersensitivity
Situational syncope (e.g. micturition)
DDx of cardiac syncope (4)
Arrhythmias
Structural cardiac pathology causing outflow obstruction (e.g. aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM))
Massive pulmonary embolism
DDx of orthostatic syncope (5)
Dehydration
Drugs (anti-hypertensives, anti-sympathetics)
Autonomic instability
Baroreceptor dysfunction (in hypertensive patients)
DDx of cerebrovascular syncope (3)
Vertebrobasilar insufficiency Subclavian steal
Aortic dissection
DDx of non-syncope loss of consciousness (6)
Intoxication (e.g. alcohol, sedatives) Head trauma Metabolic (mainly hypoglycaemia) Non-epileptic ‘seizure’ (psychologically driven) Epileptic seizure Narcolepsy
What is the pre-syncopal sensation in vasovagals
An odd sensation in the stomach, going pale and clammy, and knowing they are going to lose consciousness.
Most common cause of loss of consciousness in young people
Vasovagal syncope
Most common causes of loss of consciousness in middle-aged patients
Vasovagal syncope and cardiac arrhythmias
Why are syncopes due to cardiac arrhythmias more common in middle aged patients but not in the elderly
because cardiac arrhythmias are usually secondary to ischaemic heart disease, itself more common as patients age and accumulate an increasing burden of atherosclerotic lesions.
Many of the patients who have sufficient ischae- mic heart disease to cause arrhythmias in middle age will succumb to an atherosclerosis-related death (usually cardiac or stroke) before reaching ‘old age’
Triggers of cardiac arrhythmias related syncope?
None
Most common cause of loss of consciousness in old-aged patients
orthostatic hypotension caused by medications
Which medications can cause orthostatic hypertension (4)
Diuretics and ACEi (reduce blood volume and vasodilation)
Beta-blockers (inability to increase heart rate on standing)
Alpha-blockers (inability to vasoconstrict major capacitance veins as well as some are negatively inotropic/chronotropic)
Which questions should you ask about before the loss of consciousness? (3)
Was there any warning?
Were there any precipitating factors?
Was there any recent head trauma?
Which questions should you ask about during the loss of consciousness? (4)
How long was the patient unconscious – seconds or minutes?
Did they bite their tongue, move their limbs, or were they incontinent of urine or faeces?
Which questions should you ask about after the loss of consciousness? (3)
Did they recover spontaneously? If not, how long did it take them to recover? Were they confused after recovery?
If there is no warning before the loss of consciousness what is it most likely to be? (2)
Massive PE or cardiac arrhythmia
What can precede cardiac arrhythmias
Palpitations
What does an aura before loss of consciousness suggest?
Epileptic seizure
What does dizziness before loss of consciousness suggest?
Vasovagal syncope
What does loss of consciousness following turning your head suggest suggest?
Carotid sinus hypersensitivity
What does loss of consciousness whilst sitting or lying down suggest?
Cardiac arrhythmia
What does loss of consciousness whilst exercising suggest? (2)
Structural cardiac pathology such as aortic stenosis or hypertrophic cardiomyopathy
What does head trauma in the days preceding loss of consciousness suggest?
Subdural haemorrhages
Which precipitating factors should you ask about? (4)
Exercise, straining, standing up, fear, pain
How long does vasovagal syncope last for?
Seconds
How long does syncope due to a cardiac arrhythmia last for?
Seconds
What is tongue-biting during loss of consciousness suggestive of
Epileptic seizure
What does a spontaneous recovery from loss of consciousness indicate against and what is the exception?
A spontaneous recovery argues against a metabolic or neurological cause (other than epilepsy).
What does a slow recovery with confusion from loss of consciousness suggest?
A slow recov- ery with confusion suggests an epileptic seizure.
Length of recovery of epileptic seizure
Slow with confusion for 5-30 mins
What should you ask about in the PMHx of someone presenting with loss of consciousness (7)
Has it happened before? Diabetes Cardiac illness Peripheral vascular disease Epilepsy Anaemia Psychiatric illness
What else should you ask someone who has epilepsy who has lost consciousness?
If this resembled one of their typical seizures
Why is anaemia important to know about in someone presenting with loss of consciousness
This can contribute to hypoxia
How should you enquire about peripheral vascular disease in someone who doesn’t know what that means
Ask about claudication
Which Ix should you do in someone presenting with blackout (5)
Oxygen sats Capillary blood glucose FBC U&E's ECG
Advice for someone diagnosed with vasovagal syncope
to sit or lie down if he feels like he is going to faint. Now is also a good opportunity to encourage Mr Williams to avoid excessive alcohol consumption. You should advise him to see his general practitioner (GP) if he has recurrent episodes, but no follow-up is necessary unless these occur.
Ix for someone to confirm epilepsy (2)
EEG and MRI/CT however it is a clinical diagnosis so even if the Ix come back -ve, if the doctor thinks the Hx warrants the diagnosis we can start the patient on anti-convulsants
What medication is used for BPH
Doxazosin/tamsulosin
Three main causes of aortic stenosis
In a young patient a congenital bicuspid valve is most common. In the elderly, calcification of the valve commonly leads to stenosis. Rheumatic fever is a third cause of aortic stenosis but thankfully is relatively rare in the UK today
Mx of status epilepticus (3 drugs used, 5 steps, 2 things to monitor)
Start by giving her 2–4 mg of lorazepam IV as a slow bolus over 2 minutes. If she is still fitting 10 minutes later, you can repeat this. If 10 minutes after that she is still fitting, you should contact an intensive care consultant and start giving her a phenytoin infusion with a loading dose of 18 mg/kg at a rate of 50 mg/min. Be sure to monitor her ECG and blood pressure when starting the infusion for arrhythmias and hypotension (both side-effects of phenytoin given acutely). By this time the intensive care specialists will have taken over and, if she is still fitting 10 minutes later, may decide to give her a general anaesthetic such as thiopentone to terminate the seizure
What are Stokes–Adams attacks? How are they treated?
A Stokes–Adams attack is a sudden transient loss of consciousness induced by a slow or absent pulse and subsequent loss of cardiac output. The underlying problem is either complete (third degree) heart block or sinoatrial disease. Attacks are not associated with a change in posture or any other trigger. They usually last seconds but if they go on for more than 15–20 seconds twitching may occur due to cerebral anoxia. After an attack the patient becomes flushed as the well-oxygenated blood sat in the pulmonary capillaries during cir- culatory arrest is pumped around. The term Stokes–Adams attack comes from two physicians who described the condition but is not used much nowadays, as the terms ‘cardiogenic syncope’ or ‘syncope due to cardiac arrhythmia’ are preferred. Stokes–Adams attacks are treated with a pacemaker.
What are the 6 different types of seizures
a) Tonic–clonic (‘grand mal’): patients are initially rigid (tonic phase) and then convulse, making rhyth-
mical muscular contractions (clonic phase)
b) Absence (‘petit mal’): usually in children, the patient loses consciousness and appears vacant and
unresponsive to observers for up to 30 seconds
c) Atonic: a brief loss of muscle tone, causing the patient to fall to the ground
d) Tonic: like the tonic phase of tonic–clonic seizures
e) Clonic: like the clonic phase of tonic–clonic seizures
f) Myoclonic: an extremely brief muscle contraction (<0.1 second) seen as a jerky movement
What are the main side-effects of anticonvulsant drugs in general
All anticonvulsants are teratogenic
What side effects/interactions of carbamezapine and phenytoin
Carbamazepine and phenytoin interfere with the hepatic metabolism of the contraceptive pill by inducing cytochrome P450, therefore patients on the pill should be advised to double their dose and/or use barrier contraceptives. By the same mechanism they can interfere with warfarin dosing (requiring a greater dose of warfarin for the same target international normalized ratio (INR)).
What are the four main anti-convulsants?
sodium valproate, lamotrigine, carbamazepine, phenytoin?
What is the law when it comes to driving after an episode of loss of consciousness
If it was a simple faint with prodromal symptoms and a provoking factor can be identified that is unlikely to recur whilst sitting, there are no driving restrictions and there is no need to advise the DVLA.
• If the loss of consciousness was likely due to a transient loss of blood supply to the brain (syncope) with a low risk of recurrence, the patient can drive 4 weeks after the event.
• If the loss of consciousness was likely syncope with a high risk of recurrence, the patient can drive 4 weeks after the event if the cause has been identified and treated, or 6 months after if not identified or treated.
• If the loss of consciousness is unexplained and there are no suggestions it was a seizure, the patient cannot drive for 6 months.
• If the loss of consciousness was associated with seizure markers, the patient cannot drive for one (seizure-free) year.
If someone with epilepsy has been on anti-epileptic medication for many years and wants to stop (e.g. due to a desire to be pregnant), they cannot drive for 6 (seizure-free) months after they have stopped.
