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Oxford Clinical Cases > Blackout > Flashcards

Blackout Flashcards

1
Q

What is syncope

A

Syncope is a form of loss of consciousness in which hypoperfusion of the brain is the cause

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2
Q

Divisions of syncopal causes of loss of consciousness

A

Reflex
Cardiac
Orthostatic
Cerebrovascular

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3
Q

Explain orthostatic syncope

A

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.

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4
Q

Which patients are vulnerable to orthostatic syncope (3)

A

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.

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5
Q

Define cerebrovascular syncope

A

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.

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6
Q

Explain reflex syncope

A

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

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7
Q

DDx of reflex syncope (3)

A

Vasovagal syncope
Carotid sinus hypersensitivity
Situational syncope (e.g. micturition)

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8
Q

DDx of cardiac syncope (4)

A

Arrhythmias
Structural cardiac pathology causing outflow obstruction (e.g. aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM))
Massive pulmonary embolism

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9
Q

DDx of orthostatic syncope (5)

A

Dehydration
Drugs (anti-hypertensives, anti-sympathetics)
Autonomic instability
Baroreceptor dysfunction (in hypertensive patients)

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10
Q

DDx of cerebrovascular syncope (3)

A

Vertebrobasilar insufficiency Subclavian steal

Aortic dissection

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11
Q

DDx of non-syncope loss of consciousness (6)

A 
Intoxication (e.g. alcohol, sedatives)
Head trauma
Metabolic (mainly hypoglycaemia)
Non-epileptic ‘seizure’ (psychologically driven)
Epileptic seizure Narcolepsy
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12
Q

What is the pre-syncopal sensation in vasovagals

A

An odd sensation in the stomach, going pale and clammy, and knowing they are going to lose consciousness.

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13
Q

Most common cause of loss of consciousness in young people

A

Vasovagal syncope

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14
Q

Most common causes of loss of consciousness in middle-aged patients

A

Vasovagal syncope and cardiac arrhythmias

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15
Q

Why are syncopes due to cardiac arrhythmias more common in middle aged patients but not in the elderly

A

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’

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16
Q

Triggers of cardiac arrhythmias related syncope?

A

None

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17
Q

Most common cause of loss of consciousness in old-aged patients

A

orthostatic hypotension caused by medications

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18
Q

Which medications can cause orthostatic hypertension (4)

A

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)

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19
Q

Which questions should you ask about before the loss of consciousness? (3)

A

Was there any warning?
Were there any precipitating factors?
Was there any recent head trauma?

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20
Q

Which questions should you ask about during the loss of consciousness? (4)

A

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?

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21
Q

Which questions should you ask about after the loss of consciousness? (3)

A

Did they recover spontaneously? If not, how long did it take them to recover? Were they confused after recovery?

22
Q

If there is no warning before the loss of consciousness what is it most likely to be? (2)

A

Massive PE or cardiac arrhythmia

23
Q

What can precede cardiac arrhythmias

A

Palpitations

24
Q

What does an aura before loss of consciousness suggest?

A

Epileptic seizure

25
Q

What does dizziness before loss of consciousness suggest?

A

Vasovagal syncope

26
Q

What does loss of consciousness following turning your head suggest suggest?

A

Carotid sinus hypersensitivity

27
Q

What does loss of consciousness whilst sitting or lying down suggest?

A

Cardiac arrhythmia

28
Q

What does loss of consciousness whilst exercising suggest? (2)

A

Structural cardiac pathology such as aortic stenosis or hypertrophic cardiomyopathy

29
Q

What does head trauma in the days preceding loss of consciousness suggest?

A

Subdural haemorrhages

30
Q

Which precipitating factors should you ask about? (4)

A

Exercise, straining, standing up, fear, pain

31
Q

How long does vasovagal syncope last for?

A

Seconds

32
Q

How long does syncope due to a cardiac arrhythmia last for?

A

Seconds

33
Q

What is tongue-biting during loss of consciousness suggestive of

A

Epileptic seizure

34
Q

What does a spontaneous recovery from loss of consciousness indicate against and what is the exception?

A

A spontaneous recovery argues against a metabolic or neurological cause (other than epilepsy).

35
Q

What does a slow recovery with confusion from loss of consciousness suggest?

A

A slow recov- ery with confusion suggests an epileptic seizure.

36
Q

Length of recovery of epileptic seizure

A

Slow with confusion for 5-30 mins

37
Q

What should you ask about in the PMHx of someone presenting with loss of consciousness (7)

A 
Has it happened before?
Diabetes
Cardiac illness
Peripheral vascular disease
Epilepsy
Anaemia
Psychiatric illness
38
Q

What else should you ask someone who has epilepsy who has lost consciousness?

A

If this resembled one of their typical seizures

39
Q

Why is anaemia important to know about in someone presenting with loss of consciousness

A

This can contribute to hypoxia

40
Q

How should you enquire about peripheral vascular disease in someone who doesn’t know what that means

A

Ask about claudication

41
Q

Which Ix should you do in someone presenting with blackout (5)

A 
Oxygen sats
Capillary blood glucose
FBC
U&E's
ECG
42
Q

Advice for someone diagnosed with vasovagal syncope

A

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.

43
Q

Ix for someone to confirm epilepsy (2)

A

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

44
Q

What medication is used for BPH

A

Doxazosin/tamsulosin

45
Q

Three main causes of aortic stenosis

A

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

46
Q

Mx of status epilepticus (3 drugs used, 5 steps, 2 things to monitor)

A

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

47
Q

What are Stokes–Adams attacks? How are they treated?

A

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.

48
Q

What are the 6 different types of seizures

A

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

49
Q

What are the main side-effects of anticonvulsant drugs in general

A

All anticonvulsants are teratogenic

50
Q

What side effects/interactions of carbamezapine and phenytoin

A

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)).

51
Q

What are the four main anti-convulsants?

A

sodium valproate, lamotrigine, carbamazepine, phenytoin?

52
Q

What is the law when it comes to driving after an episode of loss of consciousness

A

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.

Oxford Clinical Cases (29 decks)

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