Blackout Flashcards
What is the commonest cause of loss of consciousness in a patient…
1) 25yrs old?
2) 55yrs old?
3) 85yrs old?
1)
- Vasovagal syncope
2)
- Arrythmias - due to increased atherosclerotic burden with age
3)
- Orthostatic hypotension - more likely due to the medications older people take such as beta-blockers, ACEI’s, CCBs, alpha-blockers etc
In which causes of blackout can you get a warning prior to the blackout episode?
- Epileptic seizure - ‘aura’ warning
- Vasovagal episode - dizziness before the episode - you know you are about to faint
What precipitating factors are there that can cause different types of blackout?
- Postural changes - orthostatic hypotension
- Upon turning head - carotid sinus hypersensitivity
- Rapid arm movement - subclavian steal
- Exercise - suggests cardiac pathology
- Aortic stenosis
- Cardiomyopathy (e.g. hypertrophic obstructive cardiomyopathy)
- Cardiac channelopathy (e.g. long QT syndrome)
Blackout following head trauma should alert you to the possibility of what?
- Subdural haemmorhages
- Subarachnoid haemorrhages
- Haematomas
- Subdural
- Extradural
What are the characteristic features in the presentation of vasovagal blackout - before, during and after?
BEFORE
- PRECIPITANT CAUSING IT e.g. fear etc
- VAGAL symptoms:
- Sweating
- Pallor
- Nausea
- Dizziness and the sense that you are about to faint just before fainting
DURING
- Lasts seconds
- Twitch / incontinence sometimes
AFTER
- Rapid recovery on sitting or lying
What are the characteristic features in the presentation of Epileptic blackout - before, during and after?
BEFORE
- ‘Aura’ symptoms in partial seizure
- No warning in general seizure
DURING
- Tongue biting is pathognomic of epileptic seizures
- Lasts minutes
- Twitching and incontinence may also occur but not specific to epilepsy
AFTER
- Slow recovery for 5-30 minutes
- Post-ictal confusion
What are the characteristic features in the presentation of arrythmia causing blackout - before, during and after?
BEFORE
- No warning
DURING
- Lasts seconds
- May twitch or be incontinent
AFTER
- Rapid spontaneous recovery
What things might you consider about the past medical history in patients who have had a blackout episode?
- Previous epileptic seizure / epilepsy?
- Diabetes? Predisposes to PVD, hypoglycaemia (cause of blackout), polyuria and dehydration (in orthostatic hypotension) and autonomic dysfunction (in orthostatic hypotension)
- Cardiac illness? Arryhtmias (cause of blackout) my arise following MI. Left ventricular outflow obstruction may occur secondary to aortic stenosis, HOCM
- PVD? Associated with CVAs such as stroke, TIA (rarely cause blackout though)
- Anaemia? Can contribute to hypoxia
- Psychiatric illness? Panic attacks → hyperventilation → loss of consciousness. anaon-epileptic seizure also more common in people with psychiatric illness
What drugs in the drug history are important in the context of blackout?
- Insulin? - hypoglycaemia as a cause of blackout
-
Anti-hypertensives? Cause hypotension
- Diuretics
- ACEIs
- Beta-blockers
- CCBs
-
Vasodilators? Cause hypotension
- GTN
- Isosorbide mononitrate
- Antiarrythmics? These can ironically predispose to arrythmias
- Antidepressants? E.g. TCAs can cause hypotension
- Warfarin / other anticoagulants? More vulnerable to subdural haemorrhages
What 2 things from the social history are important to derive that are important in the context of blackout?
- Alcohol
- Stimulant recreational drug use
- Cocaine
- Methamphetamines
- Both cause tachyarrythmias and potentially a drop in cardiac output
Why is family history important in the context of blackout?
- Some cardiomyopathies and arrythmias are hereditary
- Sudden death in any relations < 65 years old. Particularly informative regarding exercise-induced syncope
What might carotid bruits on examination in the context of blackout point towards?
- Carotid artery stenosis as a cause of blackout
How do you investigate possible orthostatic hypotension and what would you find?
- Take the BP lying down and standing up repeatedly for 3 minutes
- Orthostatic HOTN → 20mmHg SBP drop or 10mmHg DBP drop
What focal neurological signs might you find on examination in the context of blackout and what diagnoses do these point towards?
- Signs of peripheral neuropathy (e.g. due to DM, chronic alcohol abuse)
- Parkinsonism - associated with autonomic dysfunction - in some cases of orthostatic hypotension
What investigations would you carry out in a typical suspected vasovagal blackout episode (after examination), including bloods?
-
BLOODS
- Capillary blood glucose - exclude hypoglycaemia, check for DM - can lead to polyuria and dehydration or autonomic dysfunction causing HOTN or be a risk factor for CVAs - stroke, TIA - rare cause of blackout
- FBC - Anaemia may be a contributing factor
- U&Es - check for dehydration raised urea : creatinine. Exclude electrolyte abnormalities predisposing to arrythmias
- ECG
How are non-epileptic seizures different to epileptic seizures?
- Episodes are not stereotyped
- Recovery is relatively rapid
- No post-ictal confusion
What kind of past medical history or co-morbidities are common in patients with non-epileptic seizures?
- Anxiety
- Depression
What are the 3 causes of aortic stenosis?
- Congenital bicuspid (aortic) valve
- Calcification of valve
- Rheumatic fever
What investigations are there for suspected epilepsy and what results would you get, also what is an important caveat?
- MRI
- EEG
- However, you may still get negative results from these, but you can still diagnose epilepsy based on the history since epilepsy is a clinical diagnosis
1) What is status epilepticus?
2) How to manage status epilepticus?
1)
- A life-threatening neurological condition defined as 5 or more minutes of either continuous seizure activity or repetitive seizures without regaining consciousness
2)
- Airways - check patent
- Breathing - provide high flow oxygen
- Circulation - monitor ECG, BP, pulse oximetry, capillary glucose
- Disability - check pupils and GCS score
- Exposure - check for external signs of injury
- Glucose - if hypoglycaemic, treat with 250ml 0f 10% glucose
- Benzodiazepines e.g. IV lorazepam / IV or PR diazepam / IV or PR midazolam
- Phenytoin
- If persists after phenytoin, thiopentone (RSI indicution agent) to terminate the seizure
What are possible causes of status epilepticus?
- Poor compliance with anti-convulsant medication
- Metabolic causes
- Hypoglycaemia
- Electrolyte imbalance - renal or liver failure
- Alcohol or toxins
- Amphetamines
- Cocaine
- Lead poisoning
- Hypoxia
- Infection in known epileptics - encephalits, meningitis
- Hypertensive encephalopathy
- Cerebral
- Tumour
- Head trauma
- Stroke
- AVM
- Vasculitis
1) What are Stokes-Adams attacks?
2) How are they treated?
1)
- Sudden, transient loss of consciousness
- Induced by slow or absent pulse and subsequent loss of cardac output
- Underlying causes:
- 3rd degree (complete) heart block
- Sinoatrial disease
- No trigger
- Last for seconds and twitching may occur due to cerebral anoxia
- AKA ‘cardiogenic syncope’ or ‘syncope due to cardiac arrythmia’’
2)
- Implant a pacemaker
1) Define epilepsy and define seizures
2) How are seizures classified? Define the different types of seizures
1)
- Epilepsy = tendency to have recurrent, unprovoked seizures
- Seizures = transient excessive electrical activity with motor, sensory, or cognitive manifestations discernible to the patient or observer
2)
- GENERALISED SEIZURE
- Tonic-clonic (grand mal) - patients initially rigid (tonic phase) and then convulse, making rhythmical muscular contractions (clonic phase)
- Absence (petit mal) - patient loses consciousness and appears vacant and unresponsive to observers for up to 30s
- Atonic - loss of mucle tone - so patient falls
- Tonic - like the tonic phase of tonic-clonic
- Clonic - like the clonic phase of tonic-clonic
- Myoclonic - extremely brief muscular contractions (< 0.1 seconds) - jerky movements
- PARTIAL SEIZURES
- Simple - unimpaired consciousness
- Complex - impaired consciousness
- Affects different brain regions e.g. temproal lobe, olfactory / auditory aura, epigastric discomfort, frontal lobe (motor) parietal (sensory), occipital (visual)
What are the different types of atrial heart blocks (i.e. excluding things like LBBB or RBBB)? What will they shown on an ECG?
- 1st degree heart block - every atrial contraction is transmitted to the ventricles, but conduction is slower, so PR interval is >200ms. Asymptomatic usually
- 2nd degree heart block - prolonged PR >200ms, and some but not all atrial contractions are transmitted to the ventricles i.e. missing QRS waves. Due to XS vagal stimulation to AVN or damage to AVN or bundle of His
- Mobitz Type 1 - progressively increasing PR interval until a QRS is missed entirely - ‘Wenkebaching’ pattern. Normal in ultrafit athletes
- Mobitz Type 2 - missing QRS without a prolonged PR interval prior to the preceding QRS or a shortened PR interval before the next QRS. Usually there is a pattern like 2:1 or 3:1 i.e. QRS missed after every second or third p-wave
- 3rd degree (complete) heart block - NO conduction between atria and ventricles - absolutely no relationship between p-wave and QRS waves. Broad QRS complexes
1) What is a tilt table test and what is it used for?
2) When is it contra-indicated?
1)
- In patients with suspected vasovagal syncope
- Patients lose consciousness with significant drop in BP or HR upon being tilted up
2)
- In patients with orthostatic hypotension
What is carotid sinus hypersensitivity and how do you test for it?
- A cause of blackout where if pressure is applied to the carotid sinus (where the carotid artery meets the angle of the jaw) this can cause blackout
- Carotid sinus massage (massage the carotid sinus in a rotational motion for 5s and check for loss of consciousness, BP drop and bradycardia) NOTE: always check for possible carotid artery atheroma first with carotid duplex u/s
Question on rare cardiac causes of loss of consciousness - not relevant to Y3 curriculum so omitted - on pg 52 of oxford cases
Question on informing DVLA on loss of consciousness - not relevant to Y3 curriculum so omitted - on pg 51 of oxford cases
Question on side effects and interactions of anticonvulsant drugs - not relevant to Y3 curriculum so omitted - on pg 50 of oxford cases
What is…
1) Brugada syndrome?
2) Dressler’s syndrome?
3) Leriche’s syndrome?
4) Eisenmonger’s syndrome?
5) Wolff-Parkinson-white syndrome?
See pg 53 on oxford cases
Most of these are not relevant to Y3 curriculm (all irrelevant except dressler’s and wolff-parkinson-white)
