Loss of Consciousness Flashcards
What is the differential diagnosis for transient loss of consciousness?
Traumatic
Non-traumatic:
- Neurogenic (epilepsy, vertebrobasilar disease)
- Metabolic (hypoglycaemia, toxins)
- Psychogenic
- Cardiovascular (reflex syncope, orthostatic, cardiac syncope)
What is the definition of syncope?
Transient loss of consciousness caused by a disorder of the circulation
What are the methods of recording an ECG trace in someone with suspected arrhythmia?
ECG of patient when they are asymptomatic should be carried out first
- Patients who have daily symptoms should have ambulatory holter ECG for 24hrs
- Internal loop recorder used in patients who have symptoms relatively frequently - patient presses button when they have sx to record a 10 min trace
- Patients with infrequent, prolonged sx can come to GP practice for 12-lead ECG
Features of cardiogenic loss of consciousness
Pre-syncope symptoms:
- Light headedness
- Nausea
- Sweating
- Blurring of vision
Recovery from syncope = spontaneous and total, with little confusion afterwards
What are the triggers for reflex syncope?
Reflex syncope caused by particular trigger that leads to dysfunction of the heart rate and blood pressure regulation mechanism:
- Vasovagal syncope- triggers = seeing blood, emotional stress, standing up
- Situational syncope - triggers = micturition, coughing, lifting heavy weight
- Carotid sinus hypersensitivity = compression over the carotid sinus e.g. tight collar, shaving
Why does consciousness return spontaneously after syncope?
Syncope normally causes individual to fall to the ground, which means that cerebral bloodflow returns when heart is on level with the brain leading to spontaneous regaining of consciousness
Treatment for reflex syncope…
Conservative:
- Avoidance of triggers
- Increased fluid and sodium intake (increase circulating volume)
Medical:
- Fludrocortisone (corticosteroid)
- Midodrine (vasopressor)
- Discontinuation of medications thought to lower blood pressure
What is the definition of orthostatic hypotension?
From sitting to standing position:
- Drop of at least 20mmHg in systolic BP
- Drop of at least 10mmHg in diastolic BP
What is the pathophysiology of orthostatic hypotension?
Delayed vasoconstriction of the lower limbs leads to blood pooling in the lower extremities meaning there is reduced venous return and so the cardiac output is reduced which causes fall in cerebral bloodflow.
Main causes of orthostatic hypotension…
- Autonomic failure - regulatory mechanism e.g. baroreceptor reflex does not work in time(Parkinsonism, MS, spinal injury)
- Drug induced - e.g. diuretics, vasodilators
- Volume depletion (bleeding, diarrhoea)
Diagnosis of orthostatic hypotension…
- BP taken lying down for 5 minutes
- BP taken after 1 min of standing, then after 3 min of standing
SBP drop by >20mmHg or DBP drop by >10mmHg
What is Addisonian crisis?
Severe, acute emergency caused by deficiency of cortisol in the body.
What are the causes of Addisonian crisis?
- Infection/ surgery causing acute exacerbation of chronic Addison’s disease
- Haemorrhage of the adrenal glands
- Steroid withdrawal
Why does steroid withdrawal cause Addisonian crisis?
Exogenous steroids will suppress the hypothalamic CRH and pituitary ACTH, leading to suppression of the adrenal glands causing drop in cortisol levels.
When the steroids are withdrawn suddenly, there is a very low baseline of endogenous cortisol leading to crisis.
Presentation of Addisonian crisis…
- Low blood pressure
- Weakness
- Headache
- Nausea and vomiting
- Tachypnoea
- Confusion
- Syncope - could be orthostatic hypotension
- Hypoglycaemia
Why is there circulatory collapse in Addisonian crisis…
- Decreased mineralocorticoid = increased sodium loss and increased potassium reabsorption –> hyponatraemia and hyperkalaemia
- Hyponatraemia leads to decreased intravascular volume and so cardiac output will fall.
Management of Addisonian crisis…
- Hydrocortisone 100mg IM/IV STAT - then continue 100mg 6- hourly until patient is stable
- 1 litre saline IV over 30-60 mins
- Oral relacement after 24 hours
Causes of cerebral hypoxia …
Any event that disrupts the brain’s ability to gain or process oxygenated blood.
Hypoxic hypoxia = not enough oxygen entering the body - lack of exogenous oxygen - divers, altitude climbers OR pulmonary obstruction e.g. asthma, choking, strangulation
Hypaemic hypoxia = not enough oxygen entering the blood e.g. anaemia, CO poisoning
Ischaemic hypoxia = not enough oxygenated blood reaching the brain e.g. cerebral infarction, cerebral haemorrhage, cardiac arrest
Histotoxic hypoxia = oxygenated blood present in cerebral tissue but cannot be metabolised - e.g. cyanide poisoning
What is CO2 narcosis?
Dangerously elevated levels of CO2 in the blood which may lead to reduced levels of consciousness
How does CO2 narcosis cause LoC?
Cerebral autoregulation is heavily influenced by CO2:
- Increasing CO2 levels will decrease pH of CSF
- Decreasing pH causes cerebral vessels to vasodilate which causes increased cerebral bloodflow and intracranial pressure
What causes hepatic encephalopathy ?
Liver disease prevents the metabolisation of waste products such as ammonia which then build up in the systemic circulation leading to it crossing the blood brain barrrier and therefore damaging the brain tissue
Clinical features of hepatic encephalopathy…
- Confusion
- Drowsiness
- Asterixis
- Apraxia
- Raised ammonia levels
Grading of hepatic encephalopathy…
Grade 1 = irritable, minimal confusion
Grade 2 = more confused, drowsy, inappropriate behaviour
Grade 3 = incoherent, restless
Grade 4= coma
How does cerebral malaria cause LoC?
Sequestration = parasitic RBCs adhere to endothelial lining of cerebral vessels leading to clumping of multiple RBCs which may eventually prevent perfusion of the cerebral tissue leading to ischaemic hypoxia.
What are some psychogenic causes of LoC, and how do they present?
Anxiety disorder:
- Usually a history of anxiety disorder
- Rapid breathing
- Sweating
- Globus hystericus (feeling of lump in the throat)
Non-epileptic attack disorder:
- Long duration
- Violent thrashing movements
- Side to side head movement
- Able to recall events
- EEG shows no typical epileptiform changes
