Acute neurosciences Flashcards
Respiratory control centre
Medulla oblangata
- controlls most of breathing
- Dorsal Respiratory Group: integrates peripheral signals
- Ventral Respiratory Group: Excites inspiratory muscle to contract
Pons
- Controls smooth transition from inspiration to expiration
Neural control of respiration…
Automatic (metabolic) respiration – to maintain acid-base balance
Voluntary (behavioural) respiration – allows modulation of ventilation in response to voluntary acts such as speaking, singing, breath hold and straining.
Limbic (emotional) control – allows respiratory modulation to emotion such as laughing, coughing and anxiety
Automatic (metabolic) respiration
To maintain acid-base balance
Voluntary (behavioural) respiration –
Allows modulation of ventilation in response to voluntary acts such as speaking, singing, breath hold and straining.
Limbic (emotional) control
Allows respiratory modulation to emotion such as laughing, coughing and anxiety
CNS respiratory considerations
Impaired neurological control of respiration (altered rate, depth and pattern)
Muscle weakness / fatigue
Dysfunction in gas exchange leading to respiratory failure
Impaired neurological control of swallow, cough and secretion clearance leading to reduced airway protection and increased risk of aspiration
Monroe-Kellie hypothesis
“The total volume of intercranial contents must remain constant”
Brain tissue, CSF, blood
An increase in one should cause a reciprocal in one or both of the remaining two.
Intercranial pressure (ICP)
ICP depends on volume of intercranial contents. Normally 1.4kg brain, 50-70ml blood and 50-120ml CSF.
Common causes of raised ICP = brain swelling e.g. after TBI or as a result of tumour.
Raised ICP means both neural and vascular tissues are compressed and if left untreated can be fatal.
Elevated ICP can be treating with medication, drainage of CSF or changing ventilator settings.
Cerebral perfusion pressure (CPP)
Pressure at which the brain is perfused (approx. 15-20% of cardiac output)
Normal CPP = 60-80mmHg
CPP > 50mmHg results in cerebral ischaemia and tissue death
Symptoms of raised ICP
Dilated pupils
Headache
Drowsiness
Hyper or hypotension
Loss of reflexes or increased reflexes
Seizures
Shortness of breath or rapid breathing
Abnormal posturing, rigid body movements and abnormal positions of the body
Cardiac arrest
Loss of consciousness
Coma
Factors affecting ICP
- Hypercapnia
- Hypoxia
- Obstruction to venous outflow from the brain
- Increased intrathoracic or abdominal pressure
- Uncontrolled systemic BP
- Pyrexia
- External stimuli
Cushing’s triad
- 3 primary signs that often indicate an increase in ICPIncreased Systolic BP
Decreased Pulse
Decresed Respiration
Diagnosis of death using neurological criteria
Completed by two doctors on two occasions
Evidence of irreversible brain damage of known aetiology
Exclusion of reversible causes of coma and apnoea
Test for absence of brain stem reflexes
Apnoea test
Mitigation for ‘Red Flags’
Disorders of consciousness
**Coma **(usually acute and short term)
Prolonged disorders of consciousness (PDOC) (unconscious >4 weeks)
Vegetative state (VS)
Minimally conscious state (MCS)
Disordered consciousness occurs in two main contexts:
- Prolonged disorder of consciousness (PDOC) following sudden onset acquired brain injury – from which the patient may or may not regain consciousness
- Terminal decline of consciousness (TDOC) towards the end of life in patients with progressive degenerative brain damage (for example due to dementia, Parkinson’s disease or multiple strokes)