Case 10 Flashcards
What is general anaesthesia?
A medically induced comma and loss of protective reflexes resulting from the administration of one or more general anaesthetic agents
What are the purposes of General Anaesthesia?
Analgesia - loss of response to pain Amnesia - loss of memory Immobility- loss of motor reflexes Unconsciousness Skeletal muscle relaxation
How do anaesthetics work?
They will enhance inhibitory signals or block excitatory signals via interaction with ion channels
What is the purpose of anaesthetic premedication?
It improves or complements the quality of the anaesthetic
What are some anaesthetic premedications?
- Benzodiazepines - anxiolysis (relieves anxiety)
- Opioids
- Anticholinergics - antisialagogue (reduces saliva production)
- antibiotics
- antacids - neutralises excess stomach acid to relieve heartburn, acid indigestion, stomach pain
What are the monitoring systems used in general anaesthesia?
- ECG - identify heart ischaemia
- Blood Pressure
- Oxygen saturation - identify hypoxaemia
- end tidal CO2
- inspiration oxygen
- neuromuscular blockade
- airway pressures and flow
- temperature
- depth of anaesthesia
What are the stages of anaesthesia?
Induction
(Excitement stage - marked by excited and delirious activity with irregular heart and breathing rate)
Maintenance
Reversal
How can anaesthetic agents be induced?
Inhalation:
• vapour, Highly lipid soluble, recovery is via exhalation
Injection - Intravenous:
• bolus, highly lipid soluble, recovery via redistribution and elimination
Intravenous is quicker (takes 10-20sec for unconsciousness) hence avoids complications and excitement stage
What is the common intravenous induction agents?
Propofol, sodium thiopentone, etomidate and ketamine
What is the purpose of maintenance during general anaesthesia?
To prolong the duration (5-10mins) of intravenous induction agent and hence keep patient unconscious for duration of surgery
How is maintenance of induction agent achieved?
Patient breathes in a mixture of NO, O2 and volatile anaesthetic agent (isoflurane)
It can also be achieve by continuous infusion of propofol via catheter
Inhaled agents (Isoflurane, Sevoflurane, Desflurane) are supplemented by intravenous anaesthetics = opioids- fentanyl or morphine; sedative- hypnotics (propofol)
Why is a muscle relaxant used?
Eliminates the need for a deep anaesthesia to conduct surgery in body cavities and also facilitated endotracheal intubation
How do muscle relaxants works?
They inhibit the binding of acetylcholine to muscarinic receptors
E.G. atracurium, succinylcholine(sucamethonium), tubocurarine (carare), rocuronium, vecuronium
What does the endotracheal intubation do?
Protects the larynx while it is paralysed and allows maintenance of regular breathing via mechanical ventilation
How is the muscle relaxant reverted?
With an acetylcholinesterase drug
Neostigmine
What are the respiratory affects of anaesthesia?
Spontaneous breathing:
- normal negative pressure breathing
- respiratory depression - hypercapnia
- hypoxia on room air
Positive pressure ventilation:
- Increase incidence of chest infection (ventilator acquired pneumonia)
What are the cardiovascular affects of anaesthesia?
Decreased venous return, cardiac output, and force of contraction
Increase in arrhythmia potential
Vasodilation
What are the CNS affects of anaesthesia?
Unconsciousness, depression of cerebral metabolism, dreaming and awareness
What is the issue caused by low blood flow to adipose tissue?
High lipid soluble agents accumulate in body fat and produce prolonged ‘hangover’ if used for long operation
What is important to monitor and assess after the operation?
Oxygenation, pain control, fluid balance, postoperative nausea and vomiting (PONV), cardiovascular stability, conscious l‘level and urine output
What is the risk of anaesthesia?
Less than 1 in 500,000
What is the muscarinic antagonist used to prevent or treat bradycardia or reduce bronchial and salivary secretion?
Antropine or glycopyrrolate
What are the target sites of anaesthetic agents?
GABA-A receptors
Two-pore domain potassium channels
NMDA receptors
glycine, nicotinic and 5HT receptors
What type of receptors are GABA-A receptors?
Ligand-gated chlorine channels ionotropic receptors
Anaesthetic agents increase its influx of chlorine ions at extrasynaptic receptors
This enhances tonic inhibition
What are two-pore domain potassium channels?
Aka leak channels
These are only affected by inhalation inducing agents causing hyperpolarisation to reduce membrane excitability
Inhibition of which part of the CNS leads to analgesia and unconsciousness?
Thalamic sensory relay nuclei and midbrain reticular formation
What causes death innanaesthesia?
Loss of cardiovascular reflexes and respiratory paralysis
What determines the speed of induction and recovery of anaesthesia?
Properties of the anaesthetic:
- blood:gas partition coefficient (solubility in blood)
- oil:gas partition coefficient (solubility in fat)
Physiological factors:
- Alveolar ventilation rate
- cardiac output
What is anaesthetic potency?
Minimal alveolar concentration (MAC)
i.e. the concentration of vapour in the lungs that is needed to prevent movement (motor response) in 50% of patients in response to surgical stimulus
Higher lipid solubility = lower MAC = greater potency
How does propofol work and what are the side effects?
MOA: positive modulation of inhibitory function of GABA through GABA-A receptors
Side effects:
- hypotension and bradycardia
- respiratory depression
- nausea and vomiting
How does Isoflurane work and what are the side effects?
MOA: binds to GABA, NMDA, and glycine receptors
Side Effects:
- hypotension
- coronary vasodilator - increases cardiac ischaemia in CVD patients
- respiratory suppression
How does fentanyl work?
micro-opioid receptor agonist inhibiting adenylate cyclase hence inhibiting release of nociceptive substances eg Substance P, GABA, dopamine
How do non-depolarising Neuromuscular blocking agents work?
Competitive antagonists at ACh receptors of motor end plate
They block the presynaptic auto receptors, inhibiting release of ACh during repetitive stimulation of motor nerve
Effect: motor paralysis
Side effects: hypotension, bronchospasm (due to histamine release) and ganglion block
Example: Atracurium
What is the advantage of a respiratory low pH (acidosis) for Atracurium?
It reduces elimination
How do depolarising Neuromuscular blocking agents work?
Mimics ACh without rapid hydrolysation by AChE hence persistent depolarisation leading to desensitisation
Example: Suxomethonium (hydrolysed by BuChE - plasma cholinesterase)
Side Effects: bradycardia and Hyperkalemia, increased intraocular pressure
What do cholinesterase inhibiting drugs do?
Reverse action of non-depolarising neuromuscular blocking drugs and treat myasthenia gravis
Example: neostigmine
What are muscarinic receptor antagonists?
Inhibit cholinergic transmission and used to limit parasympathomimetic effects caused by neostigmine (e.g. bradycardia)
Examples: atropine (crosses BBB) and glycopyrolate
What is a osmotic diuretic?
Drug used to treat intracranial pressure e.g cerebral oedema
MOA: increase solute content of fluid in proximate tubule and collecting tubule causing fluid to be drawn from the body into the proximal tubule decreasing extra cellular fluid volume
Example: Mannitol
What is sleep?
State of physiological reversible unconsciousness - reduced responsiveness to and interaction with the environment
What is wakefulness?
Associated with awareness - The ability to integrate all sensory information from the external environnement and the internal environment of the body
What is total consciousness?
Continuous awareness of the external and internal environment, both past and present, together with the emotions arising from it
Requires short-term and explicit memory and intact emotional response
What is the Circadian Rhythm?
It is the control of human sleep through detection of decreased light levels over 24H
How is the circadian rhythm controlled?
Ganglion cells contain melanopsin which is depolarised by light provides input to suprachiasmatic nucleus (SCN) via retinohypothalamic tract
From SCN output is set to the paraventricular nucleus (PVN) to intermediolateral zone (IML) on lateral horn of thoracic spinal cord, to superior cervical ganglia (SCG) to the pineal gland
Pineal gland is stimulated to secret melatonin into the blood by decreased light
What other functions other than light synchronise the sleep-wake cycle?
Body temperatures hormone secretion, blood pressure and urine production
All governed by SCN
How is wakefulness mediated?
By the ascending arousal system flowing from brainstem to the cerebral cortex through thalamus, hypothalamus and basal forebrain
What are the two components of the ascending arousal system?
- Thalamus to the cerebral cortex
2. Lateral hypothalamus and basal forebrain to the cerebral cortex
What is the ascending arousal system through the thalamus to the cerebral cortex?
Cholinergic structures (PPT/LDT) in brainstem send acetylcholine to thalamus reticular nuclei > transmission promotes a state of excitability and wakefulness (reticular activating system)
PPT/LDT more active during wakefulness and REM sleep and less active during NREM sleep
What is the ascending arousal system through the lateral hypothalamus and basal forebrain to the cerebral cortex?
LH and BF are comprised of monoaminergic cells:
- noradtenergic neurons of locus coeruleus
- serotonergic dorsal and median raphe nuclei
- dopaminergic neurons of ventral periaqueductal grey matter
- histaminergic neurons from TMN (tuberomammillary nucleus)
Active during wakefulness, slow during NREM sleep and no activity during REM sleep
What is Orexin?
Neurotransmitter that regulates arousal, wakefulness and appetite
(Helps stabilise wakefulness and sleep)
How does orexin regulate wakefulness?
It strongly excites dopamine, noradrenaline, histamine and acetylcholine brain nuclei
Activation for orexin neurons reduces during REM sleep
What is the sleep cycle?
Moving through NREM sleep (80%) and then REM sleep (20%)
- In 8H sleep there is about 4-6 cycles (durations in NREM sleep decreases after each cycle and amount in REM sleep increases)
NREM sleep is required to survive
What induces NREM sleep?
NREM-on GABA neurones in the hypothalamus And Serotonin from Raphe Nuclei
What happens during NREM sleep?
Decreased activity of noradrenergic neurones in brainstem
Skeletal muscles relax but maintain tone
active parasympathetic nervous system w/ gastric motility and decreased HR and BP
What are the four stages of NREM sleep?
Awake:
• active mental concentration [EEG Beta, 14-30Hz]
• closed eyes [EEG Alpha, 8-13Hz]
NREM 1: light sleep [EEG Theta, 4-7Hz]
NREM 2:
• deeper sleep, bruxism [EEG Theta]
• sleep spindle (10-15Hz) and K-complex
NREM 3 + NREM 4:
• deepest sleep, sleepwalking, night terrors, bedwetting, ‘slow-wave sleep’ [EEG Delta, <3.5Hz]
What is Bruxism?
Involuntary habitual grinding of teeth
Occurs during NREM 2
What is atonia?
Loss of muscle tone
When does REM sleep start?
Once NREM sleep has completed cycle from 1-4 and back to 2 (lasts 90mins)
It is induced by cholinergic neurones in ascending arousal system
What happens during REM sleep?
EEG = synchronised to desynchronised waves (resembles awake state w/ atonia)
skeletal muscles are flaccid and muscle stretch reflexes to be absent
Sensory systems are inhibited
Increased BP, metabolism and blood flow to brain
Penile and Clitoral erection
Dreams
What are REM- off cells?
Noradrenergic and serotonergic neurones
Causes transition back to NREM sleep
What is consciousness?
Alert cognitive state in which you are aware continually of the external and internal environment, both past and present, together with the emotions arising from it
To be considered full conscious you need:
1. Intact ascending reticular activating system (awake)
- Functioning cerebral cortex (aware)
What is a concussion?
A reversible state of unconsciousness that last for only a brief amount of time, without any structural or pathological alteration
What is a coma?
Profound state of unconsciousness that is associated with depressed cerebral activity from which individual cannot be aroused
Dysfunction or injury involving both cerebral hemispheres or the reticular formation leads to coma
What is comatose?
Unconsciousness and inability to respond to verbal commands (might show motor responses to painful stimuli)
What is stuporose?
Unconsciousness but can be roused by verbal command or painful stimuli for short periods and produce verbal responses
What does the Glasgow Coma Scale look at?
Assess depression of consciousness
Records:
Pupillary responses to light
Reflex eye movement in horizontal and vertical plane
BP, respiratory rate, pulse and temperature
What is a seizure?
Extreme form of synchronous brain activity accompanied by very large EEG patterns
- Generalised - entire cerebral cortex of both hemispheres
- Partial - limited area of the cortex but can spread
What is epilepsy?
Repeated seizures
What is a convulsant?
Drugs that block GABA receptors = seizure promoting agents
Seizures can be caused by…
CNS Depressant drugs (Alcohol or barbiturate)
How do anticonvulsants work?
Prolong inhibitory action of GABA (e.g. barbiturates and benzodiazepines)
Decrease the tendency for certain neurones to fire high frequency action potentials (e.g. phenytoin, carbamazepine)
What are signs of Elevated Intracranial Pressure?
Early = drowsiness and diminished level of consciousness
Late = coma and unilateral pupillary changes
How is ICP treated?
• Emergency = intubation and hyperventilation - causing vasoconstriction and reduces cerebral blood volume
(hyperventilation must be used for short time to avoid worsening or causing cerebral ischaemia)
• high-dose barbiturates, decompressive hemicraniectomy or hyperthermia
What are the types of cranial oedema?
- Vasogenic - influx of fluid and solutes into brain through BBB
- Cytotoxic - cellular swelling
Cranial oedema represents a combination of both
How is cranial oedema treated?
Elevate head 30 degrees
Intimate and hyperventilate - to 25-30 mmHg PCO2
IV mannitol (osmotic diuretic)
Ventricular damage
What is a craniotomy?
Surgical removal of part of the cranium to help relieve excess intracranial pressure
What is the blood supply of the scalp?
Internal Carotid:
• supratrochlear- to midline forehead
• supraorbital - to lateral forehead and scalp
External Carotid:
• superficial temporal
• occipital - posterior aspect of scalp
• posterior auricular - scalp above and behind the auricle
What is a compound fracture?
Skin is also broken with the fracture
What is a linear fracture?
Impacted area bends inwards causing area around it to bend outwards
Most common cranial fracture
What is a diastatic fracture?
Fracture line transverse one or more suture lines causing a widening of sutures
What is a depressed fracture?
Inward displacement of broken bone
High risk of intracranial pressure
Surgery required
What is basilar fracture?
Breaks in bones at the base of the skull
Characteristics: blood in sinuses, CSF leaking from the nose or ears
