Case 10 Flashcards
what is general anaesthesia?
a medically-induced coma 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 - loss of consciousness
- skeletal muscle relaxation
what is the theory of general anaesthetic action?
- anaesthetics alter neuron function by interacting directly with a small number of ion channels
- upon activation, channels change the electrical excitability of neurons by controlling the flow of depolarising (excitatory) or hyperpolarising (inhibitory) ions across the cell membrane via an ion channel that is integral with the receptor that senses the initial signal
- general anaesthetics primarily act by either enhancing inhibitory signals or by blocking excitatory signals
what happens during the pre-anaesthetic evaluation?
- key factors of this evaluation are the patient’s age; body mass index; medical and surgical history; current medications and fasting time
- also, evaluation of the patient’s airway, involving inspection of the mouth opening and visualisation of the soft tissues of the pharynx, is required
- if a tracheal tube is indicated and airway management is deemed difficult, then alternative methods of tracheal intubation may be required as part of the anaesthetic management
- consent must be obtained
what is the premedication? what does it include?
- this is preliminary medication which is administered on the ward - not everyone requires it
- this is medication that is administered prior to administration of a general anaesthetic
- anaesthetic premedication consists of a drug or combination of drugs that serve to complement or otherwise improve the quality of the anaesthetic
Premedication includes:
benzodiazepines
-diazepam, midazolam, temazepam, lorzepam
-anxiolysis, amnesia, sedation
opioids
- morphine - anxiolysis, analgesia, sedation, euphoria, nausea
anticholinergics
-antivagal, antisialagogue (reduce production of saliva), antiemetic (reduce vomiting), amnesic
antibiotic
-surgical implant, endocarditis
antacids
-reflux, hiatus hernia, pregnancy
What has to be monitored when under general anaesthetic?
- ECG - also help identify early signs of heart ischaemia
- blood pressure - invasive or non-invasive
- oxygen saturation - pulse oximetry - allows early detection of a fall in a patient’s haemoglobin saturation with oxygen (hypoxaemia)
- end tidal CO2 - carbon dioxide measurement (capnography)
- inspired oxygen - low oxygen alarm
- inspired agent concentration
- neuromuscular blockade
- airway pressures and flows
- temperature - to discern hypothermia or fever
- depth of anaesthesia
what are the stages of anaesthesia?
- induction
- there is an ‘excitement stage’ that occurs after induction and before maintenance - this is marked by excited and delirious activity - there may be an irregular heart rate and breathing rate
- maintenance
- reversal
Describe the induction stage
- intravenous vs. inhalation induction
- how they work, when they used
Anaesthetic agents may be administered by various routes, including inhalation, injection (intravenous, intramuscular or subcutaneous), oral, and rectal
Intravenous induction:
- bolus of drug injected
- travels to the brain
- highly lipid soluble
- rapidly enters the brain
- onset is in one arm-brain time (less than one minute)
- initial recovery by redistribution
- ultimate recovery by elimination
Once in the circulatory system, they are transported to their biochemical sites of action in the central and autonomic nervous system, where they exert their pharmacologic effects
Inhalation induction:
- vapour breathed in via lungs
- enters the blood
- travels to the brain
- highly lipid soluble
- enters the brain
- initial recovery by exhalation
- ultimate recovery by exhalation
- minimal amounts are metabolised
- onset of anaesthesia is faster with intravenous injection than with inhalation, taking about 10-20 seconds to induce total unconsciousness
- this has the advantage of avoiding the excitatory phase of anaesthesia, and thus reduces the complications related to induction of anaesthesia
- commonly used intravenous induction agents include propofol, sodium thiopentone, etomidate and ketamine
- an inhalational induction may be chosen where intravenous access is difficult to obtain, where difficulty maintaining the airway is anticipated, or due to patient preference
Describe the maintenance phase
- duration of action of IV induction agents
- how is maintenance achieved
- what else is given
- what happens at the end of surgery
- the duration of action of intravenous induction agents is in general 5-10 minutes, after which time spontaneous recovery of consciousness will occur
- in order to prolong anaesthesia for the required duration, anaesthesia must be ‘maintained’
This is achieved by allowing the patient to breathe a carefully controlled mixture of:
- oxygen - nitrous oxide - volatile anaesthetic agent (isoflurane) - this can also be achieved by having a carefully controlled continuous infusion propofol through an intravenous catheter
- inhaled agents (e.g. isoflurane, sevoflurane, desflurane) are frequently supplemented by intravenous anaesthetics, such as opioids (usually fentanyl or morphine) and sedative-hypnotics (usually propofol)
- at the end of surgery, the volatile or intravenous anaesthetic is discontinued
- recovery of consciousness occurs when the concentration of anaesthetic in the brain drops below a certain level (usually within 1 to 30 minutes, depending upon the duration of surgery)
what is muscle relaxation during surgery? what does it allow?
- ‘paralysis’ or temporary muscle relaxation with a neuromuscular blocker is an integral part of modern anaesthesia
- muscle relaxation allows surgery within major body cavities, e.g. abdomen and thorax, without the need for very deep anaesthesia, and is also used to facilitate endotracheal intubation
how do muscle relaxants work? what are examples of muscle relaxants?
- acetylcholine, the natural neurotransmitter substance at the neuromuscular junction, causes muscles to contract when it is released from nerve endings
- muscle relaxants work by preventing acetylcholine from attaching to its receptor
- e.g. atracurium, succinycholine (suxamethonium), tubocurarine (curare), rocuronium, vecuronium
what does paralysis of muscles of respiration, i.e. the diaphragm and intercostal muscles, and muscles of larynx require?
- requires that some form of artificial respiration be implemented
- the airways usually needs to be protected by means of an endotracheal tube due to paralysed larynx muscles
how are the effects of muscle relaxants reversed?
anticholinesterase drugs
what does general anaesthesia cause the loss of?
- protective airway reflexes (such as coughing)
- airway patency
- regular pattern due to the effect of anaesthetics, opioids, or muscle relaxants
what is done to maintain an open airway and regulate breathing within acceptable parameters?
- some form of ‘breathing tube’ is inserted in the airway after the patient is unconscious
- to enable mechanical ventilation, an endotracheal tube is often used (intubation)
describe the reversal stage
- this stops what is keeping the patient asleep
- reverse any muscle relaxants (neostigmine & glycopyrrolate)
- give the patient time to recover
what are the consequences of anaesthesia?
- affects respiration, cardiovascular system, CNS, renal system, gastrointestinal tract and liver
respiratory:
- spontaneous respiration
- normal negative pressure breathing
- supine position and V/Q matching
- respiratory depression - increase in CO2 - hypercapnia
- hypoxic on room air
- positive pressure ventilation
- inspiration is now positive pressure
- expiration is passive
- needs a tracheal tube
- increased incidence of chest infection (e.g. ventilator acquired pneumonia)
Cardiovascular:
- decreased venous return
- decreased cardiac output
- decreased force of contraction
- increase in arrhythmia potential
- vasodilation
- change in regional flow patterns
CNS (central venous system):
- unconsciousness
- depression of cerebral metabolism
- dreaming
- awareness
- specific EEG (electroencephalogram) changes
- possible long-term effects
what might be the consequence of agents with high lipid solubility?
they accumulate gradually in body fat and may produce a prolonged ‘hangover’ if used for a long operation
- this is because of the low blood flow to adipose tissue, meaning it can take many hours for the drug to enter and leave the fat
what does postoperative recovery include?
taking care of the unconscious patient:
- airway management, monitoring, position, pressure points, nerve damage, lifting and handling
Monitory and assessing the following is extremely important:
- oxygenation
- pain control
- fluid balance
- postoperative nausea and vomiting (PONV)
- cardiovascular stability
- conscious level
- urine output
what is postoperative management?
- early management - ‘recovery’
- late management:
- wound infection
- deep vein thrombosis (DVT)
- chest infection
- surgical problems
what is the safety of anaesthesia?
- mortality and morbidity are principally related to the type of surgery
- mortality and morbidity are also related to the type of surgery
- risk due to anaesthesia alone < 1 in 500,000
- anaesthesia may contribute to some deaths
What are the uses of anaesthetics in combination with other drugs? (summary of drugs used)
What does this combination allow?
- an intravenous anaesthetic for rapid induction (propofol)
- an inhalation anaesthetic to maintain anaesthetic during surgery (isoflurane)
- a perioperative opioid analgesic (fentanyl)
- a neuromuscular blocking agent to produce adequate muscle relaxation (atracurium)
- other muscle relaxation agents (suxamethonium)
- a muscarinic antagonist to prevent or treat bradycardia or to reduce bronchial and salivary secretions (atropine, glycopyrrolate)
- towards the end of the procedure, an anticholinesterase agent (neostigmine) to reverse the neuromuscular blockade and an analgesic for postoperative pain relief (opioid/NSAID)
Such combinations of drugs result in much faster induction and recovery, avoiding long (hazardous) periods of semi-consciousness, and it enables surgery to be carried out with less undesirable cardiorespiratory depression
what are the different sites that anaesthetic agents act on?
- GABA-A receptors
- two-pore domain k+ channels
- NMDA receptors
- glycine, nicotinic and 5-HT receptors
what are GABA-A receptors?
how do anaesthetics act on them?
GABA-A receptors are ligand-gated ion channels (ionotropic receptors)
- they are chlorine channels
- they are the most abundant fast inhibitory neurotransmitter receptors in the CNS
Almost all anaesthetics potentiate the action of GABA at the GABA-A receptor
- they have a positive modulation of the inhibitory function by causing an increased reflux of Cl- ions into the postsynaptic neurone
- anaesthetics mainly work on extrasynaptic GABA-A receptors