Here’s a run down of what you need to know about the basics of anaesthesia for the nursing student . The triad of anaesthesia consists of three components:
- Muscle relaxant
This class of drug is used to induced sleep and maintain a patient in a state of unconsciousness. Alternatively, some anaesthetics alter the patients consciousness and perceptions without inducing sleep
An inhalant, more commonly known as laughing gas. At room temperature, it is a colorless non-flammable gas, with a pleasant, slightly sweet odor and taste. It is used in surgery and dentistry for its anesthetic and analgesic effects. It is known as “laughing gas” due to the euphoric effects of inhaling it, a property that has led to its recreational use as an inhalant drug.
Mechanism of action: Findings to date indicate that nitrous oxide induces opioid peptide release in the brain stem leading to the activation of descending noradrenergic neurones, which results in modulation of the nociceptive process in the spinal cord. Several receptor–effector mechanisms including dopamine receptors, α2 adrenoceptors, benzodiazepine receptors and -methyl- -aspartate (NMDA) receptors have been implicated although the relationship of one with the other is not known.
The mechanism of action of nitrous oxide is trifold and includes analgesia, anxiolysis, and anesthesia.
- Its analgesic mechanism of action is described as opioid in nature and may involve a number of spinal neuromodulators.
- The anxiolytic effect is similar to that of benzodiazepine and may involve gamma aminobutyric (GABA) receptors.
- The anesthesia mechanism may involve GABA and possibly N-methyl-D-aspartate receptors as well (NMDA). In general, the effect of nitrous oxide ceases as soon as the inhalation stops, with no residual effect.
Nitrous oxide is administered by inhalation, absorbed by diffusion through the lungs, and eliminated via respiration. The elimination half life of nitrous oxide is approximately 5 minutes.  It is excreted essentially unchanged (ie, nonmetabolized) via the lungs; less than 0.004% is actually metabolized in humans.
- Blurred vision
- Dizziness, faintness, or lightheadedness when getting up suddenly from a lying or sitting position
- Mild cardiac depression
- Ensure adequate ventilation of the room to avoid bystander effects
- Conduct a history and physical examination to rule out the contraindications for use of nitrous oxide/oxygen. This includes a cardio-respiratory, gastrointestinal and ear-nose-throat (ENT) exam
- Ensure client is able to follow directions
- Obtain a baseline set of vital signs, including oxygen saturation
- Monitor closely during administration; note patient responsiveness, color, respiratory status
- Nitrous oxide/oxygen is self-administered through a demand-valve with face mask or mouthpiece.
- If the pain is spasmodic or episodic, as in labour, encourage the client to stop using the gas during the pain-free periods.
- Have the client apply the mask or hold mouth piece to own face
- Encourage slow, deep breaths to allow the demand-valve to function
- If the mask falls away as the client becomes sedated, do not replace the mask
- Allow the client to use nitrous oxide/oxygen until the pain is relieved or side-effects appear
- Discontinue if cyanosis develops
To support learning see the Adult Pain Management info sheet
Desflurane is a highly fluorinated methyl ethyl ether used for maintenance of general anaesthesia.It induces muscle relaxation and reduces pains sensitivity by altering tissue excitability. It does so by decreasing the extent of gap junction mediated cell-cell coupling and altering the activity of the channels that underlie the action potential.
Mechanism of action
Desflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Desflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Desflurane also binds to and agonizes the GABA receptor, the large conductance Ca2+ activated potassium channel, the glycine receptors, and antagonizes the glutamate receptors.
Desflurane may activate GABA channels and hyperpolarize cell membranes. In addition, they may inhibit certain calcium channels and therefore prevent release of neurotransmitters and inhibit glutamate channels. Volatile anesthetics easily partition into cellular membranes and could expand the volume of the cell membrane and subsequently distort channels necessary for sodium ion flux and the development of action potentials necessary for synaptic transmission.
- Altered heart rate
- Monitor for hypersensitivity reactions, respiratory depression, cardiac arrhythmia, malignant hyperthermia, respiratory adverse reactions, disruption of hepatic function, icterus, liver necrosis, and other adverse reactions.
- Monitor HR, BP, urine flow, and serum K+ levels.
- Monitor cerebral perfusion pressure in patients w/ intracranial space occupying lesions.
Warnings: May trigger malignant hyperthermia in susceptible individuals; treat by discontinuation of triggering agents, administration of IV dantrolene sodium, and application of supportive therapy. Fatal outcome of malignant hyperthermia reported. Rare increases in K+ levels resulting in cardiac arrhythmias and death in pediatric patients during the postop period reported (may be associated w/ concomitant succinylcholine use.
Propofol is an intravenous anaesthetic agent used for induction and maintenance of general anaesthesia. IV administration of propfol is used to induce unconsciousness after which anaesthesia may be maintained using a combination of medications. Recovery from propofol-induced anaesthesia is generally rapid and associated with less frequent side effects (e.g. drowsiness, nausea, vomiting) than with thiopental, methohexital, and etomidate. Propofol may be used prior to diagnostic procedures requiring anaesthesia, in the management of refractory status epilepticus, and for induction and/or maintenance of anaesthesia prior to and during surgeries.
Mechanism of action
The action of propofol involves a positive modulation of the inhibitory function of the neurotransmitter gama-aminobutyric acid (GABA) through GABA-A receptors. Increased GABA causes post synaptic neurons to hyperpolarize through an increased influx of chloride. This prevents the propagation of an action potential, inhibiting excitability.
Rapid – time to onset of unconsciousness is 15-30 seconds, due to rapid distribution from plasma to the CNS. Distribution is so rapid that peak plasma concentrations cannot be readily measured. Duration of action is 5-10 minutes.
- Involuntary muscle movement
Propofol contains egg and soy products so ensure that patient allergies are checked before administration.
For the visual learners, check out this youtube clip.
Thiopental is a short acting barbituate used in general anesthetic. It is lipid soluable which acounts for the short duration as it is redistributed to muscle tissues.
Mechanism of action
Thiopental binds at a distinct binding site associated with a Cl– ionopore at the GABAA receptor, increasing the duration of time for which the Cl– ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. This CNS depression produces hypnosis.
- Shivering and trembling
- Prolonged somnolence (a strong desire to sleep)
Severe side effects can include emergence delirium, cardiac arrhythmia, bronchospasm and respiratory depression.
Benzodiazipines (midazalam, diazapam, and lorazapam) are used for anaesthetic as well as being antianxiety and antiepileptic agents.
Mechanism of action
Benzodiazepines bind nonspecifically to benzodiazepine receptors which mediate sleep, affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABAA) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.
Benzodiazipines can cause dependence and neurological dysfunction. Withdrawal from these can cause agitation, anxiety, tremors and headaches.
Get more info here
Muscle relaxants inhibit voluntary muscle tone and reflexes to stop muscles from contracting when stimulated. The can be divided into depolarizing and non-depolarizing drugs.
A non-depolarising neuromuscular blocker which causes flaccidity paralyis lasting up to 30 minutes. The effect of pancuronium can be reversed with anticholinesterase drugs which cause the rapid breakdown of the drug in the neuromuscular junction.
Mechanism of action
Nondepolarizing neuromuscular blocking agents inhibit neuromuscular transmission by competing with acetylcholine for the cholinergic receptors of the motor end plate, thereby reducing the response of the end plate to acetylcholine. Nicotinic receptors are a cholinergic receptor that pancuronium binds to. This type of neuromuscular block is usually antagonized by anticholinesterase agents.
- Increased cardiac output
Small muscles are affected first then the limbs neck, trunk and lastly the diaphragm and intercostal muscles. Return of function follows the reverse order with the intercostal muscles and diaphragm recovering first.
Here’s a link to a video exploring both depolarizing and non-depolarizing muscle relaxants.
A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.
Mechanism of action
The mechanism of action of Succinylcholine involves what appears to be a “persistent” depolarization of the neuromuscular junction. This depolarization is caused by Succinylcholine mimicking the effect of acetylcholine but without being rapidly hydrolysed by acetylcholinesterase. This depolarization leads to desensitization.
It is an nicotinic receptor agonist which causes persistent stimulation and maintains the depolarized state of the motor end plate. The sodium channels remain open which causes the muscle fibre to become unresponsive to electrical stimulus.
- Excessive drooling
Due to the loss of potassium from the motor end plate, serum potassium levels can increase causing hyperkalaemia causing arrhythmia.
Drugs that are injected into the body tissues to cause a localized absence of pain.
Mechanism of action
The drug is administered in an unionized form which is able to enter the neuronal cell (nociceptor). Due to the acidity of the neuron, lignocaine then becomes ionized which allows it to block the sodium channels from inside of the neuron. This inhibits the influx of sodium into the neuron ensuring that the neuron can not reach threshold potential, inhibiting depolarization. Preventing propagation of the action potential inhibits the transduction and transmission of pain signals to the brain.
Local anaesthetic has a rapid onset of action, withing 5-10 minutes and provides a nerve blockade affect for 1 hour to 1 and a half hours.
This video provides info on local anaesthetics