Commonly use rapid sequence induction drugs
Propofol injectable emulsion is a sterile, nonpyrogenic emulsion containing 10 mg/mL of Propofol suitable for intravenous administration. Propofol is chemically described as 2,6-diisopropylphenol.
Propofol is an intravenous sedative-hypnotic agent for use in the induction and maintenance of anesthesia or sedation. Intravenous injection of a therapeutic dose of Propofol induces hypnosis with minimal excitation, usually within 40 seconds from the start of injection (the time for one arm-brain circulation).
The mechanism of action, like all general anesthetics, is poorly understood. However, Propofol is thought to produce its sedative/anesthetic affects by the positive modulation of the inhibitory function of the neurotransmitter GABA through the ligand-gated GABAA receptors.
One of the main side effects of propofol is hypotension.
Dose: 1 to 2.5 mg/kg for induction. Commonly given in 20-40mg boluses and titrated to effect.
Onset: Onset: 15-45 seconds; Duration: 5 – 10 minutes.
- Rapid onset
- Rapid offset- short half life, often used in procedural sedation.
- Causes bronchodilatation
- Relatively cheap
- Causes vasodilation and negative inotropy –may not be tolerated well by patient with severe circulatory compromise.
- No provision of analgesia.
A short acting barbiturate which can act as both a hypnotic and an anticonvulsant. It acts by depressing the post synaptic sensitivity to neurotransmitters.
It is presented a yellow powder which is reconstituted with water producing a 2.5% solution.
Used as an anticonvulsant in status epilepticus when it can be given as an infusion, or in an emergency caesarean section as it has less impact on the foetus.
Dose: 3 to 7 mg/kg for induction.
Onset: Onset: 30 -45 seconds; Duration: 5 – 15 minutes.
- Negative inotrope
Both a hypnotic and an analgesic which produces a dissociative anaesthesia. It interacts with both the opioid receptors and the muscarinic receptors. The patient therefore experiences profound analgesia with a trance like state.
It is presented as a colourless solution.
Ketamine is often the drug of choice with the shocked patient as it has the least cardio-respiratory depressive effect. Doses as low as 0.25- 0.5mg/kg might be considered in the shocked patient.
Also due to its bronchodilatory effect it might be used in the COPD patient or the patient in acute bronchospasm.
Dose: IV – 1-2mg/kg (30 sec onset) for induction.
- ?Increased ICP
- Emergence delirium
- Presynaptic Terminal
- Postsynaptic Terminal
- Synaptic vesicle
- Nicotinic receptor
In order for a muscle to contract it must receive a message to do so. An electrical signal has to be converted to a chemical one in order to bridge the gap junctions between cells. In the diagram one can see the important structures involved in this process.
First there is the presynaptic terminal (1), remembering that the space between that and the post synaptic terminal (2) is called the synaptic cleft.
At the end of this terminal there are vesicles filled with the neurotransmitter chemical (3).
Awaiting the chemical is the receptor on the other side of the cleft (4).
So what happens?
- Firstly, the electrical signal moves down the presynaptic terminal. This is an electrical signal which has been generated at the other end of the cell and is now reaching the cleft over which the signal must cross.
- The electrical signal causes the vesicle to fuse with the pre synaptic membrane and release its contents in to the synaptic cleft.
- These neurotransmitters (acetylcholine) then bind to the receptors on the post synaptic cleft.
- This will then cause the post synaptic membrane to fire off an action potential as substances like calcium enter the cell changing its electrical potential.
- The neurotransmitter molecules must be cleared from the cleft, so that the muscle can relax or contract again as needed. They are cleared by a simple process of diffusion, reabsorbed in to the presynaptic membrane or cleared from the space by enzymes such as acetylcholinesterase.
Action of NMBs
Suxamethonium causes depolarization of at the post synaptic membrane whereas Rocuronium does not. So Sux is mimicking the action of acetycholine. They are both blocking the receptors ensuring that the acetycholine cannot interact and cause the muscle to move.
This is two acetylcholine receptors stuck together which bind to the acetylcholine receptors at the neuromuscular junction. This action then prevents motor neurons from triggering action potentials.
Suxamethonium causes depolarisation of the muscle- so the muscles may twitch when it is given- otherwise known as fasciculation. This can often be observed in the patient after giving the drug.
Dose- 1-1.5mg/kg IV
One of its main benefits is that it has the fastest onset and shortest duration of action of all the neuro muscular blockers. This short duration means that if the practitioner is unable to intubate the patient, the paralysis can be allowed to wear off and hopefully the patient may make some respiratory effort for themselves again. The endotracheal induction may still need to take place, but this will allow the practitioner time to think of ‘option B’. However, Life in the Fast Lane questions the necessity for this, putting the argument forward that if you needed sux to intubate them in the resus room then probably it might be better to keep them paralysed and manually ventilated whilst you think of an alternative. You should be working through your intubation plans A, B and C which should have been discussed prior to starting the procedure with a good check list.
Sux will typically take 45-60 seconds to relax the patient sufficiently to allow intubation attempts. It will take approximately 10 minutes to wear off.
There are some side effects to Sux. One of the main ones to be aware of is the potential rise in potassium that it can cause. One needs to check that the patient’s potassium levels are not already high, and it shouldn’t be used in the burns patient for example for this very reason. Sux can also trigger malignant hyperpyrexia if the patient has this genetic muscle disorder.
There is also a condition called suxamethonium apnoea where the patient lacks the enzyme which breaks down the drug and these patients can remain paralysed for many hours whilst the drug is broken down by other physiological means.
Repeat doses could cause a bradycardia and the fasciculation can cause muscle pain and increase oxygen demand.
Unlike Sux, Rocuronium is a non depolarising neuromuscular blocker. This then does not create the muscle twitch that Sux can. It does not have an action on the muscle other than stopper other neurotransmitters from being able to affect the nerves.
It takes longer to take effect compared to Sux, normally being considered to create good intubating conditions after 90 secs approximately. There is an argument that if you use bigger doses then the time to intubation is shorter and comparable to Sux.
The range of dose then goes from 0.6mg/kg where the time to intubation will be 60-90 seconds, up to 0.9-1.2mg/kg where the time to intubation will be approximately 45 seconds.
It would also seem that Rocuronium has very little side effect. Perhaps the only problem one might encounter is an anaphylactic reaction.
Recently there has also been the introduction of Sugammadex to reverse the effects of Rocuronium. Normally, with a dose of 1.2mg/kg, it could take up to 90 minutes for the Rocuronium to wear off. However, a dose of 16mg/kg Sugammadex will reverse its effects in about 2 and a half minutes.