Ep.32 – Cocaine For the FRCA Primary

Jul 17, 2025

—

James

inEduCast,Pharmacology

GasGasGas – The FRCA Primary Anaesthetics Exam Podcast

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Cocaine For the FRCA Primary

If you like a story about extensive testicular traction and hammering shins then this is the episode for you.

This FRCA Primary Podcast episode explores cocaine and the exposure patients have to it in the clinical environment, chiefly courtesy of the ENT surgeons. The episode explores mechanism, side effects, onset, implications, but also the history of spinal anaesthesia and treatment of cocaine toxicity in the A&E department.

The Local Anaesthetics Chapter:

Introduction to Local Anaesthetics

Introduction

Welcome to another episode in our Local Anaesthetics series! Today we’re covering cocaine – the drug that launched spinal anaesthesia and still finds clinical use in ENT surgery. While we don’t use it as anaesthetists very often, understanding cocaine is crucial for FRCA candidates because it illustrates fundamental local anaesthetic principles and you may encounter its complications.

This episode covers the fascinating history of spinal anaesthesia (spoiler: it really did involve testicular traction and iron hammers), cocaine’s complex pharmacology as both a local anaesthetic and sympathomimetic, and the emergency management of cocaine toxicity. We’ll explore why ENT surgeons still use it, how it differs from other local anaesthetics, and what to do when someone presents with cocaine-induced complications.

From August Bier’s painful experiments to modern emergency management with benzodiazepines and avoiding unopposed alpha activity, this episode provides essential knowledge for understanding both historical context and contemporary clinical challenges.

Duration of Episode: 23 minutes

Focus of Episode:

Historical development of spinal anaesthesia
Cocaine’s dual mechanism of action
Clinical applications in ENT surgery
Emergency management of cocaine toxicity
Pharmacokinetics and drug interactions

Links to other relevant episodes:

Local Anaesthetics Fundamentals
Prilocaine – Next episode

Quick Reference Tables

Cocaine Toxicity Management – Toxbase!

Presentation of Cocaine Toxicity	Treatment of Cocaine Toxicity
Agitation	Benzodiazepines
Seizures	Benzodiazepines
Hypertension	Benzodiazepines (avoid β-blockers), proceed to toxbase
Chest Pain	Nitrates + Benzodiazepines
VT/VF	8.4% Sodium Bicarbonate 100ml IV
Hypotension	Fluid + Consider cardiac dysfunction

Onset and Duration by Route for Cocaine

Route	Onset	Duration
Inhaled	3-5 seconds – ‘euphoria’	5-15 minutes
Nasal – local effect	5 minutes local effects –	60-90 minutes
Nasal – systemic effects	30-40 mins	100min HL for this fraction

Key Concept Principles

Why are we interested in this: Cocaine represents the prototype local anaesthetic that launched neuraxial anaesthesia. Understanding its pharmacology illustrates key principles of local anaesthetic action, sympathomimetic effects, and toxicity management. While rarely used by anaesthetists, its complications present in emergency situations requiring immediate recognition and management.

Cocaine Pharmacology

Classification of Cocaine

Name	Cocaine Hydrochloride
Class	Ester Local Anaesthetic
Chemical Name	Naturally occurring sympathomimetic alkaloid
Colour/Appearance	10% topical spray – Clear – Colourless
Molecular weight	311

PharmacoDynamics of Cocaine

Mechanism of Action	Sodium Channel Blockade (Vaughan-Williams 1C effect) Vasoconstricting Sympathomimetic via Central Monoamine reuptake inhibition by blocking post synaptic reuptake proteins< Causing increased Dopamine/noradrenaline/adrenaline/serotonin concentrations in synaptic clefts
Clinical Use	Topical Local anaesthesia – ENT Surgery<br>Not used for eyeballs as it causes corneal irritation<br>Altitude sickness (traditional use)
Dose Onset time	Topical: 1.5mg/kg Epidural: Not used Infiltration: Not used Topical: Rapid onset IV: Not used therapeutically 30% of nasal dose is absorbed Peak plasma concentration at 30-40 minutes Tracheal application shows slower uptake – effects at 2 hours Doesn’t last long enough to be clinically useful neuraxially
Side effects	CVS: Tachycardia, Hypertension, Myocardial ischaemia secondary to coronary vasospasm, Arrhythmias due to ischaemia, Positive inotropic effects, Vasospasm of other vasculature (GI ischaemia) Resp:Tachypnoea, Respiratory mucosa necrosis, Chronic crack use = Crack lung (fibrotic changes) CNS:Euphoria, Anxiety/Paranoia/Psychosis, Mydriasis (dilated pupils), Headaches, Sub-arachnoid haemorrhage (hypertension), Seizures (vasospasm/bleeding) GI: Oral ingestion = ischaemic gut, “Packing” rupture = gut necrosis if not fatal overdose Renal: – Metabolic & Endocrine: Can progress to Serotonin Syndrome (Lethal hyperpyrexia) TRIAD: CNS (agitation/altered mentation), NEUROMUSCULAR (tremulousness, excitability), AUTONOMIC (Pyrexia, Tachycardia, Hypertension) Contraindications: IHD/Vascular disease, Uncontrolled Hypertension, Porphyria

Table of Cocaine Pharmacodynamics

Pharmacokinetics of Cocaine

Pharmacokinetics of Cocaine
Absorption	Onset times: Inhalation: 3-5 seconds Nasal: 5 minutes (vasoconstriction slows uptake)
Distribution	Protein Binding: 95% protein bound PKA + (% un-ionised): pKa 8.6 Solubility: Around 6% unionised at physiological pH Volume of Distribution: –
Metabolism	Half-Life: 100 minutes Organ: Plasma and Liver Esterases Metabolites: Benzoylecgonine, Ecgonine methyl ester, Norcocaine IMPORTANT: If concomitant alcohol → Cocaethylene forms (slower breakdown, more potent than cocaine)
Elimination	Clearance: Very rapid via plasma esterases Elimination: Inhaled: 5-15 minutes, Nasal: 60-90 minutes The elimination half-life is ~100 minutes
OTHER:	Cocaine and suxamethonium prolong each other (compete for cholinesterases)<br>Cocaethylene has double the half-life of cocaine<br>17% of cocaine becomes cocaethylene when co-administered with alcohol

Table of Cocaine Pharmakinetics

Special Populations / Considerations for Cocaine use intraoperatively

Patients with Cardiovascular Disease

Absolute contraindication in patients with IHD, uncontrolled hypertension, or vascular disease
Cocaine increases myocardial oxygen demand while reducing coronary blood flow
Risk of coronary vasospasm independent of dose or frequency of use

Perioperative Patients

Consider cocaine toxicity in agitated, hypertensive patients post-ENT surgery (especially if pain free)
Avoid β-blockers in hypertensive patients (unopposed α-agonism)
Monitor for delayed systemic absorption (up to 2 hours with tracheal application)
If they have Porphyria, think again about the cocaine!

Alcohol Co-ingestion

Formation of cocaethylene (more potent, longer-lasting than cocaine)
Increased risk of complications

Common Pitfalls and Safety for Clinical Cocaine Use

Emergency Management Priorities

ABC approach always first
Benzodiazepines are first-line for most complications
Avoid β-blockers in hypertensive patients (risk of unopposed α-agonism)
Consider aortic dissection in chest pain patients
Sodium bicarbonate 8.4% 100ml IV for cardiac arrest with cocaine, lipid emulsion would be a Hail Mary
- Also utilised if there is any cocaine toxicity and QRS broadening (like tri-cyclic overdose)

Drug Interactions

Suxamethonium: Prolonged action due to cholinesterase competition
Alcohol: Forms cocaethylene (more dangerous)
SSRIs/MAOIs: Risk of serotonin syndrome
β-blockers: Unopposed α-agonism, worsened hypertension

Clinical Recognition

Early signs: Agitation, tachycardia, hypertension, mydriasis
Late signs: Seizures, hypotension, arrhythmias, cardiac arrest
Always consider in unexplained cardiovascular collapse

Key Clinical Pearls for Clinical Cocaine Use

Historical significance: First local anaesthetic used for spinal anaesthesia (August Bier, 1898)
Dual mechanism: Both local anaesthetic AND sympathomimetic effects
ENT use: Vasoconstriction provides excellent surgical field
Toxicity management: “Benzos first line for everything” except cardiac arrest (then add bicarbonate)
Cocaine ACS: simple treatments first Morphine/benzos/aspirin/nitrates
Avoid β-blockers: Can worsen hypertension via unopposed α-agonism
Cocaethylene warning: Alcohol + cocaine = more dangerous combination
Emergency dose: 8.4% sodium bicarbonate 100ml IV for cardiac arrest
Lipid rescue: Case reports suggest possible benefit in refractory cases

Three Viva Style Questions

Question 1: Historical and Mechanism (you’re a purveyor of anaesthesia in 1920 for the first half of this question!)

“Tell me about the history of spinal anaesthesia and explain cocaine’s mechanism of action.”

Model Answer: Spinal anaesthesia began with August Bier in 1898, who used 15mg of cocaine intrathecally for a patient with tuberculous ankle surgery. The technique was developed after Quincke introduced lumbar puncture in 1891. Bier famously tested the technique on himself and his assistant, using needle pricks, testicular traction, and hitting shins with an iron hammer to test the block effectiveness.

Cocaine has a dual mechanism of action. As a local anaesthetic, it blocks voltage-gated sodium channels (Vaughan-Williams Class 1C effect), preventing nerve depolarization. However, it’s also a potent sympathomimetic, blocking reuptake of dopamine, noradrenaline, adrenaline, and serotonin at central synapses. This increases synaptic concentrations of these neurotransmitters, causing euphoria, tachycardia, hypertension, and increased myocardial oxygen demand. It also causes excellent local vasoconstriction, which is why ENT surgeons still use it.

Question 2: Clinical Applications and Contraindications

“An ENT surgeon wants to use cocaine for nasal surgery. What are the contraindications and how would you manage a patient who becomes agitated postoperatively?”

Model Answer: Cocaine is contraindicated in patients with ischaemic heart disease, uncontrolled hypertension, or any vascular disease. It’s also contraindicated in porphyria. The drug increases myocardial oxygen demand through tachycardia and hypertension while simultaneously causing coronary vasoconstriction – a dangerous combination.

For postoperative agitation, I’d first ensure ABC management and consider cocaine toxicity. A ‘safe’ dose of cocaine is 1.5mg/kg topically, noting 30% nasal absorption and peak plasma levels at 30-40 minutes. If the patient is agitated, hypertensive, and tachycardic without pain, this suggests cocaine toxicity.

Management involves benzodiazepines as first-line treatment. I’d avoid β-blockers as they cause unopposed α-agonism, potentially worsening hypertension and coronary vasospasm. If chest pain develops, I’d give nitrates. The effects typically resolve within 60-90 minutes for nasal administration as cocaine is rapidly metabolized by plasma esterases.

Question 3: Emergency Management

“A 35-year-old presents to A&E with chest pain after cocaine use. They’re now in VT. How would you manage this?”

Model Answer: This is a medical emergency requiring immediate systematic management. I’d call for help and follow ABCDE approach with ALS protocols for the VT.

Specifically for cocaine-induced VT, I’d give 8.4% sodium bicarbonate 100ml IV immediately. This helps counteract the sodium channel blockade effects of cocaine on the cardiac conduction system. I’d continue with standard VT management.

I’d consult Toxbase and consider contacting the National Poisons Information Service for complex cases.

For the underlying cocaine toxicity, benzodiazepines are first-line for agitation and hypertension. If there’s ongoing chest pain, I’d give nitrates (GTN). I need to consider that cocaine increases platelet aggregation and can cause both coronary vasospasm and thrombosis.

I’d also consider aortic dissection in the differential – cocaine-induced hypertension can cause this in susceptible patients. If standard measures fail, there are case reports of lipid emulsion rescue being beneficial. The patient needs intensive monitoring as cocaethylene formation (if alcohol co-ingested) can prolong and intensify effects.

Transcript Key Moments

Timestamps:

[00:00] – Introduction and series overview
[01:03] – Historical background of cocaine
[02:00] – History of spinal anaesthesia (Bier’s experiments)
[05:37] – Basic properties and mechanism of action
[07:54] – Clinical uses and dosing
[09:40] – Pharmacodynamics and systemic effects
[13:42] – Contraindications and clinical considerations
[14:20] – Pharmacokinetics
[17:21] – Complications and management of cocaine toxicity
[21:18] – Perioperative considerations
[21:43] – Cocaethylene research
[22:18] – Conclusion

Transcript

Gas Gas Gas – Episode 32: Cocaine (Local Anaesthetics Series)

Introduction and Series Overview

00:00 – 01:03

Hello everyone, this is James at the Gas Gas Gas. Welcome to the next episode of our Local Anaesthetics series. Today we’re covering cocaine, which seems to be typically used by our ENT colleagues. The next episode in the series is going to be on prilocaine.

I’d just like to take this moment before we get stuck into the show to remind you guys there’s a donate link in the show notes and on the website – help funding podcast hosting where we’re posting etc. is very much appreciated.

Historical Background of Cocaine

01:03 – 02:00

Cocaine is derived from the coca bush called Erythroxylon coca. It’s a South American native plant, probably original to the Andes, and has been used for a very long time whereby indigenous tribes chew the coca leaf – something that still happens today. But coca leaves are probably not very useful for rubbing into tracheas or intranasal cavities.

In 1855, it was extracted and purified – the cocaine element of the coca leaf. Then Karl Koller in 1884 used it to topically anaesthetise an eyeball, and that’s probably one of the first documented uses of cocaine. We’re not really the most prolific eyeball anaesthetists as anaesthetists, but we do like spinal anaesthesia though.

The History of Cocaine and Spinal Anaesthesia

02:00 – 05:37

Before we pile into cocaine, I wanted to talk about the history of cocaine and spinal anaesthesia. You might have heard the story – this is courtesy of the Association of Anaesthetists of Great Britain and Ireland. It all bears down to: did it really involve knees and cricket bats? The answer is it involved shins and another implement.

So kicking off – who stuck local anaesthetics in the intrathecal space first? There’s an American called J. Leonard Corning, a neurologist, who injected a dog in 1885 in what he expected to be its spinal canal, and a human a bit later. But looking at the needles he was likely using and his anatomical understanding, assuming that epidural vessels would carry agent to the spinal cord, he was likely injecting in the epidural space and getting some clinical effect there.

However, a number of fortuitous events came together. Heinrich Irenäus Quincke (Quincke needle fame) in 1891 started lumbar puncturing people to drop their intracranial pressure. And in 1898, August Bier of Bier’s block and now spinal anaesthetic fame injected 15 milligrams of cocaine using Quincke’s lumbar puncture technique for a patient with a tuberculous ankle. The surgery went well, but the patient did have a headache and vomiting postoperatively, which you would somewhat expect seeing it was probably a needle the size of a scaffolding pole.

However, it worked. He did this five more times in different patients and then figured he’d best actually understand this in a bit more detail. His patients maybe weren’t the best at describing the clinical onset and depth of anaesthesia to him, so he convinced his assistant to have a go at injecting local anaesthetic into his spinal cord.

His assistant had a go. However, they anecdotally spilled a lot of CSF, and I think August Bier decided that perhaps roles should reverse here. So he successfully cocainised his assistant’s spinal cord. There were a number of testing procedures: needle pricks in the thigh, apparently some fairly robust testicular traction, and then hitting the poor assistant in the shins with an iron hammer. I’m sure there’s no parallels to draw with current practice.

However, they both did have headaches and dizziness afterwards, and as you would expect, the test subject possessed a number of new bruises. But this was perhaps the first documented evidence of spinal anaesthesia being described fairly clearly.

The last thing I want to say is Theodore Tuffier caught wind of this and took this technique and popularised it. He also went on to coin Tuffier’s line, which I hope we all know – the line that intersects the L3-4 interspace from the tops of the iliac crests, which is a great way to approximate where you are on someone’s back. Although I think there’s some evidence that says if you ask someone what interspace they just did the injection at and then count it, it appears that we’re not as accurate as we think we are.

Basic Properties and Mechanism of Action

05:37 – 07:54

Cocaine is a naturally occurring sympathomimetic alkaloid. It comes in two varieties: cocaine hydrochloride (water-soluble, crystalline powder – probably what we’re mostly using in hospitals) and freebase cocaine (crack cocaine, the version that gets smoked). I should probably take this opportunity to say that cocaine is bad, and we’re going to learn about how devastatingly bad it is for you, especially in large amounts or if you’ve got any whiff of hypertensive or atherosclerotic disease. Drugs are bad, kids. Don’t do them.

Cocaine hydrochloride is an ester-classed local anaesthetic. It classically comes as a 10% topical spray or solution, is clear and colourless, and has a molecular weight of 311.

How does it work? It actually does quite a few different things:

From a local anaesthesia perspective, it’s a sodium channel blocker (Vaughan Williams 1C effect)
It causes vasoconstriction locally – that’s why people who snort cocaine end up with nosebleeds as they damage and necrose their nasal mucosa and can eventually end up with perforated cartilages in their nose
It’s a sympathomimetic – you could describe it as a central monoamine reuptake inhibitor because it blocks post-synaptic reuptake of dopamine, noradrenaline, adrenaline and serotonin

You can imagine if we’re accumulating those four agents in your synaptic clefts in your central nervous system, a number of things are going to happen. Dopamine: reward, euphoria, feeling great. Serotonin: euphoria, feeling great, feeling like you’re on top of the world. But noradrenaline and adrenaline make you more awake and have other effects on your centrally mediated blood pressure through your locus coeruleus, whereby you end up tachycardic and hypertensive.

Clinical Uses and Dosing

07:54 – 09:40

What do we use it for clinically? I think it used to be used quite a lot in dental anaesthesia. However, now they just use those clever little glass ampoules of lidocaine and inject to their heart’s content. It’s still used a lot in ENT surgery because of its potent vasoconstricting effects that really do open up the nasal cavity and allow the surgeon to get in there without scraping along too much mucosa. It also controls bleeding in the clinical operative field – when you’re manoeuvring around a nasal concha and there’s not much room, any bit of bleeding wrecks your surgical field.

We do not use it for eyeballs because it causes corneal irritation. Those indigenous tribes – although I’m sure they’re probably somewhat addicted to the coca leaf – chewing it helps altitude sickness, but it’s certainly not first line. Can’t imagine getting tachycardic, hypertensive, with increased respiratory rate and feeling really great and on top of the world when you’re literally on Everest puts you in a very safe frame of mind.

The dose: 1.5 milligrams per kilogram as a topical dose, which has rapid onset. If we’re putting it in someone’s nose to contract that mucosa down and anaesthetise it, about 30% of the dose is absorbed and you see a peak plasma concentration of that intranasal dose at about 30 or 40 minutes into the surgical case. Interestingly, if used in the trachea during bronchoscopy, it demonstrates slower uptake and you can see effects almost two hours later. From a spinal perspective, it doesn’t really last long enough to make it useful – 30 to 40 minutes is what’s created.

Pharmacodynamics and Systemic Effects

09:40 – 13:42

From a cardiovascular standpoint, it causes tachycardia and hypertension. Those in themselves increase myocardial workload. As you know, tachycardia means less time in diastole. The heart on the left side – the left ventricle – is perfused in diastole only (right ventricle is perfused throughout the cycle). Hypertension increases afterload, meaning increased LV tension and therefore work. But then we add insult to injury because we cause coronary vasoconstriction and sometimes even coronary vasospasm.

So now we’ve got a heart that’s working harder that’s getting less blood flow – you can see that’s probably not a great combination. It also has positive inotropic effects on the heart, so it’s now squeezing harder against more pressure, faster. This is a recipe for cardiovascular problems. If they get coronary vasospasm, they’re going to get myocardial ischaemia. If they don’t get the vasospasm, they’re still at risk of ischaemia. Younger people might tolerate that, but anyone who has any whiff of coronary artery disease is at higher chance of problems.

Imagine the anecdotal person who does cocaine at a wedding – they used to do cocaine when younger and thought “one last hurrah” and then down they go as a sweaty pile and off to hospital they trot with their new chest pain. But remember, hypertension means increased tightness of vessels throughout the body, and you can get vasospasm of other vasculature (the GI tract, etc.).

From a respiratory perspective, it causes tachypnoea from the sympathomimetic effects. You can get respiratory mucosa necrosis (your nose), and for those unfortunate individuals smoking crack cocaine, chronic consumption leads to crack lung, which is a fibrotic awfulness. I haven’t read about what that mechanism may be, but I imagine if you’re causing vasoconstriction in your nose with cocaine, you might cause it in your lungs and hypoperfuse your poor little alveoli.

Central nervous system effects: you’d hope euphoria – the patient feels great. But also anxiety, paranoia, and it can trigger psychosis, cause headaches. They get mydriasis, and if you get cerebral vasospasm, you might have a seizure.

GI effects: I mentioned the potential of ischaemic GI tract. However, if you have an unlucky person who’s ended up trying to smuggle cocaine in packets that they’ve eaten and one bursts, that’s going to be very neat cocaine – it won’t have been cut because they want to transfer the largest amount of pure stuff so they can cut it on the other side. Someone who’s now ingested a load of cocaine – it’s bad news. You will certainly end up with GI tract ischaemia if you survive the physiological insult of that much cocaine.

From a metabolic or endocrine perspective, it’s a monoamine reuptake inhibitor, which means it can cause serotonin syndrome. If the patient’s already on fluoxetine and having cocaine as well, they might end up quite full of serotonin and in that agitated, altered mental state where they’re tremulous, excitable, tachycardic, hypertensive, and pyrexic – that pyrexia can be lethal.

Contraindications and Clinical Considerations

13:42 – 14:20

I’m sure you can already guess what the contraindications to cocaine use might be. Anyone with ischaemic heart disease, cardiovascular disease, or uncontrolled hypertension really should not be having cocaine in their nose courtesy of the ENT surgeons. But also porphyria – porphyria is just a spooky thing that’s intolerant to many odd things.

Pharmacokinetics

14:20 – 17:21

From a pharmacokinetics perspective, the relevant one is onset time intranasally – it takes about five minutes to start working. The vasoconstriction that it mediates slows its uptake but also prolongs the effect at the site of action.

From a distribution perspective, cocaine is 95% protein-bound, has a pKa of 8.6, and works out to be around 6% unionised, so that fraction’s quite low.

From a metabolism perspective, the important thing to remember is esters are broken down by esterases. The interesting thing about cocaine is that liver esterases can also get involved in clearance. There are metabolites of cocaine: benzoylecgonine, ecgonine methyl ester, and norcocaine.

However, the interesting thing is when someone has plasma alcohol and plasma cocaine, those two bind up quite happily and you get something called cocaethylene. This is much harder to break down than standard cocaine and is actually more potent than cocaine itself. So we return to our anecdote of someone at a wedding who shouldn’t have been doing cocaine but chose to even though they were hypertensive and on ramipril, and they’ve been drinking and have cocaine – you can imagine that’s a suboptimal situation.

Perhaps one of the saving graces of cocaine is it only lasts for about 100 minutes. If inhaled, it lasts even less – 5 to 15 minutes – because the plasma esterase system is exceedingly busy and voracious in nature. You could almost throw a sofa at it and it would probably break it down if that sofa was made of ester molecules. When administered nasally, it takes about 60 to 90 minutes to clear.

Cocaine and suxamethonium probably prolong each other as they compete for cholinesterases. Note that there are plasma esterases and plasma pseudocholinesterases. There’s always going to be crosstalk between everything, although proteins have certain preferences for molecules.

Complications and Management of Cocaine Toxicity

17:21 – 21:18

I’m now thinking you’re the anaesthetist on call and you’ve been called to someone in VT because they’ve had far too much cocaine. Remember, any cocaine is technically far too much. What are you going to do? Toxbase is really quite useful.

The important questions with anyone coming with cocaine toxicity:

If they’re agitated: give them benzodiazepines
If they’re having seizures: give them benzodiazepines
If they’ve got hypertension: give them benzodiazepines
If they’ve got hypotension: you could give them fluid, but you need to start thinking they’re going to have myocardial dysfunction – really they shouldn’t have low blood pressure, so something has happened

What do you do if the benzodiazepines aren’t working? Well, probably more benzodiazepines. From a high blood pressure perspective, if they’re having myocardial ischaemia, do not just beta-block them because you’ll end up with unopposed alpha and can actually make things worse. Toxbase mentions labetalol, although some other sources steer away from labetalol to start with.

If someone has chest pain, give them nitrates – give them GTN. If that works and their pain comes back, start a GTN infusion. Interestingly, cocaine also improves platelet function, improving how platelets respond to ADP and inhibiting plasminogen. You can imagine if someone’s got coronary vasospasm, sluggish flow in their arteries, maybe some slightly gnarly artery, and now their platelets work better, you might go from having coronary vasospasm to relieving that with benzodiazepines but then having persisting ischaemia because they’ve now got a lump of clot in their coronary that wasn’t there to begin with.

Another important thing with a patient presenting with chest pain from cocaine: don’t just immediately pile into thinking it’s coronary vasospasm or myocardial ischaemia, because someone with slightly crusty arteries who takes cocaine and gets hypertensive might end up dissecting something.

What about your patient who’s taken loads of cocaine, had chest pain, and now they’re in ventricular dysrhythmia? Toxbase suggests that bicarbonate (sodium bicarbonate 8.4%, 100 mls) either very quickly if they’re in cardiac arrest or as a more thoughtful infusion if they’re not and conscious, is a good way to try and help counter that sodium channel blockade. If they’ve got a dysrhythmia, they might have enough cocaine in their system to block the sodium channels on their cardiac conducting system.

There are reports of lipid emulsion rescue being used at a case report level to try and counter that, which sounds a bit like local anaesthetic toxicity. There’s a website for lipid emulsion rescue therapy with case reports of giving it a go when nothing else is left to do.

Perioperative Considerations

21:18 – 21:43

Bringing it back to the patient in front of you in theatre: if they’ve had their nose packed with cocaine for surgery and they’ve woken up agitated, hypertensive, maybe tremulous but tachycardic and not complaining of pain and muddled, you need to think they might be cocaine toxic. Ideally that’s been avoided because you’ve not administered too much cocaine to their intranasal space, but in that case, absolutely reach for some benzodiazepines. Clearance is about 100 minutes – hopefully they’ve not been drinking alcohol and ended up with that cocaethylene.

Cocaethylene Research

21:43 – 22:18

Cocaethylene apparently has a slightly longer half-life – approximately double that of cocaine. There’s research from Yale experimental pharmacology which found that for equimolar doses, subjects weren’t terribly able to differentiate between whether they’d been administered cocaine or cocaethylene.

There was another patient group administered cocaine as an IV infusion who were co-administered alcohol. This identified that the effects were more pronounced, and about 17% of the cocaine became this cocaethylene, with alterations in clearance of metabolites into the urine, suggesting it’s taking longer for the plasma esterase system and liver to tidy up that molecule.

Conclusion

22:18 – 23:27

That was probably everything you certainly need to know about cocaine for the FRCA exam, plus a little trip down memory lane with spinal anaesthesia, and the things you should probably be thinking about if you’re going to a cocaine-flavoured cardiac arrest or poorly person. But have a look at Toxbase as well.

Thank you very much for listening – you’ve successfully got to the end of this podcast. I hope you enjoyed it. Next week is prilocaine, and I’ll see you guys then.

Thanks for listening. I hope you found it useful, but if you found it awful, do let me know. Please like and subscribe, register with whichever podcast platform you find yourself using, and leave a comment if you think I need to square something away. I just want to make sure you guys know that every day you are getting better at this. There is a bucket of content to try and consume, and it’s like drinking from a fire hose. Take it day by day, don’t overcook yourself, don’t freak out, and keep studying.

This is the full, Raw Show Transcript – Courtesy of Whisper LLM

00:00-00:00
Please listen carefully.

00:30-00:31
And let’s get on with the show.

00:34-00:36
Hello everyone, this is James at the Gas Gas Gas.

00:37-00:40
Welcome to the next episode of our Local Anesthetics series.

00:40-00:42
And today we’re covering cocaine.

00:43-00:46
This seems to be typically used by our ENT colleagues.

00:47-00:50
The next episode in the series is going to be on prilocaine.

00:50-00:52
And I’d just like to take this moment before we get stuck into the show.

00:53-00:56
Just to remind you guys, there’s a donate link in the show notes and on the website.

00:57-01:03
like helping fund a podcast hosting where we’re posting etc very much appreciated. Anywho history

01:03-01:09
of cocaine. So cocaine is derived from the cocoa bush and that bush is called erythrozylon coca.

01:09-01:14
It’s a South American native plant and it’s probably original to the Andes and has been

01:15-01:20
used for a very very very long time whereby indigenous tribes chew the cocoa leaf and that’s

01:20-01:24
something that still happens today. But cocoa leaves are probably not very useful at rubbing

01:24-01:32
into tracheas or intranasal cavities. Then 1855 it was extracted and purified the cocaine element

01:32-01:40
of the cocoa leaf. Then Carl Coller in 1884 used it to topically anaesthetise an eyeball and that’s

01:40-01:45
probably one of the first documented uses of cocaine. Yeah but we’re not really the most

01:46-01:51
prolific eyeball anaesthetisers as anaesthetists. We do like spinal anaesthesia though and the

01:51-01:56
question is before we pile into cocaine I just wanted to talk a little bit about the history of

01:56-02:00
cocaine and spinal anaesthesia you might have heard the story I think I’ve heard parts of the story

02:01-02:05
here goes and this is courtesy of the Association of Anesthetists of Great Britain and Ireland

02:06-02:10
there’s a link to the article on their web page at the bottom of the show notes but it all bears

02:10-02:16
down to did it really involve knees and cricket bats and the answer is it involved shins and

02:16-02:23
another implement. So kicking off, who stuck white clown aesthetics in the intrathecal space first?

02:24-02:30
So there’s an American called J. Leonard Corning, he was a neurologist, and he injected a dog in 1885

02:30-02:36
in its, what he was expecting to be, spinal canal, and a human a bit later. But looking at the needles

02:36-02:43
he was likely using and his anatomical understanding, assuming that epidural vessels would carry agent

02:43-02:50
to the spinal cord, he was likely injecting in the epidural space and getting some clinical effect

02:50-02:56
there. However, a number of fortuitous events came together. So Heinrich Irenaeus Quinky,

02:56-03:02
Quinky Needle fame, in 1891 started lumbar puncturing people to drop their intracranial

03:02-03:09
pressure. And in 1898, August Beer of Beer’s Block, and now spinal anaesthetic fame, in my mind,

03:10-03:16
injected 15 milligrams of cocaine using Quinky’s lumbar puncture technique for a patient with a

03:17-03:22
tuberculous ankle. And the surgery went well, but the patient did have a headache and vomiting

03:23-03:29
postoperatively, which you would somewhat expect, seeing it was probably the needle the size of a

03:29-03:35
scaffolding pole, or thereabouts, I’m sure. However, it worked. He did this five more times

03:35-03:41
in different patients and then he figured well I best actually understand this in a bit more detail

03:41-03:50
my patients maybe aren’t the best at describing the clinical onset and depth of anaesthesia to him

03:51-03:59
so he convinced his assistant to have a go at injecting local anaesthetic into his spinal cord

03:59-04:11
So his assistant had a go. However, they anecdotally spill a lot of CSF and I think August Beer decided that perhaps roles should reverse here.

04:11-04:16
So he successfully cocaineised his assistant’s spinal cord.

04:17-04:23
And there are a number of instilling tests, needle pricks in the thigh, apparently some fairly robust testicular traction,

04:24-04:29
and then hitting a poor assistant in the shins with an iron hammer.

04:29-04:33
I’m sure there’s no parallels to draw with current practice.

04:34-04:36
However, they both did have headaches and dizziness afterwards.

04:37-04:40
And as you would expect, the test subject possessed a number of new bruises.

04:41-04:47
But this was perhaps the first documented evidence of some spinal anaesthesia being described fairly clearly.

04:47-04:55
The last thing I want to say is Theodore Tufier caught wind of this and took this technique and popularised it.

04:55-05:05
He also went on to coin Tufier’s line, which I hope we all know of, which is the line that intersects the L3-4 interspace from the tops of the iliac crests,

05:05-05:09
which is a great way to approximate where you are on someone’s back.

05:09-05:17
Although I think there’s some evidence that says if you ask someone what interspace did you just do the injection at and then count it,

05:18-05:20
it appears that we’re not as accurate as we think we are.

05:20-05:24
So that was a little sojourn into the history of spinal

05:24-05:25
anaesthesia and

05:25-05:27
cocaining eyeballs and spinal cords.

05:28-05:29
I’m sure they didn’t abuse it at all.

05:30-05:32
That would be our dear fellow Halstead, poor bloke.

05:33-05:37
Great surgeon, troubled with access to such illicit agents.

05:37-05:44
Anyway, cocaine. Cocaine is a naturally occurring sympathomimetic alkaloid. It comes in two

05:45-05:49
varieties. There’s cocaine hydrochloride, that’s water soluble, crystalline powder,

05:51-05:55
probably what we’re mostly using in hospitals I imagine. And then there’s freebase cocaine and

05:55-06:00
this is crack cocaine and this is the version that gets smoked. Yummy. Not for the faint-hearted

06:00-06:05
I’m sure. I should probably take this opportunity to say that cocaine is bad and we’re all going to

06:05-06:12
learn about how devastatingly bad it is for you, especially in large amounts or if you’ve got any

06:12-06:18
sort of whiff of hypertensive or atherosclerotic disease. Drugs are bad, kids. Don’t do them.

06:19-06:25
Cocaine hydrochloride, we’re going to be clinical about this, is an ester-classed local anaesthetic.

06:25-06:31
It classically comes as a 10% topical spray or solution and it is clear and colourless and it

06:31-06:37
has a molecular weight of 311 if you’re interested in that. How does it work? It actually does quite

06:37-06:43
a few different things. So from a local anaesthesia perspective, you’ve guessed it, it is a sodium

06:43-06:49
channel blocker and this is a Vaughan Williams 1C effect. It also causes vasoconstriction locally

06:50-06:56
and that’s why people who snort cocaine end up with nosebleeds as they damage and necrose their

06:56-07:03
nasal mucosa and they can eventually end up with perforated cartilages in their nose. It also is a

07:03-07:09
sympathomimetic as I alluded to moments ago. You could describe it as a central monoamine reuptake

07:09-07:16
inhibitor because it blocks post-synaptic reuptake of dopamine, noradrenaline, adrenaline and

07:17-07:24
serotonin and you can imagine if we’re accumulating those four agents in your synaptic lifts in your

07:24-07:28
central nervous system, a number of things are going to happen. As we all know, dopamine, reward,

07:28-07:35
euphoria, feeling great. Serotonin, again, euphoria, feeling great, feeling like you’re on top of the

07:35-07:39
world. But then noradrenaline and adrenaline, they’re going to make you more awake. But also

07:40-07:44
they’re going to end up having other effects on your centrally mediated blood pressure through your

07:44-07:49
locus, seraleus, etc. whereby you end up tachycardic hypertensive. But I’m getting ahead of myself,

07:50-07:54
we’re going to go through that in a moment. What do we use it for clinically? So I think it used

07:54-07:56
but used quite a lot in dental anaesthesia.

07:56-08:01
However, now they just use those clever little glass ampoules of lidocaine

08:01-08:02
and injects to their heart’s content.

08:03-08:05
It’s still used a lot of ENT surgery,

08:05-08:08
and that’s because of its potent vasoconstricting effects

08:08-08:11
that really do open up the nasal cavity

08:11-08:14
and allow the surgeon to get in there without scraping along too much mucosa.

08:15-08:19
It also controls bleeding in this clinical operative field,

08:19-08:23
which when you think if you’re manoeuvring around a nasal concha

08:23-08:29
and there’s not much room, any bit of bleeding wrecks your surgical field. We do not use it for

08:29-08:36
eyeballs because it causes corneal irritation. And I think those indigenous tribes, although I’m sure

08:36-08:41
they’re probably somewhat addicted to the cocoa leaf in some regards, no judgments here folks,

08:41-08:47
chewing it helps altitude sickness, but it’s certainly not first line. And can’t imagine getting

08:48-08:54
tachycardic, hypertensive, a bit of an increased respiratory rate and feeling really great and on

08:54-08:59
top of the world when you’re literally on Everest puts you in a very safe frame of mind. Anyway,

08:59-09:07
the dose. So 1.5 milligrams per kilo as a topical dose which has a rapid onset. If we’re putting it

09:07-09:13
in someone’s nose to try and contract that mucosa down and anaesthetise it, about 30% of the dose

09:13-09:20
is absorbed and you see a peak plasma concentration of that intranasal dose at about 30 or 40 minutes

09:20-09:26
into the surgical case. Interestingly if they’ve used it in the trachea during bronchoscopy it

09:26-09:31
demonstrates slower uptake and you can see effects almost two hours later. And of note from a cocaine

09:32-09:36
spinal cords perspective it doesn’t really last long enough to make it useful like 30 to 40 minutes

09:36-09:40
is what’s created. So pursuing pharmacodynamics of cocaine a bit

09:40-09:42
further we

09:42-09:43
need to think about the

09:43-09:48
profile, having spoken about its effects. From a cardiovascular standpoint, it causes a tachycardia

09:48-09:54
and it causes hypertension. Now, those in itself increase myocardial workload. As you know,

09:55-10:01
tachycardia, less time in diastole. The heart on the left side, the left ventricle, is perfused in

10:01-10:07
diastole only. Right ventricle is perfused throughout the cycle. Hypertension, increased

10:07-10:14
afterload that means increased lv tension and therefore work but then we add insult to injury

10:14-10:21
because we cause coronary vasoconstruction and sometimes even coronary vasospasm so now we’ve

10:21-10:25
got a heart that’s working harder that’s getting less blood flow and you can see that that’s

10:25-10:30
probably not a great combination it also has positive inotropic effects on the heart so it’s

10:30-10:37
now squeezing harder against more pressure faster. And you can imagine that this is a recipe for

10:38-10:42
cardiovascular problems. If they get coronary vasospasm they’re going to get myocardial ischemia.

10:43-10:47
If they don’t get the vasospasm they are still at risk of ischemia. Younger people might tolerate

10:47-10:53
that but anyone who has any whiff of coronary artery disease is at a higher chance of problems.

10:54-11:00
Imagine the anecdotal person who does cocaine at a wedding. They used to do cocaine when they

11:00-11:05
younger and they just thought one last hoorah and then down they go as a sweaty pile of spuds and

11:06-11:12
off to hospital they trot with their new chest pain daft. But also we focused a lot on the heart

11:12-11:19
there but remember hypertension means increased tightness of vessels throughout the body and you

11:19-11:26
can get vasospasm of other vasculature i.e. the GI tract etc. From a respiratory perspective

11:26-11:33
causes tachypnea. This is from the sympathomimetic side of things. You can get respiratory mucosa

11:33-11:40
necrosis, i.e. your nose, and for those unfortunate individuals who are smoking crack cocaine,

11:41-11:47
chronic consumption of crack cocaine leads to crack lung, which is a fibrotic awfulness.

11:47-11:52
I haven’t read about what that mechanism may be, but I imagine if you’re causing vasoconstriction

11:52-11:58
in your nose with cocaine, you might cause it in your lungs and hypoperfuse your poor little alveoli.

11:58-12:04
But don’t quote me on that. Central nervous system effects. So, you’d hope, euphoria. The patient

12:05-12:10
feels great. Oh, I’ve had my ENT surgery. Wow. Yeah, let’s go. But also, anxiety, paranoia,

12:11-12:22
and it can trigger psychosis, can cause people to have headaches. They get mydriasis, i.e. big

12:22-12:27
and if you get cerebral basal spasm or a sub-rack you might have a seizure. It’s not really

12:28-12:34
sounding like a strong cell here. What about GI? GI effects? So I mentioned the potential of ischemic

12:34-12:41
GI tracts however if you have an unlucky person who’s ended up having to try and smuggle cocaine

12:41-12:47
in packets that they’ve eaten and one of those packets bursts that’s going to be very neat cocaine

12:47-12:53
it’s not going to have been cut because they want to try and transfer the largest amount of pure

12:53-12:59
stuff as they can so they can cut it on the other side. So someone who’s now gone off and done a full

12:59-13:06
cocaine bear, ingested a load of cocaine, it’s bad news. You will certainly end up with GI tract

13:06-13:12
ischemia if you survive the physiological insult of that much cocaine. And then from a metabolic

13:12-13:18
or endocrine perspective. I mentioned it’s a myoamine reuptake inhibitor. That means amongst

13:18-13:24
other things it can cause, it can cause a serotonin syndrome. So if the patient’s already on floxetine

13:24-13:30
etc and then they’re having cocaine as well they might end up quite full of serotonin and end up

13:30-13:36
in that agitated altermentation state where they’re tremulous, excitable, they get tachycardic, they get

13:36-13:42
hypertensive, they get pyrexia and that pyrexia can be lethal. From a clinical perspective

13:42-13:42
I’m

13:42-13:42
sure you can

13:42-13:45
already guess what the contraindications to cocaine use might be.

13:46-13:49
And I would say that anyone with ischemic heart disease, cardiovascular disease,

13:50-13:54
or uncontrolled hypertension really should not be having cocaine in their nose

13:55-13:56
courtesy of the ENT surgeons.

13:56-14:00
But also porphyria is something to not administer cocaine to.

14:00-14:05
And porphyria is just a spooky thing that is intolerant to many the odd thing.

14:06-14:10
So that was the pharmacodynamics of cocaine for the FRCA primary exam.

14:10-14:20
I think it would be an interesting conversation to have in a viva, but I imagine it probably is fair game because it’s a local anaesthetic that is used and has an interesting side effect profile.

14:20-14:28
So from a pharmacokinetics of cocaine perspective, the real relevant one is onset time intranasally.

14:28-14:32
And we know that it takes about five minutes to start working.

14:32-14:41
The vasoconstriction that it mediates slows its uptake, but it also in some way prolongs the onset of the site of action that we’re interested in.

14:42-14:55
From a distribution perspective, cocaine is 95% protein bound, has a pKa of 8.6, and that seems to work out that it’s around 6% unionised, so that fraction’s quite low.

14:55-15:07
From a metabolism perspective, the important thing to remember is esters are broken down by esterases, and that’s a trick of the name for all you people trying to remember stuff.

15:07-15:09
Esters broken down by esterases, shocker.

15:10-15:17
The interesting thing about cocaine is that the liver esterases can also get involved in clearance.

15:17-15:21
There are a number of metabolites of cocaine, which are somewhat hard to pronounce.

15:21-15:28
So benzoyl-lechagonine, echagonine, methyl ester and norkane.

15:28-15:35
However, the interesting thing is when someone has plasma alcohol and plasma cocaine,

15:36-15:38
those two bind up quite happily.

15:39-15:44
you get something called cocaethylene. This is much harder to break down than standard cocaine

15:45-15:52
and actually is more potent than the cocaine itself. So we return to our anecdote of someone

15:52-15:57
at a wedding who shouldn’t have been doing cocaine but chose to even though they were a bit

15:57-16:03
hypertensive now and take Ramipril and they’ve been drinking and have cocaine. You can imagine

16:03-16:09
that that is a suboptimal situation. I’d like to point out that that hasn’t happened to me but it’s

16:09-16:14
of an anecdote type thing that you hear on the grapevine. Offset. So perhaps one of the saving

16:14-16:20
graces of cocaine is it only lasts for about 100 minutes. If it’s inhaled it lasts even less than

16:20-16:26
that, 5 to 15 minutes, and that’s because we need to remember that the plasma esterase system is a

16:26-16:27
exceedingly

16:27-16:34
busy metabolic system that is vacuous in nature. You could almost throw a sofa at it and

16:34-16:40
it probably would break it down if that soda was made of ester molecules and had sufficient surface

16:40-16:48
area etc. When it’s administered nasally it takes about 60 to 90 minutes to clear. I’m going to talk

16:48-16:53
a little bit more about cocaethylene in a second. Now the other thing we need to think about is what

16:53-16:59
prolongs what. So cocaine and sucks probably prolong each other as they compete for choline

17:00-17:06
esterases. Note that there are plasma esterases and plasma pseudoclon esterases. There’s always

17:06-17:11
going to be a little bit of crosstalk between everything, although we all know that proteins

17:11-17:16
have certain preferences for other molecules, but if there’s enough of that molecule around

17:16-17:20
that every now and again something binds, you’re going to see a bit of activity there.

17:21-17:26
Complications of cocaine. I’m now thinking you’re the anesthetist on call, you’ve just been called

17:26-17:32
someone who’s in VT because they’ve had far too much cocaine. And remember, any cocaine is

17:33-17:37
technically far too much. What are you going to do? So tox base is really quite useful and there’s

17:37-17:42
loads of other information on the internet. The important questions to go through your mind with

17:42-17:48
anyone who’s coming with cocaine toxicity is if they are agitated, give them benzos. If they’re

17:48-17:54
having seizures, give them benzos. If they’ve got hypertension, give them benzos. And if they’ve got

17:54-17:59
hypotension, well you could give them fluid but you need to start thinking that they’re going to have

17:59-18:04
myocardial dysfunction, impending badness because really they shouldn’t have a low blood pressure so

18:05-18:10
something has happened. What do you do if the benzos aren’t working? Well probably more benzos

18:11-18:18
from a high blood pressure perspective if they’re having myocardial ischemia do not just beta block

18:18-18:24
them because you’ll end up with unopposed alpha and you can actually make things worse. Toxbase

18:25-18:31
mentions libetolol, although some other sources steer away from libetolol to start with. If someone

18:31-18:37
has chest pain, give them nitrates, so give them some GTN. If that works and then their pain comes

18:37-18:46
back, start a GTN infusion. Interestingly, cocaine also improves platelet function, improving how a

18:46-18:52
platelet responds to ADP and inhibiting plasminogen, which as you can imagine if someone who’s got

18:52-18:57
coronary vasospasm, sluggish flow in their arteries, maybe some slightly gnarly artery,

18:57-19:01
and now you’re telling me that their platelets work better, you might go from having coronary

19:01-19:07
vasospasm to relieving that with the benzos, but then having persisting ischemia because actually

19:07-19:11
they’ve now got a lump of gunk in their coronary that wasn’t there to begin with.

19:12-19:16
Another important thing with a patient presenting with chest pain from cocaine,

19:16-19:21
don’t just immediately pile into thinking it’s the coronary vasospasm,

19:21-19:23
it’s their myocardial ischemia,

19:23-19:29
because someone with slightly crusty arteries who takes cocaine and gets hypertensive

19:30-19:31
might end up dissecting something.

19:32-19:35
So what about your patient who’s now taken loads of cocaine,

19:35-19:38
they’ve had some chest pain, and now they’re in a ventricular dysrhythmia?

19:38-19:47
Well, Tuxbase would suggest that bicarbonate, as in sodium bicarb, 8.4, 100 mils, either very quickly

19:47-19:52
if they’re in cardiac arrest or slightly more thoughtful infusion if they’re not and they’re

19:52-19:57
conscious, is a good way to try and help counter that sodium channel blockade because if they’ve

19:57-20:01
got a dysrhythmia then they might have enough cocaine in their system to block the sodium

20:01-20:07
channels on their cardiac conducting system. There’s reports of lipid emulsion rescue being

20:07-20:13
used at a case report level to try and counter that which sounds a little bit like local anesthetic

20:13-20:19
toxicity and I think there’s a website for lipid emulsion rescue therapy which has case reports of

20:20-20:24
giving it a go when nothing else is left to do. I’ll put a link in the show notes because that’s

20:24-20:29
quite interesting. Now I don’t want to go too far off piste thinking about cocaine toxicity

20:29-20:35
just bringing it back to the patient in front of you in the theatre. If they’ve had their nose

20:35-20:40
packed with cocaine for the purposes of surgery and then they’ve woken up and

20:40-20:44
they’re a bit agitated and a bit hypertensive maybe a bit tremulous but

20:45-20:48
tachycardic and not complaining of pain and muddled then you need to think that

20:48-20:53
maybe they’re a bit cocaine toxic now ideally that’s been avoided because

20:53-20:57
you’ve not ministered too much cocaine to their intranasal space courtesy of the

20:57-21:02
ENT surgeons but in that case absolutely reach for some benzodiazepines

21:02-21:08
clearance is about 100 minutes hopefully they’ve not been drinking alcohol and therefore ended up

21:08-21:09
with that cocaethylene stuff

21:09-21:11
cocaethylene

21:11-21:13
apparently has slightly longer half-life

21:14-21:18
approximately double that of cocaine there’s a little bit of research out there although not a

21:18-21:27
lot something out of yale experimental pharmacology which found that for equimolar doses the subjects

21:27-21:34
weren’t terribly able to differentiate between if they’d been administered cocaine or cocaethylene.

21:35-21:43
There was another patient group administered cocaine as an IV infusion who were co-administered

21:44-21:52
alcohol. This identified that they found that the effects were more pronounced, but also

21:52-22:02
So there was evidence to suggest that about 17% of the cocaine became this coke ethylene stuff

22:02-22:09
and that there were alterations in clearance to those metabolites into the urine,

22:09-22:17
which would suggest that it’s taking longer for the plasma esterase system and the liver to start tidying up that molecule.

22:18-22:25
Anywho, that was probably everything you certainly need to know about cocaine for the FRCA exam

22:25-22:29
and also a little trip down memory lane, spinal anaesthesia,

22:30-22:34
and the things that you should probably be having working through your mind

22:35-22:41
if you’re going to a cocaine-flavoured cardiac arrest or poorly person.

22:42-22:43
But have a look at Toxbase as well.

22:44-22:47
Anyway, I’d like to say thank you very much for listening.

22:47-22:54
you’ve successfully got to the end of this podcast. I hope you enjoyed it. And next week is

22:54-22:58
Prilocaine. And I’ll see you guys then. Cheers and thank you very much.

23:03-23:07
Thanks for listening, guys. I hope you found it useful. But if you found it awful, do let me know.

23:07-23:12
Please like and subscribe, register with whichever podcast platform you find yourself using,

23:12-23:16
and leave a comment if you think I need to square something away. I just want to make sure that you

23:16-23:20
guys know that every day you are getting better at this. There is a bucket of content to try and

23:20-23:25
consume and it is like drinking from a fire hose. Take it day by day, don’t overcook yourself,

23:25-23:27
don’t freak out and keep studying.

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