Why this poison is interesting

The plan for this library set venlafaxine aside from the SSRI page deliberately, because the SSRI page's argument does not cover it. The SSRI page explains an overdose in which the drug does more of exactly what it does therapeutically — floods the synapse with serotonin — and reaches the reassuring conclusion that pure SSRI overdose is usually benign. Venlafaxine breaks that argument in one place: it causes seizures, and it causes them in proportion to the dose swallowed. A serotonin-reuptake mechanism does not straightforwardly predict a convulsion, and the seizure is the reason this drug has its own page.

It is also the antidepressant most burdened by a reputation the data only partly support. Venlafaxine is widely taught as the SNRI with tricyclic-like cardiotoxicity, and the UK label does list ventricular tachycardia, QT prolongation, bundle branch block and QRS prolongation among reported overdose events.¹ But the largest prospective series — 369 overdoses in 273 patients — found no arrhythmias… based on continuous telemetry, a median maximum QRS of 85 ms, and a QRS above 120 ms in only 7% of admissions.³ The label is a list of everything ever reported; the cohort is what actually happens. Holding those two documents against each other is most of what this page is for.

And it is two drugs at once. Venlafaxine is biotransformed to its major active metabolite, ODV, by CYP2D6¹, and that metabolite — O-desmethylvenlafaxine, desvenlafaxine — is a licensed antidepressant sold in its own right. The parent has a half-life of 5 ± 2 hours; the metabolite, 11 ± 2 hours.¹ The thing that does the work outlasts the thing that was swallowed, and a desvenlafaxine overdose is therefore a venlafaxine overdose with the first step already taken.

A poison is a drug whose kinetics have escaped its pharmacology.

The toxic principle

The toxic principle is the reuptake block itself, carried by two molecules rather than one. Venlafaxine and its major metabolite, O-desmethylvenlafaxine (ODV), are inhibitors of serotonin and norepinephrine reuptake; venlafaxine also weakly inhibits dopamine uptake, and the two species are very similar with respect to their overall action on neurotransmitter reuptake and receptor binding.¹ In overdose the same action is simply turned up: more synaptic serotonin and noradrenaline, in a patient who cannot clear either quickly because the metabolite half-life is eleven hours.

What distinguishes venlafaxine toxicologically from the SSRIs is what it does that serotonin reuptake inhibition does not explain. The label records that venlafaxine reduces β-adrenergic responsiveness¹ and, in overdose, produces convulsion, ECG changes and hypoglycaemia¹ — a set of effects that outrun a tidy monoamine story. The seizure is the clearest example. It is dose-dependent, it is common at large doses, and it is not a feature of the SSRIs; the mechanism is not fully established, and this page does not pretend otherwise. Inferred

Why the cardiac label and the cardiac cohort disagree

The overdose section lists ventricular tachycardia, QT prolongation, bundle branch block and QRS prolongation.¹ A dedicated study of 369 overdoses measured the reality: no arrhythmias on continuous telemetry, conduction defects in seven admissions of which five were pre-existing, an abnormal QT–HR pair in 6% (95% CI 4–10), a median maximum QRS of 85 ms, and a QRS above 120 ms in only 7% (95% CI 4–10) — with larger doses being more likely to widen the QRS.³ The conclusion was that venlafaxine causes only minor abnormalities in the QT and QRS intervals, unlikely to be associated with major arrhythmias, except possibly with large doses.³ A weak, dose-dependent sodium-channel effect that becomes clinically real only at the extreme, presented on the label as an unqualified list. This is the page's clearest instance of the difference between reported and typical. Traditional teaching

That the membrane effect is real at the extreme, but rare at ordinary overdose, places venlafaxine at the mild end of the family the sodium-channel blockade page describes, rather than alongside the tricyclics at its dangerous end. The relative fatal toxicity of the antidepressants tracks that ordering: retrospective data place venlafaxine higher than the SSRIs but lower than the tricyclics¹, a position confirmed by fatal-toxicity indices in UK self-poisoning cohorts.⁶

Toxicokinetics

Two features of the kinetics decide the clinical behaviour: an active metabolite with a longer half-life than the parent, and a modified-release preparation that spreads absorption over hours. Neither makes the drug more dialysable — the volume of distribution is large — but both extend the window in which a seizure can still occur.

Venlafaxine — a large volume of distribution, a longer-lived active metabolite, and a slow-release trap
Parameter	Therapeutic	In overdose	Why it changes
Absorption	At least 92% absorbed; bioavailability 40–45% through presystemic metabolism; immediate-release peak at 2 h (venlafaxine) and 3 h (ODV)², prolonged-release at 5.5 h and 9 h¹	The prolonged-release capsule spreads and delays the peak — but the total absorbed is unchanged	The modified-release preparation is the toxicological trap. A large ingestion of prolonged-release capsules delivers its dose over many hours, so the peak concentration — and the seizure risk that tracks it — can arrive well after a reassuring early assessment.
Distribution	Vd 4.4 ± 1.6 L/kg at steady state; protein binding 27% (venlafaxine) and 30% (ODV), minimally bound¹	Large volume — most of the drug is in tissue, not plasma	A 4.4 L/kg volume is why extracorporeal removal cannot help. Low protein binding would ordinarily favour dialysis, but a poison distributed four times body-water over cannot be pulled back through the plasma fast enough to matter.
Metabolism	Extensive hepatic metabolism; CYP2D6 → ODV (major, active); CYP3A4 → N-desmethylvenlafaxine (minor, less active)¹	CYP2D6 poor metabolisers run higher venlafaxine and lower ODV — but total (AUC) exposure is similar¹	Because the parent and the metabolite are pharmacologically alike, a slow metaboliser shifts the ratio without changing the total active burden. The polymorphism that matters for other drugs is neutralised here by the metabolite being as active as the parent.
Elimination	Renal: ~87% recovered in urine within 48 h — 5% unchanged venlafaxine, 29% free ODV, 26% conjugated ODV, 27% other¹	Renal clearance dominates, but of metabolite more than parent	The half-lives — 5 ± 2 h for venlafaxine, 11 ± 2 h for ODV¹ — set the observation period. The metabolite is the reason a patient is not clear at four hours.
Half-life	Venlafaxine 5 ± 2 h; ODV 11 ± 2 h; both prolonged in hepatic impairment¹	Long enough that the active species persists into a second day	A desvenlafaxine overdose is a venlafaxine overdose with the CYP2D6 step already done — the patient starts at the metabolite and stays there for its longer half-life.
Dialysability	—	Not useful. Forced diuresis, dialysis, hemoperfusion and exchange transfusion are unlikely to be of benefit¹	The label reaches this conclusion from the large volume of distribution, and no EXTRIP recommendation contradicts it. Removal from plasma cannot touch a poison that is mostly in tissue.

Metabolism and the metabolites

The metabolic story is unusual because the metabolite is not a detoxification product and not a poison — it is a second, equally active drug. Venlafaxine is biotransformed to its major active metabolite, ODV, by CYP2D6, and to a minor, less active metabolite, N-desmethylvenlafaxine, by CYP3A4.¹ There is no NAPQI here, no glycolate, no oxon. The pathway does not create toxicity; it merely converts one active molecule into another with a longer half-life.

Venlafaxine — a metabolism that makes a second drug, not a poison

VenlafaxineSNRI; half-life 5 ± 2 h¹
CYP2D6 — the major routeO-desmethylvenlafaxine (desvenlafaxine, ODV)Equally active SNRI; half-life 11 ± 2 h¹ — a licensed antidepressant in its own right
CYP3A4 — the minor routeN-desmethylvenlafaxineLess active¹ — a side branch of no toxicological consequence
Urine — ~87% in 48 h, mostly as free and conjugated ODV¹Only 5% leaves as unchanged venlafaxine¹ — the body clears the parent by turning it into the metabolite first

Elimination and accumulation

Elimination is renal and, for a therapeutic dose, unremarkable: about 87% of a dose is recovered in urine within 48 hours, largely as ODV and its conjugate.¹ The accumulation questions that matter in overdose are not about renal failure — they are about the preparation swallowed and the metabolite that persists.

The modified-release capsule spreads the dose across the danger window

Venlafaxine is dispensed overwhelmingly as a once-daily prolonged-release capsule, and the label's own kinetics show why that matters in overdose: the prolonged-release peak arrives at 5.5 hours for venlafaxine and 9 hours for ODV, against 2 and 3 hours for the immediate-release tablet.¹ A large ingestion of modified-release capsules therefore has its concentration — and its seizure risk — still rising when many overdoses would already be resolving. A patient who looks well at two hours after a slow-release overdose has not yet reached their peak. This is the same latent-phase logic the library applies to the modified-release calcium-channel blockers, produced here by the formulation rather than by the molecule. Established

The second accumulation point is the metabolite. Because ODV has more than double the half-life of venlafaxine and is renally cleared, it is the species that lingers into the second day, and it is the reason the observation period for a significant ingestion is measured against eleven hours, not five. There is no enterohepatic recirculation and no saturable pathway to prolong it further — the persistence is simply the metabolite's own half-life. Inferred

Target organs — and why those

Brain — the seizure threshold

TargetCortical excitability; the dose-dependent lowering of seizure threshold

Why hereThis is the organ that defines the page. Venlafaxine overdose lowers the seizure threshold in proportion to the dose, and the relationship has been modelled directly: the probability of a first seizure is about 0.05 at 1000 mg, 0.19 at 5000 mg and 0.75 at 10 000 mg.⁴ The mechanism is not a serotonin-reuptake effect — the SSRIs, which share that action, do not do this — and it is not fully established at the molecular level, so this card claims a dose–effect relationship rather than a mechanism. The seizure is the reason venlafaxine is not just a stronger SSRI. Inferred

At the bedsideGeneralised tonic–clonic seizures, typically early and sometimes recurrent; the risk climbs steeply above a few grams.⁴ Convulsion is listed among the commonest overdose events on the label.¹

Heart — the conduction system

TargetCardiac sodium and potassium channels at high concentration

Why hereIncluded because it is the most over-attributed organ in venlafaxine toxicity. The label lists ventricular tachycardia, QT prolongation and QRS widening¹; the prospective cohort found the effects to be real but minor and dose-dependent — QRS above 120 ms in 7%, an abnormal QT in 6%, and no telemetry arrhythmias.³ The conduction system is a target only at the extreme of ingestion, and treating every venlafaxine overdose as a tricyclic overwrites the evidence. Traditional teaching

At the bedsideSinus tachycardia (54%) and mild hypertension (40%) are the usual findings³; genuine QRS widening and QT prolongation appear with very large doses and warrant the sodium-channel and QT approaches used elsewhere in the library.³

Autonomic and vascular tone

TargetNoradrenaline reuptake block at the sympathetic synapse

Why hereThe noradrenergic half of the SNRI action shows itself as sympathetic excess: tachycardia and hypertension are the modal vital-sign changes, present in roughly half and two-fifths of overdoses respectively.³ This is the pharmacology doing more of its therapeutic job, not an off-target lesion — which is why it is usually mild and self-limiting. It is also why the picture differs from a pure SSRI overdose, where the noradrenergic drive is absent. Established

At the bedsideTachycardia and mild-to-moderate hypertension³; occasional severe hypertension (3%) or, less often, hypotension (5%)³. Mydriasis is common.¹

The serotonergic synapse — brain and periphery

TargetSerotonin reuptake block, producing serotonin toxicity when it summates with other serotonergic drugs

Why hereVenlafaxine can produce serotonin toxicity, but the desvenlafaxine cohort puts it in proportion: serotonin toxicity was diagnosed… in 7/75 (9%) single-agent overdoses, but only one of these met the Hunter Serotonin Toxicity Criteria, and none… had seizures, were admitted to intensive care or died.⁵ The full serotonin syndrome is largely a phenomenon of co-ingestion, which is why the mechanism belongs to the shared syndrome page rather than to this molecule. Established

At the bedsideClonus, hyperreflexia, agitation, tremor and hyperthermia when serotonin toxicity develops — usually mild, usually with a second serotonergic agent on board.⁵ See SSRIs and serotonin toxicity.

Timeline of effects

Two versions of the same overdose — the immediate-release tablet declares itself early, the modified-release capsule keeps climbing

Time

What you seeWhat is happening

0–4 h (immediate release)Early effects
What you seeTachycardia, mild hypertension, mydriasis, drowsiness, vomiting; a seizure may occur here after a large dose.¹³
What is happeningImmediate-release peak at 2–3 h.¹ Sympathetic drive from noradrenaline reuptake block; the seizure threshold is already lowered in proportion to the dose swallowed.⁴
Up to 9 h (modified release)The rising slope
What you seeDeceptively settled, then not. A patient can look well while a prolonged-release ingestion is still being absorbed.¹
What is happeningProlonged-release peaks at 5.5 h (venlafaxine) and 9 h (ODV).¹ The concentration — and the seizure probability — is still climbing after an early assessment would have reassured, which is why the slow-release preparation earns a latent phase the immediate-release tablet does not.
First 12–24 hPeak toxicity
What you seeThe window for generalised seizures, for genuine QRS/QT change after very large doses, and for serotonin toxicity if a second serotonergic drug is present.³⁴⁵
What is happeningPeak active drug — parent plus the longer-lived metabolite. Seizure probability tracks dose steeply above a few grams⁴; conduction effects appear only at the extreme.³
24–48 hResolution
What you seeGradual settling as concentrations fall; late seizures are unusual once absorption is complete and the patient has been seizure-free.
What is happeningRenal elimination clears both species; ~87% of the dose is recovered in urine within 48 h¹. The metabolite's 11-hour half-life is what carries the tail into the second day.

A gap made by a capsule, not by a metabolite

Venlafaxine and the SNRIs — the slow-release capsule — a modified-release preparation whose absorption is spread over hours, so the seizure risk of a large ingestion is still climbing long after presentation

The other 39 kinds of latent phase in this library

Amphetamines and MDMA — a hormone acting normally on a kidney behaving normally, while the patient supplies the water
Anticoagulants — clotting factors that were already made, still working — the poison stops production and nothing happens until the existing stock decays
Antipsychotics — a physical object in the stomach — extended-release quetiapine forming a pharmacobezoar
Arsenic — a tissue declaring on its own timetable rather than the poison's — the arsenic is excreted within days, but the nail that was growing while it circulated does not show its white transverse line for several weeks
Arsine and stibine — a red cell mass haemolysing faster than a kidney can cope with — the exposure is over, the haemolysis is silent until the urine changes colour, and the renal failure that follows is the cause of death
Baclofen — not the poisoning but its withdrawal — an implanted pump that has silently stopped delivering, with hours to days before anything appears
Beta-blockers — a repolarisation lesion waiting for an ectopic beat to fall inside it — sotalol prolongs the QT and then, for hours, nothing happens
Calcium-channel blockers — a tablet that has not yet dissolved
Carbamazepine — reduced gut motility from its own antimuscarinic effect, forming a reservoir that delays absorption and causes relapse on the second or third day
Carbon monoxide — an inflammatory process continuing after the poison itself has gone
Chlorine and ammonia — paraquat's cause at its shortest — the time an injured alveolar epithelium takes to leak
Cocaine — a package that has not yet failed — the calcium-channel blocker's cause moved outside the tablet, where wrapping integrity cannot be measured
Colchicine — antimitotic injury to fast-dividing tissues that declares itself over 24–72 hours, after a gastrointestinal phase that can appear to settle
Death cap and the amatoxin mushrooms — the interval before amatoxin-blocked transcription starves the hepatocyte of protein
Digoxin — distribution of the drug to its target — which that page argues is not a latent phase in the paracetamol sense at all
Ethylene glycol — paracetamol's cause with a different enzyme — glycolate accumulating behind glycolate oxidase while the patient looks merely drunk
GHB and GBL — not the poisoning but its withdrawal — a half-life under an hour means admission for any reason interrupts round-the-clock redosing
Hydrofluoric acid — an ion diffusing far enough to reach a nerve ending — and the thinner the solution, the further it travels before anybody feels it
Insulin — the long-acting analogue depot — a subcutaneous reservoir of glargine or degludec that releases insulin for a day or more, so hypoglycaemia can be delayed in onset and persist long after a soluble insulin would have cleared
Iron — a true remission — the corrosive injury settling while absorbed iron moves into the cells it will poison, so the patient improves on their way to the dangerous phase
Ketamine — nitrous oxide's cause on a longer clock — urothelial damage accumulating over months to years of repeated exposure
Lead — bone giving lead back — a store with a half-life of 10 to 30 years releasing its contents when pregnancy, lactation, menopause or osteoporosis resorbs it, so the blood concentration rises after the exposure has ended
Lithium — transport across cell membranes
Local anaesthetic systemic toxicity (LAST) — the tissue depot — a large-volume block absorbed slowly, so systemic toxicity can appear well after the injection is finished, not only at the moment of an intravascular one
Mercury — distribution on two clocks — tissue concentrations peaking within 24 hours everywhere except the brain, which is not reached until 2 to 3 days, and which then cannot let the poison out again
Metformin — drug accumulation and a lactic acidosis that build over hours, so a well-looking early patient can deteriorate
Methaemoglobin inducers — paracetamol's cause at its shortest — one to four hours manufacturing the toxic species
Methanol — paracetamol's cause again — formate accumulating behind a folate-dependent disposal step that primates perform poorly
Methotrexate — antifolate injury to fast-dividing tissues that declares itself over days, after an early phase that can be silent
Nitrous oxide — damage accumulating to a threshold
Opioids — an antidote wearing off before the poison does — renarcotisation, the only gap in this set that treatment creates rather than reveals
Organophosphate insecticides — a fat store emptying — and, separately, a second and unexplained lesion declaring itself at a neuromuscular junction the first phase had already left
Paracetamol — time spent manufacturing a toxic metabolite
Paraquat — the body responding to an injury that is already complete
Sodium-channel blockade — a gap that cannot be shortened
Sulfonylureas — delayed and recurrent hypoglycaemia, because the drug keeps releasing insulin long after the first glucose correction
Thallium — hair on its own clock rather than the poison's — sensory symptoms come first and the alopecia that makes the diagnosis obvious follows them, well after the interval in which treatment is recommended
Theophylline — a prolonged-release formulation whose peak may not arrive for twelve hours, so the concentration rises while the patient is still being assessed
Valproate — hyperammonaemia and carnitine depletion that build after ingestion, so encephalopathy can lag a reassuring early examination

Most latent phases in this library are metabolic — a poison has to be turned into its toxic form, or has to accumulate, before anything happens. Venlafaxine's gap is pharmaceutical: the modified-release capsule releases its dose over hours, so a large ingestion is still being absorbed when an early assessment would reassure, and the seizure risk peaks late. It is the same shape as the slow-release calcium-channel blockers — a formulation, not a molecule, holding the danger back.

What the mechanism predicts at the bedside

Expect a seizure, not an arrhythmia, as the dangerous event. The modelled seizure probability rises from about 5% at 1 g to 75% at 10 g⁴; the largest ECG cohort found no telemetry arrhythmias and only minor, dose-dependent QRS/QT change.³ The monitoring and the anticonvulsant readiness should follow the seizure risk.
A modified-release ingestion is not excluded by a well patient at two hours. The prolonged-release peak is at 5.5–9 h¹; the seizure risk of a large slow-release overdose is still climbing after an early assessment.
Activated charcoal has overdose-specific evidence here. Decontamination modelling found that it lowered the probability of the first seizure, though it did not change the modelled time to that seizure⁴ — a stronger statement than the general-principles charcoal recommendation attached to most drugs.
Benzodiazepines are the seizure treatment, as for the poison-induced seizures elsewhere in the library; they are also the first move if serotonin toxicity or agitation dominates.
Do not reach for dialysis. The label states forced diuresis, dialysis and haemoperfusion are unlikely to be of benefit¹, and a 4.4 L/kg volume of distribution is why.
Treat genuine QRS widening as sodium-channel blockade only when it is actually present — the minority of very large ingestions — using the approach on the sodium-channel blockade page, not prophylactically on every venlafaxine overdose.³
A desvenlafaxine overdose starts one step further along. The patient has ingested the active metabolite directly, with an 11-hour half-life¹; the clinical effects are the same but usually milder in single-agent ingestion.⁵
Co-ingestants change everything. The desvenlafaxine cohort's severe effects, its seizures and its serotonin toxicity clustered in the patients who took something else as well.⁵ The history of what else was swallowed is the most important part of the assessment.

The antidote, from the poison's side

There is no antidote. The label states it plainly: no specific antidotes for venlafaxine are known¹. What the mechanism offers instead is unusually specific guidance about which supportive measures fit, because the danger is a defined event — the seizure — rather than a slow organ injury.

Activated charcoal: The one decontamination measure with venlafaxine-specific evidence: modelling of 436 overdoses found that charcoal lowered the probability of a first seizure, though it did not change the modelled time to that seizure.⁴ The label also notes charcoal may… limit absorption.¹ See activated charcoal.
Benzodiazepines: The treatment for the seizure and for agitation or serotonin toxicity — a GABA-ergic brake on an over-excited cortex. Not venlafaxine-specific, but matched to the exact danger the drug produces.
Intravenous lipid emulsion: A rescue option for cardiovascular collapse after a massive ingestion, on the general grounds that venlafaxine is lipophilic and membrane-active at the extreme — not on venlafaxine-specific evidence. See lipid emulsion; reserve it for the collapsing patient, not the tachycardic one.
Sodium bicarbonate: Applies only to the minority with genuine QRS widening, borrowing the logic of the sodium-channel blockade page. The prospective cohort is the reason this is a conditional measure, not a default.³ See sodium bicarbonate.
Dialysis and haemoperfusion: Not useful, by the label's own assessment¹ — the volume of distribution is too large for extracorporeal removal to change the plasma concentration meaningfully.

Critical appraisal

The cardiotoxicity downgrade is the load-bearing judgement, and it has a citation for the doubt. The label lists ventricular tachycardia and QRS prolongation¹; Isbister's 369-overdose series found no telemetry arrhythmias, a median QRS of 85 ms and a QRS above 120 ms in only 7%.³ The Traditional teaching badge is applied because a specific, adequately powered study contests the received teaching — which is exactly the condition the house style requires before downgrading a mechanism, and not merely an absence of evidence for it.
The seizure mechanism is badged Inferred, not Established. The dose–response relationship is well demonstrated⁴, but the molecular reason venlafaxine lowers the seizure threshold when the SSRIs do not is not established, and the page claims the relationship without claiming the mechanism.
The seizure-probability figures are a model, not a count. The 5% / 19% / 75% values at 1/5/10 g are simulated from a logistic model of 436 overdoses⁴, with wide credible intervals at the top dose (0.30–0.96 at 10 g). They are quoted as a shape, not as precise risks.
The relative fatal toxicity is confounded, and the label says so. Venlafaxine's higher fatal-toxicity index than the SSRIs is real in the data¹⁶, but the label notes venlafaxine-treated patients carry a higher burden of suicide risk factors¹ — so the number reflects the population as much as the molecule. The page states the ordering (SSRI < venlafaxine < tricyclic) and the caveat together.
The desvenlafaxine data are extrapolated to duloxetine only cautiously. Cooper 2017 studied desvenlafaxine directly⁵; duloxetine is grouped under the SNRI heading of this page on pharmacological similarity, and the specific figures quoted are venlafaxine's and desvenlafaxine's, not duloxetine's.
No toxic-dose table, no lethal dose and no concentration threshold appears here. The label's approximately 3 grams is quoted as the threshold for severe poisoning symptoms¹ — a when-to-worry figure, not a lethal dose — and risk assessment belongs to TOXBASE and NPIS.
Serotonin toxicity is deliberately handed to the shared page. The mechanism, the Hunter criteria and the management of serotonin toxicity are on SSRIs and serotonin toxicity; this page states only that venlafaxine can contribute to it and that the full syndrome is largely a co-ingestion phenomenon.⁵

References

1
Efexor XL 150 mg hard prolonged release capsules (venlafaxine) — Summary of Product Characteristics. electronic medicines compendium, product 1219. Sections 4.9 (Overdose), 5.1 (Pharmacodynamic properties) and 5.2 (Pharmacokinetic properties). medicines.org.uk/emc/product/1219
2
Venlafaxine 75 mg tablets (immediate-release) — Summary of Product Characteristics. electronic medicines compendium, product 764 (Dexcel Pharma). Section 4.9 (Overdose) and 5.2 (Pharmacokinetic properties), cited where the immediate-release peak times differ from the prolonged-release capsule. medicines.org.uk/emc/product/764
3
Isbister GK. Electrocardiogram changes and arrhythmias in venlafaxine overdose. British Journal of Clinical Pharmacology 2009 May;67(5):572–6. PMID 19552753. 369 overdoses in 273 patients; no telemetry arrhythmias, median maximum QRS 85 ms, QRS >120 ms in 7%, abnormal QT–HR pair in 6%.
4
Kumar VV, Isbister GK, Duffull SB. The effect of decontamination procedures on the pharmacodynamics of venlafaxine in overdose. British Journal of Clinical Pharmacology 2011 Jul;72(1):125–32. PMID 21306417. 436 overdoses; modelled seizure probability 0.05 / 0.19 / 0.75 at 1000 / 5000 / 10 000 mg; activated charcoal lowered and delayed seizure risk.
5
Cooper JM, Brown JA, Cairns R, Isbister GK. Desvenlafaxine overdose and the occurrence of serotonin toxicity, seizures and cardiovascular effects. Clinical Toxicology (Phila) 2017 Jan;55(1):18–24. PMID 27622824. 182 overdoses; single-agent ingestions caused minor effects, no seizures and no ICU admission; severe effects clustered with co-ingestants.
6
Hawton K, Bergen H, Simkin S, et al. Toxicity of antidepressants: rates of suicide relative to prescribing and non-fatal overdose. British Journal of Psychiatry 2010 May;196(5):354–8. PMID 20435959. Fatal-toxicity data placing venlafaxine above the SSRIs and below the tricyclics.

Venlafaxine and the SNRIs

At a glance