Why this poison is interesting

Yew is interesting because it is a false friend of the previous page. Taxus baccata is one of the most lethal plants in the British flora, and its poisoning superficially resembles the cardiac-glycoside picture: vomiting, bradycardia, conduction block, collapse, and in severe cases hyperkalaemia. A clinician who has just learned that plant glycosides respond to digoxin-specific Fab is primed to make exactly the wrong move — because yew is not a glycoside at all, and the antidote that rescues foxglove does nothing here.

The toxic principle is a group of alkaloids — the taxines — which block cardiac sodium and calcium channels. That places yew, mechanistically, alongside the sodium-channel-blockade syndrome and the calcium-channel blockers, not alongside digoxin. The resemblance to glycoside toxicity is a coincidence of the final common pathway — a poisoned, slow, wide-complex heart looks similar whatever slowed it — and the resemblance is the danger.

The toxic principle

The yew alkaloids are a mixture — taxine A, taxine B and related compounds — and the pharmacology points to taxine B (and its isomers) as the principal cardiotoxin.¹ In the classic experimental work, taxines depress the fast inward sodium current and the slow inward calcium current in cardiac tissue, slowing depolarisation and conduction and depressing contractility.

The consequence at the ECG is progressive: QRS widening as sodium-channel blockade slows ventricular depolarisation, PR prolongation and AV block, bradyarrhythmia, and then ventricular tachyarrhythmia, ventricular fibrillation or asystole in fatal cases.¹ The widened QRS is the same electrophysiological lesion described on the sodium-channel-blockade page, which is why the bicarbonate manoeuvre used there is the rational response to the QRS here — even though it does not remove the taxine.

Toxicokinetics

The taxines are poorly characterised kinetically in humans — there is no licensed product, no summary of product characteristics and no formal pharmacokinetic study, and the honest kinetic table for yew is mostly empty. What can be said is qualitative and matters clinically.

Yew taxines — what is known, and how much is not
Parameter	Therapeutic	In overdose	Why it changes
Absorption	Rapid enough that severe cardiotoxicity is reported within a few hours of a substantial ingestion¹	Chewing the seeds or ingesting foliage releases the alkaloids; an intact swallowed seed may pass without releasing much toxin	The interval from ingestion to collapse can be short, so a well-appearing patient after a significant deliberate ingestion is not reassuring.
Distribution	Lipophilic alkaloids; presumed wide tissue distribution	Not quantified in humans	The absence of a measured volume of distribution is itself the point: there is no threshold concentration to chase and no level to guide treatment.
Metabolism / elimination	Hepatic metabolism of the taxine alkaloids is described but poorly quantified. Separately, 3,5-dimethoxyphenol — the aglycone of the yew leaf's own phenolic glycoside taxicatine, not a taxine metabolite — is released on ingestion and used as a forensic marker of Taxus poisoning²	Not usefully quantified for acute management	The forensic marker matters at autopsy and for confirming ingestion, not for real-time care.
Dialysability	—	No established role. No pharmacokinetic basis to expect extracorporeal removal to help	The extracorporeal intervention that has rescued yew poisoning is mechanical circulatory support (ECLS/VA-ECMO) to bridge a poisoned heart, not dialysis to remove the toxin. Inferred

Metabolism and the metabolites

Unlike the metabolic-activation stories elsewhere in this library, yew has no toxic metabolite to form — the taxine alkaloids are active as ingested. The metabolism section is short for the same reason it is short on the digoxin page: the parent is the poison.

Yew taxines — active on ingestion, no bioactivation step

Taxine alkaloids (seed / foliage)Already the toxic species. Taxine B the principal cardiotoxin¹
Absorption; block cardiac Na⁺ and Ca²⁺ channelsNo metabolic activation required
3,5-dimethoxyphenolA plant-derived forensic marker of Taxus ingestion — not a taxine metabolite; useful post-mortem, not for acute care²

Elimination and accumulation

There is little to add here that the kinetics table has not already conceded: elimination is hepatic and incompletely described, there is no accumulation story of the digoxin kind because yew poisoning is an acute single event rather than a chronic drift, and there is no level to follow. The clinically important corollary is that the duration of danger is set by how long the myocardium takes to recover, not by a measurable falling concentration, so the decision to continue or withdraw circulatory support is a bedside cardiological judgement rather than a toxicokinetic one.

Target organs — and why those

Yew is a cardiotoxin first and almost only. The channels it blocks exist elsewhere, but the heart is where blocking them is immediately lethal.

Myocardium and conducting system

TargetCardiac voltage-gated sodium channels and L-type calcium channels

Why hereBlocking the fast sodium current slows phase-0 depolarisation and widens the QRS; blocking the calcium current depresses contractility and nodal conduction. The heart is uniquely intolerant of both at once, so a dose that produces only paraesthesia or vomiting systemically produces conduction failure in the myocardium. Inferred

At the bedsideThe clinical course is dominated by bradyarrhythmia, widening QRS, AV block, ventricular arrhythmia and refractory cardiac arrest; collapse can be abrupt after a deceptively mild prodrome.¹

Gastrointestinal tract

TargetDirect mucosal irritation by plant material

Why hereAs with most toxic plant ingestions, the leaf and seed material is irritant, producing early nausea, vomiting and abdominal pain before the cardiac phase declares itself. Inferred

At the bedsideEarly GI symptoms are common and non-specific and should never be taken as the whole picture after a known yew ingestion.

Central and peripheral nervous system

TargetPresumed channel effects; described clinically more than mechanistically

Why hereDizziness, mydriasis, muscle weakness, tremor and reduced consciousness are reported, but the mechanistic account is thinner than the cardiac one and is best treated as observed rather than explained. Inferred

At the bedsideNeurological features accompany but do not dominate; the threat to life is cardiac.

Timeline of effects

Yew ingestion — a mild prodrome that can end abruptly

Time

What you seeWhat is happening

0–2 hProdrome
What you seeNausea, vomiting, abdominal pain, dizziness, mydriasis. The patient may not look seriously ill.
What is happeningPlant material irritating the gut; taxines being absorbed. Cardiac conduction not yet visibly affected.
1–several hCardiac phase
What you seeWidening QRS, PR prolongation, bradyarrhythmia, AV block, then ventricular arrhythmia; collapse can be sudden.
What is happeningSodium- and calcium-channel blockade established across the myocardium; conduction slows and contractility falls.
Refractory phaseArrest
What you seeCardiac arrest that is characteristically resistant to standard drugs and pacing.
What is happeningProfound channel blockade; the reported survivals from this point involve mechanical circulatory support bridging recovery, not a pharmacological reversal.

What the mechanism predicts at the bedside

Do not treat yew as a glycoside. Digoxin-specific Fab does not neutralise taxines — there is no glycoside for it to bind — and reaching for it wastes the narrow window. Isolated case reports have tried Fab in yew poisoning without convincing benefit, and it is not an antidote here.¹ Inferred
Treat the widened QRS as sodium-channel blockade. A progressively widening QRS is the same lesion as on the sodium-channel-blockade page, and sodium bicarbonate is the rational response to it — a sodium load and an alkaline shift — even though it does not remove the taxine.
Expect resistance to standard resuscitation. Yew cardiac arrest is characteristically refractory to drugs and pacing; the documented survivals from severe poisoning have generally required extracorporeal life support to bridge the myocardium through the toxic period. Early escalation and transfer thinking matter more here than another round of the same drug.
A normal first ECG does not clear the patient. Because collapse follows a variable prodrome, decisions rest on the ingestion history and continuous monitoring, not on a single reassuring tracing.
There is no level to chase. Management is guided by rhythm, haemodynamics and the ingestion history, with NPIS — not by a concentration.

The antidote, from the poison's side

This is the shortest antidote section in the botanical band, because there is no specific antidote to yew, and the honest thing a mechanism page can do is explain why.

That is a genuinely different antidote philosophy from the rest of this band. Foxglove has a specific binder; the death cap has a competitive hepatoprotectant; the adder has an antivenom. Yew has time, sodium and a pump — and the recognition that a poisoning which mimics a treatable one is more dangerous precisely because it invites the wrong treatment.

Critical appraisal

The channel-blockade mechanism is inferred from experimental preparations, not demonstrated in poisoned humans. That taxine B depresses cardiac sodium and calcium currents is established in vitro and in animal tissue; that this is precisely what produces the human ECG picture is a reasonable and widely accepted inference rather than a directly demonstrated causal chain.¹ Inferred
Which taxine matters most is a simplification. Taxine B and its isomers are identified as the principal cardiotoxic fraction, but yew contains a mixture whose composition varies by species, part and season, and human toxicity cannot be attributed cleanly to a single molecule.¹ Inferred
The role of bicarbonate is extrapolated from the sodium-channel-blockade syndrome, not proven in yew. Using bicarbonate for the widened QRS is mechanistically coherent and consistent with how the syndrome is treated generally, but there is no yew-specific trial evidence, and it treats a sign rather than the poison. Inferred
ECLS survival is reported, not quantified. Case reports describe survival of severe yew poisoning bridged by extracorporeal support, which establishes that recovery is possible if the heart is sustained; they do not establish a success rate, and severe yew poisoning remains frequently fatal.

References

1
Wilson CR, Sauer J, Hooser SB. Taxines: a review of the mechanism and toxicity of yew (Taxus spp.) alkaloids. Toxicon 2001;39(2–3):175–85. PMID 10978734.
2
Musshoff F, Jacob B, Fowinkel C, Daldrup T. Suicidal yew leave ingestion — phloroglucindimethylether (3,5-dimethoxyphenol) as a marker for poisoning from Taxus baccata. International Journal of Legal Medicine 1993;106(1):45–50. PMID 8398891.

Yew (taxine alkaloids)

At a glance