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Bezold-Jarisch Reflex
Related terms:

Bradycardia, Ischemia, Faintness, Blood Pressure, Infarction, Heart Rate,

Hypotension, Acute Heart Infarction

Cardiac Physiology
Michael A. Gropper MD, PhD, in Miller's Anesthesia, 2020

Bezold-Jarisch Reflex
The Bezold-Jarisch reflex responds to noxious ventricular stimuli sensed by
chemoreceptors and mechanoreceptors within the left ventricular wall by inducing
the triad of hypotension, bradycardia, and coronary artery dilatation.80 The
activated receptors communicate along unmyelinated vagal afferent type C fibers.
These fibers reflexively increase parasympathetic tone. Because it invokes
bradycardia, the Bezold-Jarisch reflex is thought of as a cardioprotective reflex. This
reflex has been implicated in the physiologic response to a range of cardiovascular
conditions such as myocardial ischemia or infarction, thrombolysis, or
revascularization and syncope. Natriuretic peptide receptors stimulated by
endogenous ANP or BNP may modulate the Bezold-Jarisch reflex. Thus, the
Bezold-Jarisch reflex may be less pronounced in patients with cardiac hypertrophy
or atrial fibrillation.88

Cardiovascular Physiology
George J. Crystal, ... Kai Kuck, in Pharmacology and Physiology for Anesthesia
(Second Edition), 2019

Bezold-Jarisch Reflex
The Bezold-Jarisch reflex is a triad of responses (bradycardia, hypotension, and
apnea) first observed following injection of Veratrum plant alkaloids in animals by
von Bezold and Hirt in 1867.40,59–61 Seventy years later, Jarisch and Richter62,63
demonstrated that the receptor area was in the heart (not the great vessels), the
afferent pathway was in the vagus nerve, and the efferent pathway involved
inhibition of sympathetic outflow to peripheral vessels and increased activity in the
vagus nerve to the heart. The ventricular receptors underlying the Bezold-Jarisch
reflex are nonencapsulated terminals of unmyelinated vagal C-fiber afferents in the
walls of the ventricles.64 Although Veratrum alkaloids are not normally present in
animals, physiologic factors, including mechanical stimulation, can trigger the
Bezold-Jarisch reflex.65 The literature contains reports of “paradoxical” bradycardia
during severe hemorrhage in humans.66,67 Studies in a rabbit model demonstrated
that this response is mediated by the ventricular receptors and by the ability of the
Bezold-Jarisch reflex to override the arterial baroreceptor response.68,69 During
severe hemorrhage, the ventricular receptors can be excited by abnormal squeezing
of the myocardium owing to vigorous contraction around a nearly empty chamber.

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Anesthesia for Orthopedic Surgery

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Michael A. Gropper MD, PhD, in Miller's Anesthesia, 2020

Shoulder and Elbow Surgery

Over the past several decades, an increasing number of patients have undergone
shoulder surgeries, as it has been shown that these procedures have a positive
impact on the quality of life. Shoulder arthroplasty surgery can range from
extensive open repairs, hours in duration, to simple shoulder arthroscopic
procedures of short duration. Most of the surgeries are performed in the beach
chair position,as this position offers superior surgical exposure and access, less
distortion of muscle anatomy, and less tension on the brachial plexus than the
lateral position. Therefore, anesthetic considerations are mostly tailored to
counterbalance the physiologic derangements occurring in this position in
anesthetized patients. Anesthetic techniques can range from general anesthesia to
conscious sedation or monitored anesthesia care with regional block. For the most
part, open procedures require muscle relaxation and therefore, general
endotracheal anesthesia is often preferred. For arthroscopic procedures, muscle
relaxation is not necessary, and these cases can be amenable for general anesthesia
with a LMA or monitored anesthesia care with regional block. The anesthetic
approach is largely influenced by the local practice culture. Surgeons may request
controlled hypotension in arthroscopic cases, as visualization can be hindered by
local bleeding. This can be problematic, especially in patients with chronic
uncontrolled hypertension, as well as those with underlying cerebral vascular
insufficiency. Cerebral perfusion pressure (CPP) is reported to decrease by 15% in
sitting patients under general anesthesia. In patients with chronic hypertension,
cerebral autoregulation is altered, and the curve is shifted to the right (Fig. 64.10).
In patients with cerebrovascular disease, detrimental decrease in cerebral blood
flow (CBF) can occur if the systemic pressure is kept below the minimal required
CPP. Cerebral autoregulation is also influenced by ventilation via arterial PCO2.
Hypercapnia can result in cerebral vasodilation and increased CBF at a constant
CPP. Conversely, hypocapnia causes a decrease in CBF due to cerebral
vasoconstriction.181 A randomized study suggested that cerebral oxygenation can
indeed be improved with higher end tidal CO2 during surgery in the beach chair
position.182 Therefore, permissive hypercapnia may be considered during shoulder
surgery in the sitting position for patients with altered CBF. Additionally, the effects
of vasopressors, such as phenylephrine, in the sitting position should be taken into
account, as high doses of vasoconstrictors can affect CBF. In a study measuring
cerebral oxygen saturation in the sitting position, desaturation occurred with the
use of phenylephrine. The study concluded that cerebral oxygenation can be used
to provide an endpoint for vasopressor therapy.183 Another important anesthetic
factor to consider when allowing hypotension in the beach chair is the distance
discrepancy between the measurement of noninvasive blood pressure (NIBP) and
the circle of Willis. In the supine position, the height of the NIBP at the arm and
the circle of Willis are about the same. Therefore, the blood pressure reading
closely approximates the CPP. However, in the sitting position, the blood pressure
reading from the arm is different than the actual CPP at the circle of Willis. In
general, for every 10 cm rise of an organ or tissue, there is 7.5 mm Hg drop in its
mean arterial pressure. In the sitting position, the distance between the blood
pressure cuff at the arm and Circle of Willis can approximate 20 cm. A technique to
mitigate the distance is to decrease the angle of the sitting position. When
inducing hypotension in the sitting position, all these factors have to be taken into
account and discussed in a preoperative huddle with the surgeon. It is important to
note that the role of the sitting position (beach chair) on postoperative neurological
outcome remains controversial. According to the Anesthesia Patient Safety
Foundation Beach Chair Study, there were no differences in postoperative
cognition or brain injury biomarkers when compared to the supine position.184

Cardiac rhythm diseases

Anika Niambi Al-Shura BSc, MSOM, PhD, in Medical Empathy, Pharmacological
Systems, and Treatment Strategies in Integrative Cardiovascular Chinese Medicine,
2020

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Atrioventricular block
Atrioventricular (AV) block is a type of arrhythmia that involves low cardiac output,
hypotension, and end-organ hypoperfusion leading to sudden death. Symptoms
can range from having no symptoms to exercise intolerance, fatigue, shortness of
breath, weakness, or syncope. Treatment usually is a pacemaker. There is a greater
risk of atrial fibrillation and a poorer prognosis than heart failure.
Causes:
• Ischemia
• Bezold-Jarisch reflex: An inferior myocardial infarction, which may cause a
temporary increase in vagal tone leading to transient Mobitz I or complete AV
block
• Degenerative changes
• Infection seen in myocarditis
• Infiltrative processes as seen in Lyme disease and sarcoidosis
• Beta blockers and calcium antagonists that slow AV node activity
• Procaniamide and flecainamides that block His-Purkinje conduction or
lengthen AV node refractoriness
Categorizations:
• First-degree AV block
• Conduction delay or slowing in AV node and His-Purkinje system
• EKG: PR interval exceeds 0.20 s (sec)
• Intrinsic disease of the AV node, high vagal tone, or dual AV nodal
pathways (two separate PR intervals)
• Beta blockers, calcium channel antagonists, digitalis, and select
antiarrhythmic medications that prolong the PR interval
• Second-degree AV block
• Some P waves conduct while others do not
• Mobitz I (Wenckebach)
- Increased vagal tone
- Degenerative disease of the AV conduction system, seen in elderly
skilled nursing patients
- AV node–blocking medications
- Lyme disease, sarcoidosis, myocarditis
• Mobitz II/2:1 block
- Degenerative disease of the His-Purkinje system
- Damage of the conduction system
• Coronary artery disease
• Infiltrative cardiomyopathies (sarcoidosis, hemochromatosis), myxedema, Lyme
disease, neuromuscular disease
• Myocardial infarction
• Myocarditis
• Systemic diseases (ankylosing spondylitis, Reiter syndrome)
• Valve surgery
• Third-degree/AV block
• Anterior myocardial infarction causing ischemia or infarction of the
bundle branches
• Cardiac surgery, catheter ablation of the AV node, alcohol septal ablation,
or neuromuscular disease
• Reversible causes: AV node–blocking drugs and ischemia
• Pathologic causes:
- Cardiomyopathy (infiltrative, idiopathic, and infarction)

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- Myocarditis (Lyme disease)
- Endocarditis
- Hyperkalemia

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Pericardial Diseases
Douglas P. Zipes MD, in Braunwald's Heart Disease: A Textbook of Cardiovascular
Medicine, 2019

Anatomy and Physiology of the Pericardium

The pericardium is composed of two layers, thevisceral pericardium, a monolayer of
mesothelial cells and collagen and elastin fibers adherent to the epicardial surface
of the heart, and the fibrousparietal layer, which is normally about 2 mm thick and
surrounds most of the heart (Fig. 83.1).1 The parietal pericardium is largely
acellular and contains collagen and elastin fibers. The visceral pericardium reflects
back near the origins of the great vessels and is continuous with and forms the
inner layer of the parietal pericardium. The pericardial space or sac is contained
within these two layers, and normally contains up to 50 mL of serous fluid. The
reflection is a few centimeters proximal to the junctions of the caval vessels with
the right atrium; thus, portions of the caval vessels lie within the pericardial sac.
Posterior to the left atrium, the reflection occurs at the oblique sinus of the
pericardium. The left atrium is largely extrapericardial. The parietal pericardium
has ligamentous attachments to the diaphragm, sternum, and other structures.
Although its removal has no obvious negative consequences, the pericardium does
have functions.1 Its attachments maintain the heart at a relatively constant position
within the thorax, and it provides a barrier to infection. The pericardium is well
innervated with mechanoreceptors, chemoreceptors, and phrenic afferent receptors
that participate in reflexes arising from the pericardium and/or epicardium (e.g.,
the Bezold-Jarisch reflex) and transmission of pericardial pain. The pericardium
also secretes prostaglandins and related substances that may modulate neural
traffic and coronary tone.
The best-characterized mechanical function of the pericardium is itsrestraining
effect on cardiac volume.1 This reflects the mechanical properties of the parietal
pericardial tissue. At low stresses, the tissue is very elastic (eFig. 83.1, top). With
further stretch, it abruptly becomes stiff and resistant to even more stretch. The
point on the stress-strain relation (seeeFig. 83.1, top) where this transition occurs
is near the upper range of physiologic cardiac volumes. Thepressure-volume relation
(PVR) of the pericardial sac reflects the properties of the tissue (seeeFig. 83.1,
bottom, left curve) (i.e., a flat, compliant segment transitioning relatively abruptly
to a noncompliant segment around the upper limit of normal total cardiac
volume).1 Thus, the sac has a relatively small reserve volume. When exceeded, the
pressure within the sac operating on the surface of the heart increases rapidly and
is transmitted into the cardiac chambers. The shape of the pericardial PVR dictates
that once a critical level of effusion is reached, relatively small amounts of
additional fluid will cause large increases in intrapericardial pressure and have
marked effects on cardiac function. Conversely, removal of small amounts of fluid
can result in striking benefit. The shape of the pericardial PVR also suggests that
itnormally restrains the cardiac volume (i.e., the force it exerts on the surface of the
heart limits filling, with a component ofintracavitary pressure reflecting the surface
pressure). Studies with specially designed balloons demonstrate a substantial
surface pressure, especially when the upper limit of normal cardiac volume is
exceeded.1

Autonomic Nervous System and the Heart

F.J. Jaeger, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Vasovagal Syncope
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Vasovagal syncope, also called neurocardiogenic syncope,is a common reflex
syncope triggered by the Bezold–Jarisch reflex, in which an inotropically enhanced,
chronotropically-augmented relatively hypovolemic left ventricle activates
intramyocardial C fibers that travel via afferents to the brainstem initiating the
reflex. The reflex produces sympathetic withdrawal leaving the vagal output
relatively unopposed, causing vasodilatation, hypotension, bradycardia, and
ultimately syncope. Vasovagal propensity appears to be universal in humans,
occurring clinically in up to 60% of individuals. Frequent triggers include
prolonged standing, venipuncture, sight of blood, pregnancy, pain, dehydration,
and fear, but it can occur in individuals without a recognized provocative stimulus.
Recurrent vasovagal syncope with minimal prodrome, prolonged systolic pauses
and asystole has been termed ‘malignant vasovagal syncope.’ Treatment of
vasovagal syncope includes expanding fluid volume, increasing salt intake,
compression stockings, avoidance of known noxious provoking stimuli, and
avoidance of prolonged standing. In recalcitrant cases, drugs such as
fludrocortisone, midodrine, serotonin or serotonin–norepinephrine reuptake
inhibitors, and anticholinergic medications may be useful. Pacemakers may be
utilized in refractory cases or in the malignant form of the condition.

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Autonomic Nervous System

Joel O. Johnson, in Pharmacology and Physiology for Anesthesia (Second Edition),
2019

Bezold-Jarisch Reflex
This cardiac reflex is characterized by hypotension, bradycardia, and peripheral
vasodilation (see Chapter 10). The Bezold-Jarisch reflex occurs in response to
noxious stimuli detected in the ventricle; historically this was studied using
Veratrum alkaloids administered intravenously. Chemoreceptors located in the
ventricles respond to myocardial ischemia, resulting in an increase in blood flow to
the myocardium and a decrease in the work of the heart. This appears to be a
cardioprotective reflex, as coronary vasodilation occurs. The pathway for this
cardioprotective reflex begins with receptors in the ventricles of the heart, which
detect mechanical and chemical stimuli. Afferent unmyelinated C-fibers travel
through the vagus to enhance the baroreceptor reflex mechanisms, inhibit
sympathetic output, and inhibit vasomotor tone, leading to peripheral vasodilation.
The significance of this reflex in the presence of anesthetics continues to be
debated, particularly in relation to regional anesthesia. As a cardioinhibitory reflex,
the Bezold-Jarisch reflex might be functioning in parallel with the baroreceptor
reflex but is probably not a predominant cause of physiologic change in humans.35

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A worldwide yearly survey of new data in adverse drug

reactions
K. Chan, ... Z.X. Lin, in Side Effects of Drugs Annual, 2011

Rhododendron spp. (Ericaceae, rhododendron)

Cardiotoxicity of “mad honey”

Certain species of rhododendron contain grayanotoxins (andromedotoxins), which open

sodium channels. In the heart this effect can trigger the Bezold–Jarisch reflex and cause
bradycardia, heart block, asystole, and hypotension [79R].

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Case reports
There have been several reports of these complications in people who have eaten honey
prepared by bees from Rhododendron luteum, Rhododendron mucronulatum,
Rhododendron ponticum, or Castanea sativa [80A–95A];myocardial infarction has also
been reported [96A]. In the eastern Black Sea region of Turkey, where most cases have
been reported, such honey is called “bitter honey” or “mad honey”, which is often used as
a household remedy for various conditions, including stomach pains, bowel disorders,
hypertension, and erectile dysfunction [97R]. Because of variations in the plant content of
grayanotoxins, poisoning with honey made in the spring is more severe [97r]. However,
honey poisoning is rarely fatal and the effects generally last for no more than 24 hours.
This type of poisoning is thought to have been described by Xenophon 2400 years ago
[98R].
In one case poisoning from Rhododendron simsii occurred when a baby's grandmother
prepared a decoction of this plant in milk [99A]. Poisoning from eating rhododendrons
has also been reported in animals such as sheep and goats [100R].
Other Ericaceae can do likewise, as has been reported in a series of cases of poisoning
with Agauria salicifolia from Reunion Island [101c]and a case from the Mascarene
Islands, where a 28-year-old woman mistakenly drank a herbal tea made with leaves of
Agauria salicifolia and developed symptoms characteristic of grayanotoxin intoxication,
with vomiting, hypotension, and bradycardia. [102Ar].
Case series
In a retrospective series of 19 patients poisoned by “mad honey”, all had nausea,
vomiting, sweating, dizziness, and weakness several hours after ingestion [103c]. There
was hypotension in 15, sinus bradycardia in 15, and complete atrioventricular block in
four. The hypotension and conduction disorders resolved with atropine treatment,
resulting in complete recovery within 24 hours.
In 66 patients symptoms that occurred several hours after the ingestion of small
amounts of “mad honey” included nausea, vomiting, salivation, dizziness, weakness,
hypotension, bradycardia, and syncope [104c]. All had hypotension and most had
bradycardia. These features resolved completely in 24 hours with intravenous fluids and
atropine; none died.
In a review of 47 patients who had ingested “mad honey” 0.5–9 (mean 2.8) hours before
presentation, the heart rate was 30–77 (mean 47) per minute and the systolic blood
pressure was 50–140 (mean 47) mmHg [105c]. Cardiac rhythms on arrival were sinus
bradycardia (n = 37), nodal rhythm (6), sinus rhythm (3), and complete atrioventricular
block (1). All were given atropine 0.5–2 mg.
In a prospective study of 42 patients (33 men; median age 49 years) who had been
hospitalized with “mad honey” intoxication, all had nausea, vomiting, dizziness, fainting,
and sweating; five had syncope [106c]. The mean blood pressure was 73/52 mmHg and
the mean heart rate 38/minute; 18 had sinus bradycardia, 15 had complete
atrioventricular block, and nine had nodal rhythm. None needed temporary pacing and
all were discharged without complications.
In 33 patients (30 men, median age 52 years) the most common effects of poisoning
with “mad honey” were sinus bradycardia (91%), nausea and vomiting (82%), and
dizziness (79%); average heart rate was 55/minute and mean blood pressure was
78/46 mmHg [107c].
In seven cases of grayanotoxin poisoning due to consumption of wild honey that was
brought from the Himalayan belt of Nepal, most had blurring of vision, diplopia, and
nausea and vomiting; two had cardiac effects [108c].
Chronic mad honey intoxication syndrome has also been described in a prospective
evaluation of 173 patients with bradycardia or atrioventricular conduction
abnormalities; in five cases there was a history of ingestion of non-commercial honey
made by different amateur beekeepers in the eastern Back Sea region of Turkey [109c].
When they stopped taking the honey there was prompt normalization of conduction and
significant symptomatic improvement.
Although most cases of poisoning are accidental, in a few cases deliberate self-poisoning
has occurred. In 21 patients (18 men) with acute grayanotoxin poisoning, enhancement
of sexual performance was the reason for the would-be therapeutic use of “mad honey”
[110c].

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Incidence
This type of poisoning is said to be rare, but the incidence is not known. In one report 69
published reports were reviewed [111M].
Management
Muscarinic M2receptors in the vagus are involved in the cardiotoxicity of grayanotoxin
[112AE,113AE], and bradycardia and heart block in these cases respond to atropine, as in
toxicity with veratrum alkaloids. However, temporary pacing may sometimes be required
[114Ar].

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Plant Poisons and Traditional Medicines

Jeffrey K. Aronson, in Manson's Tropical Infectious Diseases (Twenty-third Edition),
2014

Gastroenteritis due to Compounds in Plants

Jequirity beans (Abrus precatorius; Figure 76.12) and castor oil beans (Ricinus
communis; Figure 76.13)) are bright and attractive and are sometimes made into
necklaces. Ricinus is the source of the purgative castor oil and Abrus has been used
to treat schistosomiasis. However, these beans contain poisons that, after a delay of
1–48 hours, can cause fatal gastroenteritis; their toxic principles, abrin and ricin,
are among the most poisonous substances known;106 one bean can kill a child.
Acute poisoning is treated by gastric lavage, demulcents and adjustment of fluid
and electrolyte balance. Abdominal pain may require analgesics. In serious cases
ventilation or haemodialysis may be needed. Modeccin, a lectin found in Adenia
digitata, the wild granadilla,107 may have similar properties to those of abrin and
ricin.108
Abrin and ricin both consist of two components, an α chain and a β chain; the
former is toxic and is carried into cells by the latter, from which it then
dissociates.109 This action has been put to use therapeutically, by conjugating the β
chain of ricin to monoclonal antibodies for use, for example, in the treatment of
leukaemias.110 The dose is limited by the risk of a vascular leak syndrome.
Because ricin is so easily prepared from castor oil beans, there has been some
concern in recent years that it might be used as a weapon of mass terror,
particularly because it was supposed to have been the agent that was used to kill
the Bulgarian dissident Georgi Markov, who was thought to have had it injected
into his leg in a metal pellet via the medium of an umbrella tip.111 However, this
fear is largely unfounded.112 Although ricin is highly toxic, oral administration
results only in effects on the gut and impracticably large amounts would be needed
(e.g. to contaminate water supplies); mass parenteral or inhalational delivery is
unrealistic. On 15 October 2003, a metal canister was found in a package in a Post
Office in Greenville, South Carolina, with a note threatening to poison water
supplies if certain demands were not met; there was ricin in the canister, but the
threat came to nothing.113
Many other plants can cause gastrointestinal disturbances, such as nausea,
vomiting, and diarrhoea. These include the Euphorbia spp., Phytolacca americana
(Figure 76.14), and all plants that contain cardiac glycosides (Table 76.2) or
cucurbitacins (such as Bacopa monnieri, Begonia heracleifolia, Bolbo­stemma
paniculatum, Bryonia aspera, Cayaponia racemosa, Citrullus colocynthis, Coutarea
hexandra, Cucurbita pepo, Ecballium elaterium, Elaeocarpus hainanensis, Gratiola
officinalis, Hemsleya endecaphylla, Kageneckia oblonga, Leucopaxillus gentianeus, Luffa
operculata, Momordica balsamina, Morierina montana, Neopicrorhiza scrophulariiflora,
Physocarpus capitatus, Picrorrhiza scrophulariaeflora, Picria fel-terrae, Trichosanthes
tricuspidata, and Wilbrandia ebracteata). Severe gastrointestinal toxicity can
sometimes cause heart block, secondary to vagal stimulation.114
The leaves of Dieffenbachia spp. cause damage to the mucosa of the gastrointestinal
tract if chewed or swallowed; this has been attributed to their oxalate content.115
The sap can also cause corneal damage.

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The attractive red berries of Arum maculatum (cuckoo-pint or lords and ladies) can
cause burning of the mouth, tongue, and oesophagus, followed by nausea,
haematemesis, and intestinal and other smooth muscle spasm.116 However,
poisoning is rarely serious.
Lectins are phytohaemagglutinins that are resistant to digestion in the gut but are
removed from food by proper cooking. They affect the integrity of the intestinal
epithelium and the absorption of dietary antigens and cause release of allergic
mediators from mast cells in vitro. Many plants, such as Jatropha macrorhiza
(Figure 76.15)117 and Euonymus europaeus, contain lectins,118 which, if not
destroyed by cooking, can cause severe vomiting and bloody diarrhoea, in some
cases followed by damage to the central nervous system, the cardiovascular system,
and the kidneys. Coral plants, Jatropha curcas, J. glandulifera, and J. multifida, grow
rapidly and are used as hedges in Africa and the West Indies. Their fruits, physic
nuts, taste like sweet almonds but have been reported to cause colic, cramps, thirst,
and hypothermia. Another species, J. gossypifolia, is known in the West Indies as
the bellyache bush. The potential uses of lectins, such as those found in Viscum
album (mistletoe), Phaseolus vulgaris (common beans), Robinia pseudoacacia (black
locust), and Agaricus bisporus (button mushrooms), in the treatment of cancers have
been investigated.119
Croton spp., which are widespread in the tropics cause violent purgation. They
contain phorbol esters, which activate protein kinase C,120 are carcinogenic, and
can cause contact dermatitis.121
The ackee, Blighia sapida Figure 76.16; (named after Captain Bligh of the Bounty) is
a native of West Africa but is common in the West Indies and South America. The
fruit has a large fleshy aril and is eaten when ripe; however, the unripe fruit is
poisonous and has caused ‘vomiting sickness’ in Jamaica and other islands.122
Unripe ackee fruits contain toxic hypoglycins, hypoglycin A (L-α-
aminomethylenecyclopropylpropionic acid) and its γ-glutamyl conjugate, the less
toxic hypoglycin B.123 Hypoglycin A is metabolized to methylenecyclopropylacetic
acid, which reduces several cofactors that are essential for β-oxidation of long-
chain fatty acids and inhibits the transport of long-chain fatty acids into
mitochondria. Accumulation of short-chain fatty acids in the serum results from
suppression of short-chain acyl-CoA dehydrogenases and β-oxidation, leading to
omega-oxidation of long-chain fatty acids in the liver. Reduced fatty acid
metabolism causes increased use of glucose and hypoglycaemia.124,125 Anaphylaxis
and cholestatic jaundice have also been reported. Typically, poisoning presents with
abdominal discomfort and vomiting, usually within 6–48 hours of ingestion, and a
few hours later convulsions and coma. Extreme hypoglycaemia occurs and unless
glucose is given promptly, death usually occurs within 12 hours of the initial
vomiting. The liver shows fatty changes, with almost complete absence of
glycogen.
Grayanotoxins in Plants
Certain species of rhododendron contain grayanotoxins (andromedotoxins), which
open sodium channels. In the heart, this effect can trigger the Bezold–Jarisch reflex
and cause bradycardia, heart block, asystole, and hypotension.126 There have been
many anecdotal reports of these complications in people who have eaten honey
prepared by bees from Rhododendron luteum, Rhododendron mucronulatum,
Rhododendron ponticum, or Castanea sativa;127–142 myocardial infarction has also
been reported.143 In one case, poisoning from Rhododendron simsii occurred when
a baby's grandmother prepared a decoction of the plant in milk.144 Poisoning with
Agauria salicifolia has also been reported in a series of cases from Reunion Island145
and a case from the Mascarene Islands.146
In the eastern Black Sea region of Turkey, where most cases have been reported,
such honey is called ‘bitter honey’ or ‘mad honey’. It is often used as a household
remedy for various conditions, including stomach pains, bowel disorders,
hypertension, and erectile dysfunction.147 Because of variations in the plant
content of grayanotoxins, poisoning with honey made in the spring is more
severe.147 However, honey poisoning is rarely fatal and the effects generally last for
no more than 24 hours.
Common adverse reactions that have been reported in case series include nausea,
vomiting, salivation, sweating, dizziness, and weakness several hours after

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ingestion and in some cases hypotension, sinus bradycardia, or complete
atrioventricular block.148–152 Blurring of vision and diplopia have also been
reported.153 Deliberate self-poisoning has been used as a means of enhancing
sexual performance.154
Muscarinic M2 receptors in the vagus are involved in the cardiotoxicity of
grayanotoxins,155,156 and bradycardia and heart block in these cases respond to
atropine, as in toxicity with Veratrum alkaloids. However, temporary pacing may
sometimes be required.157

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Complications After Peripheral Nerve Block

Joseph M. Neal M.D., James R. Hebl M.D., in Essentials of Pain Medicine and
Regional Anesthesia (Second Edition), 2005

HYPOTENSIVE/BRADYCARDIC EVENTS
Sudden-onset hypotensive/bradycardic events (HBE) may occur in about 20% of
awake, sitting patients undergoing shoulder surgery with interscalene block.34 The
purported mechanism for these events, still unproven, involves the Bezold–Jarisch
reflex. Cardiac preload, which is reduced by preoperative volume restriction and the
beach-chair position, and exogenous epinephrine35 combine to create the scenario
of a vigorously contracting empty ventricle. Resultant stimulation of
mechanoreceptors in the ventricular wall initiates reflex bradycardia and
hypotension. Somewhat analogous to the well-described HBE associated with
spinal anesthesia, this complication typically occurs 30 to 60 minutes after block
placement. Beta blockade with metoprolol (titrated to a heart rate <60
beats/minute or a maximum 10 mg dose) decreases its frequency, but
glycopyrrolate has no beneficial effects.34 For reasons unclear, HBE are infrequent
in sitting shoulder surgery patients in whom general anesthesia is administered,
with or without supplemental interscalene block.

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