Biomedical Engineering Reference
In-Depth Information
on clothing or skin rapidly evaporates. This eases the
work of resource intensive decontamination that is
required for the agents with lesser volatility.
Compared to the volatile nerve agents the oily
consistency of VX requires cutaneous absorption
for toxic effects. Though VX is an extremely
lethal the onset is slow. Because the agent that
clings to skin and clothing it requires total body
protection for rescuers and exhaustive decontami-
nation of victims and environment. As a terrorist
weapon however, the necessity for a liquid disper-
sion system makes VX an unlikely candidate for
inflicting casualties.
Table 6.2
Receptor related effects of nerve agent
poisoning
Peripheral Nervous System
Central
Nervous
System
Muscarinic
Nicotinic
Diarrhea
Mydriasis
Confusion
Urination
Tachycardia
Convulsions
Miosis
Weakness
Coma
Bradycardia
Hypertension
Bronchorrhea,
bronchospasm
Hyperglycemia
Emesis
Fasciculations
Lacrimation
Salivation, secretion,
sweating
6.2.3 Mechanism of Toxicity
Nerve agents are organophosphate cholinesterase
inhibitors that inhibit cholinesterase enzymes
(butyrylcholinesterase in the plasma, acetyl-
cholinesterase on the red cell, and acetyl-
cholinesterase at cholinergic receptor sites in
tissue). The primary clinical effect of nerve agents
is to inhibit acetylcholinesterase in the cholin-
ergic nervous system so that the neurotransmitter
acetylcholine cannot be hydrolyzed. Acetylcholine
is the neurotransmitter of the neurons to skeletal
muscle (nicotinic receptors), of the pre-ganglionic
autonomic nerves (nicotinic receptors), and
of the post-ganglionic parasympathetic nerves
(muscarinic receptors). Due to blockade of acetyl-
cholinesterase, acetylcholine cannot be metabo-
lized and continues to stimulate the receptors.
The clinical effects from nerve agent exposure are
caused by excess acetylcholine causing the signs
and symptoms of poisoning (Table 6.2).
Nerve agents combine with cholinesterase at the
esteratic site, and the stability of the bond depends
on the structure of the nerve agent. Cleavage of
the nerve agent with reactivated enzyme can only
be achieved by administration of an oxime thera-
peutic agent. Oximes are the most effective agents
for reactivation of enzymatic activity. If oximes are
not administered within a defined period of time
the nerve agent-enzyme complex becomes refrac-
tory to oxime reactivation of the enzyme. This
process is known as aging. Thus, the enzyme may
remain indefinitely inhibited and return of enzy-
matic activity occurs only with the synthesis of new
enzyme. For most nerve agents, the aging time is
longer than the time within which acute casualties
will be seen.
The initial effects of nerve agent exposure
depends on the dose (Table 6.1) and route of expo-
sure with the initial effects of differing vastly from
vapor exposure and exposure to liquid agent on the
skin (Tables 6.3 and 6.4).
Initial exposure to low concentrations of nerve
agent vapor produces local effects in the eyes,
nose, and airways and does not necessarily indi-
cate systemic absorption of the agent. These
effects start seconds to minutes after exposure and
maximal effects peak within minutes after expo-
sure. However, a small amount of liquid agent on
the skin causes localized sweating, blanching, and
fasciculations. The onset of gastrointestinal systems
indicates systemic effects after dermal exposure.
Regardless of the route of exposure lethal systemic
absorption of vapor or liquid causes a rapid cascade
of events that result in loss of consciousness and
convulsive activity, followed by apnea andmuscular
flaccidity within several minutes.
6.2.4 Signs, Symptoms and Severity of
Exposure
6.2.4.1 Ocular, Nasal and Airway effects
The characteristic signs of exposure to nerve
agent vapor is miosis that can be accompanied
