Transcript EMS/Nursing I 80612/30812 Objectives

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Poisoning: Stimulants and
Hallucinogens
Paul R. Lockman, BSN, PhD
Assistant Professor
Department of Pharmaceutical Sciences
School of Pharmacy
Texas Tech University Health Sciences Center
Amarillo, Texas
EMS/Nursing I 80612/30812
Objectives
1. Recognize the mechanism of
action of stimulant/
dissociative anesthetic drugs.
2. Identify the symptoms of drug
toxicity.
3. Identify general measures for
treating drug overdoses.
EMS/Nursing I 80612/30812
Cocaine
1.
2.
3.
Define cocaine’s mechanism of
action with regard to
neurotransmission
Identify symptoms of toxicity for
cocaine
Define a treatment protocol for
an individual with cocaine
toxicity
General Comments


Central nervous system (CNS)
stimulants: a group of drugs that are
loosely classified on their ability to
elicit sympathomimetic clinical
symptoms
Differential diagnosis for CNS
stimulant overdoses
 hypoglycemia
 hypo- or hyperthermia
 subarachnoid hemorrhage
Cocaine Background

Relevant neuroanatomy:
dopaminergic-rich areas of the
brain
 nucleus accumbens
 primary area considered in
addiction processes
Cocaine Background
Grays Anatomy 20th US Edition
Review of
Neurotransmission
Neurons communicate by
chemical signals
 Incoming action potential causes
opening of voltage-gated calcium
channels
 Calcium influx causes neuronal
vesicles to fuse with plasma
membrane

Review of
Neurotransmission
Released transmitter diffuses to
receptors on postsynaptic
membrane (e.g., ion channels)
and causes response
 Transmitters also activate
presynaptic receptors (feedback
control)

Cocaine: Mechanism of
Action
Cocaine: Mechanism of
Action
Blocks the presynaptic uptake of
the amine neurotransmitters [i.e.,
norepinephrine (NE), dopamine
(DA), and serotonin (5HT)]
 Dopamine blockade may cause
euphoria and activate the reward
system

Cocaine: Mechanism of
Action
Serotonin blockade may add to
the euphoria and agitation
 NE blockade leads primarily to
cardiovascular events


Strong correlation between DA
reuptake inhibition and clinical
CNS symptoms
 ~47% blockade = “high”
described primarily as euphoria
 ~60-77% blockade =
psychostimulation and
agitation
Cocaine: Symptoms

Cocaine CNS stimulation occurs
rostral to caudal (i.e., cortex
stimulation first followed by the
lower motor centers)
Cocaine: Symptoms

CNS symptoms
appear
in the following
order (cortex 
brain base)
restlessness
excitement
increased motor activity
hyperthermia
increased respiratory rate
vomiting
Cocaine: Neurologic/
Psychologic Effects
Significant agitation  seizures
CNS neuronal irritability along
with hyperthermia are attributed
to most cocaine fatalities
Tactile hallucinations
picking, scratching
bugs under the skin


Cocaine: Neurologic/
Psychologic Effects
Cocaine: Neurologic/
Psychologic Effects

May also have spontaneous
neurovascular accident
ruptured aneurysm
stroke
Cocaine-induced
Hyperthermia
Increased heat production
through increased motor activity
 Liver stimulation of glucose
metabolism
 Direct stimulatory effect on
thermoregulatory center in the
hypothalamus

Cocaine:
Cardiovascular Effects
Initially there is transient
bradycardia (secondary to
stimulation of the vagal nuclei):
not clinically relevant
 Hypertension: resultant from
central reuptake inhibition of
norepinephrine and epinephrine

Cocaine:
Cardiovascular Effects

Pronounced tachycardia:
increased release of
norepinephrine from adrenergic
neurons (primarily in the adrenal
medulla)
Cocaine:
Cardiovascular Effects

Chromaffin cells found in the
adrenal medulla are homologous
to sympathetic ganglia
 innervated by preganglionic
sympathetic nerve terminals 
 uses acetylcholine as stimulant 
 cells then secrete epinephrine (not
norepinephrine) into blood
Cocaine: Dysrhythmias

Primarily tachydysrhythmias
 atrial fibrillation (A-fib)
 A-flutter
 supraventricular tachycardia
 premature ventricular
contractions
 torsades
 ventricular fibrillation (V-fib)
Cocaine: Dysrhythmias

May also see conduction delays
cocaine has anesthetic
properties (for clinical use)
blocks sodium channels
Skeletal Muscle and
Pulmonary Effects
Ischemia
secondary to
vasoconstriction and increased
oxygen demand from an
increased workload may result in
rhabdomyolysis
Skeletal Muscle and
Pulmonary Effects
Pulmonary
complications
 pulmonary edema secondary to
pulmonary vasculature effects
 alveolar hemorrhage
Cocaine Toxicity
Evaluation and
Treatment
 Benzodiazepines and
thermal
cooling are the only measures
shown to have significant
efficacy in reducing cocaine
mortality!!!!!
General Measures
Protect staff and patient
Lavage/activated charcoal/
cathartic
 Probably not that effective unless
the patient has ingested a large
quantity of cocaine in an attempt
to evade arrest. Even then
cocaine is rapidly and well
absorbed from the
gastrointestinal (GI) tract.


Body Packers
J Kelly, M Corrigan, RA Cahill, and HP Redmond
Body Packers

Abdominal x-ray may reveal large
amount of drug
 usually swallowed in a condom
 charcoal and a lot of it, repeat
doses often
 whole bowel irrigation: goal is
to move the packages down the
GI tract without rupture
Body Packers

Abdominal x-ray may reveal large
amount of drug
 serial radiographs to evaluate
GI clearance
 may remove in operating room
if needed (if packages rupture,
high mortality rate)
Neurologic Symptoms
Assessment:
physical exam
agitation
tactile hallucinations

Treatment: benzodiazepines,
such as lorazepam or diazepam
(benefit is from reduction of the
seizure threshold as well as
diminishment of psychomotor
agitation)
Hyperthermia





Hyperthermia blanket
Ice
Environment
Fans
Aggressive fluid resuscitation
unless significant pulmonary
edema noted
Pulmonary Symptoms

Treatment
 primarily supportive in nature
 maintain airway as needed
 assess for respiratory rate: may
have some respiratory alkalosis
 provide supplemental oxygen:
goal is to supplement to
provide for the increased
demand and workload of the
organs
Cardiovascular
Symptoms

Myocardial ischemia
 ECG (electrocardiograph): if ST
elevation is present treat as a
typical myocardial infarction
–Morphine
–Oxygen
–Nitrates
–Aspirin
Cardiovascular
Symptoms

Myocardial ischemia
 cardiac enzymes
• evaluate CPK (creatine
phosphokinase) specifically
• must evaluate in serial fashion
(i.e., 2 and 6 hours)
• if normal, myocardial
infarction unlikely
Dysrhythmias
Evaluate ECG (again in a serial
fashion every hour)
 Benzodiazepines to reduce
workload of heart
 Atrial dysrhythmias
 origin thought to be from CNS
 should respond to cooling and
sedation

Dysrhythmias

Ventricular dysrhythmias
 early on in the management the
dysrhythmia probably
originates from the local
anesthetic effect of cocaine on
the myocardium
Dysrhythmias

Ventricular dysrhythmias
• treatment is sodium
bicarbonate
• will overwhelm the sodium
channels, providing improved
conductance
Dysrhythmias

Ventricular dysrhythmias
 late in management the
dysrhythmia may originate from
ischemic cardiac tissue:
treatment includes sodium
bicarbonate and lidocaine
Amphetamines
1.
2.
3.
4.
Define the mechanism of action
of amphetamines with regard to
neurotransmission
Identify symptoms of toxicity for
amphetamines
Define a treatment protocol for
an individual with amphetamine
toxicity
Differentiate the clinical toxicity
of various amphetamines
Mechanism of Action

Can block the reuptake of
dopamine and serotonin similar
to cocaine, however it is not
significant to major clinical
symptoms
Mechanism of Action
Regional Distribution
Lateral tegmental area, with
projections which overlap those
of the locus coeruleus but target
the hypothalamus
 Largest site of synthesis is locus
coeruleus, in midbrain (just a few
hundred cells); it sends axons to
almost every other region of the
nervous system

Regional Distribution
Grays Anatomy 20th US Edition
Clinical Symptoms in
Autonomic Nervous
System

NE release results in peripheral
stimulation of α and β receptors
in the autonomic nervous system
(ANS):
Clinical Symptoms in
Autonomic Nervous
System

results in continual fight or flight
response
 hypertension
 tachycardia
 dysrhythmias
 myocardial infarction and/or
ischemia
Clinical Symptoms in
Autonomic Nervous
System

results in continual fight or flight
response
 hyperthermia
 rhabdomyolysis
 dehydration
Clinical Symptoms
NE in the locus coeruleus
anorexia
hypervigilance
 Increased dopamine/serotonin in
mesolimbic area results in
altered perception/ psychosis
 Amphetamines do not have the
ability to block sodium channels
like cocaine

Hallucinogenic
Amphetamines:
Distinction and Symptoms

Designer amphetamines are
created by substituent
substitutions allowing the
molecule greater interaction with
the presynaptic NE transporter
(i.e., allows either greater or
lesser synaptic distribution)
Methylenedioxymethamphetamine
(MDMA)

MDMA has less stimulant effect
than regular amphetamines but
10x greater serotonergic effect
 widely abused by college and
high school students
 has many common names:
M&M, Adam, E, Ecstasy, MDM

Reported clinical symptoms (in
addition to the amphetamine
symptoms listed above)
 enhances pleasure
 euphoria
 enhancement of socialization
 ataxia
 restlessness
 confusion
Toxic Doses for
Amphetamine

Treatment should be based upon
clinical symptoms and measures
required alleviate those
symptoms
Toxic Doses for
Amphetamine

Amphetamine: low dose






increased vigilance, delayed sleep
anorexia
reduced sensation of fatigue
euphoria
increased motor and speech activity
typically, motor and intellectual tasks
can be performed more rapidly but with
more errors
Toxic Doses for
Amphetamine

Amphetamine: high dose
 paranoid psychosis, tactile





hallucinations
convulsions with potentially lethal
consequences
tachycardia
hypertension
strokes
arrhythmias
General Measures for
Treatment
Protect staff and patient
Airway, breathing, and
circulation (ABCs)
 Lavage/activated charcoal/
cathartic


Specific Measures
Hyperthermia
 ice
 fans
 environment
 aggressive fluid resuscitation
 Neurologic symptoms
assessment: physical exam
 agitation
 tactile hallucinations

Specific Measures
Treatment: benzodiazepines,
such as lorazepam or diazepam
 Benzodiazepines and thermal
cooling are excellent measures
in reducing amphetamine
mortality!!!!!!!!!!

Urinary Acidification

Principle is similar to urinary
alkalinization that aids in the
elimination of weak acids (e.g.,
aspirin, phenobarbital,
chlorpropamide, etc.)
Urinary Acidification

Amphetamines are a weak base:
acidification of the urine will
theoretically ionize the molecule
in the urine; the drug is trapped
and cannot be absorbed back
into blood, resulting in increased
elimination and decreased
toxicity
Urinary Acidification
However, acidification of the
urine requires acidification of the
blood leading to metabolic
acidosis
 This acidosis coupled with the
increased demand and ischemia
at muscles can enhance the
possibility of rhabdomyolysis

PCP and Ketamine
1.
Define mechanism of action,
clinical symptoms and treatment
for phencyclidine (PCP), and
ketamine
PCP and Ketamine
Dissociative anesthetics are
drugs which cause an altered
sensory perception without
losing consciousness
 Monoamine reuptake inhibition
 NMDA (N-Methyl-D-aspartic acid)
antagonism
 Sigma opioid receptor: PCP
associates with extremely high
doses

Clinical Symptoms:
Ketamine and PCP
Mechanism and symptoms are
similar to amphetamines and
cocaine, but must be at higher
doses to have significant clinical
effect
 Responsible for
sympathomimetic and
psychomotor effects

Clinical Symptoms:
Ketamine and PCP
Symptoms resemble that of
schizophrenia (sometimes
unable to distinguish difference,
except PCP symptoms usually
recede within 4 weeks)
 Inhibition of sensory perception:
produce a lack of response to
external stimuli

Clinical Symptoms:
Ketamine and PCP
Dissociative
 consciousness
 memory
 perception (including pain):
diminution in all 5 senses
 Increase in motor activity
 Hallucinations typically are
auditory

Clinical Symptoms
Unique to PCP

Hallmark sign of PCP toxicity is
delusion of superhuman strength
and invulnerability (result of
anesthetic and dissociative
properties of drug)
Clinical Symptoms
Unique to PCP
Other
neurologic signs
 bizarre behavior
 cerebellar signs
 dystonic reactions
Treatment of PCP and
Ketamine Toxicity
ABCs and supportive therapy as
always
 Agitation and bizarre behavior:
benzodiazepines are used to
reduce symptoms

Treatment of PCP and
Ketamine Toxicity

Decontamination
 ipecac contraindicated –
possible seizures
 lavage, probably not
 activated charcoal/cathartic
indicated if recent ingestion
Treatment of PCP and
Ketamine Toxicity

Most individuals recover within
1-2 hours; however, some
patients may be symptomatic for
weeks
Treatment of PCP and
Ketamine Toxicity
Protect the patient: primary
symptoms of toxicity are a result
of behavioral injury and or
rhabdomyolysis from significant
muscle exertion
 Acidification of urine is
theoretical BUT NOT
RECOMMENDED

Poisoning: Stimulants
and Hallucinogens
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EMS/Nursing I 80612/30812
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Paul R. Lockman, BSN, PhD has disclosed that no financial interests,
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