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134 Cards in this Set

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How do epilepsy drugs work?
They prolong the state of inactivation of Na channels or block Ca channels, or interact w/ GABA receptors
Name the epilepsy drugs.
phenytoin
valproate
carbamazepine
ethosuxamide
baclofen
Phenytoin
1. DOC for generalized tonic-clonic seizures

2. Treatment of status epilepticus (diazepam is DOC),

3. Tx of episodic clonic movements following severe head injury

4. Non-linear kinetics at large doses, i.e., at large doses elimination not first order
Phenytoin S/E’s?
1. gingival hyperplasia

2. ataxia, nystagmus, diplopia

3. psychological disturbances

4. megaloblastic anemia (interferes w/ folate metabolism)

5. osteomalacia (responds to vitamin D)

6. teratogenic (cleft lip/palate)

not much sedation
Carbamazepine MOA?
prolong the state of inactivation of the Na channels
-- no impulse propagation
Carbamazepine therapeutic use?
1. Tx of temporal lobe seizures

2. DOC for trigeminal neuralgia
Carbamazepine S/E’s?
1. Monitor LFTs, espec in young pts or pts treated w/ valproate + other seizure meds

2. can cause ↑ release of AVP and potentiate the antidiuretic effects of AVP
-- result is dilutional hyponatremia
Phenytoin and phenobarbitol?
Causes osteomalacia

MOA: induction of CYP450 which increases the metabolism of vit D and vit K (vit K a cofactor for the synthesis of osteocalcin)

Decreased vit D lowers the GI absorption of Ca++.

In order to maintain plasma [Ca++], bone is resorbed.
Primidone?
metabolized to Phenobarbital
-- probably acts directly on Na channels like phenytoin
Ethosuxamide MOA?
blocks T-type Ca channels in thalamus
Ethosuxamide therapeutic use?
DOC for absence seizures
-- blank stare
-- eyelids flutter
-- 3-sec spike wave rhythms from thalamus
Baclofen MOA?
Interacts w/ GABA-B receptors linked to K channels
-- enhanced K conductance hyperpolarizes cells presynpatic membrane of glutaminergic neurons in spinal cord to prevent the release of glutamate onto alpha-motor neurons
-- ↓ efferent excitation of spastic skeletal muscle
Baclofen therapeutic use?
Tx of spasticity from spinal cord injury, CP, and MS
Dantrolene MOA?
Inhibits release of “trigger” Ca++ from SR in skeletal muscle
Dantrolene therapeutic use?
1. spasticity from spinal cord injury

2. malignant hyperthermia

3. neuroleptic malignant syndrome
Dantrolene S/E’s?
generalized muscle weakness
Therapeutic effect of TCAs does not correlate with…?
blockade of uptake of any of the biogenic amines
Explain the specificity for amine transporters and antidepressants.
NE reuptake blocked
-- desipramine
-- secondary amine

5-HT reuptake blocked
-- SSRI’s
-- fluoxetine, paroxetine, citalopram, fluvoxamine

BOTH NE and 5-HT reuptake blocked
-- imipramine (tertiary amine)
-- clomipramine
-- venlafaxine
Tyramine-containing foods and MAOIs?
Phenelzine or Tranylcypromine

Tyramine contraindicated in these pts can cause “cheese reaction”
Antidepressant S/E’s?
1. confusion in elderly patients
2. postural hypotension (-blockade)
3. sedation (central antimuscarinic effect)
4. urinary retention
5. tachycardia (atropine-like effect),
6. fine tremor
7. AV block (direct toxic effect)
MAO inhibitor MOA?
inhibit MAO-A which degrades NE and 5-HT

(MAO-B degrades DA)
CLINICAL: Schizophrenic patient w/ depression?
SSRI like fluoxetine
CLINICAL: Depressed pt w/ hypotension?
SSRI like fluoxetine
CLINICAL: Depressed pt being treated w/ antidepressant suffers from sedation and hypotension. Which antidepressant is the likely cause?
Could be MAOI or TCA since both cause sleepiness and hypotension, but pick TCA b/c TC’s cause greater orthostatic hypotension than do MAOIs
CLINICAL: Small child w/ nocturnal enuresis?
Treat w/ TCA for atropine-like effect in urinary bladder
CLINICAL: Which NT is involved in OCD?
5-HT

Treatment for OCD – clomipramine or SSRI
CLINICAL: Depressed pt w/ CHF being treated w/ digoxin is given TCA…what happens?
Inverts or flattens T-wave

Slows conduction in fast fibers so QRS increased
CLINICAL: OD w/ imipramine?
Imipramine (tertiary amine which blocks 5-HT and NE uptake1)
-- converted to desipramine (secondary amine which blocks NE uptake1)

If OD – usual affects are:
-- ↓BP from alpha blockade
-- ↑HR from ↓BP and anticholinergic effects
-- decreased AV conduction w/ ↑ QT interval
What causes serotonin syndrome?
results from excessive stimulation of central 5-HT receptors
-- ↑ BP, HR & respiration
-- increased muscle activity (muscle twitching, shivering, myoclonus) causing hyperthermia and sweating
-- pupillary dilation
-- confusion, agitation, hallucinations

Caused by
-- SSRI (ex: fluoxetine) OR
-- TCA which blocks both NE and 5-HT uptake (ex: imipramine)
-- especially in pts taking MAOI --> prevents degradation of 5-HT in CNS and accum of 5-HT in the cytoplasm of central 5-HT neurons
What are the antipsychotic drugs?
haloperidol
clozapine
chlorpromazine
Lithium
MOA of antipsychotic drugs?
blocks D2 receptors in the mesolimbic DA pathway
Haloperidol?
least sedating

greatest likelihood of ESP

DOC for Tourette’s syndrome (vocal and motor tics, copralalia)
Clozapine?
Effective in treatment of negative symptoms
-- measure CBC weekly w/ clozapine
Chlorpromazine?
prevets emetic effects of D2 receptor stimulation at CTZ
S/E’s of antipsychotic drugs?
ALPHA BLOCK
-- dizziness
-- orthostatic hypotension
-- ↑ HR
-- nasal stuffiness
-- impotence

MUSCARINIC BLOCK
-- dry skin and mouth
-- mydriasis
-- ↑HR
-- urinary retention
-- sedation

CENTRAL D2 BLOCKADE
-- fine tremor
-- muscular rigidity
-- EPS
-- tardive dyskinesis
-- hyperprolactinemia
-- galactorrhea
-- amenorrhea
-- neuroleptic malignant syndrome
Li MOA?
inhibits enzymes important in recycling phosphoinositides, so PIP2 is depleted
HCTA and furosemide and Li?
Both enhance the reabsorption of Li in the PT causing toxicity
Li S/E’s?
1. tremor

2. motor and psychiatric disturbances

3. causes nephrogenic DI by inhibiting adenylase coupled to V2-ADH receptors in CD
Li in a female pt w/ bipolar disease?
Must discontinue Li treatment during first trimester to prevent teratogenesis

Ebstein’s anomaly
-- leaflets of mitral valve displaced downward into right ventricle
-- tricuspid regurgitation
-- right ventricular dysfxn
Which drugs can cause Parkinsonian-like side effects?
D2 receptor antagonists such as
-- haloperidol
-- chlorpromazine
-- trifluperazine
Drugs used to treat PD?
levodopa

carbidopa

benztropine

bromocriptine

amantadine

selegiline

bromocriptine
Levodopa MOA?
Dopa precursor which is pumped into brain via the aromatic amino acid pump
What can interfere w/ levodopa treatment?
Treatment w/ vitamin B6 interferes w/ therapeutic action of levodopa
-- B6 increases the peripheral decarboxylation of levodopa to Dopa
Carbidopa MOA?
inhibits DOPA (L-aromatic amino acid) decarboxylase outside brain to enhance the amount of DOPA taken up by the brain and converted to DA
Benztropine MOA?
central muscarinic receptor blockade
Bromocriptine MOA?
central D2-dopamine receptor agonist
Amantadine MOA?
antiviral drug which release DA centrally
Selegiline MOA?
selective MAO-B inhibitor, blocks breakdown of DA in CNS
Centrally acting anticholinergic drugs and levodopa?
Enhance central actions of levodopa in PD
Carbidopa + levodopa?
1. can reduce dose of Dopa

2. prevents decarboxylation of Dopa outside CNS

3. carbidopa does not enter CNS

4. carbidopa does not attenuate the orthostatic hypotension caused by levodopa
Levodopa and schizophrenics?
Can cause reappearance of psychotic symptoms in a schizophrenic pt w/ PD caused by atypical antipsychotic drugs (ex: haloperidol)
Which drugs can increase plasma prolactin?
D2 dopamine receptor blockers
Haloperidol
Reserpine
Metoclopramide
alpha-methyldopa

Hyperprolactinemia causes galactorrhea, amenorrhea, anovulatory cycles, and infertility in women; causes decreased libido and impotence in men
Bromocriptine MOA?
a D2-dopamine receptor agonist

Used to treat PD and inhibit prolactin release in hyperprolactinemia

Reverses infertility caused by hyperprolactinemia
Ethanol metabolism?
Oxidized to acetaldehyde by alcohol dehydrogenase

Acetadehyde degraded to water and CO2 by acetaldehyde dehydrogenase
Ethanol kinetics?
Alcohol dehydrogenase easily saturated at low concentrations of ethanol
-- so ethanol removed by zero-order kinetics = constant amount of drug/h metabolized
What inhibits acetaldehyde dehydrogenase?
Inhibited by disulfiram & metronidazole

Build up causes
-- peripheral vasodilation (red skin)
-- n/v
-- pulsating headache
-- sweating
-- chest pain
-- vertigo
-- syncope
-- blurred vision
-- confusion
How does EtOH enhance loss of body heat?
peripheral vasodilation
CLINICAL: Patient is being treated w/ Giardia + some other infection (bacterial) and develops n/v and headache after drinking a beer. What drug causes this?
Metronidazole
Alcoholism causes…?
1. hyperlipidemia and fatty infiltration of the liver

2. cardiomyopathy, portal hypertension, gastric ulceration, esophageal varices

3. Wernicke-Korsakoff syndrome - assoc w/ thiamine deficiency - get paralysis of external eye muscles, altered mentation and ataxia
Fetal alcohol syndrome?
flattened face, short nose, short palpebral fissures = underdevelopment of mid-facial region, microcephaly with low IQ, retarded growth
Describe methanol toxicity.
severe visual disturbance (“like being in a snow storm”) with relatively clear sensorium

headache

dyspnea

cold digits

GI pain

breath smells of formaldehyde.
Treatment of methanol toxicity?
treat w ethanol to saturate enzymes which degrade EtOH and MeOH
-- because toxic product of MeOH appears to be a formate compound produced by the sequential actions of alcohol and acetaldehyde dehydrogenases
What occurs when someone ingests ethylene glycol from antifreeze?
converted to aldehydes, acids and oxalate
-- oxalate causes acute renal failure
Describe amphetamine toxicity
nervousness, restlessness, insomnia, hypertension, tachycardia, hyperthermia, toxic psychosis = paranoid schizophrenia, weight loss, formication, tonic-clonic seizures.

EARLY USE get pupillary dilation from the release of NE in the radial muscle

PROLONGED USE can get miosis due to depletion of NE from radial muscle
Amphetamine withdrawal?
DOES NOT cause delirium tremens (DTs)
Methylphenidate use?
Treatment of ADD and ADHD in children

CAN CAUSE: depression, insomnia, loss of appetite, weight loss, slowed growth rate
Theophylline, aminophylline and caffeine therapeutic use?
normalize breathing in neonatal apnea
Phentermine therapeutic use?
suppresses appetite via release of NE in the hypothalamus
What is MDMA?
“Ectasy”
-- can cause degen of central 5-HT neurons
ALL sedative hypnotics cause…?
dependence, shortened sleep latency, suppression of REM sleep, tolerance, rebound insomnia, respiratory depression.

They are NOT analgesic.

(barbiturates, BZs, choral hydrate, glutethimide)
General effect of barbiturates?
general CNS depressants w/ low therapeutic index
Barbituate MOA?
enhance GABA-A receptor-mediated increase in Cl conductance to hyperpolarize neurons
-- enhances duration of channel opening
What predicts which barbiturate will have the most rapid onset of action?
oil:water partition coefficient predicts most rapid onset
Barbituate S/E’s?
-- can cause paradoxical excitation in older patients

-- decrease sleep latency, but decrease REM and slow-wave sleep
Phenobarbital?
active when given p.o. and is the least sedating
Thiopental?
Poor analgesic activity
-- used for induction of anesthesia
-- short duration of action due to redistribution (blood-brain/viscera --> skeletal muscle --> fat
-- transient ↓ in BP with reflex ↑ in HR and dP/dT, so CO not depressed
BZ MOA?
enhance GABAA receptor-mediated increase in Cl- conductance to hyperpolarize neurons
-- enhances rate of channel opening
BZs and older patients?
-- older patients exhibit ↑ half-life due to ↓ Cl
-- ↑ free plasma concentration from ↓ plasma protein binding

-- ↑ receptor sensitivity to BZ’s = ↑ risk of falls and hip fracture
Several BZs are converted to active metabolites…
Diazepam converted to
-- desmethydiazepam
-- oxazepam
-- temezepam
Which BZs are preferred for older pts?
lorazepam

oxazepam

-- cleared by glucuronidation rather than CYP450
-- rate of glucuronidation does not ↓ w/ age
Triazolam?
BZ w/ the shortest half-life

Used to tx insomnia

Greatest risk of rebound insomnia
Describe the BZ withdrawal syndrome.
anxiety, dysphoria, agitation, insomnia, vomiting, sweating, muscle and abdominal cramps, myoclonic jerks, convulsions.

No CV effects!
What is the BZ receptor antagonist?
flumazenil
Flumazenil therapeutic use?
Used to treat OD w/ BZs

Also precipitate BZ w/d syndrome in pts addicted to BZs
Zolpidem?
NON-BZ hypnotic drug
-- acts to increase Cl conductance
Buspirone MOA?
a partial agonist at 5-HT1A receptors linked to K channel
-- causes hyperpolarization to suppress neuronal activity

Anxiolytic but NOT addictive
Buspirone vs BZs?
Slow onset compared to BZs

No sedation or EtOH interaction

No hypnotic, anticonvulsant or muscle relaxant effects
Describe the drug schedule.
CLASS 1
-- heroin, LSD, marijuana, mescaline, PCP, psilocybin, MDA, DMT, DET, bufotenine
-- no med uses

CLASS 2
-- opiates (meperidine, methadone, fentanyl, oxycodone)
-- amphetamines (methylphenidate, etc)
-- cocaine
-- some barbiturates (amo, pento, seco), dronabinol
-- NO tel scripts/ refills

CLASS 3
-- codeine, opium, some barbiturates
-- rewrite script after 6 mos or 5 refills

CLASS 4
-- BZs, pentazocine, propoxyphene, phenobarbital
-- rewrite script after 6 mos or 5 refills

CLASS 5
-- diphenoxylate
Opiates: beta-endorphin and enkephalins
agonists at certain opiate receptors
-- found in adenohypophysis and certain nerve cells
-- suppress spinal nociceptive pathways

effects blocked by naloxone
Clinically useful opiates are relatively selective for which receptors?
Mu receptors

Larger doses affect all receptors
Mu receptor natural agonists?
beta-endorphins
enkephalins
morphine
Mu receptor analgesia?
supraspinal Mu1 (predominant effect)

spinal Mu2 receptors
Effects at Mu2 receptor?
respiratory depression

decreased GI motility
Other effects of Mu receptor stimulation?
miosis
-- increases PSNS activity from E-W nucleus to sphincter muscle of iris

-- euphoria

-- physical dependence
Kappa receptors?
Natural agonists
-- dynorphin A and K1

Analgesia
-- supraspinal kapp3
-- spinal kappa1

Dysphoria and sedation
Delta receptors?
Natural agonists
-- enkephalins

Spinal and supraspinal analgesia
-- spinal is most important
Where does the supraspinal effect occur?
1. GABA neuron normally inhibits pain-inhibiting neurons (PIN)

2. Opiates inhibit GABA neuron, so no GABA released onto PIN = no inhibition of PIN = central descending inhibition of pain pathways
-- inhibitory effect on GABA neurons can explain seizures caused by some opiates like meperidine
Where does the spinal effect occur?
Opiates block nociceptive stimuli in ascending spinothalamic pathways

1. mu2, delta2 & kappa1 stimulation decreases NT release (probaby glutamate) from presynaptic terminal of nociceptive primary afferent

2. mu receptor stimulation creates IPSP (hyperpolarization) in secondary ascending pain transmission neuron
Mu, kappa, and delta receptors are coupled to…?
G-proteins
-- mu & delta = increased K conductance = hyperpolarization

-- kappa = decreased Ca conductance
Actions of opiates?
-- analgesia
-- respiratory depression - MOA: increase in the threshold [CO2] which activates the medullary respiratory center
-- constipation = no tolerance; increases smooth muscle tone but decreases GI motility
-- miosis - no tolerance (NB: meperidine causes mydriais via atropine-like effect)
-- sedation, euphoria, physical dependence
-- sedation, dysphoria, psychotomimesis
-- cough suppression (act on cough pathways in the brainstem) - MOA of dextromethorphan & codeine does not involve opiate receptors!
Actions of opiates (cont)?
-- truncal rigidity - a spinal mechanism
-- emesis - via stimulation of CTZ
-- not much effect on BP or HR in a supine patient , but i.v. morphine can induce histamine release which can decrease BP and cause cutaneous dilation and itching (hives)
-- morphine acts centrally to decreases peripheral sympathetic nerve acivity; can cause orthostatic hypotension
-- smooth muscle contraction in biliary tract and GU tract
Toxicity triad of opiates?
1. miosis

2. coma

3. depressed respiration
What affect of morphine do we NOT develop tolerance to?
miosis

constipation
Pentazocine, butorphanol, nalbuphine, & buprenorphine?
Partial opiate agonist

1. less depression of respiration

2. causes w/d symptoms in pts addicted to morphine/heroin and pts on methadone maintenance for addiction
Symptoms of opiate withdrawal?
1. rhinorrhea, lacrimation, chills

2. n/v, diarrhea, hyperthermia

3. sweating and piloerection (“goose flesh”)

4. myalgia, tremor, urticaria,

5. mydriasis, anxiety, hostility
methadone?
1. active p.o.

2. longest duration of action (15-30h)
-- impt to keep addicts off morphine
Which opiate inhibits respiration the greatest?
morphine
Which opiate has the least potential for addiction?
diphenoxylate
-- used to treat diarrhea
CLINICAL: Morphine is DOC for…?
1. pain & pulmonary edema caused by acute MI
-- acts in CNS to decrease SNS activity
-- decreased preload and afterload
CLINICAL: Tx of female w/ acute pain from gallstones w/ morphine causes greater pain. Why?
Morphine contracts smooth muscle of gall bladder
CLINICAL: female on methadone has emergent surgery and is tx w butorphanol; patient experiences S/S of opiate withdrawal. Why?
Butorphanol is a partial agonist at mu receptors.
-- partial agonists pentazocine, nalbuphine and buprenorphine can also cause S/S of opiate withdrawal in a patient taking methadone.
CLINICAL: Which opiate does not cause a dose-related inhibition of respiration?
partial agonists

Pentazocine
Butorphanol
Nalbuphine
CLINICAL: If mom receives opiate during labor…?
Newborn baby may have respiratory depression
CLINICAL: Why do we treat MI pt w/ morphine?
Chest & arm pain  the activity of the sympathetic nervous system which constricts arterioles and venules to increase preload and afterload.

The damaged heart cannot pump the increased venous return, especially in the face of an increase in afterload.

Morphine acts centrally to decrease pain and to decrease
sympathetic outflow.
-- Decreased activity of the SNS decreases preload and afterload and improves CO.

The analgesic effects of morphine also make the patient more comfortable.
General anesthesia and partition coefficients?
Partition coefficients have actual clinical significance.

The minimum alveolar concentration (MAC) is the concentration of gas in the inspired air (in percent) which is required to cause a surgical plane of anesthesia in 50% of patients.
-- The MAC is a measure of anesthetic potency and is inversely related to the oil/gas partition coefficient.

High oil/gas partition coefficient = high lipid solubility = low MAC = high potency
Nitrous oxide and anesthesia?
Cannot be used for anesthesia b/c its MAC is >100%
-- even if N2O had MAC of 90%, it could still not be used for anesthesia b/c the pt has to breathe at least 20% oxygen to prevent hypoxia
Which drugs lower the MAC dose of volatile anesthetic agents?
nitrous oxide

BZs

ketamine

Barbituates

EtOH

NOT NMB agents!!
General anesthesia and blood/gas coefficients?
The blood/gas partition coefficient determines the rate of onset (induction)/offset of anesthesia.
-- Agents that are poorly soluble in blood have a rapid onset/offset b/c the blood (including the RBC’s) must be saturated with gas before the gas will move from the blood into the brain.

After the volatile anesthetic agents are d/c, the partial pressures of the gases will fall in exactly the same order that they rose
-- nitrous oxide drops rapidly
-- halothane drops more slowly
-- methoxyflurane drops very slowly.

***If vapor pressures are given in the question, ignore them. They will not help you answer the Q.
CLINICAL: If there is a question regarding the potency of MAC…?
Most potent drug has the smallest MAC gas with lowest MAC (most potent) = gas with the highest oil/gas partition coefficient.

gas with the highest MAC (least potent) = gas with lowest oil/gas coefficient
What is the second gas effect?
A rapidly absorbed gas ↑ the rate of uptake of a second gas

Give 70% nitrous oxide + 0.78% halothane + 29% oxygen, and the rapid uptake of nitrous oxide pulls the halothane along with it.

The arterial tension (partial pressure) of halothane rises more rapidly when given with nitrous oxide (N2O). Net effect is 2-fold:
1. 0.78% halothane +70% N2O --> the steady-state alveolar concentration of halothane is increased (2.00%)
2. the MAC of halothane is decreased (normal MAC = 0.78%; w N2O, MAC = 0.29%)
Describe diffusion hypoxia.
Nitrous oxide is very insoluble in blood. When its administration is discontinued, large volumes of N2O pour out of the blood into the lungs.

This large volume of N2O dilutes the oxygen, and the patient becomes hypoxic.

Occurs during first 10 min after D/C of N2O

Tx patient w/ 100% oxygen
N2O and air-filled cavities…?
N2O easily leaves the blood to enter any air-filled cavity in the body.

If N2O enters a compliant air-filled cavity (e.g., intestinal gas, pneumothorax, air bubbles)
-- the gas space expands.

If the air-filled cavity is non-compliant (e.g., sinuses, middle ear and cerebral ventricles)
-- intracavity pressure increases
-- Increased middle ear pressure can rupture the tympanic membrane or cause n/v after surgery
What are the factors controlling rate of INDUCTION of anesthesia?
1. alveolar ventilation rate

2. blood/gas partition coefficient

3. partial pressure of gas in lungs

4. - cardiac output

5. increase in FI (concentration of gas in inspired air) = concentration effect =  dose

6. cerebral blood flow

7. NOT potency (MAC)
What are the factors controlling rate of OFFSET of anesthesia?
1. blood/gas partition coefficient

2. hyperventilation

3. cardiac output

4. drug metabolism by the liver
What are the CV effects of halothane, isoflurane, enflurane?
ALL volatile agents decrease MAP by decreasing either CO or TPR
-- but effect to decrease BP is attenuated in the presence of N2O which tends to increase sympathetic activity

**isoflurane has little effect on CO
Volatile agents directly…?
relax skeletal muscle and potentiate the effects of the NMB’s
Methoxyflurane S/Es?
causes renal failure after surgery via release of fluoride ions
Ketamine MOA?
blocks NMDA glutamate receptor coupled to Ca channel

(NB: glutamate is an excitatory NT in the CNS)
Ketamine effects?
produces a dissociative state of consciousness, analgesia and postanesthetic hallucinations

least likely to supppress respiration (all opiates, barbiturates, BZ’s and gaseous anesthetics suppress respiration)

MAP via ↑ CO (↑LV-EDP, dp/dt, HR). Little effect on TPR
Etomidate MOA?
enhances GABAA-mediated chloride conductance to hyperpolarize neurons
Etomidate effects?
minimal effect on BP or respiration

causes myoclonic movements (not epilepsy) which can be prevented by pre-tx w BZ’s

can cause adrenal suppression w decrease in plasma cortisol
CLINICAL: Which of the following drugs decreases BP and respiration when given i.v.?
-- opiate
-- ketamine
-- etomidate
-- thiopental
OPIATE
-- nc BP
-- ↓ respiration

KETAMINE
-- ↑BP
-- nc respiration

ETOMIDATE
-- nc BP
-- nc respiration

THIOPENTAL
-- ↓BP
-- ↓ respiration
Halothane predisposes to…
Epi induced cardiac arrhythmias

Tx w/ β-blockers
N2O produces…
analgesia, amnesia, and mental confusion

DOES NOT cause anesthesia!!!