General Anesthesia, Neuromuscular Blockers, Parkinson’s Disease; Anxiety and Insomia

General Anesthesia (GA)
– Not just one medication
– Block flow of sodium into neurons or enhance GABA receptors
– Delay nerve impulses and reduce neural activity
– Exact mechanism not known, but likely that GABA receptors in brain are deactivated
– Produce unconsciousness
– Produce lack of responsiveness to painful stimuli
– Inhalation agents or intravenous agents
– Pt will need cardiopulmonary
– Stages of general anesthesia
– Inhalation agents: gaseous agents (nitrous oxide) or volatile liquids

GA – Block flow of sodium into neurons or enhance GABA receptors
Some anesthetics work through both pathways

GA – Exact mechanism not known, but likely that GABA receptors in brain are deactivated
– GABA: main inhibitors neurotransmitter in brain
– Increases chloride influx and decreases sodium

GA Combo of several medications for a BALANCED ANESTHESIA
– Med that sedates pt
– Med that paralyzes pt
* Doesn’t cause loss of pain
* Normally just used at beginning of anesthesia because they will be unconscious from sedative meds
– Analgesics (opiates)
* Prevent feeling of pain

GA – Inhalation agents or intravenous agents
Usually start through inhalation and maintain with IV

GA – Stages of general anesthesia
Stage I (induction): loss of pain; pt starts to become sedated
Stage II: excitement and hyperactivity
Stage III: surgical anesthesia
Stage IV: paralysis of medulla

GA – Stage I
– loss pain
– pt starts to become sedated

GA – Stage II
Excitement and hyperactivity
– Want to transition quickly into Stage III
– Some prolong this stage – Ketamine (Special K)
* Used because it doesn’t affect BP as much as other anesthetics

GA – Stage III
Surgical anesthesia
* Want to keep pt here
* Achieve balanced anesthesia

GA – Stage IV
Paralysis of Medulla
* Pt needs cardiovascular support
* Overdose – give pt NARCA or something else to reverse opioids/anesthetics
* Incident report required if pt enters Stage IV

GA Inhalation Agents (IA) – kinds
– Gaseous agents (Nitrous oxide)
– Volatile liquids

GA Inhalation Agents (IA) – characteristics
– Don’t always need to be on cardiovascular support – may still maintain ability to breathe (nitrous oxide)
– Prevent flow of sodium into neurons in CNS, delay nerve impulses, produce reduction in neural activity
– Primary Use: with IV agents to maintain loss of consciousness; used alone for dental procedures/short procedures
– Opiates, sedatives, sometimes hypnotics
– Gaseous agents

GA – Gaseous Agents
– Nitrous oxide

GA – Nitrous Oxide
– Fairly safe, minimal side effects
* does not lead to severe hypertension
– Risk for abuse, especially by health care providers
– Causes pt to relax enough for procedure – for short surgical procedures
– Side effects

GA Side effects of Nitrous Oxides
– Fairly safe, minimal side effects
* does not lead to severe hypertension
– Dizziness, drowsiness
– Vomiting, nausea
– Euphoria – part of excitatory period
– Malignant hyperthermia
* Rare – ICE Pt
– Apnea – Slowed RR
* Must count respirations
– Cyanosis:Hypoxemia
– Liver Damage

GA Volatile liquid
– vaporized upon inhalation

GA Contradictions of Nitrous oxide
– Impaired LOC
– Head injuries
– Inability to comply with instructions
– Abdominal pain
– Bowel obstruction
– Chest trauma with pneumothorax

GA Drug to Drug interactions Nitrous oxide
-Sympathomimetics and phosphodiesterase inhibitors may exacerbate dysrhythmias

GA Herbal Tx for Nitrous oxide
Milk-taken before or after NO to lower liver damage
-Ginger- therapeutic benefits

GA Overdoes of Nitrous Oxide Treatment
Metoclopramide- help reduce the symptoms of nausea and vomiting associated w/ inhalation of nitrous oxide

GA – Intravenous Agents
– Opioids (very high does acts as general anesthesia)
– Benzodiazepines (GABA enhancing drug), and miscellaneous agents
– Used in combination with inhalation agents
* provide greater anesthesia and muscle relaxation
* Balanced anesthesia – decreases side effects
– Used alone for procedures that take 15 minutes or less
– Miscellaneous IV general anesthetics
* GABA enhancers
* Good for patients in shock
* Need to be ready to assist during intubation – intubation kit must be at bedside in case pt needs it
* causes CNS depression
* Types (all given via IV)

GA Intravenous Agents
– Etomidate (Amidate)
– Propofol

GA Etomidate (Amidate)
-Intravenous Agent
-Give IV push
-Cause GABA enhancement (Sedation)
-Depending on dose, pt may need Cardio Support- maintain air way
-Normally pt is intubated in case pt vomits
-Doesn’t affect BP -pt hypovolemic shock benefit

GA Problem with Etomidate (Amidate)
– if pt is addisonian crisis (acute adrenal insufficiency); can cause pt to go into shock b/c cortisol deficiency

GA Propofol (Diprivan)
– Very painful – lipid based
* many pt receive a small amount of lidocaine or analgesic in vein prior to giving propofol
– Works by GABA enhancement and blocking Na channels – powerful sedative
– Can be used to both induce and maintain anesthesia
– Recommended for short-term use

GA Why can nurse give Propofol via IV push?
– out of scope of nursing practice
– can only be IV pushed (bulus) by anesthesiologist or CRNA (Certified registered nurse anesthesiologist): that would be giving an anesthetic.

GA Propofol Side effect
– Severe hypotension * causes vasodilatation
– Drowsiness
– Respiratory depression

GA Propofol Infusion Syndrome
– Toxic buildup of medication in body
* Hepatotoxicity – Rabdomyolisis
* Acidosis
* Death

GA Adverse Effect of IV Agent for General Anesthesia
– Allergic reactions, dysrhythmias, respiratory depression
* CNS depression, shivering, headache
* Nausea and vomiting, vital-sign changes
– During postoperative period: hallucinations, confusion, excitability
– Most anesthetics can give you arrhythmias/CNS depression and excitability

Neuromuscular blockers NB
– Depolarizing muscle paralyzers
– Intravenous agents
– Nondepolarizing muscle paralyzer

(NB) Depolarizing muscle paralyzers – Name the drug
– Succinylcholine (Anectine)
– Binds with acetylcholine receptors at neuromuscular joints
– Action potential goes through (depolarization occurs) but it prevents repolarization – muscle contracts until it can’t anymore and then slowly relaxes (doesn’t contract again)
– Has short half life **
– Given with anesthesia
– Do not decrease pain or anxiety
– Main side effect of prolonged contraction is malignant hyperthermia
– Along with muscle paralyzer, ppt needs sedative med and an analgesic


(NB) Main side effects of prolonged contraction
Malignant hyperthermia
– It happens often with succunylcholine (Anectine)
* black box
– Genetically linked – check family history
– Causes extremely high fever and muscle rigidity
– Causes rapid breakdown of muscle (rabdomyolysis)
– Metabolic acidosis
– Pt. needs to be intubated and mechanically ventilated
– Reversal agent is dantrolene (muscle relaxer)

NB – side effect: causes rapid breakdown of muscle

NB – reversal agent

(NB) Nondepolarizing muscle paralyzer – name the drug
– Mivacurium (Mivacron)
– Prevents depolarization/contraction of muscle **
– Compete with acelylchololine for cholinergic receptors at neuromuscular junctions
– Benefit is that there is less chance of pt developing malignant hyperthermia
* No prolonged contraction
– Need to intubate pt
– Doesn’t work as fast
– Used as drug of choice – safer profile than succinylcholine (Anectine)
– Main side effect is paralysis

NB Mivacurium (Mivacron)
(NB) Nondepolarizing muscle paralyzer

PD Parkinson’s Disease
– Causes by lack of dopamine
– Progressive condition characterized by
– Rapids swings in response to levodopa occur (“on-off phenomenon”)
– “Wearing-off phenomenon”/”on-and-off phenomenon”
– Patients with Parkinson’s needs to receive meds at SAME TIME EVERY DAY

PD Rapids swings in response to levodopa occur (“on-off phenomenon”)
– PD worsens when too little dopamine is present
– Dyskinesia (abnormal voluntary movement) occurs when too much dopamine is present

PD “Wearing-off phenomenon”/”on-and-off phenomenon”
– Able to move and all of the

PD Patients with Parkinson’s needs to receive meds at SAME TIME EVERY DAY
– Will go into “on and off phenomenon”
* Many meds just dissolved under tongue so pt doesn’t need to drink water with it

PD Parkinson’s Disease characteristics
– Tremors
– Bradykinesia
– Rigidity
– Postural Instability: Shuffle gate:leaning forward and walking without lifting legs

PD treatment goal
To increase dopamine or decrease acetylcholine

PD treatment
– Dopamine:slows down/controls movement
– Acetylcholine: increase/speeds up movement
– Need a balance between dopamine/acetylcholine
– Anticholinergics (decrease acetylcholine)
– Dopaminergics (increase dopamine)
– Dopamine replacement drugs

PD Dopamine for PD
slows down/ controls movement

PD Acetylcholine
increase/ speeds up movement

PD Anticholinergics
-Decrease acetylcholine
-Block Effects Ach
-Used to treat muscle tremors and muscle rigidity associated with PD
– DOES NOT relieve bradykenesia (extremely slow movement)

PD Symptoms causing PD tremors
these two symptoms are caused by excessive cholinergic activity

PD Benztropine Mesylate (Cogentin)
Treat extrapyramidal side effects caused by use of antipsychotic and other drugs

PD Extrapyramidal Side Effects
normally happen as result of depletion of dopamine; symptoms look like PD.

PD Diphenhydramine (Benadryl)
used for extrapyramidal s/e
-Antihistamine with anti-cholinergic side effect
-Can be used for pts with PD or extrapyramidal symptoms

PD Dopaminergics
– Increase dopamine
– Levodopa therapy
– Dopamine replacement drugs

PD Levodopa therapy
– Levodopa: precursor of dopamine
– Blood brain barrier doesn’t allow exogenously supplied dopamine to enter, but does allow Levopoda
– Levodopa is taken up by dopaminergic terminal, converted to dopamine and released as-needed; as a result neurotransmitter imbalance is controlled in pts with early PD who still have functioning nerve terminals
– Levodopa is broken down quickly
– As PD progresses, it becomes difficult to control with Levodopa (not a cure)

PD Dopamine replacement drugs
– Carbidopa is given with Levodopa
Carbidopa/Levodopa (Sinemet)
– Carbidopa does not cross blood-brain barrier and prevents Levodopa breakdown in periphery
* More Levodopa crosses blood-brain barrier,where it is converted to dopamine

PD Sinemet

(ANS) Anxiety, Insomnia and Seizure Pharmacology

(ANS) Anxiety – short term
– Short Term Anxiety is usually resolved
* meditation, listening to music, deep breathing, massage : non-pharmacological
* sometimes requires pharmacological action

(ANS) Anxiety -long term
– Chronic Anxiety is not easy to change
* altered level of neurotransmitter needs pharmacological intervention

(ANS) CNS depression
a continuum ranging from relaxation, to sedation, to induction of sleep and anesthesia

(ANS) Limbic System
– located in the middle of the brain
– responsible for emotional responses, learning, and memory
– Signals pass to hypothalamus

(ANS) Hypothalamus
– responsible for unconscious responses
– connects with reticular formation (group of neurons that branch into brainstem)

(ANS) Reticular formation
– network of neurons along length of brainstem
– stimulation causes heightened awareness and arousal
– inhibition causes general drowsiness and sleep (affects sleep cycles)

(ANS) Anxiolytics
– drugs that can relieve anxiety
– used for short term anxiety
– quite effective
– used when anxiety begins to significantly affect daily activities
– most common is benzodiazepines
– many antidepressants used for anxiety: SSRIs, SNRI’s

(ANS) Benzodiazepines
– short term anxiety and sleep inducers
* addictive/habit forming
– formerly most common prescribed sedative-hynotic drug
– GABA enhancers
– “pam” and “lam” endings
– Meant for short-periods – highly addictive
– May affect REM – some data from studies shows this: REM (Rapid Eye Movement)

– classification of antidepressants
– first line of anxiety
– maintenance of anxiety
– increase serotonin in brain
– selective serotonin reuptake inhibitor

– selective serotonin norepinephrine reuptake inhibitor
– anti-depression and anxiety

(ANS) Classes of Medications Used to Treat Anxiety and Sleep Disorders
– ALL ARE GABA ENHANCERS; GABA=main inhibitory neurotransmitter in brain
– Antidepressants
– Benzodiazephines
– Barbiturates (older)
– Nonbenzodiazepines/nonbarbiturate CNS depressants

(ANS) Barbiturates
– similar to benzodiazepines
– enhance GABA
– Definitely affect REM in negative way (lose REM) – mess up sleep cycle
– used less than benzodiazepines
– used for anxiety and insomnia

(ANS) Treating anxiety/insomnia with CNS agents
– Used when patient can’t get out of cycle of anxiety and insomnia
– Antidepressants frequently used to treat anxiety (SSRI’s,SNRIs)
– Major classes of CNS agents : Benzodiazepines

(ANS) Sedatives and Hypnotics
– used for anxiety
– CNS depressant are called:
* Sedatives due to ability to sedate or relax pt
* Hypnotics for their ability to induce sleep
*Sedative- hypnotic: calming effect (sedative) at lower doses and sleep (hypnotic) at higher doses
– category depends on dosage
– most CNS depressants can cause physical and psychological dependence

(ANS) Sleep
– normal sleep cycle is cyclic and repetitive
– sleeping person is unaware of sensory stimuli within immediate environment
– sleep architecture
– sleep stages
– need both REM and non-REM sleep cycles for memorization and storage of information

(ANS) Non-REM sleep
rest and restore

(ANS) REM sleep
dreaming; associated with memory, learning and adaptation

(ANS) Sleep Stages
3 stages (5-15 minutes each)
– stage 1: easy to wake up;awarae
– stage 2: longest stage: light sleep; body gets ready for deep sleep
– stage 4: deep sleep (relaxation); harder to wake up; body repairs tissues, builds bone/muscle, and strengthens immune system (HR SLOWS AND BODY TEMP DROPS)
– wide and deep waves of sleep

(ANS) Sleep Stages (REM sleep) 4th stage
– usually happens 90 minutes after you fall sleep
– first period usually last 10 minutes, and each later stage lasts longer
– dreams occur (brain more active)
– without REM cycle: no deep sleep, final outcome is you don’t dream, sleep debt, day dreaming occurs
– without REM cycle: unable to memorize, not able to store information in long term files

(ANS) Sleep Architecture
– Non-REM sleep
* Happens first
– Rapid Eye Movement (REM) sleep – 4th Stage
* Happens 900 minutes after you fall sleep
– REM Interference: barbiturals
– REM rebound: REM cycle length and frequency increase after sleep deprivation; also takes shorter time to reach REM cycle

(ANS) Insomnia
– short term insomnia: usually caused by stress
– long term insomnia: medical condition: depressioin, chronic pain, chronic anxiety (lack ability to sleep)
– rebound insomnia: due to abrupt discontinuation of a sedative medication
– diagnostics:
* 1st pharmacological
* EEG: monitors brainwave activity; looks at NREM and REM cycles
* REM: dreaming; associated with memory, learning and adaptation
* NREM: rest and restore
– pt may develop daytime drowsiness – can cause safety hazard

(ANS) CNS depressants: Benzodiazepines
– short term anxiety/insomnia
* addictive/habit forming
– formerly most common prescribed sedative-hypnotic drug
Nonbenzodiazepines (long term problems) currently more frequently prescribed
– favorable drug effect profiles, efficacy, and safety
– classified as either:
* sedative – hypnotic
* Anxiolytic (medication that relieves anxiety)
– long acting

Benzodiazepines name the drugs
– Long acting
* Diazepan (Valium)
– Intermediate Acting
* Alprazolam (Xanax) – oral form, Lorazapam (Ativan), Temazepam (Restoril)
* Short Acting – most end in “pam”
– Used for insommia, anxiety, antidepresants, seizures, many clinical problems
– pam and lam endings “BARS on the streets”

Benzodiazepines- mechanism of action

Leave a Reply

Your email address will not be published. Required fields are marked *