General Anesthesia, Neuromuscular Blockers, Parkinson’s Disease; Anxiety and Insomia – Flashcards
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General Anesthesia (GA)
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- 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
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GA - Block flow of sodium into neurons or enhance GABA receptors
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Some anesthetics work through both pathways
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GA - Exact mechanism not known, but likely that GABA receptors in brain are deactivated
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- GABA: main inhibitors neurotransmitter in brain - Increases chloride influx and decreases sodium
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GA Combo of several medications for a BALANCED ANESTHESIA
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- 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
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GA - Inhalation agents or intravenous agents
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Usually start through inhalation and maintain with IV
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GA - Stages of general anesthesia
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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
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GA - Stage I
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Induction - loss pain - pt starts to become sedated
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GA - Stage II
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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
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GA - Stage III
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Surgical anesthesia * Want to keep pt here * Achieve balanced anesthesia
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GA - Stage IV
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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
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GA Inhalation Agents (IA) - kinds
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- Gaseous agents (Nitrous oxide) - Volatile liquids
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GA Inhalation Agents (IA) - characteristics
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- 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
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GA - Gaseous Agents
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- Nitrous oxide
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GA - Nitrous Oxide
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- 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
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GA Side effects of Nitrous Oxides
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- 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 -
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GA Volatile liquid
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- vaporized upon inhalation
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GA Contradictions of Nitrous oxide
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- Impaired LOC - Head injuries - Inability to comply with instructions - Abdominal pain - Bowel obstruction - COPD - Chest trauma with pneumothorax
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GA Drug to Drug interactions Nitrous oxide
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-Sympathomimetics and phosphodiesterase inhibitors may exacerbate dysrhythmias
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GA Herbal Tx for Nitrous oxide
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Milk-taken before or after NO to lower liver damage -Ginger- therapeutic benefits
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GA Overdoes of Nitrous Oxide Treatment
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Metoclopramide- help reduce the symptoms of nausea and vomiting associated w/ inhalation of nitrous oxide
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GA - Intravenous Agents
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- 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)
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GA Intravenous Agents
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- Etomidate (Amidate) - Propofol
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GA Etomidate (Amidate)
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-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
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GA Problem with Etomidate (Amidate)
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- if pt is addisonian crisis (acute adrenal insufficiency); can cause pt to go into shock b/c cortisol deficiency
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GA Propofol (Diprivan)
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- 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
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GA Why can nurse give Propofol via IV push?
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- 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.
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GA Propofol Side effect
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- Severe hypotension * causes vasodilatation - Drowsiness - Respiratory depression
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GA Propofol Infusion Syndrome
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- Toxic buildup of medication in body * Hepatotoxicity - Rabdomyolisis * Acidosis * Death
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GA Adverse Effect of IV Agent for General Anesthesia
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- 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
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Neuromuscular blockers NB
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- Depolarizing muscle paralyzers - Intravenous agents - Nondepolarizing muscle paralyzer
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(NB) Depolarizing muscle paralyzers - Name the drug
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- 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
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Anectine
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Succinylcholine
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(NB) Main side effects of prolonged contraction
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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) -
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NB - side effect: causes rapid breakdown of muscle
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Rabdomyolysis
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NB - reversal agent
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Dantrolene
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(NB) Nondepolarizing muscle paralyzer - name the drug
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- 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
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NB Mivacurium (Mivacron)
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(NB) Nondepolarizing muscle paralyzer
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PD Parkinson's Disease
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- 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 -Treatment
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PD Rapids swings in response to levodopa occur ("on-off phenomenon")
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- PD worsens when too little dopamine is present - Dyskinesia (abnormal voluntary movement) occurs when too much dopamine is present
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PD "Wearing-off phenomenon"/"on-and-off phenomenon"
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- Able to move and all of the
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PD Patients with Parkinson's needs to receive meds at SAME TIME EVERY DAY
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- Will go into "on and off phenomenon" * Many meds just dissolved under tongue so pt doesn't need to drink water with it
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PD Parkinson's Disease characteristics
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- Tremors - Bradykinesia - Rigidity - Postural Instability: Shuffle gate:leaning forward and walking without lifting legs
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PD treatment goal
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To increase dopamine or decrease acetylcholine
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PD treatment
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- 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
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PD Dopamine for PD
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slows down/ controls movement
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PD Acetylcholine
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increase/ speeds up movement
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PD Anticholinergics
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-Decrease acetylcholine -Block Effects Ach -Used to treat muscle tremors and muscle rigidity associated with PD - DOES NOT relieve bradykenesia (extremely slow movement)
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PD Symptoms causing PD tremors
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these two symptoms are caused by excessive cholinergic activity
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PD Benztropine Mesylate (Cogentin)
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Treat extrapyramidal side effects caused by use of antipsychotic and other drugs
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PD Extrapyramidal Side Effects
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normally happen as result of depletion of dopamine; symptoms look like PD.
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PD Diphenhydramine (Benadryl)
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used for extrapyramidal s/e -Antihistamine with anti-cholinergic side effect -Can be used for pts with PD or extrapyramidal symptoms
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PD Dopaminergics
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- Increase dopamine - Levodopa therapy - Dopamine replacement drugs
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PD Levodopa therapy
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- 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)
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PD Dopamine replacement drugs
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- 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
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PD Sinemet
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Carbidopa/Levodopa
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(ANS) Anxiety - short term
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- Short Term Anxiety is usually resolved * meditation, listening to music, deep breathing, massage : non-pharmacological * sometimes requires pharmacological action
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(ANS) Anxiety -long term
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- Chronic Anxiety is not easy to change * altered level of neurotransmitter needs pharmacological intervention
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(ANS) CNS depression
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a continuum ranging from relaxation, to sedation, to induction of sleep and anesthesia
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(ANS) Limbic System
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- located in the middle of the brain - responsible for emotional responses, learning, and memory - Signals pass to hypothalamus
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(ANS) Hypothalamus
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- responsible for unconscious responses - connects with reticular formation (group of neurons that branch into brainstem)
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(ANS) Reticular formation
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- network of neurons along length of brainstem - stimulation causes heightened awareness and arousal - inhibition causes general drowsiness and sleep (affects sleep cycles)
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(ANS) Anxiolytics
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- 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
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(ANS) Benzodiazepines
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- 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)
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(ANS) SSRI's
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- classification of antidepressants - first line of anxiety - maintenance of anxiety - increase serotonin in brain - selective serotonin reuptake inhibitor
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(ANS) SNRI's
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- selective serotonin norepinephrine reuptake inhibitor - anti-depression and anxiety
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(ANS) Classes of Medications Used to Treat Anxiety and Sleep Disorders
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- ALL ARE GABA ENHANCERS; GABA=main inhibitory neurotransmitter in brain - Antidepressants - Benzodiazephines - Barbiturates (older) - Nonbenzodiazepines/nonbarbiturate CNS depressants
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(ANS) Barbiturates
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- 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
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(ANS) Treating anxiety/insomnia with CNS agents
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- 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 Barbiturates SSRi's SNRI's
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(ANS) Sedatives and Hypnotics
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- 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
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(ANS) Sleep
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- 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
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(ANS) Non-REM sleep
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rest and restore
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(ANS) REM sleep
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dreaming; associated with memory, learning and adaptation
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(ANS) Sleep Stages
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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
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(ANS) Sleep Stages (REM sleep) 4th stage
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- usually happens 90 minutes after you fall sleep - first period usually last 10 minutes, and each later stage lasts longer - HR AND BREATHING QUICKENS - 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
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(ANS) Sleep Architecture
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- 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
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(ANS) Insomnia
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- 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
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(ANS) CNS depressants: Benzodiazepines
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- 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
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Benzodiazepines name the drugs
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- 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"
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Benzodiazepines- mechanism of action
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