Anesthesia Flashcards
Types of Sedation
Conscious sedation - alleviates pain and anxiety without altering consciousness. Patient is able to maintain a patent airway and can respond to verbal commands.
Deep Sedation - light general anesthesia with decreased consciousness in which the person is not easily aroused. May be indistinguishable from general.
General Anesthesia - Depress the CNS causing complete loss of protective reflexes, ability to maintain a patent airway and respond to verbal commands.
5 Effects of General Anesthesia
Unconsciousness
Amnesia
Analgesia
Inhibition of autonomic reflexes
Skeletal Muscle relaxation.
No anesthetics currently available achieve all 5 alone.
Ideally should induce rapid, smooth, and reversible loss of consciousness.
Guedel’s Stages of anesthesia
Analgesia - Normal respiration, ocular movement, pupil size, reflexes, muscle tone, HR, BP. Used in labor, incisions, and minor operations
Delirium - Rapid respiration and HR, roving eye movements, dilated pupils, most reflexes, high BP, high skeletal muscle tone. Not used
Surgical Anesthesia - Respiration slows, eyes become fixed, pupil sizes from normal to dilated, loss of reflexes, decreased muscle tone, BP, HR. Stages 1 and 2 for most surgeries, 3 for some, 4 never attempted.
Medullary Paralysis - severe CNS depression resulting in death.
Anesthesia objectives
Minimize deleterious effects
Sustain homeostasis
Improve postoperative outcomes
General Hemodynamic Effects
Decreased MAP
Blunted baroreceptor reflex
Decrease in sympathetic tone.
General Respiratory Effects
Reduce or eliminate ventilatory drive and airway patency. Endotracheal intubation is necessary.
Reasons for Hypothermia
Low ambient temp, exposed body cavities, cold IV fluids, reduced thermoregulatory control, and reduced metabolic rate.
Causes of Nausea and Vomiting
Action of anesthetic on chemoreceptor trigger zone modulated by 5HT, histamine, ACH, DA, and NK1
Other Postoperative side effects
HTN
Tachycardia
Ischemia
Airway Obstruction
Balanced Anesthesia
Use of multiple classes to achieve the desired effect and depth given both preop and postop
Inhibitory Neuron Target of Anesthetics
GABAa receptor
Potassium channels
Excitatory Ion Channel Targets
NMDA receptors
Serotonin Receptors
ACH receptors
Parenteral Anesthetics
Methohexital
Etomidate
Ketamine
Propofol
Small Hydrophobic and lipid soluble
Parenteral Anesthetics that potentiate the GABA receptor
Etomidate and Propofol
Parenteral Anesthetics that inhibit the NMDA receptor
Ketamine
Redistribution: Three Compartment Model
Blood -> brain -> skeletal muscle.
Leads to termination of effects
Context sensitive half time
Elimination half time after discontinuation of a continuous infusion.
Ketamine, propofol, and etomidate show little increase in half life with prolonged infusion.
Redistribution, accumulation in fat, and drugs metabolic rate affect duration of action
Propofol
MOA: Potentiation of GABA, sodium channel blockade
Applications: Rapid onset and short duration. anesthetic induction, used in procedures for rapid return to preop mental status
Reduce dose in elderly due to reduced clearance, increase dose in young children due to rapid clearance
**Propofol infusion syndrome associated with prolonged high doses in young or head injured patients
Etomidate
MOA: Stimulates GABA
Applications: Rapid onset and short duration. anesthetic induction, used in procedures for rapid return to preop mental status
Preferred for patients at risk of hypotension or MI. Produces hypnosis and has no analgesic effects. INCREASED EEG ACTIVITY. DO NOT USE IN EPILEPSY
Ketamine
MOA: NMDA antagonist
Applications: Rapid onset and short duration. anesthetic induction, used in procedures for rapid return to preop mental status
Suited for patients with hypotension, asthma, and pediatric procedures. Increases HR, BP, CO, CBF, and ICP. Mental side effects like delirium and hallucinations
Methohexital and Thiopental
MOA: Stim GABA
Application: Anesthetic induciton
Respiratory and EEG depressant
Rapid clearance
Possible inflammatory or necrotic reaction with injection
Inhalation Anesthetics
Fluranes and NO
Most dangerous drugs in clinical use due to narrow therapeutic window
Fluranes are liquids are room temp, NO is gas
Increase in solubility slows induction of anesthesia. NO less soluble than fluranes
Inhalation Uptake
FA approaches FI fastest for the least soluble agents.
Low blood solubility leads to rapid concentration increase
Greater blood solubility causes more molecules to dissolve in the blood before the partial pressure changes, causing the arterial pressure to increase less rapidly
Effect of ventilation on FA/FI
To accelerate induction increase the inspired anesthetic pressure.
Increase tidal volume and respiratory rate
Greater increase in FA/FI ratio with an increase in ventilation for halothane when compared to NO
Minimum Alveolar concentration
Concentration of inhaled anesthetic needed to eliminate movement in 50% of patients stimulated by incision.
Inverse is a measure of potency
MAC is small for potent and large for weak.
NO cannot produce anesthesia alone
Elimination
Most soluble take longer to clear.
Insoluble prefer gas phase and rapidly diffuse to alveoli and are eliminated
Ventilation is the determining variable.
Toxicity of Inhalation Anesthetics
Acute: nephrotoxicity, hematotoxicity, genetic hyperthermia, hepatotoxicity.
Chronic: Mutagenicity, teratogenicity, reproductive effects, cardiogenicity.
Isoflurane
MOA: Increases GABA release and glutamate reuptake decreasing motor function.
Application: Maintenance of anesthesia
Highly volatile at RT. Decreases ventilation and RBF. Increases CBF. Hypotension and increased coronary blood flow, decreased myocardial O2 demand. Decreased baroreceptor reflex.
Enflurane
MOA: Positive allosteric effector of GABA receptor.
Application: Maintenance
Also volatile with slow induction. Decreased arterial BP and decreased contractility. Possible increased ICP and seizure
Sevoflurane
MOA: not fully understood, likely membrane hyperpolarization through GABA
Application: Anesthetic induction for outpatient surgery.
Ideal induction agent. Decreased AP and CO, so preferred for patients with ischemia. Sevoflurane + CO2 absorbent soda lime is nephrotoxic.
Desflurane
MOA: Same as sevoflurane
Application: Same as sevoflurane, although not preferred over it.
Highly volatile, nonflammable in mixtures of air of O2. Airway irritant
Nitrous Oxide
MOA: Unknown
Weak anesthetic with analgesic effects
Used as adjunct.
Expands volume of air containing cavities, so avoid in ear or bowl obstructions or introcular bubbles.
Administer 100% O2 rather than air when discontinuing to avoid hypoxia.
Controversial due to potential changes in DNA and protein synthesis
Neuromuscular Blocking Agents MOA
Nondepolarizing: prevents the opening of sodium channel when bound to the receptor
Depolarizing occupies the receptor and blocks the channel.
Neuromuscular Blocking Agents Uses
Surgical relaxation
Endotracheal intubation
Control of ventilation
Treatment of convulsions, although they don’t cross the BBB.
Assessment of Neuromuscular Transmission
Nondepolarizing: Fade
Depolarizing phase I: Diminished
Depolarizing phase II: Fade
Succinylcholine
MOA: Persistent depolarization at NMJ
Rapidly metabolized by plasma cholinesterase
Arrhythmias. hyperkalemia, intraocular and abdominal pressure, and postop muscle pain are possible side effects.
-curium/curonium
MOA: Competitive antagonist at nACH receptors
Application: relaxation for surgical procedures
Action is usually antagonized by Sugammadex or and ACH inhibitor when the effects is no longer desired.
Toxic Effects: Prolonged apnea
Sugammadex
MOA: Noncompetitive inhibition of rocuronium and vercuronium through encapsulation
Used to reverse neuromuscular blockade.
Side effects: Bradycardia, hypersensitivity, recurrence of neuro blockade, headache, vomiting, nausea.
Benzodiazepines
Midazolam
Diazepam
Lorazepam
Enhance GABA
Used to anxiolysis, amnesia, sedation.
Midazolam is most commonly used followed by the other two
A2 agonists
Dexmedetomidine
Short term sedation of critically ill adults or sedation prior to procedures in non-intubated patients
Side Effects: Hypotension and Bradycardia
Opioids
Reduce anesthetic requirement and minimize hemodynamic changes due to painful stimuli
Primary analgesics during perioperative period.
Administered intrathecally and epidurally.
NSAIDs
Used for minor surgical procedures to control postoperative pain
Oxygen
Used to reverse or prevent hypoxia
Excessive use decreases ventilation
HR and CO decrease
Can irritate mucosal surfaces so humidified O2 should be used.
Carbon Dioxide
Insufflation during endoscopic procedures
Flooding surgical field during cardiac procedures
Adjusting pH during bypass
Highly soluble
Respiratory acidosis
Increases CO, HR, and BP
Local Anesthetics
MOA: Bind inside ion channel and block sodium ion entrance to prevent depolarization
Extradural injection = epidural
Caudal block = needle inserted into caudal canal via sacral hiatus
Peripheral nerves = perineural block
CSF = Spinal block
Local Anesthetics Absorption
Dependent on dosage, site of injection, drug tissue binding, local tissue blood flow, and physiochemical properties of the drug.
More lipid soluble = more potent and longer duration of action + longer time to achieve effect.
Peak serum values vary based on site of injection. Intercostal is highest while femoral and sciatic are lowest
Local Anesthetic Toxicity
CNS - sedation, lightheadedness, visual and auditory disturbances
Cardio - Negative effects on conduction and overall function
Neural: Potential neruotoxicity leading to neural injury.
Transient Neurologic symptoms: possible transient pain or dysthesia
Short Duration Local Anesthetics
Lidocaine
Prilocaine
Mepivacaine
Duration 1-2h/ 2-4h with epi
Prilocaine and Mepivacaine pose a risk of methemoglobinemia
Longer Duration Local Anesthetics
Bupivacaine
Ropivacaine
Levobupivacaine
Duration 3-6 h
Possible cardiovascular collapse
Popular Dental Anesthetic
Articaine
Very Short Acting Local Anesthetics
Chloroprocaine
Procaine
30-60 min/ 60-90 with epi
Procaine not used epidurally
Spinal Anesthetic
Tetracaine
