Anesthesia II: Types and Measurements of Anesthesia
Surgery needs to be tolerated. The patient needs to be immobile, unconscious and not remember. The accepted mechanism of anesthetic action is suppression of synapses. There are many molecular targets however research has identified specific GABA A receptor subtypes that are involved in the action of intravenous anesthetics etomidate and propofol. *bookmark nature*
There are three types of anesthesia, local which is major anesthesia by the surgeon, regional like an epidural for specific nerve or plexus (brachial, lumbar) block, intravenous sedation and anesthesia allowing for awake testing and clinical correlation, a loss of bodily sensation with or without loss of consciousness, dissociative anesthesia with intravenous dissociative agents which is supplemental sedation and general anesthesia where the patient is unconscious and intubated and a combination of amnesia, analgesia and relaxation effects are required. An additional goal is anesthesia that gives the strongest implication for neuromonitoring.
The goals of anesthesia are hypnosis or loss of consciousness, analgesia or absence/insensitivity to pain, amnesia or absence of memory, immobility or muscle relaxation, the maintenance of patient vital functions (cardiovascular, pulmonary and renal) and then finally emergence from this induced and maintained state. An additional goal is to facilitate favorable conditions for neuromonitoring.
All of these goals are artificially induced by the administration of anesthetics before, during and after surgical operations. Hypnosis and amnesia are accomplished by administration of drugs that have primary site of action in the brain. Analgesia and immobility are accomplished by drugs that have primary sites of action in the spinal cord and or muscles of the periphery. Hypnosis is the loss of consciousness, analgesia is the absence of pain, amnesia is the absence of memory, immobility is muscle relaxation. All of these mechanistic actions take place while allowing for the maintenance of the patient's vital functions through the regimen of balanced anesthesia.
Types of Anesthetics
Sedative-hypnotics
Sedative-hypnotics produce relaxation and often euphoria in low doses, sleep in higher doses and possible coma and death in overdose. They are believed to exert their effect on the brain by interacting with receptors for the neurotransmitter GABA. Their effect at these receptors enhances the action of GABA as an inhibitory neurotransmitter and results in a depression of brain activity. Some may also have actions at glutamate receptors reducing the action of glutamate which is the brain's major excitatory neurotransmitter.
Synthetic pharmaceutical sedative-hypnotics include the benzodiazepines, barbiturates and other substances. General anesthetics are powerful sedative-hypnotics used to induce loss of conscious awareness and are often volatile organic compounds inhaled as part of a gas mixture during surgery. Examples of general inhalation anesthetics are the halogenated compounds desflurane, enflurane, halothane, isoflurane and sevoflurane and nitrous oxide.
Isoflurane is slow acting with high blood solubility, it might take a while to see the effects of reduction. Sevoflurane is intermediate acting with moderate blood soluability. Desflurane is fast acting with low blood soluability. Nitrous oxide is fast acting with no decrease in blood pressure
Propofol (Diprivan) used for induction and maintenance, it is a hypnotic (milk of amnesia), it's mechanism is it is a GABA agonist (ligand or drug that binds and alters the activity of a receptor; GABA is inhibitory neurotransmitter). side effects, vasodilation and hypotension, respiratory suppression, patients will often have pain/burning sensation in the arm that propofol is injected into. This is typically the last drug delivered before the patient goes to sleep and is conscious. Propofol has rapid kinetics and is extremely titratable. There is a possible issue for patient's with egg allergies. Propofol is the most common TIVA sedative. Consider reducing the Propofol concentration by adding ketamine.
Benzodiazepines
Benzodiazepines are for sedation but also have hypnosis and amnesia effect. these are things like versed (midazolam), valium (diazepam), ativan (larazepam), klonopin (clonazepam), nitrazepam, can cause respiratory suppression and mild hypotension.
Nitrous Oxide
Nitrous Oxide (N2O) is a gas widely used for its anesthetic and analgesic properties. It is used by dentists as a sole anesthetic and is a component of the inhalation anesthesia (together with potent volatile sedative-hypnotic general anesthetics) for major surgeries.
Opioids
Opioids or opiates are a group of naturally occurring and synthetic chemicals. Naturally occurring opioids are derived from the unripened seedpod of the opium poppy (papaver somniferum) which yields a milky, latex secretion when cut. Natural opium inherently contains morphine and codeine. Opioids act on opioid receptors in the brain to reduce the perception of pain (analgesia), suppress cough, constrict pupils, and slow respiration. They may also produce relaxation, euphoria, and a dreamy altered state of consciousness. Medicinally, opioids are invaluable as analgesics and cough suppressants.
Synthetic opioids either are chemical derivatives of morphine, codeine, or other related molecules inherent to opium or can be synthesized from non-opioid precursors. Heroin (diacetlymorphine) is a simple chemical derivative of morphine that allows it to cross the blood brain barrier into the brain two or three times more efficiently than morphine. Hydromorphone, oxycodone, and hydrocodone are all derived from opium precursors. Methadone, fentanyl, remifentanil, meperidine, and propoxyphene are other examples of synthetic opioids with fentanyl and remifentinil widely used in the operating room.
Also known as narcotics, they are used for analgesia/pain management. Sufentanil is 10 times more potent than fentanyl, fentanyl is ten times more potent than alfentanil, remifentanil is very short acting, morphine is very long acting. They may cause respiratory suppression at high doses.
The endogenous neurotransmitters acting at opioid receptors are a class of small peptide molecules collectively called opioid peptides or endorphins. These range in size from the 5-amino acid long enkephalins to the 31-amino acid long beta-endorphin.
Analgesics
Narcotics are for analgesia, the types and potency are sufentanil is 10 times more potent than fentanyl, fentanyl is 10 times more potent an alfentanil, remifentanil is very short acting (5-10 minutes), morphine is long acting 3-4 hours, can cause respiratory suppression at high doses.
Dissociative Anesthetics
This class of psychoactive drugs included ketamine. they are synthetic compounds introduced into medicine to produce an anesthetic loss of sensation without depressing respiration and cardiovascular function as do the general anesthetics. Ketamine is used for both human and veterinary surgical procedures. At sub anesthetic doses in humans, ketamine produces an altered state of consciousness that has some psychedelic-like characteristics and may be accompanied by a loss of body sensation.
Ketamine is an anesthetic and analgesic, it has dissociative properties where the brain is unable to process stimuli. it can increase intracranial pressure and cerebral metabolic rate and blood flow, it can cause hallucinations and can increase intracranial pressure and may induce seizures.
Dexmedetomidine (precedex) is for sedation and analgesia, has MAC sparing effects, has effect on locus ceruleus, which is involved in depression, stress and panic, can cause bradycardia and hypotension which sometimes atropine pre-dosing helps to negate effect. It is an alpha 2 adrenergic agonist.
Neuromuscular Blocking Agents
Rocuronium, vecuronium; Neuromuscular blocking agents, also called muscle relaxants, used to prevent movement, binds to acetylcholine receptors on the motor end plates blocking acetylcholine activation. there are two types, depolarizers, which depolarize the motor end plate wehn binding to acetylcholine receptors, muscle fasciculation may be noticed in response to depolarization. Succinylcholine is short acting, lasts 3-10 minutes. Non depolarizers bind the acetylcholine receptors without causing depolarization, they are immediate acting and can last for 30-60 minutes depending on the dose. atracurium, vecuronium, cis-atracuium, rocuronium, pancuronium, they are longer acting. T
Molecules that bind to nicotinic acetylcholine (Ach) receptors at the motor end plate/neuromuscular junction for complete or partial muscle paralysis to prevent patient movement. Depolarizers depolarize the motor end plate when binding to acetylcholine receptors, may notice muscle fasciculation. Succinylcholine is a short acting (3-10 minutes) depolarizer, has a negative postoperative after effect sensation. This is ideal for intubation because can quickly get a baseline without having to wait for titration of -ronium or administration of suggamadex.
Non-depolarizers depolarize the motor end plate, are immediate but potentially long-lasting (low-dose vs. high-dose). Vecuronium, rocuronium, pancuronium.
Neuromuscular Blockade Reversing Agent
Suggamadex; Removes effects of neuromuscular blockade. Can test the validity of NMB with T04 and MEP, relay to anesthesia, there is a grading system if 1/4, 4/4 depending on dose of suggamadex. depends on the molecular interaction. is typically a once per surgery kind of thing but i have been involved in surgeries where they as for it twice. just need to make sure you give enough.
Intravenous Agents
Propofol, Narcotics (Opioids), benzodiazepines, barbituates, etomidate, ketamine, dexmedetomidine, neuromuscular blocking agents
Induction Anesthetics
Barbiturates are used for neuro-protection and during induction, they are short acting, like sodium pentothal, hethohexital, phenobarbital, pentobarbial, they may cause respiratory and cardiovascular suppression.
Etomidate is used for induction, it is a hypnotic, a GABA agonist that suppresses adrenal function, its side effects can cause nausea, vomiting, myalgia and myoclonus, may have minimal cardiovascular effects.
Cardiac drugs
atropine, dobutamine, dopamine, epinephringe, heparin (anticoagulant), lidocaine, minoxidil, nitroglycerine, nitroprusside, pheynlephrine.
Antiseizure Drugs
depakene, dilantin, klonopin, tegretol, zarontine
MAC Measurements/Anesthesia Math
MAC the basic language of - minimum alveolar concentration/monitored anesthesia care. 1 MAC amount of agent required to prevent movement in 50% of patients when exposed to painful stimuli. Isoflurane 1.15%, Desflurane 6.0%, Sevoflurane 1.71%, Nitrous Oxide 104%. When inhalation agents are combined, they have an additive effect on the MAC value ex 0.5 MAC Desflurane = 0.5 MAC N20 = 1.0 MAC. The effect on SEPs when inhalation agents are combined is not additive, it is synergistic in its effects on SEP cortical waveforms. Therefore, inhalation agents should not be mixed when monitoring evoked potentials.
Factors that decrease the MAC are hypothermia, elderly patient, acute alcohol intoxication, CNS depressants such as opioids, benzodiazepines, clonidine, etc. Factors that increase the MAC chronic alcohol abuse, pediatric patients, patients with red hair. Factors not affecting the MAC are anesthetic duration, gender, PaCO2.
Effective dose, MAC for intravenous drugs is referred to as ED50, effective dose amount of IV drug required to prevent movement of 50% of the patients in response to painful stimulation.
Patient's weight is typically measured in kilograms and pump deliveries are in mcg/kg/min
Effective Dose
Effective Dose is the amount of IV drug required to prevent movement in 50% of the patient's in response to painful stimulation
General Anesthesia
Inhalational; halothane, enflurane, isoflurane, sevoflurane, desflurane, nitrous oxide +/- NMB
Balanced (Inhalational agents plus); propofol, etomidate, midazolam, dexmeditomidine; Analgesia; fentanyl, sufentanil, remifentanil
TIVA; propofol, etomidate, midazolam, ketamine, dexmeditomidine, Analgesia; fentanyl, sufentanyl, remifentanyl, ketamine, dexmeditomidine; +/-NMB
mcg/kg/min, mcg/kg/hr, how many kilos, blood pressure measurement of systolic vs asystolic, when does it mean when the patient codes, train of four, eeg for burst suppression, etcetera, MAP in mm Hg. Can see observational effects of low blood pressure on monitoring
Anesthetic Targets
Inhalational Agents; NMDA, GABA, Ach, Na+/K+, ATPase
Propofol; GABA
Opiods; opiate receptors (enkephalins)
Ketamine; NMDA, sigma opiod
Dexmeditomidine; Central alpha 2
Muscle Relaxants; Acetylcholine Recording at the neuromuscular junction; NMJ Blockade
****Revisit this power point for the wealth of imagery that describes what is the effects of anesthesia on specific neural pathways****
Anesthesia "Creep" may well be contributed to by other physiological factors which change over time: Temp, Hct, pH, pC02, Na+, K+, blood volume
There are three types of anesthesia, local which is major anesthesia by the surgeon, regional like an epidural for specific nerve or plexus (brachial, lumbar) block, intravenous sedation and anesthesia allowing for awake testing and clinical correlation, a loss of bodily sensation with or without loss of consciousness, dissociative anesthesia with intravenous dissociative agents which is supplemental sedation and general anesthesia where the patient is unconscious and intubated and a combination of amnesia, analgesia and relaxation effects are required. An additional goal is anesthesia that gives the strongest implication for neuromonitoring.
The goals of anesthesia are hypnosis or loss of consciousness, analgesia or absence/insensitivity to pain, amnesia or absence of memory, immobility or muscle relaxation, the maintenance of patient vital functions (cardiovascular, pulmonary and renal) and then finally emergence from this induced and maintained state. An additional goal is to facilitate favorable conditions for neuromonitoring.
All of these goals are artificially induced by the administration of anesthetics before, during and after surgical operations. Hypnosis and amnesia are accomplished by administration of drugs that have primary site of action in the brain. Analgesia and immobility are accomplished by drugs that have primary sites of action in the spinal cord and or muscles of the periphery. Hypnosis is the loss of consciousness, analgesia is the absence of pain, amnesia is the absence of memory, immobility is muscle relaxation. All of these mechanistic actions take place while allowing for the maintenance of the patient's vital functions through the regimen of balanced anesthesia.
Types of Anesthetics
Sedative-hypnotics
Sedative-hypnotics produce relaxation and often euphoria in low doses, sleep in higher doses and possible coma and death in overdose. They are believed to exert their effect on the brain by interacting with receptors for the neurotransmitter GABA. Their effect at these receptors enhances the action of GABA as an inhibitory neurotransmitter and results in a depression of brain activity. Some may also have actions at glutamate receptors reducing the action of glutamate which is the brain's major excitatory neurotransmitter.
Synthetic pharmaceutical sedative-hypnotics include the benzodiazepines, barbiturates and other substances. General anesthetics are powerful sedative-hypnotics used to induce loss of conscious awareness and are often volatile organic compounds inhaled as part of a gas mixture during surgery. Examples of general inhalation anesthetics are the halogenated compounds desflurane, enflurane, halothane, isoflurane and sevoflurane and nitrous oxide.
Isoflurane is slow acting with high blood solubility, it might take a while to see the effects of reduction. Sevoflurane is intermediate acting with moderate blood soluability. Desflurane is fast acting with low blood soluability. Nitrous oxide is fast acting with no decrease in blood pressure
Propofol (Diprivan) used for induction and maintenance, it is a hypnotic (milk of amnesia), it's mechanism is it is a GABA agonist (ligand or drug that binds and alters the activity of a receptor; GABA is inhibitory neurotransmitter). side effects, vasodilation and hypotension, respiratory suppression, patients will often have pain/burning sensation in the arm that propofol is injected into. This is typically the last drug delivered before the patient goes to sleep and is conscious. Propofol has rapid kinetics and is extremely titratable. There is a possible issue for patient's with egg allergies. Propofol is the most common TIVA sedative. Consider reducing the Propofol concentration by adding ketamine.
Benzodiazepines
Benzodiazepines are for sedation but also have hypnosis and amnesia effect. these are things like versed (midazolam), valium (diazepam), ativan (larazepam), klonopin (clonazepam), nitrazepam, can cause respiratory suppression and mild hypotension.
Nitrous Oxide
Nitrous Oxide (N2O) is a gas widely used for its anesthetic and analgesic properties. It is used by dentists as a sole anesthetic and is a component of the inhalation anesthesia (together with potent volatile sedative-hypnotic general anesthetics) for major surgeries.
Opioids
Opioids or opiates are a group of naturally occurring and synthetic chemicals. Naturally occurring opioids are derived from the unripened seedpod of the opium poppy (papaver somniferum) which yields a milky, latex secretion when cut. Natural opium inherently contains morphine and codeine. Opioids act on opioid receptors in the brain to reduce the perception of pain (analgesia), suppress cough, constrict pupils, and slow respiration. They may also produce relaxation, euphoria, and a dreamy altered state of consciousness. Medicinally, opioids are invaluable as analgesics and cough suppressants.
Synthetic opioids either are chemical derivatives of morphine, codeine, or other related molecules inherent to opium or can be synthesized from non-opioid precursors. Heroin (diacetlymorphine) is a simple chemical derivative of morphine that allows it to cross the blood brain barrier into the brain two or three times more efficiently than morphine. Hydromorphone, oxycodone, and hydrocodone are all derived from opium precursors. Methadone, fentanyl, remifentanil, meperidine, and propoxyphene are other examples of synthetic opioids with fentanyl and remifentinil widely used in the operating room.
Also known as narcotics, they are used for analgesia/pain management. Sufentanil is 10 times more potent than fentanyl, fentanyl is ten times more potent than alfentanil, remifentanil is very short acting, morphine is very long acting. They may cause respiratory suppression at high doses.
The endogenous neurotransmitters acting at opioid receptors are a class of small peptide molecules collectively called opioid peptides or endorphins. These range in size from the 5-amino acid long enkephalins to the 31-amino acid long beta-endorphin.
Analgesics
Narcotics are for analgesia, the types and potency are sufentanil is 10 times more potent than fentanyl, fentanyl is 10 times more potent an alfentanil, remifentanil is very short acting (5-10 minutes), morphine is long acting 3-4 hours, can cause respiratory suppression at high doses.
Dissociative Anesthetics
This class of psychoactive drugs included ketamine. they are synthetic compounds introduced into medicine to produce an anesthetic loss of sensation without depressing respiration and cardiovascular function as do the general anesthetics. Ketamine is used for both human and veterinary surgical procedures. At sub anesthetic doses in humans, ketamine produces an altered state of consciousness that has some psychedelic-like characteristics and may be accompanied by a loss of body sensation.
Ketamine is an anesthetic and analgesic, it has dissociative properties where the brain is unable to process stimuli. it can increase intracranial pressure and cerebral metabolic rate and blood flow, it can cause hallucinations and can increase intracranial pressure and may induce seizures.
Dexmedetomidine (precedex) is for sedation and analgesia, has MAC sparing effects, has effect on locus ceruleus, which is involved in depression, stress and panic, can cause bradycardia and hypotension which sometimes atropine pre-dosing helps to negate effect. It is an alpha 2 adrenergic agonist.
Neuromuscular Blocking Agents
Rocuronium, vecuronium; Neuromuscular blocking agents, also called muscle relaxants, used to prevent movement, binds to acetylcholine receptors on the motor end plates blocking acetylcholine activation. there are two types, depolarizers, which depolarize the motor end plate wehn binding to acetylcholine receptors, muscle fasciculation may be noticed in response to depolarization. Succinylcholine is short acting, lasts 3-10 minutes. Non depolarizers bind the acetylcholine receptors without causing depolarization, they are immediate acting and can last for 30-60 minutes depending on the dose. atracurium, vecuronium, cis-atracuium, rocuronium, pancuronium, they are longer acting. T
Molecules that bind to nicotinic acetylcholine (Ach) receptors at the motor end plate/neuromuscular junction for complete or partial muscle paralysis to prevent patient movement. Depolarizers depolarize the motor end plate when binding to acetylcholine receptors, may notice muscle fasciculation. Succinylcholine is a short acting (3-10 minutes) depolarizer, has a negative postoperative after effect sensation. This is ideal for intubation because can quickly get a baseline without having to wait for titration of -ronium or administration of suggamadex.
Non-depolarizers depolarize the motor end plate, are immediate but potentially long-lasting (low-dose vs. high-dose). Vecuronium, rocuronium, pancuronium.
Neuromuscular Blockade Reversing Agent
Suggamadex; Removes effects of neuromuscular blockade. Can test the validity of NMB with T04 and MEP, relay to anesthesia, there is a grading system if 1/4, 4/4 depending on dose of suggamadex. depends on the molecular interaction. is typically a once per surgery kind of thing but i have been involved in surgeries where they as for it twice. just need to make sure you give enough.
Intravenous Agents
Propofol, Narcotics (Opioids), benzodiazepines, barbituates, etomidate, ketamine, dexmedetomidine, neuromuscular blocking agents
Induction Anesthetics
Barbiturates are used for neuro-protection and during induction, they are short acting, like sodium pentothal, hethohexital, phenobarbital, pentobarbial, they may cause respiratory and cardiovascular suppression.
Etomidate is used for induction, it is a hypnotic, a GABA agonist that suppresses adrenal function, its side effects can cause nausea, vomiting, myalgia and myoclonus, may have minimal cardiovascular effects.
Cardiac drugs
atropine, dobutamine, dopamine, epinephringe, heparin (anticoagulant), lidocaine, minoxidil, nitroglycerine, nitroprusside, pheynlephrine.
Antiseizure Drugs
depakene, dilantin, klonopin, tegretol, zarontine
MAC Measurements/Anesthesia Math
MAC the basic language of - minimum alveolar concentration/monitored anesthesia care. 1 MAC amount of agent required to prevent movement in 50% of patients when exposed to painful stimuli. Isoflurane 1.15%, Desflurane 6.0%, Sevoflurane 1.71%, Nitrous Oxide 104%. When inhalation agents are combined, they have an additive effect on the MAC value ex 0.5 MAC Desflurane = 0.5 MAC N20 = 1.0 MAC. The effect on SEPs when inhalation agents are combined is not additive, it is synergistic in its effects on SEP cortical waveforms. Therefore, inhalation agents should not be mixed when monitoring evoked potentials.
Factors that decrease the MAC are hypothermia, elderly patient, acute alcohol intoxication, CNS depressants such as opioids, benzodiazepines, clonidine, etc. Factors that increase the MAC chronic alcohol abuse, pediatric patients, patients with red hair. Factors not affecting the MAC are anesthetic duration, gender, PaCO2.
Effective dose, MAC for intravenous drugs is referred to as ED50, effective dose amount of IV drug required to prevent movement of 50% of the patients in response to painful stimulation.
Patient's weight is typically measured in kilograms and pump deliveries are in mcg/kg/min
Effective Dose
Effective Dose is the amount of IV drug required to prevent movement in 50% of the patient's in response to painful stimulation
General Anesthesia
Inhalational; halothane, enflurane, isoflurane, sevoflurane, desflurane, nitrous oxide +/- NMB
Balanced (Inhalational agents plus); propofol, etomidate, midazolam, dexmeditomidine; Analgesia; fentanyl, sufentanil, remifentanil
TIVA; propofol, etomidate, midazolam, ketamine, dexmeditomidine, Analgesia; fentanyl, sufentanyl, remifentanyl, ketamine, dexmeditomidine; +/-NMB
mcg/kg/min, mcg/kg/hr, how many kilos, blood pressure measurement of systolic vs asystolic, when does it mean when the patient codes, train of four, eeg for burst suppression, etcetera, MAP in mm Hg. Can see observational effects of low blood pressure on monitoring
Anesthetic Targets
Inhalational Agents; NMDA, GABA, Ach, Na+/K+, ATPase
Propofol; GABA
Opiods; opiate receptors (enkephalins)
Ketamine; NMDA, sigma opiod
Dexmeditomidine; Central alpha 2
Muscle Relaxants; Acetylcholine Recording at the neuromuscular junction; NMJ Blockade
****Revisit this power point for the wealth of imagery that describes what is the effects of anesthesia on specific neural pathways****
Anesthesia "Creep" may well be contributed to by other physiological factors which change over time: Temp, Hct, pH, pC02, Na+, K+, blood volume