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42 Cards in this Set

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  • Back
Define anesthesia.
The loss of all sensation w/ or w/o the loss of consciousness
-- may be achieved via inhalational or intravenous agents
What are the 5 components of the “anesthetic state”?
1. amnesia

2. sedation/loss of consciousness

3. analgesia

4. hyporeflexia (sensory and automatic)

5. muscle relaxation
What are the inhalational anesthetic agents in current use?

What are the inhalational analgesics in current use?
Nitrous oxide
What are the intravenous anesthetic agents in use?
Midazolam (antianxiety benzodiazepine)

Propofol (anesthetic)

Etomidate (anesthetic)

Ketamine (dissociative agent)
What are Guedel’s Stages of Anesthesia?
I. analgesia
II. delirium

III. surgical anesthesia
-- sleep
-- sensory loss
-- muscle tone loss
-- intercostals paralysis

IV. Medullary paralysis
Newer, more potent anesthetics w/ lower blood solubility produce…?
Faster and less distinct progression through the stages of anesthesia

Awake --> analgesia and delirium --> surgical anesthesia
Describe how differential sensitivity of neuronal pathways to anesthetic agents appears to account for the stages of anesthesia.
1. selective sensitivity of neurons in the substantia gelatinosa accounts for the analgesia, Stage I (spinothalamic neurons)

2. blockade of inhibitory neurons appears to account for Stage II, delirium stage

3. progressive depression of ascending pathways in the reticular formation account for Stage III, surgical anesthesia stage

4. at higher concentrations the medullary vasomotor and respiratory centers are depressed accounting for Stage IV
The kinetics of ONSET of anesthesia depends on…? OFFSET?
Rate of change of concentration of inhalational agent in alveolus vs. blood vs. brain

Vice versa for the OFFSET of effects.
Describe inspired concentration.
1. determined by the flow of carrier gases and the vapor pressure of the anesthetic agent

2. liquid anesthetic agents require a vaporizer in order to volatize the anesthetic agent into a gas for inspiration
Describe alveolar concentration.
1. determined by the inspired concentration and the two respiratory parameters
-- minute volume
-- fxnal residual capacity

2. the rate of removal of the inhaled agent from the alveolar space (via pulmonary blood flow) also determines the alveolar concentration and is largely dependent on solubility of the agent in blood
Describe blood concentration.
1. determined by the alveolar concentration and also permeability of the alveolar mbrn

2. solubility of the inhalational agent in blood is important in determining the blood concentration and is related to the blood-gas partition coefficient

3. the blood-gas partition coefficient determines how rapidly the solubility equilibrium is reached btwn the concentrations in the alveolus vs. blood

4. induction of anesthesia w/ agents w/ low blood solubility such as SEVOFLURANE (0.65) or DESFLURANE (0.45) occurs much more rapidly than induction w/ higher solubility agents
Describe brain concentration.
1. determined by the blood concentration and solubility of the anesthetic agent in the brain

2. solubility of the anesthetic agent in the brain is related to the lipid solubility of the agent

3. the oil-gas partition coefficient is the index of solubility of the inhalational agents in brain
The rate of ONSET and OFFSET of anesthesia is dependent on…?
The SPEED with which equilibration occurs in each of the compartments
-- rate of onset/offset
-- blood solubility
How is the potency of inhalational anesthetic agents defined?
Defined by Minimal Alveolar Concentration (MAC)
-- concentration of anesthetic measured in end tidal gas which prevents response to a standard painful stimulus in 50% of the humans or test animals

Largely determines the concentrations administered
How is MAC used clinically?
In the clinical situation, anesthetics are usually administered in multiples of MAC

MAC requirement can be reduced by co-administration of either inhalation analgesic (N20) or IV narcotic analgesics, or physical status of the patient
Hepatic metabolism of anesthetic agents?
Hepatic metabolism varies w/ agent:
-- minimal biotransformation occurs w/ DESFLURANE and NITROUS OXIDE
-- approx 2-5% of administered SEVOFLURANE is metabolized
Consequences of metabolism of anesthetic agents?
1. metab of SEVOFLURANE generates fluoride ions
Elimination of anesthetic agents?
1. most agents eliminated quantitatively in expired gases

2. metabolites and organic/inorganic fluoride eliminated by kidney
What is the major correlate with potency of anesthetic agents?
Lipid solubility correlates w/ potency

1. most theories of anesthetic action are based on the physicochemical properties of the agents, including lipid solubility of the agents (MAC)

2. inhaled anesthetics possess no unique structural configuration that can be assoc w/ a particular structure-activity relationship, only lipid solubility
What are the electrophysiological changes that occur with anesthetics?
1. Decreased excitatory synaptic transmission (EPSPs)
-- enter lipid-protein matrix of neuronal mbrns and reversibly disrupt (K+, Na+, Ca++) channel fxn through either direct or indirect actions
-- it is unclear how these effects decrease excitatory synaptic transmission (decreased EPSPs) to reduce neuronal signaling

2. Increase inhibitory synaptic transmission (IPSPs)
-- low concentrations of both inhalational and injectable anesthetic agents facilitate the action of GABA to decrease GABAa-activated chloride ion flux
-- at higher concentrations these agents also directly activate GABAa-chloride ion channel-receptor complex to increase chloride flux (up to 50%) to increase inhibitory synaptic potentials leading to depression of neuronal signaling
What effect do inhalational anesthetics have on the CNS?
-- inhalational produce IRREGULARLY descending depression of the CNS
-- higher cortical centers, ascending reticular activating system and spinal cord affected first
-- medullary area is depressed at high concentrations leading to respiratory and circulatory arrest

-- most of the inhalational anesthetic agents produce a small increase in cerebral blood flow due to decreased cerebral vascular resistance
What effect do inhalational anesthetics have on the cardiovascular system?
-- sevoflurane (++) decreases contractility and cardiac output at 1 MAC concentrations
-- desflurane produces minimal depression

-- all inhalational anesthetic agents decrease vascular smooth muscle tone and therefore reduce blood pressure in a concentration-dependent manner
-- desflurane can increase blood pressure (sympathetic activation) when rapid increases in anesthetic concentration occur
What effect do inhalational anesthetics have on the respiratory system?
All inhalational anesthetic agents produce a concentration-dependent respiratory depression via:
-- direct depression of the respiratory center
-- decrese in sensitivity of the medullary respiratory center to carbon dioxide

All inhalational anesthetic agents cause a decrease in tidal volume
-- while increase in respiratory rate can occur, it is insufficient for the decrease in tidal volume
-- w/o assisted (mechanical) ventilation, these agents produce an increase in the resting PaCO2
What effect do inhalational anesthetics have on the neuromuscular system?
Concentration-dependent skeletal muscle relaxation that quantitatively varies w/ the different agents

Due to reduced signal strength in spinal polysynaptic interneurons which may be related to increased GABA effects
What effect do inhalational anesthetics have on the gastrointestinal system?
Older anesthetics, caused postoperative nausea and vomiting to a greater degree than some of the newer agents

Incidence of nausea and vomiting is quite variable from patient to patient, and depends to some extent on the length of anesthetic administration (can also occur w/ N20)
What are the adverse effects of desflurane?
-- rapid increases in anesthetic concentration produces activation of the sympathetic nervous system
-- transient increased heart rate and blood pressure

-- high incidence of airway irritation (laryngospasm, coughing, etc) when used as a single anesthetic agent, especially during induction and recovery
-- pretreatment w/ narcotics decreases this side effect

-- recent studies have demonstrated that carbon monoxide forms from the rxn of desflurane w/ the material that absorbs CO2 (sode, line, Baralyme) in the anesthetic circuit
-- the amt of carbon monoxide formed depends upon temperature and moisture of the CO2 absorption material
-- have been reports of pts experiencing a signif increase in carboxyhemoglobin
What are the adverse effects of sevoflurane?
1. Under low flow conditions (<1 L/min), can also react w/ the CO2 absorber, soda lime, in the breathing circuit

2. Compound A (an olefin) is formed from the reaction of sevoflurane w/ soda lime, especially w/ increased temperature in the gas delivery circuit
Nitrous oxide characteristics?

INADEQUATE as an inhalational ANESTHETIC and is used most often in combo w/ either intravenous or inhalational anesthetic agents

Due to limited solubility in blood, NO has rapid onset and offset of effects
(blood-gas partition coefficient = 0.45)
NO analgesia?
Occurs w/ inspired concentrations of 20% and is used clinically in concentrations up to 70%

Used to lower the concentration of inhalational anesthetic required to produce the same level of anesthesia

The mechanism of analgesic action is not known
NO effects on organ systems?
1. NO has no significant effects on the CV, respiratory, hepatic, renal or autonomic nervous systems

2. CNS effects largely due to disinhibition of inhibitory pathways, hence the “laughing gas” descriptor
Limitations to use of NO?
1. occurs when NO concentrations greater than 80% are administered
2. “diffusion hypoxia” occurs when NO admin is rapidly terminated w/o supplemental oxygen
-- rapid diffusion of NO from the blood into the alveolar space
-- NO from the blood dilutes the amt of alveolar oxygen which is around 20% w/o supplemental oxygen

1. NO diffuses over 30 times more rapidly than oxygen to increase the volume or pressure in air-filled cavities
2. increased in volume of pneumothorax, tympanic mbrn rupture and increased gastric volume/pressure have been reported

1. nausea and vomiting can occur in a percentage of pts following prolonged administration w/ high concentrations
2. studies have demonstrated that women exposed chronically to high levels of NO (due to lack of scavenging of expired gasses) have decreased fertility
1. Reduces anxiety and sedates patient (enhances GABAa chloride current flow) but does not produce analgesia

2. Combo of benzodiazepines w/ regional anesthesia, NO, or a potential narcotic can produce effective clinical anesthesia

3. Minimal cardiovascular and respiratory depression

4, Midaxolam is more water soluble, thus less injection site irritation
Characteristics of Propofol?
1. induction of anesthesia is rapid and comparable to tiopental

2. maintenance of anesthesia can be achieved w/ either continuous intravenous infusion or intermittent bolus injections

3. regional anesthesia, NO or potent narcotics are required since propofol is NOT analgesic

4. induction and recovery are rapid w/ less “hang over” compared to thiopental
Propofol MOA?
1. appears to increase inhibitory synaptic transmission via facilitation of GABAa receptor-ion channel fxn

2. produces dose-dependent CNS depression
Propofol organ system effects?
1. dose-dependent depression of respiration w/ possible apnea

2. depression of the cardiovascular system
-- hypotension due to reduced systemic vascular resistance
-- infusions of propofol have produced a 15-30% reduction in various cardiac indices (CO, stroke work, stroke index)

3. anti-emetic properties reduce nausea and vomiting

4. vehicle is a problem and produces injection site irritation (burning) and potential allergic reactions (lecithin vehicle)
Etomidate characteristics of anesthesia?
1. rapid onset of sleep and recovery (t1/2 = 2-5 hrs)

2. lacks analgesic properties (requires N2O or narcotic analgesic)
Etomidate MOA?
1. increases inhibitory synaptic transmission by interacting with the GABAa receptor

2. does not reduce excitatory transmitter release
Etomidate organ system effects?
1. minimal cardiovascular and respiratory system depression

2. produces high incidence of excitatory phenomenon including spontaneous involuntary muscle movement and tremor (myoclonus)

3. patients who receive it, especially by continuous infusion, exhibit marked adrenocortical suppression for as long as 4 days after discontinuation

4. relatively high incidence of postop nausea and vomiting
Ketamine characteristics of anesthesia?
1. produces a cateplectic trance-like state

2. patient may appear awake with his eyes open (“dissociative anesthesia”)

3. relatively rapid acting w/ a return of consciousness in 15min (t1/2 2-3 hrs)
-- complete recovery can be slow and protracted

4. profound analgesia (even at sub-anesthetic concentrations)
Ketamine MOA?
1. non-competitive antagonist of the NMDA subtype of the glutamate receptor

2. decreased excitatory synapic transmission by reducing synaptic Ca++ channel conduction
Ketamine organ system effects?
1. CV system stimulation
-- increased bp
-- increased heart rate
-- increased cardiac reflex

2. most likely due to direct stimulation of CNS and increased sympathetic outflow

3. increased cerebral blood flow and intracranial pressure

4. minimal respiratory depression occurs and pharyngeal and laryngeal reflexes are maintained

5. muscle tone is frequently increased

6. adult patients may experience disagreeable dreams and hallucinations which may occur days or weeks after admin