Twenty Five Flashcards
What are 4 phases of anesthesia?
Stage 1: Induction with dizziness and reduced sensitivity to touch
Stage 2: Excitation including delirium and muscle contraction
Stage 3: Surgical level with depression of CNS to allow surgery
Stage 4: Coma and death
What are 7 properties of an ideal anesthetic? Why are most inhalational anesthetics less than ideal?
Anesthesia – reversible loss of sensation and consciousness
Analgesia – reduction or prevention of perception of pain
Amnesia – loss of memory
Akinesia – loss of movement (motor activity)
Minimal cardiovascular and respiratory depression
Non-flammable
Rapid induction and recovery
Anesthetics suppress consciousness reversibly by suppressing cortical function. Some anesthetics have significant amnesic effects but few have suitable analgesic properties. The volatile anesthetics have a very low therapeutic index (low safety margin) which has limited their use more recently compared to intravenous agents. They are still very effective often in combination with injectable agents.
What is the potency or MAC? Why is it clinically relevant?
The potency of volatile anesthetics is defined as the minimum alveolar concentration (MAC) or the concentration of anesthetic that will inhibit responses to noxious stimuli in 50% of patients. Specifically, the MAC
refers to the alveolar partial pressure of a volatile agent at one atmosphere that prevents skeletal muscle movement in response to a noxious stimulus (skin incision) in 50% of patients. Agents with high MAC are less potent than agents with a low MAC.
What are 2 general ways in which general anesthetics work?
General anesthetics work by different mechanisms. The volatile anesthetics hyperpolarize neurons reducing excitability. For example, several intravenous and inhalational agents enhance the actions of inhibitory neurotransmitters on GABAA (halogenated anesthetics, nitrous oxide, barbiturates, propofol, etomidate) and glycine receptors (halothane,propofol, barbiturates). Therefore, many anesthetics target ligand-gated ion channels, particularly the chloride channel regulated by GABA.
Many anesthetics also affect synaptic transmission. For example, halogenated anesthetics inhibit excitatory synapses and enhance the actions of inhibitory neurotransmitters (e.g. GABA described above). In contrast, ketamine inhibits the excitatory actions of glutamate on NMDA receptors. Likewise, nitrous oxide, cyclopropane and xenon inhibit NMDA currents. Some volatile agents inhibit K+ channels, too.
What are 4 factors that alter the rate of induction of a volatile anesthetic?
Alveolar partial pressure
Blood:gas coefficient
Cardiac output
Blood flow distribution
What is the alveolar partial pressure? Why is it important? What things will increase the input to the alveoli and thus speed up induction? What 3 things will affect the output from the alveoli from the blood?
The concentration of anesthetic in the alveoli is critical for induction and maintenance of anesthesia. This concentration determines the amount of anesthetic that is in the brain, the site of action. The alveolar partial pressure is the amount of drug in the alveoli and closely approximates the partial pressure in the CNS but is easier to monitor. The alveolar partial pressure reflects the amount of anesthetic that gets to the alveoli (input) in combination with the amount that is removed (output). The input is dependent on:
Inspired partial pressure
Alveolar ventilation rate
Anesthetic breathing circuit volume
Anesthetic induction occurs faster with a greater inspired partial pressure of the drug, increased ventilatory rate, smaller volume or lower solubility of the agent in the anesthetic breathing circuit. The opposite changes would reduce the rate of induction and the level of anesthesia.
The uptake (output) of anesthetic from the alveoli is dependent on:
Blood: gas coefficient
Cardiac output
Alveolar to venous partial pressure difference
What determines the blood: gas coefficient? What effect will greater solubility have on alveolar uptake and thus the alveolar partial pressure and thus the rate of induction? What about lower solubility?
The blood: gas coefficient is determined by the solubility of the anesthetic in the blood. Greater solubility in the blood will increase uptake from the alveoli slowing the increase in alveolar concentration and reducing the rate
of induction. Lower solubility would reduce uptake but increase the rate of alveolar partial pressure and increase the rate of induction of anesthesia.
What effect does cardiac output have on alveolar uptake?
Cardiac output determines pulmonary blood flow and, therefore, the rate of clearance from the alveoli. Higher cardiac output will more rapidly remove anesthetic from the alveoli resulting in a slower rise in alveolar partial pressure and a reduced rate of induction of anesthesia. In contrast, lower cardiac output (e.g. heart failure) would impede the uptake of anesthetic from the alveoli resulting in greater alveolar partial pressures and more rapid induction of anesthesia.
What is the venous to alveolar partial pressure and how does it affect alveolar uptake? How does it change during the course of anesthesia?
The alveolar to venous partial pressure difference is the partial pressure difference between the alveoli and the venous blood coming to the lungs through the pulmonary artery. This gradient determines the rate of uptake. For example, during the beginning of anesthetic induction, the gradient is large because there is no anesthetic in the blood. This gradient will remain great for some time because the tissues in the body will remove much of
the anesthetic before it returns to the lungs. As the anesthesia continues, the anesthetic levels equilibrate in the tissues and venous partial pressureincreases as less anesthetic is absorbed.
How does the distribution of cardiac output affect the rate of equilibration of anesthetics?
The distribution of cardiac output also affects the rate of equilibration of
anesthetics. Vessel rich tissues such as brain, kidneys, heart and liver,
represent only 10% of body mass, but receive 75% of cardiac output.
Therefore, these tissues are saturated by the anesthetic agent more rapidly
than other tissues. Skeletal muscle represents 50% of the body mass, but
typically receives only 10% of the cardiac output. These tissues are the
second group saturated by the volatile anesthetics. Fat tissue represents
approximately 20% of body mass but receives only 5% of cardiac output.
This, coupled with the high solubility of most agents in lipids, makes it
difficult to saturate these tissues. Finally, approximately 20% of tissues
are categorized as vessel-poor because they receive only 1% of cardiac
output. These tissues are virtually impossible to saturate at normal
anesthetic doses.
What is the rate of recovery from anesthesia determined by? Explain.
Recovery depends on the rate at which the alveolar concentration decreases. The more soluble the agent, the slower the recovery. The less soluble the agent, the faster the recovery. The rate of recovery is
determined by:
Tissue concentrations
Alveolar ventilation
Metabolic rate
Tissue concentrations are important because they act as a reservoir for the anesthetic agent. During recovery, the anesthetic can be removed but the tissues will slowly release anesthetic until all anesthetic has been expired
or metabolized. Alveolar ventilation determines how fast the anesthetic is returned to the alveoli so it can be expired in the air. The anesthetic that is not metabolized, will be lost by pulmonary expiration. Some volatile
anesthetics are metabolized in the liver. More soluble anesthetics are more dependent on metabolism since they remain in the tissues longer. Less soluble agents are more dependent on alveolar ventilation.
What are the 4 planes of stage 3 of anesthesia? What are 4 effects of general anesthesia?
n Plane 1 – ocular movement stops
n Plane 2 – lose response to incision
n Plane 3 – ideal surgical plane
n Plane 4 – respiration depressed
General Anesthesia
n Analgesia
n Amnesia
n Hypnosis
n Muscle atonia
What are 5 common side effects of volatile anesthetics?
n Respiratory depression
n Cardiovascular depression
n Hypothermia
n Nausea
n Increased intracranial pressure
What is the prototype halogenated anesthetic? What is its potency and solubility? What is its MAC? What are its side effects? Does it irritate the bronchi? How commonly is it used?
Halothane
n Highly potent and soluble, slow induction
n MAC =0.75%
n Side effects
n Suppresses respiratory drive
n CV depression (↓SNA, ↓cardiac function)
n Cardiac sensitization (arrhythmias)
n Increase cerebral blood flow (↑ICP)
n Halothane hepatitis & malignant hyperthermia
n Little irritation to bronchi
n Rarely used except pediatric use
How do enflourane and isoflourane differ from Halothane in solubility and MAC? In use? Side effects? irritation to bronchi?
Less soluble than halothane, MAC 1.2% (Iso) 1.6% Enfl
n Muscle relaxant
n Significant ↓ systemic vascular resistance & ↑CBF
n All side effects less severe than halothane
n More irritating to bronchi
