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50 Cards in this Set
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44. What are transmembrane signaling systems? What is their net effect?
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44. Transmembrane signaling systems describe the way in which receptors exert their effect after interacting with, or being activated by, a drug. The portion of the receptor that lies outside the cell membrane interacts with the drug, whereas the portion of the receptor that faces the inside of the cell exerts the cellular effect after activation. The collective end result of receptor activation most often is a change in transmembrane voltage and neuronal excitability. Receptors are therefore transmembrane signaling systems. (23; 38-39)
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53. What does the pharmacokinetics of inhaled anesthetics describe?
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53. Pharmacokinetics is the study of the absorption, distribution, metabolism, and elimination of inhaled or injected drugs and their metabolites. The pharmacokinetics of inhaled anesthetics describes their absorption from the alveoli, distribution in the body, and metabolism via the liver or elimination via the lungs. (25; 1S)
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54. How does the inspired partial pressure (PI) of an inhaled anesthetic influence the onset of anesthesia?
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54. The onset of anesthesia is dependent on achieving an appropriate partial pressure of anesthetic in the brain. The achievement of this relies on the concentration gradient of anesthetic from the anestl'oesia machine to the brain. By controlling the inspired partial pressure (PI) of an ifu_aled anesthetic the clinician is able to manipulate that concentration gradient. An increased PI will result in a greater concentration gradient, and a quicker achievement of the optimal patial pressure of anesthetic in the brain. This ultimately results in a more rapid onset of anesthesia. (25; 74, 77-78)
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55. How do the tissues of the body equilibrate with the inspired partial pressure (PI) of an inhaled anesthetic?
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55. The tissues of the body equilibrate with the inspired partial pressure of an inhaled anesthetic through the blood. The blood is responsible for the distribution of inhaled anesthetic to the various tissues of thf body. The partial pressure of anesthetic in theuterial blood, or Pa, is thm an intermediary between the partial pressure of anesthetic in the alveoli (PA) and the partial pressure of anesthetic in the brain (Pbr), this is reflected in the equilibrium equation PA-'='Pa-'='Pbr. (~5-26; 7~78)
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56. What is a clinical use of the alveolar partial pressure of an anesthetic?
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56. The alveolar partial pressure (PA) of an anesthetic is used clinically as a .on of the partial pressure of anesthetic in the brain (Pbr). The PA of an anesthetic is therefore a useful clinical indicator of anesthetic depth. Maintaining a constant and optimal PA allows the anesthesiologist to achieve e same with the Pbr. It is also useful in monitoring the induction and recovery of anesthesia when administering an inhaled anesthetic. Another clinical use of the PA of an anesthetic is that it provides a means by which inhaled anesthetics can be compared at equal potencies. (26)
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57, What are some factors that act simultaneously to determine the alveolar partial pressure of an anesthetic?
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57. In general terms the partial pressure of an anesthetic in the alveoli is a function of its input into the alveoli minus its uptake into the arterial blood. There are three things that influence the input of an aresthetic. These include the inspired partial pressure of the anesthetic, alveolar ventilation, and the characteristics of the anesthetic breathing system. There are also three things - characteristics of the anesthetic breathing system. There are also three things These include the blood:gas partitio[ coefficient of the anesthetic gas, the .illC:>\: llluuae me Olooa:gas partItIOn ccefficient of the anesthetic gas, the Together, these six factors determine the partial pressure of an anesthetic in the alveoli
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58. What are some factors that act simultaneously to determine the partial pressure of an anesthetic in the brain?
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;8. The partial pressure of an anesthetic in the brain is determined by its blood partition coefficient cerebral blood flow, and the arterial-tovenous partial pressure difference. (26; 75-76)
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59. How much does the metabolism and percutaneous loss of inhaled anesthetics influence the alveolar partial pressure of an anesthetic during the induction and maintenance of anesthesia?
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59. The metabolism and percutaneous loss of inhaled anesthetics do not significantly influence the alveolar partial pressure of an anesthetic during the induction and maintenance of anesthesia. (26; 79)
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60. What is the concentration effect? Clinically, with which inhaled anesthetic agent is the concentration effect solely possible? Why?
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60. With the administration of a given concentration of inhaled anesthetic, a certain amount of the anesthetic will be taken up by the blood. By administering a high inspired partial pressure (PI) of anesthetic initially, the impact of the uptake of anestbetic into the blood will be offset. The result is an accelerated rate of the induction of anesthesia. The rate of induction is reflected by the rate of increase in the alveolar partial pressure of the inhaled anesthetic. This effect of the high PI of anesthetic on the rate of rise of the alveolar concentration of the anesthetic is known as the concentration effect. The concentration effect occurs for two reasons. One is that the uptake of a large volume of anesthetic in:o the blood results in the remainder of the anesthetic gas being left in a smaller volume. The remainder of the gas is thus concentrated to a greater partial pressure than it otherwise would have been. The second reason why the concentration effect occurs is because of the augmentation of inspired ventilation. I\ugmentation of the inspired ventilation refers to the greater influence of the inspired gases when replacing larger volumes of lost gases in the alveoli. A high concentration of anesthetic must be given to produce the concentration effect. Oinically, this is only possible with nitrous oxide
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61. Why is the inspired partial pressure of an anesthetic often decreased after the induction of anesthesia?
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61. With the administration of a given concentration of inhaled anesthetic, a certain amount of the anesthetic will be taken up by the blood. The administration of a high inspired partial pressure (PI) of anesthetic initially offsets the impact of the uptake of anesthetic into the blood. The result is an accelerated rate of the induction of anesthesia. After the induction of anesthesia, the uptake of anesthetic into the blood will decrease. At this point the PI of anesthetic should be decreased from the high initial PI in order to maintain a constant and optimal partial pressure of anesthetic in the brain. If the PI of the anesthetic were maintained constant as the uptake of anesthetic into the blood decreased, the partial pressures of anesthetic in the alveoli and the brain would continue to increase. This could result in a greater than necessary, and even potentially totic, partial pressure of anesthetic in the brain.
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62. What is the seccnd gas effect? Does this depend on or occur independent of the concentraton effect? Give an example of the second gas effect
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62. When two gases exist in the alveoli, a large volume of uptake of the first gas from the alveoli results in an increase in the rate of rise of the partial pressure of the second gas in the alveoli. This is because the second gas remaining in the alveoli is concentrated in a smaller total volume of gas in the alveoli. The uptake of the second gas into the blood is then increased as well. This I is known as the second gas effect. The second gas effect occurs independent of the concentration effect. The classic example of the second gas effect is when the first and second gases are nitrous oxide and oxygen, respectively. The initial large volume of uptake of nitrous oxide into the blood accelerates the uptake of oxygen. (
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63. Is the second gas effect clinically significant?
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63. The second gas effect is not considered clinically significant.
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64. What is alveolar hyperoxygenation? By what percent does t'1e arterial partial pressure of oxygen increase during alveolar hyperoxygenation?
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64. Alveolar hyperoxygenatilln refers to the increase in the uptake of oxygen when oxygen is administered with nitrous oxide due to the second gas effect. The increased uptake of oxygen in the blood results in a transient increase in the arterial partial pressure of oxygen by about 10% during the early phase of nitrous oxide administration. Although this phenomenon may be seen clinically, it is not considered to be clinically significant
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65. How does increasing alveolar ventilation affect the rate of the induction of anesthesia with an inhaled anesthetic?
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65. An increase in alveolar ventilation helps to offset the impact of the uptake of alveolar ventilation is a more rapid rate of increase in the partial pressure of alveolar ventilation is a more rapid rate of increase in the partial pressure of an inhaled anesthetic in the alveoli and a more rapid rate of the induction of anesthesia. This is particularly true when the inhaled agent has a high · blood:gas partition coefficient or is highly soluble in blood. Under these conditions there is a greater degree of uptake of anesthetic in the blood, and the more beneficial is the increase in alveolar ventilation in offsetting this.
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66. How can controlled ventilation of the lungs affect the rate of increase of the alveolar partial pressure of an inhaled anesthetic during its initial administration?
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66. Controlled ventilation of the lungs can cause an increase in the rate of the increase in the alveolar partial pressure of an inhaled anesthetic and a corresponding increase in the rate of induction of anesthesia. This may occur for two reasons. First, controlled ventilation of the lungs may result in an increase in alveolar ventilation, thereby increasing the input of anesthesia. Second, controlled ventilation of the lungs may decrease venous return. A corresponding decrease in cardiac output also results in a decrease in the uptake of an inhaled anesthetic into the blood. The net result of these is a · more rapid rate of increase of alveolar partial pressure of the inhaled anesthetic.
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67. How can switching from spontaneous to controlled ventilation of the lungs during the administration of an inhaled anesthetic affect the anesthetic depth?
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67. Switching from spontaneous to controlled ventilation of the lungs during the initial administration of an inhaled anesthetic may result in an increase in the increase in alveolar ventilation and a decrease in cardiac output. Also of note ' increase in alveolar ventilation and a decrease in cardiac output
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68. Why might the brain be theoretically protected from a high inspired partial pressure of anesthetic ~ith the institution of controlled ventiRtion? Why is the heart not similarly protected on a theoretical basis?
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L With the institution of controlled ventilation of the lungs there may be corresponding alveolar hyperventilation, as reflected by a decrease in the arterial carbon dioxide partial pressure. This, in turn, results in a decrease in cerebral blood flow. Alveolar hyperventilation of the lungs increases the rate of increase of the alveolar partial pressure (PA) of the anesthetic with a potential increase in the delivery of anesthetic to the tissues. Because the brain relies on cerebral blood flow for the delivery of anesthetic, during hyperventilation the impact of the rate of increase of the PA of the anesthetic may be offset. Coronary blood flow is unlike cerebral blood flow in that coronary blood flow is not altered with hyperventilation. The myocardium is, therefore, not inherently protected from the possible increased input of anesthesia with the institution of controlled ventilation, and myocardial depression lay result.
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69. What are the three characteristics of the anesthetic breathing system that influence the rate of increase of the partial pressure of anesthetic in the alveoli?
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69. The three characteristics of the anesthetic breathing system that influence the rate of increase of the alveolar partial pressure of anesthetic are the volume of the system, the solubility of inhaled anesthetics in the components of the · system, and gas inflow from the anesthetic machine.
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70. How does an increased volume in the anesthetic breathing system affect the rate of increase of the alveolar partial pressure? How is this overcome?
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70. An increased volume in the anesthetic system slows the achievement of an optimal partial pressure of anesthetic in the brain by acting as a buffer. This can be overcome by using high gas inflows. (27; 85)
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71. How does the solubility of inhaled anesthetics in the components of the anesthetic 0n induction
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71. The solubility of inhaled anesthetics in the plastic or rubber components of the anesthetic breathing system leads to absorption of anesthetic into the components. This results in slowing in the rate of increase in the alveolar partial pressure (PA) of anesthetic on the induction of anesthesia, as well as slowing in th~ rate of decrease in the PA of anesthetic upon the termination of anesthesia. Trace concentrations of anesthetic still remain in the components of the anesthetic breathing circuit at the conclusion of anesthesia. (27;
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72. What does the partition coefficient define? What does a blood:gas partition coefficient of 10 mean? Does temperature influence a partition coefficient?
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72. The solubility of an inhaled anesthetic in blood and tissues is quantified as partition coefficients specific to the inhaled anesthetic. A partition coefficient describes how an inhaled agent will distribute itself between two phases when the partial pressures of the inhaled aneslhetic in each phase are equal. For example, a blood:gas partition coefficient of 10 means that at equilibrium the ratio of the concentrations of anesthetic in hlood:gas is lO:1. Therefore, the concentration of the anesthetic in the blood will be 10 times the concentration of the anesthetic in the gas. Partition coefficients are defined at a specific temperature, and are thus temperature dependent. Partition coefficients conventionally used in anesthesia have been defined at a temperature of 37°C. When temperatures are greater than this, the solubility of a gas in a liquid decrease
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73. What is the single most important determinant of the rate at which the alveolar concentration (FA) of an inhaled anesthetic Increases toward the constant inspired concentration (FI) of the anesthetic?
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73. The single most important determinant of how quickly the alveolar concentration (FA) of an anesthetic increases toward the constant inspired concentration (FI) of the anesthetic is the solubility of the inhaled anesthetic in blood. The solubility of the inhaled anesthetic in blood is defined by the anesthetic's blood:gas partition coefficient. Therefore, the rate of induction of anesthesia with an inhaled anesthetic is reflected by its blood:gas partition coefficient. The lower the blood:gas partition coefficient, the more quickly the FA of the anesthetic increases toward its FI, and the more rapidly the induction of anesthesia will be achieved.
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74. Why is the rate of increase of the alveolar partial pressure of an inhaled anesthetic, and therefore the rate of induction of anesthesia, influenced by the anesthetic's solubility in blood?
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74. The rate of increase of the alveolar partial pressure CPA) of an inhaled anesthetic is influenced by the solubility of the anesthetic in blood. This is based on the premise that a gas that is highly soluble in blood will have a higher concentration of the gas taken up by the blood than a gas that is less soluble in blood. Likewise, an inhaled anesthetic with a high blood:gas partition coefficient will have a greater amount of anesthetic dissolved in the blood before reaching equilibrium. The inhaled anesthetic dissolved in blood does not quickly move to the tissues. The blood can therefore be considered an inactive reserv(lir that takes up anesthetic but does not contribute to anesthesia. An anesthetic that is highly soluble in blood will have a slower rate of increase of its PA and a slower rate of induction of anesthesia, secondary to the greater amount of anesthetic that must dissolve in the blood before it can equilirate with the tissues. (27; 75-7:
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75. When an inhaled anesthetic has a low solubility in blood, is the rate of increase of the partial pressure of anesthetic in the alv:!oli rapid or slow?
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75. When the blood solubility of an inhaled anesthetic is low, minimal amounts of anesthetic will have to be dissolved in the blood before the anesthetic can equilibrate with the tissues. For this reason, the rate of increase of the partial pressures of the anesthetic in the alveoli and brain are rapid.
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76. How can the impact of a high blood:gas solubility on the rate of increase of alveolar partial pressure be offset clinically?
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6. An anesthetic that is highly soluble in blood will have a slower rate of increase of its alveolar partial pressure (PA) and a slower rate of induction of anesthesia, secondary to the greater amount of anesthetic that must dissolve in the blood before it can equilibrate with the tissues. The impact of an anesthetic's high solubility in blood and its subsequent relatively slower rate of increase of its PA can be offset clinically to some extent by increasing the inspired concentration of the anesthetic. Increasing the inspired concentration of anesthetic will increase the amount of anesthetic delivered to the alveoli per unit of time, more rapidly fill the inactive blood reservoir with the soluble anesthetic, and decrease the amount of time required for equilibration with the tissues
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77. What are the three factors that influence the uptake of anesthetic at the tissues from the blood? What does a tissue:blood partition coefficient describe?
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77. The three factors that influence the uptake of anesthetic at the tissues from the blood include the blood flow to the given tissue, the arterial-to-tissue cor..centration gradient, and the tissue:blood partition coefficient of the anesthetic. The solubility of an inhaled anesthetic in blood and tissues is quantified as partition coefficients specific to the inhaled anesthetic. The tissue:blood partition coefficient describes how an inhaled agent will distribute itself between tissues and the blood when the partial pressures of the inhaled anesthetic in each phase are equal. The value of tissue:blood partition coeffidents is that they are useful in predicting the time it will take for the anesthetic in the tissue to equilibrate with the anesthetic in the blood.
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78. How can the time necessary for the equilibration of an inhaled anesthetic between a given tissue and the blood be predicted?
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78. The time necessary for the equilibration of an inhaled anesthetic between a anesthetic in the given tissue. The time constant is defined as the capacity of anesthetic in the given tissue. The time constant is defined as the capacity of the system or tissue divided by the flow to the system. In the case of inhaled anesthetics and a specific tissue, the time constant is the amount of inhaled anesthetic that can be dissolved in a specific tissue divided by the blood flow to that tissue. Given this, tissues in which anesthetics do not dissolve well and tissues with a high volume of blood flow will have the shortest time constants and equilibrate most rapidly with the blood. For complete equilibration of anesthetic in the tissue and the blood, at least three time constants are I required.
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79. How does the time constant for isoflurane compare with the time constant for destlurane with respect to brain tissue?
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79. The approximate time constant for isoflurane with respect to the brain is 3 to · 4 minutes, whereas for desflurane it is about 2 minutes. Because cerebral lses is equal, the difference in the time constants for each of these agents is based solely on the difference in the solubility of the inhaled agents in the brain. The brain:blood partition coefficients are reflective of the solubility of these two agents. Three time constants, or the time required for almost complete equilibration of isofturane with the tissue, results in equilibration of the partial pressures of anesthetic between the blood and the brain in 10 to 15 minutes. Inhaled anesthetics that are less soluble in blood, such as desflurane and nitrous oxide, require less time for the arterial partial pressure to equilibrate with the partial pressure of anesthetic in the brain. For this reason, desflurane and nitrous oxide require about 6 minutes for almost complete equilibration of their partial pressures in the blood and the brain. (27)
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80. Why does nitrous oxide transfer into air-filled cavities with its administration?
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80. The transfer of nitrous oxide into air-filled cavities with its administration occurs as a result of the difference in solubility between nitrous oxide and nitrogen. The blood:gas partition coefficient of nitrous oxide is 0.46, and that of nitrogen is 0.014. Nitrous oxide is therefore 34 times more soluble in blood than nitrogen. Because nitrogen does not enter blood readily, nitrogen tends to remain in the air-filled cavity. Nitrous oxide is likely to enter the airfilled cavity until an equilibrium is established between the partial pressures of nitrous oxide in the air-filled cavity and the blood_ Because of this preferential transfer of nitrous oxide, and the subsequent net transfer of gas into the air-filled cavity total amount of gas in the air-filM cavity increases.
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81. How does the transfer of nitrous oxide into air-filled cavities affect the cavity? What are some of the potential risks that can occur as a result?
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81. The air-filled cavity that is undergoing the net transfer of nitrous oxide may be surrounded by a compliant wall or a noncompliant wall. If the wall is compliant, as the gas enters the cavity the volume of the air-filled cavity will increase. Examples of potential compliant-walled, air-filled cavities include the intestines, pulmonary blebs, or blood vessels. If the wall is noncompliant, as the gas in the cavity increases the pressure in the air-filled cavity will increase. Examples of potential noncompliant-walled, air-filled cavities include the middle ear, cerebral ventricles, and supratentorial subdural space. The potential risk of the transfer of nitrous oxide into an air-filled cavity is that there may be expansion of the volume or an increase in the pressure of the cavity that can result in harm to the patient. For example, a contraindication to the administration of nitrous oxide is a closed pneumothorax or when an air embolus is suspected. When bowel gas volume is increased preoperatively, as in a small bowel obstruction, nitrous oxide administration is best limited to an inspired concentration of 50%. By following this guideline, bowel gas vohune has been shown to double at most, even with prolonged operations.
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84. How does a patient's cardiac output influence the rate of induction of anesthesia.
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84. A patient's cardiac output influences the rate of induction of anesthesia by influencing how much anesthetic is carried away from the alveoli. For example, a high cardiac output will result ill more rapid uptake of anesthetic by the blood. This is because more blood is exposed to the alveoli per unit time, and thus more of the anesthetic will be taken up by the blood. Less inhaled anesthetic remains in the alveolus under these conditions. Therefore, the rate of increase of the alveolm- partial pressure (PA) of anesthetic and the rate of induction of anesthesia are both slowed in patients with a high cardiac output. On the other land, a low cardiac output, as in the shock state, results in less rapid uptake of anesthetic by the blo(d. This is because less blood is exposed to the alveoli per unit time, and thus less of the anesthetic will be taken up by the blood. More inhaled anesthetic remains in the alveolus under these conditions. Therefore, the rate of increase of the PA of anesthetic and the rate of induction of anesthesia are both rapid in patients with a low cardiac output.
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85. How do intracardiac shunts affect the rate of induction of anesthesia?
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85. The effects of shunts on the rate of induction of anesthesia are intuitively obvious. A right-to-left shunt, whether intracardiac or intrapulmonary, results in blood from the venous system returning to the left ventricle of the heart without passing ventilated alveoli. This blood is not exposed to the anesthetic present in the alveoli. The partial pressure of (i(\esthetic is decreased in the blood that will be relivered to the tissues because of the dilutional effect of the shunted blood, and the rate of induction of anesthesia is slo'hed in the results in blood that has passed ventilated alveoli returning to the venous circulation without delivering the anesthetic.
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86. How does wasted ventilation influence the rate of induction of anesthesia?
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86. Wasted ventilation is the ventilation of alveoli that are not perfused. Under these conditions the rate of induction of anesthesia is not affected provided difference between the alveolar partial pressure of anesthetic and the partial pressure of anesthetic in the arterial blood. This effect is similar to the observed difference between the end-tidal partial pressure of carbon dioxide :PC02) and partial pressure of arterial carbon dioxide (Paco2) seen in cases of wasted ventilation, such as in the case of a pulmonary embolus.
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89. How does the uptake of anesthetic in skeletal muscle and fat compare with the uptake of anesthetic in the vessel-rich organs? How does the uptake of anesthetic in skeletal muscle am fat influence the equilibration of the partial pressures of anesthetic between these tssues and the blood?
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89. Skeletal muscle and fat together comprise about 70% of body mass but only receive less than 25% of cardiac output. As a result, these tissues act as reservoirs that slowly take up anesthetic for several hours after the induction of anesthesia. Because of the relatively low blood flow to these organs, equilibration of these organs with the partial pressure of anesthetic in the arterial blood is much slower than the equilibration of the tissues comprising the vessel-rich group. In fact, equilibration of the partial pressure of anesthetic Ie blood with fat, which receives only 5% of the cardiac output, is probably not ever achieved. (29; 76)
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90. How might the recovery from anesthesia be defined?
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90. The recovery from anesthesia might be defined as the rate at which the alveolar partial pressure of anesthetic decreases with time. With the tennination of the delivery of anesthetic, the partial pressure of the tissues will decrease as the anesthetic moves along its concentration gradient from tissues to the alveolus. The alveolar concentration is a reflection of the anesthetic that remains in the tissues. Initially, the partial pressure of anesthetic in the alveolus falls rapidly, followed by a slower rate of decline.
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91. What are three common factors that influence both the rate of induction of anesthesia and the rate of recovery from anesthesia? What are three factors that influence the rate of recovery from anesthesia that are unique to this phase, and do lot influence the rate of induction of anesthesia?
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91. Three common factors that influence both the rate of induction of anesthesia and the rate of recovery from anesthesia include alveolar ventilation, the mlubility of the anesthetic in blood, and the c:u-diac output. Three factors that influence the rate of recovery from anesthesia that are unique to this phase of anesthesia include the absence of a concentration effect on recovery, variable tissue concentrations of anesthetics at the start of recovery, and the potential importane of metabolism on the rate of decrease in the alveolar partial pressure of anesthetic.
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92. How do tissue concentrations of inhaled anesthetics affect the alveolar partial pressure CPA) of anesthetic at the conclusion of anesthesia? What two factors will determine how much impact tissue concentrations will have on the rate of recovery of anesthesia?
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92. At the conclusion of anesthesia the variable tissue concentrations of anesthetic will serve as a source, or reservoir, that will maintain the alveolar partial pressure (PA) of anesthetic. The partial pressure gradient is reversed and anesthetic slowly comes off the tissues at varying rates, depending on the partial pressure of the anesthetic in the tissue. The PA of anesthetic during the recovery of anesthesia can never be zero. This is different than the induction of anesthesia, when all the tissues begin with a partial pressure of anesthetic of zero. The degree of impact that the partial pressures of anesthetic in tissues will have on the rate of recovery of anesthesia depends on the
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93. Which volatile anesthetics undergo a significant amount of metabolism?
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93. During the recovery phase of anesthesia metabolism may contribute to the removal of the volatile anesthetic from the tissues in addition to alveolar ventilation. The role of metabolism is only significant, however, with anesthetics that are highly lipid soluble. Of the volatile anesthetics in clinical use today, halothane alone undergoes a significant degree of metabolism such that the rate of decrease of the alveolar partial pressure (PA) of halothane at the conclusion of anesthesia is dependent on both metabolism and alveolar ventilation. For methoxyflurane, a highly lipid soluble volatile anesthetic that is not widely used clinically today, meubolism is a principal determinant in the rate of decrease of its PA. As opposed to methoxyflurane and halothane, ! less lipid-soluble anesthetics isofiurane, desfturane, and sevofiurane principally rely on alveolar ventilation for recovery from anesthesia.
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94. What is the clinical utility of the context-sensitive half-time in evaluating the time to recovery from an inhaled anesthetic?
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94. The context-sensitive half-time refers to the time required for the concentration of a particular drug to reach a specific percent after the discontinuation of its administration as a continuous intravenous infusion for a specific luration. For inhaled anesthetics the context-sensitive half-time depends on the anesthetic's blood:gas solubility and the duration of its administration. As with intravenous drugs, computer-simulated models of the context-sensitive half-time of an anesthetic may be useful clinically in anesthesia to predict the duration of a particular drug's effects after its discontinuation.
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95. What is diffusion hypoxia? When is diffusion hypoxia likely to occur? How can diffusion hypoxia be prevented?
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95. Diffusion hypoxia refers to the hypoxemia that may occur at the conclusion of a nitrous oxide anesthetic in a patient breathing room air. Diffusion oxide in blood is so low, nitrous oxide will move quickly from the tissues oxide in blood is so low, nitrous oxide will move quickly from the tissues to the alveoli down its concentration gradient when its administration is discontinued. Initially, the outpouring of nitrous oxide into the alveoli can displace the oxygen in the alveoli and dilute the alveolar partial pressure of oxygen (PAOz) so greatly that the arterial partial pressure of oxygen (Paoz) decreases. The second reason why diffusion hypoxia may occur is because the dilution of carbon dioxide in the alveoli that can occur by the same mechanism may decrease the patient's respiratory drive. Diffusion hypoxia " can be prevented by administering 100% oxygen to the patient at the conclu- 1 sion of a nitrous oxide anesthetic.
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96. What is the minimum alveolar concentration (MAC) of an anesthetic? How does the MAC of an anesthetic relate to the anesthetic's dose-response curve?
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96. A dose-response curve for an inhaled anesthetic is a graph of the alveolar concentration of an anesthetic and a phannacologic response. The MAC of sphere that prevents skeletal muscle movement in resnons.p tn " nnY;rm" sphere that prevents skeletal muscle movement in response to a noxious · such as surgical incision, in 50% of patients. The MAC of an inhaled anesthetic is one point on an inhaled anesthetic's dose-response curve for which the desired effect is no skeletal muscle movement on surgical incision. While a MAC of 1.0 prevents skeletal muscle movement in about 50% of patients undergoing surgery, the administration of approximately 1.3 MAC prevents skeletal muscle movement in nearly all patients undergoing surgery
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7. How has the determination of the minimum alveolar concentration of various inhaled anesthetics enabled comparisons between the various anesthetics? How is the therapeutic index of an inhaled anesthetic derived?
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97. The MAC of an anesthetic is a reflection of the partial pressure of anesthetic required in the brain for a specific effect. The MAC can then be used as an index for comparing anesthetics for their potency by comparing the partial pressure of each anesthetic required at MAC. In addition, since a given MAC reflects a specific potency, inhaled anesthetics can be compared with regard to their other effects (e.g., decreases in blood pressure) at equal potency. This can be done by calculating the therapeutic index of the anesthetic for a given effect. The therapeutic index for an inhaled anesthetic is the alveolar concentration producing a given effect divided by its MAC. Through this use of MAC, comparisons of the effect of inhaled anesthetics on vital organs I may facilitate the rational selection of a specific inhaled atesthetic for an individual patient.
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98. What inhaled anesthetic is often administered concomitantly with volatile anesthetic agents to increase the potency of anesthesia? How is the combined minimum alveolar concentration calculated when two or more inhaled anesthetics are being administered?
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98. Because the MAC of nitrous oxide is 105%, it cannot be used as a sole anesthetic agent while allowing a sufficient alveolar oxygen concentration. Because nitrous oxide has minimal depressant cardiovascular and ventilation effects, it is often administered in combination with a volatile anesthetic to increase the MAC without increasing the negative effects of the volatile anesthetic. The effective MAC that is achieved when two or more inhaled anesthetics are being administered to a patient is the added MAC of each individual inhaled mesthetic agent. For ex.ample, the administration of 0.6 AC of nitrous oxide and 0.5 MAC of isoflurane together produces an effect of 1.1 MAC
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99. Name some physiologic or pharmacologic factors that increase the minimum alveolar concentration for an individual patient.
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99. Physiologic or pharmacologic factors that increase the MAC for an individual patient include hype:thtrmia, infant age, hypernatremia, chronic ethanol abuse, and drugs that increase catecholamines in the central nervous system. Examples of drugs that increase central nervous system catecholamines inelude MAO inhibitors, cocaine, and amphetamines. c:
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100. Name some physiologic or pharmacologic factors that decrease the minimum alveolar concentration for an individual patient.
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100. Physiologic or pharmacologic factors that decrease the MAC for an individual patient include hypothermia, preoperative medication, intravenous anesthetics, neonatal age, elderly age, pregnancy, alpha-2 agonists, a.:ute ethanol ingestion, lithium, cardiopulmonary bypass, opioids, and an arterial partial pressure of ox:.ygen <38 nun Hg.
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101. How do the duration of anesthesia, gender, anesthetic metabolism, and thyroid gland dysfunction each iLfect the minimum alveolar concertration of anesthesia for an individual patient?
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101. The duration of anesthesia, gender, anesthetic metabolism, and thyroid gland dysfunction each have no effect on the minimum alveolar concentration of ani!sthesia for individual patients.
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102. What are some of the effects of inhaled anesthetics at the molecular level? Which of these is the mechanism by which inhaled anesthetics produce their depressant effects on the central nervous system?
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102. Some of the effects that anesthetics have at the molecular level include alterations in membrane properties, in the activity of neurQtransmitters, in receptor responsiveness, and in chemical- and voltage-gated ion channels and enzymes. It has been difficult to generate a 1beory for the mechanism of action of general anesthetics ilia: incorporates all these alterations. The precise mechanism by which inhaled anesthetics proiuce their depressant effects on the central nervous system is not known.
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103. Name some theories that have been proposed to explain the production of anestheSla by inhaled agents.
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103. Three theories that have been proposed to explain the production of anesthesia by inhaled agents include the Meyer-Overton theory (critical-volume hypothesis), the protein (receptor) hypothesis, and alterations in the availability of the neurotransmitter gamma-aminobutyric acid (GABA).
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105. Inhaled anesthetics may alter the availability of which neurotransmitter? How is this applied as a theory for the mechanism of action of inhaled anesthetics?
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lOS. The inhibition of the metabolic breakdown of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by inhaled anesthetics has led to speculation that anesthesia may result from enhanced inhibition of central nervous system activity by GABA.
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106. What is the Meyer-Overton theory? What is the evidence to support this theory? What is the basis for the opposition to tlle Meyer-Overton theory?
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106. The Meyer-Overton theory, or critical volume hypothesis, suggests that anesthesia occurs when a critical volume, or number, of anesthesia molecules dissolve in lipid cell membranes. The evidence for this theory is the close correlation between the lipid solubility of inhaled anesthetics and their MAC (potency). Lipid cell membrane expansion by a critical volume of 0.4% has been shown to result in anesthesia, lending further support to the MeyerOverton theory. Subsequent exposure of these membranes to high pressures (40 to 100 atmospheres) partially reverses the action of inhaled anesthetics,
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