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Pharm of Inhalates
Pharm of Inhatation Agents
| Question | Answer |
|---|---|
| What is the partial pressure of a gas? | The force exerted by the gas on the liquid it is dissolved in. |
| Partial Pressure of gas | A force that attempts to drive molecules out of a solution and into the gas phase. |
| PA | Alveolar Partial Pressure |
| Pb | Brain Partial Pressure |
| Pa | Arterial Blood |
| Why is the PA used as an index of the depth of anesthesia? | It is an indirect measure of Pb, therefore is used to index depth of anesthesia |
| Is a factor that will effect the partial pressure gradients necessary for anesthesia? | Transfer of inhaled anesthetic from machine to alveoli (anesthetic input) |
| Is a factor that will effect the partial pressure gradients necessary for anesthesia? | Transfer of inhaled anesthetic from alveoli to arterial blood |
| Is a factor that will effect the partial pressure gradients necessary for anesthesia? | Transfer of inhaled anesthetic from arterial blood to brain (anesthetic loss) |
| What factor will effect alveolar partial? | Input into the alveoli minus the loss into the arterial blood. |
| Input factor | Inspired partial pressure |
| Input factor | Alveoli ventilation |
| Input factor | Characteristics of breathing |
| Input factor | Functional residual capacity |
| loss factor | blood gas partition coefficient |
| loss factor | cardiac output |
| loss factor | alveolar to venous partial pressure difference |
| How does the inspired concentration of inhaled anesthetic effect the rate of increase of the alveolar concentration? | A high PI (Inhaled partial pressure) from the anesthetic machine is needed during initial administration to offset the impact of uptake. Time helps accelerate induction of anesthesia. |
| Second gas effect | ability of high volume uptake of one gas to accelerate the rate of increase on PA of a concurrently administered companion gas |
| Second gas effect | simultaneous adm. of slower agent (halothane) with a faster drug (nitrous oxide) in high concentrations can speed the onset of the slower agent. |
| How does the inspired concentration of inhaled anesthetic effect the rate of increase of the alveolar concentration? | A high PI (inhaled partial pressure) from the anesthesia machine is needed during initial adm. to offset the impact of uptake. This helps accelerate induction of anesthesia. |
| How does alveolar ventilation effect the rate of the increase in PA? | Increased ventilation promotes input of inhaled anesthetic to offset uptake into blood. |
| Increased ventilation | net effect is more rapid rate of increase in the PA and thus an increase in induction |
| Controlled ventilation as hyperventilation and decreased venous return | accelerates rate of increase in PA by increased input (increased VA) and decreased uptake (decreased cardiac output) |
| Spontaneous ventilation of inhaled anesthesia | produces a dose dependent depressant effect on alveolar ventilation |
| Spontaneous ventilation | has a protective negative feedback mechanism that prevents excessive depth of anesthesia when ventilation is decreased |
| Spontaneous ventilation | when concentration of partial pressure in the brain decreases to a certain threshold then ventilation increases to deliver more anesthesia |
| Mechanical ventilation | the protective mechanism against development of an excessive depth of anesthesia is lost |
| Mechanical ventilation | it may be appropriate to decrease the PI of volatile anesthesia to maintain PA similar to spontaneous |
| Volume of Anesthetic Breathing System | acts as a buffer to slow the attainment of PA |
| Solubility of inhaled anesthetics in the rubber or plastics components of the Breathing System | initially slow the rate at which PA rises, and at conclusion of anesthesia may slow the rate at which PA decreases. |
| Gas inflow from anesthetic machine | helps to negate the buffering effect |
| Subsequent reuse of same breathing system | can lead to malignant hyperthermia |
| What is FRC? | Functional residual capacity |
| The greater the alveolar ventilation to FRC ratio | the more rapid is the rate of increase in PA |
| The greater the alveolar to FRC ratio | the quicker the induction |
| Arterial tension | is directly dependent on both the rate and depth of ventilation |
| An increase in ventilation | can increase arterial tension of anesthetics of moderate to high blood solubility (halothane) but only slightly increase that of one with low blood solubility (nitrous oxide) |
| What factors of pulmonary ventilation effect the rate of PA | hyperventilation or hypoventilation |
| hyperventilation by mechanical control | increases the speed of induction with inhaled anesthetics that would normally have a slow onset |
| depression of ventilation | may slow onset of anesthesia of SOME inhaled agents |
| increase in pulmonary blood flow | decreases the induction rate |
| in shock patients | decreased CO and increased ventilation may accelerate the induction process |
| slows induction rate | more soluble gases |
| low blood solubility | few molecules are needed to raise its partial pressure and the arterial tension rises quickly |
| Intermediate soluble | Isoflurane |
| Poorly Soluble | Nitrous Oxide |
| Poorly Soluble | Desflurane |
| Poorly Soluble | Sevoflurane |
| blood:gas PC Isoflurane | 1.46 |
| brain:blood PC Isoflurane | 1.6 |
| muscle:blood PC Isoflurane | 2.9 |
| fat:blood PC Isoflurane | 44.9 |
| oil:gas PC Isoflurane | 98 |
| blood:gas PC Nitrous Oxide | 0.46 |
| brain:blood PC Nitrous Oxide | 1.1 |
| muscle:blood PC Nitrous Oxide | 1.2 |
| fat:blood PC Nitrous Oxide | 2.3 |
| oil:gas PC Nitrous Oxide | 1.4 |
| blood:gas PC Desflurane | 0.42 |
| brain:blood PC Desflurane | 1.3 |
| muscle:blood PC Desflurane | 2 |
| fat:blood PC Desflurane | 27.2 |
| oil:gas PC Desflurane | 18.7 |
| blood:gas PC Sevoflurane | 0.69 |
| brain:blood PC Sevoflurane | 1.7 |
| muscle:blood PC Sevoflurane | 3.1 |
| fat:blood PC Sevoflurane | 47.5 |
| oil:gas PC Sevoflurane | 55 |
| oil gas PC | parallels anesthetic requirements |
| MAC | 150/oil:gas PC |
| 150 constant | average value of the oil:gas solubility and MAC for several inhaled anesthetics with widely divergent lipid solubilities |
| high cardiac output | results in rapid uptake which slows PA |
| low cardiac output | speeds up PA since there is less uptake into the blood |
| Alveolar to venous partial pressure differences | tissue uptake of the inhaled anesthetics |
| highly perfused tissue | brain, heart, kidneys |
| equilibrate rapidly with PA | vessel rich group (high perfused) |
| poorly perfused tissues | skeletal muscle |
| how inhalant agents are eliminated | once inhalant agents of gas ceases the alveoli-blood-brain gradients are reversed and the pulmonary epithelium becomes the channel of elimination |
| drug characteristic has greatest effect on elimination | lower the solubility the faster the rate of elimination |
| drug characteristic that effects elimination | higher the solubility, the higher the extent of accumulation over the same exposure of time |
| how inhalant agents are metabolized | liver metabolism is significant for halothane (15%) but only 2-5% for enflurane and 0.2% for isoflurane |
| MAC | that concentration at 1 atmosphere pressure which causes immobility in 50% of patients when exposed to a noxious stimuli |
| 1.3 MAC | effective in 99% of patients |
| MAC bar | the dose that blocks adrenergic and cardiovascular response in 50% of individuals |
| increases MAC | hyperthermia |
| increases MAC | chronic alcohol use |
| increases MAC | drug induced increases in CNS catecholamine levels (MAOI, cocaine, ephedrine, levodopa) |
| increases MAC | hypernatremia |
| increases MAC | hyperthyroid |
| decreases MAC | hypothermia |
| decreases MAC | increasing age |
| decreases MAC | pre-op meds |
| decreases MAC | drug induced decreases in CNS cathecolamine levels |
| decreases MAC | alpha 2 agonist |
| decreases MAC | acute alcohol ingestion |
| decreases MAC | post-partum (returns to normal in 24-72 hrs) |
| decreases MAC | pregnancy |
| decreases MAC | lithium |
| decreases MAC | neuraxial opioids |
| decreases MAC | lidocaine |
| decreases MAC | hypoxia |
| decreases MAC | blood pressure < 40mmHG |
| decreases MAC | cardiopulmonary bypass |
| decreases MAC | hyponatremia |
| decreases MAC | anemia |
| decreases MAC | metabolic acidosis |
| decreases MAC | opioids |
| decreases MAC | opiod agonist-antagonist |
| decreases MAC | diazepam |
| decreases MAC | methyldopa |
| decrease MAC | reserpine |
| decreases MAC | chronic dextroamphetamine |
| decreases MAC | alpha-2 agonist |
| decreases MAC | lithium |
| decreases MAC | ketamine |
| decreases MAC | pancuronium |
| decreases MAC | physostigmine (10x clinical dose) |
| decreases MAC | lidocaine |
| decreases MAC | chlorpromazine |
| decreases MAC | verapamil |
| decreases MAC | hydroxyzine |
| decreases MAC | ^9 tetrahydrocanabinol |
| Isoflurane vapor pressure | 240 |
| Desflurane vapor pressure | 681 |
| Sevoflurane | 160 |
| Isoflurane MAC | 1.2 |
| Desflurane MAC | 6 |
| Sevoflurane MAC | 2 |
| highly perfused tissues | equilibrate rapidly with the Pa. |
| after 3 time constants | 95% of the returning venous blood is at the same partial pressure as the Pa |
| uptake of gas is decrease | after 3 time constants |
| continued uptake of gases after saturation of vessel rich groups | leads to anesthesia of the skeletal and fat tissues |
| sustained tissue uptake of the anesthestic into the large tissue mass (skeletal/fat) | causes the returning venous blood to be at a lower partial pressure than the Pa |
| when the returning venous blood is at a lower partial pressure than the Pa | the (alveolar to venous) Av-D difference is maintained and the uptake from the lungs continues for several hours. |
Created by:
albaker32
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