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Barry Inhaled Meds
Inhaled Meds, kays lecture on passing gas
| Question | Answer |
|---|---|
| General Anesthesia is characterized by: | altered state reversible loss of consciousness analgesia amnesia muscle relaxation |
| Three Phases of General Anesthesia | Induction Maintenance Emergence |
| Meyer-Overton Rule | Anesthetic potency correlates with lipid solubility. Implies when a specific hydrophobic region is occupied-anesthesia results. |
| Unitary Hypothesis | Proposes all inhalational anesthetics share a common mechanism of action at the molecular level |
| Critical Volume Hypothesis | anesthesia occurs when a “critical region” volume is sufficiently changed. Anesthesia binding to sites on cell mem cause an expansion of the bilayer |
| Membrane Hypothesis | membrane channels behavior is changed by anesthetic agents some channels slowed, some speed up, different channels with different effects, with different agents. |
| Receptor Theory | Enhancement of GABA receptor is thought to be a target in the CNS GABA-A & GABA receptors with a alpha-5-sub-unit. |
| Newer theories | Supraspinal effects on the brain: amnesia and hypnosis. Thalamus,midbrain, and reticular formation more depressed. Spinal cord level: suppression of nociceptive motor responses/immobilization of skeletal muscle |
| Stage I | Amnesia occurs with induction and LOC, no pain remembrance, lightest stage, patient still feels pain |
| Stage II | Delirium with period of excitement, muscle movement, irritability, and pupils dilated, disconjugate gaze, increased RR and HR, risk of laryngospasm |
| Stage III | Surgical plane (target depth), fixed gaze of eyes, constricted pupils and no response to pain |
| StageIV | Overdose, absent or shallow RR, hypotension, profound CV compromise |
| FGF | determined by the vaporizer and flowmeter settings |
| FI: inspired gas concentration | determined by FGF, breathing circuit volume, and circuit absorption |
| FA: alveolar gas concentration | determined by uptake, ventilation, the concentration effect and second gas effect |
| Fa: arterial gas concentration | affected by ventilation/perfusion mismatch |
| the more soluble the anesthetic agent is in the blood the ________ the patient becomes anesthetized | Slower |
| The more soluble the anesthetic agent is in the blood the ____ the drug goes into the body | More |
| Insoluble agents have a slower uptake by the blood so a _____ induction | Faster |
| If CO decreases what happens to the alveolar concentration | Decreased blood flow through the lungs, less anesthetic taken up by the blood therefore the alveolar concentration increases |
| If CO increases what happens to the FA | Increase in CO, more blood travels through the lungs, thereby removing more anesthetic from the gas phase, decrease alveolar concentration and slower FA increase |
| What determines PA-Pv/Partial Pressure difference in Alveolar gas and Venous blood | tissue solubilitytissue blood flowarterial blood/tissue partial pressure difference |
| How does ventilation affect FA/Alveolar Concentration | Decreased alveolar partial pressure by uptake can be countered by increasing ventilation |
| Brain uptake is _______ related to the alveolar ventilation: the greater the ventilation, the faster the uptake | Directly |
| What is it called when "increasing the inspired concentration can increase alveolar concentration" | Concentration Effect |
| Increasing the concentration will _____ the rate of equilibrium of the agent | Speed |
| Uptake _______ as tissues become saturated, plateaus in about an hour | Declines |
| Second Gas Effect | Uptake of large volumes of a first or primary gas(usually N2O) from alveoli increases the rate of increase in alveolar concentration of a second gas given at the same time |
| factors that are responsible for the concentration effect and also control the second gas effect | increasing ventilation and concentration |
| Ventilation/Perfusion Mismatch will | increase the aveolar-arterial difference |
| Factors Affecting Wake Up | Agent used Length of procedure Patient age, mental state, medical conditions, other medications(benzo’s, opiates, neuroleptics, intoxicants)Obesity |
| Metabolism/Elimination of gases | *Exhalation, increasing ventilation and FGFlow, anesthetic circuit volume decreased, Biotransformation: cytochrome P-450(CYP) |
| Respiratory effects of inhaled agents | Tidal Volume decreased,Respiratory rate increased,Minute ventilation decreased,Chemoreceptor response to CO2 is blunted. |
| More Respiratory effects of inhaled agents | All are great bronchodilators by direct action on smooth muscle.Good for bronchospasm. |
| CVS effects of inhaled agents | All cause cardiac depression, causes an increased rate of concentration rise, which can cause even more cardiac depression--Halo=Enfl>Des=Iso=Sevo Desflurane >Isoflurane can cause initial tachycardia, Halothane reduces HR, Sevo and Enf are neutral |
| More CVS effects of inhaled agents | All inhaled agents are smooth muscle relaxants. All cause vasodilation(decreased SVR) leading to hypotension except Nitrous Oxide Coronary Dilators--Iso>Sevo=Des Arrhythmias can be induced by the agents, Halothane the worst>enfl>iso>des |
| EEG changes due to inhaled agents | decreased Amplitude, increased Latency |
| ICP and cerebral blood flow changes | Increased Cerebral Blood flow, autoregulation of cerebral blood is impairedIncreased ICP due to increased blood flow and induced hypercapnea(prevented by hyperventilation) |
| Intraoperative Awareness risk factors | age, gender, substance abuse/use, underlying medical conditions, ALSO Paralytic use Type of surgery Poor Machine maintenance estimated at 0.15% |
| Renal risk factors induced by inhaled agents | renal function usually returns to normal after stopping anesthesia does dependent decreases in renal blood flow, GFR, Urine outputSevo potentially produces Compound A which is renal toxin but not really shown in humans |
| Liver problems associated with inhaled agents | Hepatic blood flow decreased, drug metabolism slowed, so agents are hepatotoxic Most agents cause a transient increase in LFT’s |
| MAC | alveolar concentration at one atmosphere of an inhalational agent at which 50% of patients do not move in response to skin incision or similar noxious stimuli |
| Why is the Alveolar concentration used as the measure of anesthetic concentration | because the partial pressure in the aveolus quickly equilibrates with that in the blood and brain because of the brains high blood flow |
| How is MAC related to potency? | MAC is INVERSELY related to POTENCY |
| What is ED95 | ED95= 1.3 MAC of any volatile anesthetic has been found to prevent movement in 95% of patients |
| What is MAC awake | MAC of volatile anesthetic at which a patient will open their eyes (0.3-0.4 MAC) |
| What is MAC BAR | concentration required to block autonomic reflexes to nociceptive stimuli (1.7-2.0 MAC) |
| Factors that increase MAC | Hyperthermia Drugs that increase CNS catecholamine levels (monoamine oxidase inhibitors, tricyclic antidepressants, acute cocaine use,Infants (6-12 months)Hypernatremiachronic ethanol abuse |
| Factors that decrease MAC | Hypothermia Preoperative medications and IV anesthetics Neonates and the elderlyPregnancyAlpha-2 blockers, calcium channel blockersacute alcohol ingestion |
| Factors that have no efect on MAC | Duration and GenderAnesthetic metabolism Thyroid gland dysfunctionHyper/HypokalemiaPaCO2 15-95 mm HgPaO2 above 38Blood pressure above 40 mm Hg |
| What is compound A | formed from the reaction between Sevo and soda lime, Compound A is a renal toxin, and large amounts are produced at low gas flow ratesRecommended FGF of 2 or more liters, little evidence of harm unless low flows or long exposure |
| Signs of MH | Increased ETco2, increased heart rate and temperature |
| primary pathophysiologic event in MH | The release of excessive calcium from the sarcoplasmic reticulum(SR) |
| What is MH | Fulminant HYPERMETABOLIC state of skeletal muscle induced by volatile anesthetics, succinylcholine, and, perhaps by stress and exercise |
| ISOFLURANE(Forane) | Advantages: cheap, very soluble-slow to leave pt, cardio-protective Disadvantages: Solubility-high residual at end of case, risk of awareness, may slow OR turnover, can’t be used for gas inductionBlood:Gas coefficient= 1.4MAC:1.2 |
| DESFLURANE(Suprane) | Insoluble, fast on and off, easy to use, faster turnover, low residual at end of case, patient more awake pungent smell, cost, SNS stimulation, can’t be used for induction, careful with irritable airways, asthma, smokers, requires special vaporizerBl |
| SEVOFLURANE(Ultane) | non-pungent smell, good for induction, less SNS activation, cardio-protective, can be used with N2O to decrease need of Sevo, quicker wakeupDisadvantages: cost, solubility, compound ABlood:Gas coefficient= .65MAC:2.0 |
| Nitrous Oxide (N2O) | Only inorganic gas in clinical usecolorless, pleasant smell, non-explosive, non-flammableusually used in combination with inhaled gas or with O2Blood:Gas coefficient= 0.47No respiratory irritation, good for inductionCheapLow solubility |
| Cardiac and respiratory effects of Nitrous | slight myocardial depression usually offset by the SNS(increased endogenous catecholamines)Increased RR, decreased TV, reduced ventilatory response to CO2 and hypoxiaNOT a triggering agent for MH |
| Disadvantage of Nitrous | Major drawback is the diffusion of N2O into closed air Avoid N2O use in bowel cases/obstruction, pnuemothorax/blebs, venous air emboli, middle ear surgery, some eye surgeries, |
| Toxicity of Nitrous | N2O activates methionine synthetase by oxidizing the cobalt in Vit B12 and can affect DNA, spontaneous abortions in women working in the OR/dental offices (Unproven) |
Created by:
jenbirne69
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