Inhaled Anesthetic Agents Flashcards
Not exactly "top shelf", but we need to know it anyway...
What is the most important factor in ventilatory drive?
PCO2; VAA attenuate the vent. response to hypercarbia and hypoxia
What are the inhalation anesthetic agents we use?
N2O, isoflurane, sevoflurane, desflurane (halothane and enflurane are supposedly still commercially available, but rarely used)
Define MAC
Minimum Alveolar Concentration: concentration at 1 atm. in which 50% of subjects do not respond to painful stimulation (surgical incision)
Effects of nitrous oxide?
- may stim. sympathetic nerv. sys.2. direct depression of myocardial contractility (stimulation of catecholamines keeps bp, co, hr in check though)3- myocardial depr unmasked in CAD or hypovolemic pts4-constricts pulm vasc. smooth muscle5-PVR not significantly altered6-may see epi-induced dysrhythmias d/t catecholamine release
Effects of halothane?
1- Dose-dependent reduction of art BP is d/t direct myocardial depression (b/c of interference w/ intracellular calcium utilization)2- 2.0 MAC = 50% decrease of bld pressure and CO3- Though it is a coronary artery vasodilator, coronary bld flow decreases b/c of the drop in systemic arterial pressure4- Adequate myocardial perfusion is maintained b/c O2 demands also drop5- Blunts vagal stimulation leading to a increase in HR6- Prolongs the QT interval7- Sensitizes the heart to the dysrhythmogenic effects of epinephrine8- SVR is unchanged
Effects of enflurane?
1- Depresses myocardial contractility2- Art BP, CO, and myocardial O2 consumption are lowered3- Decreases SVR4- Sensitizes the heart to the dysrhythmic effects of epi; doses up to 4.5mcg/kg are usually well tolerated
Effects of isoflurane?
1- Causes minimal cardiac depression2- CO is maintained by a rise in HR d/t partial pressure preservation of carotid baroreflexes.3- Mild B-adrenergic stimulation increases skeletal muscle bld flow, decreases SVR, lower art BP4- Dilates coronary arteries, though not as potent as NTG or adenosine (May lead to coronary steal syndrome)5- Should avoid in pt’s with CAD
Effects of desflurane?
1- Similar to isoflurane2- Increased dose=decline in SVR=fall in art BP (esp. q/ rapid changes in dose)3- CO remains relatively unchanged or slightly depressed at 1-2 MAC4- Does not increase coronary artery bld flow
Effects of sevoflurane?
1- Mildly depresses myocardial contractility2- SVR and art BP decline slightly less than w/ iso or des3- Causes little if any rise in HR (but CO is not as well maintained as w/ iso or des)4- Not assoc w/ coronary steal syndrome5- May prolong the QT interval
Which agent(s) most associated with cardiac dysrhythmias?
Mostly halothane (although the rest of the agents, save for iso & des, have the potential to produce these effects)
Which ones be stank?
Des & Iso ( Sevo, Halo, and N2O are not)
What are some major effects inhaled anesthetic agents have on ventilation?
- Inhaled anesthetics increase freq of breathing and decr TV w/ incr. anesthetic concentrations- Minute ventilation is relatively preserved- Decr TV leads to greater proportion of dead space ventilation relative to alveolar ventilation- Gas exchange becomes progressively less efficient at deeper levels of anesthesia- PaCO2 incr proportionally w/ anesthetic concentration- All volatile anesthetics blunt the ventilatory stimulation evoked by arterial hypoxemia.
What do inhaled anesthetics do to CO and BP?
MAP decreases. (All VAAs besides halothane decrease SVR. Halothane directly decreases CO.)Nitrous oside either does nothing to the MAP or increases it slightly, just like the little bitch it is.
Any VAA lead to nephrotoxicity?
Sevo metabolites have exhibited some nephro problems in lab mice, but rarely significant in clinical practice. Just know it’s a theoretical possibility… (compound A)
Let’s talk about halothane-associated hepatic dysfunction… what it is?
Halothane is the most metabolized VAA, and the metabolites can (but rarely) lead to hepatic necrosis. Usually these people have recent frequent exposure to halothane, meds that enhance CYP450, middle aged, obese, female, and genetically predisposed to the condition.Most likely an antibody-mediated problem; preop admin of disulfiram inhibits oxidation of halothane and may provide prophylaxis.