1. Inhalation Anesthetics
Aden Bronstein, MD

2. MAC
• Decreased: Hypoxia, Hypotension,
Hypothermia, Anemia, Age, Acute etoh,
pregnancy, chronic amphetamines
• Unchanged: Thyroid function, gender,
Paco2 15-95, Beta blockers
• Increased: Hyperthermia, Hypernatremia,
acute amphetamines, Chronic etoh

3. Alveolar Partial pressure
• Alveolar partial pressure ~rate of
input/removal
• Rate of induction affected by:
– FiAA
– Alveolar ventilation
– Characteristics of anesthetic breathing circuit
– uptake

4. Uptake = (Λ)(Q)(PA-PV)
Barometric pressure
• Denver, Colorado

5. Uptake
• Uptake = (Λ)(Q)(PA-PV)
– Barometric pressure
Λ: B.G. partition coefficient
• Decreased solubility decreases uptake:
anemia,hypoalbuminemia,fever
– Uptake most dependent on Alveolar partial
pressure difference

6. Uptake = (Λ)(Q)(PA-PV)
Barometric pressure
• RL Shunt
– Accelerated rise of FA/FI
– Slows rate of induction b/c of dilution
– Uptake of highly soluble volatile anesthetics is
sufficient to partially negate the dilutional effect

7. Uptake = (Λ)(Q)(PA-PV)
Barometric pressure
• Dead space
– Profound impact on soluble anesthetic gases
– Small impact on insoluble agents

8. Uptake = (Λ)(Q)(PA-PV)
Barometric pressure
• LR shunt
– Faster increase in FA/FI due to higher partial
pressure of anesthetic gas in blood returning to
the lung
• Clinically insignificant

9. MAC B/G solubili Vapor press
Halothane 0.75 2.3 240
Enflurane 1.68 1.8 175
Isoflurane 1.15 1.4 238
Methoxyflu
rare
0.15 12 22
Ether 2.0 12 450
Nitrous 105 0.47 ----
Desflurane 5.70 0.42 665
Sevoflurane 2.0 0.60-0.65 200

10. Metabolis
m
Deflurinati
on
Methoxyflu
rane
40% Methoxyflu
rane
Halothane 20% Sevoflurane
Sevoflurane 3% Halothane
Enflurane 2% Enflurane
Isoflurane .2% Desflurane
Desflurane .02% N2O

11. Fluoride nephropathy
• Diabetes insipidus:
• Renal tubule damage
• Fluoride and lithium in appropriate
concentrations are capable of causing
nephrogenic diabetes insipidus

12. Hemodynamics
HR SVR CI
Halothane NONE NONE Dec
Sevoflurane Dec Dec Dec
Desflurane Inc Dec Dec (min)
Isoflurane Inc Dec None
N2O Inc (min) Inc Increased

13. Hemodynamics (cont)
• Mechanism of decrease BP
– 1. Decreased SVR—2-3x increase in skeletal
muscle blood flow
– 2. Myocardial Depression/decreased C.O.
– 3. Decrease sympathetic nervous system tone

14. Respiratory Affects
• Rapid/shallow
• Elevated PaCO2

15. Desflurane
• Low B/G partition coefficient (.42)rapid
induction of anesthetics
• Pungency, Airway irritation
• Airway irritiationcoughing, salivation, breath
holding, laryngospasm
• Abrupt increase in concentration increased
sympathetic dischargeHTN and tachycardia
– If increased slowly or prior narcotic---HTN and tachy
may not occur

16. Sevoflurane
• Biotransformationcompound A, fluoride renal
toxicity
• Compound A: Renal tubular necrosis
– Sevo is degraded in a temp-dependent fashion in both
sodalyme and baralyme
– Factors that lead to increased concentration of
Compound A:
• Fresh absorbent
• Baralyme>sodalyme
• Higher absorbent temperatures
• Higher concentrations of sevo in anesthetic system
• Closed circuit or LOW FLOW anesthesia
– Gas flows >2L/m prevent rebreathign

17. Nitrous Oxide
• Dose dependent myocardial depressant
• Sympathetic stimulation obscures myocadial
depressant effects
• Sympathetic stimulationIncrease in PVR, C.O.
HR, circulating catecholamines
• Contraindications: Air embolus, bowel
obstruction, COPD, CHF, PTX/pneumocephalus,
chest wall trauma, eye/ear surgery

18. Second gas effect
• Alveolar uptake of a second gas (ie N2O)
creates a subatmospheric intrapulmonary
pressureincreased tracheal inflow
• Alveolar uptake of a second gas (ie N2O)
increases Alveolar Concentration of 1st
gas
(concentrating affect)