1. Nurcan Kızılcık Sancar YTUH Anesthesiology Dept.
VOLATILE ANESTHETICS
Nurcan Kızılcık Sancar
YTUH Anesthesiology Dept.

2. Anesthetics are divided into two classes:
Inhalation Anesthetics
Gasses or Vapors
Usually Halogenated
Intravenous Anesthetics
Injections
Anesthetics or induction of agents

3. Pathway for General Anesthetics

4. Rate of Entry into the Brain: Influence of Blood and Lipid Solubility

5. MAC (minimal alveolar concentration)
A measure of volatile potency
1 MAC is the concentration necessary to prevent movement in response to painful stimulus in 50% of the patients.

6. FACTORS THAT INFLUENCE MAC
Increased central neurotransmitter levels
(MOI, acute amphetamine intake, cocain, ephedrine, levodopa)
Hyperthermia
Chronic ethanol abuse
Hypernatremia
INCREASE the Volatile MAC VALUE

7. DECREASE the Volatile MAC Value
OLD age
Metabolic acidosis
Hypoxia
Induced hypotension
Decreased central neurotransmitter levels (α-methyldopa, reserpine)
α-2 agonists
Hypothermia
Hyponatremia
Lithium
Hypoosmolality
DECREASE the Volatile MAC Value

8. DECREASE the Volatile MAC
Pregnancy
Acute ethanol intake
Ketamine
Lidocaine
Opioids, agonist-antagonist analgesics
Barbiturates, Diazepam
Hydroxyzin
Verapamil
Anemia
DECREASE the Volatile MAC

9. MAC Agent [agent] 1 MAC Halothane 0.75 % Isoflurane 1.46 % Sevoflurane
1.80%
Desflurane
6.60 %
Nitrous Oxide
104%

10. General Actions of Inhaled Anesthetics
Respiration
Depressed respiratory depth, increased RR
Kidney
Decreased renal blood flow, GFR & urine output
Hepatic:
Decreased blood flow
Neuromuscular
High concentrations will relax skeletal muscle
Prolong the effect of non-depolarizing neuromuscular blockade

11. Cardiovascular System
Decreased arterial blood pressure.
Variable effects on heart rate & cardiac output
Central Nervous System
Increased cerebral blood flow, increased ICP & decreased cerebral metabolic rate (except N2O)

12. METABOLISM RATE OF THE VOLATILES
N2O
Halothane
Isoflurane
Desflurane
Sevoflurane
0.004%
15-20%
0.2%
<0.1% 5%
Least metabolized
most metabolized

13. Nitrous Oxide (inorganic anesthetic)
Prepared by Priestly in 1776
Anesthetic properties described by Davy in 1799
Colorless, odorless, tasteless

14. Nitrous Oxide Major difference is low potency MAC value is 105%
Weak anesthetic, powerful analgesic
Combination with other agents for surgical anesthesia is required
Low blood solubility (quick recovery)

15. Nitrous Oxide Systemic Effects
Minimal effects on heart rate and blood pressure
May lead to myocardial depression in susceptible patients
Little effect on respiration

16. Nitrous Oxide Side Effects
Generally combined with other volatile anesthetics or opioids
It tends to diffuse into air containing cavities and air buubles in the blood rapidly
For example: If a patient with a 100 ml pneumothorax inhales 50% N2O, the gas content of the pneumothorax expands until it contains 100 mL of air and 100 ml of N2O.
N2O diffused into the middle ear can lead to hearing loss postoperatively.

17. Beginning of the case: Second gas effect
When two volatile agents are delivered to the patient simultaneously (N2O & a potent volatile) the uptake, therefore, the alveolar concentration of the volatile anesthetic will be increased due to the high N2O uptake.

18. At the end of the case: diffusion hypoxia

19. DIFFUSION HYPOXIA
Observed within first 5-10 mins of recovery, when large volumes of N2O is released into the lungs.
The blood gas solubility of N2O is very low. It is even more soluble than Nitrogen in blood.
At the end of the anesthesia, N2O diffuses back into alveoli from blood down to a concentration gradient and this is even more rapid than the uptake of Nitrogen.
Result of the rapid diffuse of pure N2O into the alveoli is hypoxia.

20. Nitrous Oxide Side Effects
Inhibits methionine synthetase (precursor to DNA synthesis) & vitamin B12 metabolism
Dentists, OR personnel, abusers are at risk

21. Halothane Synthesized in 1956 by Suckling Halogen substituted ethane
Volatile liquid easily vaporized, stable, and nonflammable

22. Halothane Most potent inhalational anesthetic MAC of 0.75%
Efficacious in depressing consciousness
Very soluble in blood and adipose tissue

23. Halothane Systemic Effects
Inhibits sympathetic response to painful stimuli
Sensitizes myocardium to exogenous catecholamines-- ventricular arrhythmias
Depresses myocardium-- lowers BP and slows conduction, mild peripheral vasodilation
Decreases respiratory drive-- central response to CO2 and peripheral to O2
Respirations- shallow-- atelectasis
Depresses protective airway reflexes

24. Halothane Side Effects
“Halothane Hepatitis” -- 1/10,000 cases
fever, jaundice, hepatic necrosis, death
metabolic breakdown products are hapten-protein conjugates
immunologically mediated assault
exposure dependent
Malignant Hyperthermia- 1/60,000 with succinylcholine to 1/260,000.

25. Enflurane Developed in 1963 by Terrell, released for use in 1972
Stable, nonflammable liquid
Pungent odor
MAC 1.68%

26. Enflurane Systemic Effects
Sensitizes myocardium to effects of exogenous catecholamines– arrhythmias
Metabolism 1/10 that of halothane-- does not release hepatotoxic metabolites
Metabolism releases fluoride ion-- renal toxicity
Epileptiform EEG patterns

27. Isoflurane İsoflurane is a halogenated methyl ethyl ether Cheap
Very soluble – slow emergence
Cardio-protective
Risk of awareness
It is not suitable for volatile anesthesia induction

28. Coronary vasodilation is a characteristic of isoflurane and in patients with coronary artery disease there has been concerns about the coronary steal ? –experimental-

29. Desflurane Insoluble Fast on-off Easy to use Loss of potency
Faster turnover of OR & PACU
Low residual at end of case
High cost
CNS stimulation (minor)
Pollution of environment (minor)
Can’t be used for gas induction
CO production (not relevant)

30. Sevoflurane It is suitable for volatile anesthesia induction
Potent bronchodilator
Less CNS activation
Cardio-protective
High-cost
Solubility
Compound A

31. Toxicity - Hepatitis
First described with Halothane use.

32. complications of surgery. The estimated rate is: 1: 1 000 000
Hepatitis and Pancreatitis are known
complications of surgery. The estimated rate is: 1:

33. Fluoride Nephrotoxicty
F- is a nephrotoxic byproduct of metabolism in liver and kidney
Fluoride nephrotoxicity
F- opposes ADH leading to polyuria
methoxyflurane 2.5 MAC-hours (no longer used)
enflurane 9.6 MAC-hours

34. Potency of renal injury
Methoxy > enflur > sevoflur > isoflur >desflur
Lead to potentially permanent renal injury

35. Toxins – Sevoflurane and Compound A
Sevoflurane reacts with CO2 absorbant of the anesthetic circuit “soda lime” to form “compound A”
fluoromethyl-2-2-difluoro-1-(trifluoromethyl) vinyl ether
There are some reports of fire & explosions
Compound A is renal toxin
Large amounts are produced at low gas flow rates
≥2 L/min flow rate is recommended
Little evidence of harm
unless
Low flows
Long exposure

36. Anesthetics and CO
All anesthetic agents react with sodalime to produce CO
CO is toxic and binds to Hgb in preference to oxygen
Desflurane > enfl >>> iso > sevo >halothane
Risk Factors
Dryness & Temperature of soda lime
Barylime produces more CO than soda lime & withdrawn from the market
In general, it is not clinically significant
No deaths are reported