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Lectures > Volatile anesthetics > Flashcards

Volatile anesthetics Flashcards

1
Q

Modern inhaled anesthetics

A

Volatile anesthetics

  • isoflurane
  • desflurane
  • sevoflurane
  • –> all have ether moiety
  • –> liquid at room temp
  • –> desflurane has unique vapor pressure, uses own vaporizer

N2O is a gas at room temp

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2
Q

Why use inhalend anesthetics?

A
  • Reliable effects
  • Hallmark of general anesthesia –> cause unconsciousness, amnesia, immobility
  • Level and effect of anesthesia can be safely monitored
  • Inexpensive
  • Ease of administration
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3
Q

Monitoring effects of anesthesia

A

Vital signs

  • EKG rhythm, heart rate
  • BP
  • O2 sat
  • with spontaneous respiration –> resp rate, tidal vol, pattern of respiration

Movement in response to surgery

Levels of exhaled gases –> O2, N2, CO2, N2O, volatile anesthetics

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4
Q

Goal of inhaled anesthetics

A
  • To produce the anesthetic state by establishing a specific concentration of anesthetic molecules in the CNS
  • Achieved by establishing the specific partial pressure of the agent in the lungs, which ultimately equilibrates with the brain
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5
Q

Mechanism of action

A
  • poorly understood
  • immobility –> acts on spinal cord
  • amnestic effects –> acts on brain (hippocampus, amygdala, cerebral cortex)
  • CNS depression
  • –> enhance inhibitory neurotransmitters (GABA + glycine)
  • –> block excitatory neurotransmitters (NMDA)
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6
Q

Definition

  • partial pressure
  • solubility
A

Partial pressure –> for any mixture of gases in a closed container, each gas exerts a pressure proportional to its fractional mass

Solubility –> used to describe tendency of a gas to equilibriate with a solution, hence determining its concentration in solution
- implications –> anesthetic gases administered via the lungs diffuse into blood until the partial pressures in alveoli and blood are equal

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7
Q

Minimum alveolar concentration (MAC)

A

Effects of inhaled anesthetics must be based on a dose –> this dose is the MAC

  • MAC is the alveolar concentration of an anestetic at one atmosphere that prevents movement in response to a surgical stimulus in 50% of patients
  • it is analogous to the ED50 expressed for IV drugs
  • MAC>0.5 = amnesia
  • MAC =1 = surgical anesthesia
  • MACs are additive
  • MAC declines 6% per decade of life –> highest at 6 months
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8
Q

Blood:gas partition coefficient or solubility
Blood brain partition coefficient
Blood:fat partition coefficient or solubility
oil-gas partition coefficient

A

Blood:gas partition coefficient or solubility –> solubility of a gas in blood

Blood brain partition coefficient –> mirrors blood-gas solubility

Blood:fat partition coefficient or solubility –> solubility of gas in tissue/fat

Oil-gas partition coefficient –> correlates lipid solubility with potency

  • potency is roughly equivalent to MAC
  • N2O <iso
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9
Q

MACs and solubilities

A

N20

  • MAC = 104
  • blood-gas partition coefficient = 0.46
  • oil-gas partition coefficient = 1.4
  • fat-blood solubility = 2.3

Isoflurane

  • MAC = 1.17
  • blood-gas partition coefficient = 1.46
  • oil-gas partition coefficient = 91
  • fat-blood solubility = 45

Sevoflurane

  • MAC = 1.8
  • blood-gas partition coefficient = 0.69
  • oil-gas partition coefficient = 147
  • fat-blood solubility = 48

Desflurane

  • MAC = 6.6
  • blood-gas partition coefficient = 0.42
  • oil-gas partition coefficient = 19
  • fat-blood solubility = 27
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10
Q

Factors that increase and decrease MAC

A

Factors that increase MAC

  • increased central neurotransmitter levels –> MAO inhibitors, cocaine, levodopa, ephedrine, acute detroamphetamine administration
  • chronic alcohol abuse
  • hyperthermia
  • hypernatremia

Factors that decrease MAC

  • increased age
  • metabolic acidosis
  • hypoxia
  • decreased CNS NT levels –> a-methyldopa, reserpine, chronic detroamphetamine administration, levodopa
  • hypothermia
  • hyponatremia
  • pregnancy
  • acute alcohol intoxication
  • drugs –> lithium, lidocaine, opioids, barbiturates, alpha 2 agonists, ketamine
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11
Q

Pharmacokinetics of inhaled anesthetics

A

At equilibrium = PA = Pa = Pbr

Based on concentration gradient

  • uptake from alveoli into systemic circulation
  • uptake from circulation into brain
  • redistribution of anesthetic throughout the body

Induction –> Pbr equilibrates with PA (and Pa) within 6-12 minutes
- highly perfused tissues equlibrate faster

The vascular system delivers blood to 3 physiologic tissue groups –> the vessel rich group, the muscle group and the fat group

  • VRG = brain, heart, kidney, liver, digestive tract and glandular tissues
  • anesthetic is delivered most rapidly to the VRG because of high blood flow –> here it diffuses according to partial pressure gradients
  • CNS tissue takes in the anesthetic according to the tissue solubility, and at a high enough tissue concentration, unconsciousness and anesthesia are achieved
  • increasing CNS tissue conc cause progressively deeper stages of anesthesia

PA mirrors the Pbr

  • index of anesthetic depth
  • reflection of rate of induction and recovery from anesthesia
  • measure of potency

Thus, monitoring MAC of inhaled anesthetics provides an index of their effects in the brain –> anesthesia machine measures level of inspired and exhaled anesthetic gas

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12
Q

Factors determining PA

A

Inspired anesthetic partial pressure (PI)

  • higher PI accelerates induction, offsets uptake into blood
  • as uptake into the blood decreases, PI can be decreased to maintain a constant Pbr

Alveolar ventilation

  • increased ventilation accelerates induction by more rapidly increasing PA
  • offsets uptake into blood

Cardiac output

  • influences uptake into the blood by controlling how much anesthetic is carried from the alveoli
  • low CO speeds induction
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13
Q

Uptake and distribution

A

Uptake - follows ratio of fractional concentration of alveolar anesthetic to inspired anesthetic (FA/FI) over time
- the faster FA rises relative to FI, the faster the speed of induction since FA is proportional to PA

Solubility = main factor controlling rate of induction and emergence
- N2O<iso

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14
Q

Recovery from anesthesia

A

Inhaled anesthetic turned off

  • PA = 0
  • Patient breathes 100% oxygen

Partial pressure gradient reversed
- stored anesthetic in tissues diffuses down its concentration gradient into the blood and is exhaled

Similar to induction

  • solubility of agent –> less soluble agents will allow faster emergence
  • depends on alveolar ventilation –> more ventilation allows faster emergence
  • depends on CO –> lower CO allows faster emergence

Different than induction

  • tissue concentration –> tissues serve as a reservoir of inhaled anesthetics
  • –> concentration depends on solubility and duration of anesthesia
  • –> can have variable concentrations in different tissue
  • metabolism –> minimal with modern anesthetics

Diffusion hypoxia

  • occurs with N2O administration
  • high initial outpouring of N2O from blood to alveoli can dilute and decrease PaO2
  • hypoxia if patient breathes room air and not given enough high concentrations of O2
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15
Q

Desirable properties of an inhaled anesthetic

A

Anesthesia machine and breathing circuit

  • lack of flammability
  • ease of vaporization at room temp
  • chemical stability

Lungs and breathing

  • rapid induction and emergence
  • lack of airway irritation
  • bronchodilation
  • lack of resp depression

Other requirements

  • maintenance of MAP + HR
  • low solubility in skeletal muscle and fat
  • potency
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16
Q

Effects of inhaled anesthetics on circulatory system

A

MAP - decrease in MAP due to decrease in systemic vascular resistance
- N2O little change in MAP and SVR

HR –> small increase, iso>des
- no effect with N2O and sevo

Desflurane - transient circulatory stimulation with abrupt increase >1 MAC –> increase in HR + MAP

Little effect on CO
Few cardiac arrhythmias
Sevo may prolong QT interval
N2O - increases pulm vascular resistance

Cardioprotection –> ischemic preconditioning

  • a preconditioning stimulus such as brief coronary occlusion and ischemia initiates a signaling cascade of intracellular events that reduces ischemia and reperfusion myocardial injury
  • ischemic preconditioning seen with volatile anesthetics in patients with compromised regional perfusion
17
Q

Effects of inhaled anesthetics on ventilation

A
  • increase RR and decrease tidal vol –> minute ventilation preserved (RRxTV)
  • decrease in FRC
  • increase in dead space
  • less efficient gas exchange with deeper anesthesia, PaCO2 increases
  • less responsive to CO2 at higher MAC –> apnea
  • inhalation induction –> best with seco and N20 (they are non-pungent)
  • bronchodilation
  • depression of pharyngeal and laryngeal reflexes

second gas effect of N2O

  • ability of high volume uptake of one gas, N2O, to accelerate rate of increase of PA of concurrently administered “companion gas”
  • “concentrating effect” - conc of second gas in smaller lung vol due to high vol uptake of the first gas
18
Q

Effects of inhaled anesthetics on CNS

A

All cause cerebral vasodilation

  • increased cerebral blood flow
  • increased intracranial pressure

Uncoupling of CBF and CMRO2 –> decrease in CMRO2

Dose dependent EEG depression

N2) –> some mild analgesic properties

19
Q

Other effects of inhaled anesthetics

A

Neuromuscular effects

  • dose related skeletal muscle relaxation
  • enhance activity of all paralytics

Decreased renal blood flow –> decreased GFR, decreased urine output

Decreased hepatic blood flow

20
Q

Adverse effects - Compound A formation

A

Sevoflurane undergoes degradation in CO2 absorbents to form a vinyl ether called compound A

  • production enhanced in low flow or closed circuit breathing systems, also warm or very dry CO2 absorbents
  • well-defined species differences in the threshold for compound A induced nephrotoxicity
21
Q

Adverse effects - CO and heat

A

Inhaled anesthetics degraded by CO2 absorbents to CO when normal water content of the absorbent (13-15%) is markedly decreased ( significant heat production, fires and patient injuries

22
Q

Adverse effects - hepatic

A

Postop liver dysfunction associated with volatile anesthetics, commonly halothane

2 mechanisms

  • more common form –> hepatocyte toxicity, relatively mild
  • with repeat exposure, probably immune reaction to metabolites –> severe liver damage and fulminant hepatic failure

Unlike halothane, current volatile anesthetics have minimal adverse effects on the liver and might afford some protection for hepatocytes from ischemic and/or hypoxic injury

23
Q

N2O toxicity

A

N2O decreases activity of vit B12 dependent enzymes = methionine synthetase and thymidylate synthetase
- Use > 24 hours –> megaloblastic anemia, pernicious anemia, neuropathy

Ability of N2O to expand air filled spaces –> most clinically relevant concern

  • due to its greater solubility in blood compared to nitrogen
  • N2O diffuses from blood into closed gas spaces (bowel, middle ear) easily
  • 75% N2O can expand a pneumothorax to double or triple its size in 10 and 30 min, respectively
24
Q

Malignant hyperthermia

A

Hypermetabolic reaction due to exposure to VA or succinylcholine

  • 1/15,000 children, 1/50,000 adults
  • 80% mortality without treatment, 5% with
  • can occur during or a few hours after surgery

Mechanism

  • autosomal dominant inheritance
  • aberrant RYR1 receptor in skeletal muscle voltage gated Ca channel in T tubule
  • uncontrolled CA release from SR
  • sustained contractility and rigidity
  • myocyte ischemia and cell death
  • very increased CO2 production, anaerobic metabolism, severe acidosis
  • hyperkalemia, myoglobinuria, renal failure
25
Q

Signs of malignant hyperthermia

A 
Exhaled CO2>55mmHg
Metabolic and respiratory acidosis 
    pH<7.25
Hyperthermia up to 43 °C
\+/- muscle rigidity
Hyper-/hypotension
Tachycardia, dysrhythmias
Renal failure
Disseminated intravascular coagulation (DIC)
Death:
Cardiac arrest, pulmonary/cerebral edema
26
Q

Treatment of malignant hyperthermia

A

Discontinue triggering agents
Dantrolene 2.5 mg/kg, followed by infusion
Hyperventilate pt with 100% O2
Cool pt
Treat hyperK+, dysrhythmias, metabolic acidosis
Maintain good UO
Call for help

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