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Advantages?
- Control of airway
- High FiO2 (fraction of inspired oxygen)
- Rapid changes in depth
- Rapid recovery - ventilation
- Compatible with renal or hepatic disease
- Cost effective
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3 Basic Steps
- 1. Breathed in
- 2. Absorbed - alveoli into blood
- 3. Absorbed - blood to brain
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Uptake and Distribution
Goal of Inhalant Anesthesia?
To acheive an adequate partial pressure in the brain to cause the desired level of CNS depression.
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Alveolar Partial Pressure
What are the components?
- What is added
- -Inspired Concentration
- -Alveolar Ventilation
- What is taken away
- -Solubility of anesthetic in blood
- -Cardiac output
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Alveolar Partial Pressure
Inspired Concentration?
- Directly proportional
- Higher % concentration - faster to desired partial pressure
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Alveolar Partial Pressure
What does it depend on? How is it set?
- Function of vaporizer setting and fresh gas flow into the circle system
- % concentration at induction is higher than at maintenance
- -The higher the inspired partial pressure, the more rapidly the alveolar partial pressure approaches the inspired partial pressure
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Alveolar Partial Pressure
Alveolar Ventilation - how does it affect it?
- Better ventilation = faster increase in alveolar %
- Depends on tidal volume and RR
- Rapid shallow breathing = slow rise of alveolar pressure (dead space rebreathing)
- Spontaneous vs. Mechanical (much more efficient)
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Alveolar Partial Pressure
Time Constant - what is it?
- Time required for flow through a container to equal the capacity of the container
- Lung = FRC/ValveolarAnesthetic circuit = circuit capacity/FGF
- (FRC = functional residual capcity, FGF = fresh gas flow)
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Alveolar Partial Pressure
Factors that offset the rise of PA?
- Anesthetic Solubility
- Cardiac Output
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Alveolar Partial Pressure
Anesthetic Solubility
- Capacity of blood to take up anesthetic
- High solubility = more drug moves into blood from alveoli
- Drug dissolved in blood = not available as a diffusible gas
- High Sol = more molecules required to saturate blood before PP can increase
- Speed of onset is closely related to anesthetics solubility
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Alveolar Partial Pressure
Blood:Gas Partition Coefficient
- Index of solubility of anesthetic agent in the blood
- Measured at equilibrium
- -PP are equal
- -Concentrations are not equal
- High number = high solubility
- Methoxyflurane>Halothane>Isoflurane>Sevoflurane
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Alveolar Partial Pressure
Cardiac Output
- Blood flow through lungs removes inhalant from alveoli, lowers PA, delays onset
- High CO = large distribution throughout body
- = less than 8% total to brain
- Low CO = Heart-Lung-Brain perfusion preserved
- = very high % of total CO goes to brain
- = large amount of anesthetic to brain
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Clinical Onset of Anesthesia
- Rapid in
- -sick/debilitated animals
- -CV compromise
- Slow in
- -stressed/excited animals
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Alveolar Partial Pressure
When does it increase/when does anesthesia occur faster?
- Good alveolar ventilation
- Low CO
- Low anesthetic solubility
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Adequate Plane of Anesthesia?
- PA high enough to guarantee sufficient PBrMAC = minimum alveolar concentration
- % at which 50% of animals will not move in response to surgical stimulus
- more than 1 MAC to guarantee surgical anesthesia in 100% of patients
- 1.2-1.3 x MAC required for most animals
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Alveolar Partial Pressure vs. Alveolar Concentration
- Gas phase - partial pressure = % conc x atmospheric pressure
- Use alveolar concentration in MAC determination for convenience
- -vaporizer setting delivers a percent concentration
- -do not need to know barometric pressure
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Relative MAC of anesthetics?
halothane<isoflurane<sevoflurane
comparison of potency (halothane has lower MAC and is more potent)
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Factors that Decrease MAC
- hypothermia
- pregnancy
- old age
- hypothyroidism
- hypoxemia (<40mmHg)
- hypercarbia (>95mmHg)
- concomitant anesthetic drugs (inj, inhal, sed, analgesics)
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Factors that INCREASE MAC
- hyperthermia
- hyperthyroidism
- hypernatremia
- CNS stimulants
- -increase catecholamines
- -ephedrine, amphetamines
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What does anesthetic recovery depend on?
- Movement of drug from brain back into blood
- Movement from blood to alveolus
- Removal from alveolus into breathing system and out scavenger
(same factors influence anesthetic uptake)
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Physiologic Effects of Inhalant Anesthetics
Which ones, margin of safety, what happens with OD?
- Isoflurane, Sevoflurane, Desflurane - potent!
- Low margin of safety (TI 2-4)
- OD
- -severe ventilatory depression
- -severe cardiovascular depression
- -severe CNS depression
- -Death
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CNS - Mechanism?
- unknown!
- collection of many end points that are site specific
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CNS Effects
EEG (Electro encephalogram) , etc
- EEG wave changes
- -awake: low amp, high freq
- -inhalation anesthesia: high amp, low freq
- -ISO, Sevo, Des 2 MAC or > = isoelectric pattern
- All agents depress seizure activity
- No analgesia
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What happens to cerebral blood vessels?
- VASODILATION
- increased CBF
- decreased CMR (metabolic rate)
- increased ICP
- hyperventilation (PaCO2 < 30mmHg) reduces CBF with iso, sevo, des
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Cardiovascular effects
Contractility
- Dose dependent
- Contractility
- -not myocardial depressants around MAC in health
- -may decrease contractility in pt w/heart dz
- -may decrease contractility at conc > 1xMAC
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Cardiovascular effects
Systemic Vascular Resistance
SV
HR
Arterial BP
- Dose dependent vasodilation (decreased resistance)
- Decreased SV
- Dose dependent increase in HR (suppressed w/opioids)
- usually remains CONSTANT
- Arterial BP decreases (less dramatic w/Des)
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CV Effects: Arrythmogenesis
- Sensitization of myocardium to catecholamine induced arrhythmias
- -stress/excitement can increase endogenous catecholamine levels
- Iso, Sevo, Des - least effect
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Factors Influencing CV Effects
- 1. Mode of Ventilation and PaCO2
- 2. Noxious Stimulation
- 3. Duration of Anesthesia
- 4. Concurrent drug administration
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CV Effects: Mode of Ventilation
- Spontaneous vs. Mechanical
- Mechanical or IPPV (Intermittent positive-pressure ventilation)
- -increased intrathoracic pressure
- -decreased venous return
- PaCO2 if increased
- -direct depressant on heart and peripheral vessels - dilation
- -indirect via SNS increasing arterial BP
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CV Effects: Noxious Stimulation
- Sympathetic stimulation
- Increase arterial BP
- Increase HR and CO
- Decreased or prevented by inhaled anesthetics
- 1.5 to 2 x MAC
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CV Effects: Duration of Anesthesia
- After several hours: CO and HR may increase
- Cause unknown - dose? body position?
- More important in research than clinically
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CV Effects: Concurrent Drug Administration
- Sedatives and Injectables
- -decreases anesthetic requirements (MAC)
- -decrease effects from inhalant
- -may accentuate CV depression
- Positive Inotropes or Vasopressors
- -do not affect anesthetic requirements
- -counteract unwanted CV depression
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Respiratory Effects
- Decrease minute ventilation (dose-dep) (Apneic index)
- Decrease sensitivity to PaCO2
- -depress resp. control center in medulla and peripheral chemoreceptors
- Severely depress hypoxic drive
- Depress hypoxic pulmonary vasocontstriction
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More Respiratory Effects
- Decreased lung volume (FRC)
- -atelectasis is common
- Bronchodilation
- -increased dead space ventilation
- Airway irritation d/t pungency
- -Des>Iso
- -prevents mask induction w/Des
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Hepatic Effects
- Depression of hepatic function and hepatocellular damage
- -mild and transient or permanent
- Reduce intrinsic hepatic clearance of drugs
- Reduced blood flow
- Iso, Sevo, Des - maintain adequate O2 supply so liver injury less likely
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Renal Effects
- Dose-Depending decrease
- -renal blood flow
- -glomerular filtration
- -urine output
- Primarily pre-renal corresponding to decreased BP
- Reversed after anesthesia
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Renal Effects - Sevoflurane
- Breakdown of Sevo causes increased serum fluoride concentration
- -potentially nephrotoxic
- -horses? no effect
- Sevo degradation in CO2 absorbents produces Compound A (nephrotoxic to rats)
- -no evidence in dogs, cats, horses
- -avoid low O2 flow rates w/prolonged anesthesia
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Biotransformation
- Varying degrees of metabolism in liver
- relative % metabolized by drug
- Des<Iso<Sevo
- Recovery mainly dependent on elimination through lung
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Skeletal Muscle Effects
- Malignant Hyperthermia
- -potentially life threatening genetic myopathy
- -swine and humans
- -other species too
- -any agent can cause this
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Skeletal Muscle Effects
Malignant Hyperthermia: Signs
- Rapid rise in body temp (treat quick, may cause death)
- Increased RR, dyspnea, apnea
- Tachycardia
- Metabolic acidosis
- Muscle rigidity
- Increase in end tidal CO2
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Skeletal Muscle Effects
Malignant Hyperthermia: Treatment
- Dantrolene IV (muscle relaxant, antipyretic)
- Stop inhalant anesthesia
- 100% O2
- Body cooling
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Summary: Highly Soluble Inhalant
- Slow rise in alveolar partial pressure
- Slow to reach MAC
- Slow to achieve adequate brain concentration
- Slow to overdose
- Slow to recover
- More metabolism of drug
- More hangover
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Summary: Low Solubility Inhalant
- Rapid rise in alveolar partial pressure
- Fast to reach MAC
- Fast to achieve adequate brain concentration
- Fast to overdose
- Fast to recover
- Less drug metabolism
- Less hangover
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Relative MAC of drugs
halothane<isoflurane<sevoflurane<desflurane
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