Inhalational Agents Flashcards

1
Q

What are some terms for inhalational agents?

A

Anaesthetic gases, anaesthetic agents, volatiles.

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2
Q

What affects the uptake and distribution of volatile agents?

A

(1) DELIVERY of the agent to the lungs
(2) UPTAKE of the agent from the lungs to the bloodstream
(3) UPTAKE of the agent into other tissues (besides the brain

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3
Q

What governs the partial pressures of anaesthetic in all body tissues?

A

The alveolar partial pressure

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4
Q

What is the relationship between alveolar concentration of an agent and alveolar partial pressure?

A

Direct proportionality.
Factors decreasing alveolar concentration slow down induction of anaesthesia,
and vice versa

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5
Q

Relationship between ability to dissolve in blood and induction? Provide a reason.

A

Agent that dissolves easily=slow induction
Agent that is insoluble in blood=faster induction
If insoluble in blood–> fat soluble, like the brain tissue. Thus, agent is ready to bind to the fatty tissue in the brain.

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6
Q

Relationship between the cardiac output and rate of induction? Provide a reason.

A

Faster cardiac output= slower rate of induction.
Blood needs enough time to travel through the capillary/alveolar interface to pick up enough agent… if the cardiac output is higher, blood will not be as saturated with agent
SHUNTING (blood passing through alveoli that are not ventilated) will adversely affect induction

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7
Q

List the factors that leads to a faster induction of an agent

A
High inspired concentration of agent
Increased ventilation
Less soluble agent (in blood)
Decreased cardiac output
Decreased shunting
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8
Q

List the factors that leads to a slower induction of an agent

A
Lower inspired concentration of agent
Decreased ventilation
More soluble agent (in blood)
Increased cardiac output
Increased shunting
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9
Q

How does solubility affect recovery from anaesthesia?

A

Recovery is slow from soluble agents e.g. halothane.

Recovery is fast from poorly soluble agents eg desflurane and sevoflurane

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10
Q

Harmful metabolites from volatile agents

A

CF3 group causes “Halothane Hepatitis”
Fluorides from older agents like methoxyflurane and enflurane renal impairment
“Compound A” from Sevoflurane (renal impairment in rats

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11
Q

Explain potency of volatiles

A

Potency is the measure of a drug’s efficacy at a given dose
A more potent agent requires a lower dose to achieve the same effect; a less potent drug requires more
The concept of MAC is a measure of volatile potency

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12
Q

What does MAC stand for and how does it relate to potency of a volatile agent?

A

MAC (%): Minimum Alveolar Concentration (in %) required to prevent 50% of patients from moving in response to a standard surgical stimulus (incision) at sea level.
Hence a low MAC = more potent (e.g. Halothane = 0.75%) and a high MAC – less potent (e.g desflurane =6 %)

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13
Q

Which factors leads to a decrease in the MAC?

A
Sedatives 
N2O 
Analgesics 
Increased age 
hypotension 
hypothermia 
myxoedema 
Less effect: hypoxia, anaemia, pregnancy
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14
Q

Which factors leads to an increase in the MAC

A

Alcoholism
Increased in children
Hyperthermia
Thyrotoxicosis

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15
Q

What colour is nitrous oxide?

A

Blue

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16
Q

MAC of nitrous oxide

A

105%

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17
Q

Nitrous oxide- CNS effects

A

Potent analgesic
Poor anaesthetic
> 80% = hypoxic gas mix, always give max 70%
Second gas effect (need less [AA]) and speeds up induction

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18
Q

Nitrous oxide- CVS effects

A

Negative inotrope

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19
Q

Nitrous oxide- Resp effects

A

Augment depression of other agents

Diffusional hypoxia – after switch off NO2 from blood diffuse into alveoli and displace O2

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20
Q

Nitrous oxide- Muscle effects

A

no MH trigger

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21
Q

Nitrous oxide- additional info

A

Only ‘gas’ – stored as liquid.
Flow meter control

Diffuses into air filled cavities = rapid expansion (think pneumothorax and middle ear)

22
Q

Colour and MAC of sevoflurane

23
Q

sevoflurane- CNS Effects

A

Low sol = fast induction
Slight incr. CBF and ICP (Monroe Kelly doctrine)
Decr O2 consump

24
Q

sevoflurane- CVS Effects

A
Mild -ve inotrope
Slight BP drop
No HR compensate = CO not maint
Prolong qT 
No dysrhythm
25
sevoflurane- Resp Effects
Dose dependant depression
26
sevoflurane- Muscle Effects
Adequate relaxtion for intubation w children Rigidity on induction
27
sevoflurane Additional Information
``` Sweet smelling Best gas induction *ideal for cardiac pt Caution renal pt (compound A and floride) Possible emergence delirium ```
28
Colour and MAC of Isoflurane
Purple | 1.14-1.2%
29
Isoflurane- CNS effects
ICP stable Decr cerebral met rate/O2 consumption Decr CSF prod *ideal neurosurgery
30
Isoflurane- CVS Effects
Min depression Peripheral vasodilate = decr BP Pulse maintained
31
Isoflurane- Resp effects
Irritant to airway | Not suitable for induction
32
Isoflurane- Muscle effects
Relax. Potentiates NDMRs Relax uterus
33
Isoflurane- Liver toxicity
Low toxicity potential | Isolated enzyme elevations
34
Isoflurane- Additional Information
Halogenated ether Good eye op condition *ideal for liver pt
35
Colour and MAC of Halothane
Red | 0.75%
36
Halothane- CNS effects
Potent anaesthetic | Incr. CBF and ICP (min by hyperventilation)
37
Halothane- CVS Effects
Depressant Hypotension via vasodilate | Dysrhythmias – dose related
38
Halothane- Resp effects
Depressant (dose related) | Increase RR but decr tidal vol
39
Halothane- Muscle Effects
Some relaxation | Decr. uterine tone (risk C/S)
40
Halothane- Liver toxicity
Mild incr. in enzymes
41
Halothane- Additional Information
Decomposed by light Incr sol, slow induction Rare halothane hepatitis
42
Colour and MAC of Desflurane
Sky blue | 6%
43
Desflurane- CNS Effects
CNS stable | insoluble = rapid induction and emergence
44
Desflurane- CVS Effects
Min depression
45
Desflurane- Resp Effects
Irritant - Not suited for induction
46
Desflurane- Muscle Effects
Some relax
47
Desflurane- Liver toxicity
Toxic carbon monoxide - exposed to dry soda lime
48
Desflurane- Additional Information
Special vaporizer (BP close to room temp
49
Malignant hyperthermia and its triggers.
• Acute hypermetabolic state within muscle tissue during induction of GA (defect in muscle Ca receptor – calcium stays in cells) = increase in metabolic rate, CO2 and O2 consumption. Sympathetic activation (increase CO by incr HR and vasodilate) Triggers- All inhalational agents and suxamethonium
50
How to recognise malignant hyperthermia
Early: muscle rigidity b. High temp is a LATE sign c. Blood gas will show: metabolic/resp ACIDOSIS = +++ K/Ca/creatinine kinase d. Myoglobinuria and acute renal failure e. ECG changes: hyperkalaemia (peaked T wave, widened QRS, flat P) can lead to VF
51
Immediate Mx for malignant hyperthermia
a. STOP all triggering agents b. Call for HELP (get antidote = DANTROLENE) c. Change to clean breathing system and hyperventilate pt (elimination of AA) d. Maintain anaesthesia w IV agent e. Abandon/finish surgery ASAP
52
Mx and monitoring for malignant hyperthermia
a. Give dantrolene (2.5mg/kg bolus, repeat 1mg/kg as needed to max 10mg/kg) b. Initiate active cooling (antipyretics not useful) & avoid vasoconstriction c. Treat: hyperkalaemia (CaCl), arrhythmias (Mg/amiodarone, avoid Ca channel blockers), metabolic acidosis (hyperventilate), myoglobinaemia (forced alkaline diuresis), FIC (FFP, cryoprecipitate, platelets) d. Check plasma CK ASAP e. Admit ICU, monitor renal fxn, repeat CK, look at alt dx, counsel pt and fam (genetic factors)