Inhaled Agents Flashcards
Normobaric oxygen therapy causes
T/F
Alveolar changes after 6 hours when the FiO2 is 1.0
False. In the critically ill patient, oxygen related pulmonary damage may be seen as early as 12 hours. It may take up to 24 hours for similar changed to be seen in a normal subject.
Normobaric oxygen therapy causes
T/F
Alveolar changes after 48 hours when the FiO2 is 0.4
False. At a FiO2 of 0.4 oxygen related pulmonary damage is unlikely. This pathological process becomes a clinical problem once oxygen concentrations are above 50%.
Normobaric oxygen therapy causes
T/F
A reduction in functional residual capacity when the FiO2 is 1.0
True. When breathing oxygen at 100%, absorption atelectasis is a significant complication resulting in a reduction of both FRC and vital capacity.
Normobaric oxygen therapy causes
T/F
Absorption atelectasis at high concentrations
True. Absorption atelectasis occurs at high concentrations.
Normobaric oxygen therapy causes
T/F
Convulsions at high concentrations
False. Normobaric oxygen therapy does not typically cause convulsions. This is a complication of hyperbaric oxygen therpay (Bert effect).
Toxicity from hyperbaric oxygen therapy can cause: A. Painful joints B. Pulmonary oedema C. Acute tubular necrosis D. Convulsions E. Bradycardia
A. False. This may be a symptom of ‘the bends’, for which hyperbaric oxygen therapy is used to treat.
B. True. The ‘Smith effect’.
C. False. Hyperbaric oxygen therapy is not directly associated with renal dysfunction.
D. True. The ‘Bert effect’.
E. False.
Regarding Oxygen therapy:
T/F
The Bert effect describes the neurological complications caused by normobaric oxygen toxicity
False. The Bert effect describes convulsions secondary to hyperbaric oxygen therapy.
Regarding Oxygen therapy:
T/F
The Smith effect describes the pulmonary dysfunction caused by oxygen toxicity
True
Regarding Oxygen therapy:
T/F
Retrolental fibroplasia occurs in neonates up to 64 weeks post-conceptual age
False. The neonate is at risk of oxygen associated retrolental dysplasia up to 44 weeks post conceptual age.
Regarding Oxygen therapy:
T/F
It is not causative of neonatal bronchopulmonary dysplasia
False
Regarding Oxygen therapy:
T/F
Hyperoxia is beneficial post cardiac arrest
The agent is highly soluble in blood
False. Recent evidence suggests that hyperoxia post cardiac arrest is related to a worse outcome. This may be related to the negative effects of oxygen free radicals and reduced coronary blood flow. However, adequate oxygenation after cardiac arrest is obviously essential.
A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
False. A high blood partial pressure is reached more quickly if the agent is less soluble in blood with a low blood:gas coefficient.
A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
The patient has a low cardiac output
False. Although a high blood partial pressure is reached more quickly in patients with a low cardiac output, this effect is minimal with modern agents and outweighed by the quicker effect site transit time seen with higher cardiac output states
A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
The patient has a low FRC
True. A low FRC means that there is a lower volume that needs to be filled by inspired anaesthetic agent to produce a high alveolar fractional concentration.
A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
The agent has a low blood:gas solubility coefficient
True. Low agent solubility means that a high arterial and effect site partial pressure is achieved more rapidly, speeding the onset of anaesthesia.
A more rapid induction of anaesthesia will occur using inhalational agent if:
T/F
There is a carrier gas used in low volumes
False. Carrier gases are non-potent and must be used in high volumes.
Regarding the concentration effect:
T/F
It has a greater effect when low volumes of carrier gas are used
False. The concentration effect requires high volumes of carrier gas.
Regarding the concentration effect:
T/F
It is not responsible for the second gas effect
False. The opposite is true.
Regarding the concentration effect:
T/F
It has no effect upon alveolar ventilation
False. The concentration effect increases alveolar ventilation for each tidal breath. It is this process that is involved in ‘concentrating’ the ‘carried’ gases within the alveolus. This is known as ‘augmented ventilation’.
Regarding the concentration effect:
T/F
A potent agent is used to gain its benefits
False. A high volume of non-potent carrier gas is used. The low potency of a carrier gas allows it to be used at a high fractional inspired concentration.
Regarding the concentration effect:
T/F
May result in emergence hypoxia
True. This is one of the important complications of nitrous oxide and can be prevented by the use of oxygen post emergence.
Regarding GABA receptor
T/F
Its natural ligand is glutamate
False. It is GABA.
Regarding GABA receptor
T/F
It consists of 5 subunits, most commonly 2 alpha, 2 beta and 1 echo
False. It is 2 alpha: 2 beta: 1 gamma. There are around 18 different subunit types
Regarding GABA receptor
T/F
Its A subtype is metabotropic
False. It is ionotropic. GABA receptors are ligand-gated ion channels.
Regarding GABA receptor
T/F
It has over 30 isomers
True
Regarding GABA receptor
T/F
When opened it increases the conductance of calcium ions
False. Opening of the channel pore increases Cl conductance.
Regarding CNS receptors
T/F
N-Methyl-D-Aspartate receptors are inhibitory in action
False. They are stimulatory. Ketamine, xenon and nitrous oxide probably produce their anaesthetic actions by modulating the NMDA receptor.
Regarding CNS receptors
T/F
Benzodiazepines act via positive allosteric modulation
True. The binding of benzodiazepines to their GABA site increases the chance of ion pore opening.
Regarding CNS receptors
T/F
Ketamine binds competitively to NMDA receptors
False. Ketamine binds in a non-competitive manner.
Regarding CNS receptors
T/F
NMDA receptors are metabotropic
False. They are ionotropic. The binding of glutamate increases the conductance of cations such as Ca2+.
Regarding CNS receptors
T/F
Magnesium blocks the central pore of NMDA receptors
True. Mg2+ is an NMDA modulator. It binds to the open NMDA pore inhibiting current passage.
Regarding CNS receptors
T/F
Ionotropic receptors are ligand-gated ion channels
True
Regarding CNS receptors
T/F
Examples of metabotropic receptors include glutamate and GABAB
True. Glutamate is also the ligand for ionotropic receptors such as NMDA and AMPA.
Regarding CNS receptors
T/F
GABAA activation promotes Cl- conductance
True. GABAA is an ionotropic receptor. The binding of GABA promotes chloride conductance hyperpolarizing the postsynaptic membrane and inhibiting pathway transmission.
Regarding CNS receptors
T/F
Alcohol inhibits NMDA function
True. Alcohol mediates its effects of tolerance, dependence and withdrawal syndrome via its effects on NMDA receptor numbers and function.
Regarding CNS receptors
T/F
The glycine receptor is found in high concentration with the cerebral cortex
False. Glycine receptors are found in the brainstem and spinal cord, where they function as the analogue of GABAA. Inhalation agents may markedly potentiate the effect of glycine within the spinal cord.
Isoflurane:
Is a stereoisomer of enflurane
False. It is a structural isomer.
Isoflurane:
Causes vasodilatation without reflex tachycardia
False. A reflex tachycardia suggests that baroreceptor function remains intact with isoflurane use. The main cause of isoflurane induced hypotension is a reduction in systemic vascular resistance. Myocardial function and cardiac output see only a small decrease.
Isoflurane:
Has a saturated vapour pressure of 23.3 kPa at 20 degrees Celcius
False. This is the SVP of enflurane. The SVP of isoflurane is 32 kPa.
Isoflurane:
0.2% of isoflurane undergoes hepatic metabolism
True. Hepatic cytochrome P450 metabloizes the C - F bond. Renal toxicity is rare due to the low levels of fluoride ions produced.
Isoflurane:
The chloride group is attached to the chiral centre
True
Factors that increase Minimum Alveolar Concentration:
Alpha-2 agonists
False. These decrease MAC.
Factors that increase Minimum Alveolar Concentration:
Hypernatraemia
True
Factors that increase Minimum Alveolar Concentration:
Chronic alcohol intake
True
Factors that increase Minimum Alveolar Concentration:
Acute alcohol intake
False. Acute alcohol intake decreases MAC.
Factors that increase Minimum Alveolar Concentration:
The premature neonatal period
False. The MAC is low in preterm neonates. For most agents MAC value peaks at 1-6 months.
Sevoflurane:
Has a chiral centre
False. It is achiral
Sevoflurane:
Produces hydrofluoric acid if stored in glass
True. This is highly toxic. Lewis acids degrade the ether and halogen bonds if sevoflurane is stored in water at concentrations less than 100ppm. The highly toxic hydrofluoric acid corrodes glass, driving Lewis acid production.
Sevoflurane:
Has a blood:gas coefficient of 1.4
False. This is the blood:gas coefficient of isoflurane. 0.7 is the correct answer.
Sevoflurane:
Causes coronary steal syndrome
False. This is a side effect of isoflurane use.
Sevoflurane:
Is metabolised by cytochrome isoform CYP3A4
False. This cytochrome isoform is responsible for the metabolism of opiates and benzodiazepines. CYP2E1 is responsible for sevoflurane / isoflurane / halothane metabolism.
Minimum alveolar concentration:
Is above 6% for desflurane
True
Minimum alveolar concentration:
Is above normal atmospheric pressure for nitrous oxide
True
Minimum alveolar concentration:
May be as low as 0.7 for sevoflurane in 70% nitrous oxide
True
Minimum alveolar concentration:
Is 0.95 for Halothane
False. MAC of halothane is 0.75
Minimum alveolar concentration:
Is lower for enflurane than it is for isoflurane
False. Isoflurane 1.17, Enflurane 1.68
Halothane:
Is an halogenated ether
False. Halothane is a halogenated hydrocarbon. There is no ether ‘link’.
Halothane:
Has a SVP at 20 degrees celcius, similar to isoflurane
True. Halothane 32.3 kPa, Isoflurane 33.2 kPa.
Halothane:
May be given safely with adrenaline infiltration at doses of 100 micrograms per minute
False. This dose of adrenaline should be administered over a 10 minute period. Halothane sensitises the heart to catecholamines, which may lead to arrhythmias - particularly ventricular tachycardias and bradyarrhythmias.
Halothane:
Its C-Br bonds are metabolised with greater ease than its C-F bonds
True. C-F bonds are the most stable carbon-halogen bond.
Halothane:
Is metabolised under hypoxic conditions to produce trifluoroacetyl chloride which is implicated in halothane hepatitis
False. This metabolite is produced under oxidative conditions. In a hypoxic state reduced metabolites are produced e.g. inorganic fluoride.
Desflurane:
Has a boiling point of 39 degrees celcius
False. Its boiling point is 23.5 degrees celcius.
Desflurane:Is administered via the Tec 5 vaporiser
False. Is administered via the Tec 6. This heats the volatile to 39 degrees celcius under a pressure of 2 atmospheres.
Desflurane:
Induces tachycardia and hypertensions at MAC values greater than 1
True
Desflurane:
Produces carbon monoxide on contact with soda lime
True. Volatile agents that contain a -CHF2 molecule (isoflurane, enflurane, desflurane) may produce carbon monoxide upon reaction with dry soda lime.
Desflurane:
Has a blood gas coefficient higher than nitrous oxide
False. Blood gas coefficient of desflurane is 0.42; nitrous oxide 0.47
Nitrous Oxide
Has a critical pressure of 72 bar
True. In addition to this, the critical temperature is 36.5 degrees celcius.
Nitrous Oxide
Is stored in cylinders with a pin index configuration of 2 and 5
False. This is the pin index of oxygen. The configuration for nitrous oxide is 3 and 5.
Nitrous Oxide
Increases cerebral blood flow
True. It may also increase intracranial pressure.
Nitrous Oxide
Inhibits methionine synthetase by reducing the cobalt ion in vitamin B12
False. It oxidises this cobalt ion. It may also inhibit methionine synthetase directly. Nitrous oxide therefore inhibits methionine, thymidine, tetrahydrofolate and DNA synthesis.
Nitrous Oxide
Reduces that MAC of isoflurane to 0.5 when used at 70%
True
Halothane:
Increases cerebral blood flow less than enflurane
False. In descending order; halothane, enflurane, nitrous oxide, isoflurane
Halothane:
Has a sweet odour
True
Halothane:
Has two bromide atoms
False. 1 bromide, 1 chloride and 3 fluoride ions.
Halothane:
Is prepared with 0.01% thymol to prevent combustion
False. It is prepared with 0.01% thymol to prevent decomposition by light.
Halothane:
Causes vagal stimulation
True. It may also cause bradycardia by inhibiting atrioventricular conduction / activity.
In reference to inhaled anaesthetic agents:
Isoflurane does not increase cerebral blood flow at concentrations below 1 MAC
True
In reference to inhaled anaesthetic agents:
Xenon is hepatically metabolised
False. All clearance is by lung elimination.
In reference to inhaled anaesthetic agents:
Oxygen has a critical pressure of 50 bar
True
In reference to inhaled anaesthetic agents:
Entonox seperates into its constituent parts below 7 degrees celcius
False. This is likely to occur at temperatures below -7 degrees celcius (pseudo-critical temperature) at pressures of 117 bar.
In reference to inhaled anaesthetic agents:
0.1% of nitrous oxide is metabolised
False. Less than 0.01% of nitours oxide undergoes metabolism.
