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Anaesthetics > Lecture Notes in Anaesthesia - Chapter 3 > Flashcards

Lecture Notes in Anaesthesia - Chapter 3 Flashcards

1
Q

Which premedications (+doses) are given to increase gastric pH and reduce gastric contents(4)?

Which high-risk patients require them (4)?

Which physical method is also used to reduce gastric contents?

A

​Ranitidine - 150mg PO 12 & 2hrs pre-operatively

Omeprazole - 40mg 3-4hrs pre-operatively

Metoclopramide - 10mg pre-operatively (given with ranitidine)

PO sodium citrate 0.3M - 30ml PO (C-sections)

  • women who are pregnant, particularly in the later stages of pregnancy
  • patients who require emergency surgery
  • patients with a hiatus hernia, who are at an increased risk of regurgitation
  • patients who are morbidly obese

Aspirate NG/OG tube

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2
Q

Intravenous anaesthetic drugs

How are do they distribute initially? And then subsequently? How does this affect plasma concentration?

A

Quickly cross BBB. Re-distribute to other tissues (muscles then fat) so plasma and brain concentrations fall and the patient regains consciousness.

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3
Q

Propofol

Induction dose (mg/kg)

Speed of induction (s)

Duration of action (mins)

Effects on:

  • cardiovascular system
  • respiratory system
  • CNS (2)
  • other side effects (3)

Cumulative or not? Other comments (1)?

A

Induction dose - 1.5-2.5 mg/kg

Speed of induction - 30-45s

Duration of action - 4-7 mins

Effects on:

  • cardiovascular system - hypotension (worse if hypovolaemic/cardiac disease)
  • respiratory system - apnoea, depression of ventilation
  • CNS - decrease cerebral blood flow & intracranial pressure
  • other side effects - pain on injection, involuntary movements, hiccups

Other comments - Non-cumulative, repeat infections/infusion used for TIVA

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4
Q

Etomidate

Induction dose (mg/kg)

Speed of induction (s)

Duration of action (min)

Effects on:

  • cardiovascular system
  • respiratory system
  • CNS (2)
  • other side effects (3)

Cumulative or not? Other comments (3)?

A

Induction dose - 0.2-0.3 mg/kg

Speed of induction - 30-40s

Duration of action - 3-6 mins

Effects on:

  • cardiovascular system - relatively less CV depression
  • respiratory system - depression of ventilation
  • CNS - decrease cerebral blood flow/ICP, anticonvulsant
  • other side effects - pain on injection, involuntary movement, hiccups

Other comments - non-cumulative, emulsion less painful, no histamine release, suppresses steroid synthesis.

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5
Q

Thiopental

Induction dose (mg/kg)

Speed of induction (s)

Effects on:

  • cardiovascular system
  • respiratory system
  • CNS (2)
  • other side effects (1)

Cumulative or not? Other comments (1)?

A

Induction dose - 2-6mg/kg

Speed of induction - 20-30 s

Duration of action 9-10 mins

Effects on:

  • cardiovascular system - dose-dependent hypotension
  • respiratory system - apnoea, depression of ventilation
  • CNS - decreases CBF/ICP, anticonvulsant
  • other side effects - Rare but serious adverse reactions (arrhythmia, circulatory collapse)

Cumulative - delayed recovery after repeat doses. Patients taste garlic or onions.

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6
Q

Ketamine

Induction dose (mg/kg)

Speed of induction (s)

Duration of action (mins)

Effects on:

  • cardiovascular system
  • respiratory system (3)
  • CNS (2)
  • other side effects (1)

Other comments (3)

A

Ketamine

Induction dose - 1-2 mg/kg

Speed of induction - 50-70s

Duration of action - 10-12 mins

Effects on:

  • cardiovascular system - minimal in fit patients
  • respiratory system - minimal depression of ventilation, laryngeal reflexes better preserved, bronchodilatation
  • CNS - CBF maintained, profound analgesia
  • other side effects - vivid hallucinations

Other comments - Subanaestheic doses used as anaesthetic, can be used as sole anaesthetic pre-hospital.

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7
Q

Midazolam

Induction dose (mg/kg)

Speed of induction (s)

Duration of action (mins)

Effects on:

  • cardiovascular system
  • respiratory system (1)
  • CNS (1)

Other comments (1)

A

Induction dose 0.1-0.3 mg/kg

Speed of induction 40-70s

Duration of action - 10-15 mins

Effects on:

  • cardiovascular system - dose-dependent hypotension
  • respiratory system - depression of ventilation, worse in elderly
  • CNS - mildly anticonvulsant

Other comments - causes amnesia

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8
Q

Inhaled anaesthetic drugs

What determines depth of anaethesia?

Induction speed relative to IV anaesthetic agents?

A

Depth of anaesthesia produced is directly related to the partial pressure that the vapour exerts in the brain, and this is closely related to the partial pressure in the alveoli.

Even the most rapid induction using these drugs takes several minutes to achieve the same depth of anaesthesia that is achieved within seconds of giving an IV anaesthetic drug.

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9
Q

Sevoflurane

MAC in oxygen/air (%)

Solubility

Effects on:

  • cardiovascular system
  • respiratory system
  • CNS

Comments (1)

A

MAC in oxygen/air 2.2 %

Solubility - Low, rapid changes of depth

Effects on:

  • cardiovascular system - hypotension, vasodilatation
  • respiratory system - depresses ventilation
  • CNS - minimal effect on CBF

Comments - Popular for inhalation induction

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10
Q

Desflurane

MAC in oxygen/air (%)

Solubility

Effects on:

  • cardiovascular system
  • respiratory system
  • CNS

Comments (2)

A

MAC in oxygen/air 6.0%

Solubility - low (rapid changes of depth)

Effects on:

  • cardiovascular system - hypotension, tachycardia
  • respiratory system - depession
  • CNS - minimal effection CBF

Comments - Pungent, boils at 23 degrees

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11
Q

Isoflurane

MAC in oxygen/air (%)

Solubility

Effects on:

  • cardiovascular system
  • respiratory system
  • CNS

Comments (1)

A

MAC in oxygen/air 1.3%

Solubility - Medium

Effects on:

  • cardiovascular system - hypotension, tachycardia, vasodilation
  • respiratory system - depression
  • CNS - slight increase in CBF/ICP

Comments - Pungency limits use for induction

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12
Q

How does blood solubility relate to partial pressure?

How does this relate to rate of change of depth of anaesthesia?

How does it affect recovery from anaesthesia?

A

An agent that is relatively soluble in blood (isoflurane) will dissolve readily in plasma and not exert a high partial pressure. Therefore a large amount has to diffuse from the alveoli before PP in the blood and then brain begin to rise.

High solubility = slow rate of change

Low solubility = rapid rate of change (faster induction & revoery)

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13
Q

Which factors govern the speed at which alveolar concentration of an inhaled anaesthetic agent can rise (4)?

A
  • Solubility
  • High inspired concentration (limited by irritation cause by vapour)
  • Alveolar ventilation (increased ventilation means drug being removed from alveoli (high solubility drugs) are replaced rapidly)
  • Cardiac output - if high, then greater pulmonary blood flow, increased uptake and reduced alveolar partial pressure.
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14
Q

How is minimum alveolar concentration (MAC) defined?

How does MAC relate to potency?

A

MAC = the concentration required to prevent movement following a surgical stimulus in 50% of subjects

Compounds with a low potency (such as desflurane) will have a high MAC; those with a high potency (such as isoflurane) will have a low MAC.

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15
Q

How does combining two inhalational anaesthetics affect MAC?

A

The effects of inhalational anaesthetics are additive, therefore two values for MAC are often quoted – the value in oxygen and the value when given with a stated percentage of nitrous oxide (which has its own MAC), which will clearly be less.

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16
Q

Which patient factors increase MAC of inhalational anaesthetics (7)?

A
  • Infants or children
  • Hyperthermia
  • Hyperthyroidism
  • Hypernatraemia
  • Chronic alcohol intake
  • Chronic opioid use
  • Increased catecholamines
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17
Q

Which patient factors decrease MAC of inhalational anaesthetics (8)?

A
  • Neonates/ elderly
  • Hypothermia
  • Hypothyroidism
  • Acute alcohol intake
  • Acute intake of opioids, benzodiazepines, TCAs, clonidine
  • Lithium, magnesium
  • Pregnancy
  • Anaemia
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18
Q

How do the analgesic and anaesthetic properties of nitrous oxide compare?

What is its MAC?

What is the maximum safe inspired concentration?

A

Nitrous oxide (N2O) is a colourless, sweetsmelling, non-irritant vapour with moderate analgesic properties but low anaesthetic potency (MAC 105%). The maximum safe inspired concentration that can be administered without the risk of causing hypoxia is approximately 70%, therefore unconsciousness or anaesthesia sufficient to allow surgery is rarely achieved.

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19
Q

Effects of nitrous oxide

  • Cardiovascular
  • Respiratory (2)
  • CNS
  • Effects of rapid diffusion (3)
  • Bone marrow
A
  • CV depression (worse if pre-existing cardiac disease)
  • Increase resp rate and decrease in tidal volume, decreases response to hypercarbia and hypoxia
  • Cerebral vasodilatation, increasing ICP
  • Diffuses into air-filled cavities faster than nitrogen can escape
    • Increasing pressure (middle ear)
    • Increasing volume (gut or air embolus)
    • Diffusion hypoxia
  • Bone-marrow suppression by inhibiting the production of factors necessary for the synthesis of DNA. The length of exposure necessary may be as short as a few hours, and recovery usually occurs within 1 week.
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20
Q

How do neuromuscular blocking drugs work (broadly)?

What are the two types?

A

These work by preventing acetylcholine interacting with the postsynaptic (nicotinic) receptors on the motor end plate on the skeletal muscle membrane (and possibly other sites).

Depolarizing and non-depolarizing

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21
Q

Which is the only depolarizing neuromuscular blocker in regular use?

A

Suxamethonium

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22
Q

Suxamethonium

​Concentration of preparation?

Dose in adults?

Time of onset?

Recovery mechanism? And recovery time?

Effects of cardiovascular, respiratory and CNS?

A

50mg/ml

Dose in adults 1.5mg/kg IV

After injection, short period of fasciculation followed by paralysis in 40-60s.

Recovery spontaneous as sux is hydrolysed by plasma pseudocholinesterase. Normal neuromuscular transmission in 4-6 mins.

No direct effects on CV, resp or CNS. Bradycardia secondary to vagal stimulation in large/repeat doses.

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23
Q

Important side effects of suxamethonium (7)

A
  1. Malignant hyperpyrexia in susceptible patients
  2. Increased intraocular pressure which may cause loss of vitreous in penetrating eye injuries
  3. Muscular pain around the limb girdles, most common 24 h after administration in young adults
  4. Histamine release: usually localized but may cause an anaphylactic reaction
  5. Prolonged apnoea in patients with pseudocholinesterase deficiency
  6. A predictable rise in serum potassium by 0.5–0.7 mmol/L in all patients
  7. A massive rise in serum potassium may provoke arrhythmias in patients with:
  • Burns (maximal 3 weeks to 3 months after the burn)
  • Denervation injury, e.g. spinal cord trauma, maximal after 1 week
  • Muscle dystrophies, e.g. Duchenne’s
  • Crush injury
24
Q

Most significant genotypes relating plasma cholinesterase production (3)?

Effect of suxamethonium on each?

A
  • Normal homozygotes: sufficient enzyme activity to hydrolyse suxamethonium in 4–6 min (950 per 1000 population)
  • Atypical heterozygotes: slightly reduced enzyme activity levels; suxamethonium lasts 10–20 min (50 per 1000)
  • Atypical homozygotes: marked deficiency of active enzyme; members of this group remain apnoeic for up to 2 hours after being given suxamethonium (<1 per 1000)
25
Q

Non-depolarising neuromuscular blocking drugs

Examples (6)

Mechanism of action?

Time of onset?

Two main uses?

Mechanism of recovery?

A

Atracurium, cisatracurium, rocuronium, vecuronium, mivacurium, pancuronium.

  • Mechanism of action - Block access of acetylcholine to post- synaptic receptor sites.
  • Time of onset - 1.5-3 mins
  • Two main uses
    • following suxamethonium to maintain muscle relaxation during surgery;
    • to facilitate tracheal intubation in non-urgent situations.
  • Mechanism of recovery - will eventually occur spontaneously but anticholinestarase often administer
26
Q

Atracurium

Dose for intubation

Maintenance dose

Time to intubation (s)

Clinical duration of action (min)

Systemic effects (2)

Comments (1)

A

Dose for intubation - 0.5– 0.6 mg/kg

Maintenance dose - 0.15–0.2 mg/kg; 30–50 mg/h infusion

Time to intubation - 90–120s

Clinical duration of action - 40 min

Systemic effects - Cutaneous histamine release, drops BP

Comments - Spontaneous degradation in plasma.

27
Q

Cisatracurium

Dose for intubation

Maintenance dose

Time to intubation (s)

Clinical duration of action (min)

Systemic effects (1)

Differences from atracurium (3)

A

Dose for intubation - 0.1– 0.15mg/kg

Maintenance dose - 0.03 mg/kg; 6–12 mg/h infusion

Time to intubation - 120–150s

Clinical duration of action - 50 min

Systemic effects - Minimal

Comments - Single isomer of atracurium. Greater potency, longer duration of action. Minimal histamine release.

28
Q

Rocuronium

Dose for intubation (and for RSI)

Maintenance dose

Time to intubation (and for RSI) (s)

Clinical duration of action (and for RSI) (min)

Systemic effects (1)

Comment (1)

A

Dose for intubation (and for RSI) - 0.6– 0.7 mg/kg (For RSI 1.0– 1.2 mg/kg)

Maintenance dose - 0.15–0.2 mg/kg, 30–50 mg/h infusion

Time to intubation (and for RSI) 60–90s after 0.6 mg/kg, (40–50s after 1.2 mg/kgs)

Clinical duration of action (and for RSI) 30–40, (60–70)min

Systemic effects (1) - Minimal

Comment (1) - Alternative to suxamethonium for RSI

29
Q

Vecuronium

Dose for intubation

Maintenance dose

Time to intubation (s)

Clinical duration of action (min)

Systemic effects (1)

Comment (1)

A

Dose for intubation - 0.1 mg/kg

Maintenance dose - 0.02–0.03 mg/kg; 6–10 mg/h infusion

Time to intubation - 120–150s

Clinical duration of action 30–35 min

Systemic effects (1) - Minimal, no histamine release

Comment (1) - White powder, dissolved before use

30
Q

How are non-depolarising neuromuscular blockers reversed? Mechanism?

What is the accepted practice for the timing of administration? Why?

A

Anticholinesterases inhibit the action of the enzyme acetylcholinesterase, leading to an increase in the concentration of acetylcholine within the synaptic cleft of the neuromuscular junction.

It is accepted practice that anticholinesterases are only used once there is return of at least two twitches on peripheral nerve stimulation using the train-of-four assessment. If used in the presence of more profound neuromuscular block there is an increased chance of residual muscle paralysis in the immediate postoperative period.

31
Q

Unwanted effects of anticholinesterases?

How is these prevented?

Most common anticholinesterase used?

Dose? Max effect? Duration of action?

Given with which drugs (2)? Doses?

A

Increase the amount of acetylcholine within parasympathetic synapses (muscarinic receptors), causing:

  • bradycardia
  • spasm of the bowel bladder and bronchi
  • Increased bronchial secretions.

They are always administered with a suitable dose of an anti-muscarinic.

Neostigmine, 2.5mgIV, max effect 5 mins, lasts 30 mins.

Given with atropine 1.2mg or glycopyrrolate 0.5mg

32
Q

What is sugammadex used for?

Dose range and time of onset?

Mechanism?

Benefits over anticholinesterases?

Main use?

A

Reverses any intensity of neuromuscular block induced by drugs of the aminosteroid group, i.e. rocuronium and vecuronium.

Dose needed depends on intensity of block, range from 4-16mg/kg. Time taken 1-3 mins

Doughnut shaped, surrounds blocker and inactivates, then excreted in urine.

Avoids need for antimuscarinic.

Not routinely used for reversal as too expensive. Used in emergencies to reverse blockade in can’t intubate, can’t ventilate.

33
Q

Meaning of opioid vs opiate?

Where are opioid receptors located?

What are the classes of opioid receptor (4)?

A

This term opioid is used to describe all drugs that have an
analgesic effect mediated through opioid receptors
including both naturally occurring and synthetic
compounds. The term ‘opiate’ is reserved for naturally
occurring substances, such as morphine.

They act on opioid receptors distributed throughout the CNS in particular the substantia gelatinosa of the spinal cord and the periaquaductal grey matter of the mid-brain.

MOP (mu), KOP (kappa), DOP (delta) and NOP (not named previously)

34
Q

Effects of opioids

CNS (8)

Respiratory (2)

Cardiovascular (2)

Urinary (1)

GI (2)

Endocrine (1)

Skin (1)

A
  • Central nervous system - Analgesia, Sedation, Euphoria, Nausea and vomiting, Pupillary constriction, Depression of ventilation (rate more than depth, reduced response to carbon dioxide), Depression of vasomotor centre, Addiction
  • Respiratory system - Antitussive, Bronchospasm in susceptible patients
  • Gastrointestinal tract - Reduced peristalsis causing constipation and delayed gastric emptying, constriction of sphincters.
  • Cardiovascular system - Peripheral venodilatation, Bradycardia due to vagal stimulation
  • Endocrine system - Release of ADH and catecholamines
  • Urinary tract - Increased sphincter tone and urinary retention
  • Skin - Itching
35
Q

Morphine

Dose (IM/IV)

Speed of onset (IM/IV)

Duration of action (mins)

Effective against?

Less effective in?

A

Dose - 0.2-0.3 mg/kg IM / 0.1-0.15mg/kg IV

Speed of onset - 20-30 min IM / 5-10 min IV

Duration of action - 60-120 min/ 45-60 min

Effective against visceral pain

Less effective in trauma.

36
Q

Fentanyl

Doses (2 + indications)

Speed of onset (2)

Duration of action (2)

A

Short procedures, spontaneous ventilation

1–3 mcg/kg, 2–3 min, 20–30min

Long procedures, controlled ventilation

5–10 mcg/kg, 1–2 min, 30–60min

37
Q

Remifentanil

Dose? Route?

Speed of onset?

Duration of action?

Comments (2)?

Widely used in?

A

IV infusion 0.1–0.3 mcg/kg/min

Speed of onset: 15–30 s

Duration: Infusion dependent

Very rapid recovery. Profound respiratory depression.

Widely used in TIVA

38
Q

Tramadol

Dose?

Receptor? Agonist or antagonist?

2nd mechanism?

% of morphine’s potency?

Side effects vs morphine?

Reversal?

A

PO (or IV/IM) 50–100mg 4 hourly.

MOP receptor - weak agonist

10% of morphine potency

Respiratory depression/constipation less severe at equivalent doses.

Blocks noradrenaline/5-HT re-uptake augmenting descending inhibitory pathways (naloxone only blocks MOP mediated actions)

39
Q

Buprenorphine

Receptor? Agonist or antagonist?

Potency versus morphine?

Duration of action?

Route?

Side effects(1)?

Reversal?

A

Partial agonist

30 times more potent than morphine

Duration of action up to 8 hours.

It is well absorbed when given sublingually.

Nausea and vomiting may be severe and
prolonged.

Not completely reversed by naloxone.

40
Q

Naloxone

Mechanism of action?

Dose?

Time of onset?

Duration of action? Versus opioids?

When may very high doses be required?

A

Opioid receptor antagonist

Initial dose: 0.1-0.4mg

Time of onset: <60s

Lasts 30-45 mins. Shorter than most opioids so may require repeat doses or infusion.

Limited effect vs opioid with partial or mixed actions. May require very high doses up to 10mg.

41
Q

What do the different schedules of controlled drugs correspond to (5)?

A

Schedule 1: hallucinogenic drugs, including cannabis and lysergic acid diethylamide (LSD), which currently have no recognized therapeutic use

Schedule 2: this includes opioids, major stimulants (amphetamines and cocaine);

Schedule 3: drugs thought less likely to be misused than those in schedule 2, and includes barbiturates, minor stimulants, buprenorphine, and
temazepam;

Schedule 4: this is split into two parts:

  • benzodiazepines (except temazepam), ketamine, which are recognized as having the potential for abuse
  • androgenic steroids, clenbuterol and growth hormones.

Schedule 5: Preparations which contain very low
concentrations of codeine or morphine, such as cough mixtures.

42
Q

Parecoxib

Mechanism?

Route?

Initial IV dose? Subsequent doses? Max dose? Reduce in who?

Example uses (2)?

CVS/resp effect?

A

A selective COX-2 inhibitor, with predominantly
analgesic activity.

Usually given IV, but can be given IM.

Initial IV dose 40 mg, subsequent doses
20–40mg, 6–12 hourly, maximum 80 mg/day
for 2 days – reduce dose by 50% in elderly;

Opioid sparing effects after abdominal surgery; effective in orthopaedic surgery.

No effect on ventilation or cardiovascular
function;

43
Q

Four independent risk factors for PONV?

How is incidence of PONV affected by risk factors?

Scoring system? Above which score should a change in approach be considered?

A
  • emale sex;
  • being a non-smoker;
  • previous history of PONV or motion sickness;
  • opioids as part of the anaesthetic technique.

The incidence of PONV increases with the number of risk factors and is approximately 10%, 20%, 40%, 60%, and 80% in patients with zero, one, two, three or four risk factors respectively.

Apfel score (1 point per RF). Scores of 2 & above.

44
Q

Metoclopramide

Mechanism?

Dose?

Timing?

Other effects (2)?

A

​Dopamine antagonist

10mg orally or IV
End of surgery

Pro-kinetic, extrapyramidal side effects

45
Q

Ondansetron

Mechanism?

Dose?

Timing?

A

5-HT3 antagonist

4–8mg orally or IV

End of surgery
More effective at treating established vomiting

46
Q

Cyclizine

Mechanism?

Dose?

Timing?

A

H1 histamine antagonist

50mg IM or IV
End of surgery
Cyclizine has anti-vagal properties, may cause a
tachycardia

47
Q

Resting potential of a polarised cell?

How do nerve cells depolarise in response to stimuli? How do they repolarise?

What determines the strength of a nervous impulse?

A

Resting potential of a polarised cell is -70mV.

Noxious stimuli cause sodium to enter the cell. If the stimulus reaches threshold, depolarisation occurs and propagates along the nerve. The membrane repolarises by loss of K+ from within followed by active pumping out of Na+.

The strength of a nervous impulse is solely dependent
on the frequency of action potentials (as action potentials are all-or-nothing events).

48
Q

By what mechanism do local anaesthetics work?

What two forms do LAs exist in?

How do these forms affect entry into the cell?

Which form is active against their target?

A

LA works by blocking voltage-gated sodium channels from within the nerve cell preventing depolarisation so no action potential can be initiated or propagated.

Local anaesthetic drugs exist in two forms: ionized and unionized.

When a local anaesthetic is given, the majority will exist as the ionized form but, in order to cross the cell membrane, they have to be in the unionized form. This change occurs after injection because of a relatively higher pH in tissues (7.4 compared to 6.0 in solution). However, intracellular pH is lower (7.1) and so a greater proportion returns to its ionized form. It is this form that is attracted to, and then blocks, the sodium channels.

49
Q

Which factors determine the duration of action of local anaesthetic(4)?

A

Degree of un-ionised drug (pKa)

Protein binding (binding to membrane proteins = longer action)

Local blood supply (more supply, faster wash out)

Lipophilicity (more lipophilicity greater membrane penetration but greater toxicity)

50
Q

When local anaesthetic is injected:

  • are small or large diameter nerves blocked first?
  • are myelinated or unmyelinated nerves blocked first?

When a regional anaestheic technique is used, what is the order of onset of the block (5)?

A

Following the injection of a local anaesthetic drug, there is always a predictable sequence to the onset of effects as small diameter nerves are blocked before large diameter ones, and unmyelinated nerves are blocked before myelinated ones.

Consequently when a regional anaesthetic technique is used, the order of onset of the block is:

  1. autonomic fibres – vasodilatation;
  2. temperature;
  3. pain;
  4. touch;
  5. motor – paralysis.
51
Q

Two groups of local anaesthetics defined by chemical structure (2 x 3 examples)?

Which is the older group and what are its drawbacks (3)? What is the main use for this group?

A
  • esters: amethocaine, benzocaine, cocaine;
  • amides: lignocaine, bupivacaine, prilocaine.

The esters were the first drugs to be introduced into clinical practice. They are relatively more toxic, allergenic, and unstable than their modern counterparts the amides. Their main use today is to provide topical anaesthesia.

52
Q

What is the main use of amethocaine?

A

Available as a 4% gel (Ametop) that is applied topically at the site of intended intravenous cannulation, and is effective in 45 min. More dilute solutions are available to provide topical anaesthesia of the conjunctiva.

53
Q

What are the maximum safe doses of lidocaine with and without adrenaline (in mg/kg and max dose in mg)?

When should doses be reduced?

How is it metabolised?

A

The currently accepted maximum safe dose is:

  • 3mg/kg, maximum 200mg (without adrenaline);
  • 6–7 mg/kg, maximum 500mg (with adrenaline).

These doses should be reduced if the patient is elderly, frail or shocked. It can also be used in the treatment of VF/VT refractory to defibrillation (100mg IV) when amiodarone is unavailable. As with all amide local anaesthetics it is metabolized in the liver.

54
Q

Bupivacaine

Onset and duration vs lignocaine?

Which % solutions are used for:

  • Nerve blocks
  • Spinal anaesthesia
  • Epidurals

Maximum safe dose? Over what period?

Risk of overdose?

What forms of the drug are available and how do they differ?

A

Bupivacaine has a slower onset but a longer duration
of action than lignocaine.

  • Nerve block - 0.25 or 0.5%
  • Spinal anaesthesia - 0.5% with 8% dextrose (Marcain Heavy)
  • Epidural infusion - 0.125%

Maximum safe dose is 2mg/kg (with or without adrenaline) in a 4hr period.

More cardiotoxic than other amides. Toxicity hard to treat.

Chiral molecule -L/D forms. Racemic mixture and pure L-isomer (chirocaine) available. Same doses but L0isomer has reduced toxicity.

55
Q

What does EMLA stand for?

What does it contain?

A

EMLA, a eutectic mixture of local anaesthetics.

This is a cream that contains lidocaine and prilocaine in equal proportions
(25mg of each per gram).

56
Q

The relationship between concentration, volume and dose is given by the 0formula?

A

Concentration (%) x Volume (ml) x 10 = dose (mg)

57
Q

Volume of a unit of blood? How much should a unit of blood raise a patient’s Hb?

Volume of a unit of platelets? How much should 1 bag increase platelet count?

A

A unit of blood (300ml) should raise a patient’s Hb by 10 g/L.

A unit of platelets (50-60ml) supplied as 1 bag of 4 units. A bag should increase count by 30-40 x 109/L.

Anaesthetics (7 decks)

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