Anaesthesia Flashcards
What are the three stages of general anaesthesia?
- Induction
- Maintenance
- Emergence
What are the three A’s of general anesthesia?
- AMNESIA - lack of response and recall to noxious stimuli – Unconsciousness
- ANALGESIA - pain relief
- AKINESIS - Immobilisation/paralysis
What are the three types of drugs that make up the ‘triad of anaesthesia?’
- Hypnotic agents
- Analgesics
- Muscle relaxants
What are induction agents and what is there aim? What are the two ways in which an individual can be induced?
Transition from an awake to an anesthetised state.
- IV - induce loss of consciousness in one-arm brain circulation time (10-20 secs; lasting for 4-10 mins)
- Inhalational Induction - usually amnesia maintenance
What are the IV induction agents?
- Propofol
- Etomidate
- Ketamine
- Thiopentone
What are the characteristics of propofol?
- Dose
- Mechanism
- Advantages
- Disadvantages
- CIs
‘Milk’ (MJ overdose!) - most common
- 1.5 – 2.5 mg/kg: titrated against patient response (anaesthesia onset)
- Enhances inhibitory function of the GABA through GABA-A receptors
-
Rapid induction (<30 secs) and emergence (lasts 2-5 mins)
- Anti-emetic properties (↓ incidence of postop N&V (PONV))
- Excellent suppression of pharyngeal reflexes and good brochodilator
-
Rapid induction (<30 secs) and emergence (lasts 2-5 mins)
- Lipid based - pain on injection
- Marked ↓BP (systemic vasodilatation), ↓HR ↓RR (act on respiratory centre),
- Involuntary movements
- Allergies/rashes - contains soya, eggs
- Lipid based - pain on injection
-
Children - “propofol infusion syndrome”
- metabolic acidosis, lipidaemia, cardiac, arrhythmias and increased mortality
-
Children - “propofol infusion syndrome”
What are the characteristics of Thiopentone?
1 Dose
2Type of drug and Mechanism
3 Advantages
4 Disadvantages
5 CIs
‘Pale yellow powder’
- 4-5 mg/kg
- Barbituate - Binds to GABA-A receptor and enhances inhibitory effects of GABA
-
Rapid induction (<30sec) (∴ main use = rapid sequence induction)
- Anticonvulsant properties
- Can imprvoe neurological outcomes ( ↓cerebral blood flow (↓ICP), ↓metabolic rate and ↓oxygen demand - ‘Barbitutate coma’
-
Rapid induction (<30sec) (∴ main use = rapid sequence induction)
- Depresses heart contractile force (↓BP/Q BUT ↑HR) - caution in hypovolaemia
- ↓RR
- Depresses heart contractile force (↓BP/Q BUT ↑HR) - caution in hypovolaemia
- Airway reflexes well preserved (vs propofol) - coughing/laryngospasm
- Rash/bronchospasm (causes histamine release)
- Intrarterial Injection - thrombosis and gangrene
5. Porphyria (overproduction and excretion of porphyrins) - can precipitate prophyria due to hepatic enzyme induction
What are the characteristics of etomidate?
Dose
Mechanism
Advantages
Disadvantages/CIs
- Non-barbituate - 0.3 mg/kg
- Binds to GABA-A receptor and enhances inhibitory effects of GABA
- Haemodynamic stability - minimal ↓BP/Q
- Lowest incidence of hypersensitivity reactions
- Haemodynamic stability - minimal ↓BP/Q
- Pain on injection (lipid emulsion)
- Involuntary movements
- High incidence of post-op N&V
- Adreno-cortical suppression (suppressed for up to 72hrs) - ∴
- Pain on injection (lipid emulsion)
CI in critically ill/septic shock patients (↑ mortality)
What are the characteristics of Ketamine?
Dose
Mechanism
Advantages
Disadvantages/CIs
Dose: 1 - 1.5 mg/kg. Slow onset (90 secs) and lasts 5-10 mins
Mech:
- Anatagonises NMDA (↓effects of glutamate (main excitatory NT) ► dissociative anaesthesia (conscious but insensitive to pain) - anterograde amnesia
- Acts on opioid and muscarinic receptors. Also effects Na/Ca movement across cell membranes ► Profound analgesia
- Inhibits monoamine reuptake ► anti-depressant effects
- Because of above, can be used as sole anaesthetic for SHORT procedure
Advan:
- minimal effect on resp drive, protective airway reflexes = intact ∴ good preshopital
- ↑HR/BP/Q - useful in shocked, unwell patients
- Bronchodilator - role in management of severe asthma
Disadvan:
- Hypersalivation ► airway obstruction (Tx with anti- muscarinic e.g. glycopyrrolate)
- N&V
- Catalepsy - open eyes, slow nystagmus gaze. Intact corneal/light reflexes
- Emergence phenomenon: vivid dreams, hallucinations
- Hypertonus, occassional purposeful movements
What are the inhalation/volatile agents for maintaining (usually) /inducing amnesia?
- Sevoflurane
- Desflurane
- Isoflurane
- Enflurane - rare
What is the definition of minimum alveolar concentration (MAC)?
- Minimum alveolar concentration of vapour (%) at steady state
- That prevents the reaction to a standard surgical stimulus (traditionally a set depth/width of skin incision)
- In 50% of subjects
What factors can increase MAC? (i.e. anaesthesia requirements)
Things that increase metabolism
- Infancy (peaks at 6 months)
- High temp
- Pregnancy
- Chronic Alcoholism
- Stimulants (cocaine/amphetamine)
What factors reduce the MAC (i.e. anaesthestic requirement)
Things that REDUCE metabolism…
- Hypoinatraemia
- Hypothermia
- Elderly
- Acute alcohol intoxication
- Pregnancy
- Anemia
- CNS depressant drugs e.g. benzo, opioids
What are the characteristics of Sevoflurane?
- Colour/characteristics
- Uses
- Route and MAC
4 Effects on CV, resp and CNS
SEs
- Clear, colourless, sweet smelling, non- irritant
- Popular for inhalational induction. Maintenance.
- Route: Inhalation, via calibrated vaporiser. MAC: ~2%
- ↓BP (vasodilation), ↓RR, minimal effect on cerebral blood flow
- Malignant Hyperthermia, nephrotoxic (↓ renal blood flow)
What are the characteristics of Isoflurane?
- Colour/characteristics
- Uses
- Route and MAC
4 Effects on CV, resp and CNS
- SEs
- Clear, colourless liquid. Pungent smell
- Maintenance. Pungent smell limits use for induction.
- Routes: Inhalation via calibrated vaporiser. MAC: 1.15%
- Least effect on organ blood flow ↓BP (vasodilation), ↑HR, ↓RR, slight ↑cerebral blood flow/ICP
- Malignant hyperthermia.
What are the characteristics of Desflurane?
- Colour/characteristics
- Uses
- Route and MAC
4 Effects on CV, resp and CNS
- SEs
- Clear colourless liquid. Low lipid solubility (∴ rapid induction and elimination). High volatility.
- Long operations e.g. organ donation. Unsuitable for induction.
- Inhaled via electrically heated vaporiser - dual circuit gas/vapour blender. MAC: 6%
- ↓BP, ↑HR, ↓RR, min effect of cerebral blood flow/ICP
- Malignant hyperthermia. Reduces renal blood flow.
What is the MAC of Enflurane? Why isnt it really used anymore
- MAC: 1.6%
- Potentially causes hepatotoxicity
What is the pathohpysiology of malignant hyperthermia? What triggers it?
Triggers: ALL volatile inhalation agents, Suxamethonium
Pathophysiology:
- Autosomal genetic condition of ryanodine receptor gene
- Triggering agent causes uncontrolled release of cytoplasmic free calcium from skeletal muscle SR
- Causes muscle rigidity ► ↑ metabolism ► body temp
What are the CFs of malignant hyperthermia?
Due to uncontrolled ↑ in intracell Ca ion conc, there is:
- Muscle rigidity
- ↑ metabolism (↑ end tidal CO2 first, ↑ body temp occurs later )
- Rhabdomyolysis - renal failure
(Arrythmias, ↑K+, and DIC may develop)
What are the two types of general analgesias used in anaesthetics?
- Short Acting - rapid acting, high potency (fentanyl = 100x more potent than morphine)
- Long Acting
Name three short acting analgesics. When/why are they used?
- Fentanyl, Remifentanil, Alfentanil
- Intra op analgesia - suppresses response to laryngoscope, reduces surgical pain
Name two long acting analgesics. When/why are they used?
- Morphine, Oxycodone
- Intra-op and post-op analgesia
What other types of analgesics are commonly used?
Most commonly used analgesic
- Paracetamol
Most commonly used oral opioid in adults
- Codeine
Intravenous NSAIDS
- Ketorolac, Parecoxib
What are the two main groups muscle relaxants? How do they exert there action?
-
Depolarising
-
PHASE I: Cause depolarisation by mimicking the effect of Ach to nicotinic receptor. Contraction; fasciculations are seen and repolarisation is inhibited
- Not hydrolysed by acetylcholinesterase, therefore…
- PHASE II:‘Persistent depolarisation’ = desensitisation (end plates lose sensitivity)
-
PHASE I: Cause depolarisation by mimicking the effect of Ach to nicotinic receptor. Contraction; fasciculations are seen and repolarisation is inhibited
-
Non-depolarising
- Competitive antagonist - bind to nicotinic ACh receptors causing gradual muscle paralysis
- Compete with ACh for nicotinic receptor binding, preventing end plate depolarisation and impulse propagation
- Name one depolarising muscle relaxant.
What is:
- It used for
- It’s dose
- The SEs
Suxamethonium
Use: 1. Rapid intubation of the trachea and short periods of neuromuscular blockade. 2. Rapid sequence induction
Dose: 1 - 1.5 mg/kg
SEs:
- Bradycardia
- Muscle pains (due to fasciulations before paralysis)
- Hyperkalaemia
- ↑ICP, IOP and gastric pressure
- Anaphylaxis - skin rash ► bronchospasm
- Malignant hyperthermia
- Suxamethonium apnoea
What is the cause of suxamethonium apnoea?
- Suxamethonium = metabolised by plasma cholinesterase (usually 5-10mins) - some PTs lack /have an altered enzyme ∴ ↓ metabolism
- ∴ PTs may = paralysed for many hrs after administration
- Pts must be anaesthetised/ventilated until after sux eliminated (slow!)
What drug is used to reverse Suxamethonium?
None!
Name the a) short, b) intermediate and c) long acting non-depolarising muscle relaxants
Short: Atracurium, mivacurium (aka nevercurium - hardly used!) (10 letters, earlier in alphabet!)
Intermediate: vecuronium, rocuronium** (10 letters, later in alphabet)
Long: Pancuronium (11 letters!)
What are the SEs for non-depolarising muscle relaxants?
- Slow onset and variable duration, therefore less side effects
- Stimulate histamine release - ↓BP (vasodilation), ↑HR, Flushing
Which population should you caution the use of non-depolarising muscle relaxants?
- Myasthenia gravis or myasthenic syndrome
- Extremely sensitive to their effects.
What drug is used to reverse the action of ALL non-depolarising drugs? What is the mechanism and its SEs?
Neostigmine
Mech: Reversible, anti-cholinesterase ► prevents ACh breakdown ∴ ↑ACH
SEs: Stimulates both nicotinic and muscarinic receptors (parasynp)
- Nicotinic: low dose: muscle contraction. High dose: block neuromuscular transmission (↑↑↑acetylcholine)
- Muscarinic: ↓HR, bronchoconstriction (↑bronchial secretions), miosis, salivation, ↑GI tone/secretions/motility, N&V,

What drug is neostigmine usually combined with to reverse the muscarinic SEs?
- Anti-muscarinic agent: Glycopyrrolate
- ∴ prevents muscarinic SEs ass with neostigmine:
- ↓bradycardia
- ↓ salivary, tracheabronchial, pharyngeal, gastric, secretions
- SEs: cant see, cant pee, cant spit, cant shit,
What is the physiology of PONV?

What drugs and procedures are used to treat/prevent post operative N&V?
Anti-emetic agents:
- 5HT3 blockers: Ondansetron - prevention and Tx of PONV (esp chemo/RT)
- Anti-histamine: Cyclizine - opioids, GA, RT and vestibular.
- Steroids: Dexamethasone (8mg Adults, 150mg/kg children) ► unclear mech. Tx for chemo and PONV.
- Dopamine antagonists: Phenothiazides (e.g. Prochlorperazine)
- Anti-dopaminergic: Metoclopramide
- Benzodiazepines - Lorazepam - sedative/amnesic/antiemetic
Acupuncture
- Point P6 (2.5-5cm proximal to distal wrist crease. Between flexor carpi radialis and palmaris longus tendons).
- 5 mins manual/electical stimulation ↓ vomiting incidence
What factors can increase the risk of PONV?
Patient factors - young, female, history motion sickness, anxious, non smoker
Anaesthetic factors - opioids, etomidate, N2O, volatile
Surgical factors - gynae, abdominal, middle ear, neurosurgery, ophthalmic (e.g. squint), prolonged op times, poor pain control post op
What types of drugs are used to Tx hypotension in A) commonly in surgery B) Severe Hypotension/ICU
Vasoactive agents
Commonly used:
- Ephedrine
- Phenylephrine
- Metaraminol
Severe hypotension / ICU
- Noradrenaline
- Adrenaline
- Dobutamine
What do alpha (I & II) beta (I & II) adreno receptors do?

What are the: effects, doses mechanisms and SEs of ephedrine?
Mech: Activates α1 (indirectly), β1, β2
Effects: HR ↑, MAP ↑ (contractility), CO ↑ PVR ±
SEs: Repeated doses less effective (tachyphylaxis)
What are the: effects, doses mechanisms and SEs of Phenylephrine?
Mechs: α1 (weak α2, weak β1)
Effects: HR ↓, MAP ↑↑, CO ↓, PVR ↑↑
SEs:
What are the: effects and mechanisms of Metaraminol?
Mechs: Activates α1 (indirectly), β1, β2
Effects: Vasoconstriction - ↑ systolic/diastolic BP, ↑PVR
What is the total body water as % of total body weight in:
a) neonates
b) 6 months old
c) 1 yr olds
d) young adult
e) elderly
Neonate - 80%
6 Months - 70%
1 yr - 60%
Young Adult - 60%
Elderly - 50%
How is total body water distributed throughout the body? What are the different fluid compartments?
- Distributed into different compartments/spaces - seperated by membranes that regulate flow of water between compartments
- Intracellular Fluid (ICF) - 2/3s (30L) of total body water
-
Extracellular Fluid (ECF) - 1/3 (15L)
- Interstitial fluid (ISF) (10L) - occupies spaces between cells
- Intravascular fluid (3.5L) - blood plasma
- Transcellular Fluid (1.5L) - intraocular fluid, CSF, urine in bladder, fluid in bowel lumen

What is the definition of a solvent and solute?
A liquid/ solid/gas which is able dissolve another solid/liquid/gas (solute*) to form a solution e.g. water + salt
Solute - a dissolved substance e.g. glucose
What is the difference between osmolarity and osmolality?
Both quantify how much of a solute is dissolved in a solution i.e. the solute concentration of a solution
- Osmolarity: the number of osmoles of solute particles per unit volume of solution (milliosmole)
- Osmolality: the number of osmoles of solute particles per unit weight of solvent (milliosmoles/kg)
What is the definition of tonicity?
- Describes the relative solute concentration of two solutions seperated by a selectively permeable (semi-permeable) membrane (e.g. ICF and ECF)
- Tonicity = influenced by number of solute particles within a solution (which cannot cross membrane)
- Hypertonic (contains a higher concentration of solute on one side of the membrane)
- Isotonic (contains the same concentration of solute on both sides of the membrane)
- Hypotonic (contains a lower concentration of solute on one side of the membrane)
What is the definition of osmosis? WHat is osmotic pressure?
- Movement of water from less concentrated solution (hypotonic) to a more concentrated (hypertonic) solution across a semipermeable membrane
- Semi-permeable membrane - allows free passage of water, but NOT any solutes
Osmotic pressure - minimum pressure which needs to be applied to a solution to prevent the inward flow of its solvent across a semi-permeable membrane
How does fluid move between different compartments?
a) Interstitial and intravascular
B) Intracellular and extracellular
Interstitial and intravascular compartments
- Seperated by capillary wall (water crosses via gaps/through cell membrane)
- Movement of H2O/solutes = largely passive (simple diffusion/filtration)
Cell membrane - allows passive movement
- Water/small uncharged/lipid soluble molecules able to cross via passive diffusion
- Ions, glucose (facilitated diffusion), proteins via transmembrane proteins or ion channels (act to provide different permeability to different solutes)
- Steady state - ECF and ICF = isotonic
- Any difference in EC/IC tonicity = due to change in solute concentration in either fluid compartment
- H2O then moves from area of relative hypertonicity ► hypotonicity
What is the main ion that governs movement of fluid between ICF and ECF compartments? What controls its conc?
- Na+ - memebrane = impermeable to Na+ ions so extracell conc governs movement between ECF and ICF
- Extracell Na conc = controlled by kidneys and neuroendocrine controls
- K+ = major intracell ion
What are the sources of fluid input and output? (70kg man)

What is the definition of insensible losses?
- Loses from non-urine sources - insensible losses incease in unwell patients (febrile, tachypnoeic, increased bowel movements/stoma output)
What is the physiology of water and sodium homeostasis?

How are IV fluids broadly categorised?
- Crystalloids - NaCl 0.9%, Dextrose, Dex/Sal, Hartmanns
- Colloids - gelatins (Gelofusine, voluven, Volulyte), RBCs, Albumin (HAS)
What parameters are used to assess patient fluid status?
- Thirst
- Dry mucous membranes
- ↓Skin turgor (sturnum)
- Urine output <0.5ml/kg/hr (Oliguria)
Ongoing losses
- ↑Cap refill time
- ↓BP ↑HR
- ↓JVP/CVP
Monitor fluid input-output chart, daily weight chart and U&Es regularly
How is fluid loss classified?
Mild - ↓weight (4%), ↓skin turgor, dry mucous membranes
Moderate - ↓weight (5-8%), oliguria, ↓BP ↑HR
Severe - ↓weight (>8%), profound oliguria, CVS collapse
What are crystalloids? What are their uses?
- Balanced salt/electrolyte solutions. Forms true solution and is capable of passing through semi-permeable membranes
- Can be isotonic, hypertonic or hypotonic
- Uses: Plasma expanders
- ↑ the intravascular/circulatory volume via movement of intracellular and interstitial water into intravascular space
- e.g. haemorrhage, dehydration or surgical fluid loss
What are the advantages and disadvanatges of crystalloids?
Advantages
- Short half life (30-60mins)
- Inexpensive, readily avaliable
- Non-allergenic
Disadvantages
- 3x volume needed for replacement (Molecules = small enough to freely cross capillary walls ∴ 2/3s of infused volume fluid will move into tissues)
- Excessive use: peripheral and pulmonary oedema
What are the characteristics of saline solution NaCl 0.9%?
- 9 g of NaCl/L water
- 154 mmol/L sodium
- 154 mmol/L chloride
- Osmolality = 308 mosm/L
- Does not contain the same electrolytes in the same concentrations as extracellular fluid (135- 145)
• Potential problem = hyperchloraemic metabolic acidosis, more likely with renal insufficiency
Name 4 crystalloid solutions
- Normal saline (0.9% NaCl)
- Hartmanns solution
- Lactated Ringer’s
- Hypertonic Saline (3, 5, 7.5%)
- Ringer’s solution
WHat are the characteristics of Hartmanns solution?
- Na+: 131 mmo/l
- Cl = 111 mmol/l
- Lactate = 29 mmol/l
- K = 5 mmol/L
- Ca = 2mmol/L
- Isotonic - distributes across extravascular space
- Potential SEs: K+ may accumulate
What are the characteristics of hypertonic solutions?
- Hypertonic saline solutions include 1.8%, 3%, 5%, 7.5% and 10% sodium chloride solutions
- Osmolality = exceeds intracellular water. the extracellular fluid (ECF) becomes slightly hyperosmolar thus gradient formed i.e. cell water ► extravascular space
- Comps: ↓intracellular volume (cellular dehydration), hypernatraemia?
What are the characteristics of 5% dextrose?
- Only water and dextrose (5% i.e. 50g/L) - Glucose taken up by cells and water distributes quickly across all fluid compartments
- Contains no electrolytes so decreases blood osmolality by dilution
- 1 g Dextrose 3.4 Kcal
- Calorific value approx. 170 kcal
What are colloids?
- Contain NaCl and large chemicals (proteins/starches) which are incapable of passing across a semi-permeable membrane.
- Thought to increase oncotic pressure ► increase intravascular volume
- Synthetic:
- Gelatine based - dextrans
- Starch based - Glesofusin (banned in 2013 - hyperoncotic ►AKI; anaphylaxis, coagulopathy)
- Human protein products
- Blood products: RBS, platelets, FFP
- Human Albumin Solution (HAS)
What are the main problems associated with colloids?
- Anaphylactic reactions
- Coagulopathy
- Cost
What are the five principles of clinical fuluid management?
- Individualise to the particular patient
- Assess current fluid status
- Replace any deficit
- Maintenance fluids / electrolytes
- Replace ongoing losses
What are the daily requirements? (Water, Na, K+, Energy, glucose)
Water - 30-40 ml/kg (35ml/kg if elderly)
Energy - 30-40 kcal/kg
Na - 1-2 mmol/kg
K - 1mmol/kg
Glucose - 50g/day
What arenthe daily requirements for a 70kg man? What would be a typical maintenance fluid regime?
- Water = 70 x 40 = 2800ml
- Na = 70 x 1-2 = 70-140 mmol
- K = 70 mmol
- 50g Glucose/day
1st bag: 1L 0.9% saline/Hartmanns over 8hrs
2nd Bag: 1L of 5% dextrose + 20mmol/L K
3rd: 1L of 5% dextrose + 20mmol/L K
Total:
- 3000ml Water
- Saline: 154 mmol Na/Hartmanns: 131 mmol Na
- 40 mmol K
-
What are sources of fluid loss in patients?
Reduced intake (high urea:creartinine, high PCV)
- Elderly, dysphagia, unconscious
Increased Requirements
- Trauma, burn, post-operative
Increased Loss
- Fever/sweating
- Hyperventilation
- GI loss: vomiting (low K, low Cl, alkolosis), diarrhoea (low K, acidosis)
- Renal loss (↑ diuresis - e.g. diuretics)
- Third space losses e.g. lumen (bowel obstruction), retroperitoneum (e.g. pancreatitis),
What is the fluid Tx for ongoing losses?
- Prescribe for routine maintenance requirement plus additional fluid and electrolyte supplements to replace the ‘measured’ abnormal ‘ongoing’ losses
- (refer to table and prescribe according to source of loss)
What are the 2 main ways in which fluid resuscitation is used? What is the aim?
- To maintain intravascular volume (in order to maintain blood pressure) e.g. hypovolaemic/cardiogenic/distributive shock
- To replace massive fluid losses (may require blood transfusion + other blood products)
- AIM: ↑volume to ↑BP
What is the dose for resus fluids?
- Crystalloids (0.9% sodium chloride) 500 ml fluid bolus over less than 15 minutes.
- If fluid resus still required, repeat bolus.
- If >2000ml given and fluid resus still required, seek expert help