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186 Cards in this Set

  • Front
  • Back
Fasting guidelines pre-op
8hr
6hr
4hr
2hr
8hr: meat, fried or fatty food
6hr: light meal (toast, cracker, clear fluid)
4hr: breast milk, jello
2hr: clear fluid (water, black coffee, black tea, carbonated beverages, juice without pulp)
genetic condition causing adverse anaesthetic reaction
malignant hyperthermia
GORD: risk, mgt
Aspiration
Mgt: sodium citrate 30mL PO or ranitidine 150-300mg PO 30 min preop
which antihypertensives do you withhold preop?
diuretics: volume depletion reaction with anesthetic agents
B-blockers: if it is a new drug because increases hypotension and increases risk of stroke
what drugs should be withheld preop
diuretics
b-blockers
potassium supplements
oral hypoglycaemics (eg. metformin)
insulin: easier to fix hyperglycaemia in sx
what monitoring is needed for a pt undergoing sedation?
oxygenation: pulse oximetry, inspired O2 (FiO2)
ventilation: correct position ETT, chest movement, breath sounds, tidal CO2 analysis, end tidal anesthesia analysis
circulation: pulse, heart sounds, BP, telemetry, oximetry, CVP
temperature: temperature probe
what are the different components of anaesthesia
analgesia
amnesia
muscle relaxant
abolition of autonomic reflexes
maintenance of homeostasis
triad of GA
1. unconsciousness (anaesthesia)
2. loss of reflexes (muscle relaxant)
3. analgesia
four stages of anaesthesia
Stage 1: Anaelgesia 'induction' phase
Stage 2: Excitement stage
Stage 3: Surgical anaesthesia
Stage 4: Overdose (severe brain stem or medullary depression)
What happens in the analgesia 'induction' stage of anaesthesia
the patient progresses from analgesia without amnesia to analgesia with amnesia
What happens in the excitement stage stage of anaesthesia
following loss of consciousness and marked by excited and delirious activity
- heart rate may become irregular
- uncontrolled movements
- vomiting
- breath holding
- pupillary dilation
how do you reduce the adverse effects of the excitement stage stage of anaesthesia
rapidly acting drugs are used to minimize time in this stage and reach stage 3 as fast as possible
What happens in the surgical anaesthesia stage stage of anaesthesia
Patient ready: the skeletal muscles relax, vomiting stops , and respiratory depression occurs
1. eyes initially rolling, then becoming fixed
2. loss of corneal and laryngeal reflexes
3. pupils dilate and loss of light reflex
4. intercostal paralysis, shallow abdominal respiration
What happens in the overdose stage stage of anaesthesia
This results in a cessation of respiration and potential cardiovascular collapse. This stage is lethal without cardiovascular and respiratory support.
What is the risk of the excitement stage of anaesthesia?
airway compromise
what are some IV induction drugs?
propofol
sodium thiopental
benzodiazepines
ketamine
what are the volatile induction drugs?
Fluranes: sevofluranem desflurane, isoflurane, enflurane
Halothene
NO: but need too much, so its crap
what is NO? benefit? downside?
Nitrous oxide is an inorganic inhalation agent
Benefit:
- rapid onset of the inhalation agents
removed by the body through the lungs by exhalation- spares liver and kidney
- has a rapid off set as well
- minimal cardio/ resp effects
- provides additional analgesia

Downside:
- High MAC (mean alveolar conc) >100, thus it can't be used alone
- danger of hypoxia: reduces inspired O2 to 33%
- can't be used if there is respiratory disease
assess patency of airway principles
look
listen
feel
anatomical causes of airway obstruction
Tongue and pharyngeal tissues, airway oedema
foreign causes of airway obstruction
Introduced objects (false teeth, food, ect)
Body fluids (Vomitus, Blood)
Basic airway maneuvers
Position: Recovery positon

Manouvers:
- Head Tilt/Chin lift
Triple Airway Manouver (head tilt + forward displacement of mandible and seperation of lips with thumbs)
Modified Jaw thrust to protect C-Spine

Oro/Nasal-pharyngeal airways:
- Guedel
- Naso-pharyngeal tube
size of a Guedel
flange is aligned with the centre of the lips and the tip to the angle of the jaw

Large Adult 100mm (guedel size 5)
Medium Adult 90mm (guedel Size 4)
Small adult 80mm guedel size 3
complications of Guedel airways
mucosal trauma
worsening obstruction by pressing the epiglottis against the laryngeal outlet or displacing tongue more posteriorly
not to be used if gag reflex present
no protection from aspiration
complications of nasopharyngeal airways
epistaxis, aspiration
laryngospasm
oesophageal mis-placement
contra-indicated in c-spine injury or base of skull fractures, does not protect against aspiration
when are nasopharyngeal airways contraindicated
c-spine injury
base of skull fractures
why would you use a laryngeal mask airway?
to maintain airway after failed intubation before re-attempt or surgical airway insertion
good alternative to bag mask ventilation because less air enters the stomach and decreases but does not eliminate risk of aspiration
What patient factors and surgical factors affect the choice of airway management
Patient: Reactivity of patient airway, aspiration risk, history of difficult airway, use of positive pressure ventilation

Surgical:
- Position of patient
- Area of surgery
- Availability of equipment
- Length of procedure
- Use of muscle relaxants
Indications, advantages and disadvantages of endotracheal intubation
Indications:
- the need to deliver positive pressure ventilation
- protection of the respiratory tract from aspiration of gastric contents
- all situations involving neuromuscular paralysis

Advantages: patent protected airway

Disadvantages: hard to be inserted, requires use of muscle relaxant, complications
ETT sizes for adult male and female patients
Male: 8.0-9.0mm
Female: 7 .0-8.0mm
Pediatric: (age/4) + 4 mm
LMA sizes for adult male and female patients
40-50kg: 3
50 - 70kg: 4
70 - 100 kg: 5
Mallampati Classification of Oral opening
I – full view of uvula (body and base of uvula, tonsils and tonsillar pillars
II – body and base of uvula, partial view of tonsils and tonsillar pillars
III – Base of uvula, post-pharngeal wall
IV – hard palate and tongue, other structures not visable
aids for intubation: MDSOLES
Monitors
Drugs
Suction
Oxygen source and Bag-mask + nasopharyngeal or Guedel airway
Laryngoscope
ET tube
Stylet
Syringe for tube cuff inflation
how do you tell that an ETT has been placed in the trachea
- visualise the ETT passing through the cords
- bronchoscopic visualisation of ETT
- end-tidal CO2 in exhaled gas (capnograph)
- breath sounds/ chest movement
- condensation of water vapour in ETT
- refilling of reservoir bag during exhalation
- Xray- lateral is more sensitive and specific
worried about oesophageal intubation: what are the signs
end tidal CO2: zero, or near zero
wrong breath sounds, impaired chest movement
hypoxia/ cyanosis
gastric contents in ETT
distended stomach
consequences of endobrachial intubation
associated with left-sided atelectasis
right-sided tension pneumothorax
How is the airway in a child (< 1year) different from that of an adult?
o Larger tongue in proportion to mouth
o Smaller pharynx
o Larger and more flaccid epiglottis
o Larynx is more superior and anterior
o Narrowest point at cricoid cartilage
o Trachea is more narrow and less rigid
which patients are at risk of aspiration under GA
pregnant women
gastric sphincter incompetence: GORD, hiatus hernia
full stomach: emergency sx
decreased level of consciousness
steps in rapid sequence induction
1. pre-oxygenation/ denitrogentate: 100% O2 for 3-5 mins
2. Selick's manoeuvre: compress oesophagus
3. administration of induction agent then fast acting muscle relaxant
4. intubate within 45-60sec after muscle relaxant
5. must use cuffed ETT to prevent aspiration
6. inflate cuff, verify correct placement of ETT, release cricoid cartilage pressur
7. ventilate when ETT in place and cuff inflated
selick's manoeuvre
pressure on cricoid cartilage to compress esophagus between cartilage and C6 to prevent reflux/aspiration
drugs are commonly used in a rapid sequence induction
IV induction agent (usually propofol or thiopental, but can use ketamine or Etomidate, never benzos)

Rapid acting muscle relaxant (suxamethonium (sux) used primarily or rocuronium (roc))
Precautions with rapid sequence induction with potential cervical spine injury?
minimum of 3 people, but you really need 4
- cervical spine in-line immobilization should be maintained
- manual in-line axial traction
- patient lies supine with the head in neutral position; an assistant applies manual in-line immobilization by grasping the mastoid processes
C.I. to rapid sequence induction
- total upper airway obstruction
- total loss of facial/oropharyngeal landmarks
- contraindications for drugs to be used- like hyperkalaemia CI for paralytic agents like suxamethonium
Midazolam
- use
- MOA
- dose
- adverse
use: pre-op relxation, conscious sedation, IV induction
MOA: increased CL channel opening, facilitating inhibitory GABA
Dose:
- conscious sedation: 1-2.5mg
- IV induction: 0.15-0.2mg/kg
adverse: Sedation/resp depression, decreased BP, HR
Dependence
Propofol
- use
- MOA
- dose
- adverse
Use: IV induction agent and Total IV anaethesia
MOA: uncertain, thought to be at GABA
Dose: 2.5-3mg/kg
Adverse:
- allergy: soy, eggs
- hypotension
- burning feeling
Thiopentone
- use
- MOA
- dose
- adverse
Use: IV induction agent + decreases seizures
MOA: facilitates GABA be decreasing Cl- opening time (barbituate)
Dose: 3-5mg/kg
Adverse:
- barbituate allergy
- hypotension and decreased CO
- arrhythmias
- laryngospasm
Atropine
- use
- MOA
- dose
- adverse
Use: anti muscarinic, thus decreases salivation and bronchial secretions
MOA: muscarinic antagonist
Dose: 300-600mcg IM, SC, IV
Adverse: anticholinergic SE
Suxamethonium
- use
- MOA
- dose
- adverse
- reverse
Use: rapid intubation
MOA: short acting depolarising muscle relaxant, mimics ACh and binds to receptors causing prolonged depolarisation
Dose:
Adverse:
- bradycardia
- hyperkalaemia (because works at a NA/K channel)
- raised ICP
- anaphylaxis
Reverse: none
Fentanyl
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: opioid, Mu receptor agonist, same as morphine but shorter acting
Dose: 2-3 ug/kg IV
Adverse: resp depression, nausea, vmiting, dizziness, constipation, drowsiness, confusion, euphoria, miosis, hypotension, urinary retention, ECG changes, tolerance, dependence.
Morphine
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: opioid, Mu receptor agonist
Dose: 0.2-0.3mg/kg IV
0.4-0.6mg/kg PO
Adverse: Resp depression, nausea, vmiting, dizziness, constipation, drowsiness, confusion, euphoria, miosis, hypotension, urinary retention, ECG changes, tolerance, dependence.
Paracetamol
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: COX-2 inhibition
Dose: 500mg TID, q4h
Adverse: dyspepsia, nausea, allergy, hepatotoxic
Tramadol
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: weak Mu binder and inhibitis NA and 5HT reuptake
Dose: 50-100mg PO q4-6hr PRN
Adverse:
Mild: dizziness, nausea, constipation
Serious: serotonin syndrome, seizures and respiratory depression
Oxycodone
- use
- MOA
- dose
- adverse
Use: oral analgesic
MOA: opioid, Mu receptor agonist
Dose: 5-15mg PO
Adverse: same as morphine
Parecoxib
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: Cox-2 selective inhibitor
Dose: 40mg IV
Adverse: GI, N&V, renal toxicity, increased risk of MI
Ibuprofen
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: COX-1 and COX-2 inhibition
Dose: 200-600mg TID
Adverse: nausea, tinnitus, vertigo, rash, dyspepsia, GI, renal toxicity
Ketamine
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: acts on NMDA, opiate and other
Dose: induction 1-2mg/kg
Adverse: arrhythmias, increased/decreased BP & HR, apneoa, laryngospasm, diplopia, nystagmis, hallucinations
Codeine
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: opioid, Mu receptor agonist
Dose: 15-30mg PO
Adverse: same as morphine
Hydromorphone
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: opioid, Mu receptor agonist
Dose: 40-60ug/kg IV, 2-4mg PO
Adverse: same as morphine
Methadone
- use
- MOA
- dose
- adverse
Use: analgesic
MOA: opiod, Mu receptor agonist
Dose: 5-10mg q6-8hr
Adverse: same as morphine
Metoclopramide
- use
- MOA
- dose
- adverse
Maxolon
Use: antiemetic
MOA: D2 antagonist
Dose: 10mg IM q2-3 PRN
Adverse: drowsiness, fatigue, insomnia, headache, dystonic reactions
Prochlorperazine
- use
- MOA
- dose
- adverse
Use: antiemetic
MOA: dopamine antagonist
Dose: 5-10mg PO/N/ IM BD, TID PRN
Adverse: constipation, dry mouth, drowsiness, akathisia, parkinsonism, blurred vision, EPSE (especially in children), hypotension, hyperprolactinaemia
Ondansetron
- use
- MOA
- dose
- adverse
Use: antiemetic
MOA: 5HT3 antagonists
Dose: 8mg PO BD
Adverse: headaches, flushing, constipation, seizures, movement disorders
Tropisetron
- use
- MOA
- dose
- adverse
Use: antiemetic
MOA: 5HT3 antagonists
Dose: 2mg IV
Adverse: headache, fatigue, dizziness, GI upset, anorexia, hypersensitivity
Droperidol
- use
- MOA
- dose
- adverse
Use: antiemetic
MOA: D2 antagonist, neuroleptic
Dose: 2.5-10mg IVI 30-60mins preop
Adverse: hypotension, drowsiness, extrapyramidal SE
Dexamethasone
- use
- MOA
- dose
- adverse
Use: antiemetic, chemotherapy-induced nausea and vomitin
MOA: steroid
Dose: 2.5mg PO
Adverse: steroid side effects
Lignocaine
- use
- dose
- duration of action
Use: local anaesthetic, rapid onset (5-10mins)
Dose: 5mg/kg
Duration of action:1-3hr
Bupivacaine
- use
- dose
- duration of action
Use: local anaesthetic, slow onset (10-15mins)
Dose: 2.5mg/kg
Duration of action: 3-8hr
Ropivacaine
- use
- dose
- duration of action
Use: local anaesthetic, moderated onset (10-15mins)
Dose: 3-4mg/kg
Duration of action: 8-13hr
What are the non-depolarising muscle relaxants?
Use:
Reversal:
Rocuronium
Mivacurium
Vercuronium
Cistracurium
Pancuronium

Use: longer acting, used during sx
Reversal: cholinesterase inhibitors: neostigmine, pyridostigmine, edrophonium
Symptoms of LA toxicity?
CNS: numbness of tongue, metallic taste, disorientation, drowsiness, tinnitus, visual disturbances, muscle twitching, tremors, unconsciousness
CVS: vasodilation, hypotension, decreased myocardial contractility, arrhythmias, CVS collapse
Mgt of LA toxicity
100% O2 and aBC
Increase seizure thresh hold: diazepam, propofol, sodium thiopental
Level for lumbar puncture?
L3-4, L4-5
Malignant hyperthermia: pathology
calcium channel ryanodine receptor mutation.

If given sux or certain volatile agents, there will be a drastric increase in skeletal muscle O2 consumption
Prophylaxis for GORD
Risk: aspiration
Prophylaxis:
- sodium citrate 30mL PO or
- ranitide 150-300mg PO
30-60mins preop
continuous monitoring (pt under sedation)
1. oxygenation: pulse oximetry, FiO2
2. ventilation: ETT properly placed, chest movement, tidal CO2 analysis
3. Circulation: pulse, heart sounds, BP, telemetry, CVP, pulmonary capillary wedge pressure
triad of GA
unconsciousness
loss of reflexes
analgesia
defn: loss of consciousness
amnesia
propofol: use
IV induction agent: provide amnesia and blunt reflexes
Maintenance
Total IV anaesthesia
propofol: MOA
inhibitory at GABA synapse
decreases cerebral metabolic rate and blood flow
decreases ICP
decreases BP
propofol: dose, special paramaters
IV: 2.5-3.0mg/kg, less with opioid or premed
propofol: affect on BP
0-30% decrease in BP due to vasodilation
sodium thiopental: use
IV induction agent
control of convulsive state
propofol: t 1/2
0.9hr
sodium thiopental: class
ultra short acting thiobarbiturate- hypnotic
sodium thiopental: MOA
decreased Cl opening time, enhancing GABA and suppressing glutamic acid
sodium thiopental: dose
3-5mg/kg
sodium thiopental: t1/2
t1/2: 5-12 hr
which muscle relaxant can you not use sodium thieopental with and why?
thiopental + rocuronium causes precipitate to form
ketamine: use
IV induction agent
maintenance agent
ketamine: MOA
acts on NMDA, opiate and other receptors
increases HR,
increases BP
increases SVR
increases coronary flow
increases myocardial O2 uptake
produces CNS and resp depression and bronchial smooth muscle relaxation
ketamine: dose
induction 1-2mg/kg
ketamine: t1/2
t1/2: 3hr
which induction agent can be used for severe asthma?
ketamine: bronchial smooth muscle relaxation
midazolam: use
sedation
amnesia
anxiolysis
midazolam: MOA
benzo
increases glycine inhibitory neurotransmitter, facilitating GABA
anti anxiety effects
skeletal muscle relaxant
minimal cardiac depression
midazolam: t1/2
variable, somewhat unpredicatble
MAC
minimal alveolar concentration:
the alveolar concentration of an agent at one atmosphere of pressure that will prevent movement in 50% of patients in response to surgical stimulus
least soluble in blood to most of volatile induction agents
least:
- NO
- desflurane
- sevoflurane
- isoflurane
- halothane
Most
which type of induction agents are most used surgically, and which in ICU?
surgical: inhalation
ICU: injectable
what determines the speed on onset of volatile induction agents?
1. solubility
2. cardiac output
3. partial pressure difference between alveolar and venous blood
4. inspired gas concentration
5. alveolar ventilation
6. second gas effect: when two gasses are administered together, eg. NO and desflurane
who is at greater risk of atlantoaxial subluxation?
RA
DS
complications of guedel airway
mucosal trauma
worsening obstruction- epiglottis, tongue lodged wrong
no protection from aspiration
when do you use a guedel instead of a nasopharygneal airway
when the gag reflex is present
when do you use a nasopharygneal instead of a guedel airway
semi conscious pt
suspected c-spine injury
suspected base of skull #
what kind of basic airway eliminates the risk of aspiration?
laryngeal mask airway
what is central venous cannulation?
a large cannula placed in a large venous branch (femoral/ neck/ thoracic) for administration of drugs/ fluids and to measure central venous pressure
where can you put a central venous cannulation?
internal jugular
subclavian vein
femoral vein
what site of central venous cannulation accurately represents intrathoracic central venous pressures? when does this not apply?
femoral

not in pregnant patients
complications of central venous cannulation?
insertions stuff: pneumothorax, haemothorax, chylothorax
vein thrombosis
thrombophlebitis
infection
which site of central venous cannulation has the highest risk of DVT and bacterial colonisation?
femoral
what are the three modes of mutli-modal analagesia
1. reduce nociceptive input: NSAIDs, local anaesthetics
2. spinal cord inhibition: opioids, NSAIDs, gabapentanoids, NMDA receptor antagonists or the others that act on the descending pathway
3. central acting: opiates, paracetamol
Pain: cv and resp risks
CV: sympathetic nervous system activated releases adrenaline and noradrenaline, resulting in increased HR and BP

Resp: decreased depth of breathing can lead to atelectasis and predispose to pneumonia
Pain: stress response and why its bad
increased cortisol release: impair immune function and increased glucose tolerance
advantages of patient controlled analgesia
better pain control
fewer side effects
accommodates patient variability of pain response
accommodates changes in opioid requirements
disadvantages of patient controlled analgesia
not appropriate for all patients: confused, critically ill, mentally disabled
features of opioid overdose
decreased consciousness
decreased respiratory rate
respiratory acidosis
mgt opioid overdose
ABC
Naloxone administration (t1/2: 1hr)
Naltrexone (t1/2: 10hr)
10mg morphine IV= ? PO
20mg PO
10mg morphine IV= ? fentanyl IV
100ug Fentanyl IV
how is hypothermia related to blood loss
blood loss is increased due to reduced platelet function and impaired activation of coagulation cascade
how does the body regulate body temp?
hypothalamus receives input about body temp and adjusts the internal thermostat accordingly
four ways that heat is lost from the body
conduction
convection
radiation
evaporation
define hypothermia
body temp <36
negative impact of hypothermia on the body
1. increased infection risk: immune function impaired at low temp
2. delayed healing
3. increased blood loss: reduced platelet function and impaired activation of coagulation cascade
4. 3x risk of VT and morbid cardiac events
5. decreased metabolism of anaesthetic agents, prolongs post-op recovery
how to minimize heat loss in unconscious pt
warming blankets
warmed replacement fluids and blood products
3 components of emesis pathway
1. afferent inputs to the CNS, from emetic stimuli
2. CNSL receives, recognises and processes the signal
3. motor and chemical efferent pathways produce a coordinated respiratory, GI and abdo muscle expulsion action
what are the two centres for vomiting in the brain
1. chemoreceptor trigger zone: recognizes the stimuli and sends stimuli to the intergrative vomiting centre
2. integrative vomiting centre: coordinates the action
where are the vomiting centres in the brain? how many are there?
medullary centres, there are 2:
1. chemoreceptor trigger zone
2. integrative vomiting centre
is vomiting controlled by somatic or autonomic systems?
both
what surgical, anaesthetic and patient factors increase the risk of post op nausea and vomiting?
surgical: abdo and gynae sx
anaesthetic: inhalation anaesthetics, opioids, large dose neostigmine
patient factors: motion sickness, female, non-smoker, young adult and childhood after infancy
Metoclopramide: MOA
D2 antagonist
Prochlorperazine: MOA
D2 antagonist
Ondansetron: MOA
5HT3 antagonist
Tropisetron: MOA
5HT3 antagonist
Droperidol: MOA
D2 antagonist
Neuroleptic
Dexamethasone: MOA
steroid
Which antiemetics can produce hyperprolactinaemia?
metoclopramide and prochlorperazine
what space does a spinal anaesthetic go into?
subarachnoid space: between the arachnoid membrane and the pia mater
what space does an epidural go into?
epidural space: between the ligamentum flavum and the dura mater
how to local anaesthetics work?
bind to cytosolic receptor site of Na channels, inhibiting Na influx into tissues

they block the generation and propagation of impulses in excitable tissues, nerves, skeletal muscle, cardiac muscle and brain
why is adrenaline added to local anaesthics
adrenaline causes vasoconstriction - reduces bleeding and drug clearance which therefore prolongs the effects of the local anaesthetics
LA toxicity: seizures not controlled with diazepam, propofol or sodium thiopental, what can you do?
Need to intubate: use succinylocholine to aid this
Also:
Manage arrythmias
LA toxicity + circulatory arrest: emergency mgt
IV lipid emulsion 20% to bind local anaesthetic
if you use spinal anaesthetic, does the patient need more or less peri-operative analgesia?
less
when are epidural blocks used?
procedures involving the lower limbs, pelvis, perineum and lower abdomen
a cathetor for anaesthesia is used for spinal or epidural anaesthesia?
epidural, this can allow for patient controlled anaesthesia as well.
O2 in air and expired gas/breath
air: 21%
expired gas: 15%
Fixed or variable performance?
- nasal prongs
- hudson mask
- venturi mask
- non-rebreather mask
Variable
- nasal prongs
- hudson mask
- non-rebreather mask

Fixed
- venturi mask
Nasal prongs: max flow and FiO2
max flow: 5L
max FiO2: ~0.4
Hudson mask, aprox FiO2 for 2L, 4L, 6L, 10L
2L: 0.28
4L: 0.35
6L: 0.40
10L: 0.55
benefit of a venturi mask?
fixed performance device, thus you can control the FiO2

important in CO2 retainers or to control FiO2 to measure blood gases
CO2 retainers and O2 delivery: what are we afraid of?
hypercarbic respiratory failure
cause of hypoxic hypoxia
decreased O2 saturation of normal heamoglobine: high altitude, hypoventilation, V-Q mismatch, diffusion abnormality
cause of stagnant hypoxia
blood flow is insufficient
causes of anaemic hypoxia
low concentration of heamoglobin
causes of histotoxic hypoxia
inability of cells to take up or utilize oxygen from the bloodstream eg. in cyanide poisoning
crystalloid vs colloid fluids
crystalloid: salt containing solutions that distribute within the ECF
colloid: donor blood products or synthetics that distribute within the intravascular volume
plasma osmolality
285-295 milli-osmoles/kg
70kg male:
total body water?
intracellular fluid volume?
extracellular fluid volume?
plasma volume?
70kg male:
total body water: 50-60%- 45L
intracellular fluid volume? 2/3- 30L
extracellular fluid volume? 1/3- 15L
plasma volume? 1/4 vascular- 3L
ADH: what does it do?
incorporates water channels in the kidney collecting ducts to increase reabsorption of water.
ADH regulation:
increases:
receptors in hypothalamus and stretch receptors in the aorta and carotid bodies

decrease:
stretch receptors in the atria
aldosterone
aldosterone increases sodium reabsorption at the distal tubule, and thus water reabsorption
what are a pts required electrolyte needs per day
Na: 3mEq/kg/day
K: 1 mEq/kg/day
fluid replacement: maintenance amounts
4:2:1
4ml/kg/h first 10kg
2ml/kg/h next 10kg
1ml/kg/h for all the other kg
assessing dehydration: mild
dry oral mucosa
thirst
mild decrease in skin turgor
urine output decreased
assessing dehydration: moderate
heart rate increased
oliguria
assessing dehydration: severe
tachycardia
pulse weak
hypotensive
slow cap refill
% blood loss per grade
I: <15%
II: 15-30%
III: 30-40%
IV: >40%
level of consciousness by grade of blood loss
I: anxious
II: agitated
III: confused
IV: lethargic
define massive transfusion
more than 1x blood volume in 24hr
or
more than 50% blood volume in 4hr
complications of massive transfusion
infection risk
hypervolaemia
electrolyte changes- K+ is increased in stored blood
dilutional coagulopathy or thrombocytopeania
hypothermia
anticoagulant reactions
iron overload
transfusion related immunosuppression
immune transfusion reactions
types of shock
1. hypovolaemic
2. septic
3. cardiogenic
4. neurogenic
most common causes of anaphylaxis in the operating theatre
inhalation anaesthetics
injectable anaesthetics
pain meds
any drug
latex
transfusion of blood product
mgt moderate anaphylaxis in ot
adrenaline (1:1000) 0.3-0.5mg SC
antihistamines
salbutamol nebulised
mgt of severe anaphylaxis in ot
ABC
EET
adrenaline (1:1000) 0.3-0.5mg IV push PRN
antihistamines IV
steroids: hydrocortisone 100mg IV
crystalloid resus
vasopresser
any medications that raise blood pressure
inotrope
any medication that increases contraction of the heart
adrenaline: receptors
a-1
a-2
B-1
B-2
noradrenaline: receptors
a-1 & a-2 primarily
B-2: weak
dobutamine: receptors, action
a-1
B:1: main
inotrope
Metaraminol: receptor, use
B-1
Dopamine: receptor, use
B-1: main
a-1
a-2

inotrope at high dose
Phenylephrine: receptor, use
a-2
vasopressor
Ephedrine: receptor, use
a-1
vasopressor
mostly used for nasal congestion
how are adverse events documented in NSW
NSW health incident information management system (IIMS)
MET criteria
SBP<90 or mean <70
HR >140 or <50
O2sat <90% despite O2 therapy
RR >30 or <8
GCS <12 or drop by 2 points
Urine <0.5ml/kg/hr
concerned experience nurse