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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) |
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genetic condition causing adverse anaesthetic reaction
|
malignant hyperthermia
|
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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?
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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 |
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what are the different components of anaesthesia
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analgesia
amnesia muscle relaxant abolition of autonomic reflexes maintenance of homeostasis |
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triad of GA
|
1. unconsciousness (anaesthesia)
2. loss of reflexes (muscle relaxant) 3. analgesia |
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four stages of anaesthesia
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Stage 1: Anaelgesia 'induction' phase
Stage 2: Excitement stage Stage 3: Surgical anaesthesia Stage 4: Overdose (severe brain stem or medullary depression) |
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What happens in the analgesia 'induction' stage of anaesthesia
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the patient progresses from analgesia without amnesia to analgesia with amnesia
|
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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 |
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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
|
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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 |
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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.
|
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What is the risk of the excitement stage of anaesthesia?
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airway compromise
|
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what are some IV induction drugs?
|
propofol
sodium thiopental benzodiazepines ketamine |
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what are the volatile induction drugs?
|
Fluranes: sevofluranem desflurane, isoflurane, enflurane
Halothene NO: but need too much, so its crap |
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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 |
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assess patency of airway principles
|
look
listen feel |
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anatomical causes of airway obstruction
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Tongue and pharyngeal tissues, airway oedema
|
|
foreign causes of airway obstruction
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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 |
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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 |
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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 |
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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 |
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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 |
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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 |
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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
|
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sodium thiopental: dose
|
3-5mg/kg
|
|
sodium thiopental: t1/2
|
t1/2: 5-12 hr
|
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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 |