anaesthetics Flashcards
structure for dealing with anaesthetic related exam question?
A: airway - patent, or obstructed? do they need an ETT or can they sustain own airway - Mask
B: breathing: breathing on their own? maintained - - mask or LMA.
need mechanical ventilation: ETT
C: CVS - anaesthetic drugs - decrease CVS + resp - therefore monitor
LMA means?
laryngeal mask airway
ETT means?
endotracheal tube
3 steps prior to anaesthetic + op?
considerations
pre-op assessment
optimising
Considerations (pre-op)
Pt: risk - assess, high risk, minimise risk.
Info: informed consent - reduce anxiety etc
surgery: deal with the stress, blood loss, fluid shifts,
anaesthetic - ADRs, coma, CVS,CNS, resp problems
pre-op assessment
hx - known + unknown co-morbs - severe? control.
d+a
prev surg + prev anaesthetic problems
ex - ASA grading
exercise tolerance:
METs
investigations
exercise tolerance within pre op assessment?
MET - metabolic equivalents
2: walk around house
5: walk up hill , stairs
9: strenuous exercise
point of investiigations in pre-op assessment
establish baseline for post op monitoring.
aspects of optimisation
- optimise: IHD, DM, COPD, HTN, asthma, epilepsy
- do not stop
anti epileptics, inhalers,
anti-anginas - stop DM meds - pts done 1st
- anticoagulants stopped if secondary
triad of anaesthesia
hypnosis (unconscious)
analgesia
muscle relaxants
if muscle relaxants used must have?
mechanical ventilation - ETT
and hypnosis - unconscious pt
Rapid onset IV induction agent?
propofol - readily distributes, fat soluble and crosses BBB
inhaled agent - for maintenance?
halogenated hydrocarbons - want a low MAC - minimum alveolar concentration - potent drug
common side effects of anaesthetic drugs - what should always be monitored
- CVS: cause vasodilation (decreased TPR + BP) & venodilation (decreased venous return + CO)
- resp: increased RR + decreased tidal volume/
reduce hypoxic and hypercapnic drive
what anaesthetic drug doesn’t depress the CVS + resp systems?
ketamine
indications for muscle relaxants
- neurosurgery (tight control of sats)
- open cavity surgery - laparotomy
- microscopic surgery
- when ventilation + intubation are required
local anaesthetic - limiting factor
toxicity
aspects to help induction
quiet room /anaesthetic room
noise can trigger laryngospasm
how do you monitor consciousness?
loss of verbal contact lack of movement resp pattern EEG stages of anaesthesia
1st stage of anaesthesia?
stage 1: induction - between induction of agents + loss of consciousness
can still be communicating
2nd stage of anaesthesia?
excited + delirious - resp + CVS become irreg.,
rapidly acting drugs are used to minimise the time spent in this stage
3rd stage of anaesthesia?
surgical anaesthesia - skeletal m relaxes, resp depression,
4th stage of anaesthesia?
overdose
severe brainstorm/medulla depression - resp ceases, potential cvs collapse
simple airway management options?
- face mask (triple airway manoeuvre)
- oropharyngeal airway (feudal) must be unconscious
- nasopharyngeal airway
advanced airway management?
- LMA: supraglottic - therefore does not protect the airway from aspiration or laryngospasm (where the vocal cords adduct)
ETT allows for…
protection from gastric contents
muscle relaxants to be used
neurosurg - tight blood gas control
airway complications?
aspiration
airway collapse - laryngospasm
risks of unconsciousness?
hypothermia pressure sores hypoxia loss of protective reflexes VTE airway collapse
monitor what?
Sp02, ECG,BP, Fi02, ETCO2, resp parameters, agent monitoring, temp, Urine output, NMJ, invasive venous / arterial monitoring, ventilator disconnect
emergence substance?
sevoflurane
gas - commonly used in paeds + emergencies
types of pain?
chronic (>3wks), + acute
cancer + non cancer
nociceptive pain is?
obvious tissue injury or illness, normally well localised
neuropathic pain description?
damaged or abnormal nervous system - described as burning, numbness, not well localised
neuropathic pain tx?
does not respond to WHO pain ladder
example of causes of neuropathic pain
nerve trauma
dm
fibromyalgia
chronic tension headache
physiology of peripheral pain
tissue injury –> release of prostaglandin - stimulation of nociceptors - signal A delta + C fibres to spinal cord
spinal cord pain physiology
dorsal horn (1st delay) fibres synapse - decuss at that level. ascend spinothalamic tract
brain physiology of pain
thalamus –> cortex - pain perception
physiology of pain modulation
descending pathway - gate theory: activation of inhibitor interneurone between nociceptor fibres and large distractive nerve fibre
spinal cord pain tx
local anaesthetic
opioids
ketamine
WHO pain ladder
- non opioid - aspirin, paracetamol
- weak opioid: codeine
- strong opioid: morphine,fentanyl