Anaesthetics notes Flashcards
Mendelson’s syndrome and main RF
chemical pneumonitis due to aspiration of reflux during anaesthesia.
Main RF = pregnancy
what is sellick’s maneovre
This involves digital pressure against the cricoid cartilage of the larynx, pushing it backwards. The oesophagus is thus compressed between the posterior aspect of the cricoid and the vertebrae behind. The cricoid is used because it forms the only complete ring of the larynx and trachea.
The cricoid is located at the level of C6. Moderate pressure may be applied before loss of consciousness, and firmer pressure maintained until the cuff of the tracheal tube is inflated.
risks of anaesthesia in early and late pregnancy
early - teratogenicity of drugs, spontaneous miscarriage
late - preterm labour, reflux, failed intubation
mandatory manovres for people with reflux
RSI with cricoid pressure
starvation for 6hrs
if obstetric, also use h2 antagonist and ppi (evidence is sparse)
what physical airway problems can there be in pre-op assessment
congenital (pierre robin/treacher collins) neck fusion (ank spond/arthritis) neck instability (fractures, atlantoaxial instability)
can you have halothane more than once in your life?
Yes, but not more than once in any 3 month period
it is rarely used in uk anymore
important things to elicit in family history
suxamethonium apnoea
malignant hyperthermia
inherited porphyria
dystrophia myotonia
what is suxamethonium apnoea
Sux is a neuromuscular blocker
plasma cholinesterase activity is reduced in some people due to either genetic variation or acquired conditions, which results in a prolonged duration of neuromuscular block.
physiology of malignant hyperthermia
mutation of the ryanodine receptor (type 1), located on the sarcoplasmic reticulum (SR), the organelle within skeletal muscle cells that stores calcium.[10][11] RYR1 opens in response to increases in intracellular Ca2+
level mediated by L-type calcium channels, thereby resulting in a drastic increase in intracellular calcium levels and muscle contraction.
symptoms of malignant hyperthermia
Symptoms include muscle rigidity, high fever, and a fast heart rate.[1] Complications can include rhabdomyolysis and high blood potassium
what does smoking increase the risk of in terms of anaesthetic worry
bronchospasm due to reactivity of airways and increased mucus production
and the carboxyhaemoglobin doesn’t help
how does chronic alcohol use affect anaesthetic
tolerance to sedation so may need more
what is thyromental distance
Thyromental distance (TMD) measurement is a method commonly used to predict the difficulty of intubation[1] and is measured from the thyroid notch to the tip of the jaw with the head extended.[2] If it is less than 7.0 cm with hard scarred tissues, it indicates possible difficult intubation
how to do pre-op assessment
- confirm patient details and procedure and consent
- how are you doing today
- SR (incl pregnancy)
- PMH/PAH
Anything you see GP for
Breathing problems (COPD,asthma)
Circulatory problems (heart, lungs, kidneys, peripheral arterial)
Diabetes and stroke
Everything else (haematology)
ANY PREVIOUS REACTIONS TO ANAESTHESIA - DH. current med, allergies
- FH. anaesthetics, malignant hyperthermia, sux reaction, porphyria
- SH. how are you getting home. alcohol. smoking.
- ICE
examination
- general
- airway (dentition, thyromental distance, mallampati score, range of neck movement)
- lungs, heart, pulse
Main anaesthetic risk factors
ASS PRICHAD
age (risk of death doubles every 7 years over the age of 10) sex (men 1.7x) socioeconomic status (poor 2x) (conditions 1.5x) peripheral arterial disease, renal disease ischaemic heart disease, cerebrovascular disease, heart failure, aerobic fitness, diabetes (3x for type 1, 2x for type 2)
do you stop aspirin before surgery
only if on the brain, spinal cord or prostate. in which case you stop it 5 days before
do you stop statins
no
do you stop amlodipine
no
do you stop ACEi
why
often omit the morning dose prior to surgery
Patients taking ACE inhibitors are more likely to have profound hypotensive episodes with regional and general anaesthesia.
Many anaesthetists will stop ACE inhibitors in patients at risk of major haemorrhage or those planned for epidural anaesthesia.
do you stop diuretics
no
do you stop warfarin
you can continue it in following scenarios because of low risk of bleeding:
- eye
- dental
- endoscopies
otherwise, replace warfarin with SC heparin and INR should be <2 before surgery
do you stop clopidogrel
yes, 5 days before surgery
do you stop digoxin
depends, check toxicity prior to surgery and plasma K+
do you stop diabetic drugs
long acting drugs are normally stopped, yes. Often around surgery permissive hyperglycaemia is allowed as risk of hypo is too great.
do you stop steroids (e.g. in adrenal insufficiency)
no, you give extra to account for the stress
do you stop anticonvulsants
no, you give the normal dose 1hr before surgery
do you stop COCP/HRT
why
yes, 4 week prior to surgery
for risk of VTE
do you stop SSRIs
no
but in high risk CNS surgeries, you should stop it 3 weeks prior
should you stop smoking and why
YES. perioperative chest infection is 6x more likely
risk of surgery =
underlying fitness (ASA/6) + extent of surgery (surgical score/4)
to whom do you do the following pre-op investigations:
- fbc
- U/E
- G/S
- LFT
- glucose
- clotting
- virology
- sickle cell test
- tft
- ABG/pul function
- ECG
- CXR
- echo
- pregnancy
- cardiac investigation
fbc = 60+SS2, SS3
U/e = 60+SS3, SS4, major trauma, burns, on diuretics
G/S = SS2
LFT = in jaundice, alcohol abuse, malignancy
glucose = in diabetes
clothing = if bleeding or if on warfarin/heparin
virology = if HIV or hepatitis
sickle test = patients of african or asian descent or if family history
tft = thyroid disease
abg/pulfun = ASA3
ECG = 60+SS3
CXR = rest disease or pathology
echo = murmur or HOCM
pregnancy = any woman of child bearing age
cardiac investigation if can’t walk up stairs or if surgical grade is 4
what’s involved in ‘cardiac investigations’ pre-op
exercise testing
treadmill ECG
dobutamine stress echo
myocardial perfusion scanning
ASA grading
1 = normal healthy patient 2 = mild systemic disease 3 = severe systemic disease 4 = threat to life 5 = moribund patient (will die regardless of surgery) 6 = braindead
surgery severity grading
1 = endoscopy/laparoscopy/biopsy 2 = hernia repairs, arthroscopies 3 = hysterectomy, TURP, thyroidectomy 4 = joint replacement, colonic resection, artery reconstruction, neck dissection
what to do if needlestick injury
wash wound with soap and water immediately
let it bleed
consult local policy
what are the 3 checklist stages in an operation
Check-in = before aneathesia
Time-out = before knife to skin
Check out = after last suture
3 types of coma
- with focal neurology
- with meningism
- coma alone
when do you put a collar on if worried about C-spine
although you can do MIL straight away, you only put a collar on once airway is secure
what conservative B management is there
sit patient up
fluid challenge dose
500ml warmed hartmans solution over 15 mins
how many fluid challenges can you give until you do something else
2L can be given before you need to cross-match blood
GCS calculation
Eyes /4 A = 4 V = 3 P = 2 U = 1
Voice /5 oriented = 5 confused = 4 words don't make sense = 3 noises = 2 nothing = 1
Motor /6 commands = 6 localises to pain = 5 flexes to pain = 4 abnormal flexion = 3 abnormal extension = 2 nothing = 1
walk me through basic life support
DRABC
danger response "hello can you hear me" airway = head tilt chin lift breathing = listen for 10s CPR = 120bpm at 30:2 with ventilations coming from a bag valve mask with 15L oxygen running into bag
defibrillator (one pad under right clavicle and other on apex of heart). if shockable give it and then CPR for 2 mins and shock again if poss
what are 2 shockable and 2 non-sociable rhythms
VT and VF are shockable
pulseless electrical activity and asystole are non-shockable
what is the shock algorithm if shockable
If shockable:
- shock
- cpr for 2 mins
- shock
- cpr for 2 mins
- shock
- cpr for 2 mins and give adrenaline 1mg and amiodarone 300mg
what do you do if not shockable
continue CPR
give 1mg adrenaline every 3-5 mins
check for rhythm every 2 mins
8 reversible causes of cardiac arrest
4H’s and 4T’s
hypoxia
hypothermia
hyperkalaemia
hypovolaemia
tamponade
thombosis
toxins
tension pneumothorax
what is the apacheII score
looks at:
age
chronic health status
12 physiological values
to determine mortality in intensive care
what are the two ways to approach treating a critically ill patient
resus drill (ABCDE)
systemic drill (doing each system one by one - better for more stable patients)
CPAP vs BiPAP
CPAP helps recruit alveoli that are closed and so is good for hypoxia and LV failure.
BiPAP cycles between high pressure when patients starts a breath and resting CPAP pressure. this increases the tidal volume and helps get rid of CO2. this is good in type II respiratory failure (COPD, fatigue in asthma, neurological causes).
type 1 vs type 2 resp failure
Type 1 = hypoxic
- VQ mismatch (air is getting to alveoli but can’t get to blood)
- pneumonia, pul oedema, PE, asthma, emphysema, pul frbosis, ARDS
type 2 = hypoxic & hypercapnia
- alveolar hypoventilation
- fatigue in asthma/COPD. neuromuscular stuff, opioids, thoracic wall problems like flail chest.
think that type 1 has 1 thing wrong, type 2 has 2 things wrong.
calculating oxygen delivery
The oxygen of blood can be calculated by:
O2 content = O2 in Hb + O2 dissolved
O2 content = (Hb (g/dL) x SaO2/100 x1.34) + (PaO2 (KPa) x0.0225)
Oxygen delivery can be calculated by:
O2 delivery = CO (L/min) x O2 content (ml/100ml)
MAP =
2 equations
MAP = CO x TPR
MAP = 2/3(diastolic) + 1/3(systolic)
what type of shock is hypotension, bradycardia and warm skin
neurogenic shock (loss of sympathetic tone)
systemic vascular resistance in: - hypovolaemic shick cardiogenic shock - septic shock - anaphylactic shock
high
high
low
low
treating haemorrhagic shock
1. ABCDE • Stop bleeding if possible • Pelvic binder? Tourniquet? Pressure 2. High flow oxygen 3. IV access 4. Fluid challenge 5. Major haemorrhage protocol 6. Cross-matched blood • 1:1 ratio of RBC: Platelets 7. Discuss with haematology
treating anaphylactic shock
- ABCDE (Airway important – intubate if obstruction imminent)
- 100% oxygen
- Remove cause + raise feet
- Adrenalin IM 0.5mg (0.5mL of 1:1000)
• Repeat every 5 min if needed (guided by observations) - Secure IV access
- Chlorphenamine (antihistamine) 10mg IV and hydrocortisone (steroid) 200mg IV
- IVI Saline
• 500mL over 25min (up to 2L may be needed)
• Titrate against BP - Wheeze -> treat for asthma
- No improvement refer to ITU
- Further management
• Mast cell tryptase
treating septic shock
- ABCDE
- Titrate O2 to give saturation of >94%
- Insert two large bore cannulas and take 2x peripheral blood cultures (plus urine,
sputum, CSF depending on source – but don’t delay) - Lactate
- Antibiotics within 1h
• Empirical if no clear source: Tazocin, Gentamicin and vancomycin (if MRSA) - Fluid bolus
• 500mL over 25min (challenge) – crystalloid (Hartmann’s, 0.9% saline) - Monitor urine output
SIRS criteria
HR >90
RR >20
WCC >12
temp >38 or <36
Abx in sepsis 6 if no clear source
tazocin, gentamicin and vancomycin
what does BE represent
the amount of acid you need to add to get the blood sample back to normal acidity. + means you add that amount, - means you need to remove acid
So the more negative it is, the more acidic the sample is
average deadspace in a man
150ml
what is total headspace made up of
anatomical deadspace (airways) and physiological deadspace (unopened alveoli)
normal V:Q ratio
0.95
what is Hypoxic pulmonary vasoconstriction
lung vasculature, in areas of hypoxia, constrict to prevent V/Q mismatch occuring
does increasing FiO2 in a shunt area help?
No, because if V/Q is very low, no inhaled air is getting to the area anyways so it doesn’t matter if you raise FiO2
sats in arterial and venous normal blood
100%
75%
what is the Haldane effect
deoxy blood has higher CO2 affinity than oxy blood.
this is good because in the peripheries when O2 is low, it will pick up CO2. And in the lungs when O2 is high, CO2 will be offloaded
what is the Bohr effect
describes the oxy-affinity curve shifting right when there is:
- high temperature
- acidity
- CO2
- 2,3-DPG.
this is useful because all these things are around metabolically active cells, and they all cause affinity of Hb to decrease, therefore giving oxygen to the cells that need it
what increases 2,3-DPG
chronic hypoxia
how does hypoxia affect:
- coronary arteries
- peripheral vascular resistance
- HR and CO
- kidneys
- brain
- coronary vasodilation
- decreased (predominantly through splanchnic)
- increased
- kidneys activate RAAS and EPO
- dilation and increased blood flow
how do you give oxygen in a critically unwell patitnt
15L non-rebreathe.
do ABG and titre down to target sats (esp. if CO2 retainer) when more stable
so don’t worry about COPD target sats in first instance.
normal fluid losses in a day
1800-2500ml
fluid requirement per hour for adults based on weight
4ml/kg/hr for first 10kg
2ml/kg/hr for next 10kg
1ml/kg/hr for rest
this is v similar to the pads calculation of:
100ml/kg/day for first 10kg
50ml/kg/day for first 10kg
20ml/kg/day for rest
crystalloid vs colloid fluid
Crystalloids and colloids are the primary options for intravenous fluid resuscitation. Crystalloids fluids such as normal saline typically have a balanced electrolyte composition and expand total extracellular volume. Colloid solutions (broadly partitioned into synthetic fluids such as hetastarch and natural such as albumin) exert a high oncotic pressure and thus expand volume via oncotic drag. Colloids contain large proteins so therefore do not pass from the plasma to the interstitial to keep infused fluid largely in circulation.
Restoring the circulation with these fluids is rapid and sustained.
crystalloids are the hartmans, saline, 5% glucose
colloids are blood, starch or gelatin based
why are the 5% and 4% glucose crystalloids not suitable for resus
glucose is taken rapidly into the cells to the fluid left has no oncotic pressure and so very little stays in the plasma - it all goes into the intracellular space
what 3 things control [H+]
ventilation
renal bicarb
buffering by bicarb, sulphate, haemoglobin
how does malignant hyperthermia affect ABG
causes an acute respiratory acidosis
standard vs actual bicarbonate
standard bicarbonate is the bicarbonate concentration under standard conditions of 40 mmHg pCO2, temperature of 37 degrees Celsius and saturated with oxygen. The term standard bicarbonate was introduced by Jorgensen and Astrup in 1957.
The actual bicarbonate is the concentration of bicarbonate in the blood. In acid-base measurements, the bicarbonate concentration is not measured but is calculated from the pH and the pCO2 using the Henderson-Hasselbach equation.
what happens to standard and actual bicarbonate when CO2 drops
The actual bicarbonate decreases as a physiochemical response to the fall in CO2, but not the standard bicarbonate.
remember CO2 + H2O becomes bicarb so it makes sense that when CO2 drops so does bicarb
which of the fluids is basically just water
5% glucose - because the glucose is rapidly take up and metabolised, leaving just the water and no electrolytes
number of ATP for each glucose in aerobic and anaerobic respiration
38
2
in what regions (in terms of V/Q) does increasing FiO2 actually help arterial o2
when V/Q is low (but not zero as with shunts)
if a CO2 retainer is started on oxygen, how long should it be before an ABG is done
30-60mins
when should you reduce a patient off oxygen
when sats have been stable for 4 hours
how do you monitor when reducing oxygen
check sats after 5 mins and after 1 hour
what is fixed performance device vs variable performance device in terms of oxygen delivery mean
fixed = constant FiO2 no matter how hard patient is breathing. Venturi mask, thanks to Bernoulli effect/
variable = if you breathe hard and fast, amount of oxygen % goes down because it is diluted. nasal cannula, hudson,, non rebreathe
why is it dangerous to give lots of oxygen to a COPD CO2 retainer (3 reasons)
1
- they chronically have CO2 high, so they rely on hypoxia to breathe
- when you give lots of oxygen, they stop needing to breathe
2
- giving so much oxygen also opens up all the useless parts of the lungs that were previously shut down thanks to hypoxic pulmonary vasoconstriction. By giving loads of oxygen, it creates a VQ mismatche
3
- Haldane effect - by giving lots of oxygen, the haemoglobin suddenly can’t hold as much CO2 anymore, so that also contributes to increase in PaCO2
what are the 3 WHO stages of analgesia
- paracetamol/aspirin
- diclofenac/NSAID
- fentanyl/morphine
what is the triad of anaesthesia
- hypnosis (i.e. induce sleep)
- muscle relaxation
- analgesia
why is analgesia important in anaesthetics
otherwise, despite being asleep, the patient will still have pain responses in terms of HR and BP, which you want to eliminate
how strong is fentanyl
100x stronger than morphine
fentanyl:
- short or long acting
- long or short half life
- accumulates where?
- lipid soluble?
- metabolised where?
short acting (5 mins to take effect) short half life (lasts 15-30min) accumulates in fat lipid soluble metabolised in liver
what is remi-fentanyl
also a synthetic opioid
it is even shorter acting than fentanyl (10mins half life)
unlike fentanyl, it does not accumulate in tissues and so is good for long cases (repeated doses)
is morphine natural
yes, its found in poppy seeds
is morphine lipid soluble
yes, but less so than fentanyl. hence why it crosses BBB slower and has slower onset of action and longer lasting effect
what metabolises morphine and into what. and why is this important
liver, into morphine-6-glucuronide.
this has more analgesic effect than morphine so is an important metabolite.
it can also build up readily in renal failure so you need to be careful in these patients
SEs of morphine
respiratory depression nausea and vomiting urinary retention/constipation itching can cause bronchospasm in asthmatics due to histamine release
how long does morphine last
30-40min
how can paracetamol affect your use of opioid
opioid sparing effect - paracetamol use intraoperatvely can reduce need for opioids by 10-20%
how much more potent is diclofenac than ibuprofen
8x
contraindications of NSAIDs
special CI of just diclofenac
previous or existing GI bleeds
asthmatic who is aspirin intolerant
care in renal impairment
porphyria
summarise how long each opioid takes to work and how long its lasts
morphine = 10-15 to act, lasts 30-40
fentanyl = 5 to act, lasts 15-30
remi-fentanyl = almost immediate to act, lasts 10-15
what is parecoxib
a COX-2 selective inhibitor (compared to NSAIDs that are COX1/2).
sometimes used as adjunct to opioids
should opioids be used post-op in day cases
no, diclofenac is a good choice
codeine ok too if needed but only for 72 hours
how does PCA work
1-2mg of morphine can be given on demand with a 5 min lockout to prevent overdose
what are the 4 main causes of post-operative nausea and vomiting (PONV)
hypotension
dehydration
hypoxia
anaesthetic drugs (opioids, volatile agents, N2O)
what are the 4 main types of antiemetics for PONV and give examples
(remember they can’t be PO or they won’t work)
- 5HT3 antagonist (ondansetron IV)
- H1 antagonist (cyclizine IV) - anticholinergic SEs
- D2 antagonist (prochlorperazine IM) - slow onset
- Dexamethasone
which is the best anti-emetic for acute PONV and why
which is best for prophylactic PONV
ondansetron because it has rapid onset, minimal SE and is effective.
dexamethasone has a long half life but slow onset so is best for prophylaxis
how can you subdivide types of LA
nerve blocks and neuraxial anaesthesia
what is a Bier’s block and what LA do you use with it
putting LA IV and using a tourniquet to achieve a regional block
you use prilocaine
mechanism of LA
blocks voltage gated sodium channels in nerve axons to prevent conduction.
relationship between how lipophilic LA is and how potent it is
more lipophilic = more potent because it penetrates into nerve axons better
Why do LAs comparatively leave motor fibres more functional then nociceptive or somatosensory fibres?
LAs are more effective on small diameter fibres (C>B>Aδ>Aγ>Aβ>Aα), and so at low doses LAs block Aδ and C fibres (pain). At high concentrations, LAs will effect larger diameter fibres and have effects on things like the heart (hence why LAs can treat arrhythmias).
what is pKa
The pKa value is one method used to indicate the strength of an acid.
pKa is the negative log of the acid dissociation constant or Ka value.
A lower pKa value indicates a stronger acid. That is, the lower value indicates the acid more fully dissociates in water.
HA <=> A- + H+
Ka, the acid dissociation constant, is how much that equation sits to the right (i.e. a strong acid)
Are LA’s weak acid or weak bases and what does this mean.
weak bases, with a pKA or 8-9. This means that most of the LA stays as HA, with only some as A- + H+
HA <=> A- + H+
How do you calculate the % of ionized:unionised LA at a given pH and pKA?
o Using the Henderson-Hasselbalch equation, given the pH and pKa: o pH = pKa + log(base/acid) o pH – pKa = log(base/acid) o pKa – pH = log(acid/base) o pKa – pH = log([LAH+]/[LA])
Why does whether it is ionised or unionised LA matter?
unionised LA cross lipid membranes quicker so have quicker onset of action.
what factors influence how well a LA works
the pKa of the drug AND the pH of the environment (think of henderson-haselbach)
the pH of the solution of the LA (if you raise the pH, more will be unionised an
what effect does the LA being a weak acid or weak base have?
weak bases ionise when pH is below their pKA
weak acid ionise when pH is above their pKA
hence if an LA is a weak base (which it is), it means that at pH 7.4 (body), the weak base is mainly ionised (which is good for action)
why does lidocaine work quicker than bupivicaine
because lidocaine has more unionised molecules (25%) compared to bupivicaine (15%).
unionised means it travels across membranes quicker.
Are most LAs more or less effective on inflamed tissue/abscesses?
Less, because inflammed tissue is more
acidic and LAs are less effective in more acidic conditions. this is because:
If pH is lower, there will be even
less LA compared to LAH+, meaning it will find it even harder to get into the nerve cell and hence LAs
will become less effective
can you use adrenaline with bupivicaine
no, because cardiotoxicity is the limiting factor
structure of a LA
- Aromatic group -
Lipophilic, so it’s important in getting the LA through the membrane and into the nerve fibre - ester or amide link - s
- Amino group - When protonated (i.e. has an extra H+ on it) it is charged and so is water soluble. Important for LA interaction with Na+ channel
Sx of lidocaine overdose
circumoral tingling
seizures
coma
what does a 1% solution mean
it means there are 10mg/ml
so a 0.5% solution there is 5mg/ml
which LA is used for obstetric epidurals
bupivicaine - slower onset and longer duration than lidocaine (half life of 3hrs)
which LA is used in spinal blocks and why
heavy marcain - this is used because it is hyperbaric and so floats down. this means by tilting you can ensure it doesn’t go too high and numb breathing nerves
when can you not remove an epidural
if LMWH has been given in past 10 hours
complications of epidural
inadequate analgesia (give more)
pruritus (chlorphenamine)
leaking epidural (redress)
disconnection (remove rest and restart)
hypotension (fluids and vasopressors)
motor block (stop infusion as there is clearly too much and restart at lower infusion rate once it wears off)
spinal epidural abscess = triad of fever, backache, focal deficit (broad spectrum Abx)
ECG artefact:
- mimics VF
- HR really high
surgical diathermy can mimic VF
If P or T waves are large, software can count them as R wave which doubles the displayed HR. Palpate to check accuracy.
why is palpation not adequate for measuring BP with a cuff
you can only feel for systolic. since things like sepsis lowers diastolic more this is unsafe
cuff width should be ?% of mid arm circumference
40
if cuff is too small, BP is under or overestimated?
BP overestimated if too small
small = big reading big = small reading
shape of arterial waveform from invasive transducer
what does it mean if trace is squiggly or if trace is flat
smooth dicrotic notch
if too flat, trace is over-damped
if trace is squiggly, trace is under-damped
if invasive arterial trace is over damped, then:
- systolic is …
- diastolic is …
if invasive arterial trace is under damped, then:
- systolic is …
- diastolic is …
over damped = underestimated systolic, overestimated diastolic
under damped = overestimated systolic, underestimated diastolic
when is invasive BP monitoring indicated
unstable patient and NIBP is insufficient
during transfer (there would be too much movement artefact)
deliberate induced hypotension in middle ear surgery
critical perfusion states like carotid stents
how does pulse oximetry work
two wavelengths of light (Red and infrared) detect relative oxy- and deoxy-haemoglobin as the molecules have special absorption characteristics
why is pulse oximetry NOT a measure of oxygen delivery to tissues
because all it does is measure relative oxy and deoxy states of Hb. it does not tell you:
a) how much blood there is
b) how much Hb is in the blood
e.g. you can have a severely anaemic person with 100% sats with inadequate oxygen delivery
what factors can make the sats measurement inaccurate
- being cold and having poor perfusion in fingers
- diathermy
- extraneous light
- COHb (carbon monoxide) as it reads like HbO2
- movement
what things are proportional to flow rate through cannula
what things are inversely proportional to flow rate through cannula
Poiseuille’s formula
PROPORTIONAL
pressure gradient
radius of tube^4 - so increasing radius by 2 increases flow rate by 16
INVERSELEY PROPORTIONAL
length of tube
fluid viscosity
flow rate of:
blue (22G)
orange (14G)
blue (22G) = 42ml/min
orange (14G) = 270ml/min
name of technique for central venous access
Seldinger technique - uses 2D USS
where can you get central venous access:
- routinely
- in emergency
routinely
femoral vein - abduct and external rotate leg. find artery and go 1cm medially (NAVY)
internal jugular - high and low approach (high has lower incidence of pneumothorax and is at level of cricoid cartilage)
in emergency
external jugular
saphenous vein cut down over medial malleolus
concentration of Na in normal saline
154mmol
remember body is 135-145 - this is why giving loads of normal saline can cause hypernatraemia
NBM rules:
- clear fluids
- breast milk
- meals (incl. milk)
- chewing gum
- oral medication
2hr 4hr 6hr gum counts as clear fluid oral medication can be given with 30ml of water up to 30min before surgery
what drug can help the anxious patient
midazolam
describe the induction process
- analgesia (fentanyl)
- drug to reduce awareness (propofol/thiopental)
- muscle relaxant
- bag the patient until reliant has taken effect
- intubation
- switch to volatile agent to maintain decreased awareness
describe the process of waking someone up from anaesthesia
- give post-op analgesia
- give PONV prophylaxis
- switch off volatile agent
- decrease minute ventilation as PCO2 stimulated breathing response
- give muscle relaxant reversal agent (neostigmine) - watch out for bradycardia. can give atropine/glycopyrrolate for this)
- extubate and insert oral airway adjunct
emptying rate of stomach for fat, protein and carbs
from fastest to slowest emptying
carbs > protein > fat
what 4 drugs can be given to reduce the risk of aspiration
immediately before surgery
1. antacids (aluminium chloride)
90 min before surgery:
- PPI
- H2 antagonist
- pro kinetic (erythromycin [via motion receptors], metoclopramide)
virchows triad
3 factors contributing to VTEs
- hyper coagulability
- vessel wall injury
- venous stasis
how to split up risk factors for VTE in surgery
- patient factors (age, previous VTE, pregnancy, puerperium, HRT/OCP, obesity, immobility, travel)
- associated diseases (heart failure, respiratory failure, CVA/MI, varicose veins, trauma, haematological disease, nephrotic syndrome, IBD)
- operation factors (>30min surgery, major joint replacement, abdominal or pelvic surgery)
how do we reduce risk of peri-operative VTE
advice (avoid dehydration, encourage early mobilisation)
mechanical things (stocking, intermittent pneumatic calf devices)
drugs (LMWH, fondaparinux)
surgical things (vena cava filter - if recent VTE in last month and anticoagulation is CI)
mechanism of LMWH and heparin
they both bind to and activate antithrombin 3. This:
inactivates FXa
Since heparin is bigger, when it binds to antothombin 3 it makes it do more things. It also makes AT3:
inactivates thrombin (FIIa)
LMWH is therefore more subtle and has a larger therapeutic window
revision of blood thinners.
say whether the following is antiplatelet or anticoagulant and say mechanism:
aspirin clopidogrel abciximab warfarin rivaroxaban dabigatran heparin LMWH fondaparinux
first 3 are antiplatelets (acts on platelet plug formation, which is v relevant in arteries which have platelet rich clots), rest are anticoagulants (acts on coagulation cascade, which is v relevant in veins which have fibrin rich clots)
aspirin = COXi. COX1 inhibits thromboxane A2, inhibiting platelets
clopidogrel = P2Y12
abciximab = glycoprotein 2b3a
warfarin = vit K antagonist so blocks factors 2, 7, 9, 10
rivaroxaban = FXa
dabigatran = direct thrombin inhibitor (F2a)
heparin = inhibits antithrombin 3 –> Xa inhibition AND thrombin inhibition
LMWH (enoxaparin) = inhibits antithrombin 3 –> Xa inhibition ONLY
fondaparinux = a LMWH-like drug that does the same thing as LMWH
immediate management of hypovolaemia (post-op complication)
elevate legs give fluids assess for bleeding measure FBC transfuse
immediate management of arrhythmia (post-op complication)
measure BP and perfusion
ECG
measure K and Mg
treat arrhythmia according to type
immediate management of left ventricular failure (post-op complication)
oxygen
fluid restrict
diuretics
inotropic support on HDU/ICU
immediate management of septic shock (post-op complication)
sepsis 6
+/- central venous pressure monitoring +/- inotropic support
management of pulmonary oedema
POD MAN
position (sit up)
oxygen (high flow)
diuretics (IV 50mg furosemide)
morphine (venodilation and reduces preload)
anti-emetic (metoclopromide)
nitrates
oliguria definition
<0.5ml/kg/hr
most common cause of hypoxia post-surgery
atelectasis
Mx for post-op atelectasis
humidified oxygen
nebuliser bronchodilators
physio
analgesia
causes for post-op oliguria
pre-renal (hypovolaemia, heart failure)
renal (ATN, neprhotoxic drugs like gentamicin)
post-renal (obstruction catheter or BPH)
Mx for post-op oliguria by cause
pre-renal
fluid challenge +/- treat underlying cause
renal
ask med reg or anaesthetist
post-renal
flush catheter to exclude blocked catheter. or put in catheter if BPH is blocking.
when can a patient be discharged from recovery area
all physiological parameters must be within 20% of normal patient:
A - patient must be fully conscious and maintaining airway
B - normal sats
C - stable obs
D - PONV and analgesia controlled. temp normal.
E - notes complete
who is followed up on the ward by anaesthetist following surgery
ASA 3+
they still have PCA, epidural or central venous line in place
complications
is BP measured in peri-operative assessment
it probably still is, but GP readings should be used to better estimate patients normal BP
if, from previous records, patient is not easy to intubate, what should you do?
an awake fibreoptic intubation
can you use isofluorane for surgeies again and again
yes (unlike halothane with the 3hr rule)
are repeated nitrous oxide anaesthetics safe
no, if repeat exposures within hours occurs, folate synthesis may be inhibited
half life of water in stomach
10-20 min.
they are completely emptied within 2 hours
what factors can predispose regurgitation (and increase risk of aspiration)
abnormal peristalsis (peritonitis, post-op ileus, metabolic ileus in DKA or hypokalaemia, drug-induced ileus like with anticholinergics)
obstructed peristalsis (bowel obstruction, tumour, pyloric stenosis)
delayed gastric emptying (shock, trauma, fear/pain/anxiety, opioids)
other factors: increased intrabdominal pressure hiatus hernia oesophageal stricture pharyngeal pouch drugs reducing GOJ tone (anticholinergics, opioids, ethanol)
a person eats breakfast at 8am. they are in an RTA at 11am. surgery is at 3pm (so >6hrs since breakfast). is it safe from an aspiration point of view?
No
Although 6 h have elapsed since oral intake, trauma is a cause of delayed gastric emptying, so the patient is at risk of regurgitation and aspiration.
Management of intra-arterial injection of a drug that is causing badness
Management of intra-arterial injection of a drug involves leaving the cannula in the artery and giving a vasodilator (such as 20 mg papaverine) through it. If the artery is in the upper limb, then a brachial plexus block may reduce arterial spasm. Intravenous heparin should be given.
which IV drugs cause badness when injected into an artery by accident
propofol atracurium ketamine phenytoin thiopental
cause blanching, vasoconstriction, gangrene
why is the right internal jugular vein chosen over the left in central venous access?
The right internal jugular is normally chosen because of the straighter course of the vein.
how do epidural drugs affect blood pressure
they cause hypotension
common effect on vital signs with fentanyl
- HR down
- BP sometimes down
- tidal volume down (but RR same)
if you give diclofenac or paracetamol PR for post-op pain, when should you put it in
At the beginning of surgery, to allow time for absorption
