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4th Year > Anaesthetics notes > Flashcards

Anaesthetics notes Flashcards

1
Q

Mendelson’s syndrome and main RF

A

chemical pneumonitis due to aspiration of reflux during anaesthesia.

Main RF = pregnancy

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2
Q

what is sellick’s maneovre

A

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.

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3
Q

risks of anaesthesia in early and late pregnancy

A

early - teratogenicity of drugs, spontaneous miscarriage

late - preterm labour, reflux, failed intubation

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4
Q

mandatory manovres for people with reflux

A

RSI with cricoid pressure
starvation for 6hrs

if obstetric, also use h2 antagonist and ppi (evidence is sparse)

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5
Q

what physical airway problems can there be in pre-op assessment

A 
congenital (pierre robin/treacher collins)
neck fusion (ank spond/arthritis)
neck instability (fractures, atlantoaxial instability)
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6
Q

can you have halothane more than once in your life?

A

Yes, but not more than once in any 3 month period

it is rarely used in uk anymore

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7
Q

important things to elicit in family history

A

suxamethonium apnoea
malignant hyperthermia
inherited porphyria
dystrophia myotonia

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8
Q

what is suxamethonium apnoea

A

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.

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9
Q

physiology of malignant hyperthermia

A

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.

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10
Q

symptoms of malignant hyperthermia

A

Symptoms include muscle rigidity, high fever, and a fast heart rate.[1] Complications can include rhabdomyolysis and high blood potassium

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11
Q

what does smoking increase the risk of in terms of anaesthetic worry

A

bronchospasm due to reactivity of airways and increased mucus production

and the carboxyhaemoglobin doesn’t help

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12
Q

how does chronic alcohol use affect anaesthetic

A

tolerance to sedation so may need more

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13
Q

what is thyromental distance

A

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

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14
Q

how to do pre-op assessment

A
  • 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
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15
Q

Main anaesthetic risk factors

A

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)
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16
Q

do you stop aspirin before surgery

A

only if on the brain, spinal cord or prostate. in which case you stop it 5 days before

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17
Q

do you stop statins

A

no

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18
Q

do you stop amlodipine

A

no

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19
Q

do you stop ACEi

why

A

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.

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20
Q

do you stop diuretics

A

no

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21
Q

do you stop warfarin

A

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

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22
Q

do you stop clopidogrel

A

yes, 5 days before surgery

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23
Q

do you stop digoxin

A

depends, check toxicity prior to surgery and plasma K+

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24
Q

do you stop diabetic drugs

A

long acting drugs are normally stopped, yes. Often around surgery permissive hyperglycaemia is allowed as risk of hypo is too great.

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25
Q

do you stop steroids (e.g. in adrenal insufficiency)

A

no, you give extra to account for the stress

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26
Q

do you stop anticonvulsants

A

no, you give the normal dose 1hr before surgery

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27
Q

do you stop COCP/HRT

why

A

yes, 4 week prior to surgery

for risk of VTE

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28
Q

do you stop SSRIs

A

no

but in high risk CNS surgeries, you should stop it 3 weeks prior

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29
Q

should you stop smoking and why

A

YES. perioperative chest infection is 6x more likely

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30
Q

risk of surgery =

A

underlying fitness (ASA/6) + extent of surgery (surgical score/4)

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31
Q

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
A

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

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32
Q

what’s involved in ‘cardiac investigations’ pre-op

A

exercise testing
treadmill ECG
dobutamine stress echo
myocardial perfusion scanning

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33
Q

ASA grading

A 
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
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34
Q

surgery severity grading

A 
1 = endoscopy/laparoscopy/biopsy
2 = hernia repairs, arthroscopies
3 = hysterectomy, TURP, thyroidectomy
4 = joint replacement, colonic resection, artery reconstruction, neck dissection
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35
Q

what to do if needlestick injury

A

wash wound with soap and water immediately
let it bleed
consult local policy

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36
Q

what are the 3 checklist stages in an operation

A

Check-in = before aneathesia
Time-out = before knife to skin
Check out = after last suture

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37
Q

3 types of coma

A
  1. with focal neurology
  2. with meningism
  3. coma alone
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38
Q

when do you put a collar on if worried about C-spine

A

although you can do MIL straight away, you only put a collar on once airway is secure

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39
Q

what conservative B management is there

A

sit patient up

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40
Q

fluid challenge dose

A

500ml warmed hartmans solution over 15 mins

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41
Q

how many fluid challenges can you give until you do something else

A

2L can be given before you need to cross-match blood

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42
Q

GCS calculation

A 
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
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43
Q

walk me through basic life support

A

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

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44
Q

what are 2 shockable and 2 non-sociable rhythms

A

VT and VF are shockable

pulseless electrical activity and asystole are non-shockable

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45
Q

what is the shock algorithm if shockable

A

If shockable:

  • shock
  • cpr for 2 mins
  • shock
  • cpr for 2 mins
  • shock
  • cpr for 2 mins and give adrenaline 1mg and amiodarone 300mg
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46
Q

what do you do if not shockable

A

continue CPR
give 1mg adrenaline every 3-5 mins
check for rhythm every 2 mins

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47
Q

8 reversible causes of cardiac arrest

A

4H’s and 4T’s

hypoxia
hypothermia
hyperkalaemia
hypovolaemia

tamponade
thombosis
toxins
tension pneumothorax

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48
Q

what is the apacheII score

A

looks at:
age
chronic health status
12 physiological values

to determine mortality in intensive care

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49
Q

what are the two ways to approach treating a critically ill patient

A

resus drill (ABCDE)

systemic drill (doing each system one by one - better for more stable patients)

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50
Q

CPAP vs BiPAP

A

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).

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51
Q

type 1 vs type 2 resp failure

A

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.

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52
Q

calculating oxygen delivery

A

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)

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53
Q

MAP =

2 equations

A

MAP = CO x TPR

MAP = 2/3(diastolic) + 1/3(systolic)

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54
Q

what type of shock is hypotension, bradycardia and warm skin

A

neurogenic shock (loss of sympathetic tone)

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55
Q 
systemic vascular resistance in:
- hypovolaemic shick
cardiogenic shock
- septic shock
- anaphylactic shock
A

high
high
low
low

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56
Q

treating haemorrhagic shock

A 
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
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57
Q

treating anaphylactic shock

A
  1. ABCDE (Airway important – intubate if obstruction imminent)
  2. 100% oxygen
  3. Remove cause + raise feet
  4. Adrenalin IM 0.5mg (0.5mL of 1:1000)
    • Repeat every 5 min if needed (guided by observations)
  5. Secure IV access
  6. Chlorphenamine (antihistamine) 10mg IV and hydrocortisone (steroid) 200mg IV
  7. IVI Saline
    • 500mL over 25min (up to 2L may be needed)
    • Titrate against BP
  8. Wheeze -> treat for asthma
  9. No improvement refer to ITU
  10. Further management
    • Mast cell tryptase
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58
Q

treating septic shock

A
  1. ABCDE
  2. Titrate O2 to give saturation of >94%
  3. Insert two large bore cannulas and take 2x peripheral blood cultures (plus urine,
    sputum, CSF depending on source – but don’t delay)
  4. Lactate
  5. Antibiotics within 1h
    • Empirical if no clear source: Tazocin, Gentamicin and vancomycin (if MRSA)
  6. Fluid bolus
    • 500mL over 25min (challenge) – crystalloid (Hartmann’s, 0.9% saline)
  7. Monitor urine output
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59
Q

SIRS criteria

A

HR >90
RR >20
WCC >12
temp >38 or <36

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60
Q

Abx in sepsis 6 if no clear source

A

tazocin, gentamicin and vancomycin

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61
Q

what does BE represent

A

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

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62
Q

average deadspace in a man

A

150ml

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63
Q

what is total headspace made up of

A

anatomical deadspace (airways) and physiological deadspace (unopened alveoli)

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64
Q

normal V:Q ratio

A

0.95

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65
Q

what is Hypoxic pulmonary vasoconstriction

A

lung vasculature, in areas of hypoxia, constrict to prevent V/Q mismatch occuring

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66
Q

does increasing FiO2 in a shunt area help?

A

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

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67
Q

sats in arterial and venous normal blood

A

100%

75%

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68
Q

what is the Haldane effect

A

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

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69
Q

what is the Bohr effect

A

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

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70
Q

what increases 2,3-DPG

A

chronic hypoxia

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71
Q

how does hypoxia affect:

  • coronary arteries
  • peripheral vascular resistance
  • HR and CO
  • kidneys
  • brain
A
  • coronary vasodilation
  • decreased (predominantly through splanchnic)
  • increased
  • kidneys activate RAAS and EPO
  • dilation and increased blood flow
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72
Q

how do you give oxygen in a critically unwell patitnt

A

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.

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73
Q

normal fluid losses in a day

A

1800-2500ml

74
Q

fluid requirement per hour for adults based on weight

A

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

75
Q

crystalloid vs colloid fluid

A

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

76
Q

why are the 5% and 4% glucose crystalloids not suitable for resus

A

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

77
Q

what 3 things control [H+]

A

ventilation
renal bicarb
buffering by bicarb, sulphate, haemoglobin

78
Q

how does malignant hyperthermia affect ABG

A

causes an acute respiratory acidosis

79
Q

standard vs actual bicarbonate

A

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.

80
Q

what happens to standard and actual bicarbonate when CO2 drops

A

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

81
Q

which of the fluids is basically just water

A

5% glucose - because the glucose is rapidly take up and metabolised, leaving just the water and no electrolytes

82
Q

number of ATP for each glucose in aerobic and anaerobic respiration

A

38

2

83
Q

in what regions (in terms of V/Q) does increasing FiO2 actually help arterial o2

A

when V/Q is low (but not zero as with shunts)

84
Q

if a CO2 retainer is started on oxygen, how long should it be before an ABG is done

A

30-60mins

85
Q

when should you reduce a patient off oxygen

A

when sats have been stable for 4 hours

86
Q

how do you monitor when reducing oxygen

A

check sats after 5 mins and after 1 hour

87
Q

what is fixed performance device vs variable performance device in terms of oxygen delivery mean

A

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

88
Q

why is it dangerous to give lots of oxygen to a COPD CO2 retainer (3 reasons)

A

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

89
Q

what are the 3 WHO stages of analgesia

A
  1. paracetamol/aspirin
  2. diclofenac/NSAID
  3. fentanyl/morphine
90
Q

what is the triad of anaesthesia

A
  1. hypnosis (i.e. induce sleep)
  2. muscle relaxation
  3. analgesia
91
Q

why is analgesia important in anaesthetics

A

otherwise, despite being asleep, the patient will still have pain responses in terms of HR and BP, which you want to eliminate

92
Q

how strong is fentanyl

A

100x stronger than morphine

93
Q

fentanyl:

  • short or long acting
  • long or short half life
  • accumulates where?
  • lipid soluble?
  • metabolised where?
A 
short acting (5 mins to take effect)
short half life (lasts 15-30min)
accumulates in fat
lipid soluble
metabolised in liver
94
Q

what is remi-fentanyl

A

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)

95
Q

is morphine natural

A

yes, its found in poppy seeds

96
Q

is morphine lipid soluble

A

yes, but less so than fentanyl. hence why it crosses BBB slower and has slower onset of action and longer lasting effect

97
Q

what metabolises morphine and into what. and why is this important

A

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

98
Q

SEs of morphine

A 
respiratory depression
nausea and vomiting
urinary retention/constipation
itching
can cause bronchospasm in asthmatics due to histamine release
99
Q

how long does morphine last

A

30-40min

100
Q

how can paracetamol affect your use of opioid

A

opioid sparing effect - paracetamol use intraoperatvely can reduce need for opioids by 10-20%

101
Q

how much more potent is diclofenac than ibuprofen

A

8x

102
Q

contraindications of NSAIDs

special CI of just diclofenac

A

previous or existing GI bleeds
asthmatic who is aspirin intolerant
care in renal impairment

porphyria

103
Q

summarise how long each opioid takes to work and how long its lasts

A

morphine = 10-15 to act, lasts 30-40

fentanyl = 5 to act, lasts 15-30

remi-fentanyl = almost immediate to act, lasts 10-15

104
Q

what is parecoxib

A

a COX-2 selective inhibitor (compared to NSAIDs that are COX1/2).

sometimes used as adjunct to opioids

105
Q

should opioids be used post-op in day cases

A

no, diclofenac is a good choice

codeine ok too if needed but only for 72 hours

106
Q

how does PCA work

A

1-2mg of morphine can be given on demand with a 5 min lockout to prevent overdose

107
Q

what are the 4 main causes of post-operative nausea and vomiting (PONV)

A

hypotension
dehydration
hypoxia
anaesthetic drugs (opioids, volatile agents, N2O)

108
Q

what are the 4 main types of antiemetics for PONV and give examples
(remember they can’t be PO or they won’t work)

A
  1. 5HT3 antagonist (ondansetron IV)
  2. H1 antagonist (cyclizine IV) - anticholinergic SEs
  3. D2 antagonist (prochlorperazine IM) - slow onset
  4. Dexamethasone
109
Q

which is the best anti-emetic for acute PONV and why

which is best for prophylactic PONV

A

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

110
Q

how can you subdivide types of LA

A

nerve blocks and neuraxial anaesthesia

111
Q

what is a Bier’s block and what LA do you use with it

A

putting LA IV and using a tourniquet to achieve a regional block

you use prilocaine

112
Q

mechanism of LA

A

blocks voltage gated sodium channels in nerve axons to prevent conduction.

113
Q

relationship between how lipophilic LA is and how potent it is

A

more lipophilic = more potent because it penetrates into nerve axons better

114
Q

Why do LAs comparatively leave motor fibres more functional then nociceptive or somatosensory fibres?

A

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).

115
Q

what is pKa

A

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)

116
Q

Are LA’s weak acid or weak bases and what does this mean.

A

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+

117
Q

How do you calculate the % of ionized:unionised LA at a given pH and pKA?

A 
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])
118
Q

Why does whether it is ionised or unionised LA matter?

A

unionised LA cross lipid membranes quicker so have quicker onset of action.

119
Q

what factors influence how well a LA works

A

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

120
Q

what effect does the LA being a weak acid or weak base have?

A

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)

121
Q

why does lidocaine work quicker than bupivicaine

A

because lidocaine has more unionised molecules (25%) compared to bupivicaine (15%).

unionised means it travels across membranes quicker.

122
Q

Are most LAs more or less effective on inflamed tissue/abscesses?

A

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

123
Q

can you use adrenaline with bupivicaine

A

no, because cardiotoxicity is the limiting factor

124
Q

structure of a LA

A
  1. Aromatic group -
    Lipophilic, so it’s important in getting the LA through the membrane and into the nerve fibre
  2. ester or amide link - s
  3. 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
125
Q

Sx of lidocaine overdose

A

circumoral tingling
seizures
coma

126
Q

what does a 1% solution mean

A

it means there are 10mg/ml

so a 0.5% solution there is 5mg/ml

127
Q

which LA is used for obstetric epidurals

A

bupivicaine - slower onset and longer duration than lidocaine (half life of 3hrs)

128
Q

which LA is used in spinal blocks and why

A

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

129
Q

when can you not remove an epidural

A

if LMWH has been given in past 10 hours

130
Q

complications of epidural

A

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)

131
Q

ECG artefact:

  • mimics VF
  • HR really high
A

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.

132
Q

why is palpation not adequate for measuring BP with a cuff

A

you can only feel for systolic. since things like sepsis lowers diastolic more this is unsafe

133
Q

cuff width should be ?% of mid arm circumference

A

40

134
Q

if cuff is too small, BP is under or overestimated?

A

BP overestimated if too small

small = big reading
big = small reading
135
Q

shape of arterial waveform from invasive transducer

what does it mean if trace is squiggly or if trace is flat

A

smooth dicrotic notch

if too flat, trace is over-damped

if trace is squiggly, trace is under-damped

136
Q

if invasive arterial trace is over damped, then:

  • systolic is …
  • diastolic is …

if invasive arterial trace is under damped, then:

  • systolic is …
  • diastolic is …
A

over damped = underestimated systolic, overestimated diastolic

under damped = overestimated systolic, underestimated diastolic

137
Q

when is invasive BP monitoring indicated

A

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

138
Q

how does pulse oximetry work

A

two wavelengths of light (Red and infrared) detect relative oxy- and deoxy-haemoglobin as the molecules have special absorption characteristics

139
Q

why is pulse oximetry NOT a measure of oxygen delivery to tissues

A

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

140
Q

what factors can make the sats measurement inaccurate

A
  • being cold and having poor perfusion in fingers
  • diathermy
  • extraneous light
  • COHb (carbon monoxide) as it reads like HbO2
  • movement
141
Q

what things are proportional to flow rate through cannula

what things are inversely proportional to flow rate through cannula

A

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

142
Q

flow rate of:
blue (22G)
orange (14G)

A

blue (22G) = 42ml/min

orange (14G) = 270ml/min

143
Q

name of technique for central venous access

A

Seldinger technique - uses 2D USS

144
Q

where can you get central venous access:

  • routinely
  • in emergency
A

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

145
Q

concentration of Na in normal saline

A

154mmol

remember body is 135-145 - this is why giving loads of normal saline can cause hypernatraemia

146
Q

NBM rules:

  • clear fluids
  • breast milk
  • meals (incl. milk)
  • chewing gum
  • oral medication
A 
2hr
4hr
6hr
gum counts as clear fluid
oral medication can be given with 30ml of water up to 30min before surgery
147
Q

what drug can help the anxious patient

A

midazolam

148
Q

describe the induction process

A
  1. analgesia (fentanyl)
  2. drug to reduce awareness (propofol/thiopental)
  3. muscle relaxant
  4. bag the patient until reliant has taken effect
  5. intubation
  6. switch to volatile agent to maintain decreased awareness
149
Q

describe the process of waking someone up from anaesthesia

A
  1. give post-op analgesia
  2. give PONV prophylaxis
  3. switch off volatile agent
  4. decrease minute ventilation as PCO2 stimulated breathing response
  5. give muscle relaxant reversal agent (neostigmine) - watch out for bradycardia. can give atropine/glycopyrrolate for this)
  6. extubate and insert oral airway adjunct
150
Q

emptying rate of stomach for fat, protein and carbs

A

from fastest to slowest emptying

carbs > protein > fat

151
Q

what 4 drugs can be given to reduce the risk of aspiration

A

immediately before surgery
1. antacids (aluminium chloride)

90 min before surgery:

  1. PPI
  2. H2 antagonist
  3. pro kinetic (erythromycin [via motion receptors], metoclopramide)
152
Q

virchows triad

A

3 factors contributing to VTEs

  1. hyper coagulability
  2. vessel wall injury
  3. venous stasis
153
Q

how to split up risk factors for VTE in surgery

A
  1. patient factors (age, previous VTE, pregnancy, puerperium, HRT/OCP, obesity, immobility, travel)
  2. associated diseases (heart failure, respiratory failure, CVA/MI, varicose veins, trauma, haematological disease, nephrotic syndrome, IBD)
  3. operation factors (>30min surgery, major joint replacement, abdominal or pelvic surgery)
154
Q

how do we reduce risk of peri-operative VTE

A

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)

155
Q

mechanism of LMWH and heparin

A

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

156
Q

revision of blood thinners.

say whether the following is antiplatelet or anticoagulant and say mechanism:

aspirin
clopidogrel
abciximab
warfarin
rivaroxaban
dabigatran
heparin
LMWH
fondaparinux
A

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

157
Q

immediate management of hypovolaemia (post-op complication)

A 
elevate legs
give fluids
assess for bleeding
measure FBC
transfuse
158
Q

immediate management of arrhythmia (post-op complication)

A

measure BP and perfusion
ECG
measure K and Mg
treat arrhythmia according to type

159
Q

immediate management of left ventricular failure (post-op complication)

A

oxygen
fluid restrict
diuretics
inotropic support on HDU/ICU

160
Q

immediate management of septic shock (post-op complication)

A

sepsis 6

+/- central venous pressure monitoring +/- inotropic support

161
Q

management of pulmonary oedema

A

POD MAN

position (sit up)
oxygen (high flow)
diuretics (IV 50mg furosemide)

morphine (venodilation and reduces preload)
anti-emetic (metoclopromide)
nitrates

162
Q

oliguria definition

A

<0.5ml/kg/hr

163
Q

most common cause of hypoxia post-surgery

A

atelectasis

164
Q

Mx for post-op atelectasis

A

humidified oxygen
nebuliser bronchodilators
physio
analgesia

165
Q

causes for post-op oliguria

A

pre-renal (hypovolaemia, heart failure)
renal (ATN, neprhotoxic drugs like gentamicin)
post-renal (obstruction catheter or BPH)

166
Q

Mx for post-op oliguria by cause

A

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.

167
Q

when can a patient be discharged from recovery area

A

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

168
Q

who is followed up on the ward by anaesthetist following surgery

A

ASA 3+
they still have PCA, epidural or central venous line in place
complications

169
Q

is BP measured in peri-operative assessment

A

it probably still is, but GP readings should be used to better estimate patients normal BP

170
Q

if, from previous records, patient is not easy to intubate, what should you do?

A

an awake fibreoptic intubation

171
Q

can you use isofluorane for surgeies again and again

A

yes (unlike halothane with the 3hr rule)

172
Q

are repeated nitrous oxide anaesthetics safe

A

no, if repeat exposures within hours occurs, folate synthesis may be inhibited

173
Q

half life of water in stomach

A

10-20 min.

they are completely emptied within 2 hours

174
Q

what factors can predispose regurgitation (and increase risk of aspiration)

A

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)
175
Q

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?

A

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.

176
Q

Management of intra-arterial injection of a drug that is causing badness

A

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.

177
Q

which IV drugs cause badness when injected into an artery by accident

A 
propofol
atracurium
ketamine
phenytoin
thiopental

cause blanching, vasoconstriction, gangrene

178
Q

why is the right internal jugular vein chosen over the left in central venous access?

A

The right internal jugular is normally chosen because of the straighter course of the vein.

179
Q

how do epidural drugs affect blood pressure

A

they cause hypotension

180
Q

common effect on vital signs with fentanyl

A
  • HR down
  • BP sometimes down
  • tidal volume down (but RR same)
181
Q

if you give diclofenac or paracetamol PR for post-op pain, when should you put it in

A

At the beginning of surgery, to allow time for absorption

4th Year (10 decks)

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