ANAESTHESIA A (38) Flashcards Preview

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1
Q

KIDS ETT SIZES & DEPTHS

A

At birth, a N kid weighs 3.0kg and takes a 3.0 ETT, then:

  • At 6/52: 3.5
  • At 6/12: 4.0
  • from 1y: (age/4 +4)
  • (go down a size if cuffed)
  • ET Depth = 10 cm at birth, then : 1/2 age + 12cm (+15cm if nasal)
2
Q

3 CONSIDERATIONS FOR SAFE USE OF CUFFED ETT IN CHILDREN

A
  1. correct size: go down a size
  2. correct depth: must be below cricoid
  3. correct pressure: not >25 cm H2O, pref <15
3
Q

KIDS WEIGHT FORMULA

A
  • At birth, the typical kid weighs: 3kg
  • At 1yr: 10kg
  • From 1-10yr: ‘twice age + 8kg’
4
Q

KIDS MAINTAINENCE FLUID FORMULA

A

Maint =

  • 4ml/kg/h for first 10kg
  • 2ml/kg/h for next 10kg
  • 1ml/kg/h then on

Ie, a 30 kg kids needs 70ml/hr

5
Q

KIDS CVS PARAMETERS

A
  • Neonates: HR = 160, BP = 70/
  • Infants: HR = 120, BP = 90/
  • Small children: HR = 100, BP = 100/
  • Adolescents: HR = 80, BP = 120/
6
Q

KIDS RESPIRATORY RATES

A
  • Neonates/infants = 40
  • Small children = 30
  • Adolescents = 20
  • Adults = 15

All breathe with a tidal volume of 7ml/kg, of which 3ml/kg is anatomical deadspace. We ventilate at 10 ml/kg to allow for circuit dead space

7
Q

ADULT, INFANT & CHILD, AND NEONATAL ALS* RATIOS

A
  • ADULT ALS: begin with 30 compressions at 2/sec, then 2 breaths, and repeat
  • INFANT & CHILD ALS: begin with 15 compressions at 2/sec, then 2 breaths and repeat
  • NEONATES: begin with 15 breaths over 30s, then 3 compressions and one breath every 2s

* BLS, however, uses the same 30:2 ratio for all ages

8
Q

FASTING KIDS

A
  • <6/12: 4h for milk and solids, & 2h for clear fluids
  • >6/12: 6h for milk and solids, & 2h for clear fluids
  • Adults: 6h for solids, & 4h for clear fluids
9
Q

NG vs NJ FEEDING TUBES AND FASTING

A

as a general rule, GASTRIC feeds (NG, OG and PEGS) need to be stopped 6h before surgery whereas JEJUNAL feeds do not

10
Q

CLASSIC LMA SIZES

A
  • 1 = <6kg
  • 2 = 6-20kg
  • 2.5 = 20-30kg
  • 3 = adult female
  • 4 = adult male
  • 5 = Shrek
11
Q

OPA AND NPA SIZING

A
  • OPAs are “ANGLE to ANGLE” *
  • NPAs are “NOSTRIL to EAR’” **
  • * angle of the mouth to angle of the jaw*
  • ** nostril to EAM*
12
Q

MINIMUM AGE AND WEIGHT LIMITS FOR AED*s USING ADULT PADS

A
  • not <8y
  • not <12kg

* realising few collapsed children will have defibrillatable rhythms anyway

13
Q

FIRST AID FOR THE CHOKING CHILD OR ADULT

A
  1. if coughing effectively, leave alone to cough
  2. if not, give 5x (single*) back blows, pausing after each to check effect
  3. if still obstructed, give 5x chest thrusts**, again pausing after each to check effect
  4. if loses consciousness, commence CPR and attempt larngoscopic clearance ASAP

  • * the aim being to clr the obstruction with each one*
  • ** each like a CPR chest compression*
14
Q

LARYNGOSPASM

A
  • is caused by spasm of the false cords, not the true cords, so it’s a powerful deep obstruction that cannot be overcome by forced intubation without risking severe damage
  • can often be broken by applying painful pressure with the fingertips holding the mask around the angle of the jaw
15
Q

DESIRABLE TEMPERATURE FOR A TRAUMA THEATRE?

A
  • HOT, at least 30 C! …. KAF was 33C
16
Q

ANGIOEDEMA

A
  • Angioedema = localised swelling of the mucosa of the lips and upper airway, most commonly due to HISTAMINE mediated allergic reactions to food or drugs, and thus responsive to normal anaphylaxis treatment (esp neb Adrenaline)
  • Less commonly, PERIODIC ANGIOEDEMA may be caused by a Hereditary defect in the ‘C1 ESTERASE INHIBITOR’ enzyme, leading to excess BRADYKININ activity. Such cases do not respond to usual anaphylaxis treatment* and instead require
    • airway support (but rarely intubation, however swollen)
    • C1 Esterase Inhibitor replacement with donor concentrates or FFP
    • Bradykinin receptor blockers eg ICATIBANT
  • ACE Inhibitor associated Angioedema is increasingly seen and may also be Bradykinin related

* Teubner still thinks neb Adrenaline is useful

17
Q

4 Causes of PPH

A
  1. TONE (uterine atony)
  2. TEARS
  3. TISSUE (retained placenta)
  4. THROMBUS (coagulation defect)
18
Q

THE HAEMATOLOGY OF PPH

A
  • Pro-thrombotic changes occur in preparation for delivery, with a doubling of clotting factor levels, and concommitant reductions in APTT & INR.
  • In consequence:
    • Coagulopathy develops late in PPH (although still early in abruption & AFE)
    • [FIBRINOGEN] targets in PPH have now doubled to 2.0g/l
19
Q

OXYTOCIN, SYNTOCINON, ERGOMETRINE and SYNTOMETRINE

A

These are all uterotonic agents:

  • OXYTOCIN is a Posterior Pituitary Hormone responsible for milk ejection during lactation, and uterine contraction.
  • Synthetic Oxytocin (SYNTOCINON) may be administered to drive labour or reduce PPH, typically in a dose of 5-10u IV at delivery, +/- an infusion of 40u in 1000mls @ 250 mls/h
  • ERGOMETRINE is a uterotonic agent derived from the toxin of the ERGOT fungus, which caused epidemics of gangrene and miscarriage in the middle ages. In addition to its uterotonic effect, it’s also a powerful VENOCONSTRICTOR (!) so its usually given IMI, in a dose of 500mcg, but can be given slow IV in emergency
  • SYNTOMETRINE combines the 2 agents, with 5u of Synthetic Oxytocin and 500mcg of Ergometrine
20
Q

WHATS CARBETOCIN?

A
  • CARBETOCIN is a single shot long acting synthetic Oxytocic now replacing SYNTOCINON at delivery in FMC, although its not approved for GA sections (? why)
  • DOSE : 100 mcg slow IV x1
21
Q

POST PARTUM PULMONARY OEDEMA

A
  • following a natural delivery, the placenta detaches and the uterus contracts in a relatively slow process which returns ~ 1000 mls of blood to the maternal circulation over ~ 1/2 an hour
  • artificially accelerating this process with bolus oxytocics can precipitate failure in a mother with a cardiac Hx
22
Q

DURAL TAP PROTOCOL

A

PDPHA can be much reduced by:

  1. feed catheter to +2cm (prox hole is at +1.5)
  2. label “Anaesthetist top up only”
  3. topup 1/24 prn with 1-2mls R2F4
  4. remove at +24h and culture tip

(the catheter reduces initial CSF loss, and initiates the inflammation which will subsequently seal the hole)

23
Q

WHAT IS AFE?

A

AFE is thought to be an ANAPHYLACTOID response to the entry of AMNIOTIC FLUID into the maternal circulation, with:

  • bronchospasm
  • hypotension
  • coagulopathy
  • seizures

treatment is supportive

24
Q

WHICH LSCS DRUGS CROSS THE PLACENTA?

A
  • Lipid soluble drugs, like Propofol, opiods and Vapors easily cross the placenta, but muscle relaxants do not
  • so infants born by GA SECTION may be anaesthetised but they will not be paralysed
25
Q

MATERNAL HAEMODYNAMIC CHANGES IN PREGNANCY

A
  1. modest rises in HR & CO
  2. modest falls in BP
  3. blood volume rises by 40%, but red cell mass by only 30%, producing a relative anaemia
26
Q

HOW MUCH BLOOD IS NORMALLY LOST AT NVD AND CAESARIAN?

A
  • up to 500mls at NVD
  • up to 750 mls at caesarian

healthy parturients can accomodate up to 1000mls loss without significant clinical symptoms

27
Q

ROLE OF UTERINE MASSAGE IN PPH?

A
  • Uterine massage is an important first aid measure in PPH, producing uterine contraction, ? via local PG release.
28
Q

WHAT IS HELLP SYNDROME?

A

HELLP SYNDROME = the combination of

  • Haemolysis
  • Elevated LFT
  • Low platelets

sometimes seen in pregnancy (cause?)

29
Q

MATERNAL RESPIRATORY CHANGES IN LATE PREGNANCY

A
  • pCO2 falls to ~30mmHg in late pregnancy due to increased minute volume:
  • ‘normal’ pCO2 can indicate incipient respiratory failure!
30
Q

SUGAMMADEX

A

REVIEW:

  • conventional reversal of NM Blockade uses ACETYLCHOLINESTERASE inhibitors like NEOSTIGMINE to increase ACHO concentrations in the synaptic cleft, where it competes with the blocker molecules for access to the Nicotinic receptors of the NMJ.
  • this sort of COMPETITIVE REVERSAL is only effective at modest depths of blockade
  • SUGAMMADEX is a direct acting reversal agent which binds and inactivates Aminosteroid relaxants (Roc>Vec>>Panc, but not Atrac) and so can reverse even profound block. DOSE:
    • Normal reversal: 200mg (4mg/kg)
    • Emergency : 16mg/kg (both are effective in 1-2 mins)
31
Q

SCOLINE APNOEA

A
  • SUCCINYL CHOLINE mimics ACHO, binding to the NMJ and triggering contraction (then exhaustion). It occupies the receptor for 1-2 minutes before being metabolised by circulating PSEUDOCHOLINESTERASE, and muscle function returns.
  • 1 person in 33 has one defective copy of the pseudocholinesterase gene, prolonging the action of scoline to 5-10m, although this is rarely evident clinically, & 1/1000 have 2, prolonging duration to many hours.
  • DIAGNOSIS:
    • failure to regain muscle power after administration of Scoline (and despite Reversal - given for co-administered NONDEPOL relaxants)
    • no twitches
    • subsequent low activity on Pseudocholinesterase assay
  • TREATMENT: supportive: ventilate until resolves
32
Q

THYROID HORMONES, TFTs AND THYROID REPLACEMENT THERAPY

A
  • Anterior Pituitary TSH drives the thyroid to produce its 2 main* hormones:
    • T3 - TRI-IODOTHYRONINE
    • T4 - THYROXINE
  • Production is predominantly the long lasting T4, and this is converted peripherally to the short lived active form, T3, which drives metabolic rate.
  • THYROID FUNCTION is principally assessed by measuring TSH & T4 levels.
    • normal TSH levels indicate N thyroid function (or adequate replacement) whereas raised levels indicate Thyroid failure (or occasionally Pituitary Tumour)
    • normal T4 levels indicate adequate thyroid hormone production (or replacement)
  • THYROID REPLACEMENT therapy is usually solely (synthetic) T4, with subsequent peripheral conversion to T3 in the usual manner.

* the thyroid also produces the minor Calcium regulating hormone CALCITONIN, but this is secondary in importance to PARATHYROID hormone and Ca metabolism remains normal after thyroidectomy.

33
Q

ADRENAL CORTEX FUNCTION AND ADDISONS DISEASE

A

Anterior Pituitary ACTH drives the Adrenal Cortex to produce 2 steroid hormones:

  • CORTISOL, which regulates BSL & metabolism
  • ALDOSTERONE, which regulates salt and water balance

ADDISONS DISEASE occurs when the Adrenal cortex stops producing these hormones, due to either:

  • Loss of central drive
  • Adreno-cortical failure, eg due to autoimmune attack or severe illness

It results in

  • Hypoglycaemia
  • Hypovolaemia, hyponatrema and hyperkalemia → may present with circulatory collapse, an ‘ADDISONIAN CRISIS’
  • Skin hyperpigmentation
  • Nausea and vomiting
  • Muscle pain and weakness

Rx

  • Address hypoglycaemia and dehydration
  • Replace CORTISOL with HYDROCORTISONE*
  • (consider) ALDOSTERONE replacment with FLUDROCORTISONE (often unneccesary)
  • Address the cause if able

*Cortisol = Hydrocortisone,

34
Q

HOW TO INSERT DOUBLE LUMEN TUBES

A
  1. chose the correct tube, a LEFT* 39 French for the typical M, and 37 for F
  2. put stylet into ENDOBRONCHIAL Lumen and bend Left
  3. rotate tip anteriorly, place thru cords & remove stylet
  4. holding well proximally, corkscrew L 90 degrees whilst pushing firmly home to ~ 29cm at the teeth
  5. inflate TRACHEAL cuff (5-10ml) & check bilat AE**
  6. inflate BRONCHIAL cuff (1-2ml) & check bilat AE**
  7. isolate and check each side - if wrong sided, insert fibrescope to tip of Bronchial lumen and pull back to carina under direct vision then direct into opposite side (if lost: recall that the cartilage arch is deficient posteriorly)

  • * Left sided tubes are generally suitable for procedures on either lung, R sided tubes are only for surgery on the L main bronchus*
  • ** loss of one side, as per normal ETT, usually = too far in*
35
Q

DEALING WITH HYPOXIA DURING ONE LUNG ANAESTHESIA

A

assuming the DLT is correctly sided and not too deep, (the usual cause) hypoxia likely represents ongoing shunting through the collapsed upper lung: manage via

  • start with no lower lung PEEP (reduces blood diversion to upper)
  • add 5 cm lower lung PEEP
  • add 5 cm upper lung CPAP
  • discuss with the surgeon clamping the upper lung vessels or returning to 2 lung ventilation
36
Q

MINUTE AND TIDAL VOLUMES DURING ONE LUNG ANAESTHESIA

A
  • normal minute volumes can generally be achieved with only modest decreases in TV and increases in rate, so NORMOCAPNOEA can usually be maintained
37
Q

2012 FIBREOPTICS WITH DEVILBISS

A
  1. DRY UP FIRST
    • Atropine 1.2mg O with a sip 1/24 prior
    • Glyco 200 IV on arrival
  2. SEDATE AS NEEDED
    • Fentanyl 75-100 mcg, not Midaz (Currie)
  3. TOPICALISE ORAL
    1. Gargle 4% Lignocaine
    2. consider cricoid puncture
    3. Load DeVilbiss with 10mls 4% Lignocaine and 5 lpm
      • spray 2m back of throat (til gag lost)
      • spray 2m around corner (till voice change)
      • use reversed guedel between molars as bite block and proceed
  4. IF NASAL
    1. as above, plus topicalise nose with atomizer or buds
    2. use 6.0 and just feed scope to start
    3. stand in front, keep tight, advance under constant vision
38
Q

TYPE 1 VS TYPE 2 RESPIRATORY FAILURE, DEF AND MECH

A
  • TYPE 1 Respiratory Failure = HYPOXIC, and is generally due to:
    • Shunt/V/Q mismatch
    • Hypoventilation*
  • TYPE 2 Respiratory Failure = HYPERCAPNOEIC, and is generally due to:
    • hypoventilation.

* hypoventilation increases alveolar CO2, ‘crowding out’ oxygen

39
Q
A