facts learned from mcqs Flashcards
Does blood for epidural blood patch spread predominantly cranially or caudally?
cranially, so do epidural blood patch at same level or the level below initial dural puncture
Are mastocytosis, anaphylaxis, ACS, lymphomas/leukemias/myeloproliferative disorders & CKD associated with raised mast cell tryptases?
Yes, tryptases often reduced in chronic liver disease)
*What’s the IM dose of carboprost?
250microg, repeat q15-minutely up to 8 doses (2mg)
:) What lead changes correspond to which coronary arteries?
V1, V2 = septal = proximal LAD
V3, V4 = anterior = LAD
V5, V6 = apical = distal LAD, L) circumflex or RCA
I, aVL = lateral = L) circumflex
II, III, aVF= inferior = 90% RCA, 10% L) Cx
V7-9 (reciprocal ST depressions frequently seen in V1-3) = posterior = RCA or L) Cx
Reciprocal changes: PAILS (P->A, A->I, I->L, L->S/I, S->P)
*What techniques may improve the speed of onset & spread of a peribulbar block?
hyaluronidase 5-70IU/mL (hydrolysis of hyaluronic acid, a GAG molecule forming part of the ECM) increases tissue permeability & promotes dispersion of LA
lignocaine (faster onset 5-10 min vs bupiv/ropivacaine 10-15 min)
gentle digital or compression device (eg. honan balloon limits to 30mmHg; improves spread, avoid ocular massage which can increase IOP to >400mmHg)
LA injectate volume
*What ASA is an ESRD patient on haemodialysis?
3 (severe systemic disease)
*definition & examples of ASAIII?
severe systemic disease, substantive functional limitations
one or more moderate to severe diseases
poorly controlled DM or HTN
COPD
BMI >=40
active hepatitis
ETOH dependence or abuse
implanted pacemaker
moderately reduced EF
ESRD undergoing regular scheduled haemodialysis
H/o (>3/12) post MI/CVA/TIA/CAD/stents
severe OSA
oncologic state
CF
Hx organ transplant
premature infant PCA <60wks
autism with severe limitations
difficult airway
full-term infants <6/52 of age.
Pre-eclampsia with severe features
gestational DM with complications or high insulin requirement
thrombophilic disease requiring anticoagulation in pregnancy
*What’s the sensory innervation to the breast? and motor?
Supraclavicular nerve (C3-4)- skin from clavicle to 2nd rib
Intercostobrachial (T2)- axilla & medial upper arm
segmental somatic sensory innervation from the T2-6 intercostal nerves which are from the anterior rami of these Tx spinal nerves:
-Lateral breast: lateral cutaneous branches of the T2-6 intercostal nerves (pierce SAM, anterior divisions serve lateral breast)
-Medial breast: anterior cutaneous branches of the T2-6 intercostal nerves (pierce PM near sternum)
Motor:
Long thoracic nerve C5-7 (SA)
Thoracodorsal nerve C6-8 (LD)
Lateral pectoral nerve C5-7 (PM/m)
medial pectoral nerve C8-T1 (PM)
subscapular nerve C5-6 (TM)
upper/lower subscapular nerves C5-8 (subscapularis)
*What’s a derived value from an ABG & from what is it calculated?
HCO3-; from CO2 & H+ using H-H equation
Base excess (HH & Siggaard-Anderson equation)- either base excess (the amount of alkali that must be added to the sample to return it to a normal pH at roome tem (37degC) & PaCo2 40mmHg, or standard base excess calculated for the blood with a Hb [] 50g/L (thought to better represent ECF as a whole)
pH (electrode with HCl, blood & buffer solutions), pO2 (clark electrode), pCO2 (Severinghaus electrode), Hb & some biochem are measured.
What are some features consistent with SIADH?
hypoosmolar hyponatraemia
urine osmolality >100mOsmol/kg, ie. concentrated urine despite hypotonic blood (plasma osmolality <275mosb/kg))
urine Na >20mmol/L
normal renal/hepatic/cardiac/pituitary/adrenal/thyroid
absence of hypoT/hypovolaemia/oedema/ADH-influencing drugs (vasopressin, desmopression, terlipressin. Carbamazepine, cyclophosphamide, SSRIs also promote ADH release), hyponatremia corrects with H2O restriction. Na+, inhibit ADH (demeclocycline, tolvaptan)
Causes: MADCHOPS
major OT, ADH from tumour (eg. SCLC), drugs, CNS, hormone deficiency
*What are some causes of SIADH?
MADCHOPS:
major OT
ADH from tumour
Drugs
CNS (trauma, SDH)
Hormone deficiency
Others
Pulmonary
*How to treat hypoosmolar hyponatremia?
FR, Na+, decrease ADH secretion (demeclocycline, tolvaptan)
*what are some risk factors for OIVI?
Pt:
obesity
sleep-disordered breathing
Age >65yo
female
COPD
renal/neuro/cardio disease
DM
HTN 2+ comorbidities
opioid dependence
ASA 3/4
CYP450 enzyme polymorphisms
external:
concomitant administration of sedatives (BZD, gabapentanoids, antipsychotics)
different routes of opioid administration
continuous opioid infusions
multiple prescribers
inadequate nursing Ax or responses
SR opioids
*What are some benefits of robot-assisted laparoscopic prostatectomy surgery in comparison with open prostatectomy?
Risks with robot-assisted:
Pneumoperitoneum: physiological effects, venous air embolus (CO2), subcut or mediastinal emphysema, pTx, CO2 retention, pain related to intra-abdo gas
Steep head down (well leg compartment syndrome)
Problems during surgical access, including small bowel, iliac artery, colon, iliac vein damage (bleeding may not immediately be obvious as bleeding into retroperitoneum may occur)
Mechanical failures (eg. uncontrolled movements, arcing from diathermy causing burns to surrounding tissue)
Robot less bleeding, transfusion & shorter LoS, less postop med/surg complications cf laparoscopic/open
*What are some complications of pneumoperitoneum?
decr PL, incr SVR, decr CO, venous pooling + DVT, incr BP, incr ICP, incr CO2, atelectasis, VQ mismatch, incr VD alveolar, incr PaCO2-PE’CO2, incr PaO2/FiO2, decr renal BF, incr RAAS/ADH, IAP - =<10mmHg incr VR/CO, 10-20mmHg decr CO incr SVR, >20mmHg decr MAP/CO), trendelenburg, surgical access (50% complications at this time, SB>iliac a>colon >iliac vs)
*What are some complications & rates with US-guided L) IJ CVC insertion?
arterial puncture 6.3-9.4%, CLABSI 1.4%, DVT 0.9%, PTX <0.1-0.2%, haematoma <0.1-2.2%, higher rate lymphatic injury due to anatomic location of thoracic duct
*What’s the most common complication of subclavian cannulation?
arterial puncture (3.7%)
mechanical complication 2.1% (subclavian has the highest mechanical complication rate)
then PTx 1.5%
CLABSI &DVT 0.5% (lowest infection/DVT risk w subclavian but highest rate mechanical complications)
*What are some complications & rates of femoral vein cannulation?
Arterial puncture most common w fem lines (10%) so they have overall higher complication rate
DVT 1.4%
CLABSI 1.2%
*What type of drug is benztropine & what are it’s uses?
anticholinergic (selective M1)/antihistamine agent, increases dopamine availability by blocking it’s reuptake/storage
Adjunct in Parkinsonism, Tx of EPS except tardive dyskinesia from neuroleptic drugs
Ameliorates side effects of drugs that antagonise the dopamine receptor
*Regarding healthcare research, the PICO framework describes what?
Patient/problem/population
Intervention
Comparison/control/comparator
Outcome
Used to frame and answer a clinical or health care related question
*What drug (& dose) is used to treat duct dependent congenital heart disease?
Alprostadil (synthetic PGE1), infusion to maintain ductal patency. important for both right & left heart lesions.
Most effective within 96hrs of birth (before anatomical closure), palliative therapy until surgery, 0.1microg/kg/min, see effect in 30-60 min, reduce dose to 0.01-0.02microg/kg/min
causes vasodilation of all arterioles & inhibition of platelet aggregation
side effects incl apnoea, hypotension
0.05mcg/kg/min if ductus restrictive or status unknown (the dose used for transport). max 0.1mcg/kg/min.
*What are some adverse effects of alprostatil?
apnoea (dose-dependent- have intubation equipment on-hand), fever, cutaneous flushing, bradycardia, hypoT, oedema, seizures, decreased platelet aggregation, thrombocytopenia
necrotising enterocolitis (mesenteric hypoperfusion combined cyanosis & low diastolic BP- monitor infants for abdo distension, bilious vomit, bloody stools).
cyanotic baby DDx sepsis; if not yet proven duct-dependent, start alprostadil 0.05mcg/kg/min & start BS Abx (amp. &gent) once blood cultures taken.
*If a pt sustains blunt chest trauma, after how much immediate blood drainage after closed thoracostomy is a thoracotomy indicate?
1500mL (>=20mL/kg) or 200mL/hr in the first 3hrs or 100mL/hr in the first 6hrs
*What factors are used to calculate the Child-Pugh score?
INR
Bilirubin
Ascites
Albumin
Encephalopathy
ABCDE: albumin, bilirubin, cogs, distended abdo, encephalopathy
each scored out of 3, total 15
*What are the points for Child-Pugh classification?
each of INR, Bilirubin, Ascites, Albumin & encephalopathy gets 1-3 points. 5-6= Child-Pugh A, 7-9= C-P B, 10+= C-P C
*What’s the abdo surgery perioperative mortality & life expectancy for Childs A, B & C?
A= 10%, 15-30yrs
B= 30%, eval for transplant
C= 82%, life expectancy 1-3yrs
*What’s the pKa of bupivacaine? how does this influence it’s onset?
8.1, only 17% unionised @ physiological pH, lower degree of transfer across lipophilic membranes so slower onset cf other LAs eg. lignocaine pKa 7.9, 25% unionised @ physiology pH. (Adding bicarb speeds onset)
Also, bupivacaine has large MW which slows onset but there’s little difference in MW btwn LAs.
- What property does protein binding impart for LAs?
duration of action; highly PB (eg. bupiv 95%) = longer duration cf lower PB (lignocaine 70%)
*What property does lipid solubility impart to LAs?
potency. Bupivacaine more lipid soluble cf lignocaine so more potent.
*how does indocyanine green influence pulse vs cerebral oxygen tissue saturation?
decrease SpO2, increase SctO2 (a strong near-infrared absorber)
*what did CRASH-2 show that TxA did for trauma victims?
Reduces risk of death in bleeding trauma patients if given in the first 3hrs (all cause mortality @ 28d, death due to bleeding)
without increase in vaso-occlusive events
Did not reduce blood product use
What’s the dose of lignocaine in mg/kg for a bier’s block?
3mg/kg (eg. for a 30kg child, 18mL of 0.5% lignocaine)
What should the fluid prescription be for a 25kg NBM child overnight?
65mL/hr 0.9% saline with 5% dextrose
What lifestyle modifications are effective in reducing essential HTN?
Effective lifestyle modifications=
weight loss
dietary salt restriction (limit to 65mmol/day)
potassium supplementation (preferably by diet) unless contraindicated by CKD
DASH diet (high vegetables, fruit, low-fat dairy, nuts & low in red meat & sweets- rich in K+, Mg++, Ca++, protein & fibre, low in fat saturated fat & cholesterol)
smoking cessation
exercise (aerobic, dynamic resistance & isometric- 3-4 sessions/week of moderate-intensity aerobic exercise)
reduced ETOH
What’s sensory innervation of the cornea?
Nasociliary (from the ophthalmic (V1) branch of trigeminal nerve), meets ciliary ganglion & gives off long & short ciliary nerves supplying cornea
ie:
Trigeminal–> nasociliary (of the ophthalmic)–> long & short ciliary nerves (which are the terminal supply)
What are some laboratory findings with haemophilia?
prol APTT, normal platelets/bleeding time/PT
How is haemophilia A, B & C inherited? incidence & what deficiencies?
A is XLR, f8 def, 1/5000 male births
B is XLR, f9 def, 1/25000 male births
C is AD/AR, f11 def
How is vWD inherited? lab findings? And lab findings for haemophilia?
AD>AR
normal/reduced plt, normal or prolonged bleeding time, normal/prol APTT, normal PT
can do VWF:Ag & VWF:RCx, F8
VWF:RCx & F8 should both be 100IU/dl periop & >50IUl/dl immediately postop
vWf qual/quant defect clinically significant in 1/10,000
for haemophilia may have prol APTT
What are some conditions for which volatile inappropriate?
Increased risk MH: known MH, FHx MH, congenital myopathy, exertional rhabdomyolysis, exertional heat illness, idiopathic hyperCKaemia, carrier of RYR1 variant of unknown significance
What are lab findings indicating inadequate or low iron stores? what are the Hb targets & Fe replacement?
Serum ferritin <30ug/l
In the presence of inflammation (CRP>5mg/l) and/or transferrin saturation <20%, serum ferritin <100ug/l
Target Hb>=130g/l in both sexes
PO iron 6-8/52 preop
IV iron <6/52 preop or non-responder/not tolerating PO iron
(International Consensus Statement Ass of Anaesthetists 2017)
Globe perforation during eye block is more common in myopic eyes because:
Staphylomas (sclera outpouches) are more common in myopes (increased axial length >26mm)
Other risk factors for globe perforation: thinner eye, deep set eyes, previous scleral buckle, posterior staphyloma (staphyloma more common in myopes), retrobulbar (intraconal) or peribulbar > subtenon’s
What does adenosine do to pt w heart transplant?
enhance Brady effect
What do atropine & glyco do to pt w heart transplant?
no effect
What does neostigmine do to pt w heart transplant?
bradycardia may develop, esp if >6/12 post-transplant
what do B-blockers do to pt w heart transplant?
effective (but caution as heart reliant on circulating catecholamines to increase CO)
What does lignocaine do to pt w heart transplant?
effective
What does dopamine do to pt w heart transplant?
normal response
What do Adr & NAdr do to pt w heart transplant?
exaggerated effect as increased adrenoceptor density
What do metaraminol & phenylephrine do to pt w heart transplant?
effective but no reflex bradycardia
What does ephedrine do to pt w heart transplant?
decreased effect- indirect mechanism
What does dobutamine do to pt w heart transplant?
exaggerated effect
What does digoxin do to pt w heart transplant?
inotropic effect intact, conduction effects on AVN likely absent
What does isoprenaline do to pt w heart transplant?
effective
Normal A-a gradient?
Normal A-a gradient <15mmHg
What are some features NOT consistent with SIADH?
Low urine osmolality (<100mOsmol/kg)
High serum osmolality
Low urine sodium
Hypovolaemia
Abnormal thyroid, adrenal function
Which conditions may be associated with MH susceptibility?
myopathies with RYR1 abnormalities (or STAC3)- central core myopathy, multiminicore disease, King-Denborough syndrome, periodic paralysis, idiopathic hyperCKemia, carrier of RYR1 variant of unknown significance
conditions associated with rhabdo:
exertion rhabdoymolysis
severe statin-induced myopathy
some muscle disorders don’t confer higher risk of MH but are associated with significant rhabdo & hyperkalemia following sux or volatile eg. Duchenne or Becker muscular dystrophy (both X-linked, recessive leading to abnormal formation of dystrophin)- treat with non-triggering agents
Immediate action if peaked T waves, raised eTCO2 in pt w suspected Duchennes:
-stop volatile & give calcium
Duchenne= most common childhood musc dystrophy. X-linked recessive. 1:3500 live births. lack dystrophin (anchor muscle cells to ECM), sarcolemma becomes incr permeable, incr intracellular Ca++
progressive wasting/weakness prox muscles, fatal late adolescence from resp/cardiac failure. waddling gait, calf pseudohypertrophy by age 3-5, inh anaes rhabdo sec incr Ca++ not MH but avoid triggers
What ARE some high-risk transthoracic echo findings associated with aortic dissection?
intimal flap
SEVERE PROXIMAL AORTIC DILATATION
regurg
pericardial effusion
Type A associated features and complications:
aortic regurgitation (acute dilatation of the aortic root, aortic leaflet prolapse, dissection flap prolapse, pre-existing disease, e.g. bicuspid valve)
pericardial effusion and/or CARDIAC TAMPONADE
REGIONAL WALL MOTION ABNORMALITIES or SEVERELY IMPAIRED LVEF
intramural haematoma, aortic ulcer.
colour flow Doppler:
identifies true and false lumen
detect aortic branch occlusion/ dissection (absent flow)
TTE is considered limited inthe Dx of aortic dissection BUT recent contrast-TTE thought to have similar accuracy to TOE for Dx type A (sens 93%, spec 97%) but more limited in type B (sens 84%, spec 94%).
Still useful as availability, rapidity, additional info on cardiac status. useful for emergency room but has low negative predictive value so can’t rule out dissection (further tests if the TTE is -ve).
limited if abnormal chest wall, obesity, emphysema, mech vent.
Which ingested objects are high-risk & require imaging?
button batteries & magnets, a metal object & magnet or >1 magnet, lead objects (may lead to systemic absorption)
What should be offered to children >12 months old with suspected button battery ingestion?
honey at regular intervals
what size objects may become trapped in the pylorus?
> 2cm wide & >6cm long
Which metal is only variably detected on X-ray?
aluminium
Which children should NOT have honey after button battery ingestion?
Those aged <12 months (rare risk of botulism with honey)
Battery ingested >12hrs ago (higher risk oesophageal perforation)
What should children >12 months with suspected battery ingestion <12hrs ago take enroute to definitive care? then, upon hospital arrival once XR has confirmed oesophageal location of battery, what to administer?
Honey 10mL q10min if >12 months old & ingestion was within the last 12hrs
Sucralfate suspension (10mLs q10mins)
Battery removal by endoscopy shouldn’t be delayed- ideally within 2hrs of battery ingestion, anaesthesia can proceed regardless of PO honey intake
irrigate. ifno perf (sterile acetic acid)
if in stomach, minimal risk complications (consider removing if remains for 4 days)
What are some contraindications for stellate ganglion block?
unable to consent
local infection or neospasm
anatomical or vascular anomalies
recent MI
anti-coagulated pts or those with coagulopathy
glaucoma
severe emphysema
cardiac conduction block
pre-existing contralateral phrenic nerve palsy (may precipitate resp distress)
Indications:
head/neck pain (sympathetically mediated) eg. CRPS, facial herpes zoster, phantom UL/ischaemic pain, vascular disease (Reynaud’s, vasospasm), scleroderma, arrhythmia (eg. VF, VT) refractory to other therapy.
stellate ganglion is fusion inf Cx with 1st-2nd SNS ganglion
AEs= Horner’s, tracheal/oes injury, haemorrhage, brachial plexus/RLN/phrenic palsy, PHx, intrathecal
ant paratracheal approach, head extended, needle 2-3cm above & 2cm lat to suprasternal notch, 2-3cm above & 2cm lat to suprasternal notch
Is it safe to do neuraxial in a pt with MS?
little conclusive evidence for or against
epidural considered safer than spinal as demyelinated fibres more susceptible to toxic effects from LA- inform pt of risk of new/worsening neurologic Sx
Regional is OK as long as pt understands potential for relapse, have follow-up in place
PRISMS study 2004- slight reduction in relapse during pregnancy, significantly increase in relapse @ 3/12 postpartum regardless of anaesthetic technique or mode of delivery, no difference in relapse rates epidural vs no epidural
What are the heart sounds?
S1= closure of MV/TV
S2= closure AV/PV
S3= tightening of papillary muscles (rapid diastolic filling)
S4= atria contracting against stiffened ventricle eg. with AS, PS, PHTN, HOCM
What’s normal QRS axis on an ecg? L)? R)? extreme?
-30 to +90 deg
LAD= -30 to -90
RAD= +90 to 180
extreme is 180 to -90
What’s a more reliable clinical indicator of early OIVI? sedation score or decrease RR? What’s the most reliable way to detect OIVI at an early stage? Why is SpO2 unreliable?
sedation score. APMSE book: “best early clinical indicator is increasing sedation”
continuous CO2 monitoring is the most reliable way to detect OIVI at an early stage BUT this is limited to OT/PACU/ICU/some HDU
Pts may have reasons other than OIVI to have low SpO2 & use of supplemental O2 makes SpO2 unreliable for early detection of OIVI
What do we see with middle cerebral artery syndrome: non-dominant MCA? how does this contrast with Gerstmann (dominant MCA)?
contralateral arm weakness, sensory loss, HEMI-NEGLECT, homonymous hemianopia, apraxia, spatial disorientation
dominant: global receptive & expressive aphasia, agraphia, acalculia, finger agnosia, R)/L) disorientation,
What’s the purpose of the 4th bottle in the 4-chamber pleural drain?
protect against the consequences of suction failure/blockage- protecting the pt from pneumothorax.
Which anaesthetic medications are CONTRAINDICATED while breastfeeding?
codeine
aspirin (analgesic doses- can use low dose for anti-platelet action if strongly indicated)
parecoxib
use caution with:
tramadol (observe child for unusual drowsiness)
oxycodone (greater risk drowsiness in doses >40mg/day)
What’s static compliance? and dynamic?
change in volume/final change in pressure @ points of no gas flow (total compliance when all alveoli @ equilibrium w external environment)
= (VT) / (Pplat -PEEP)
in mL/cmH2O
dynamic is pulmonary compliance during periods of gas flow. always less than or equal to static compliance as peak insp pressure is always greater than Pplat.
Cdyn = (VT) / (PIP - PEEP)
What are the borders of the cubital fossa?
What is the median cubital vein & it’s surrounding structures?
epicondylar line= superior border. brachioradialis= lateral border. pronator teres= medial border.
Median cubital vein connects the cephalic (lateral) & basilic (medial) veins
median nerve (giving off antebrachial cutaneous nerve of the forearm) lies underneath & to the medial edge of it.
Radial nerve (giving off superficial & deep radial nerve) lies underneath & to the lateral edge of it.
MCNF is a branch from median nerve, LCNF from medradial, both may be damaged w cannulation
separated from brachial artery (which bifurcates into radial & ulnar arteries) by bicipital aponeurosis
biceps tendon lies deep to the median cubital vein & lateral to brachial artery.
ulnar nerve lies outside of it
How to control seizures due to LAST?
small incremental doses of benzodiazepine, thiopental or propofol
What’s ANOVA used for?
check if the means of or 2 more groups are significantly different from each other- normally distributed interval data (it CAN be used for 2 groups but more commonly use t-test). can use it for categorical independent variable w normally distributed interval dependent variable
OME of 50mg tapentadol?
15mg ( x 0.3)
What’s the gold standard test for establishing tolerance to penicillin? What test first? whats the NPV & PPV of these tests?
graded drug provocation test (DPT) using the index penicillin.
First skin test using SPTs and IDTs- skin tests for penicillin have a NPV approaching 100% & pts who don’t react to SPT or IDT are unlikely to have severe immediate reaction on the DPT. PPV is <50%.
In a pt who’s had a clinical reaction, a +ve skin test, with immediate readings, can identify presence of IgE sensitisation so then avoid DPTs.
Delayed readings required for Dx of non-immediate type IV hypersensitivity reactions but predictive value of these readings isn’t well established.
What are some limitations of skin tests?
reduced sensitivity over time in Dx of immediate reactions
low S&S in pts with non-severe, non-immediate & vague reactions
What’s an alternative to skin testing? pros/cons?
serum-specific IgE assay
low sens & spec but some pts can have -ve skin test, +ve serum-specific IgE & have anaphylaxis when exposed to the drug
What accounts for cross-reactivity between penicillins & cephalosporins? What should occur for pts who have suspected cefazolin anaphylaxis?
Probably mainly the R1 side chain, however cefazolin has different R1 side chain to other penicillins and cephalosporins (except ceftezole).
Cross-reactivity may also occur through IgE antibodies that recognise neodeterminants of the B-lactam ring structure.
After a diagnosis of cefazolin anaphylaxis, SPT to the culprit (only small numbers of pts with cefazolin anaphylaxis have a PST), then penicillin DPT. If negative DPT, penicillins can be prescribed.
Low ++ risk cross reactivity penecillin & 3rd gen cephalosporin
What are cardiovascular physiological changes seen in the first 24-48 hours & from 48-72hrs following significant burn?
Early hypodynamic phase (1st 24-48hrs):
increased SVR & PVR (ADH, catecholamines, haemoconcentration)
reduced intravascular volume, fluid loss from circulation & hypoperfusion
responds to fluid challenge, may need stress dose steroids IV hydrocortisone q6h
reduced CO, even before reduction in plasma volume
decreased SvO2
later hyper dynamic hyper metabolic phase (from 48-72hrs):
reduced SVR (impaired vasoconstriction)
limited response to fluid resus (may need inotropes)
increased ++ CO (2-3x)
tachycardia
massive energy expenditure
increased SvO2 (peripheral AV shunting)
can last days to weeks
if left untreated, multi-organ failure= the inevitable result
pathophysiology, symptoms & common causes of intracranial hypotension?
imbalance in production, absorption or flow of CSF leads to low ICP & sagging of the brain within the skull, . Usually postural headaches worse upright, eased by recumbency (or agg by coughing/strain, jugular venous compression) but they may be nonpostural & other neurologic symptoms can occur (or N&V, neck pain/stiffness, tinnitus, dizziness). May get more severe symptoms due to brainstem compression. Most commonly due to persistent CSF leak after lumbar puncture, may be spontaneous (eg. due to dural weakness).
Next step if a pt presents with headache, typically orthostatic, +/- associated symptoms, without Hx of dural puncture?
Brain MRI shows diffuse meningeal enhancement & “brain sagging” (SEEPS: subdural fluid, enhancement of pachymeninges, engorgement of venous structures, pituitary enlargment, sagging of brain). Next step is MRI brain with & without gadolinium & MRI spine without gadolinium, looking for CSF leak. If no evidence CSF leak but still strong clinical suspicion, could do heavily T2-weighted MR myelography without dural puncture or gadolinium (benefit as doesn’t risk gadolinium exposure, radiation or risks of intrathecal injection) or CT myelography (if noninvasive studies nondiagnostic- this involves contrast infusion via dural puncture also uses ionising radiation) or MR myelography with gadolinium injection or, if nondiagnostic or suspect CSF-venous fistula, digital subtraction myelography (useful for rapid leaks) & if still no evidence, proceed to radioisotope cisternography (intrathecal injection). If still no evidence of CSF leak, consider other causes.
What’s low CSF pressure?
<60cmH2O, it may be normal even if active CSF leak.
Is head CT useful for Dx spontaneous intracranial hypoT?
no- it’s often normal.
Is head CT useful for Dx spontaneous intracranial hypoT?
no- it’s often normal.
Whats normal CSF opening pressure in lat decubitus?
6-20cmH2O in adults or children, may be up to 25cmH2O in obesity
DDx for spont intracranial hypotension?
migraine, cervicogenic headache, Chiari I malformation (low-lying cerebellar tonsils), postural tachycardia syndrome (orthostatic intolerance), PDPH
Once diagnosis established, what is the Rx for spontaneous intracranial hypotension?
lumbar epidural blood patch effective in 64%- do with 10-20mL autologous blood, at “blind” lumbar level vs attempting the site of leak if the leak is above to SC terminus or site unknown, but if mild/moderate symptoms <2/52 (and NO Hx precipitating injury or connective tissue disease), consider conservative therapy (bedrest/minimise upright posture, oral hydration, caffeine PO 200-300mg 2-3x/day, abdo binder, analgesia). Approx 50% will require >1 EBP. If sysmptoms persist, could try location of leak & EBP there.
contraindications to EBP? Adverse effects?
pt refusal, localised infection at the site, increased ICP, coagulopathy, taking anticoagulants, active systemic infection (pt must be afebrile).
Adverse effects: back pain, radiculopathy, leg paraesthesia, fever. Rarely transient bilat paraplegia & cauda equina syndrome from arachnoiditis if high-volume EBP, may develop headache/other symptoms from intracranial HTN.
How to tell if an image is T1 or T2?
For T2, the grey-white matter will be switched (ie. grey lighter than white). Usual (grey darker than white)= T1-weighted. Fat bright on T1, fluid brighter on T2.
mechanism of EBP?
tamponade of the leak (immediate symptom improvement may occur) then fibrin deposition & scar formation (within 3/52)
mechanism of EBP?
tamponade of the leak (immediate symptom improvement may occur) then fibrin deposition & scar formation (within 3/52)
is efficacy of EBP lower for spont intracranial hypoT or PDPH?
spontaneous intracranial hypotension, up to 57% may require repeat blood patch
How to manage a pt with persistent symptoms of spontaneous intracranial hypoT despite EBP?
diagnostic evaluation to lacate site of CSF lead & guide targeted treatement of EBP at the spinal level of the leak or surgical/endovascular repair.
which conditions are NOT associated with raised baseline serum mast cell tryptase level?
liver failure
ETOH consumption
What’s response surface modelling used for in anaesthesia?
evaluating the interaction of (typically 2) drugs for a given endpoint
does tracheal tube size refer to internal or external diameter?
internal
to which side should I face the ett bevel for the best view?
left
to which side should I face the ett bevel for the best view?
left
What’s the reduction in renal blood flow with infrarenal aortic XC? Why?
up to 40%, due to incr renal vascular resistance of up to 75%
Why may renal & hepatic flow be relatively preserved with infrarenal aortic XC in modern anaesthesia cf splanchnic?
kidney has intrinsic autoregulation, liver has dual supply of blood flow (hepatic arterial buffer response), GI region may lack these mechanisms
What happens to descending aortic blood flow & cardiac index during infrarenal aortic XC?
significant decrease, likely due to increased afterload & myocardial dysfunction
what’s the clinical importance of splanchnic hypoperfusion (which occurs with descending aortic blood flow reductions during XC)?
associated with delayed postop recovery of GI function, prolonged GI intramucosal acidosis is ass’d with periop M&M
What’s the outer diameter of the ETT connector for the breathing system?
15mm
what are some safety features of laser ETTs?
may be wrapped in laser resistant metal foil, cuff may be filled with saline, which may be coloured with methylene blue dye, may have 2 cuffs
benefits of fenestrated tracheostomy tubes
allows pt to speak. Breathing around the cuff & through fenestration as well as stoma reduces airway resistance & assists weaning when spont breathing
another name for laryngectomy tube? Benefits?
Montandon tube, offers better surgical access as breathing system connected well away from surgical field
contraindications to methylene blue?
G6PD deficiency (lack of NADPH prevents methylene blue from working & leads to haemolysis)
renal impairment
methaemoglobin reductase deficiency
nitrite-induced methaemoglobinemia due to cyanide poising
hypersensitivity
Also methylene blue may precipitate serotonergic crisis in pts taking serotonergic meds (MAO inhibition)
what CAN methylene blue be used for?
methemoglobinaemia
catecholamine-refractory vasoplegia
septic shock
hepatopulmonary syndrome
antimalarial
antineoplastic
dye/stain (eg. enhance surgical visualisation of parathyroid glands, place in ETT cuff of laser tubes)
neutralises heparin
priapism
treating ifosfamide neurotoxicitysympt or asympt w»_space;20% metHb (>10% if risk factors eg. anaemia or IHD)
Dose of methylene blue for vasoplegia?
1.5-2mg/kg IV over 20-60mins
what clinically important enzyme can methylene blue inhibit? Clinical implications?
monoamine oxidase with high selectivity for MAO-A, the isoform responsible for serotonin metabolism.
Doses as low as 1mg/kg may –> severe serotonin toxicity.
What are signs of Horner’s syndrome?
ptosis (& may have “reverse ptosis” elevation of lower lid)
miosis (pupillary near & light responses preserved but may be lag at dilating in dim conditions)
anhydrosis
flushing face
warm arm
What does a successful stellate ganglion block produce?
Horner’s syndrome, since it causes sympathetic blockade of the ipsilateral face & arm.
What are WHO IV pregnancy categories (pregnancy not recommended)?
pulmonary arterial HTN
severe systemic ventricular dysfunction (EF <30%)
severe MS
severe symptomatic AS
severe aortic dilatation (>50mm) in aortic disease associated with bicuspid aortic valve
vascular ehlers-danlos
Marfan with aorta dilated >45mm
native severe coarctation
complicated Fontan
At what fibrinogen level should replacement be started during PPH?
2g/L
What are the ANZCOR recommendations for tachycardia with a pulse if the pt stable with narrow QRS & irregular rhythm?
rate control with B blocker or IV digoxin. Consider amiodarone if onset <48hrs (300mg IV over 20-60mins then 900mg over 24hrs (consider reduced dose if pt on digoxin))
What are the ANZCOR recommendations for tachycardia with a pulse if the pt stable with narrow QRS & irregular rhythm?
rate control with B blocker or IV digoxin. Consider amiodarone if onset <48hrs (300mg IV over 20-60mins then 900mg over 24hrs (consider reduced dose if pt on digoxin))
what classes a pt with tachycardia as “unstable”?
reduced consciousness
SBP <90mmHg
chest pain
heart failure
rate-related symptoms uncommon @ <150bpm
what’s the simplest approach for rapid AF in acute setting?
B blocker (metoprolol 5mg IV) BUT contraindications= bronchospasm or evidence decompensated heart failure
OR
digoxin 250-500microg IV or PO(which is the drug of choice fro rate control in heart failure however has slower rate of onset- IV 5-30mins, PO >30 mins, vs B blocker 3-7mins))
What energy is used for synchronised cardioversion?
70-120J biphasic but in AF an initial larger shock (120-150J biphasic) recommended
risks of using amiodarone & digoxin together?
risk dig toxicity due to reduced digoxin clearance (risk severe bradycardia, conduction disturbances, idioventricular rhythm
risks torsades
What’s MINS? significance?
myocardial injury during the first 30 days after non cardiac surgery, of ischaemic etiology.
There is evidence of elevated cTn with at least one value above the 99th percentile upper reference limit.
Independently associated with mortality.
includes MI (symptomatic & non symptomatic) or post-op troponin elevation with no evidence of non ischaemic etiology.
What’s medical management for asymptomatic troponin elevation (MINS)?
control BP, HR
consider aspirin & statin
consider, for risk stratification/management: cardiac enzyme trends until falling, lipid panel, HbA1c, echo, functional stress test
What’s the medical management for type 1 NSTEMI?
control BP, HR (goal 50-70bpm if able to tolerate this BP & no concern for depressed LVEF), pain
consider aspirin
consider P2Y12 inhibitor (only if ischaemic benefit outweighs bleeding risk)
heparin drip
B-blocker
atorvastatin 80mg
What is NOT a complication from dural puncture and resultant intracranial hypotension?
encephalitis
Differential diagnosis for postpartum headache (in order of prevalence) & their Rx?
tension (simple analgesia, massage, physiological) & migraine (usually recurring, unilateral, may be pulsating & with nausea/photophobia/visual disturbances, may have “aura”- NSAIDs, 5-HT agonists (sumatriptan)) headache
pre-eclampsia (headache a serious premonitory sign & is present in 50% who go on to develop eclampsia) or eclampsia (hypertensive encephalopathy w headache, visual disturbance, N&V, seizures, stupor which may –> coma). analgesia & control underlying condition
PDPH
cortical vein thrombosis (headache often ass’d w focal neurology & seizures. may have a postural component- may be ass’d w PDPH (?secondary to cerebral vasodilation after CSF leak & prolonged dehydration). Dx with MRI & MR venography. Mx with anticoagulation, symptom control with focus on seizure prevention)
SAH (more common if an arteriovenous malformation, cerebral aneurysms or hypertensive encephalopathy. Acute onset intense, incapacitating unilateral headache accompanied by nausea, neck stiffness & altered consciousness). diagnose with CT, seek urgent neurosurgeon opinion.
posterior reversible leucoencephalopathy syndrome: severe, diffuse headache, may have focal neurological deficit, may be an association with pre-eclampsia (loss of cerebral autoregulation compromises BBB)- imaging shows symmetrical cerebral oedema.
space-occupying lesions (tumour, subdural haematoma): dull headache ass’d with symptoms of raised ICP (N&V). may have focal neurology & altered consciousness. Neurosurg if bleed or tumour.
cerebral infarction/ischaemia
sinusitis
meningitis (neck stiffness, photophobia, fever, +ve Kernig & Brudzinski & may have petechial rash, do CT to exclude other Dx & confirm with CSF culture, early ABx)
What’s the risk of accidental dural puncture with epidural?
1:100-1:200, 50% of these will get PDPH.
what causes the pain of PDPH?
CSF leak–> intracranial hypotension & pain is from traction on intracranial structures or compensatory cerebral vasodilation. with standing, increased hydrostatic pressure gradient augments CSF leakage.
symptoms associated with PDPH?
postural headache (worse upright, strain, cough & improves with lying down)
associated: neck stiffness, nausea, visual disturbance, photophobia, auditory symptoms
in severe cases, cranial nerve palsy of abducens (susceptible to traction when CSF volumes are low)
symptoms associated with PDPH? significant complications?
postural headache (worse upright, strain, cough & improves with lying down)
associated: neck stiffness, nausea, visual disturbance, photophobia, auditory symptoms
in severe cases, cranial nerve palsy of abducens (susceptible to traction when CSF volumes are low) may occur. CN VII may also be affected. only do EBP if other causes of cranial n palsy (haemorrhage & thrombosis) excluded.
cortical vein thrombosis or cerebral venous sinus thrombosis may be associated with PDPH (cerebral vasodilation after CSF leak, damage to cerebral venous endothelium & prolonged dehydration)
cranial-subdural haematoma: caudal shift of brain may–> rupture of the fragile subdural bridging veins
seizures
what effects do caffeine & 5-HT agonists (eg. sumatriptan) have on cerebral vasculature?
vasoconstriction
what’s the chance of complete headache cure from a single epidural blood patch? how many cases require a repeat blood patch?
50%
40%
How soon after accidental dural puncture should EBP be performed?
48-72hrs, higher failure rate if within 24hrs of dural puncture.
what volume of blood should be injected for an epidural blood patch?
up to 20mL; inject until the pt feels back or buttock or leg pain/pressure (nerve root irritation)
what advice should be given post EBP?
lie flat for…, have stool softeners, admit overnight for observation, avoid strain or too much physical exertion
early complications after EBP?
backache (which may be severe) during injection, neck or backache may persist for 24hrs even if get instantaneous relief of headache, fever, bradycardia, seizures. Late= meningitis, spinal-subdural haematoma or intrathecal haematoma, arachnoidits, cerebral venous sinus thrombosis, radicular pain, seizures, infection (either localised to the lower back or meningitis)
What are some signs/symptoms & examination findings in acromegaly?
pituitary adenoma on brain MRI or CT
visual field defects
prominent supraorbital ridge
large nose & jaw
teeth separated or lacking
abnormal glucose tolerance test, glycosuria, polyuria
hypertrophy of sebaceous & sweat glands
galactorrhea (prolactin)
cardiomegaly
HTN
spade-shaped hands & feet
arthrosis
peripheral neuropathy
sexual dysfunction
What are the findings of growth hormone tests for a patient with acromegaly?
They’d have elevated growth hormone (>0/4microg/L) and/or elevated IGF-1
during the OGTT, growth hormone will NOT be suppressed to <0.4microg/L
paediatric dosing for IM adrenaline?
150microg (0.15mL of 1mg/mL) if <6yo
300microg (0.3mL) if 6-12yo
every 5 mins prn
which body weight should be used for tidal volumes in ARDS?
predicted body weight based on gender & height; not ideal body weight.
5mL/kg predicted body weight.
equations for predicted body weight in males & females?
males:
PBW= 50 + 0.91 x (height in centimetres - 152.4) kg
females:
= 45.5+ 0.91 x (height in cm - 152.4) kg
Goal Pplat for ARDs?
<30cmH2O
Goal VT for ARDS?
6mL/kg predicted body weight in absence of severe acidosis
ARDs diagnostic criteria?
PaO2/FiO2 <=300mmHg with PEEP >=5cmH2O
within 1 wk of known clinical insult
billet opacities on chest imaging
not fully explained by cardiac failure or fluid overload
ARDs diagnostic criteria?
PaO2/FiO2 <=300mmHg with PEEP >=5cmH2O
within 1 wk of known clinical insult
billet opacities on chest imaging
not fully explained by cardiac failure or fluid overload
What should probably not be done for ARDs?
systematic recruitment maneouvers
What should be applied for moderate-severe ARDS (P/F <200mmHg)?
PEEP >12cmH2O if it improves oxygenation without haemodynamic compromise or significant decrease in lung compliance; must maintain Pplat <30cmH2O
What should be applied for ARDS with P/F ratio <150mmHg?
continuous NMB infusion (within first 48hrs of ARDS Dx ideally) & prone positioning >16hrs/day for several consecutive days
What to consider if P/F <80mmHg?
discussion of V-V ECMO (refractory hypoxaemia or where protective ventilation can’t be applied)
Which muscle group has the greatest resistance to action of NDMRs?
diaphragm- contains a high proportion of type II fibres (diaphragm= 45% type I) with relatively high density of nAChR (conferring some resistance to NMBDs), relatively large muscle fibres attenuate rapidity of onset, yet high perfusion along with the higher density of glycolytic type II fibres helps speed offset
Mnemonic for colour of doppler?
BART
blue= flow away from transducer
red= flow towards transducer
Do plasma components (FFP, cryo, cryodepleted plasma) have to be ABO compatible? how about RhD type?
yes (as they may contain donor anti-A or anti-B)
however plasma components of any RhD type can be given regardless of the RhD type of the recipient & RhD immunoglobulin isn’t required in these situations
Do platelets have to be ABO compatible? how about RhD type?
ideally- since incompatible plasma may cause haemolysis (eg. a group A pt given group O platelets- the ABO is compatible but plasma not compatible). Apheresis platelets have low-titre anti-A/B.
If the RhD is incompatible (RhD +ve platelets given to a RhD negative pt), there may be sensitisation to residual red cell antigens so prophylactic RhD Ig may be needed if RhD +ve puts given to a RhD -ve pt, esp female children or women of childbearing age.
What’s the first & 2nd choice for plasma components for a group A pt?
A (-ve or +ve)
then AB
What’s the equation for NNT?
1/ARR
What’s absolute risk reduction?
incidence in control - incidence in treatment group
When should the aortic balloon pump be inflated? why?
onset of diastole. it gives rise to a start “V” on the art waveform (then diastolic augmentation). aims to increase coronary perfusion.
when should aortic balloon pump be deflated? why?
end of diastole, reduces aortic EDP & systolic pressures which decreases afterload, cardiac work, myocardial consumption & increases CO. it’ll reduce aortic end-diastolic pressure cf unassisted.
what’s the problem with balloon pump being inflated before dicrotic notch?
diastolic augmentation encroaches on systole & may cause premature closure of AV, increase LVEDV/P, incr LV wall stress or afterload.
what’s the problem if IABP inflated after dicrotic notch?
trace shows lack of sharp V. suboptimal coronary perfusion.
problem of deflating IABP early?
sharp decrease after diastolic augmentation, making the diastolic augmentation suboptimal which reduces coronary perfusion & there may even be retrograde carotid blood flow, plus the afterload reduction may be suboptimal
problem with deflating IABP too late?
incr afterload (the assisted aortic EDP may be equal to unassisted) may impede LV ejection, there may be a prolonged rate of rise & reduced assisted systole & the augmented diastole may appear prolonged.
with what should the IABP deflation correspond in pts with arrhythmia?
While electrical triggers are better, if arrhytthmias use art pressure waveform instead of ecg. R wave, mechanical event is just prior to AV opening, just before upstroke on systolic pressure waveform (inflation is just at dicrotic notch if ecg reliable, T wave ecg (TIN))
What’s a sentinel event? examples?
subset of adverse patient safety event that is:
wholly preventable
resulted in serious harm to or death of a patient
the most serious incidents
surgery at wrong site, wrong pt or wrong surgery that led to serious harm or death.
retention of foreign object–> serious harm or death
haemolytic blood transfusion reaction from ABO incompatibility–> serious harm or death
suspected suicide of pt on acute psych unit/ward
med error–> serious harm or death
physical/mech restraint–> SHOD
d/c or release of an infant to an unauthorised person
use of incorrectly positioned oral or NGT–> serious harm or death
what’s malefeasance?
wilful & intentional act injuring a party
what’s an adverse event?
incident leading to pt harm
what’s medical misconduct?
Behavior that is professionally unethical and/or illegal, e.g., negligence, incompetence, impairment from drugs or alcohol, egregious substandard care.
What’s the most likely case of collapse & LL weakness immediately on standing following foam sclerotherapy?
thromboembolic event
which anticoagulant most effectively cleared by haemodialysis?
dabigatran
Which tooth most commonly damaged during laryngoscopy?
L) central maxillary incisor
What’s a benefit of cefazolin?
superior gram-positive antimicrobial activity compared with cephalosporins of later generations
which generation cephalosporin is cefazolin?
1st
What are absolute contraindications to drug provocation test?
drug reaction with eosinophilia & systemic symptoms (DRESS), Stevens-Johnson syndrome, toxic epidermal necrolysis & other severe cutaneous reactions, severe IHD, pregnancy
What’s the estimated rate of anaphylaxis to cefazolin in a pt with IgE-mediated reaction to penicillin?
1%
What are some of the early (first 24-48hrs) physiological changes with burns?
“hypodynamic” phase
hypoperfusion (fluid loss)
decreased intravascular volume
incr SVR & PVR (ADH, catecholamines, haemoconcentration)
reduced CO
decreased SvO2
responsive to fluid challenges
side effects of adenosine administration in order of likelihood?
facial flushing (36%)
dyspnoea (35%)
chest pain (35%)
GI discomfort
headache
AV block
ST-T changes
arrhythmias
bronchospasm rare (0.1%)
also likely have:
impending sense of doom
coronary steal
Overal there are higher risks of what soon after TAVI? SAVR? How about mortality & disabling stroke @ 2yrs?
TAVI: HIGHER rates of short-term re-intervention, AV conduction disturbances & need for a PPM, major vasc complications, paravalvular leak (AR), mod-severe HF symptoms. Does have lower rates of major bleeding & AF.
SAVR: higher gradient across valve & smaller valve area, new AF, major bleeding, AKI, 30-day transfusion requirement.
All-cause mortality & disabling stroke similar across groups (nominally but not significantly higher in the TAVI group).
What does power mean in research?
the probability of correctly finding a given, existing difference as significant. Is 1-B (type II error) & represents the sensitivity. Arbitrarily set @ 80% (ie. if a difference or effect exists, there’s 20% probability of type II error).
What’s a type II error?
the null hypothesis incorrectly accepted
How to increase the power of a study?
increase the sample size, have a larger minimum effect size or difference representing clinical importance, having a smaller standard deviation in the population (hence smaller sample size needed), p value, (?higher incidence of outcome of interest in the population)
4 determinants of power calculation
p value
standard deviation (variance) in population
difference to be detected
sample size
What’s the type 1 error rate usually set at?
What’s the type 1 error rate usually set at?
If there’s more than one outcome of interest, is the probability of a type 1 error (false +ve) higher or lower? How to account for this?
higher. Can reduce risk by lowering the significance level. Bonferroni correction lowers the threshold for significance by dividing the overall type 1 error rate by the number of comparisons or hypotheses tested.
Epidural filters are designed to retain particles down to a diameter of
0.2 micrometers (200 nanometers)
What’s the HR goal in AF?
reduce it to 80bpm, usually with rate slowing therapy eg. oral B blocker or CCB as outpt if no or mild symptoms. If pt is haemodynamically unstable after rate control, could use rhythm control.
which pts with new onset AF should not have immediate anticoagulation?
if bleeding risk exceeds benefits or CHA2DS2-Vasc score of 0 in men or 1 in women & short paroxysms of AF that self-terminate.
What’s the most important initial therapeutic intervention in DKA?
fluid replacement followed by insulin administration- use crystalloid with sodium 130-154mmol/L
which lobe of lung has a medial & lateral segment?
R) ML
with which medication is a pt with known sux allergy most likely to demonstrate cross-reactivity?
rocuronium
what’s a condition associated with an elevated A-a gradient that CAN’T be corrected with incr FiO2?
shunt, eg. atelectasis, ARDs
what’s the alveolar gas equation?
PAO2 = FiO2 x (Pb-PsvpH2O) - (PaCO2/RQ)
In experienced operators, what’s more sensitive for detecting PTx? CXR or lung PoCUS?
lung US
setup position for PoCUS for Dx of PTx?
pt supine/semi-recumbent, probe anterior chest wall @ 2nd ICS MCL, sagittal orientation, marker cephalad
in M mode, what would we see with normal lung movement vs PTx?
seashore sign (motion of lung) for normal
bardode/stratosphere sign if no lung motion (PTx)
What are the A lines on lung US?
horizontal, reverberation artefact of the pleural line, indicate dry interlobular septa, if they are predominant, it suggests PCWP <=13mmHg (90% sens, 67% spec) & suggests IVT may safely be given without concern for pulm oedema
what are B lines on lung US?
indicate alveolar/interstitial fluid or fibrosis at the lung surface (if >-3 B lines). B lines are sensitive for pulm oedema & are ABSENT IN PTx.
what sign on PoCUS is pathognomonic for PTx?
lung point- on M mode, transition btwn where there is & isn’t lung sliding
What’s a parachute device
aka ventricular partitioning device, percutaneously inserted cardiac device aimed at improving cardiac output and reducing cardiac remodeling in patients following MI.
Improves compliance, reduces LVEDP & improves ventricular filling, reduces wall stress, helps maintain SV & CO
The brachial plexus is formed from what?
anterior rami of the C5-T1 spinal nerves
what does the brachial plexus (ant rami of C5-T1 spinal nerves) pass between as it enters the base of the neck?
anterior & middle scalene muscles
what do the posterior rami of spinal nerves supply?
skin & musculature of intrinsic back mm
what are the 3 trunks of the brachial plexus & of what do they comprise?
superior (C5&6)
middle (C7)
inferior (C8, T1)
what’s the posterior triangle of the neck & which anatomical structures are contained within?
SCM, middle 1/3 of clavicle, trapezius
contains divisions of brachial plexus (ant & post)
what do the divisions (ant & post) of the brachial plexus form when they have left the posterior triangle & entered the axilla?
cords
what are the cords of the brachial plexus named relative to?
axillary artery
lateral (ant divisions of sup & middle trunk)
posterior (posterior division of sup, middle & inf trunk)
medial (ant division of inferior trunk)
What are the branches of the brachial plexus & their sensory/motor supply?
axillary (C5,6): teres minor (stabilise GHJ, ER shoulder) & deltoid (stabilise HOH & abduct GHJO, superior lat cutaneous nerve of arm (regimental badge area)
musculocutaneous (C5-7): brachialis (pure flex), biceps brachii (flexion & supination), coracobrachialis (flex & adduct shoulder & stabilise humeral head (w deltoid & triceps)), sensory lateral forearm
median (C5-T1): forearm flexors, thenar mm, 2 lateral lumbricals (index & middle fingers), sensory to lateral palm & lateral 3.5 fingers of palmar surface of hand
radial (C5-T1): triceps, wrist & finger extensors, sensory to posterior arm & forearm, posterolateral hand
Ulna (C8-T1): hand muscles aside from thenar mm & 2 lateral lumbricals, FCU & medial FDP. medial 1.5 fingers & associated palm area.
from what is the cervical plexus formed?
anterior rami of C1-4 spinal nerves
What’s erb’s point?
the “nerve point” of the neck, where the cutaneous branches of the cervical plexus exit the middle of the posterior border of SCM, utilised for cervical plexus blocks
What are the sensory branches of cervical plexus? (pic in “on hand”)
greater auricular from C2-3, sensation to external ear & skin over parotid gland
transverse cervical nerve from C2-3, curves around SCM & supplies anterior neck, anterolateral skin & upper sternum
lesser occipital nerve C2-3, posterosuperior scalp
supraclavicular: C3-4, supplies skin of supraclavicular fossa
From what is the lumbar plexus formed?
anterior rami of T12-L4
What are the six major peripheral nerves of the lumbar plexus?
iliohypogastric- T12-L1, IO & TA, posterolateral gluteal skin
Ilioinguinal- L1, IO & TA, supplies antero-medial thigh, genital branch: scrotal & root of penis, labia/mons
genitofemoral- L1-2, cremasteric, skin of scrotum, mons & labia, femoral branch: upper anterior thigh
lateral cutaneous nerve of thigh: L2,3, no motor, anterolateral thigh down to knee
obutrator: L2-4, medial thigh muscles (OE, AL, AB, AM & gracilis), sensory to medial thigh, branches to hip & knee
Femoral: L2-4, anterior thigh muscles (iliacus, pectineus, sartorius, quads femoris), sensory anterior thigh–> medial leg
From where does the sacral plexus originate?
anterior rami of L4-S4 spinal nerves (the sacral plexus S1-4 join L4-5 to form the lumbosacral trunk)
What are the major peripheral branches of lumbosacral plexus?
superior gluteal- L4-S1, glute min, med & TFL, no sensory
inf gluteal- L5-S1, glute max
post fem cutaneous: S1-3, skin posterior thigh, leg & perineum
pudendal: S2-4, perineal skeletalmuscles incl sphincters, penis & clitoris & most perineal skin (S2,3&4 keeps poo off the floor)
sciatic: L4-S2, tibial innervates muscles of posterior compartment of thigh (aside from SH BF), hamstring component of add magnus & all muscles of post compartment of leg & sole of foot. common fibular (L4-S2) for SHB, muscles of ant/lat leg & EDB. tibial (L4-S3) supplies skin of posterolat leg, lateral foot & sole of foot. common fibular supplies lateral leg, dorsum of foot (sup fibular) & btwn 1st & 2nd webspace (deep fibular)
diagnostic cutoffs for OSA severity in children?
AHI or RDI 1-4.9= mild
5-9.9= mod
>10= severe
adults mild 5-14, mod 15-30, severe >30
What’s the S1 heart sound? and S2?
S1= closing of atrioventricular valves (mitral & tricuspid)
S2= closure of semilunar (aortic & pulmonic) valves
What’s the normal pattern of S2 splitting with respiratory cycle?
A2 is heard before P2, increased split with inspiration
What may cause wide splitting of S2 (ie. splitting during expiration, wider with inspiration)?
Anything delaying R) heart emptying:
-delayed closure of the pulmonary valve
-may occur with delayed conduction down the R) bundle (R) BBB, pre-excitation LV, pacing LV, LV prem beats)
-pulmonary stenosis
-PAH
what may increase intensity of P2?
pulmonary HTN
ASD
first rule out causes of a lower intensity A2, eg. MR, AR, low diastolic arterial pressure, severe immobile aortic valve
what causes fixed splitting of S2 (ie. split w both insp & exp & doesn’t lengthen with insp’n)?
ASD, R) heart failure, pulm HTN
What causes paradoxical splitting?
delayed conduction down L) bundle branch (L) BBB, pre-excitation RV, RV pacing, prem RV beats)
aortic stenosis
what causes a single S2?
loss of either A2 or P2, eg:
severe AS or AR
congen absence of pulm valve
may be difficult to hear P2 w obesity, emphysema, pericardial fluid
which vascular access is most commonly used for cardiac catheterisation to obtain haemodynamic data?
radial- less bleeding complications
often use the antecubital vein for R) heart cath when using radio for arteriography & LV haemodynamics
when may the transseptal approach to accessing LA or ventricle be desirable?
accurate decision making in MS, where PCWP is unreliable as surrogate for LA pressure
name of balloon passed through fossa ovalis, under fluoroscopic guidance, to Ax MV disease, access for mitral balloon valvuloplasty & perc repair of sec MR?
Brockenbrough
How does the pressure trace of the fem artery compare with aortic root?
delayed & higher systolic pressure, overshoot (by <20mmHg) due to summation effect of reflected waves within arterial system
In which situations is the femoral trace overshoot inaccurate? what should do?
young pts, aortic insufficiency or evidence of PVD (which would markedly reduce the overshoot)- should measure central aortic pressure above the AV (simultaneous with LV pressure)
normal mean RA pressure?
1-8mmHg
normal mean RA pressure?
1-8mmHg
what does the RA A wave follow on ecg?
p wave
what does the RV systolic upstroke immediately follow on the ecg?
qrs
normal RV diastolic & peak pressures?
1-8 & 15-30mmHg
what’s the dicrotic notch or incisura on the pulm artery pressure waveform?
pulmonic valve closure
normal PA pressures?
15-30/4-12mmHg
How does LA & pulm cap wedge pressure tracings vary?
nearly identical but the PCW is lower & slightly delayed due to transmission of pressure backward through pulm capillaries
normal mean LA pressure?
4-12mmHg
what is peak LV systolic pressure coincident with on the ecg?
T wave
what is peak LV systolic pressure coincident with on the ecg?
T wave
what’s normal LVEDP?
4-12mmHg
in the normal situation, are mean PCWP & end-diastolic PA pressure equal?
yes
With what does the LVEDP correspond on the ecg? what’s it known as on the LV pressure trace?
R wave, “z point”, situated @ the downslope of LV “a” wave
How would the LV pressure tracing appear in diastolic dysfunction?
abnormal- continuing pressure decline over mid-diastole (rather than the rapid, then slow phases of diastolic filling followed by the “a” wave generated by atrial contraction)
what are some factors that may raise LVEDP (normally <12mmHg)?
volume overload (AR, MR, high-volume shunts)
reduced LV contractility
concentric hypertrophy (eg. HTN, valvular stenosis, restrictive or infiltrative cardiomyopathy)
If aortic pressure trace showed reduced diastolic pressure, likely DDx?
AR
findings on LV pressure trace of pt with HOCM?
elevated & abnormal LVEDP waveform, may also have elevated LVEDP in MR
What generally & specifically needs to be anaesthetised for successful awake intubation?
Nasal passages (if nasal route) or oral
gag and cough reflexes need to be suppressed effectively and laryngospasm prevented
Nerves that need to be topicalised prior to awake nasal fibreoptic intubation?
Upper airway supplied by:
TRIGEMINAL
GLOSSOPHARYNGEAL
VAGUS nerves
Sensation to the nasal cavity ALL from trigeminal nerve:
anterior ethmoidal (from ophthalmic (V1)–> nasociliary–> ant ethmoidal) provides anterior 1/3 of septum & ant nasal cavity (eg. nares)
the greater & lesser palatine & nasopalatine nerves, branches of maxillary (V2) which travel through pterygopalatine ganglion (in sphenopalatine fossa posterior to middle turbinate) supply remainder of nasal cavity (turbinates, post 2/3 nasal septum)
Glossopharyngeal (CNIX) provides sensory to most of pharynx (pharyngeal branch), post 1/3 tongue/anterior surface epiglottis/vallecula (lingual branch), fauces, tonsils (tonsilar branch), & most of the pharynx
branches of vagus (CNX)
-posterior & lateral walls of the pharynx are from pharyngeal nerve (branch of vagus- joins with pharyngeal branch of glossopharyngeal to form pharyngeal plexus)
-sup laryngeal nerve has ext branch (cricothyroid) & internal branch (sensory to skin above VCs incl base of tongue, laryngeal surface of epiglottis, aryepiglottic folds & arytenoids)
-RLN: motor to other VC muscles aside from cricothyroid & sensory below glottis
ant 2/3 tongue is from lingual nerve (from V3, mandibular, not nec for nasal approach to fibreoptic)
What minimum macroshock current could cause VF if pass through heart?
100mA (current is from surface contact)
microshock current (direct contact with myocardium): 100microamps (0.1mA)
How to spot a posterior MI?
Posterior MI is suggested by the following changes in V1-3:
Horizontal ST depression
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio > 1) in V2
In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.
How soon after spinal cord injury is return of reflexes generally seen?
1-3 days (following the initial flaccid paralysis & areflexia/neurogenic shock)
What’s spinal shock? what happens after that?
loss of reflexes below level of SCI, results in flaccid areflexia, usually along with hypotension of neurogenic shock
gradual return of reflex activity when reflex arcs below redevelop, often–> spasticity & autonomic hyperreflexia
areflexia days 0-1
initial reflex return days 1-3
early hyperreflexia days 4-28
late hyperreflexia 1-12/12
If giving 8.45% sodium bicarb for hyperkalaemia cardiac arrest, what dose?
1mmol/kg, initially given over 2-3 minutes then as guided by arterial blood gases
1mmol/mL therefore 60mL for a 60kg adult
what causes the coagulopathy due to intrahepatic cholestasis of pregnancy?
lack of fat-soluble vitamin (K) absorption (due to impaired bile acid excretion), required for manufacture of coag factors II, VII, IX & X; water-soluble vit K prescribed for obstetric cholestasis.
Adverse effects of mild hypothremia
coagulopathy
incr risk surgical wound infection
incr stay in PACU & hospital LoS
incr ventricular arrhythmias
prol DoA vecuronium & rocuronium, increases plasma [] propofol (mainly due to reduced hepatic blood flow), decreases MAC
postop shivering (which augments metabolic rate)
increased myocardial O2 consumption (HTN, incr metabolic rate)
incr pain
What’s the CXR level of the cavo-atrial junction?
2 vertebral bodies below the carina
Hip adduction in pt undergoing TURBT most likely due to
stimulation of obturator nerve
what rate averaged over 48hours risks propofol infusion syndrome?
5mg/kg/hr for >48hrs (product recomends no >4mg/kg/hr)
what should be monitored if concerned re: propofol infusion syndrome?
pH, lactate, CK after 48hrs (CK [] takes 12-24hrs to peak after onset rhabdo so earlier measurement not of benefit), limit infusion rate to lowest possible, use multimodal sedation.
Signs of cholinergic poisoning (eg. organophasphates, physostigmine, carbamate insecticides, mushrooms, sarin nerve gas)
SLUDGE, Bradycardia/bronchorrhoea/bronchospasm. Confusion, CNS depression, weakness, miosis, GI cramping, vomiting, sweating, brady or tachy
Rx for cholinergic toxicity
100% O2, atropine 0.02mg/kg boluses (for brady, hypoT, secretions). BZD for seizures/agitation, may use bicarb for acidosis, for organophosohates use pralidoxime choride for muscle weakness. Activated charcoal NOT recommended. Avoid sux since the organophosphates inhibit acetylcholinesterase so prol NMB. can use NDNMBDs but they may be less effective due to competitive inhibition @ NMJ (likely need incr doses).
Draw the waveforms for PCV. Pros & cons of this mode?
pros:
higher mean airway pressures & duration of alveolar recruitment- may be better for oxygenation & gas exchange
less risk barotrauma
better @ compensating for leak (higher initial flow)
WOB & pt comfort may be improved
cons:
harder to get consistent TV (depends on compliance) so minute ventilation variable, disadvantageous if need tight PaCo2 (eg. TBI)
may get volutrauma
Draw the waveforms for VCV. Pros & cons of this mode?
more stable MV, useful for tight control of PaCo2 (eg. TBI)
cons:
lower mean airway pressure, may not be as good for hypoxia (insp pause doesn’t really help)
poorer recruitment of lung units with poor compliance, greater risk atelectasis
constant flows may not compensate for leak
Draw the waveforms for PCV-VG. Pros & cons of this mode?
decelerating flow main difference
takes 3 breaths (VCV) to calculate dynamic compliance & then works out the pressure required to delivery desired volume
pros= fuses benefits without magnifying cons of the other modes, ie:
square pressure waveform, favours alveolar recruitment
same relatively high mean airway pressures as with PCV- good for oxygenation
low risk of barotrauma as pressure minimised for prescribed volume
guaranteed MV, preserves PaCo2 control
cons: may get variable TV with variable pt effort as each breath depends on the pressure characteristics of the preceding breath
pressure goal for ARDS ventilation?
<30cmH2O (higher RR, lower TV)
The ANZCA guidelines regarding pre-operative oral intake for infants under 6 months of age
having an elective procedure under anaesthesia are
clear fluids (no more than 3mL/kg) up to 1hr prior to anaesthesia, breastmilk up until 3 hours, formula 4 hours, all else 6 hrs prior to procedure
ANZCA chn >6/12 pre-op oral intake guidelines?
clear fluids (no >3mL/kg) up to 1 hr b4 anaesthesia, limited solids, formula, breastmilk up to 6hrs pre- anaesthesia
The commonest primary cause of death from anaesthesia airway events in the NAP4 report was
aspiration
A patient has bipolar disorder and is on long term lithium therapy. An analgesic which should be avoided is
NSAIDs (eg. indomethacin COX-1 selective & diclofenac COX-2 selective- increase SS lithium [], risks lithium toxicity)
should discontinue lithium 24hrs before surgery
also, metronidazole may incr ss lithium [] & risk lithium toxicity
ACE inhibitors
AII RBs
Diuretics (thiazides, potassium-sparing, loop)
all –> lithium accumulation w supratherapeutic concentrations
risks for lithium tox= change dosing regimen, acute renal failure, hyponatremia
purely excreted by kidneys, narrow therapeutic index, interferes w ADH, cardiac dysrhy, GI disturbance, tremor.
Prolong NMB & reduce Anaes requirement.
Stop lithium >=24hrs prep.
Benzatropine ameliorates the side effects of drugs that antagonise
D2 receptor
D2 receptor blocking drugs may cause acute dystonic reactions (involuntary contraction of extremities, face, neck, larynx- intermittent or sustained.
Thought to be due to imbalance of dopaminergic & cholinergic transmission
what are some drugs withOUT CYP2D6 contributing to metabolism?
hydromorphone (but hydrocodone metabolism IS by CYP2D6, as is tramadol, codeine, oxycodone, amitryptilline, methadone, beta blockers
The catheter type most likely to be associated with bloodstream sepsis per days insertion is
Femoral CVC, then IJ then subclavian
Other factors related to risk of CLABSI?
tunnelled lower risk
placement emergent vs non-emergent
lack of asepsis
skill of operator
catheter care, surveillance, infection control with use (eg. disinfect hub)
prolonged duration in situ
what’s a central line-associated bloodstream infection (CLABSI)
laboratory-confirmed bloodstream infection not related to an infection at another site that develops within 48 hours of a central line placement
what’s the order of pathogens responsible for CLABSI?
GP (eg. coagulase negative staph, enterococci, s. aureus)
then
GN (klebsiella, enterobacter, pseudomonas (more common if neutropenic or severe illness))
candida (more likely with femoral catheterisation, TPN, haematologic malignancy)
To where are PICC lines advanced?
superior cavo-atrial junction (2 vertebral bodies below carina)
what are atypical presentations of sepsis (eg. elderly or immunocompromise)?
hypotension, lethargy, fatigue, altered mental state
How usually treat MRSA? anti-staph that’s not MRSA? and how treat pseudomonas?
vancomycin
cefazolin
beta-lactam & aminoglycoside (eg. cefepime or carbapenem)
Rx for a pt with hysteroscopy syndrome?
3% NaCl 100mL
what’s operative hysteroscopy intravascular absorption (OHIA) syndrome?
fluid overload complications from operative hysteroscopies
example manifestations (& their management) of OHIA syndrome?
altered consciousness
acute pulmonary oedema (CPAP, frusemide, ?GTN): desaturation, creps on lung auscultation
metabolic acidosis (sodium bicarb), hyponatremia
measures to limit risk of OHIA syndrome?
isotonic electrolyte-containing distension media
bipolar electrosurgical instruments
closely monitor fluid status every 30 mins (net & total irrigation fluid amounts should be <3L & <8L, respectively (in these cases, the probability of OHIA is >10%); monitor fluid deficit (fluid overload considered when the fluid deficit is >1L with hypotonic solutions or >2.5L with isotonic solutions in healthy pts, based on expert opinion)
Minimise intrauterine pressure to reduce intravascular & intraperitoneal absorption
What causes metabolic acidosis?
increase in weak acids (eg. serum proteins, albumin, inorganic phosphate) or decrease in the strong ion difference
What’s the strong ion difference?
presence of an excess strong cations (Na+, K+, Ca++, Mg++) over strong anions (Cl-) (the normal value in plasma is 42mEq/L, strong anions or cations are those that exist in a fully ionised state in body fluids)
which approach should be used to quantify acid-base status in critically ill patients?
base excess is equivalent to Stewart’s SID approach
what causes the metabolic acidosis in DKA?
B-hydroxybutyrate & acetoacetate, strong anions produced from the hepatic metabolism of fatty acids
why is lactate a strong anion? which conditions may be associated with lactic acidosis?
lactate is more than 99% ionised
lactic acidosis may be observed in cardiogenic or hypovolaemic shock, severe HF, severe trauma, sepsis
What’s a cause of hyperchloraemic metabolic acidosis?
administration of fluids which reduce the strong ion difference (eg. NaCl which has no SID, cf plasma-lyte which has SID of 47.5
what’s normal SID?
42mEq/L
what’s cardiac index? normal?
CO / BSA
2.5-4 L/min/m2
What are the management principles for a metabolic acidosis?
treat the underlying cause of the acidosis
may give sodium bicarbonate if concern for suppressed cardiac function due to the metabolic acidosis
what’s the rationale for using sodium bicarbonate for a metabolic acidosis?
administering a solution with high SID may increase the pH, improving cardiac function
CXR findings in acute pulmonary oedema?
prominently increased opacity in both lung fields, increased hilar markings, figure 2 in useful tables/figures
actions if concerns arise for OHIA?
communicate w surgeons
ABG
prophylactic diuretics
initial treatment for symptomatic hyponatraemia (whether mild, moderate or severe)?
100mL bolus 3% saline, repeat twice more as needed if symptoms persist.
monitor the serum sodium hourly until it’s increased by 4-6mmol/L after which frequency of monitoring can reduce
General measures= identify & Rx underlyinc cause, identify drugs that may contribute, reduce intake of electrolyte-free water (impose FR, eliminate hypotonic IVT, incr dietary salt)
if SIADH or chronic hyponatremia consider loop diuretics, oral salt tabs & urea.
contraindications to blind NGT insertion in adults include:
BOS#
caustic ingestion or oesophageal stricture (risk perforation)
coagulopathy (epistaxis risk)
severe mid-face trauma (risk cribriform plate destruction)
recent nasal surgery
oesophageal varices
suspected epiglottis
emergency intubation/significant hypoxia
orogastric if coagulopathy or facial truama
what’s Le Fort I? (leforts are fig III)
separation of hard palate from upper maxilla
transverse # through maxilla & pterygoid plates @ level just above floor of nose
what’s LeFort II?
transects nasal bones, anterior/medial orbital walls/floor/inferior orbital rings, posterior maxilla & pterygoid plates
what’s Le Fort III?
separates maxilla from skull base (craniofacial dysjunction), traverses the nasofrontal suture, medial orbital wall, lateral orbital wall (zygomaticofrontal suture), zygomatic arch & pterygoid plates
for which drug should total body weight dosing be used in morbidly obese?
suxamethonium
how should propofol & thiopentone be dosed for maintenance & induction in morbidly obese pts?
LBW for induction, TBW for maintenance
on what dosing scalar should fent & remi be based in morbidly obese?
lean body weight
on what dosing scalar should NDMRs be based in morbidly obese?
ideal body weight
how to calculate ideal BW? what is it?
males ht - 100
females ht -110
the BW associated with maximum life expectancy for a given height
how to calculate lean BW?
males: 50 + 0.9 per cm above 150cm
females: 45 + 0.9 per cm above 150cm
disadvantage of dosing based on ideal BW?
assumes that everyone of a certain height should receive the same dose & doesn’t take body composition into account; in morbidly obese may lead to under-dosing, ideal BW will be < lean BW for a given height
strengths of using lean body weight?
more useful in morbidly obese as LBW increases as TBW increases, albeit not proportional (as TBW ultimately incr out of proportion to LBW)
correlates to CO (important in early distribution kinetics) & drug clearance
mg/kg dose of lignocaine IV for Biers block?
3
benefit of adductor canal block for TKR cf FNB?
comparable analgesia, less motor weakness
cardiovascular effects of hyperthyroidism
Increased resting HR
AF
incr LV contractility
incr CO (incr peripheral O2 needs & incr cardiac contractility)
incr blood volume (reduced MAP incr RASS activation & renal Na+ resorption), preload
decreased SVR & diastolic BP/afterload
may have systolic HTN
may develop high- or normal-output CCF
LVEF doesn’t appropriately increase during exercise, suggesting cardiomyopathy
Incr red cell mass (EPO synthesis promoted by T3)
cardiovascular effects of hypothyroidism?
endothelial dysfunction & impaired VSM relaxation–> incr SVR
diastolic HTN & incr afterload
reduced CO
slower resting HR
how do we calculate the confidence interval for low probability events?
“rule of 3’s”, so the 95% CI is zero + 3/n
what’s sick euthyroid?
low serum thyroid levels in a pt who is clinically euthyroid but sick from another cause; Rx is for the underlying illness vs thyroid replacement
Typically low or low-normal T3, T4, may have rel high rT3 (ie. low T3:rT3). Normal or low-normal TSH.
what are the blood test results for subclinical hypothyroidism?
high TSH, normal T3 &T4
what’s the smallest size ETT manufacturer recommends fit over aintree intubation catheter?
ID >=7.0mm
Which drugs may increase bleeding risk with DOACs?
Those that inhibit CYP3A4 incr risk bleeding with apixaban, eg. fluconazole, a moderate CYP3A4 inhibitor, has a 3.5x incr risk of bleeding on apixaban cf when having apixaban sans fluconazole (esp GI bleeding)- systemic fluconazole only.
Strong dual CYP3A4 & P-gp inhibitors can increase apixaban & rivaroxaban effect.
P-gp inhibitors can increase dabigatran effect.
Examples of strong CYP3A4 inhibitors: clarithromycin, ketoconazole, voriconazole)
Moderate CYP3A4 inhibitors: amiodarone, diltiazem, verapamil, cyclosporine, cimetidine, erythromycin, grapefruit juice
Pgp inhibitors: amiodarone, carvedilol, larrythromycin, itraconazole, ivacaftor, ketoconazole, quinidine
For which pts is dose reduction of apixaban recommended?
low CrCl (avoid if CrCl <15mL/min), body wt & higher age
Those taking strong dual inhibitors of CYP3A4 & P-glycoprotein
what inheritance is hereditary angioedema?
autosomal dominant
what are the signs/symptoms of hereditary angioedema?
well-demarcated angioedema without urticaria or pruritis (cutaneous)
may cause debilitating abdominal pain (GI), nausea or vomiting due to intestinal oedema, or life-threatening laryngeal oedema (upper airway)
symptoms usually take several hours to develop, resolve in 2-4 days sans Rx
what’s the etiology of HAE?
rare autosomal dominant condition
deficiency or dysfunction of the C1 esterase inhibitor which leads to excessive bradykinin, episodic increase in vascular permeability & angioedema
how is the presentation of HAE fundamentally different from the angioedema of allergic reactions?
not mediated by histamine or other mast cell mediators, not responsive to epinephrine, antihistamines or glucocorticoids, must be managed by replacing C1 inhibitor (C1 inhibitor concentrate infusion) or blocking production or functioning of bradykinin
What are some potential triggers for hereditary angioedema?
Dental & medical procedures, intubation/oral surgery/major dental work are particularly high risk, emotional stress, hormonal changes, infections, medications (incl oral contraceptives & ACE-inhibitors)
What Rx should be given to pts with hereditary angioedema prior to dental work, surgery as prophylaxis? (high risk procedures= those involving head & neck incl intubation or any airway/head& neck instrumentation)
Intravenous C1-INH concentrate (Berinert), 1-6hr before procedure, aiming for functional C1-INH level of >=50% of normal at the time of procedure (usually get this with 20IU/kg body wt)
2nd line if C1 inh n/a: attenuated androgens, danazol (androgenic hormone) in incr doses for 5 days pre & 3 days post procedure is an alternative if berinert n/a
3rd line= FFP if C1 inhibitor n/a, or solvent/detergent-treated plasma
The pt should have access to on-demand therapies as swelling often occurs 1 day or so AFTER procedure
alt icabitant is a bradykinin receptor antagonist, has short half life so not ideal prophylactic agent
What are adverse effects of pdC1-INH concentrate?
Headache, nausea, fever, anaphylaxis
when should surgery for pts with hereditary angioedema be scheduled?
Early in the day as swelling often happens a day or so AFTER procedure, airway symptoms can be slower to recognise if begin @ night
what do the Society of NeuroInterventional Surgery and the Neurocritical Care Society recommend for endovascular Rx of acute ischaemic stroke?
SBP >140 <180mmHg, DBP <105mmHg
what’s the maximum warm ischaemia time for procuring kidneys following donation for cardiac death?
60mins (from SBP <50mmHg)
maximum warm ischaemia time heart/liver/pancreas?
30 mins (if greater for liver, risks biliary stricture), (from SBP <90mmHg)
max warm ischaemia time lungs?
90mins (from SBP <50mmHg)
max cold ischaemia time various organs?
heart 4hrs
lung 6-8hrs
liver/pancreas 12hrs (DBD), 6hrs (DCD)
kidneys 18hrs (DBD), 12hrs (DCD)
what’s warm ischaemia time?
the time from treatment withdrawal to the start of cold perfusion of the donated organs
what’s the recommended cleaning protocol for a laryngoscope handle which has been used but which has no visible soiling?
washed with detergent & water but if contaminated, wash & disinfect (semi-critical devices)
what classification of equipment are laryngoscope blades considered & how should they be cleaned?
critical (penetrate skin or mucous membrane) so require sterilisation
what’s asepsis?
prevention of microbial contamination of living tissues or sterile materials
what’s disinfection?
inactivation of non-sporing organisms using thermal or chemical means
what’s sterilisation?
complete destruction of all micro-organisms including spores
what’s a critical device?
one that penetrates skin or mucous membranes, enter vascular system or a sterile space
these devices require sterilisation
what’s a semi-critical device?
semi-critical device will be in contact with intact mucous membranes or may become contaminated with readily transmissible organisms. they require high level of disinfection or sterilisation.
what’s a semi-critical device?
semi-critical device will be in contact with intact mucous membranes or may become contaminated with readily transmissible organisms. they require high level of disinfection or sterilisation.
what’s a non-critical device?
one that comes in contact with intact skin or doesn’t contact the pt directly, these devices require low level disinfection or cleaning
what are the feature of brown sequard syndrome?
lose ipsilateral motor power (CST), vibration/proprioception, light touch & contralateral pain/temp (beginning 1-2 segments below the lesion)
retain contralateral vibration/proprioception, ipsilateral pain/temp
hyperreflexia & spastic paralysis BELOW level of lesion ipsilateral (UMN lesion)
flaccid paralysis of muscles supplied by the nerve of the level of lesion (LMN affected)
if lesion above T1 will get ipsilateral Horner’s with involvement of oculosympathetic pathway
In a Blalock–Taussig shunt, blood passes to the pulmonary artery via what?
subclavian artery
how much does 10mm on the Y axis of ecg measure?
1mV (2 big squares)
What’s the most common arrhythmia in maternal cardiac arrest?
PEA (this was in 50%, followed by asystole in 25%. Only 12% had shockable rhythm)
Which agents are the most commonly implicated in periop anaphylaxis?
NMBAs
what’s central to the allergenicity of the reacting NMBAs?
positively-charged quaternary & tertiary ammonium ions
what proportion of pts with NMBA anaphylaxis have cross-sensitisation?
50%
how long after an anaphylactic reaction should skin testing be delayed? why?
4-6wks (possible immune refractory period & may get false -ve & only +ve results are considered valid during that time)
Are sIgE assays subject to the 4-6/52 refractory period as are skin tests? utility of this?
no
may therefore be useful if urgent surgery is required within this period following an anaphylactic reaction
do morphine & pholcodine have ammonium groups similar to NMBDs?
yes- at physiologic pH they have substituted ammonium groups similar to those present on NMBAs; morphine contains one while pholcodine contains two amine groups of which one is more protonated @ physiologic pH
are sIgE to morphine & pholcodine of value in the detection of antibodies to NMBAs?
Yes, but it’s unclear whether these assays have equal diagnostic value for investigating allergic reactions to different classes of NMBAs (thought to be more reliable in detecting sensitisation to benzylisoquinoline NMBAs)
management of intracranial aneurysm rupture?
MANAGEMENT DEPENDS ON WHETHER OR NOT THE ANEURYSM IS EXPOSED.
If exposed, goals are:
-create a bloodless field to facilitate clipping & protect the brain
–>induce hypoT- esmolol 10-20mg IV as needed to achieve MAP 50-60mmHg to reduce bleeding & facilitate clip placement
–>induce temporary flow arrest with adenosine 0.5mg/kg
–>reduce CMR with propofol 20-60mg IV (if using prop for maintenance, incr rate to 125-200cmg/kg/min- aim to achieve burst suppression on BIS)
-volume resuscitation may be necessary once the clip placed; IVT & blood aiming for euvolaemia & Hb >=80g/L
-once clip in place, lighten anaesthesia
if ruptures prior to exposure, may be difficult to detect (may be heralded but unexplained incr BP & ICP. rapid decision necessary re: Surg, imaging or angio. Support pt with:
-optimising CPP by allowing permissive HTN, aim CPP 50-70mmHg if ICP monitor, if not, MAP >90mmHg. vasopressors as needed to incr BP (NAdr pref)
-manage intracranial HTN
–> optimise O2 (aim PaO2 >80mmHg, PaCO2 32-38mmHg) & ventilation
–> osmotheray, mannitol 0.25-1g/kg or HTS 100mL 3% NaCl, aim serum Na <=155mmol/L or osmolality <320mmol/L
–> improve venous drainage with head elevation 15 degrees head-up, neutral position, tape vs tie of the ETT
beware that opening of ventriculostomy abruptly may worsen bleeding (acutely elevates transmural pressure gradient)
–> neuroprotection with propofol 20-60mg IV or incr rate to >125mcg/kg/min, titrate EEG to burst suppression
IAR occurs with an endovascular procedure for an aneurysm (uncommon, if so it’s most likely with coil deployment), reverse heparinisation with protamine.
if bleeding during endovascular coiling of an aneurysm, should coiling continue?
no, not until bleeding controlled
what may be signs of ruptured aneurysm during endovascular procedure?
sudden rise ICP
sudden incr BP or decr HR
extravasation of contrast
goals of management of bleed during endovascular coiling?
reduce coagulability (protamine to reverse heparin, IF REQUESTED BY RADIOLOGIST; 1mg protamine per 100 units heparin given)
reduce BP to level before HTN due to bleeding
reduce ICP (gentle hyperventilation, reverse trendelenburg, would’ve taped not tied ETT, consider mannitol or HTS)
control seizures
reduce CMR (prop)
only continue coiling once BP controlled
what are some risks of mannitol in renal failure?
retention may cause hyperosmolality & osmotic movement of water & K out of cells. May get vol expansion, hyponatremia, metabolic acidosis & hyperK.
Dose of protamine for heparin reversal?
1mg protamine per 100 units heparin
difference required for orientation of quincke or atraucan vs whitacre or sprotte?
the quince or atraucan require orientation of bevel along with the dural fibres so less likely trauma, while it doesn’t matter with Whitacre or sprotte
does early (<12 hrs) vs delayed (48hrs) renal replacement therapy in pts with sepsis & AKI result in survival benefit?
no
Patients with obstructive sleep apnoea undergoing surgery, have been shown to have an increased incidence of what?
- neurocognitive (childhood OSA may impair learning skills), psychiatric (eg. depression), endocrine (impaired glucose tolerance, dyslipidaemia, incr cortisol [], testicular/ovarian dysfunction), cardiovascular morbidity (HTN & Brady- and tachyarrhythmias are more common, pulm HTN, CHF & biventricular dysfunction incr risk of haemodynamic instability perioperatively- OSA IS AN INDEPENDENT RISK FACTOR FOR MI- dyslipidaemia, increase pro-inflammatory cytokines, endothelial dysfunction, incr platelet aggregation) & mortality in all age groups.
they are @ incr risk of CVA with poorer outcome.
difficult intubation, obstructed breathing, OPIOID SENSITIVITY
Pulmonary complications
postop delirium
**POSTOP CARDIAC EVENTS ((Composite outcome of myocardial injury, cardiac death, heart failure, thromboembolism, AF & stroke) within 30/7 of surgery) = sig incr HR IN SEVERE BUT NOT MILD/MOD OSA
When are pts with obesity @ highest post risk?
Sleep architecture disturbances greatest on PN1 but breathing disturbances during sleep greatest PN3
Death & anoxic brain damage/other critical evnents within 24hrs. More likely if on ward vs ICU. More likely if not use CPAP.
Highest risk= SEVERE UNTREATED.
Minimise risk by:
Routine post O2
Minimise opioids
Extubatne awake
Incr intensity post-op monitoring (routine pulse ox or capnography)
Referral for sleep studies:
STOP-BANG 6-8 OR stop-bang 3-5 & MP 3-4 or neck >50cm2 or SpO2 <94% or bicarb >20 or NYNA III—> sleep studies
Non-supine positioning where possible
Continue CPAP if already on CPAP; those with severe OSA but not compliant w CPAP—> HDU invasive monitor. If not on CPAP or on CPAP + compliant OR mod risk based on screening or diff airway—> low-opioid & overnight SpO2
What are some pt factors associated with increased risk of BCIS? Surg factors?
increasing age
ASAIII-IV
male
poor physical reserve
cardiopulmonary dysfunction
pre-existing pulmonary HTN
PFO
OP
bony mets
hip fractures (esp pathological or intertrochanteric), warfarin use & diuretic use
surg factors: long-stem arthroplasty, prev uninstrumented femoral canal NOT revision surgery, ?femoral canal diameter >21mm
What are the 3 grades of BCIS? What’s bone ceme t
1: hypoxia SpO2 <94% & hypotension with SBP decrease >20% 2: SpO2 <88% or SAP drop >40% or LOC 3. cardiovascular collapse requiring CPR
Features BCIS: hypoxia, hypoT, arrhythnias, cardiac arrest
Reversible, time-limited
Limit risk by identifying high-risk pts (CEMENTED HIP ARTHROPLASTY), modify surg technique to reduce CV compromise (prep & dry canal, venting hole, bone-vacuum cement, avoid pressurisation, consider cementless)
Anaes: vigilance (prepare for cement with 100% O2, normal BP, open IVDT) to haem changes, R) heart protection, normovol, adequate MAP, art line, incr FiO2 during @ risk times (reaming, insertion cement, insertion prosthesis, reduction joint, release tourniquet), appropriate depth (not excess @ risk times), avoid N2O (air embolism).
Mx: early identification, 100% O2, aggressive resus, manage PAH & RV failure, pulm VD (prostacyclin) & inotropes (dob & milrinone, ephedrine), consider higher-level monitoring (TOE) & CVC
ICU postop.
Early post-op Ax (possible delirium w cerebral emboli)
According to National Audit Project (NAP) 5, the incidence of awareness during general anaesthesia for lower segment caesarean section should be quoted as
1:670
Piped O2 supply to major hospitals is sourced mainly from what?
VIE (vacuum insulated evaporator)
what’s 1 bar in KpA?
100KpA
The water capacity of an oxygen transport cylinder is 2 litres. The gauge is reading 150 bar. At an oxygen flow rate of 10 litres per minute, the number of minutes the cylinder will last is?
Boyle’s Law:
P1V1 = P2V2
P1= 150bar
V1= 2L
P2= 1bar (atmospheric)
so, V2= (2 x 150) / 1 = 300L
300L at 10 L/min = 30mins
What are the specifications of a normal transport size C cylinder?
2.9L water capacity
440L oxygen at 13700kPa
According to PS50, after an absence of more than 12 month from practicing clinical anaesthesia a re-entry program should be offered. The duration of the program for every year of absence would usually be at least
1 month per 12 months
Why is perioperative overheating most likely to cause worsening of symptoms of multiple sclerosis?
demyelinated axons are more sensitive to heat & symptoms can deteriorate with increase in temperature
does aspirin for primary prevention (in adult non-diabetic pts) reduce risk of cardiovascular mortality or all cause mortality? does it provide benefit on nonfatal stroke? does it increase the risk of major bleeding?
no
no
yes (incr (50%) risk of major nonfatal extracranial bleeding
likely may reduce nonfatal MI over 10 yrs
possible reduction colon Ca incidence over 20yrs
what does the ACC/AHA recommend regarding low-dose (75-100mg/day) aspirin for primary prevention of atherosclerotic cardiovascular disease?
consider it for adults aged 40-70 with high risk of ASCVD but NOT at incr bleeding risk
do not give it on routine basis for primary prevention of ASCVD in adults >70yo
don’t give it to adults at any age @ incr risk bleeding
what’s COPD GOLD3?
FEV1/FVC <70% & FEV1 30-49% predicted
what’s the maximum FiO2 that can be delivered through a Venturi mask? nasal cannula? non-rebreather?
60%
36%
85%
which agent has the highest capacity to absorb IR radiation?
?desflurane, since GWP is the product of radiative efficiency & atmospheric lifetime & N2O has much longer atmospheric lifetime than des yet lower GWP
when do most cardiac arrests after cardiac surgery occur?
within first 5 postop hours
what are some critical differences with cardiac arrest after open cardiac surg cf standard ACLS?
-external cardiac compressions aren’t immediately initiated (concern for disruption of the surgical repair)
-avoid administration of full 1mg epinephrine; may –> extremely high BP which may disrupt arterial suture lines; rather, if indicated at all, give 50mcg increments of epinephrine as needed with continuous reassessment
-avoid atropine for asystole or severe brady, instead, initiate pacing (rate of 90, DDD, if pacing wires available)
-if they are paced & in PEA, turn off pacing to “unmask” VF
if VF or pulseless VT, give 3 successive defibrillator shocks & 300mg amiodarone IV
initiate pacing for asystole or severe bradycardia- set pacemaker for dual chamber pacing (DDD mode) at 80-100bpm, max output voltage 20mA atrial & 25mA ventricle (deranged phys says max output)
if PEA, external cardiac compressions while opening chest (within 5 mins); do manual cardiac massage 100-120bpm.
internal defibrillator at 20J/s during attempts to treat VF.
what’s MEN2A? how differ from MEN2B?
characterised by medullary thyroid cancer, pheochromocytoma/paraganglioma, primary parathyroid hyperplasia
MEN2B no hyperparathyroidism
what may NF1 be associated with?
cafe au lait spots
peripheral neurofibromas
neurocognitive abnormalities
CNS tumors
soft tissue sarcomas
other tumors incl pheochromocytomas/paragangliomas
how do you calculate the est RVSP from TTE?
Bernoulli equation:
4v2 + RAP (using the continuous wave doppler trace through tricuspid valve), where v is the TR jet VTI
what are the physical properties of normal saline?
Na+ & Cl- 154, osmolarity 308mOsmol/L (considered isotonic), SG 1.0046 (plasma 1.02)
what are air bronchograms & what might they signify?
air-filled bronchi (dark) made visible by opacification of the surrounding alveoli, suggest a pathologic process going on filling alveoli w something other than air. they won’t be visible if the bronchi themselves are opacified (eg. filled w fluid).
Ddx:
pulmonary consolidation
pulmonary oedema
pulmonary haemorrhage
non-obstructive atelectasis
severe interstitial lung disease
neoplastic process
pulm infarct
how to differentiate causes of a complete hemithorax whiteout on CXR?
position of trachea.
pulled toward opacified side: pneumonectomy, total lung collapse (eg. endobronchial intubation), pulmonary genesis or hypoplasia
remains central: consolidation, pulm oedema/ARDS, pleural mass, chest wall mass, being on ECMO
pushed away: pleural effusion, diaphragmaticc hernia, large pulm mass, diaphragmatic rupture
According to the Australian and New Zealand Resuscitation Guidelines the immediate treatment for an adult conscious victim with a severe airway obstruction due to a foreign body inhalation is:
send for help
up to 5 back blows (Heel of hand middle of back btwn sh blades, aim is to relieve obstruction, check between each to see if dislodged the FB)
Infant head downwards across rescuers lap
if not successful
up to 5 chest thrusts, same hand position as CPR but thrusts slower rate & sharper. infant head down on back across rescuers thigh, adult sitting or standing. therafter, alternate 5 back blows & 5 chest thrusts.
what’s the mean (SD) lip-carina distance for males & females?
24 (2) & 22 (1)
what’s the length of the aintree catheter? Fr & ID? with which tubes can it be used? and scope? LMA?
56cm long
19Fr
ID 4.7mm
contains 15mm adapter & luerlock
can be used with an ETT ID >=7mm (as it has 6.5cm OD)
can be loaded onto fiberoptic scope with OD 4.2mm or smaller
LMA 2 or larger
length of Cook exchange catheter? French?
83cm, 11-19Fr
length of DLT exchange catheter? Fr?
100cm, 11-14Fr
length of bougie?
70cm
lesion causing L) homonymous hemianopia is due to lesion of what?
posterior cerebral artery, supplying the R) occipital lobe
which is the most commonly-affected cerebral artery for CVA?
MCA
what’s MCA syndrome?
contralateral hemisensory loss (UL, LL, lower 2/3 of face)
contralateral motor weakness, spasticity, hypertonicity/hyperreflexia
ipsilateral eye deviation & contralateral homonymous hemianopia
if dominant (usually L)-sided), Broca’s aphasia (difficulty forming words) if superior part of MCA, wernicke’s (difficulty understanding words & they may speak in fluent but unintelligible sentences & be unaware of this) if inferior part & if non-dominant, hemineglect/agosognosia/apraxia
along with contralateral homonymous hemianopia (due to occipital infarct), with what may a pt with PCA stroke present?
contralateral hemisensory loss, due to thalamic infarct, may also have memory impairment & decr consciousness
ACA: CL LL weak, executive dysfunction
brainstem: crossed sensory or motor findings, nystagmus, diplopia, vertigo, horner’s
cerebellar: ataxia, nystagmus, vertigo, nausea, headache, rapid deterioration consciousness
what is unilateral homonymous hemianopia & hemisensory loss, without motor manifestation, considered diagnostic of?
PCA territory infarct
What may rapid development of proptosis, tense eye, extra-ocular movement deficiencies & markedly decreased visual acuity suggest? major concern? treatment?
elevated IOP due to retrobulbar haematoma
visual loss
lateral canthotomy- decompressing the orbit, relieving pressure to prevent compartment syndrome & permanent vision loss
other Mx: acetazolamide, mannitol, emerg orbital decompression
don’t see chemosis with retrobulbar haemorrhage
how soon after development of orbital compartment syndrome must lateral canthotomy be performed before irreversible visual loss may occur?
2hrs, possibly less
which substance should be avoided in pts with a Hx of anaphylaxis to MMR vaccine?
gelofusin
what’s the most important complication of gelation-based colloids?
possibility of allergic reaction
for which children is MMR vaccine not advised?
those with known severe systemic allergic reaction to gelatin or neomycin
The anti-emetic action of aprepitant is via receptors for what?
Substance P (NK1 is the receptor, substance P is the ligand, aprepitant antagonises the receptor)
are opioids likely to impact MEPs? or ketamine?
neither
what’s the main cause of airway compromise following anterior C-spine surgery?
retropharyngeal OEDEMA
risk factors for airway compromise following anterior procedures on cervical spine?
multilevel surgery
blood loss >300mL
duration >5hrs
combined ant & posterior operation
previous Cx surgery
what are the 2 most common causes of metabolic alkalosis? management approach? further diagnostic approach if the cause unclear?
external loss of gastric secretions (vomiting, NG suction) or diuretics
management approach= to treat the underlying cause- eg. treat cause of vomiting, stop or slow removal of gastric secretions, stop loop or thiazide diuretics then correct the factors maintaining the disorder (eg. Cl- administration, repletion of Cl-, K+ & ECF volume will promote renal bicarb secretion & return plasma bicarb to normal).
if the metabolic alkalosis is due to persistent vomiting or gastric suction, drugs that reduce gastric HCl secretion may help (H2 blockers, PPIs)
if the ethology unclear from Hx/exam, measurement of urine chloride & Na may help as may looking at the potassium-
- low urine Cl occurs with vomiting or NG suction (unless the pt also on diuretics), spot urine Na also often low in these pts due to volume contraction
- if the pt is hypokalaemia, this is usually due to urinary potassium losses, even if the pt has concurrent vomiting, since there is little K+ in gastric secretions
what does acetazolamide do?
carbonic anhydrase inhibitor, promotes renal loss of bicarb along with sodium, water & potassium
for how long should SGLT2-i be withheld preop?
3 days; 2 days & day of OT
for how long should SGLT2-i be withheld preop for procedures involving 1 or more days in hospital or bowel prep? what about day stay procedures, including gastroscopy (no bowel prep)?
3 days; 2 days & day of OT
can withhold just for the day of the procedure but fasting before & after the procedure should be minimised
in which situations should I suspect eDKA?
pts taking SGLT2i who have one or more of:
• symptoms of abdo pain, nausea, vomiting, fatigue or metabolic acidosis – a normal or only modestly elevated plasma
glucose level does not exclude the diagnosis.
• finger prick capillary blood ketone (or blood beta-hydroxybutyrate) levels >1.0 mmol/L with or without hyperglycaemia
• low (negative) base Excess (BE) < -5mmol/l indicating metabolic acidosis on arterial or venous blood gasses.
what to do if a pt hasn’t stopped their SGLT2i as per guidelines?
course of action depends on urgency of procedure, pt factors eg. HbA1c (>9% indicates higher risk of insulin insufficiency & risk of eDKA in this setting)… if:
ketones <1 & BE > -5, there’s no ketosis or metabolic acidosis so consider proceeding w day surgery with hourly monitoring of ketones intra-op & 2-hourly postop until E&D normally. provide written post-D/C info. more extensive surgery requires considering goals of care, collaboration with endocrine & critical care.
if ketones >1 & BE > -5, ketosis without metabolic acidosis. get endocrine advice. it may be due to starvation (esp if the pt has HbA1c of <9%). could consider proceeding with periop insulin & dextrose infusions to mitigate risk of DKA.
if ketones >1 & BE < -5, ketosis with metabolic acidosis. strongly consider postponing non-urgent surgery, escalate w endocrine & critical care.
what’s the management of eDKA or DKA?
in collaboration with endocrine & critical care:
rehydration
IV insulin infusion (with added dextrose once BGL <15mmol/L)
hourly BGL, ketones & blood gas
what’s the best US probe for median nerve block?
high-frequency linear 10-14MHz
what does higher frequency confer on US?
better resolution but less penetration (ie. better for superficial)
what does lower frequency on US confer?
better tissue penetration but poorer resolution; allows visualisation at greater depth
what’s gain on ultrasound?
uniform amplification of the returning US waves; higher gain= higher signal of reflected sound waves & image whiter.
optimal depth for US images?
as shallow as possible to still see all the structures of interest, since the image quality varies inversely w penetration depth
what are the components of US that we can manipulate?
mode
depth
focus (at or 0.5cm below target nerve)
gain
frequency
doppler
for a pt with normal renal function, for how many days should apixaban be ceased prior to neuraxial block?
3 days
for how many days should dabigatran be withheld prior to neuraxial block?
5 days, however if there is NORMAL renal function (CrCl >=80mL/min) & no additional risk factors for bleeding (age >65, HTN, antiplts), may consider 3 days or if CrCl 50-79mL/min consider 4 days.
if CrCl <30mL/min, avoid neuraxial block if pt has been on dabigatran.
for how many days should rivaroxaban be held prior to neuraxial block?
3 days
for how many days should prasugrel be withheld prior to neuraxial?
7-10 days
for how many days should ticagrelor be withheld prior to neuraxial?
5-7 days
for how many days should clopidogrel be withheld prior to neuraxial?
5-7
for how many hours should we wait after catheter removal prior to restarting dabigatran, apixaban, rivaroxaban, ticagrelor & prasugrel? how about clopidogrel?
6hrs for all, immediately for clopidogrel provided no loading dose (in which case 6hrs)
with what would hypoglossal nerve damage manifest?
ipsilateral tongue deviation (LMN) or contralateral (UMN)
which cranial nerves DO decussate?
II, IV, VII & XII
how to convert hydromorphone to OMEs?
x5
what’s 12mg PO hydromorphone conversion to parenteral morphine?
20mg parenteral morphine
on what is a Fontan circulation dependent?
preload (? this may be achieved w decr volatile?) & pulmonary resistance
Keep Fontan pressure <20mmHg
Transpulmonary gradient <5mmHg
PVR <2WU/m2
for optimal circulation
what’s the most common cause of visual loss after spinal surgery?
ischaemic optic neuropathy (higher freq than pressure causing occlusion of retinal vessels).
ischaemic optic neuropathy causes are uncertain but may relate to low arterial pressure, low hct, long surgery, large IV fluid volume.
what’s ERAS?
multimodal perioperative care pathway aiming for early recovery for pts undergoing major surgery, includes pt optimisation, anaes, surg & OPD support. limit fasting, carb loading, education, normothermia, limit intraop IVT, multimodal analgesia, PONV & antibiotic prophylaxis, in/out IVC, d/c instructions & f/up plan.
What’s differential hypoxaemia & when can it occur?
is a complication specific to the use of V-A ECMO for severe cardiorespiratory failure, where the upper half of the body is perfused by blood of relatively low oxygen saturation from the heart, cf the lower body, where well-oxygenated blood is supplied via the peripheral femoro-femoral VA ECMO system.
what’s the most common complication of ECMO? then?
BLEEDING & COAGULOPATHY; 5-79% of ECMO patients
Answer= HAEMORRHAGE- particularly since most pts are on continuous anticoagulation. half of these haemorrhages relate to the cannulation site, arterial cannulation= highest bleeding risk.
Risk intracranial haemorrhage (so avoid HTN)
Thrombosis
then infection
what would the PFTs in restrictive lung disease of myasthenia gravis show?
reduced FEV1 & FVC, normal DLCO, ratio normal or high
what’s the factor to most effectively reduce mortality in early SAH?
prevent rebreeding by securing the aneurysm, ideally within 24hrs
which parameter of respiratory physiology decreases during pregnancy?
FRC, 20% by term (both RV & ERV decrease)
You are inserting a pulmonary artery catheter in an intubated patient prior to cardiac surgery, and a significant amount of blood appears in the endotracheal tube. The most appropriate specific initial management is to
aim to maintain oxygen & ventilation, identify site of haemorrhage, position pt with suspected bleeding side down (R)-side down decubitus) to limit soiling of “good lung”, isolate the non-bleeding lung to protect it from soiling & optimise oxygenation, most practically & rapidly with large-bore (at least size 8) single-lumen ETT & L) mainstem endobronchial intubation or DLT (less likely time for this) with bronchial cuff inflated, tracheal lumen clamped- also DLTs are difficult to insert w brisk bleeding & aren’t large enough for passage of a flexible bronchoscope w suction capability.
?+/- tamponade the bleeding lung with bronchial blocker such as Arndt endobronchial blocker (theoretical risk mucosal ischaemia)
?suction with bronchoscope- flexible is less efficient cf rigid, flexible can be used to instil topical vasoconstrictors or haemostat agents, ?cooled saline
volume resuscitate, manage hypoxaemia-related arrhythmia (primarily by treating cause- optimising gas exchange) manage any coagulopathy/bleeding diathesis/replace blood products
apply PEEP to the bleeding lung if possible
transport pt to medical imaging for diagnosis & embolisation if feasible
correct position of bronchial cuff with L)-sided DLT?
5mm distal to carina without herniation across it
if develop massive haemoptysis from a PA catheter, which lung likely to have haemorrhage?
L)
how long is a PA catheter usually?
110cm
How do I define massive haemoptysis?
any volume of blood that could obstruct the airway or cause significant haemodynamic compromise (“magnitude of effect” definition preferred over blood volume- ie. could be described as “haemoptysis that impairs gas exchange, causes haemodynamic instability or is >100mL/24hrs (the minimum volume reported to be life-threatening due to asphyxia))
what is the source of most cases of massive haemoptysis?
bronchial circulation (supplies bronchial tree @ systemic pressure)
disadvantage of rigid bronchoscope for pulmonary haemorrhage?
only gets to the level of main bronchi (may not get distal bleeding)
How may hyperbaric oxygen help with carbon monoxide poisoning?
reduces the half life of carboxyHb (from 90mins at normobaric, down to 30mins) so HBO can prevent neurocognitive deficits associated with severe CO poisoning
What’s normal carboxyhemoglobin?
<1.5%, may be up to 9% in smokers
What are indications for the use of HBOT in acute CO toxicity? (note: it’s NOT recommended for those with mild-mod CO toxicity, who should receive high flow O2 until CO<5%)
CO>25%
CO >20% if pregnant
LOC
severe metabolic acidosis (pH <7.1)
evidence of end-organ ischaemia (ECG changes, chest pain, altered mental status)
when is the greatest benefit of HBOT for CO poisoning?
if Rx initiated within 6hrs (benefit >12hrs after exposure is unproven)
what are the differential diagnoses of deranged LFTs in pregnancy?
intra-hepatic cholestasis of pregnancy
PET with hepatic impairment (highest proportion of deranged LFTs in pregnancy are due to this)
HELLP syndrome
acute fatty liver pregnancy
management of acute fatty liver of pregnancy?
assess for encephalopathy
manage coagulopathy (plt function tends to remain stable, unlike HELLP, however use of regional may be precluded by coagulopathy)
manage hypoglycaemia
expedite delivery once pt stabilised as high maternal & foetal mortality
Pt must be in HDU, particularly postop as symptoms can deteriorate post partum with worsening liver, renal function & coagulopathy for 48hrs
poor prognostic indicators with severe liver disease in pregnancy?
lactate >2.8mg/dL & presence of encephalopathy
when may regional anaesthesia be considered in pregnant women with liver disease?
mild, stable disease, balancing risks & benefits to mum & Bub
normal trend of LFTs during pregnancy?
ULN transaminases is reduced by 25% in all trimesters
ALP increases in the 3rd trimester due to placental production
what’s the pattern of LFT changes with intrahepatic cholestasis of pregnancy?
elevated ALT (>1.5x normal), elevated bile acids (>1.5x normal), bilirubin is usually NORMAL
what’s the pattern of LFT derangement in PET with hepatic impairment?
raised ALT (>2x normal), BA & bilirubin usually normal
what’s the pattern of LFT derangement in HELLP syndrome?
raised ALT (>2x normal), BA usually normal, Bilirubin elevated (>1.5x normal)
what’s the pattern of LFT derangement in acute fatty liver of pregnancy?
elevated ALT (>3x normal), elevated bilirubin (>4x normal), bile acids usually normal
What’s HELLP, symptoms & management?
haemolysis, elevated liver function (ALT >2x ULN, elevated bilirubin >1.5x ULN, bile acids usually normal) & low platelets
can present in late 3rd trimester, can also present post-partum
occurs in 4-20% of pts with PET
The BP elevation may be mild, as may be the proteinuria
Pt may c/o upper quadrant pain/epigastric pain (in which case the pt should have abdo imaging as hepatic haematoma or rupture are rare but significant complications ass’d w high (up to 60%) mortality)
LFT derangement may lag behind abdo pain so the LFTs should be repeated if not elevated
N&V is common
may c/o dyspnoea/chest pain & have tachypnoea due to concomitant metabolic acidosis
The haemolysis is not usually severe enough to cause anaemia
DIC occurs in about 20% of cases
The trend in platelets should be monitored, replace if active bleeding or for operative delivery/placement of invasive lines
acute renal failure is more common in HELLP than in other forms of PET & morbidity is often ass’d with AKI
Pts should be managed in HDU given the course can be unpredictable
complications= placental abruption, APH/PPH, pneumonia, liver haematoma, pulmonary oedema, ICH
TREATMENT = Stabilisation & deliver foetus, timing of which balances risks to mother & foetus
what usually recovers first after HELLP? thrombocytopenia or liver function?
liver function
when does AFLP usually present?
late in 3rd trimester (30-38wks & up to 4.7 postpartum)
what are some associations with acute fatty liver of pregnancy (AFLP)?
more common in women with multiple pregnancies, lower BMI & children with disorders of B-fatty acid oxidation
why is acute fatty liver of pregnancy (rare!) an important diagnosis for which it is worth developing a protocol?
maternal mortality is high, ranges from 20-50%
foetal mortality also high
20% have concurrent HELLP
how is the diagnosis of acute fatty liver of pregnancy made?
Swansea criteria, there must be @ least six of the listed clinical features in the absence of another explanation:
Vomiting
Abdo pain
Polydypsia/polyuria
Encephalopathy
Hypoglycaemia
Elevated bilirubin
Ascites/bright liver on US
Leukocytosis
Coagulopathy
Renal impairment (develops in about 90% of pts)
Elevated urate
Elevated transaminases
Elevated ammonia
Microvesicular steatosis on liver biopsy
Imaging (CT or MRI), liver biopsy or fat stain may support the Dx
Other complications include: pancreatitis, ARDS, metabolic acidosis & elevated lactate
Urgent delivery then Mx of liver failure
what is the pattern of platelet function in AFLP? can regional be done with AFLP?
tends to be stable, unlike with HELLP
it’s often precluded by the presence of coagulopathy but it has been described & may improve hepatic blood flow
ALT/AST all raised, bili, ammonia & WBCs can also be raised
What’s obstetric cholestasis, what’s the general approach to management & what are anaesthetic considerations?
pregnancy-related impairment of bile acid excretion
causes pruritus, typically affecting hands & feet (palms & soles, worse @ night)- may be severe but rarely requires HDU
LFTs typically show raised ALT & bile acids (both >1.5x ULN), normal bilirubin
vitamin K malabsorption may occur (steatorrhoea) so the pt should have coagulation (raised PT, INR) assessed before proceeding with regional anaesthesia (<1.4 within 24hrs acceptable, changes slowly)
neuraxial opioid may worsen pruritus but this must be balanced against need for effective pain control
obstetric cholestasis may be a marker of other liver disease (eg. AFLP, hepatitis) so the collection of symptoms should be considered
mum treated with ursodeoxycholic acid (a synthetic bile acid)- 300mg BD or TDS until delivery- timing of delivery depends on total bile acid level, hepatic function, severity of the pruritus balanced against foetal risks
two broad classifications of liver disorders in pregnancy- which more common?
gestational-related conditions (more common) or liver disorders incidental to pregnancy
example viruses that can cause hepatitis?
hep A, B, C, D, E & G, along with HSV, CMV & EBV
what’s more common? hep B or C?
hep B
which hepatits-causing viral infections have a worse course in pregnancy?
hep E & HSV
hepatic encephalopathy & hepatorenal syndrome caused by viral hepatitis have higher incidence during pregnancy
viral hepatitis ass’d with obstetric complications eg. PROM, IUGR, prem delivery
clinical features of viral hepatitis?
fever, nausea, jaundice
what’s the usual course of autoimmune hepatitis in pregnancy? management implications?
usually improves during pregnancy (as with many other autoimmune conditions)
management= immunosuppressive therapy which should be continued in pregnancy; AZA, cyclosporine & tacrolimus considered safe but not mycophenalate (contraindicated, teratogenic)
for drug-induced liver injury, what tends to be the clinical picture for methyldopa/paracetamol/highly active antiretroviral therapy? oestrogens/progesterones/amoxicillin/psychotropic drugs? trimethoprim/nitrofurantoin/carbamazepine?
-hepatocellular damage: raised transaminases & sometimes bilirubin
-cholestatic picture (raised ALP & GGT)
-mixed picture (hepatocellular & cholestatic)
considerations for the rare occasion when a cirrhotic pt is pregnant?
10% mortality rate
portal HTN worsens so oesophageal varicies= major bleeding risk (lower if Rx before pregnancy)- potential for strain makes LSCS preferred mode for delivery
use Bilirubin, INR & Cr for prognosis
implications for liver transplant pts in pregnancy?
generally favourable outcomes but higher risk pre-term delivery, LBW, PET & GDM.
must continue immunosuppression (low risk teratogenicity with commonly-used agents)
consider side-effects of immunosuppressants (neuropathy, electrolyte imbalance)
what’s budd-chiari?
obstruction to hepatic venous outflow causing ascites & hepatomegaly +/- R) UQ pain. most cases are due to thrombosis.
general management considerations for pregnant women with severe liver disease?
individualised care plan
liaise with liver unit, ICU (requires MDT planning & management)
monitor carefully for complications & identify those @ risk of fulminant hepatic failure (for which liver transplantation may be considered- best predictors for deterioration necessitating liver transplant or resulting in death= lactate >2.8mg/dL with encephalopathy)
what are some signs of worsening hepatic synthetic function?
prolonged INR
hypoglycaemia
hypoalbuminaemia
lactic acidosis
how does cirrhosis alter propofol’s pharmacokinetics?
It doesn’t. And it doesn’t reduce hepatic blood flow so it’s a suitable induction agent.
what are the NDMRs of choice in liver disease?
actrac & cistatrac; duration of roc unpredictable but can be reversed with sugammadex.
considerations for neuraxial in pregnant pts w liver disease?
severe disease coagulopathy & need for resus will make regional unsuitable
mild disease: balance risks based on plt count & +INR. only do epidural in very mild, stable disease (issues w placement, catheter removal & that all LA undergoes hepatic metabolism)
periop steroid replacement for pt @ risk of HPA axis suppression due to tertiary adrenal insufficiency (eg. pred >=5mg for >=4/52):
100mg IV hydrocortisone with 200mgIV/24hrs OR 6-8mg dexamethasone
what does hepcidin do?
an acute phase reactant.
binds to ferroportin, stopping release of ferritin from enterocytes & macrophages.
what may inhibit hepcidin production?
Anaemia. EPO & other erythrocyte stimulation agents, decr body Fe stores, hypoxaemia, incr erythropoietic demand
in contrast, infection, inflammation & malignancy may increase serum hepcidin levels, as does increase in body iron stores
Effects of N2O abuse?
a few hrs exposure= megaloblastic changes to bone marrow
more prolonged exposure= agranulocytosis
neurological symptoms from chronic B12 inactivation (resembles subacute combined degeneration of spinal cord, from damage to the posterior (fine touch/vibration/proprioception loss) & lateral (motor from lateral corticospinal tract) columns: general weakness, tingling and numbness in the hands and feet, and stiff limbs and may become irritable, drowsy, and confused.. may also get visual changes)
The Brain Trauma Foundation guideline for management of severe head trauma recommend the treatment of intracranial pressures greater than?
22mmHg (as they recommend treating >=22mmHg)
IIa: Treating ICP above 22 mm Hg is recommended because values above this level are associated with increased mortality
To perform regional anaesthesia suitable for a fourth toe amputation, it is essential to block the
posterior tibial (to block lateral plantar nerve)
also need
superficial peroneal nerve (L4-S1) to block dorsal surface
what are the roots for the superficial perineal nerve?
L4-S1
potential interventions for postictal agitation after ECT? is remi useful?
IV BZD, donepezil or propofol at the end of a seizure, dexmed may be useful if refractory, pre-med olanzapine helps
remifentanil is NOT useful for agitation after ECT
on gastric US, how does empty stomach appear?
small, flat & collapsed (2-3cm diameter), either round or ovoid in XC & often appears as “bull’s eye” target and the muscular propriae (hypo echoic) appears thick.
What’s appropriate prophylaxis for surgical TOP?
Doxycycline 400mg PO 60mins before procedure (has been administered 10-12hrs b4 procedure so can have w food to limit risk nausea) or 100mg PO 60mins b4 then 200mg PO, 90 mins postop
-NO evidence for adding metronidazole prophylaxis
what acid/base disturbance would you see with acetazolamide?
lower pH promotes bicarb loss kidneys
hypokalaemia, hyponatraemia
Of the following, the procedure that is most commonly associated with chronic pain after surgery is
risk factors for chronic post-surgical pain include:
surgical factors= surgical approach with risk nerve damage):
amputation (30-85%)
sternotomy (30-50%)
thoracotomy (5-67%)
mastectomy (11-57%, breast surgery 13-35%)
inguinal herniotomy (5-63%)
LSCS (6-56%)
knee replacement 19-43%
pt factors:
psychological vulnerability (eg. catastrophising), pre-op anxiety
female
younger age (adults)
pre-op pain, mod-severe, lasting >1/12
repeat surgery
prev opioid use (esp if inefficient)
worker’s comp
genetic predisposition
others:
poorly controlled postop acute pain
radiation therapy to the area
neurotoxic chemotherapy
For breast Ca surgery, PVB, local infiltration, IV lignocaine reduce incidence CPSP. sparing of intercostobrachial nerve doesn’t decrease chest wall hypersensitivity.
What’s CPSP?
CPSP is pain developing or increasing in intensity after a surgical procedure, in the area of the surgery, persisting beyond that time for expected wound healing (ie. 3 months) but not better explained by another cause (eg. infection, malignancy, pre-existing pain)
which anion contributes most to the anion gap?
albumin (other unmeasured anion is phosphate under normal conditions, critically ill= lactic & keto acids)
indications for prothrombinex?
prevention or control of bleeding in pts with factor IX deficiency (haemophilia B) ** but due to risk of thrombosis, better to use specific factor concentrate eg. monofix-VF
or
life-threatening haemorrhage associated with warfarin is off-label)
could also use for pts with deficiencies of factor II or X
where should the tip of a PICC line sit? risks if too high? too low?
at the cavoatrial junction
thrombus
arrhythmia
SBP goal during ext cardiac compressions in a pt after cardiac surg?
60mmHg
what’s moclobemide? anaesthetic implications?
MAO-A inhibitor, reversible
avoid indirect-acting sympathomimetics & pro-serotonergic drugs
Can withold (normal return to MAO activity in 24hrs)
Interacts with:
pethidine (norpethidine serotonergic), tramadol, dextromethorphan, Fentanyl causes efflux of serotonin & binds to serotonin receptors. methadone, oxycodone, fentanyl & tapentadol are intermediate risk opioids. Tramadol & pethidine high risk.
ABx: linezolid
MDMA (releases serotonin)
indirect sympathomimetics can precipitate fatal hypertensive crisis. slowly titrate direct (Adr/norad/phenyl) due to incr receptor sensitivity.
M relaxants: phenelzine decr plasma cholinesterase & prolongs sux. Panc releases stored NAdr.
LAs: avoid cocaine, care w Adr mix.
bzd, volatiles, antichol/nsaids all OK.
what are the major causes of cardiac arrest after cardiac surgery?
VF, cardiac tamponade & major bleeding
up until what time point is a patient considered a cardiac surgical pt (during which the algorithm for arrest includes resternotomy)? why?
10 days. thereafter, pericardium is more difficult to access due to adhesions so open resus more challenging
what’s the survival after in-hospital cardiac arrest? chance of success of a 4th stacked shock?
50%
10% so no point in continuing after 3 stacked shocks- then amiodarone (VF or VT), ext cpr w opening chest within 5mins
what’s the only cardiac arrest rhythm within 10/7 of cardiac surgery for which we’d immediately perform external cardiac massage?
PEA
why not atropine for post cardiac surgery arrest due to extreme bradycardia or asystole?
pacing is the treatment. atropine delays that.
what adjunctive measures should be taken for cardiac arrest post cardiac surgery?
take pt off ventilator, manually ventilate
increase FiO2 to 100%
drop PEEP to zero to optimise preload
exclude tension PTx
stop sedating infusions & other infusions
switch IABP to trigger mode (which assists CPR)
what are the different isoenzymes of monoamine oxidase (which breaks down NAdr)?
MAO is bound to the outer mitochondrial membrane. It breaks down NAdr, serotonin & dopaimine.
Monoamine oxidase A is found in GI mocosa, liver, noradrenergic & serotonergic nerves- moclobemide is reversible & specific to MAO-A
MAO-B is found in platelets, liver & dopaminergic nerves, selegiline is specific to MAO-B
Phenelzine is a traditional MAO inhibitor inhibiting MAO nonselectively & irreversibly (worse reaction), duration weeks
reversible moclobemide
with which type of drugs do MAO-Is interact?
indirect-acting sympathomimetics (direct still has incr effect but preferred since also metabilised by COMT so less dependent on MAO, ie. phenylephrine good, ephedrine & metaraminol avoid), due to an exaggerated response to increased NAdr release from nerve endings
SSRI or tricyclics and tramadol & pethidine (latter cause serotonin & norepinephrine reuptake inhibition)- excessive amount of serotonin (MAO inhibition results in reduced breakdown & increased activity of serotonin)
they also interact with foods high in biogenic ingested amines such as tyramine (hypertensive crisis may occur due to loss of protective effect of MAO-A in the gut)
orthostatic hypotension can occur
may get excitatory (inhibition of serotonin reuptake by pethidine) or depressive (decreased breakdown of pethidine)
preferred vasopressor for obstetrics & why?
phenylephrine- more rapid onset & short DO, ideal for continuous infusion, no adverse effect on foetal acid:base cf ephedrine
What’s nephrogenic diabetes insipidus? example causes?
decrease in urinary concentrating ability resulting from resistance to the action of ADH, either due to resistance at the ADH site of action or interference with the countercurrent mechanism
causes include hereditary such as V2 gene mutations, aquaporin-2 gene mutations, lithium toxicity, hypercalcemia, hypokalaemia
what’s central diabetes insipidus? causes? manifestations? lab results?
characterised by decreased release of ADH–> polyuria due to deficiency in ability to concentrate urine
idiopathic, primary or secondary tumours, infiltrative diseases, neurosurgery, trauma
polyuria, nocturia, polydipsia, may have neurologic symptoms related to the underlying neurologic disease, may develop decreased BMD (even those treated with desmopressin)
elevated serum Na (high normal except if pt can’t express or access (eg. postop) the hypernatremia may become severe)
elevated serum osmolality
dilute urine (osmolality <600msomol/kg) low in Na
how to treat central diabetes insipidus?
correct free water deficit (if the pt has chronic >48hrs) hypernatremia, only want to lower the serum sodium by 10mmol/L in 24hrs (3mL/kg electrolyte-free water lowers serum Na by 1mmol/L), while acute hypernatremia want to replace entire water deficit within 24hrs (5% dextrose in water 3-6mL/kg/hr up to 666mL/hr, monitoring serum Na & glucose 1-2 hourly until serum Na <145mmol/L then reduce rate to 1mL/kg/hr until normal Na+)
*as per RCH, use 0.9% NaCl w 5% dextrose to prevent hyponatremia!
increase activity of ADH, with desmopressin (ADH analogue); oral 100mcg (start with 0.5microg & titrated, intranasal 10mcg (equivalent to 0.5microg PO is 5mircog intranasal), subcut 1microg
low-solute diet (low-sodium, reduced protein) which may be combined with a thiazide
side effect of Rx with desmopressin?
hyponatremia–> symptoms such as nausea, vomiting, headache, lethargy, seizures
What’s the main advantage of using noradrenaline over phenylephrine for the prevention of hypotension as a result spinal anaesthesia for elective Casearean Section?
less maternal bradycardia; similar agars, hypotension & use of rescue vasopressors
what are manifestations of HF (hydrofluoric acid) burns?
Hx: glass etching, electronic industries, cleaning solutions- highly corrosive acid
Local injury + potentially fatal systemic reaction
Fluoride complexes with Ca++ & Mg++ –> hypoCa & hypoMg. hypocalcaemia may cause K+ efflux–> hyperKalaemia. May get prolonged QTc.
fluoride directly cardiotoxic (arrhythmias, primary cause of death with HF burns)
inhalation can–> severe pulmonary injury
A patient with a purely metabolic acidosis has a serum bicarbonate of 14 mmol/L and a lactate of 3.8 mmol/L. What’s the expected PaCO2?
1.5x (bicarb) +8
21 + 8 = 29
what’s the most common arrhythmia in maternal cardiac arrest?
PEA (50%), asystole 25%
complications of hyperbaric O2 therapy?
Claustrophobia
Hypoglycaemia
Middle ear barotrauma
Sinus squeeze
Oxygen toxicity seizure
Progressive myopia – typically reverses completely in days to weeks.
Cumulative pulmonary oxygen toxicity
Pulmonary barotrauma +/- air embolism
Exacerbation of congestive heart failure in patients with severe disease, due to:
a. Sinus bradycardia from stimulation of vagal activity and stimulation of a further measurable, nonoxygen dependent bradycardia that is associated with hyperbaric pressures.
b. Systemic vasoconstriction causing increased afterload.
Increased rate of maturation of cataracts with very long courses of HBOT.
advice for woman on hormonal contraception who gets sugammadex?
if taking the pill, follow “missed pill advice” on packaging leaflet
if using hormonal implant/innjection, use barrier contraception for next 7/7
what are some benefits of volatile-based anaesthesia compared to total intravenous anaesthesia for maintenance during cardiac anaesthesia?
Meta-analysis 2020 Anaesthesiology (RCTs 8200 participants): pts receiving volatile had lower incidences of one-year mortality & MI along with less need for inotropic medications & cardiac troponin release, higher cardiac output or index measurements & shorter extubation times
NEJM RCT 2019: 5400pts randomly assigned to VA vs TIVA, no difference in mortality at 1 year or other outcomes incl MI.
histological evidence preconditioning (no mortality benefit in vivo)
what are disadvantages of volatile anaesthesia for cardiac surgery? and of TIVA?
difficulty controlling the volatile uptake with different oxygenators & difficulty maintaining steady state plasma [] with variable FGFrates during different phases of CPB, poor correlation between oxygenator exhaust volatile [] & BIS
inefficient scavenging & risk of OT environment pollution
TIVA problem with changes in PPB capacity & variations in the free fraction of plasma propofol due to haemodilution, effects of hypothermia on hepatic clearance of propofol, absorption of propofol into the CPB circuit
how does hypothermia during CPB impact anaesthetic requirement? risk of this?
hypothermia reduces anaesthetic requirement & if using volatile, there’s greater uptake & plasma solubility during hypothermia. to avoid inadequate anaesthesia during rewarming, dose of IV or volatile should increase (blood propofol [] rapidly decreases during rewarming.
what’s the most sensitive test of liver synthetic function? why?
INR, tests extrinsic & common pathways & if prolonged, suggests impaired clotting factor synthesis or deficiency of vit K; it’s non-specific (eg. prol in warfarin use, DIC). The clotting factors have relatively short half-lives (eg. VII 4-6 days).
how is albumin useful in evaluating liver synthetic function?
marker of chronic liver impairment due to relatively long half life (20/7)
while very non-specific, how may anaemia & low platelets be a marker of impaired liver function?
liver produces TPO & 10% of EPO so low Hb & plt may occur w hepatocellular damage
why may high ammonia & low urea (non-specifically) suggest impaired hepatic metabolic function?
liver converts toxic NH3 to the less toxic urea (for excretion via the urea cycle)
along with high ammonia & low urea, high bilirubin, what’s another indicator of impaired hepatic metabolic function?
low glucose
what may be the findings with bilirubin with different forms of liver metabolic derangement?
pre-hepatic cause (eg. haemolysis, Gilbert’s) may have high unconjugated bilirubin given there’d be exhaustion of the liver’s conjugating capacity (most common causes unconj hyperbili are Gilberts, haemolysis, resolution of haematoma or portal HTN)
high direct bilirubin suggests biliary obstruction
mixed (both high) suggests hepatic disease & impaired hepatic uptake & conjugation of bilirubin
Where are AST & ALT found?
both are found in hepatocyte mitochondria so elevation suggests hepatocellular damage
AST is also found in heart, rbc, skeletal muscle
ALT therefore more specific to hepatocytes so elevated ALT:AST more suggestive of hepatocellular damage
aside from serum aminotransferases, what else may be elevated with hepatocellular injury?
LDH (found in hepatocytes, also in heart, pancreas, rbc, lungs, placenta so can be elevated if MI, Ca, haemolysis etc.
where are GGT & ALP found & what’s the significance of their elevation?
enzymes found in hepatocytes AND ductal cells along bile duct/canaliculus; high ALP & GGT suggest hepatobiliary disease (intra- and extra-hepatic cholestasis)
in isolation, GGT is non-specific (raised with ETOH)
Also, ALP is non-specific (bone, placenta)
what are the markers of cholestasis?
elevated conjugated bilirubin, GGT, ALP
What’s pacemaker nomenclature?
position 1: chamber paced (A, V or D (dual))
position 2: chamber sensed (A, V, D or O if sensing is turned off)
postion 3= response to sensing; inhibited, triggered (no clinical purpose), D (response can be I or T), O if no response to sensed events
position 4= rate modulation (eg. with accelerometer, responds to perceived increased physiological demand eg bicycling)
position 5= multi-site pacing
what does asynchronous pacing mean?
heart’s intrinsic conduction system & artificial pacemaker are firing independently of what the other is doing; the paced beat only generates a contraction if it occurs outside of the absolute refractory period. only used as a temporary mode during surgery (only use on pacing-dependent pt. risk of R on T (pacing spike occurring on a T wave))
what’s VVI mode & when is it useful or not?
has both ventricular sensing & pacing; if it senses ventricular conduction it will inhibit pacing, which avoids the risk of R on T. if a prolonged period has passed without ventricular activity, it will pace. no synchrony between the atria & ventricles, so risk having an atrial contraction during a paced ventricular beat (“pacemaker syndrome”), inadequate cardiac output, not useful for pts in sinus rhythm, more useful for a pt with AV block & chronic AF.
what’s AAI? indication? does it risk R on T?
theoretically a single lead in RA (but this is VERY RARE, since most pts with sinus node disease have some degree of AV block- it’d be more common to have dual chamber pacing wires & set it to AAI mode with the potential to have some ventricular pacing were AV block to occur), rather than sensing & pacing QRS complexes it senses & paces P waves.
used for pts with isolated sinus node disease without AV block.
even if it paces during the T wave doesn’t risk v fib as it’s pacing the A not V.
what’s the indication for VDD mode?
AV block without sinus node dysfunction- this mode will pace the ventricle but senses both A & V, response can be inhibit or trigger. eg. if senses a p wave but there’s AV block, it’ll trigger a ventricular depolarisation (appears as wide, abnormal QRS). if senses ventricular premature contraction it will inhibit ventricular pacing.
when is DDD mode used? what beats can be generated?
pt with AV block & sinus node dysfunction, in sinus rhythm. this is also the mode used for pacing in bradycardia arrest after cardiac surgery
Can be:
presence of a & v activity are both sensed so pacing inhibited to both
a activity is sensed hence activity inhibited & lack of v activity sensed hence it’s ventricular triggered (paced)
lack of a activity sensed hence it’s is paced & v activity is sensed hence inhibited
neither a or v activity sensed hence both triggered
what’s the lower rate limit of a pacemaker?
lowest rate at which the device will allow the heart to beat
what’s the maximum tracking rate for a pacemaker?
fastest rate at which the device will track the heart- it’ll track with the atrial rate up until the max limit set (typically 120-130bpm, may be higher in young/middle aged)
what’s the maximum tracking rate for a pacemaker?
fastest rate at which the device will track the heart- it’ll track with the atrial rate up until the max limit set (typically 120-130bpm, may be higher in young/middle aged)
what’s the AV delay setting on a pacemaker?
used in VDD or DDD modes- it’s the maximum time that it’ll allow for delay between either sensing or paced atrial depolarisation before it’ll trigger ventricular activity (if intrinsic activity isn’t sensed beforehand), usually 150-200ms but this can be modulated ie. if a paced atrial activity the AV delay will be longer, or the it can be rate adaptive with the AV delay shorter during perceived exertion, as in the case of a natural pacemaker
what’s the post ventricular atrial refractory period on a pacemaker?
a safety feature- minimum time after ventricular depolarisation paced or sensed, during which the pacemaker will ignore sensed atrial depolarisation- this prevents the pacemaker tracking excessive atrial impulses (eg. retrograde impulses) & causing dangerously high ventricular rates; typically 250-300ms & can be rate adaptive
placing a magnet over a ventricular pacemaker is expected to switch it to which mode?
VOO
which areas require analgesia for thoracotomy?
posterolateral thoracotomy (traverses 6 dermatomal levels, starting at T3 posteriorly & going to approx T8 anteriorly) provides good access to lung, oesophagus, mediastinal structures, descending aorta, diaphragm
anterolateral & axillary thoracotomies are used for specific lung resections (typically 5th ICS= lung resection), thoraco-abdominal for oesophageal (often @ 7th ICS for oesophageal), aortic or upper abdo, clamshell for bilateral (eg. lung transplant)
chest drains are usually inserted around T8-9 ICS post thoracotomy.
require coverage of the impulses from:
-skin & intercostal muscles
-parietal pleura (highly sensitive, from intercostal & phrenic nerves); visceral pleura insensate
-lung & mediastinum (carried via vagus nerve)
-also the lat dorsi (thoracodorsal, C6-8) & serratus anterior (long thoracic, C5-7)
at which level is a Tx epidural sited?
mid-point of dermatomal distribution
at which level is a Tx epidural sited?
mid-point of dermatomal distribution
at which level is a Tx epidural sited?
mid-point of dermatomal distribution
what’s the warm ischemia time for procuring heart/liver/pancreas? kidneys? lungs?
30 mins/ 60 mins / 90 mins
max cold ischaemia time various organs?
heart 4hrs / lungs 6-8hrs /liver or pancreas 6hrs DCD or 12 hrs DBD / kidneys 12hrs DCD or 18hrs DBD
whats the Rx for an adult developing seizures following a brachial plexus block with ropivacaine?
CONTROL SEIZURES with a BZD (midazolam 2-5mg (0.05-0.1mg/kg) or diazepam 2-5mg) or this (1mg/kg) or careful boluses of propofol (NOT if CV instability)
then intralipid (20% lipid emulsion), 1.5mL/kg over 1 min (this is 100mL in a 70kg adult), then an infusion of 15mL/kg/hr (1000mL/hr in adults)
if refractory, can do a max 2 further boluses, 5 mins apart, or can double the rate (30mL/kg/hr) after 3 mins
BUT the max cumulative dose is 12mL/kg (ie. for a 70kg, don’t give > 840mL)
what are some considerations for circulatory arrest with LAST?
recovery from LA-induced cardiac arrest may take >1hr
lidocaine should not be used as anti-arrhythmic therapy
what condition should be monitored for following administration of lipid rescue?
pancreatitis; daily lipase & amylase
What’s ANZTADC & WebAirs?
Aust/NZ tripatriate Anaesthetic Data Committee, representing 3 organisations (ANZCA, ASA, NZ Society of Anaes), developed the WebAirs online reporting database for adverse anaesthetic incidents, can link into hospital system assisting Anaesthetists to report, evaluate & receive info re: adverse incidents- the info can be fed back to the system for closing the QI loop.
why is propofol an unsuitable substitute for lipid emulsion?
significant cardiovascular depression with propofol
on what should intralipid dosing be based in extremely obese pts?
lean body weight
what does indocyanine green do to SpO2?
brief, artefactual reduction (typically to low 90s)
wavelength of absorption peak of red & IR radiation? and indocyanine green?
660 & 940nm
805nm (indocyanine green increases the absorption of light, interpreted as increased oxyHb & falsely elevating NIRS readings)
what accounts for the clinical manifestations of congenital diaphragmatic hernia?
pathologic effects of the herniated viscera on lung development- with lung compression there are decreases in bronchial & pulmonary artery branching & pulmonary hypoplasia ensues, then there’s muscular hyperplasia of the pulmonary arterial tree & risk of pulmonary HTN.
postnatally the infant often presents with resp distress
what’s a common endocrine finding in infants with CDH?
adrenal insufficiency
which therapy is most likely to decrease mortality in neonates with congenital diaphragmatic hernia? how do this?
lung-protective ventilation, they avoid further injury to damaged lung tissue & decrease mortality
limit peak Pinsp to 25cmH2O, keep PEEP 3-5cmH2O & allow permissive hypercapnia
what’s the role of high freq oscillatory ventilation in CDH?
reserved as a rescue when hypoxia & severe hypercapnia persist despite maximal conventional ventilation; as the initial mode of ventilation in CDH, HFOV has no difference in mortality but conventional ventilation has shorter time of ventilation, lower NO requirements, sildafenil & ECMO & less inotropic requirement.
why is CDH repair not necessarily considered a surgical emergency?
because the main risk/prognostic factor is the degree of pulmonary hypoplasia so emergency surgery confers little benefit
there’s much debate & little consensus re: optimal timing of surgery, prior to surgery the pt should have:
-normal MAP for gestation
-pre-ductal SpO2 consistently 85-95% on FiO2 <0.5
-lactate <3mmol/L
-UO >1mL/kg/hr
haemodynamic change expect to see in 1st 24hr following major (adult >10%TBSA) burn?
incr SVR
via what is an Ivor lewis oesophagectomy performed?
abdo phase: upper midline (T6-10) laparotomy or rooftop abdo incision (T8-9 bilaterally)
Tx phase: R) posterolateral thoracotomy at the 4th-5th ICS
what’s the recommended maximum cuff pressure for insufflating a classic LMA?
60cmH2O
what are the classic LMA sizes, pt weight ranges & max cuff volumes?
1 - neonate/infant up to 5kg - 4mL
1.5 - 5-10kg - 7mL
2 - 10-20kg - 10mL
2.5 - 20-30kg - 14mL
3 - 30-50kg - 20mL- max tube size 6
4 - 50-70kg - 30mL
5 - 70-100kg - 40mL
6 - adults >100kg - 50mL
what is the max size ETT that can fit in each of the ambu LMAs?
1 - 3.5
1.5 - 4
2 - 5
2.5 - 5.5
3- 6.5
4- 7.5
5 & 6 - 8
What’s the hunsacker mon-jet used for? benefits? how differ to laser jet double-lumen catheter?
trans-glottic ventilation
all infra-glottic ventilation options have the advantages of:
-minimising glottic movement
-ensuring debris is blown away from vs into the tracheobronchial tree with exp flow
-minimal entrainment of air (allows consistently delivered FiO2)
-can measure airway pressures & EtCO2
-hunsacker mon-jet has a basket to help secure it’s position within trachea during jet ventilation & limit risk of mucosal trauma however risk of shearing a laryngeal lesion on insertion which may seed tumour or virus (use of videolaryngoscope may limit this risk)
-laserket is also a double-lumen, laser-resistant tube for trans-glottic ventilation (and EtCO2 can be measured), has a rounded tip & no basket so may be less traumatic with insertion/removal but not stabilised in trachea.
What’s the hunsacker mon-jet used for? benefits? how differ to laser jet double-lumen catheter?
trans-glottic ventilation
all infra-glottic ventilation options have the advantages of:
-minimising glottic movement
-ensuring debris is blown away from vs into the tracheobronchial tree with exp flow
-minimal entrainment of air (allows consistently delivered FiO2)
-can measure airway pressures & EtCO2
-hunsacker mon-jet has a basket to help secure it’s position within trachea during jet ventilation & limit risk of mucosal trauma however risk of shearing a laryngeal lesion on insertion which may seed tumour or virus (use of videolaryngoscope may limit this risk)
-laserjet is also a double-lumen, laser-resistant tube for trans-glottic ventilation (and EtCO2 can be measured), has a rounded tip & no basket so may be easier to traverse the glottis but potentially more traumatic in the trachea.
-laserjet is smaller (3.4 vs 4.3mm ED) but either could interfere w access to posterior glottic lesion
According to international perioperative guidelines, what plasma ferritin concentration, among pts presenting for major surgery, is diagnostic of inadequate or low Fe stores?
<100microg/L
What’s the parasternal short axis view useful for on TTE?
info re: the overall contractility of the heart or regional abnormalities (since it images all 3 territories), volume status (eg. collapsibility of the ventricle), may see evidence of large pericardial effusion or intracardiac mass, deviation of the inter ventricular septum.
place L) of sternum, 3-4th ICS, marker to R) hip & US marker will be to L) of screen
what are the 3 views of focussed transthoracic echo?
apical
subcostal
parasternal
what’s the apical 4-chamber view useful for in focussed TTE?
comparing ventricle sizes- evidence of RHF or RV dilation (eg. if PE)
what are the 3 branches of the posterior tibial nerve?
medial & lateral plantar, calcanea
which nerves need to be blocked for complete anaesthesia for amputation of 5th toe?
sural, lateral plantar & superficial peroneal
which actions are provided by C8-T1 via the median nerve, NOT the ulnar nerve, thereby being the movements for distinguishing C8-T1 radiculopathy from ulnar nerve lesion (eg, cubital tunnel syndrome)?
the ulnar nerve does all intrinsic hand movements EXCEPT:
thumb ABduction (APB), thumb flexion (flexor pollicis brevis), thumb opposition (opponens pollicis), lateral 2 lumbricals; these are innervated by C8-T1 via the median nerve
which muscles provide shoulder external rotation? internal?
infraspinatus & teres minor
internal is subscapularis
abduction initiated by supraspinatus
what innervates infraspinatus, supraspinatus?
suprascapular nerve, C5-6
what innervates teres minor?
axillary nerve, C5-6
innervation supraspinatus?
supra scapular nerve, C5-6
what does corrugfator supercilli do? and orbiculares oculi?
eyebrow movements, eg. frown
close eyelids
why is the onset of non-depolarising neuromuscular blockade faster at the larynx & diaphragm (central muscles) vs periphery?
central with high perfusion, small fibre size (larynx moree so), despite the fact that these muscles have high proportion of type II fibres & relatively high density of nAChR, conferring some resistance to NDMBs.
adductor policis has predominantly type 1 slow twitch hence lower density nAChR, is more sensitive to NDNMBDs. The APM is more sensitive to nondepolarizing NMBAs, so recovery is delayed in comparison to central muscles (diaphragm, laryngeal muscles.
offset sequence:
diaphragm > larynx > corrugated supercilii (correlates well w larynx) > abdo mm > orbiculares oculists > geniohyoid (upper airway, very sensitive to NDNMBs) > AP (very sensitive)
what’s the management for an unstable pt with tachycardia?
synchronised DC shock, up to 3 attempts; 70-120J biphasic is the most common initial energy (except for AF, where 120-150J biphasic is recommended)
what synchronised DC cardioversion energy should be given for unstable tachycardia? should it be done under sedation or GA? what medication then give?
initial energy 70-120J biphasic (up to 3 attempts)
do under sedation or GA
if AF, 120-150J biphasic
give amiodarone 300mg IV over 10-20mins (dose reduction may be reasonable if also on digoxin), then 900mg over 24hrs (*or if the rhythm was torsades, give Mg++ 2g over 10 mins)
how to manage a stable pt w narrow complex regular tachycardia?
with continuous ecg monitoring:
vagal maneouvers (valsalva +/- leg lift or knees to chest, carotid sinus massage, diving reflex (cold ice on face))
adenosine 6mg rapid IV bolus; repeat 12 up to 2x more
once sinus rhythm restored, consider it’s probably re-entry PSVT, 12-lead ecg to be recorded, if recurs, repeat adenosine Rx, consider anti-arrhythmic prophylaxis
if sinus not restored, seek expert help
how to manage pt w narrow complex irregular tachycardia?
most likely AF
IV B blocker or digoxin
or if <48hrs onset, cardiovert with amiodarone 300mg IV over 20-60mins then 900mg over 24hrs (dose reduce if on digoxin)
what are the differentials for broad complex, regular tachycardia (stable pt)?
VT or SVT with BBB, former is Rx with amiodarone, latter with adenosine
what are the differentials for broad complex irregular tachycardia?
AF with BBB (if so, Rx as for narrow complex)
pre-excited AF (consider amiodarone)
polymorphic VT (eg. torsades, Mg++ 2g over 10 mins)
would seek expert help for this
In the POISE trial, what were the outcomes for pts with or at risk of atherosclerotic disease (RCRI 1 or 2) undergoing non cardiac surgery, receiving prophylactic B blockers DoS?
Reduced MI (which overwhelmingly contributed to a sig reduction in their composite outcome of CV death/nonfatal MI/non-fatal cardiac arrest), new clinically significant AF & cardiac revascularisation
BUT
increased:
total mortality
nonfatal stroke
clinically important hypotension (showing a significant link with death & stroke) & bradycardia
what’s the aseptic technique for central neuraxial blockade?
education to pt & staff re: the sterile field, thorough handwashing with surgical scrub solution, barrier precautions (cap/mask/gown/gloves/drape & eye protection, sterile drape), chlorhexidine in alcohol (0.5% chlorhexidine in alcohol, given that there’s no evidence of superiority of 2% vs 0.5% for antimicrobial superiority & clear evidence of the neurotoxicity of chlorhexidine. For chn <2yo, volume should be absolute minimum necessary while still ensuring antisepsis) applied moving in to out. Prior to skin asepsis which is allowed to dry completely before skin palpated or punctured. Meticulous measures must be in place to ensure the chlorhexidine does not reach CSF (eg. use of swabsticks, dyed solution, equipment covered or protected while the antiseptic is applied).
what’s the recommended skin decontamination for central VENOUS access?
2% chlorhex in ETOH
for how long does isopropyl alcohol provide antimicrobial activity? And chlorheexidine?
ETOH at least 6hrs, chlorhexidine more effective @ 24hrs.
for how long does isopropyl alcohol provide antimicrobial activity? And chlorheexidine?
ETOH at least 6hrs, chlorhexidine more effective @ 24hrs.
2nd line antiseptic solution forsaken prep before neuraxial blockade?
10% povidone iodine
what breaks down remifentanil?
non-specific plasma esterase’s
normal PCWP?
4-12mmHg
PAP 20-30/8-15mmHg
*PCWP>15mmHg ass’d w LV dysfunction
if a pt has R) heart Cath to Ix new-onset dyspnoea, PCWP 10mmHg & waveform showing PAP 74/28, most likely Dx?
PE, since PCWP normal it’s not related to L) heart & acute more likely PE vs empysema
infraclavicular blocks the BP at the level of the…
cords
is ecg essential to use for GA & major regional?
no but it must be immediately available & may be used if clinically indicated
PS18:
-breathing system MUST have O2 analyser
-GA/sedation MUST have pulse ox
-whenever auto ventilator, disconnection/vent failure alarm MUST be on & continuous & auto activated,
-CO2 monitor foall GA, avail for sedation
-ECG must be avail for all anaes; use if GA/major RA as indicated
-NIBP avail for all pts; when used, @ least 10 minutely. IABP avail
-BIS when clinically indicated
-for all pts undergoing GA or if using inhalational; must have inhaled anaes agent monitor
-temp monitor avail for all pts having GA, use it if using warmer
-quant NMT avail for all pts w NMB, use whenever extubating pts after NDNMBAs
-other equip (eg. oximetry) avail as indicated
what’s thrombin time? what factors do influence it? do warfarin & direct Xa inhibitors influence it?
measures the final step in coagulation, conversion of fibrinogen to fibrin.
usually 14-19secs.
prolonged if fibrinogen levels are low or if an agent inhibiting thrombin is present (eg. dabigatran, heparin/LMWH/bivalirudin)
warfarin & direct Xa inhibitors don’t influence thrombin time.
what’s prothrombin time? what influences it?
lab test measuring the extrinsic & common coagulation pathways.
used to monitor LT use of anticoagulant through INR, evaluate liver function & evaluate coagulation disorders; may be prolonged by vit K antagonists, direct Xa inhibitors, vit K insufficiency, liver disease (esp obstructive jaundice), DIC
normal range 11-13 seconds.
INR = (PTtest/PTnormal)^ISI
what’s aPTT, what influences it?
lab test of intrinsic & common pathways
best test for coagulation disorder, if performed properly it’s abnormal in 90% of pts with a coagulation disorder
used to monitor heparin, screen for haemophilia A (def VIII), B (lack of IX) & to screen for clotting inhibitors. Also prol in liver disease, deficiency of any coagulation factor other than VII, massive transfusion with plasma-depleted red cells, DIC.
N range 25-38 secs
what magnitude of impact does an airway obstruction have to be to produce the fixed airway obstruction pattern with truncation on both inspiration & expiration?
lesion must restrict trachea to <1cm
What ARE some complications from dural puncture and resultant intracranial hypotension? what do they NOT include?
seizure
cortical vein thrombus
subdural haematoma
stroke
NOT encephalitis
what are the segments of the R) middle lobe? lingual?
medial & lateral
superior & inferior
what are Sgarbossa’s criteria?
used to diagnose myocardial infarction in pts with L) BBB or ventricular paced rhythms
in such pts, its common to see “appropriate discordance” where abnormal ventricular depolarisation is followed by abnormal depolarisation (eg. ST depression/TWI with +ve complexes, STE & T waves normal hight in -ve complexes)
the 3 criteria to raises suspicion of infarction in pts with L) BBB:
- concordant STE >1mm in leads with +ve QRS (score 5)
- concordant ST depression >1mm in V1-3 (score 3)
- excessively discordant STE >5mm in leads with a -ve QRS (score 2)
a total score >= 3 has high specificity for diagnosing MI
signs of arterial retrobulbar haemorrhage?
rapid development proptosis
reduced visual acuity
deficiency in extra ocular movements
tense eye or other signs of raised IOP
for Parkland, when use 4mL/kg/%TBSA?
if electrical/inhalational burn, dehydrated or trauma
what’s the usual source of allergy to egg?
proteins in the white, not the yolk (propofol has egg lecithin, from the yolk)
do you give propofol to pts with egg anaphylaxis?
adults- yes, but be prepared for anaphylaxis
children, prob not (but would give if mild egg allergy)
idarucizumab reverses anticoagulant effect of?
dabigatran
During the 21st century, the dominant ozone-depleting substance emitted as a result of medical usage to date has been?
N2O
During the 21st century, the dominant ozone-depleting substance emitted as a result of medical usage to date has been?
N2O
do narcotics/opioids have impact on SSEPs? ketamine?
opioids don’t really, ketamine may increase SSEPs (but neither ketamine nor opioids impact MEPs)
does dexmed impact SSEPs or MEPs?
evidence is conflicting, MEPs may be lost @ higher doses, impact on SSEPs is minimal
how to calculate QTc?
QT / square root of the cardiac cycle in secs. therefore, if the HR is 60, R-R interval is 5 squares so the QTc is the same as QT (RR = 60/HR)
what condition ass’d w loss of a waves on CVP trace?
AF
what condition(s) ass’d w cannon a waves (fusion of a & c waves) on CVP trace?
junctional rhythm (atrial contraction occurs @ same time as ventricular so there’s a fusion of a & c waves; atria contracting against closed TCV so cannon a wave)
VT
ventricular pacing
*any conditions where there may be retrograde conduction of ventricular action potentials
complete heart block
these situations create a mechanical disadvantage for the cardiac output- expect a SBP drop- as the ventricle robbed of preload
what may the CVP trace look like in significant TCR?
fused C & V waves; backflow of blood obliterates the X descent
what’s ass’d with prominent A waves on CVP trace?
tricuspid stenosis (the Y wave is slow & lazy due to attenuated ventricular filling)
also seen w pericardial disease (eg. tamponade)- anything restricting myocardial compliance & restricting filling of the chambers
RV failure, pulmonary stenosis or pulm HTN may also cause this (anything that causes a loss of compliance beyond the TCV)
canon a waves in junctional rhythm, V-tach, 3rd degree block from RA contraction against closed TCV
in pericardial constriction the CVP would be raised & there’d be abrupt X & Y descent, while in cardiac tamponade the Y descent is prolonged
What 3 perioperative factors impair host defence against recurrence during cancer surgery?
-surgical stress response
-use of volatile anaesthetic
-opioids for analgesia
what was the crux of Sessler’s Lancet study (2019) re: recurrence of breast Ca following potentially curative surgery for breast Ca with regional anaesthesia-analgesia with PVB + propofol vs sevo & opioid? and their 2nd hypothesis re: regional reducing & persistent pain?
no sig difference in cancer recurrence (median follow-up 36 months)
no sig difference in incisional pain at 6 months
no difference in incisional pain @ 12 months
neuropathic breast pain didn’t differ with regional at 6 or 12 months
what does forest plot show?
graphically the studies included in a meta-analysis (statistical combo of numerical results from individual studies), demonstrate differences btwn studies & provide an estimate of overall result
central vertical line= line of equity. indicates no difference btwn intervention/control (risk ratio 1). To the L) indicates benefit, to the R) indicates no benefit (some the other way around)
horizontal scale @ bottom
n/N= number of events / total number of pts
%, weight of each trial in additional column to the R)
each study a blob, size proportional to study’s weight. CI extends horizontal from blob, if crosses line of equity, no difference.
diamond pooled analysis of all studies.
which nerves supply the ear?
auriculo-temporal from V3 (of trigeminal nerve)= tragus, anterior lobe & skin anterior to ear (to temporal area)
auricular nerve of vagus= inside ear
greater auricular= C2-3 = most of the helix, all of the ante helix, antetragus & earlobe
lesser occipital= C2-3 = tiny bit of upper/posterior helix, area posterior to ear
how manage suspected autonomic dysreflexia (eg. pt with C6 tetraplegia, remove bladder stones under GA, BP 166/88? most worrying complications? signs? risk factors?
emergency situation, requires rapid management
stop trigger (a stimulus below the level of the lesion, eg. bladder or bowel distension or constipation/pressure sores)-eg. relieve distension of hollow viscus
deepen anaesthesia
head up- taking advantage of orthostatic BP drop
administer 100% O2
rapid-onset, short-acting vasodilators (eg. GTN infusion 5mcg/min)- caution with longer-acting as risk hypoT when AD resolves. hypotensive effects of nitrates may be exaggerated in pts on sildefanil for erectile dysfunction.
treat arrhythmias with B-blockers, anticholinergics
treat myocardial ischaemia (eg. with GTN infusion)
invasive monitoring if doesn’t resolve quickly
the disordered SNS response can –> severe HTN, raised ICP & risk of seizures & ICH
cardiac complications= ischaemia, arrhythmias, pulm oedema
incr BP at least 20%
Brady- or tachycardia or heart block; may gen myocardial ischaemia/infarction/acute heart failure
headache, nasal congestion
flushing, sweating above the lesion (VD)
pallor/blanching/vasoconstriction below the lesion
chills
piloerection
may get ICH & seizures
risk of ADR is higher with higher level sessions (above T6)
incr frequency with more complete lesions
generally observed 1yr after injury but can occur within wks of injury
*due to risk of ADR, pts with high SCI may require deep GA or RA, even if they don’t have sensory function @ the surgical site
*ALWAYS ask pts with SCI Hx re: AD episodes- inciting events, regimens, prev surg & anaes Hx
How many domains on the Edmonton Frailty Scale? what are they? max score?
9
Overall health status (eg. number of hospitalisations in past year)
social support
functional dependence
continence
functional performance (TUG)
cognition
mood
nutritional status (weight loss)
medication use
17
What type of extinguisher for power board on back of anaesthesia machine?
CO2 (liquid & electrical fires)
what should occur if identify OT fire?
alert room & stop surgery, simultaneously briefly attempt to douse it (usually only effective in the first few seconds of the fire)
then execute plan, incl appropriate fire extinguisher, cease oxidising gases/fuel removal which can be instantly done, plan for evacuation, activate fire alarm (which activates visual & audible alarms, closes fire doors, notifies local fire dept)
best extinguisher for combustibles (paper, wood)?
water
best extinguisher for both combustibles & flammable liquids (eg. petrol)?
foam
extinguisher that can be used for combustibles, flammable liquids AND gases AND metals AND electrical equipment?
dry powder (but only up to 1000V for electrical)
extinguisher for flammable liquids AND ELECTRICAL EQUIPMENT?
CO2
what are the red sockets backed up by?
backup battery & generator (ie. they are UPS-the battery should be constantly engaged & be in immediate action, seeing supply through until the generator powers on which can take mins to half an hour)
what’s the benefit of blue power points?
they activate an alarm indicating loss of ground power
what’s NNT for analgesics? which analgesic may have the most favourable NNT for neuropathic pain?
number of pts that need to be treated to achieve @ least 50% pain relief in 1 pt cf placebo over 4-6hrs
Etiologies may be peripheral or central
Characterised by burning, p&n, tingling, numbness, electric shocks/shooting, crawling, itching, temp intolerance. allodynia or hyperalgesia.
DN4 questionnaire 7 pain discriminators & 3 exam findings; score of 4+ indicates neuropathic pain likely. S&S 83 & 90%.
Multi-D nonpharmacologic care & nonopioids (TCAs, SNRIs, gabapentanoids, topicals, transdermals)= first line. Trial 3-8 wks, change if no effect or side effects.
first line + tramadol (1st line acute neuropathic) & tapentadol= 2nd line
serotonin-specific reuptake inhibitors/anticonvulsants/NMDA antagonists & interventional therapies 3rd line
neurostimulation 4th line
low-dose opioids (no >90mg morphine equivalent units)= 5th line
TCAs NNT 3.6 for moderate pain relief, NNH 28 (9 for minor adverse effects). Risk falls, arrhythmias, orthostasis, urinary retention in elderly.
duloxetine/venlafaxine (SNRIs): NNT 6.4, NNH 11.8
gabapentin better evidence post-herpetic neuralgia & diabetic peripheral neuropathy, weak evidence other neuropathic pain conditions. NNT 6.3, NNH 25.6
pregabalin NNT 7.7, NNH 13.9
tramadol- NNT 4.4 (other ref combined NNT of 4.7)
Gabapentin (specifically postherpetic neuralgia)- NNT 5.9
membrane stabilisers eg. systemic lidocaine reasonable for acute neuropathic pain (based on evidence for use chrnoic neuropathic)
tramadol effective for neuropathicpaketamine useful for neuropathic pain after SCI
reasonable to use alpha-2 delta ligands in Mx of acute neuropathic pain; they have evidence for efficacy w chronic neuropathic pain.
bain
why may the splitting of S2 be increased with inspiration?
more blood fills the R) heart, delays systolic ejection, greater time until the pressure above the valve > the pressure in ventricle below.
why may the splitting of S2 be increased with inspiration?
more blood fills the R) heart, delays systolic ejection, greater time until the pressure above the valve > the pressure in ventricle below.
what’s unstable angina?
ischaemic symptoms suggestive of ACS but no elevation of troponin, with or without ECG changes of ischaemia (NSTEMI is the same but with trop rise)
what’s bullying?
unreasonable behaviour directed towards an individual or group that creates a risk to health & safety
it’s repeated & occurs as part of a pattern of behaviour
what’s harassment?
unwanted behaviour that offends, humiliates or intimidates a person & targets them on the basis of a characteristic set out in anti-discrimination law (eg. gender)
what’s discrimination?
treating a person with an attribute set out in legislation less fairly than a person who does not have that attribute.
what type of fluid should be administered to a pt with TBI?
warm, non-glucose-containing, isotonic crystalloid to maintain euvolaemia
why AVOID ALBUMIN in pts with TBI?
colloids may increase ICP in pts with altered BBBs as per the SAFE study (saline vs Alb fluid evaluation)- incr mortality among pts with TBI who got albumin, particularly among pts with severe TBI. Among TBI pts who received ICP monitoring, resus w alb ass’d w incr ICP.
risk for AAGA with cardiac surgery (NAP5)?
1:8,600
overall incidence of pt reports of AAGA in NAP5? how about with NMBD? and without?
1:19,000
1:8000 NMBD
1:136,000 without NMBDs
what does the “sail sign” suggest on CXR? other signs of this condition?
L) LL collapse- it’s a triangular opacity @ the posteromedial aspect of L) lung (retrocardiac sail sign)
edge of the collapsed lung may create a double cardiac contour
L) hemidiaphragm & desc aorta may be obscured but can clearly see L) heart border
CXR findings for R) ML collapse?
AP: obscures R) heart border
lateral: triangular opacity in anterior aspect of chest overlying cardiac shadow, apex @ R) hilum
CXR findings for R) ML collapse?
AP: obscures R) heart border
lateral: triangular opacity in anterior aspect of chest overlying cardiac shadow, apex @ R) hilum
how does serum GH usually respond to a glucose load?
in normal subjects, serum GH suppressed to <=1ng/mL within 2hrs of glucose load. the post-glucose values in acromegaly are generally >2ng/mL.
features of Apert syndrome?
premature closure cranial sutures–> limited growth skull (*raised ICP)
mid-face hypoplasia, choanal atresia, cleft palate, OSA (difficult BMV)
increased secretions
low-Cx fusion (reduced neck ROM)
may have fused tracheal rings (reduced ETT size)
beaked nose/small nasal passages
cardiac defects
PCKD
syndactyly (webbed/conjoined fingers/toes)
which drug has the highest rate of anaphylaxis (events per exposure)?
teicoplanin (16 per 100,000)
patent blue (14.6 per 100,000)
sux is 11 per 100,000 (*NDNMBDs have similar incidences of anaphylaxis so concern for anaphylaxis shouldn’t be a major reason for choice)
co-amoxiclav 8.8
roc 6 per 100,000
vanc 6
atrac 3 (miv also 3)
chlorhex 0.78 per 100,000
what does the brain trauma foundation guidelines recommend for BP guidelines?
SBP >=100mmHg for pts 50-69yo, >=110 for everyone else
CPP should be 60-70mmHg
what’s the goal for management of ICP in severe TBI?
<22mmHg (22mmHg= threshold for Rx)
what’s the Aldrete score used for?
suitability for discharge from stage 1 recovery
5 domains (ROCCA: respiration, O2 sats, circulation, consciousness, activity):
activity level
respiration
circulation (BP)
consciousness
O2 saturation by pulse oximetry
need score >9
further modified incl 5 additional elements useful during phase II prior to discharge home (FUPAD):
dressing
pain
ambulation
feeding
UO
Minimum PACU:
sedation 15min, GA 30min, LA could go immediately to stage 2
