Physiology Flashcards
Aortic cross-clamping (RCoA new book, past Q)
Physiological effects - SVR/afterload up, SV/CO/venous return down; renal, spinal cord, metabolic effects
Reperfusion injury (direct and indirect)
Anaesthetic management - vasodilators and fill during clamping; inotropes post release; staged reperfusion; up to 30m XCT; aorto-femoral shunt; reactive oxygen species scavengers e.g. NAC
Monitoring - invasive BP, CVP, TOE, PAFC
What organs are at risk
Oxyhaemoglobin dissociation curve (RCoA old book)
Oxygen delivery (Mendonca)
Fetal Hb has a lower P50 (left shift) so loads with O2 more readily. It has a higher SpO2 at a given PO2 than adult Hb. Fetal Hb is 2 alpha and 2 gamma subunits. It is the beta subunits that bind to 2,3DPG and cause the curve to move rightward, hence the fetal curve remains leftward.
Lactic acidosis type A: caused by tissue hypoxia. Type B: absence of hypoxia e.g. DM, renal failure, hepatic failure, biguanides, salicylates, isoniazid.
Hyperbaric O2: CO poisoning (e.g. preg/MI), severe anaemia, anaerobic sepsis/gas gangrene, decompression sickness, gas embolism, compromised skin grafts/flaps, osteomyelitis. Increases dissolved O2 in arterial blood, reduces gas bubble size, causes vasoconstriction, increases BP and SVR, promotes new vessel formation and wound healing, prevents growth of anaerobic bacteria and production of clostridial toxins, reduces oxygen free radicals thereby reducing reperfusion injury.
SEs of hyperbaric O2
High pressure: tympanic perforation, decompression sickness.
High FiO2: pulmonary, neurological and systemic toxicity. Pulmonary (Lorrain Smith) = absorption atelectasis, oedema, alveolar haemorrhage, inflammation, fibrin deposition and alveolar thickening. Neuro (Paul Bert - Bert for brain) = muscle twitching, nausea, tinnitus, vertigo, hallucinations, dysphoria, visual field defects; seizures occur at 2-3atm. Systemic = due to arterial PO2 rather than alveolar. Retrolental fibroplasia in premature neonates occur with PaO2 10-20kPa for a few hours. Reversible myopia. Hypoxic drive in 10% COPD pts.
FiO2 1.0 for 12-24h causes irritation and sternal discomfort.
FiO2 1.0 for 24-36h causes reduced vital capacity, reduced compliance and diffusing capacity, reduced surfactant production, V/Q mismatch and increased capillary permeability.
Bleomycin causes pulmonary toxicity which is exacerbated by O2. Aim SpO2 88-92%.
BTS guidance O2 prescribing - rx on admission and specify target SpO2.
CO poisoning: CO has 200x affinity than O2 for Hb. Left shift. Reduces Hb available for O2 transport.
CNS - headache, dizziness, seizures, LOC. CVS - tachycardia, MI, arrhythmias. RS - tachypnoea, pulmonary oedema. Metabolic acidosis. False high SpO2 reading.
100% reduces half life from 5h to 1h. Hyperbaric O2 reduces it to 20m, and also provides alternative oxygenation via dissolved O2. Also dissociates CO from cytochrome oxidase.
Hypothermia and blood gases (RCoA old book)
pH rises by 0.0147 units/degree C fall in blood temp (Rosenthal factor) as pCO2 falls
Favours heart and brain flow during hypothermia on CPB
Can add CO2 to oxygenator
Hibernating animals hypoventilate for this reason
Alpha stat and pH stat
Consequences of hypothermia
CVS - increased myocardial O2 demand, ischaemia, arrhythmias/brady/J etc, vasoconstriction, high SVR
RS: increased VO2 with shivering, increased PVR, V/Q mismatch, impaired HPV, reduced ventilatory drive, increased dead space, increased gas solubility
Haem: coagulopathy (enzymes temp dependent), reduced plt function, L shift of curve
Metabolic: BMR reduces 5-7% per degree C if not shivering, metabolic acidosis, hyperglycaemia (reduced insulin), K+ rise on rewarming
Renal: low RBF/GFR
GI: low blood flow, reduced gut motility
mild: 32-35 C
moderate: 28-32 C
severe: < 28 C
Hypothermic arrest
- No adrenaline or other drugs until >30C
- Between 30-35C double the dose intervals
- Shock VF up to 3 times if necessary, then no further shocks until T>30C
- ‘Not dead until warm and dead’ (30-32C)
Morbid obesity (RCoA old book)
Airway: short neck, large chin, large thoracic fat, reduced ROM of atlanto-axial joint, fat in pharyngeal wall, tendency to airway collapse and OSA. Higher risk difficult airway.
RS: elevated O2 consumption, low FRC (can encroach on CC), shorter time to apnoeic desaturation, OSA, OHS, pulmonary hypertension, cor pulmonale, reduced compliance, difficult airway, higher PE risk
CVS: higher blood volume/CO/SVR, HTN, high cholesterol, LVH, IHD, CCF, cerebrovascular disease, polycythaemia, VTE
GI: HH, GORD, gallstones, fatty liver
Endo: DM
Pharmacokinetics altered as high fat, low muscle, low TBW. Fat soluble drugs have higher VD (BDZ). Protein binding increased. Renal/hepatic excretion may be reduced. Relative OD if using total weight.
Other: difficult venous access, regional techniques and NIBP cuff fit. Landmarks obscured. Difficult positioning, higher risk of nerve/skin injury.
Postop: delayed recovery, resp depression, LRTI, wound infection, VTE.
62% of UK population are overweight or obese (BMI>25)
25% are obese (BMI>30)
Acute blood loss (RCoA old book, Mendonca)
Clinical symptoms and signs
Bilirubin metabolism (Dr Barry)
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Pulmonary vascular resistance (Mendonca)
- Factors that increase/decrease PVR
- HPV
Factors that increase PVR/HPV: hypoxia (inc altitude), hypercapnoea, acidosis, PEEP, hypothermia, stress, sympathetic stimulation/catecholamines, serotonin, protamine, ketamine, N2O, PGs, increasing alveolar pressure and volume (compression of corner capillaries).
Factors that reduce PVR/HPV: opposite of the above, + nitric oxide, prostacyclin, ACEi, PDE, histamine, volatiles > 1 MAC.
Treat high PVR with: hyperventilation, NO, morphine, GTN/SNP, prostacyclin, aminophylline, CCBs.
Pul vasodilators are used in ARDS.
NO - start at 5ppm, usual range 5-20, max 80. SEs: formation of NO2 which can cause pul oedema, MetHb, reduced plt aggregation.
HPV: PaO2<9 causes reflex vasoconstriction within seconds. Arterioles account for 80%, veins 20%. Improves V/Q matching. Occurs in denervated lungs so not neurally mediated; several theories, likely chemical mediators - endothelin, reduced NO, smooth muscle contraction. It is biphasic (2nd phase after 1h). Active in fetus, and becomes relevant in OLV and lung pathology.
HPV relevant in: OLV, fetal circulation, altitude, ARDS, GA, PHTN
Arterial tourniquet (Mendonca, past Q)
Double SBP or max 150mmHg above in LL, 50 above in UL. Max 2h.
Indications: surgical field, reducing blood loss, isolated forearm, Bier’s.
CI: abs (DVT, AV fistula), rel (SCD - exsanguinate first, PVD, poor skin).
Give abx 5m before tourniquet up to ensure adequate conc at surgical site.
Inflation: mild rise in SVR and BP from auto-fluid challenge (could push cardiac disease into LVF). Could dislodge DVT/disseminate ca or infection. Acidosis/metabolic product accumulation. Tourniquet pain and hypertension occur after 30-60m.
Deflation: release of cold blood with low pH/high PaCO2/K+/H+/lactate - hence these rise in blood. Transient rise in EtCO2 (8mmHg for thigh tourniquet) - undesirable in TBI. Transient fall in core temp 0.7C within 90s. HR up by 5-10bpm. SBP falls 15-20mmHg. Other changes peak at 3m and resolve by 30m.
Damage to skin/vessels/muscles/nerves (more in UL; radial and sciatic most vulnerable; more in high BMI). Post-tourniquet syndrome (muscles) = stiffness, weakness and pallor, without paralysis.
Pregnancy (Mendonca)
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Pre-eclampsia (Mendonca, Krishnachetty)
140/90 and proteinuria PCR>30mg/mmol (or >300mg/24h or two samples of pro 2+ >4h apart) after 20/40 (up to 30% cases postpartum)
Oedema and raised uric acid common but not part of criteria.
5% of all pregnancies a/w eclampsia (1-2%), HELLP, acute fatty liver of preg
RFs: primip, PHx or FHx PET, age <25/>35, multiple pregnancy, GDM, pre-existing HTN/DM/kidney disease, obesity, new partner Probably a genetic predisposition and possibly autoimmune
Pathophys: 1. Abnormal placentation 2. Endothelial dysfunction.
Failure of trophoblastic invasion of spiral arteries –> high resistance vascular bed (low in normal pregnancy) –> placental ischaemia/hypoxia. Immune response is triggered: release of inflammatory mediators, endogenous vasoconstrictors (TXA2), plt aggregation, coagulation cascade activation and fibrin deposition occur. Result = vasoconstriction, fluid shifts, reduced placental blood flow.
RFs: personal/FHx PET, age>35, obesity, multiple pregnancy, GDM, pre-existing HTN.
Airway: higher risk difficult intubation (facial/tongue oedema; voice changes may signify)
CVS: BP up, SVR up, CO down
RS: pul oedema, airway oedema
CNS: SNS activity up, cerebral oedema, hypertensive encephalopathy, ICH, vasospasm, visual disturbance
Haem: plt activation/consumption, DIC, haemoconcentration
Renal: ischaemia –> GFR down, proteinuria, clearance down
Hepatic: subcapsular haemorrhage, spontaneous rupture, deranged LFTs, reduced drug metabolism
Fetus: IUGR/low birthweight, abruption, mortality
Severe PET: BP>160/110 or additional features e.g. proteinuria >5g/24h, oliguria, cerebral irritability, epigastric/RUQ pain, pulmonary oedema.
HELLP: a/w DIC, abruption, hepatic ischaemia and MOF. Presents as AP, N&V.
Up: soluble endoglin (SEng)
Down: VEGF, PAPP-A
Rx: early diagnosis, BP control, vigilance for eclampsia, timely delivery, steroids before 34/40 BP: if >150/100 –> labetalol (2nd: methyldopa, nifedipine, hydralazine). MgSO4 prevents progression to eclampsia. Restrictive fluid strategy.
Anaes: early epidural, bloods <6h for neuraxial, obtund pressor response if GA
Therapeutic 2-4 mmol/L
Loss of reflexes >5
Respiratory depression 6-7
Cardiac arrest >10-12
Cerebral circulation (Mendonca, Krishnachetty)
Cerebral circ affected by head up/down position and bypass.
Factors affecting CBF: pCO2, pO2, CMRO2, CPP, drugs, temperature
Autoregulation: metabolic (H+/K+/lactate/adenosine), myogenic, neurogenic
Mx raised ICP: reduction of blood, brain or CSF
Measurement of CBF
- Transcranial Doppler (MCA)
- Kety-Schmidt technique - applies Fick principle using N2O. Pt breathes 10% N2O for 10m; paired peripheral arterial and jugular venous bulb samples are taken. Speed of equilibration = measure of delivery to brain.
- PET
- SPECT
All volatiles above 1.5 MAC abolisn autoregulation except sevo (where it is preserved up to 2 MAC). Sevo also increases CBF to a lesser extent than other volatiles, so is preferred in neuro.
All induction agents reduce CMRO2 except ketamine. Opiates indirectly increase CBF because resp depression raises CO2.
Cerebral steal: vasodilatation diverts blood away from damaged areas of brain. Inverse steal: inducing vasoconstriction of normal areas may divert blood towards damaged areas of brain (e.g. thiopentone and hypocapnoea).
Weaning from ventilation (Mendonca)
Cause of resp failure resolved FiO2 <0.5 PEEP <10 Able to breathe and cough Minimal inotropic support RR<35
SBT: T-piece, CPAP or low level PS for up to 30m. Terminate if RR>35, SpO2<90%, HR>140, SBP>180 or <90, agitation, sweating, anxiety.
Trache pros: better tolerated, reduced sedation, reduced dead space and WOB, better mouth hygiene, faciliates wean, can potentially talk and eat.
Coagulation cascade (Mendonca)
Cell-based
Initiation: tissue factor exposed
Amplification: platelets and cofactors activated
Propagation: thrombin generated
(Classical: I/E pathways then FCP - X to Xa, prothrombin to thrombin, fibrinogen to fibrin)
Tissue damage –> tissue factor exposed –> makes contact with circulating factor 7 –> forms a complex which triggers cascade by activating factors 9 and 10 –> 10 binds to 2 to form thrombin.
Then amplification - thrombin burst
Propagation - clot formation
Stabilisation - cross-linked fibrin meshwork
Tissue factor = a transmembrane glycoprotein receptor, ubiquitous in body. Also involved in inflammation, atherosclerosis and metastasis.
Fibrinolysis - breakdown of fibrin by plasmin into soluble FDPs (one type of which is D-dimers) which can then be eliminated.
TEDS - graded circumferential pressure - highest at distal portion; increases blood velocity
Heparin may increase tissue factor pathway inhibitor production.
PONV (Mendonca)
Adverse outcomes: surgical wound dehiscence, dehydration, electrolyte disturbance, unplanned admission, pt dissatisfaction (worse than pain), aspiration
Minimal fasting, fluids, avoid gastric insufflation, avoid N2O/volatiles, antiemetics, opioid-sparing techniques
RFs: patient, anaesthetic, surgical
Brainstem death and organ donation (Krishnachetty, past Q as short case in old RCoA book)
BSD changes: occur due to rising ICP then predictable pattern of changes and MOF. CVS - MAP rises to maintain ICP; sympathetic storm - HTN, ECG changes, high SVR, myocardial ischaemia, reflex bradycardia (Cushing). Herniation/coning –> loss of spinal cord sympathetic activity, vasodilatation, low CO. Pituitary ischaemia causes cranial DI. Hypothalamic ischaemia causes loss of thermoregulation. Dying brain releases tissue factor –> coagulopathy.
BSD: irreversible loss of all brain functions. Coma, apnoea, absence of brainstem reflexes.
Preconditions: irreversible brain damage of known aetiology, coma off all sedation/analgesia/paralysis, apnoea, absence of mitigating factors (T>35, MAP>60, absence of severe metabolic/electrolyte disturbance), ability to do BST (no severe oxygenation problem or high C spine injury, at least one eye and ear). Test at least 6h after loss of last reflex.
Red flag conditions: neuromuscular, prolonged fentanyl infusion, posterior fossa pathology.
BST: GCS 3, pupils fixed/unreactive (CN II, III), corneal reflex (CN V, VII), oculo-vestibular reflexes (CN III, IV, VI, VIII), gag (CN IX, X), cough (CN X), positive apnoea test (after preoxygenation, starting PaCO2>6 and rise to 6.65). 1/11/12 not tested. Excluded from BST: babies <2/12.
Ancillary tests: 4 vessel angiography, radionuclide imaging, CTA.
Organ donation: SNOD ref, check ODR, approach NOK. Specific organ testing, tissue typing, viral screening.
CI: absolute (prion disease and AIDS), relative (disseminated ca, age>70, active TB)
Organ specific criteria: heart/lung >65, chronic disease e.g. IHD, cirrhosis, ESRF, IDDM or previous malignancy of that organ.
Care: general ICU measures (feeding, abx, turning, electrolytes, insulin, VTE, warming, correct coagulation).
CVS: fluids, vasopressin, short acting drugs during catecholamine storm e.g. GTN, esmolol. HR 60-120, MAP70-90, CI>2.1, ScvO2>60%
RS: LTVV, methylpred 15mg/kg, PaO2>8
Endo: consider T3, desmopressin, insulin
Renal: avoid fluid overload, match polyuric losses
Pneumoperitoneum (Krishnachetty, Mendonca, past Q)
CVS: IVC compression –> reduced venous return, reduced CI, aortic compression –> raised SVR, increased MAP, ischaemia, arrhythmia, cardiac failure
RS: reduced FRC, atelectasis, shunt/increased V/Q mismatch, hypoxaemia, hypercapnoea, raised Paw, barotrauma, PTX, VAE, endobronchial intubation
Renal: reduced RBF and GFR
GI: reflux and aspiration
C/PNS head down: raised ICP, eye damage, brachial plexus injury
CNS head up: cerebral hypoperfusion
Up to 20mmHg tolerated in healthy pts.
Pros of lap: faster recovery, suitable for day case, less pain, lung function preserved, aesthetics
Cons: more PONV, shoulder tip pain, vagal responses, longer op time
VAE: 0.5ml in LAD or 2ml in brain fatal. Morbidity dependent on volume, rate and position. Causes pressure, inflammatory and V/Q mismatch effects.
Apnoeic oxygenation (Krishnachetty, past Q)
VO2 continues at 250ml/min - this volume continues to cross the alveoli. Only up to 20ml/min CO2 diffuses out (rest is buffered), so net 230ml in/min which creates subatmospheric pressure. If airway patent, more gas is drawn down from pharynx without any activity from diaphragm or lung expansion. Nasal cannulae can create an O2 reservoir in pharynx. Apnoeic oxygenation (mass transfer of O2) can be maintained for 100m in healthy pts as an O2 deficit of only 20ml/min occurs. Technique limited by CO2 buildup and acidosis, and dependent on airway patency.
Factors influencing time to apnoeic desaturation:
- Reservoir (pre-O2, FRC)
- Rate of use (higher in children, critical illness)
- Duration of apnoea
- Hb
- Airway patency (loss –> atelectasis)
Pre-O2
If FRC 2.5L, at FiO2 0.21, O2 reservoir is about 500ml (2 mins’ worth). If de-nitrogenated, 2.5L O2 = 10 mins’ worth.
Liver disease (Krishnachetty, past Q)
Tests of liver function: enzymatic, synthetic
Decompensation: sepsis, GI bleed, electrolyte dist, excess protein
Pathophysiology of liver disease: steatosis, hepatitis, cirrhosis.
O/E: peripheral stigmata, EJAC, portal HTN, poor nutrition
Hepatorenal syn: renal imp a/w liver disease (diagnosis of exclusion). Type 1 - rapid, severe. Type 2 - slow, progressive.
Preop - fluid/nutrition/electrolytes/coagulopathy, consider paracentesis, antacids
Intraop - increased sensitivity/reduced drug clearance, increased Vd, altered PPB, caution with neuraxial, invasive monitoring, abx, glycaemic control
Postop - ICU
Denervated heart (Krishnachetty, Mendonca, past Q)
Heart innervation: PNS from vagus, SNS from T1-4 cardioaccelerator fibres. SNS = positive chronotropy, inotropy and dromotropy (electrical conductivity across AVN). PNS opposite. Deep and superficial cardiac plexi innervate atria and ventricles.
Ind: end stage heart disease e.g. congenital, CM, valvular. Also combined lung/heart for lung disease impacting heart.
Criteria: imp LV, NYHA 3/4, on optimal medical tx, CRT done if indicated, evidence of poor prognosis (e.g. high BNP, VO2 max <12 on BB, poor prognosis on Heart Failure Survival Score).
CI: PHTN, irreversible end organ damage (lung/liver/kidney), DM with end organ damage, active smoking/alcohol/substance misuse.
90% 1y survival, 50% at 10y.
Denervated heart: no SNS/PNS innervation (some SNS might restart 1y post tx). Resting HR 90-110. Poor response to hypovolaemia - cannot increase HR. No response to drugs acting via ANS e.g. atropine, glyco, digoxin. No response to baroreceptors/CSM, Valsalva, light anaesthesia or pain. No pressor response to laryngoscopy/intubation. No ischaemic pain - need regular angiograms. Need to maintain preload. Sensitive to catecholamines; reduced response to ephedrine as lower stores of NA in myocardial neurones. Still use glyco with neo for reversal as counteracts peripheral effects e.g. nausea/salivation/bronchospasm.
Anaes concerns: denervation issues, original pathology, accelerated atherosclerosis/silent ischaemia, likely to have PPM/ICD, difficult vascular access (avoid RIJ - endomyocardial biopsy route), immunosuppression and drug SEs (need CMV -ve irradiated blood, abx, strict asepsis, steroid supplementation, drug levels, renal dysfunction - avoid NSAIDs), extensive workup/intraop monitoring needed.
Rejection: acute (first 3/12), chronic (allograft vasculopathy - reduced by statins, leading cause of late death).
Immunosuppressants: SCAT
Ventilator associated pneumonia (Krishnachetty, past Q)
Clinical diagnosis >48h IPPV (NICE). Most common hospital acquired infection in ICU - up to 28% of pts, peak at 5 days. Mortality up to 50%.
Features: fever, purulent secretions, worsening gas exchange, rising inflammatory markers, new pul infiltrates on CXR, growth of an org.
Clinical Pulmonary Infection Score: clinical, physiological, micro and radiographic evidence added - score 0-12, 6 or more = VAP but low sens/spec.
Orgs: mainly Gram -ves overall. Early: Strep pneumoniae, H.influenzae, MSSA, Gram -ve bacilli, E.coli, Klebsiella, Enterobacter, Proteus, Serratia. Late: drug-resistant orgs - MRSA, Acinetobacter, Pseudomonas, ESBL.
RFs: pt factors (age, COPD/lung disease, ARDS, low albumin, impaired LOC, trauma, burns, URT colonisation, high aspirates), intervention factors (duration of MV, level of sedation, NMBs, antacids/PPI/H2Bs, NGT, supine, frequent circuit changes, transfer outside ICU).
Path: URT colonisation –> infected secretions enter distal bronchi around ETT cuff, via suction catheter, vent tubing. ICU pts often immunosuppressed, have natural barriers breached and impaired protective reflexes.
Prevention: general (handwashing, sterile equipment, barrier nursing/universal precautions, reducing unnecessary contact).
Specific
* Reducing colonisation (chlorhex mouthwash, SDD (but risk of C.diff, abx resistance)
* Reducing aspiration (head up, subglottic suctioning, cuff pressure >20)
* Early liberation from MV (early trache, sedation holds)
* Choice of GI drugs (?H2B over PPI, stopping when on full feed)
Pulmonary hypertension (Krishnachetty)
PH = MPAP>25mmHg at rest (>35 mod, >50 severe)
Exertional dyspnoea, lethargy, fatigue, syncope - vague sx, often delayed dx
Signs: PR/TR murmur, high JVP with V waves (TR), hepatomegaly, ascites, oedema, fixed/split S2.
ECG: RAH, RAD, RVH, ST dep/TWI. Echo determines systolic pul pressure and diagnoses CHD, valve disorders etc. Gold standard cardiac catheter. CPET, VTE scans. CXR: RAH/RVH, bulky hila, oligaemic lung fields, Kerley B lines.
WHO classification: group 1-5 according to aetiology. Group 1 is PAH (arterial), 2-5 are PH (venous; heart/lung/VTE/unclear respectively).
Path: hypertrophy and intimal fibrosis of pulmonary vasculature –> vessel narrowing and increased pressures. RVF occurs when MPAP>50. LVF can then ensue as reduced venous return and septal interdependence.
Rx: general, medical, surgical. Treat underlying cause, exercise. Medical: O2, prostacyclin agonists (epoprostenol), NO-CGMP enhancers (sildenafil), endothelin antagonists (bosentan), CCBs, NO (for reactivity testing), digoxin, diuretics, anticoagulation. Surgical: lung transplantation, atrial septostomy.
Anaes: all induction/NMB drugs ok except ketamine (increases PVR). Avoid N2O. Invasive BP, CVC, CO/PAFC. Aims: full, slow, tight. Avoid dropping SVR - caution with neuraxial. Avoid increased PVR, myocardial depression and arrhythmias.
Immune response (past Q)
Barrier, innate, acquired Cellular/humoral What are antibodies IgA/D/E/G/M Monoclonal abs - what are they When do we give IVIG
Nutrition and starvation, refeeding syndrome (past Q, Krishnachetty)
See Prezi
pH for NGT: <5.5
Broca Index - precursor to ideal body weight calculations.
Calories: 25-35kCal/kg Carbs: 4g/kg (as 50% glucose) Protein: 1.5g/kg (as 10% amino acid solution) Fat: 1g/kg (as 10% lipid emulsion) H2O 30ml/kg + losses (or 2ml/kg/h) Na+ 1-2 mmol/kg Cl- 1-2 mmol/kg K+ 1 mmol/kg Ca2+ 0.1 mmol/kg Mg2+ 0.1 mmol/kg PO4- 0.4 mmol/kg
Vit B complex, B12, C, E, folate, ADEK
Glutamine, arginine, omega 3
Trace elements: Fe, Cu, Zn, Se, I, Mn, Cr
Smoking (past Q)
COHb
Cherry red - supermarket meat!
RS: COHb reduces Hb for O2 carriage, shifts curve left, CO inhibits cytochrome oxidase (needed for aerobic metabolism), airway irritability, coughing/breathholding/laryngospasm, impaired mucociliary clearance, high risk postop LRTI, COPD, ca
CVS: HTN, IHD, AAA, CVD, PVD, higher resting catecholamines so increased SNS response to desflurane, periop MI risk
Haem: polycythaemia and VTE risk
GI: GORD, PUD
Cessation 1y: risk of ca/COPD etc declines 6/12: postop complications less 1/12: possible less postop LRTI 1/52: reduced airway irritability 12-24h: clearance of CO
Thyroid (past Q, Mendonca)
Myxoedema - 300-500mcg T4 IV loading dose then 50-100mcg IV OD
Hyper: Graves’, toxic multinodular goitre, solitary adenoma. Hypo: Hashimoto’s, post radio/surgical.
Preop: FBC (agranulocytosis from tx), ensure clinically and biochemically euthyroid (TFT), any other autoimmune disease, degree of airway compromise/retrosternal extension (CXR/thoracic inlet AP/lateral/CT/nasendoscopy). Stridor/dysphonia/orthopnoea suggest risk of airway compromise on induction.
Intraop: GA vs RA/LA (cervical plexus + midline SC infiltration) +/- sedation. Gas induction (may be prolonged in obstruction) vs. AFOI vs. awake trache. If stridor present, avoid AFOI (cork in bottle). Spray cords so less pressor response and to surgical manipulation. RLN monitoring tube (–> remi, no MR), reinforced, taped, protect eyes, head up, bolster between shoulders. Dex. Valsalva at end for haemostasis. Reverse. Leak test. Awake extubation vs. deep with LMA exchange.
Postop problems: haemorrhage and airway compromise, laryngeal oedema, RLN palsy, hypocalcaemia, tracheomalacia, thyroid storm, PTX.
RLN monitoring: special ETT has EMG electrode to detect vocal cord movement. Electrodes have to be in contact with vocal cords.
Dietary iodide –> oxidised to iodine in thyroid follicular cells by thyroid peroxidase –> iodine iodinates tyrosine residues –> MIT and DIT formed –> combine to make T3 and T4, stored bound to thyroglobulin in colloid –> endocytosed and cleaved when stimulated by TSH. Carbimazole prevents iodide oxidation. PTU prevents iodination of tyrosine and peripheral conversion of T4 to T3.
Thyroid storm: cold fluids, antipyretics, PTU then Lugol’s iodine (prevents further release of thyroid hormones), beta blockers, steroids. Consider plasma exchange and dantrolene.
Respiratory function tests
Spirometry
Flow volume loops
DLCO (=TLCO)
High: polycythaemia, pulmonary haemorrhage, asthma, L to R shunt
Low: emphysema, CO-Hb (inc. smoking), CF, bronchiectasis, ILD, heart failure, pulmonary arterial HTN, anaemia
Head/neck flap surgery (past Q)
Free vs. pedicle
HCT
Vasodilators/constrictors
Causes of failure
Breast - serratus anterior block
Prone positioning (past Q)
Indications - surgical (spine, Achilles, pilonidal), SRF/ARDS
Reinforced tube
Simple prone vs. tuck
Min 6 ppl (airway, feet, +2 each side; 1 to be the surgeon)
Procedure: bed to table, secure lines/tape ETT/protect eyes etc first, disconnect, ABC (ETT may become endobronchial), top to toe, ABC, surgery start
CVS: CO falls, mainly due to lower SV from reduced preload (IVC compression)
RS: FRC/PaO2 rise, better V/Q matching
Injuries: MSK (pressure sores, dislocation e.g. joint replacements, compartment syndrome/rhabdo), nerves (SOF, brachial plexus, ulnar, lat cut nerve of thigh), ocular (direct pressure or underperfusion), abdominal (compartment syndrome, organ ischaemia, pancreatitis), airway (tongue/mouth swelling)
Montreal mattress (hole for abdo)/wedge under chest/pelvis - decrease abdo pressure
One lung ventilation (past Q)
Indications: absolute (lung isolation/prevention of contamination (e.g. unilateral BAL), ventilatory control (e.g. BPF), relative (surgical access).
DLT: check cuffs, lubricate, preload on stylet. DL with Mac 3 (for max space), stylet out once past glottis. Rotate 90 degrees, advance until resistance. Inflate tracheal cuff, confirm 2LV. Inflate bronchial cuff slowly to abolish leak. Confirm 2LV with both cuffs up (i.e. not obstructing opposite bronchus). Finally, clamp each lumen separately and confirm OLV each side.
Hypoxia: equipment or patient. 100% O2, call for help. Exclude O2 delivery failure, tube displacement/obstruction - check capnograph and pulse ox position, bronchoscopy. Exclude unrelated B problem or low cardiac output. If other causes excluded: PEEP to ventilated lung, CPAP/insufflation to non-ventilated lung (2L/m), intermittent 2LV, early PA ligation if pneumonectomy. Last resort abandon.
TRALI preferentially affects dependent lung.
Diabetes
What happens in DKA? No insulin, so glucose cannot enter cells. Metabolism switches from carbohydrate to fats (as per starvation). FFAs are broken down into ketoacids by liver, hence rise in ketone bodies. Stress hormones rise and exacerbate the hyperglycaemia by glycogenolysis and gluconeogenesis. The hyperglycaemia causes an osmotic diuresis and electrolyte imbalance, exacerbated further by vomiting.
Main causes of death in DKA = K+ disturbance, cerebral oedema and aspiration due to low GCS. Poor prognostic features = impaired GCS, hypokalaemia, oliguria and pH<7.
Prevalence of DM = 9%! 90% of which is type 2. Increases with age (24% of >75s). Male preponderance.
Fluids in paediatrics/hyponatraemia (past Q)
4-2-1 rule
5% dex with 0.45% saline for maintenance (half saline as kidneys immature, cannot handle Na load)
CSL for replacement
Serum bicarb <17 is sensitive for moderate-severe hypovolaemia
Pancreatitis (past Q)
Exo/endocrine functions of pancreas
What is a pseudocyst?
Complications
Multi-system effects
Anaemia (past Q, Krishnachetty)
Microcytic anaemia
- Iron deficiency
- Chronic blood loss
- Bone marrow failure e.g. haem malignancy
- Malabsorption
- SCD, thalassaemia
Macro: B12 or folate deficiency, hypothyroidism, alcoholism, chemo, anticonvulsants
Normo: blood loss, dilutional, BM failure, Addisonian, renal/liver disease
Options:
- Proceed with surgery regardless (higher periop risk MACE)
- Transfuse (concerns over allogenic transfusion and cancer recurrence, higher postop complications and mortality in retrospective data) - only if symptomatic (angina, dyspnoea, failure)
- Iron replacement PO or IV (latter ideal)
TRICC study - Hb 7 vs 9, no mortality difference
Sodium homeostasis (past Q)
DI - central/nephrogenic. Urine >3L/day. High serum Na+>145 and serum osm >300mOsm/kg. Urine osm <300mOsm/kg. Rx DDAVP for central, water replacement and thiazides for nephrogenic.
SIADH - serum Na+<135, serum osm <280mOsm/kg, low urine Na+, high urine osm. Rx water restriction, hypertonic saline, diuretics, vaptans (ADH receptor antgonists). ADH causes water resorption via insertion of aquaporins into CD mems.
Aortic regurgitation (past Q)
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Spinal cord injury and autonomic dysreflexia (past Q, Krishnachetty)
Commonest C-spine # = C6/7 then C2. Most fatal ones C1/2.
Spinal shock: initial phase of flaccidity, areflexia, loss of sphincter tone, priaprism. Lasts hours-weeks. Not a true form of shock as it is neurological, not cardiovascular.
Neurogenic shock: hypotension, paradoxical bradycardia, vasodilatation. Due to SNS damage from lesions above T6. Above T4, cardiac sympathetic supply is also lost.
Anaes concerns post SCI: difficult airway, AD/labile BP, severe brady on tracheal suctioning, sux hyperkalaemia, aspiration risk, latex sensitivity. Art line, temp monitor, urinary catheter.
Autonomic dysreflexia/hyperreflexia refers to a small stimulus below the level of a spinal cord lesion resulting in an exaggerated autonomic response. Occurs 3/52 to 9/12 post injury in lesions above T6 (91% in complete injury, 27% in incomplete injury). Triggered by surgical stimuli, bladder/bowel distension. Results in vasoconstriction below injury and severe HTN - risk of SAH and seizures. Below injury - SNS predominant; pale, cold skin. Above injury - PNS predominant; flushed skin, bradycardia. Mechanism not fully known - possibly alpha receptors become hyper-responsive due to low resting catecholamine levels. Possibly also loss of descending inhibition. Rx: short-acting drugs e.g. GTN, remi, labetalol, volatiles. Very high levels of NA and A are seen during episodes.
Why T6? This level controls autonomic supply to largest blood reservoir - the splanchnic circulation. Above T6, SNS activation is uninhibited. Below T6, the PNS counteracts to prevent HTN.
SCI: 40-50% colonised with multi-drug resistant organisms. Often ESBL Gram negatives associated with urinary catheters. Also MRSA, VRE.
