Thoracics Flashcards

Question

Why do SpO2 drop after the initiation of OLV?

Answer 1

HPV- biphasic, phase 1 begins within seconds & peaks @ 15 mins, phase 2 begins from 30-40mins & peaks at 2hrs

Answer 2

Increase FiO2 to 1.0, NOT for pts who've received bleomycin for malignancy

Answer 3

-if urgent, significant hypoxaemia, resume 2 lung vent If gradual desaturation: -FiO2 1.0 provided no bleo Hx -recheck DLT/BB position w FOB & ensure no lobar obstruction -ensure haemodynamics acceptable & CO optimal (eg. surgeon hasn't compressed IVC), treat any fall in CO & stop vasodilators (ensure MAC <1) -recruitment maneouver to ventilated lung to eliminate atelectasis (risks worsening hypoxaemia if transient hypoT & more blood diverted to non-ventilated lung)- 20cmH2O for 15-20 seconds -adjust PEEP to the ventilated lung. need to recruit before apply PEEP (would have recruited & put PEEP on when commenced OLV). effectiveness will depend on the patient (not for emphysematous pathology)- those with normal lung mechanics or restrictive pattern due to incr elastic recoil will have their end-exp volume brought toward the FRC so PaO2 likely imporve but not possible to predict the optimal PEEP for each pt- titrate. Aim PEEP 5-10 with driving pressure (required for alveolar opening, Pplat-PEEP) 15cmH2O or less. PEEP has the benefit of not interrupting the surgical field. PEEP is as effective as CPAP for improving PaO2 during OLV for pts with normal lung function. -can do apneoic oxygenation to the nondependent lung (3L/minO2 via a suction catheter to the non-ventilated lumen of DLT) -If a DLT, insufflate the non-ventilated lung with oxygen to recruit it (need 20cmH2O to open alveolitic lung areas for CPAP to be effective) then apply 1-5cmH2O CPAP with O2. CPAP may not be completely effective eg. if bronchus of operated lung is obstructed or if open to atmosphere, CPAP won't improve oxygenation. CPAP also can interfere w surgery for VATs. -Could try intermittent re-inflation of the non-ventilated lung (pre-condition the HPV reflex). -could try intermittent positive airway pressure (eg 2 secs on, 8 secs off with 2L/min via CO2 port with HME filter over non ventilated lumen, or could selectively oxygenate specific segments remote from site of surgery (eg. intermittent insufflation of O2 using fiberoptic scope), or could put a blocker just for the lobe being resected while continuing to ventilate the other lobes or could do small TV ventilation eg. 70mLs with RR 6/min. -if pneumonectomy or lung transplant planned or temporarily in emergency, surgeon could clamp a pulm artery to restrict perfusion to the non-ventilated lung. -systemic vasoconstrictor (eg. phenylephrine) with inhaled pulm VD (eg. epoprostenol) to ventilated lung. -dexmedetomidine may improve oxygenation index. -VV ECMO if no other option. -Resume 2-lung ventilation asap if severe desat.

Answer 4

FiO2 as low as possible, low TVs (6mL/kg pred BW) to maintain peak airway pressures as low as poss not >35cmH2O, PEEP 5-8cmH2O (nil in COPD), frequent recruitment, permissive hypercapnia

Answer 5

O2, suction, LA injection

Answer 6

9+(height/10)cm

Answer 7

non-emergent approach to expected difficult airway, particularly anticipated difficult intubation, ventilation or unstable C-spine

Answer 8

T5, angle of Louis

Answer 9

Patient: generally young, male (3:1 to 9:1). predominantly idiopathic & isolated, few (<5%) are associated with connective tissue disorders (eg. Marfan's) or musculoskeletal disorders (eg. Poland syndrome). May have psychological distress re: body image as indication for surgery. Few are symptomatic (breathlessness, palpitations, chest or back pain, pre-syncope/syncope); cardiac +/- lung compression. Pathology: PE more common (87%) than PC (5%). Severity of pectus excavatum graded by Haller index; CT, divide lateral chest diameter by AP diameter, normal 2.56, considered significant if >3.25. Procedure: Nuss= video-assisted thoracoscopc. Bilateral mid-axillary incisions. Retrosternal metallic bars inserted. Bars usually removed within a few years of placement. Potential complications: -intraoperative major haemorrhage: cardiac/vascular/liver injury or perforation -bar slippage or misplacement- may cause trauma, cardiac compression or RVOTO -minor pericardial tears, lung trauma & pleural or pericardial effusions (can be managed conservatively) -CO2 insufflation into the chest can be used to generate a PTx; may be used in addition to OLV or as an alternative to lung isolation- monitor to avoid excessive intrapleural pressure/tensioning/mediastinal shift -brachial plexus injury with arms abducted & Tx bolster- care w UL abduction (open repair doesn't always require UL abduction) -expectation of significant pain -residual PTx (require a CXR in PACU) PRE-OP: C: Hx of allergies (particularly to metals), cardioresp systems, genetic syndromes Exam: cardiorespiratory Ix: -ECG -FBC -U&Es -G&H (high risk major haemorrhage) -chest imaging particularly wrt position of heart & great vessels (displacement/compression), RV compression is common but not usually clinically significant, if severe may develop outflow obstruction. Mitral valve prolapse with MR is also common (20-40%) due to mechanical distortion of the mitral annulus. Additional tests MAY be warranted depending on particular symptom indication: -echo useful for vent fn, valvular (esp mitral) insufficiency, detect RV compression -PFTs: useful for pts c/o resp symptoms, may be normal or may show restrictive defect O: Premed/planning: -Tertiary centre Explain/consent: INTRA-OP: Monitoring: art line, CVC or TOE usually unnecessary unless complex repair/pt comorbidities Assistant Drugs -premed case-by case; anxiolysis, consider a single dose of gabapentin (10-15mg/kg max 900mg PO, 1hr preop) as may reduce postop pain & opioid use REGIONAL: either pre-op thoracic epidural T3-5 (benefit of intra & postop analgesia, failure rate approx 30% across all specialities), bilateral PVB (lower incidence adverse effects incl urinary retention & hypoT), ITM (only useful for up to 24hrs), pecs or SAP blocks, ?ESP blocks TIVA or volatile, avoid N2O (risk expanding pneumothoraces) NMBD (relax diaphragm) Multi-modal analgesia: paracetamol, NSAID, dex, ketamine, ?lignocaine, clonidine, Mg++ Equipment -choice of tracheal tube dictated by surgery- Ravitch doesn't require lung isolation (open OT), Nuss does (thoracoscopic) A B- OLV if Nuss C- lg bore IVC D E F G P- supine with bolster behind Tx spine POST-OP: -CXR in PACU (residual PTx) -Adequate analgesia vital for pt recovery, participation in PT etc; continue multimodal along with PCA (pain often significant into day 2-3 so ensure don't de-escalate PCA too early). incentive spirometry, physio, encourage early mobilisation. -generally disposition= ward

Answer 10

1. optimal gas exchange during OLV 2. allow operative lung to collapse 3. integrity of isolation: no spill over of ventilation, blood, pus

Answer 11

0.9, always leave some nitrogen 5-6mL/kg TVs RR to potentially allow some permissive hypercapnia some PEEP 0-5mmHg (lung protective vent, NO insp pressure >30mmHg)

Answer 12

probably, particularly for transplant pts who don't have the pulmonary reserve to survive. Not as crucial for other lung surg if some resp reserve.

Answer 13

probably, particularly for transplant pts who don't have the pulmonary reserve to survive. Not as crucial for other lung surg if some resp reserve.

Answer 14

analgesia (minimise nadir with resp function) fluid balance mediastinum position physiotherapy avoid atelectasis/infection

Answer 15

Pt booked for pleurodesis, he is a readmit 1/52 after a spont PTx- he has a 15% PTx, undrained. Issues are that may get a tension PTx or if the air leak is significant I may not be able to ventilate the pt. Therefore, I'll change my anaesthetic by: avoiding PPV- spont vent induction most likely sevo or with TIVA. I'd have the surgeon scrubbed in the room ready to assist if needs be with scrubbed field who could but in chest tube in (ideally their desired location of a VATS port). If the pt has an IC tube in situ, I'd still do a spont vent induction as I can't say for sure if the drain will swing/is patent/draining or if I can definitely ventilate the pt.

Answer 16

single lumen tube then railroad bronchocath DLT.

Answer 17

cervical mediastinoscopy (midline transverse incision immediately above clavicular heads); 3cm, suprasternal notch anterior mediastinoscopy (chamberlain procedure)- transverse incision immediately lateral to L) of sternum @ angle of Louie along 2nd CC Procedure: Chamberlain procedure more invasive Pt positioned supine with shoulder roll under scapulae & neck extended position of the mediastinoscope may impinge on nominate artery so may loose R) UL pulses, BP more accurately monitored on the L), can monitor R) UL pulse ox or art line to detect nominate compression Potential complications: all more common in anterior mediastinoscopy procedures vascular injury, tracheal or oesophageal injury, PTx, RLN injury Cervical relatively contraindicated in SVC syndrome (risk bleeding with distended vv), prev mediastinoscopy @ same site rel CI. severe trach deviation, cerebrovasc disease, severe C spine disease w limited neck E, prev chest RTx, thoracic aortic aneurysm all other rel CIs. Thoracoscopy: induction & intubation for single-lung ventilation (DLT or bronchial blocker), pt in lat decubitus with table broken to open intercostal spaces Potential complications: PTx, chylothorax (tx duct), phrenic nerve injury, oesophageal perforation, bleeding from vascular injury (consider pre-op access all LL due to risk of disruption of vessels driaining into SVC), RLN injury, stroke, air embolism, oesophageal tear, tracheobronchial lac, conversion to open to improve surgical exposure is not uncommon. Open approaches incl thoracotomy, sternotomy; anterior mediastinal masses crossing the midline require a sternotomy while those in one side only may be exposed adequately with hemi-clamshell incision, masses extending below pulmonary hill on both sides require a clamshell incision Preop considerations: bronchogenic carcinoma: often smokers, multicomorbid incl HTN, CAD, PVD mediastinal mass concerns as above (most asymptommatic) tracheobronchial compression predisposes to persistent RTI, wheeze, stridor Awake or inhalational to maintain spont vent & -ve Pip (lost if decr chest wall tone & cephalic displacement of diaphragm) if symptomatic w resp obstruction, AFOI, whole team see level ov obstruction, pass tube distal to obstruction. If very distal, have rigid bronch available. Could use inhalational induction alternative w pt 20 deg head up (pre-oxygenate in position of safety) d/w surgeons nature of lesion, ?stent before mediastinoscopy if significant obstructive symptoms? sandbag, head up 20 deg. reinforced may be useful to risk kinking intra-op. if long-standing mass, fibreoptic at end to rule out tracheomalacia prop/remi, NMBA if no MG. wound LIA, superficial Cx plexus block or intercostal block help. paracetamol/nsaid. CXR postop in PACU to exclude PTx. HDU or ward depending on pt/procedure (day case if very minor), postop complications RLN injury or paratracheal haematoma. PCV detects early rise in Paw.

Answer 18

central femoral line PRIOR to induction (or 2x large-bore LL peripheral catheters) If difficult IV access could place one draining into IVC (eg. femoral) & SVC (eg. IJ), so the IVC used during surgery until mass resected then SVC postoperatively

Answer 19

When the surgeon places an ETT directly into the main conducting airway to ventilate airway distal to disrupted trachea (eg. Iatrogenic injury), run TIVA in this instance (depth of anaesthesia, limit VA to surgical team, discontinue N2O & FiO2 <30% or a minimum to avoid hypoxia (fire risk), allow adequate time for reduction in both FiO2 & FeO2 to safe level before electrosurgery or other ignition source.

Answer 20

Those who may develop airway obstruction +/- haemodynamic compromise from anaes or surgery

Answer 21

-spont vent -open chest -high end-exp pressures (eg. >40mmHg) -TVs <8mL/kg Visualise respirophasic variation on art line trace- adequate estimate & may be comparable to automated values

Answer 22

Restrictive, since <=3mL/kg/hr hasn’t been ass’d w AKI after Tx surgery & excessive fluid ass’d with ALI & delayed recovery (don’t need to reverse oliguria with fluid administration) Replace red cells only if Hb <80g/L, otherwise use colloids to replace blood loss

Answer 23

Surgical: no factor requiring ongoing intubation eg. Excessive airway swelling, high bleeding risk, excessively prolonged surgery Anaesthetic: full recovery of neuromuscular function to TOFR >0.9 & sedative/hypnotics adequately washed out Pt: Not hypoxaemic (ie. P:F ratio >=150, SpO2 >=90% on FiO2 <=40% & PEEP <=5 Normothermic Acid-base status normal Haemodynamic stability (no or minimal pressor) Able to initiate resp effort Hb >=70g/L Mental status awake & alert or easily rousable

Answer 24

1. lung mechanical function 2. pulmonary parenchymal function 3. cardiopulmonary reserve

Answer 25

alert warm comfortable

Answer 26

smoking cessation physiotherapy thoracic epidural analgesia

Answer 27

preoperative exercise capacity cardiac arrhythmias & other cardiac complications

Answer 28

not with IV anaesthetic or volatile <=1MAC

Answer 29

High TVs (10mL/kg)

Answer 30

Secure lung isolation before PPV & positioning for surgery

Answer 31

PTs symptoms, preop CT, echo findings. Don’t burn your bridges

Answer 32

Continuous paravertebral with multimodal analgesia- while Tx epidural has been shown to consistently decrease post-thoracotomy resp complications in high-risk patients, continuous PVB is a reasonable alternative, comparable analgesia with fewer side effects & lower rate of block failure (refs 2 & 79 in Miller ch 53)

Answer 33

Resectable= disease that’s local or loco-regional in scope Operable= patient, someone who can tolerate the proposed procedure with acceptable risk

Answer 34

Respiratory complications- atelectasis, pneumonia, respiratory failure- in 15-20% of patients.

Answer 35

Simple spirometry

Answer 36

respiratory mechanics gas exchange (parenchymal function) cardiopulmonary interactions (exercise capacity)

Answer 37

FEV1 FVC maximal voluntary ventilation (MVV)- in the normal subject, this value (the maximum MV the subject can maintain for 12-15secs), is about 15-20x the resting MV RV/TLC ratio (higher suggests worse airflow obstruction)

Answer 38

age sex height

Answer 39

post-op predicted FEV1 % = ( pre-op FEV1 (%) ) x ( 1 - %functional tissue removed / 100 )

Answer 40

>40% low risk 30-40% moderate risk patients with ppoFEV1 <30% are at high risk

Answer 41

DLCO, correlates with functioning surface area of alveolar-capillary interface

Answer 42

a value of <40% correlates with increased respiratory & cardiac complications it is, to a large degree, independent of FEV1 ppoDLCO = pre-op DLCO x (1-%functional lung removed/100) may be negatively impacted by pre-op chemo

Answer 43

20%, considered absolute minimum value compatible with a successful outcome. Pts with homogenous emphysema also have very poor outcome.

Answer 44

1, 3.5mL/kg/min

Answer 45

3m (20 feet)

Answer 46

6MWT, maximal distance a pt can walk in 6 mins, simple, just need markers & stopwatch. shows excellent correlation with VO2 max.

Answer 47

6MWT, maximal distance a pt can walk in 6 mins, simple, just need markers & stopwatch. shows excellent correlation with VO2 max.

Answer 48

Divide total distance (m)/30, ie. 450m distance is VO2 max of 15mL/kg/min.

Answer 49

Incremental shuttle walking (walk at a gradually increased rate between 2 markers 10m apart, total distance <250m correlates with VO2max of <10mL/kg/min) Exercise-oximetry: decrease in blood SpO2 >4% during exercise are at increased risk The gold standard= cardiopulmonary exercise testing

Answer 50

VO2 max of 15mL/kg/min (maximal O2 consumption during aerobic exercise) If pre-op VO2 max is <15mL/kg/min, high risk of M&M If pre-op VO2 max is <10mL/kg/min (35% predicted), risk is very high Very few patients with VO2max >20mL/kg/min (75% predicted) have respiratory complications

Answer 51

Right ventricular dysfunction, which appears to be in proportion to the amount of functioning pulmonary vascular bed removed. Tends to be more evident with exercise vs rest, there is the absence of the normal decrease in PVR usually seen with exertion- there’s instead elevated PVR & limitation of CO.

Answer 52

For pts having a pneumonectomy & pre-op FEV1 or DLCO <80%, since if the lung to be resected has minimal function the prediction of ppoFEV1 or DLCO can be adjusted accordingly Not useful for predicting post-lobectomy function

Answer 53

30% 40% for thoracotomy (there's a threshold ppoDLCO of 60% for open procedures below which the incidence of respiratory complications much higher) Extubation plan. If a pt has ppoFEV1 >40%, the pt can be extubated in OT provided alert warm and comfortable. If the ppoFEV1 is >30% and the exercise tolerance & lung parenchymal function exceed the increased-risk thresholds, can extubate in OT depending on other medical conditions. If the pt has ppoFEV1 20-30%, consider their cardioresp & parenchymal function, presence of Tx epidural & whether VATS or open when deciding re: timing of extubation.

Answer 54

0=3.9% 1=6% 2=10.1% >=3=15%

Answer 55

high >5% intermediate 1-5% low <1% risk of perioperative adverse cardiac event (death or non-fatal MI)

Answer 56

those with major (unstable angina, recent MI, severe valvular disease, decamp CCF, significant arrhythmia) and intermediate (previous CCF, diabetes, remote infarction, stable angina) predictors of myocardial risk

Answer 57

diseased lung, part of pericardium, part of diaphragm & part of parietal pleura

Answer 58

arrhythmias, particularly AF higher with greater extent of resection, intrapericardial dissection, intraop blood loss, higher pt age extrapleural pneumonectomy particularly high risk incr pulmonary vascular resistance (lung resection, atelectasis/hypoxaemia) increased SNS stimulation & O2 requirements (maximal postop D2 when pts more mobile)

Answer 59

diltiazem B blockers may be the most effective but concern about use in pts with reactive airways disease continue B blockers if on them. all pts to have magnesium if low or suspect low total body stores. high risk pts (eg anterior mediastinal mass, lobectomy, pneumonectomy & esophagectomy) get diltiazem if not on a B blocker & if preserved cardiac function. consider amiodarone & statins.

Answer 60

OLV= obligatory 20-30% shunt through non-ventilated lung (it's not > this, due to surgical manipulation to atelectatic lung, lateral positioning (incr perfusion to dependent lung), HPV, if baseline CO decreased, the fall in SmvO2 --> exaggerated fall in PaO2 monitor SmvO2 & may need inotropes to support CO.

Answer 61

no, not according to Miller :)

Answer 62

avoid hypotensive & vasodilating anaesthetic agents wherever possible use pulmonary vasodilators (NO, prostacyclin) in preference to IV vasodilators where possible ketamine does not exacerbate pulmonary HTN monitor CO if considering a thoracic epidural, titrate cautiously with low dose LA & inotropes or vasopressors, since sympathectomy may impair tonic cardiac SNS innervation (important for haemodynamic stability in pulm HTN due to lung disease)

Answer 63

inhaled NO 10-40ppm nebulised prostacyclin 50ng/kg/min

Answer 64

better haemodynamic stability with PVB

Answer 65

trans thoracic echo to Ix pulmonary HTN

Answer 66

ABG to see baseline PaCO2 to avoid hypoxaemia with the postop fall in FRC

Answer 67

home oxygen

Answer 68

resting PaO2 of <55mmHg & decreases to <44mmHg with exercise (pts with COPD don't increase their RV EF with exercise as in normal patients)

Answer 69

findings of restrictive as well as obstructive disease during spont vent there's slightly -ve pressure in the bull but then PPV used, pressure in a bulla becomes +ve & it'll expand, risk rupturing & causing tension PTx & bronchopleural fistula. Keep airway pressures low & ensure adequate expertise & equipment available to insert a chest drain & isolate lung if necessary.

Answer 70

severe haemodynamic collapse with PPV due to dynamic hyperinflation of lungs

Answer 71

end-exp flow interruption

Answer 72

bronchospasm (if pt poorly controlled on beta agonist & anticholinergic, consider trial of corticosteroids) pulmonary oedema atelectasis respiratory tract infections

Answer 73

fewer postop pulmonary complications cough, DB, incentive spirometry, PEEP, CPAP are the options, none is proven superior, improvements if done for >1/12 prep (so less feasible prior to OT for resectable malignancy).

Answer 74

4 weeks 12 hrs intensive smoking cessation interventions

Answer 75

strongly linked to cigarette smoking tend to grow large in size & metastasise later than others symptoms tend to be due to local effects of the large tumour eg. haemoptysis, obstructive pneumonia, SVC syndrome hypercalcaemia may be associated with squamous cell carcinomas due to parathyroid-like factor

Answer 76

most common NSCLC tend to be peripheral & metastasise early esp to brain, bones, liver, adrenals almost all pancoast tumors (at apex of lung, can cause horner's syndrome, brachial plexus, RLN) are adenocarcinomas can be ass'd with paraneoplastic metabolic factors eg. growth hormone & corticotropin, may be associated with hypertrophic pulmonary osteoarthropathy. bronchioalveolar carcinoma isn't related to cig smoking, low potential to spread outside of the lungs so may be treated with lung transplantation.

Answer 77

uncommon often large caveatting peripheral tumor rapid growth, widespread mets

Answer 78

neuroendocrine in origin usually central lesions usually a medical vs surgical disease, considered metastatic on presentation treatment of limited stage SCLC with chemo, aggressive radiotherapy paraneoplastic syndromes common eg. hyponatremia (SIADH), ectopic ACTH--> hypercortisolism (Cushing syndrome). rare Eaton-Lambert myasthenia syndrome (impaired release of ACh from nerve terminals)- proximal LL weakness & fatiguability what may temporarily improve with exercise. Dx by EMG. similar to MG wrt very sensitive to NDMR & respond poorly to anticholinesterase reversal agents. There may be subclinical involvement of diaphragm & rest mm.

Answer 79

neuroendocrine in origin usually central lesions usually a medical vs surgical disease, considered metastatic on presentation treatment of limited stage SCLC with chemo, aggressive radiotherapy paraneoplastic syndromes common eg. hyponatremia (SIADH), ectopic ACTH--> hypercortisolism (Cushing syndrome). rare Eaton-Lambert myasthenia syndrome (impaired release of ACh from nerve terminals)- proximal LL weakness & fatiguability what may temporarily improve with exercise. Dx by EMG. similar to MG wrt very sensitive to NDMR & respond poorly to anticholinesterase reversal agents. There may be subclinical involvement of diaphragm & rest mm.

Answer 80

often proximal, endobronchial, may present with bronchial obstruction & distal pneumonia often highly vascular no association with smoking high 5-year survival following resection of typical carcinoid tumours (90%) systemic mets rare atypical carcinoid tumours more aggressive & may metastasise carcinoid syndrome (due to ectopic synthesis of vasoactive mediators) is rare since they are usually metabolised by the liver; more often seen with carcinoid tumors of gut origin that met to the liver. carcinoid crisis may occur- be prepared with octreotide

Answer 81

dyspnoea on exertion from pleural effusion may have symptomatic improvement with thoracocentesis but pleural biopsy by VATs= most efficient way to obtain diagnosis, often receive talc pleurodesis during the same anaesthetic to receive the effusion strongly associated with asbestos exposure

Answer 82

4M's: metastases: esp brain, bone, liver, adrenal mediations: bleomycin pulm toxicity (bleomycin used for mets from germ cell tumours); association btwn prev bleomycin therapy & pulmonary toxicity with high FiO2 is well-known but the safe doses & safe period after exposure unknown so safest= use lowest FiO2 consistent w pt safety & closely monitor oximetry, doxorubicin cardiotoxicity, cisplatin renal toxicity (avoid postop NSIADs) mass effects: obstructive pneumonia, lung abscess, SVC syndrome, tracheobraoncial distortion, pan coast, RLN or phrenic paresis, chest wall or mediastinal extension metabolic effects: eaton-lambert, hypercalcemia, hyponatremia, cushing syndrome

Answer 83

for prophylactic LMWH, 12 hrs after 24hrs after therapeutic LMWH

Answer 84

all: Ax functional capacity, spirometry, discuss postop analgesia, smoking cessation if ppoFEV1 or DLCO <60%, exercise test Ca: 4M's COPD: ABG, physic, bronchodilators incr renal risk (prep HTN, ARBs, open procedures, use of starch): measure Cr, BUN

Answer 85

1. review of initial Ax & test results 2. anticipate potential for difficult lung isolation (CXR, CT chest) 3. assess risk of desaturation during OLV

Answer 86

CXR, CT chest (eg. for saber-sheath trachea or extrinsic compression or intraluminal obstruction).

Answer 87

anaesthetic: poor SpO2 on 2-lung ventilation, esp in lateral position. Lower PaO2 on two-lung ventilation (eg. 200mmHg vs 400mmHg). surgical: R)-sided thoracotomy, since the L) lung is 10% smaller than the R), there's less shunt when the L) lung collapsed (mean PaO2 70mmHg higher in L) vs R) thoracotomy). supine position during OLV patient: normal PFTs pre-op, restrictive lung disease; patients with more severe airflow limitation on pre-op spirometry tend to have better PaO2 during OLV than pts with normal spirometry. High % V or Q to the operative lung on prep V/Q scan. CPAP (2-5cmH2O or O2) to the non ventilated lung, PEEP to dependent lung

Answer 88

increases, so PetCO2 is a less reliable indicator of PaCO2. CALHN payroll number 3025831

Answer 89

longer, shorter cuff, can advance into mainstream bronchus under fiberoptic guidance uncured paed ETT advanced into mainstream bronchus under guidance with infant bronchoscope

Answer 90

auscultation and bronchoscopy after placement & repositioning. with the FOB through tracheal lumen, ensure the endobronchial portion in correct main bronchus, no bronchial cuff herniation over carina after inflation (cuff should sit 5mm below tracheal carina for L) bronchus), identify takeoff of the R) UL bronchus (the only structure in tracheobronchial tree w 3 orifices. then FOB through endobronchial lumen to check tube potency & margin of safety, visualise orifices of L) upper & lower lobes.

Answer 91

run down posterior tracheal & mainstem bronchial walls, then the L) lower lobe (useful landmark to distinguish from L) UL)

Answer 92

cohen the arndt does in the size 9Fr

Answer 93

5-8%, usually in the epiglottic area, many have had previous radiation therapy on neck or prev airway surgery

Answer 94

AFOI nasal or oral with SLT then pass bronchial blocker could alternatively do a SLT then tube exchange

Answer 95

at least 83cm long 14Fr for size 39 & 41 Fr DLTs 11Fr exchange catheter for size 35 & 37 Fr DLTs

Answer 96

No deeper than 24cm @ lips sniffing position helps video laryngoscope to guide the 2nd tube, assistant holding scope confirm with auscultation & bronchoscopy if doing a SLT for DLT tube exchange, test the SLT, AEC & DLT combo in vitro

Answer 97

Unilateral bronchiectasis or haemoptysis (diseased lung down) until lung isolation achieved, then diseased lung to nondependent side.

Answer 98

Move head, neck, ETT “en bloc” with TL spine

Answer 99

Compression injuries- dependent arm directly under thorax, pressure clavicle, caudal migration of Tx padding Stretch injuries- lat flexion of C-spine, excessive abduction of arm >90deg, rotation of torso & traction on fixed arm

Answer 100

Suprascapular nerve

Answer 101

Judicious- risk exacerbating shunt &  pulmonary oedema, particularly during prolonged surgery, vital to avoid since dependent lung responsible for all the gas exchange. Total +ve fluid balance in the first 24hrs periop should not exceed 20mL/kg for pulmonary resection. Average adult: no >3L crystalloid. Do not need to titrate to UO >0.5mL/kg/hr. inotropes preferable to fluid overload to incr tissue perfusion postop.

Answer 102

HPV is inhibited during hypothermia (as are most of the body’s physiological functions)

Answer 103

limit airway manipulation while in light plane of anaesthesia Use BD anaesthetic Avoid histamine-releasing drugs Props or ketamine diminish bronchospasm, sevo the most potent BD of the volatiles but prop TIVA or volatile fine

Answer 104

Myocardial O2 supply/demand (preserve DBP, Hb, avoid tachy, ensure comprehensive analgesia)

Answer 105

Pre-oxygenate with 100% O2 as nitrogen lower solubility will delay collapse (esp if pts have emphysema & decr elastic lung recoil)- the dependent lung will develop atelectasis so recruit after OLV.

Answer 106

No universally accepted figure, >=90% commonly accepted, high 80s briefly accepted for pts sans sig comorbidity.

Answer 107

Maximise PVR in the nonventilated lung while minimising it in the ventilated lung; HPV promoted blood flow to the ventilated lung, PPV tends to do the opposite, surgical manipulation & cardiac output changes have variable effects on proportional flow to ventilated lung. Aim to keep the ventilated lung as close as possible to FRC as at high or low volumes, incr PVR (hyperbolic relationship). Aim to keep the nonventilated lung collapsed.

Answer 108

It can decr blood flow to nonventilated lung by 50%

Answer 109

Initial immediate & plateaus after 20-30mins, 2nd phase begins after 40 mins & plateaus @ 2hrs

Answer 110

Worsen it- vasodilators tend to cause deterioration in PaO2 during OLV

Answer 111

Not directly, but may indirectly impact oxygenation if hypotension & reduced CO occur

Answer 112

No clinical benefit on oxygenation using one over the other if the VA is <=1MAC, although the modern volatiles do slightly impair HPV it’s to a less extent that prev volatiles & is not clinically sig (reduce HPV by 20% @ 1 MAC< equivalent to reducing total AV shunt 4% which is negligible in most situations. On the flipside, there may be less pro-inflammatory cytokines & lower incidence of postop pulm complications & lower 1-year mortality with volatiles.

Answer 113

Ass’d with more atelectasis of dependent lung, increases PAP in pts with pulm HTN, impairs HPV, may expand air-filled spaces.

Answer 114

Even with optimal anaesthetic management there’s a shunt of 20-30% during OLV, so vital to maintain CO but not supranormal (excess CO increases shunt but also SvO2 but there’s a ceiling effect to SvO2 incr so ultimately that may cause hypoxaemia, low CO reduces both shunt & SvO2 which leads to hypoxaemia).

Answer 115

Depends on the patient. Patients with COPD & auto-PEEP will tend to be pushed further away from the lower inflection point of FRC hence PaO2 may suffer, while pts with normal elastic recoil or restrictive lung disease (high recoil) may be pushed towards FRC inflection point & gas exchange benefits from PEEP.

Answer 116

5-6mL/kg IBW TVs, PEEP 5cmH2), Pawpeak no >35cmH20 (Pplat approx. 25cmH2O). lateral positioning will require approx. a 20% increase in MV to maintain PaCO2- PetCO2 is a less reliable monitor of PaCO2 during OLV as the gradient becomes larger.

Answer 117

PCV ass’d with lower peak airway pressures but not improved oxygenation. PCV does avoid sudden increases in peak airway pressure with surgical manipulation of the chest which is of benefit if a bronchial blocker or if at risk for lung injury (eg. After pneumonectomy or lung transplant) but given the frequent manipulation, check volumes achieved with PCV as it may be suboptimal.

Answer 118

R) lung is larger & 10% better perfused than the L)

Answer 119

fall in arterial oxygenation, nadir 20 mins then stabilise & may rise with the increase in HPV over the next 2hrs.

Answer 120

Glycine can build up in the HME filter, increasing airflow resistance. Need to change HME filter every hour when nebulised epoprostenol used.

Answer 121

The first lung is impaired from mechanical trauma and HPV offset may be delayed after reinflation of the first lung collapsed. Therefore for bilat procedures, operate fist on the lung that has better gas exchange (usually the R) lung since larger & higher proportion of blood flow)

Answer 122

The risk of airway compression or compression of vital vasculature (IVC, PA) due to mass effect with induction of anaesthesia, which obliterates the awake patient's compensatory mechanisms (compression of airway structures & great vessels with sitting to supine, loss of airway patency after administration of NMBAs, increased Pit with decreased VR to heart during transition from spont -ve pressure vent to controlled PPV, arterial & venodilation & myocardial depression caused by administration of anaesthetic induction agents) surgical manipulation & resection of mass incl. compression of airway structures/great vessels, risk to airway continuity or patency due to injury to trachea or other airway structures major haemorrhage due to injury to structures adherent to or proximate to the mass History: -Nature & history of the mass, predominantly to assess risk of AIRWAY or RESPIRATORY compromise +/- HAEMODYNAMIC INSTABILITY due to mass effect on airways & lungs or major cardiovascular structures which may occur with induction (loss of awake/upright compensatory mechanisms, loss of muscle tone, incr Pit with spont to PPV) -where is it? -how large & rapidly growing is it? -what is it thought to be? (impacts how likely it is to be adherent, ass'd w mets, secreting) -are there symptoms related to effects of the mass on adjacent intrathoracic organs? -SVC obstruction of progressive grades: facial oedema or plethora, Pemberton's +ve (eg. retrosternal thyroid extension or lung carcinoma, lymphoma, thymoma or some aortic aneurysms ("nutcracker" effect where medial clavicles impinge major venous structures within a narrowed Tx inlet against a relatively fixed & enlarged mass)), UL oedema, hoarseness (vocal cord oedema), dysphagia or cough, visual disturbances (ocular oedema), dizziness/headache from cerebral oedema, syncope or near-syncope after bending, stridor (significant laryngeal oedema), significant haemodynamic compromise such as hypoT or syncope without trigger. Hypotension may also raise possibility of cardiac compression or tamponade. -can they lie flat (and for how long/are there positional changes that alleviate this? Haemoptysis, chest pain, dyspnoea?) -Are there systemic symptoms due to paraneoplastic syndromes (eg. thymic mass secreting anti ACh receptor antibodies--> MG, parathyroid adenoma secreting PTH (primary hyperparathyroidism)--> hyperCa++) -Has the patient completed chemo or radiotherapy to reduce mass effect/optimise successful resection? if so, adverse effects of chemo & impacts of radiotherapy on anaesthesia (dry mouth/airway swelling, airway friability, mucositis, oesophagitis and dysphagia/reduced PO intake/dehydration are considerations, as is scarring fibrosis of thoracic connective tissue potentially resulting in need for high airway pressures (peak pressure >30mmHg) during PPV) -Other general & anaesthetic Hx & systems review, functional status Examination: -walking into waiting room, vital signs, signs of work of breathing/preferred postures, plethora/cyanosis/oedema/venous engorgement -auscultating lungs and heart -pedal oedema/other signs of right heart failure Investigations: -CT, MRI +/- radio nucleotide studies- imaging to assess relationship of mediastinal mass to airway, lungs, heart & major blood vessels (*in an awake pt so the imaging may not predict changes after induction) -echo -pulmonary function tests have minimal utility (poor correlation with airway obstruction) -exercise tolerance- stress test or quantify w METs DASI -ECG Planning: -multi-D discussion with surgeons; plan OT to be @ tertiary centre, daylight hours, senior operators, ICU aware/present -if the mass is associated with high likelihood of cardiovascular collapse or complete tracheal obstruction during induction or surgical intervention, may employ cardiopulmonary bypass (having them on standby likely futile as time to cannulate major vessels is at least 10 mins) or ECMO. -IV access & art line monitoring plan (pre-induction, location particularly if SVC obstruction or if risk compression of arterial supply to either limb) -blood products- if large mass in critical location, d/w surgeons EBL -regional techniques pre-incision- approach & US, haemodynamic considerations (may just place opioid pre-incision) Discuss plan & risks w pt, verbal informed consent Pre-team brief re: surgical & anaesthetic concerns, contingency plans Eg. if CPB or ECMO are initiated pre-induction, anaesthetist must be ready to sedate for cannulation, heparin administration prior to CPB, administration of vasoactive agents & protamine during & after CPB weaning- if this is planned, do a femoral CVC & art line, sedate with midaz or ketamine for cannulation, heparin prior to partial CPB, GA induction once CPB established, if haemodynamic instability then initiate full CPB. Monitoring: appropriate site & size (considering actual or potential vessel obstruction) Assistant: skilled, briefed Drugs: Sedation for lines & regional LA +/- adjunct for regional Induction agents with minimal or favourable effects on haemodynamics if IV induction (eg. Ketamine, may consider spont breathing volatile induction for anterior mediastinal mass) Preventive/opioid sparing analgesics (ketamine, paracetamol, parecoxib, dexamethasone) Adequate volume to maintain CVP & arterial BP Vasoactive infusions Equipment: for CVC, art line (bilateral if risk vascular occlusion in an upper extremity, LL if risk of vascular occlusion both ULs), warming, airway equipment choice depends on the mass, eg: consider awake or asleep (eg spont breathing) bronchoscopy, reinforced ETT, longer microlaryngoscopy tube if distal trachea compressed, DLT if lung isolation needed, ensure rigid bronchoscopy available if loss of airway patency is possible. TOE if ant mediastinal mass compressing heart or major vessels or is attached to myocardium or pericardium (provided no contraindication eg. Mass impacting oesophagus, Hx UGI bleeding or other severe oesophageal or gastric disorder). Induction: Surgeon present- if loss of airway patency during induction & unable to advance flexible bronch or ETT, surgeon could use rigid bronchoscopy w JV. other emergency alternatives are repositioning the pt (if a "position of safety" identified pre-op) Plan depends on (for anterior mediastinal masses): -risk of airway & respiratory compromise (obstructive or restrictive)- "don't burn your bridges" if airway safety uncertain if "unsafe” (ie. severely symptomatic, CT tracheal/bronchial diameter <50% of normal irrespective of symptoms), options may be awake LA biopsy if diagnostic. loss of the awake pts compensatory mechanisms, relaxation of bronchial smooth muscle & reduced lung volumes, effect of NMBAs (loss of diaphragm caudal movement) all reduce the normal -ve transpleural pressure gradient that usually holds airways patent; transition from spont vent to controlled PPV also a time of risk (spont breathing induction technique, may maintain spont breathing after intubation if pt becomes haemodynamically unstable since it avoids the reduction in preload with PPV). step-by-step induction w careful monitoring. only give muscle relaxant once know PPV will be possible (ie gently bag manually first). -risk of cardiovascular collapse Pre-O2 in the pts preferred position which has least symptoms (may be upright or lat decubitus) Consider AFOI with spont breathing eg. If vocal cord oedema or other symptoms due to SVC syndrome Maintenance: Continuously monitor airway patency, oxygenation & ventilation- communicate with surgeon Emergence: Consider a final bronchoscopy/suction after adherent mass removed, during the transition from PPV to spont NPV- if a DLT was used, this may not be possible until after extubation (extubate deep, place a SGA & examine with flexi bronch) Smooth, coughless particularly if significant tracheomalacia or tracheobronchial tree disruption since coughing incr airway pressure & risk compromising any anastomoses or cause bleeding/airway leak, eg. Remi 0.1-0.3mcg/kg/min, lignocaine 1mg/kg. Postop: Disposition HDU, MAY be intubated if pt or surgical factors prohibiting extubation- if DLT, replace it with a SLT using a tube exchanger prior to ICU. If extubated in recovery, mindful of complications postop (airway compromise (oedema, nerve damage, tracheobronchial obstruction), haemorrhage); keep rigid bronch, diff airway trolley & surgeons on hand until know recovered

Answer 123

often ASA2, young with hyperhidrosis, also can be done on multicomorbid pt w refractory angina GA with or without DLT (surgeons will often use CO2 to have some long collapse to access the sympathetic chain; cauterise or ligate or LA). Large IVC, only needs IAL if significant co-morbidities (and beachchair type position with arms up so care with position & MAP to defend cerebral perfusion. Uni or biportal. intercostal block by surgeons, often a day procedure, use multimodal analgesia. Minimal postop pain (multimodal), postop may have PTx or compensatory hyperhidrosis below level of correction.

Answer 124

high (normal) FEV1 supine OLV L)-sided OLV (smaller left lung) low pO2 prior to OLV

Answer 125

divided by line from sternal angle to inf border T4 inferior mediastinum ant/middle/post by heart & pericardium.

Answer 126

ELS is a proximal myopathy ass'd w small cell carcinoma. reductions in ACh from presynaptic motor n terminals. incr sensitivity to ALL NMBAs. muscle weakness improves w exercise, no improvement w acetyl cholinesterase inhibitor.

Answer 127

<20% if not compromised

Answer 128

Pneumothorax: Primary- no known underlying disease, generally bullae Secondary- underlying condition eg. COPD, asthma, CF, marfans, ARDS, pneumonia, trauma Iatrogenic- Pneumoperitoneum, thoracoscopy, PPV, CVC, nerve blocks, surgery lower neck Awake spot breathing pts pleuritic chest pain & dyspnoea. If underlying lung disease, severe dyspnoea & sig hypoxaemia. ABGs: incr A-a gradient, acute Resp alkalosis. In critical illness, deterioration in rep & CV variables, physical exam. XR/US; small (<15%) often normal physical findings aside from mild tachycardia (the commonest finding) larger: dear chest expansion, hyper resonant percussion, tracheal shift, decreased or absent breath sounds on affected side. Tension: systemic hypotension, central cyanosis. Ventilator shows decreased TVs & compliance. High CVP. Late= distended neck veins, displaced apex beat. Upright XR: radiolucent thoracic air w absent lung markings btwn shrunken lung & parietal pleura. PA XR is poor method of quantifying size of PTx, usually underestimates it. supine XR: deep sulcus sign, Lucent upper quadrants of abdomen, sharp superior surface of duaphragm. Chronic lung conditions w pleural adhesions may restrict lung collapse. Tension: mediastinal shift US sens 95% & spec 100% cf CT as standard. CT indicated to differentiate PTx from bullies disease, to Dx supine PTx, if XR obscured by emphysema. Allow Dx of other pleural/lung pathologies. It’s the gold standard for PTx imaging but impractical/unsafe in critically ill, impractical for repeated imaging. Management: Small primary spont PTx in spont breathing asymptomatic pts: conservative, adding high FiO2 may speed resolution by reducing partial pressure nitrogen in pulmonary capillaries. Incr partial pressure for reabsorption air pleural cavity—> pulmonary capillaries, rate is 1.5% of the volume of the hemithorax/24hrs. Must treat symptomatic pts, those needing PPV or altitude (reduction in Bar may expand a PTx). Avoid N2O (expands a PTx). Symptomatic or >3cm or all but the tiniest (<1cm or apical) secondary PTx: Small bore chest drain (large-ore if blood). In “safe space” mid axillary line; away from internal mammary, scarring breast tissue, distant to viscera. Keep in until bubbling ceased & CXR shows lung inflation. If non-resolving or after chemical pleurodesis, high-vol/low-pressure suction (with underwater seal, 10-20cmH2O). If symptoms persist after 10 days, consider foreign body/tumour/mucus plug, CTS R/V for VATs. Tension: immediate decompression, 14g IVC 2nd ICS MCL, keep in until bubbling on formal UWSD. Intraop considerations: airway plan (DLT/BB) for VATs is chest draining adequtely (bubble, swing) surgeons present as backup (ready for 2nd ICC) spont breathing TIVA/volatile or AFOI to maintain -ve PiP until isolated, vs RSI bype with gentle intro of PPV considerations re: plan/target SpO2 for OLV (reasons desat gen inadequate FiO2, alv hypoven, large shung) pressure areas fluids Inot excessive), ABx, vasopressors LPV noromotheria & Hb (DO2) & metabolics

Answer 129

Highest postop mort of all pulm resections, only consider once all surg options excluded 40% get pulm HTN within 1 yr- important to know R) heart function (RV failure unsuitable for pneumonectomy) 20% resp comp, 10% cardiac complications peak ischaemia 72hrs postop Complications due to shunting of whole pulm circ, compromosed gas exchange Preop Ax: -often Ca, M's -Pulm parenchymal function (gas exchange: national emphysema trial ppoDLCO<20% cancel, >40% no probs, 20-40% greyzone open surgery, traditional ABG cutoffs PaO2<60, PaCO2>45) -Lung mechanical function: FEV1 >2L pneumonectomy >1.5 lobectomy vent esp FEV1; ppoFEV1 >40%--> OT *all pts need PFTs; for those where need to distinguish borderline & contribution of lung to be resected, schntigraphy considerd Cardiopulmonary reserve: SO, if FEV1 was <2L (pneumo) or <1.5 (lob), and if ppoFEV1 or ppoDLCO were <40, exercise testing. VO2 max >15mL/kg/min--> OT <15mL/kg/min, consider other options all pts having pneumonectomy need TTE Functional capacity, why liited, consider the implications (eg. COPD or m weakness less likely to improve vs obstructing lesion) Shuttle walk: 400m correlates w peak O2 consumption >15mL/kg/min consider if pt able to tolerate the OT if it proceeds & were advanced to a bigger OT, if can withstand the recovery/postop; generally age >70 & pulm HTN unsuitable (esp R) pneumonectomy, pulm HTN a relative CI Optimisable factors: ?prehab manage any infection/secretions bronchodilators smoking cessation diuretics if +ve fluid balance (high mort if pulm oedema during Tx surgery) Hb/Fe Plan: discussion multiD re suitability consent ICU bed Xmatch 2U red cells (ensure G&H) Intra-op: Analgesia: painful, posterolat thoracotomy 5th ICS may excise 5th rib, will have thoracostomy tube postop or VATs MMA (incl ketamine), PVB VATs, consider TEA open (but similar pain efficacy, no diff sig comp/LoS/mortality), consider SNS effects of neuraxial Choice of airway, lung isolation technique (if BB, withdraw before stapling) Ventilation strategy: 4-6mL/kg, max peep 8-10) Circulation: careful communication esp when clamp R) or L) main pulm artery to anticipate this & ensure stable CO (entire circulation diverted to one lung, pressure for heart esp if R) lung) FLUIDS: high mortality if intra-op pulm oedema; balance between restrictiive to limit pulmonary but need adequate perfusion for heart/kidneys; no >2mL/kg/hr for first 24hrs OR prev hours UO + 20mL, UO 0.5mL/kg/hr acceptable, but dynamic Ax normothermia: hypothermia impairs HPV Monitoring: IABP, CVC (may need vasopressors) IDC & temp probe TIVA useful as rigid bronch at start of case Position lateral w table break, pressure areas VTE prophylaxis Normothermia Postop: awake, warm & comfortable adequate analgesia for cough, mobility ongoing invasive monitoring (ICU) APS complication surveillance: haemorrhage, pulm odema (>50% mort, more common oafter R) pneumo), bronchopleural fistula (also more common R) pneumo), airway plugging, cardiac arrhythmias- up to 40% get AF cardiac herniation, mort >50% dedicated thoracic ward after step down from ICU incentive spirometry, physiotherapy *drain care- clamped only check 1 in evry hour for haemorrhage, risk mediastinal shift.

Thoracics Flashcards

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