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LUNG MECHANICS Airways Resistance
Measurement at 30 l/min a. b. c. d. e. awake paralysed partially paralysed + ETT PEFR FEV1 males females ~ 0.6-3.2 ~ 6.0 ~ 10-15 cmH2O/l/s cmH2O/l/s cmH2O/l/s (AB says 5-10 cmH2O/l/s)
~ 450-700 l/min ~ 300-500 l/min ~ 50-70 ≥ 70% ml/kg of FVC
Factors a. b. c. d. airway narrowing lung volume posture neural factors i. constriction - oedema, congestion - inflammation, FB, etc. - expiration > inspiration - closing volume - supine FRC ≤CC - smoke, dust, chemicals - hypoxia, hypercarbia, hypothermia - pulmonary emboli - ↑ PNS activity - systemic hypertension - inspiration - ↑ SNS activity - catechols, histamine, PG's, leukotrienes - histamine, methacholine - alveolar hypocarbia - ACh-esterase inhibitors - anaphylactoid reactions - catechols (β2-agonists) - PDE inhibitors, aminophylline - anticholinergics - steroids - volatile anaesthetic agents - nitric oxide
e. f.
hormonal factors drugs i. constriction
ICU Respiratory
Anatomical Site a. b. c. nasal passages larynx large airways ~ 50% ~ 25% ~ 15%
NB: airways resistance is maximal at segmental bronchioles, → ≥ 5th generation / ≤2mm
Lung Compliance
Def'n: the change in lung volume per unit change in transpulmonary pressure
Posture Upright Supine GA & NMB'd Lung 200 150 100-150 75 * all values in ml/cmH2O 80 Respiratory 100 Lung 180
Respiratory 100 55
Factors Affecting Static Lung Compliance 1. ↑ FRC → ↑ CL i. age ii. body size iii. posture *see below factors affecting FRC ↓ lung volume → ↓ CL i. lobar, lung resection ii. collapse or consolidation iii. diffuse atelectasis changes in lung elasticity i. ↑ lung elasticity ii. ↓ lung elasticity - emphysema - pulmonary oedema, congestion, fibrosis
ICU - Respiratory
Nunn: 1. 2. 3. 4. 5. 6. 7. Lung Compliance lung volume posture pulmonary blood volume age restriction of chest expansion recent ventilatory history pulmonary disease ? this is chest wall C, not lung * monotonous ventilation - absolute and relative
Factors Affecting Dynamic Lung Compliance 1. 2. 3. 4. airways resistance respiratory rate peak flow rate & inspiratory time for ventilated patients autoPEEP
actually should refer to time constant, τ = R x C the concept of dynamic compliance is flawed, as it is resistance & flow rate dependent resistance includes in its definition the time frame (cmH2O/l/s), compliance does not ergo, compliance should be time independent, but dynamic compliance is not Factors Affecting Chest Wall Compliance 1. 2. muscle tone and phase of respiration diaphragmatic movement i. neural input ii. muscle performance, fatigue iii. abdominal hypertension - pregnancy, ascites, obesity chest wall diseases i. spine & costo-vertebral joints ii. obesity iii. pleural disease, space occupying lesion iv. skin & overlying tissues
ICU Respiratory
Factors Affecting FRC 1. 2. 3. 4. body size sex age - FRC - females ∝ height ~ 90% of male FRC (~ 32-51 ml/inch) (≡ height)
- Nunn → no correlation ! - others have shown small increase
diaphragmatic muscle tone originally, FRC believed to represent equilibrium for lung/chest wall system diaphragmatic tone maintains FRC ~ 400 ml above true relaxed state → ↓ FRC with anaesthesia / ventilation ↓ FRC in the supine position ~ 0.5-1.0 l → → → → → → ↓ FRC ↓ FRC ↑ FRC ↑ FRC ↓ FRC ↓ FRC
5. 6.
lung disease consolidation, collapse, atelectasis ↑ blood volume, alveolar oedema loss of lung ER with emphysema increased expiratory resistance chest wall increased abdominal contents pleural space occupying lesion alveolar-ambient pressure gradient PEEP increases the FRC
ICU - Respiratory
Closing Volume
Def'n: lung volume in which closure of dependent airways begins, or more precisely, lung volume in which dependent lung units cease to contribute to expired gas, ie., the beginning of phase IV of the washout curve to RV normal values ~ 15-20% of VC, ie. a part of the VC manoeuvre ~ 10% of the FRC in a young adult ~ 40% of FRC at 40 years of age this is distinct from closing capacity, which is the difference between the onset of phase IV and zero lung volume = CV + RV, expressed at a % of TLC measured by either a bolus or resident gas technique, 1. bolus technique originally xenon or argon, usually now helium inspiration from RV to TLC creating differential tracer gas composition apical areas contain most of the gas cf. bases resident gas technique also dependent upon a pre-expiration concentration gradient, but i. N2 already present, and ii. normally little difference in [N2] between apex & base at TLC therefore, inspiration of O2 is used to dilute the already present N2 this results in an apical to base concentration difference of ~ 2x may result in smaller values cf. bolus technique in the presence of asthma or bronchoconstriction, probably due to air trapping (??) single breath (100% O2) nitrogen washout 4 phases I II III IV dead space transitional zone alveolar plateau (~ 1.5% rise) closing volume →
as CV represents a portion of the VC manoeuvre, it is usually expressed as a percentage of such expiration must be performed slowly to prevent dynamic airways collapse ~ 0.5 l/sec changes in CV may represent small airways disease, or loss of elastic recoil and parenchymal supportive tissue loss of elastic recoil results in the gradual increase in CV with age, such that at 65 yrs CC > FRC young children similarly have decreased elastic recoil & relatively increased CC's minimal values for CV/CC are seen in late the late second decade sensitive marker of early dysfunction, but difficulty defining normal limits NB: closing capacity ~ FRC in the supine position at 6 & 44 years
ICU Respiratory
Factors CV is increased by, 1. 2. 3. age smoking lung disease
tidal volume encroaches upon CV in, 1. 2. 3. children < 6 years of age adults progressively over the age of 45 where FRC is decreased - obesity - pregnancy - postoperatively - paralysed/ventilated without PEEP - ascites
most lung diseases
ICU - Respiratory
Pulmonary Dead Space
Def'n: Anatomical: that fraction of the inspired gas volume which, is contained in the conducting airways, is ineffective in arterialising mixed venous blood, and is exhaled unchanged at the beginning of expiration Alveolar: that fraction of the inspired gas volume which, enters the alveoli, but is ineffective in arterialising mixed venous blood alveolar + anatomical dead space
Factors Affecting Anatomical Dead Space 1. 2. 3. 4. 5. 6. 7. 8. body size age lung volume posture drugs lung disease IPPV flow pattern - high flows and turbulence increase VD - bronchodilators / bronchoconstrictors - anaesthetic agents - emphysema, asthma, CAL
Additional Factors Affecting Alveolar Dead Space 1. 2. 3. 4. 5. 6. 7. blood volume pulmonary artery pressure lung disease IPPV including waveform and PEEP anaesthesia respiratory rate and minute volume oxygen - rise in PAO2 vasodilatation & increased VD
ICU Respiratory
Bohr Equation (1891)
originally used to measure F ACO2 , using estimates of V DAnat from autopsy cast specimens not used to estimate V DAnat until the constancy of alveolar air was established by Haldane and Priestly (1905) following this, 1. 2. FACO2 is estimated from ETCO 2 with a rapid gas analyser the mean expired concentration from a Douglas bag
this estimated anatomical V D as ETCO2 estimates mean, not "ideal" alveolar CO2 subsequently modified by Enghoff to estimate total, or physiological VD, viz. Enghoff Modification (1938)
P aCO 2 − P ECO P aCO 2
Ventilation/Perfusion Relationships
Perfusion Physiological
Causes of Non-Uniformity Ventilation airway closure (FRC < CC) V vs. Q mismatch posture exaggeration of above regional compliance differences regional airway resistance change collapse, consolidation mucosal oedema, plugging diffusion block
gravity PA pressures posture exercise hypovolaemia hypervolaemia, LVF embolism regional ↑ PVR PEEP drugs
ICU - Respiratory
CXR lung scan spiral CT + contrast pulmonary angiography Xe133 washout calculation of VD/VT Pa-ETCO2 difference
Assessment Ventilation
clinical assessment CXR single breath N2 test N2 washout Xe133 venous admixture PA-aO2 difference pulmonary function tests
The Shunt Equation
Cc Cc
− C aO 2 − C vO 2
Alveolar-Arterial Oxygen Tension Gradient
Def'n: normal PA-aO2 ≤20 mmHg where the PAO2 is given by the alveolar air equation, simplest form,
P AO 2 = P iO 2 −
rearranging the shunt equation, QS/QT CaO2 = also, CaO2 ~ =
P aCO 2 R
(CcO2 - CaO2) / (CcO2 - CmvO2)
CcO2 - (Ca-mvO2 x QS / [QT - QS]) ([Hb] x 1.34 x SaO2) + (0.003 x PaO2)
ICU Respiratory
therefore, the PA-aO2 is dependent upon, 1. 2. 3. 4. 5. 6.
O2 and PAO2
- hyperbolic relationship - inverse relationship - linear relationship - linear relationship
mixed venous PmvO2 cardiac output DO2 & VO2 pulmonary shunt
minor factors i. [Hb] & position of dissociation curve ii. respiratory quotient iii. hypovolaemia
Pulmonary Gas Exchange
O2 diffusion is dependent upon, a. b. c. d. e. f. g. FIO2 alveolar ventilation effective alveolar/capillary exchange area effective diffusion distance pulmonary capillary blood flow mixed venous Hb saturation position of Hb-O 2 dissociation curve
normal Hb "fully" saturated in 0.3 sec, with a normal transit time of 0.75 s factors affecting diffusing capacity, a. b. c. d. increased diffusion path length decreased area posture exercise - definition of emphysematous lung disease - increased in supine position
ICU - Respiratory
CO2 Transport
Content a. b. c. arterial mixed venous ~ 49 ~ 53 ml/100ml ml/100ml ml/100ml ml/100ml ml/100ml ml/100ml ml/100ml ml/100ml 65% 35% 65% 26% 8% < 1%
added to capillary blood ~ 3.75 by where, i. plasma ~ 2.35 ii. rbc ~ 1.4 by form, i. CO2 as HCO3~ 2.43 ii. carbamino Hb ~ 1.0 iii. dissolved CO2 ~ 0.3 iv. carbamino plasma protein
Haldane Effect Def'n: the shift of the Hb-CO2 dissociation curve with variations in the SaO2 effectively reduces the rise in PaCO2 in venous blood, thereby limiting the fall in mixed venous pH
Arterial PCO2 CCO2 pH PO2 SO2
40 mmHg 49 ml/100ml 22 mmol/l 7.4 100 mmHg 97.5%
Mixed Venous
46 mmHg 53 ml/100ml 24 mmol/l 7.37 40 mmHg 74 %
ICU Respiratory
Effects of Hypocapnia 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. ↑ TPR cerebral vasoconstriction placental vasoconstriction ↓ cardiac output ↓ ICP ↑ pain threshold hypoventilation respiratory alkalosis left shift of the HbO 2 dissociation curve hypokalaemia → ICF shift ↓ HCO3- reabsorption by the kidney ↓ plasma ionized Ca++ → tetany
Effects of Hypercapnia 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. cerebral vasodilatation ↑ ICP ↑ CNS sympathetic outflow ↑ cardiac output & BP cardiac arrhythmias hyperventilation respiratory acidosis right shift of the HbO 2 dissociation curve hyperkalaemia ↑ HCO3- reabsorption by the kidney - indirect effect direct depressant effect upon the CVS
ICU - Respiratory
Feedback Mechanism 1. 2. 3. sensory mechanisms central integration effector systems - central / peripheral
Brainstem Influences a. b. c. d. carotid and aortic chemoreceptors - PaO2 / PaCO2 / pH central CSA cerebral blood flow lung reflexes i. Hering-Breuer reflex - inhibito-inspiratory reflex ii. paradoxical reflex of Head - inspiratory triggering iii. chest wall/parenchymal reflexes muscle spindles carotid and aortic baroreceptors thoracic chemoreceptors peripheral receptors - pain - temperature - mechanoreceptors - emotion - voluntary control - speech - SNS - olfactory sense - speech - progesterone - almitrine, ? aminophylline - respiratory muscles - not diaphragm - PaCO2 - CSF pH
e. f. g. h.
cerebral cortex
reticular activating system
k. l.
hormones drugs
ICU Respiratory
Peripheral Chemoreceptor Stimulation a. b. c. d. e. ischaemia hypoxia increase PaCO2 decrease in pH drugs - rectangular hyperbola - inflexion at ~ 60 mmHg & maximal ↑ VM ~ 32 mmHg ~ 10 mmHg ~ 0.1-0.2 - cyanide, nicotine - lobeline, doxapram - anaemia - carbon monoxide - methaemoglobinaemia - Effects - Factors
NB: not by
*ie. responds to P aO2 not CaO2
Chemoreceptor Stimulation a. b. c. d. e. ↑ VT, frequency & VM bradycardia tachycardia hypertension bronchoconstriction
- carotid body - aortic body - systemic & pulmonary vasoconstriction
Effects of Apnoea NB: PaCO2 → → → initial rise ~ 6 mmHg in first minute → subsequent rise ~ 1-3 mmHg/min falls dependent upon FIO2, FRC and VO2 lung "washin"
body stores of O 2 are small, being ~ 1550 ml on air, which corresponds to only 6 mins consumption at a basal VO2 thus, with changes in V A the P aO2 rapidly assumes its new value, the half time of change being only 30s in contrast the body stores of CO 2 are large, being ~ 120 l, or 600 mins of the basal output the time course of change for P aCO2 is slower for a reduction of V A than for an increase the half time of rise for P aCO2 ~ 16 mins thus, during the acute phase of hypoventilation, the P aO2 may be low while the PaCO2 is still within the normal range NB: ∴ during acute hypoventilation, the respiratory exchange ratio may fall far below the respiratory quotient, which it equals at steady state, as CO2 production is partly diverted to the body stores
ICU - Respiratory
CO2 & Ventilation
NB: ↑ VM ~ 2.0 l/min/mmHg ∝ ↑ PaCO2 CSA
the predominant effects are upon the central chemosensitive area large interpatient variation in slope of the VM/PaCO2 line Factors Shifting the VM-CO2 Curve Left hypoxia acidosis hyperthermia catecholamine release Right
sleep ↑ work of breathing ↑ resistance ↓ compliance drugs - narcotics - barbiturates, etc.
Isobaric a. fixed performance high flow low flow variable performance small capacity large capacity
- venturi masks - anaesthetic machine - nasal specs, Hudson - O2 tent, cribs
Device Nasal Canulae1 Hudson Mask
FGF (l/min) 2-6 4 6 8 10 12 7-10 3-8 4-8
O2 Tent Incubator Head Hood
increase F IO2 ~ 4% / litre flow of O2 up to 44%
ICU Respiratory
Venturi delivered FIO2 is estimated as follows, 1. 2. 3. 6-8 l/min FGF 8 l/min O2 10 l/min O2 + entrainment gas + 21% of (40-8) l/min + 21% of (60-10) l/min ~ 40-60 l/min total flow ~ 30% F IO2 ~ 35% F IO2
the actual delivered FIO2 is determined by, 1. 2. 3. 4. 5. O2% of FGF and variability of flow maximal FGF entrainment ratio size of O2 reservoir patient peak inspiratory flow rate and minute ventilation
MW BP H2O solubility 37°C1 H2O solubility 0°C Critical temperature Critical pressure Liquid:gas volume ratio Specific gravity (gas) Cylinders 32 -182.5°C 2.4 vol% 4.9 vol% -118.4°C 50.14 atm. 1:840 1105 (air = 1000) pressure vol. at STP colour code 132 atm. 682 l C black/white
Ostwald solubility coefficient for O2 in blood at 37°C = 0.0034 ml/100ml blood/mmHg
∴ at 760 mmHg = 2.58 ml / 100 ml
Methods of Preparation 1. 2. 3. fractional distillation of air by pressure / cooling electrolysis of H2O Brin process using BaO2
ICU - Respiratory
Oxygen Toxicity
1. hyperoxic syndromes i. optic - neonatal retrolental fibroplasia ii. neural - hyperbaric O2 seizures iii. pulmonary - tracheobronchitis, ARDS ? bronchopulmonary dysplasia normoxic syndromes presence of factors enhancing formation of free radicals at normal O2 tension i. excessive phagocytic activity ii. reperfusion following ischaemia iii. drugs / toxins - paraquat, bleomycin
Mechanisms a. b. c. d. e. free oxygen radicals oxidation of glutathione lipid peroxidation glycolytic GPDH inhibition altered glutamate & GABA metabolism
species generated, a. b. c. superoxide hydrogen peroxide hydroxyl radical O2•
superoxide dismutase → catalase → catalase, or glutathione peroxidase →
hydrogen peroxide water water
factors influencing O2 toxicity, a. increased tolerance with increased levels of, i. SOD ii. catalase iii. glutathione peroxidase pulmonary levels are increased with endotoxin may reduce O2 lung injury in sepsis decreased tolerance with, i. nutritional deficiency ii. hyperthyroidism iii. hypercortisolism iv. drugs / toxins - vit. E, C, selenium, glutathione & SH-compounds
ICU Respiratory
Pulmonary Oxygen Toxicity first described by J.L. Smith in 1899 difficult to distinguish from the effects of hypoxia in critically ill patients CXR changes are non-pathognomonic inspired oxygen tension is more important than F I O2 tracheobronchitis & ↓ VC may occur after 12-24 hours breathing 100% O 2 at 1 Atm. the pulmonary endothelial cell is most sensitive, progressing to → type I alveolar cells showing damage at ≥ 48 hrs
there is considerable patient variation an absolute "safe level" of O2 has not been established, but ≤50% tolerated for prolonged periods two phases, 1. acute exudative phase endothelial oedema, capillary damage & haemorrhage cellular infiltrate reduced compliance & VC ? type I alveolar damage late proliferative type II alveolar proliferation with type I cell destruction leukocyte infiltrate, interstitial fibrosis and septal thickening
pulmonary oxygen toxicity is hastened by, 1. 2. 3. 4. 5. higher FIO2 inhalation of CO2 radiation paraquat, bleomycin chemotherapy
pulmonary oxygen toxicity is delayed by, 1. 2. brief intermittent exposure to F IO2 = 21% a high PA-aO2 gradient
secondary cardiovascular changes, 1. 2. ↑ SVR & PVR ↓ cardiac output
ICU - Respiratory
Pulmonary Changes in Early Oxygen Toxicity 1. 2. 3. 4. 5. ↓ VC ↓ FRC ↓ compliance ↓ CO-diffusing capacity ↑ respiratory rate *most useful
the following factors are not altered in early oxygen toxicity, 1. 2. 3. RV airways resistance PA-aO2 gradient
Complications 1. chemical toxicity - tracheobronchial tree, alveolar & endothelial cells - pulmonary damage, atelectasis - hypoxia, acidosis
2. 3. 4. 5. 6. 7. 8.
retinal damage erythrocytic damage, haemolysis hepatic effects myocardial damage endocrine effects renal damage CNS enzyme / cell toxicity - twitching, convulsions, cell necrosis
Organ Systems Susceptible to Oxygen Damage a. b. c. d. e. f. g. h. i. blood-brain barrier, cognition, neuromuscular function glomerular function endocrine function, reproduction vision, auditory-vestibular function hepatic function respiratory function myocardial function haemopoietic function temperature regulation
ICU Respiratory
Oxygen Limits in Normal Man 1. 2. 3. FIO2 ≤55% 1 Atm. / 24 hours ≥ 2 Atm. / 24 hours - safe for indefinite periods ~ 10% fall in VC - CNS toxicity
Other Factors: a.
Animal Studies
factors hastening toxicity i. corticosteroids, ACTH ii. CO2 iii. convulsions iv. drugs - paraquat - dextroamphetamine - adrenaline, noradrenaline, insulin v. hyperthermia vi. thyroid hormones vii. vitamin E deficiency factors delaying toxicity i. acclimitization to hypoxia ii. adrenergic blocking agents, ganglionic blocking agents, reserpine iii. antioxidants iv. general anaesthesia v. chlorpromazine vi. GABA, glutathione vii. hypothermia, hypothyroidism viii. starvation ix. vitamin E x. immaturity
ICU - Respiratory
Oxygen Cost of Breathing
Def'n: normal ~ 0.5-1.0 ~ 2-4 ml.O2 / litre of ventilation ml.O2 / min
this is increased by, 1. 2. 3. 4. exercise asthma, CAL cardiac failure obesity
NB: lung disease (↓ compliance / ↑ resistance) increases both the baseline O2 consumption and the slope of the graph
SIMV Work of Breathing demand flow SIMV systems factors in this increase are, a. b. c. d. e. f. g. h. work during IMV triggering of the demand valve circuit/ETT resistance isometric contraction prior to reduction of airway pressure auto-PEEP inefficient action of the diaphragm with hyperinflation states low compliance disease states of the lung insufficient peak flow rates during inspiration → ↑ VO2 ~ 6-46% (mean ~ 16%)
ICU Respiratory
Hyperbaric Oxygen
Clinical Uses a. b. c. d. decompression sickness gas gangrene other severe anaerobic infections severe carbon monoxide poisoning i. COHb > 40% ii. associated cardiorespiratory limitation cerebral air embolism research with DXRT as cancer chemotherapy surgery - to prolong cardiac arrest time - superseded by hypothermia *not really hyperbaric O2
e. f. g. h.
Dissolved Plasma Oxygen sea level sea level 2 atm. 3 atm. 21 % 100 % 100 % 100 % ~ 0.3 ~ 2.1 ~ 4.2 ~ 6.3 ml ml ml ml (~ total VO2)
αO2 ~ 0.003 ml / 100ml / mmHg Other Effects a. hypercarbia PvO2 ≥ 50 mmHg → ↓ buffering capacity → ↑ work of breathing pulmonary vasodilatation systemic vasoconstriction cerebral vasoconstriction ↓ HR ↓ cardiac output - reflex baroreceptor ? reflex / direct
~ no CO2 bound to Hb ↑ minute ventilation - ↑ gas density
Haldane effect
b. c. d. e. f. g. h.
left shift of HbO2 dissociation curve - ↑ Qs/Qt ∝ loss of HPV - ↑ diastolic BP
ICU - Respiratory
Other Effects 100% O2 a. absorption atelectasis - lung - middle ear - pneumothorax
b. c. d. e.
↑ PA-aO2 gradient reduces the effect of low V/Q areas but increased shunt fraction ↑ O2 stores, apnoea time O2 toxicity ~ FRC/VO 2
Hazards a. b. c. d. e. f. g. h. fire, explosion pulmonary O 2 toxicity cerebral O2 toxicity barotrauma - convulsions, coma - middle ear - lung avascular bone necrosis head of femur
"bends" if removed rapidly retrolental fibroplasia CO2 narcosis - CAL - high altitude dwellers * loss of hypoxic drive
HYPOXIA Cause
low FIO2 hypoventilation V/Q mismatch low DO2 R→ L shunt
low high normal normal normal
δ A-aO2 P
low normal high high very high
δ aO2 100% P
large increase large increase large increase increase small increase
ICU Respiratory
Complications 1. 2. bulk, complexity condensation "rain-out", drowning ↑ resistance scalding circuit valve malfunction decrement in filter function over-spill of water bacterial contamination high compliance high resistance overheating electrocution disconnection sites - scalding - pulmonary oedema
3. 4. 5. 6. 7. 8. 9.
Consequences of Dry Gases 1. 2. heat loss ≤1-3°C/hr
water loss impaired mucociliary escalator mucociliary damage mucosal desquamation, ulceration drying of secretions, sputum retention altered lung mechanics ↓ FRC ↓ compliance ↑ shunt fraction ↓ PaO2 bronchoconstriction increased incidence of respiratory infections
ICU - Respiratory
Heat & Moisture Exchangers
Advantages a. b. c. d. cheap, simple, lightweight, silent, reliable disposable, no energy source bacterial filtration, low dead space & resistance useful for, i. children and adults ii. transport, retrievals iii. tracheostomy, spontaneous ventilation via ETT
Disadvantages a. b. c. d. inefficient with high minute volumes & gas flows inefficient after 1-2 hours airways resistance / dead space significant for small children potential for disconnection or obstruction
ICU Respiratory
CVS Response a. b. c. d. e. hypertension tachycardia arrhythmias ↑ ICP ↓ uterine blood flow - up to 100% - ↑ MAP ~ 20-40 mmHg * may have up to 60% ↑ MAP - ↑ HR ~ 50%
NB: potential for, i. ii. iii. iv. v. myocardial ischaemia / infarction LVF intracranial hypertension / haemorrhage foetal hypoxia eclampsia
methods for minimising CVS changes, a. b. rapid laryngoscopy avoid vasoconstrictors ≤45 secs - ketamine - cocaine - adrenaline, POR8
c. d. e. f. g. h. i.
adjuvant dose of STP deep volatile anaesthesia fentanyl lignocaine nitroprusside hydrallazine ~ 5-10 µg/kg ~ 1.5-3.0 mg/kg ~ 0.5 µg/kg ~ 5-10 mg 15 mins 20 mins 30 secs - phentolamine 1-5 mg - propranolol 1-4 mg - esmolol 2-4 mg bolus or infusion - 0.7 mg/kg bolus - then 0.1-0.4 mg/kg over 10 mins 5-7 min pre-ETT 2-3 min pre-ETT 30 secs pre-ETT 5-10 min pre-ETT
GTN i. paste 5cm (30 mg) ii. infusion 0.1% iii. IV bolus 50-250 µg α / β-blockade
ICU - Respiratory
Indications 1. 2. 3. 4. 5. upper airway obstruction airway protection - gastrointestinal contents - blood or secretions
application of mechanical ventilation inability to clear secretions to enable specific therapy i. induced hypocapnia ii. high F IO2 / PEEP iii. pulmonary toilet / lavage iv. BAL
Complications a. immediate i. laryngoscopy
ii. iii.
ETT cuff
- trauma - aspiration - autonomic reflexes - misplacement - obstruction / kinking / disconnection - herniation - overinflation - perforation, leakage
short-term (hours-days) i. obstruction - endobronchial misplacement - obstruction / kinking - overinflation, herniation ii. dislodgement / disconnection iii. colonization - sinusitis, tracheitis - nosocomial pneumonia iv. dry gases - dehydration - hypothermia - thickened secretions, inspissation long term (days-weeks) i. laryngeal trauma ii. tracheal trauma iii. infections - sinusitis, otitis - tracheitis, nosocomial pneumonia - microaspiration, lung abscess - septicaemia
ICU Respiratory
Difficult Intubation
Physiological a. b. c. d. e. f. g. h. i. j. k. short muscular neck receding mandible prominent upper teeth narrow mouth with high arched palate limited jaw opening large breasts anterior larynx effective mandibular length - thyromental distance receding lower jaw / maxillary protrusion short occipito-atlantis distance short C1-C3 distance
Pathological a. TM joint disease - RA - trismus - fracture - trauma, fracture - spondylitis - RA - tumours - oedema - abscess, cysts - burns, scars - tumours - mandibular, facial bones - cervical spine - larynx - airway bleeding - craniofacial disorders - macroglossia, Down's - encephalocele - cleft palate - obesity - acromegaly - goitre
limited cervical extension
oropharyngeal masses
d. e.
contractures of face/neck trauma
ICU - Respiratory
Assessment of Airway
1. history i. letters etc. re previous difficult intubation ii. previous anaesthetic records examination i. →
thyromental distance > 6 cm, or > 3 "finger-breadths" alveolar-mental distance < 2 cm "receeding", length subluxation obtuse mandibular angles
ii. iii. iv.
incisor gap > 4 cm - as per Samsoon & Young
Mallampati grades I-IV
prominent upper incisors, "buck" teeth solitary incisors, "nuisance" teeth loose teeth crowns, caps, plates & dentures
Head & Neck
flexion, extension, lateral flexion & rotation tracheal position, neck masses, upper mediastinal masses
obesity Dowager's hump "no neck" craniofacial anomalies
investigations i. awake laryngoscopy - direct or indirect ii. fluoroscopy iii. XRays (Bellhouse) mediastinal masses & tracheal position / diameter effective mandibular length atlanto-occipital distance & C1-C2 interspace anterior-posterior thickness of the tongue iv. CT scan tracheal deviation, luminal diameter intrathoracic trachea, mediastinal masses
ICU Respiratory
claimed advantages of IMV over CMV, a. b. c. d. e. f. g. minimises respiratory alkalosis minimise sedative/relaxant requirements lower mean airway pressures more uniform gas distribution expedite weaning process reduce muscle atrophy & dis-coordination reduce cardiac decompensation with weaning
possible disadvantages, a. b. c. d. e. risk of hypercarbia, cf. with AMV increased work of breathing respiratory muscle fatigue prolonged ventilation if rate reduced too slowly cardiac decompensation in patients with compromised cardiac function →
Groeger (CCM, 1989), SIMV vs. assist control 1. 2. lower PIP improved - CO & MAP - DO2 - LVSWI
advantages of SIMV
less alkalosis
NB: SIMV was associated with a higher respiratory rate, despite similar minute volumes and oxygen consumption
ICU - Respiratory
IPPV and Muscle Relaxants
Short Term 1. masking of clinical signs i. level of consciousness ii. epilepsy, neurological change iii. acute abdomen, etc. inadequate analgesia and sedation impaired secretion clearance asphyxia from circuit malfunction - loss of cough reflex histamine release, anaphylaxis / anaphylactoid reactions
2. 3. 4. 5.
Long Term 1. muscle wasting & atrophy ↑ negative nitrogen balance difficulty in weaning ? myopathy associated with steroid use, especially in status asthmaticus ?? predisposition to CIP, but EMG changes are dissimilar DVT & pulmonary emboli pressure sores drug metabolite accumulation - laudanosine - M6G - need for prophylaxis/anticoagulation
2. 3. 4.
Advantages 1. 2. 3. tolerance of mechanical ventilation tolerance of hypercarbia avoidance of - breath stacking - high peak PAW ? theoretically may not matter - inadequate ventilation - improved oxygenation - reduced inspiratory time ? reduced barotrauma ? evidence for this - particularly PCIRV
4. 5.
reduction in VO2 in infants
6. 7. 8.
RX in patients with raised ICP less baro/volutrauma ? neurophysiological studies
ICU Respiratory
Special Indications a. infant respiratory distress syndrome, decreased pneumothorax rate no change in intraventricular haemorrhage rate no change in mortality cerebral disorders less rise in ICP with various stimuli no change in ICP rise with pain less sedation required therefore aiding CNS assessment less indication now propofol allows adequate sedation & periodic assessment recent article in ?J.Trauma showing ↑mortality in NMJ paralysis group for management of severe head injury tetanus severe acute asthma severe restrictive respiratory deficits, ARDS ? cardiogenic shock to reduce VO 2
c. d. e. f.
ICU - Respiratory
Adverse Effects
respiratory i. barotrauma
ii. iii.
iv. v. b.
alveolar overdistension surfactant loss / inactivation ↓ FRC and encroachment of CC on FRC ↑ lung water ∝ ? ↓ lymphatic drainage ? ↑ LAP disproportionate effect on PV & PA pressures → ↑ PPC ↑ V/Q mismatch - ↑ QS , VD & regional alkalosis - low flow areas & regional ischaemia frequently associated with potentially toxic FIO2
- alveolar rupture, PIE - pneumomediastinum / pneumothorax - hyaline casts, ? fibrosis
cardiovascular i. RV effects
LV effects
iii. iv. v. c.
dual effects
↓ venous return ↑ PVR & RV afterload ↑ RVEDV ↓ RV perfusion pressure ↓ LV afterload ↓ LVEDV * ventricular interdependence - global cardiac compression ? ↓ coronary blood flow (most studies → no change)
↓ VO2 ↓ inspiratory muscle blood flow
renal i. ↑ ADH / ↓ ANF secretion → ↓ urine output and Na+ excretion ii. redistribution of intrarenal blood flow iii. ↑ IVC & renal vein pressure CNS i. ↑ ICP unpredictable, but clinically insignificant at levels of PEEP ≤10 cmH2O ii. ↓ cerebral blood flow ∝ induced hypocapnia hormonal i. ↑ plasma adrenaline and noradrenaline ii. ↑ ADH / ↓ ANF iii. ↑ renin & aldosterone most of these effects are reversed with volume replacement
ICU Respiratory
Assessment of Respiratory Function During IPPV
1. clinical i. signs of hypoxia ii. signs of hypercarbia shunt fraction dead space lung volumes respiratory rate compliance
- tachycardia, hypertension, cyanosis - bounding pulse, tachycardia
2. 3. 4. 5. 6.
- AaDO2, PaO2:FIO2 ratio - shunt equation ∝ PaCO2 :: VM * VC ≥ 15 ml/kg ≤30 bpm ~ δ L/(PMAW - [PEEP + autoPEEP]) V ≥ 75 ml/cmH2O
intrinsic PEEP present in most ventilated patients, i. ARDS ≥ 8 cmH2O ii. ARF ~ 4 cmH2O → 7. 8. 9. 10. resistance MMV → underestimation of compliance by ~ 20-30% ~ (Pmax - Pp1)/flow ~ 2-6 cmH2O/l/s ~ 2 x VM MIP0.1 ≥ -20 cmH2O (VT in litres) not ready to wean ≤10-15 cmH2O (NMJB/ETT)
maximal inspiratory occlusion pressure f / VT > 100
Pressure Support
optimal pressure support is influenced by, a. ventilator factors i. size of ETT ii. ventilator circuit
iii. iv. b.
- demand valves - tubing resistance / compliance ± humidifier ventilation mode - CMV, IMV, CPAP trigger method & sensitivity
patient factors i. airways resistance ii. respiratory compliance iii. respiratory rate iv. minute volume v. muscle strength
ICU - Respiratory
CPAP Circuits
Benefits a. b. c. d. ↑ FRC → alveolar recruitment
improved V/Q match improved oxygenation ↓ work of breathing i. ↑ compliance ii. ↓ inspiratory muscle work iii. ↓ autoPEEP * some, not all patients "open lung" theory
Other Effects a. b. c. ↓ LV afterload ↓ venous return in CCF, acute LVF redistribution of lung water out of alveoli however, total lung water increases
Clinical Uses 1. low FRC states i. ARDS ii. IRDS iii. acute pulmonary oedema iv. diffuse interstitial lung disease v. pneumonitis vi. bronchiolitis high autoPEEP states i. asthma ii. CAL
ICU Respiratory
CPAP a. b. c. d. e. f. Potential Disadvantages excessive ↑ FRC ↑ work of breathing ↓ venous return patient discomfort gastric distension / aspiration skin / nasal bridge necrosis
P NB: the work of breathing is proportional to the δ AW , where, δ AW ∝ resistance & reactance P resistance = pressure / flow reactance = (inertia x acceleration) - (volume / compliance) therefore, the work of breathing through a CPAP circuit is affected by, 1. 2. flow ↑ resistance < PIFR > PIFR → ↑ WBR → ↑ turbulence
- narrow tubing - demand valves - flow resistors
3. 4. 5.
gas inertia & circuit geometry gas acceleration bag compliance
ICU - Respiratory
Inverse I:E Ratio
claimed advantages, a. b. c. adequate ventilation without high peak inspiratory pressures less barotrauma not substantiated in RCTs where mean PAW has been equal use of a lower FIO2 → peak PAW > 60 cmH2O and a FIO2 > 0.6, probably cause damage unless very brief
NB: assumption,
Lachmann, lung lesion index, LLI = PaO2 / (FIO2 x PAW) ≤ 4 suggests high probability of lung damage main aims of ventilation during ARDS are, a. b. c. restoration/maintenance of FRC maximise recruitment of functional gas exchange units minimise barotrauma
the respiratory pressure/volume curve changes throughout the disease process, therefore one ventilator setting may not be the best the justifications for reversing the I:E ratio include, a. b. c. overcome the critical opening pressure during inspiration sustain opening pressure expiratory time short enough to prevent closure of lung units
additional PEEP is usually required but is low, ~ 4-8 cmH2O NB: the autoPEEP produced may be profound, ~ 8-16 cmH2O Lessard et al. (Anaesthesiology 1994) review of PCIRV versus conventional ventilation, controlling for mean airway pressures & PEEP, showed no advantage for the former with respect to, 1. 2. oxygenation barotrauma
ICU Respiratory
Positive End-Expiratory Pressure
NB: the important therapeutic change is an increase in FRC Possible Beneficial Effects NB: dependent upon the level of PEEP a. respiratory ↑ transpulmonary pressure → ↑ end-expiratory lung volume / FRC ↑ lung compliance ↓ V/Q mismatch / ↓ shunt → ↑ PaO2 /CaO2 ??DO2 conflicting information on VD/VT reduced apnoeic periods in infants and sleep apnoea patients CVS ↑ stroke volume / ↓ LVESV ?? reversal of LVF
Adverse Effects NB: especially if excessive PEEP a. respiratory adverse redistribution of blood flow
→ →
diseased lung ↑ V/Q mismatch / ↑ shunt
↓ lung compliance ↑ in total lung water barotrauma, alveolar rupture/pneumothorax inactivation of surfactant b. CVS ↑ pulmonary capillary pressure PC = LAP + 0.4(PmPA - LAP) PEEP increases LAP & PmPA PC increases ~ 0.5 x PEEP, assuming CL ~ CCW ↑ RV afterload ↓ cardiac output / ↓ venous return ventricular interdependence humoral factors → ↓ ANF / ↑ ADH global cardiac compression ? decreased coronary blood flow - disproved in most studies
ICU - Respiratory
c. renal ↓ urine output / Na + excretion ↑ ADH, ↓ ANP ↑ IVC, renal vein pressure redistribution of intrarenal blood flow CNS ↑ ICP - unpredictable ? decrease in CBF hormonal ↑ adrenaline, noradrenaline ↑ renin, aldosterone ↑ ADH (conflicting data) ↓ ANP ~ 3x after 5 min of 20 cmH 2O
NB: most of these effects are reversible with volume replacement
ICU Respiratory
Optimal PEEP
Def'n: "that level of PEEP which provides the maximal increase in O2-flux " first coined by Suter et al., NEJM 1975 schools of thought actually vary as to the end-point, 1. Suter (NEJM, 1975) Gallager, Civetta
- maximum DO2 - also happened to equate with best compliance * however, this was not substantiated by later studies - pulmonary shunt fraction ≤15% - used fluid loading and inotropes to maintain cardiac output - PEEP required ranged from 15-65 cmH2O !!! - minimal PEEP with PaO2 > 60mmHg / FIO2 ≤0.5 - aimed at avoidance of hypoxia and barotrauma - claimed "maximal" PEEP of no benefit and increases the risk of barotrauma
(Chest, 1988)
other terms i. best PEEP ii. minimal effective PEEP§ practically, where PEEP ≤10cmH2O, most patients benefit in terms of FRC and PaO2 without significant adverse effects adverse effects are minimal if the patient has an adequate BP, peripheral perfusion and renal output (UO, Cr/Ur) where PEEP > 10cmH2O, or the patient is critically-ill (sepsis, MODS, multiple trauma), O2 flux and haemodynamic variables should be calculated to optimise PEEP
Consensus Statement ICM 1994 beneficial effects of PEEP, 1. 2. 3. lung recruitment elevation of PmAW improved oxygenation
NB: assessment of "best" level of PEEP depends upon physiological response desired; "most agree that in ARDS the lower limit should be set at, or slightly above the inflexion point of the pressure-volume curve"
ICU - Respiratory
causes of dynamic hyperinflation, 1. ↑ airways resistance - bronchospasm, asthma, CAL - bronchomalacia - dynamic airways collapse - foreign body
2. 3. 4. 5. 6.
tachypnoea inspiratory muscle activity during expiration (asthma) glottic closure during expiration mechanical ventilation resistance of ETT, circuit → underestimates of compliance by 20-30%
present in most ventilated patients a. b. ARDS ARF ~ 8 cmH2O ~ 4 cmH2O
(AB says virtually zero in ARDS patients)
static autoPEEP monitored by measurement of airways pressure after end-expiratory occlusion P dynamic autoPEEP monitored by oesophageal balloon or intrapleural catheter & δ IP prior to the onset of gas flow dynamic autoPEEP generally 2-3 cmH2O < static, and thought to be more clinically relevant effects of end-expiratory occlusion, a. b. dynamic hyperinflation decrease compliance & under-estimation of static compliance by ~ 50%, Compliance = δ L/[P2 - (PEEP + autoPEEP)] V ~ δ L/PAW V ~ 75 ml/cmH2O (N) c. d. e. ↑ work of breathing barotrauma CVS and renal effects of conventional PEEP
Treatment 1. 2. 3. 4. treat bronchospasm & clear secretions ↓ I:E ratio → CPAP long expiratory times - maintain airways open - ↓ inspiratory activity & ↓ inspiratory threshold load - ↓ LV afterload - facilitate weaning ↓ circuit resistance
ICU Respiratory
High Frequency Ventilation
IPPV HFPPV HFJV HFO < 60 60 - 110 110 - 400 400 - 2400 bpm bpm bpm bpm < 1.0 Hz
1.0 - 1.8 Hz 1.8 - 6.7 Hz 6.7 - 40 Hz
Advantages a. b. c. less movement of the operating field adequate O2 & CO2 exchange adequate gas exchange where IPPV complicated or impossible, i. bronchopleural fistula ii. communicating lung cyst iii. tracheal surgery lower peak airway pressures i. less barotrauma ii. no studies showing more beneficial than IPPV/PEEP in ARDS surfactant not damaged less effect upon cardiac function volume and ? clearance of secretions increased
e. f. g.
Disadvantages a. b. c. d. e. f. requires expensive equipment and trained personnel the increased volume of secretions may be detrimental humidification difficult CO2 exchange dependent upon resistance to mass flow and diffusion, → → → limited at high frequencies, ? > 20Hz mean intrathoracic pressure similar to IPPV/PEEP ? resulting in increased barotrauma O2 exchange proportional to mean lung volume, ie. maintenance of FRC important resonant frequency may be reached in some alveoli,
NB: high frequency ventilation appears very effective at removal of CO2 over a wide range of frequencies, however oxygenation appears more dependent upon lung volume and therefore mean airway pressure
ICU - Respiratory
Mechanisms of Gas Movement 1. 2. 3. convection diffusion pendelluft - simple in large airways - complex at bifurcations & in expiration
Extracorporeal Membrane Oxygenation
the overall average mortality from ARDS ~ 50-70% hypoxia is rarely the cause, usually due to MODS or septicaemia this implies that current ventilation modes either, 1. 2. are adequate and other factors need to be addressed prevent more rapid lung recovery and allowing more time for extrapulmonary complications to develop
in ARDS to main problem is hypoxia due to increased shunting the small areas of near normal lung have to do the "work" of the whole lung this requires therapy with a high F IO2, high PEEP, and high P IP, with their iatrogenic complications Extracorporeal Lung Assist (ECLA) Terminology a. b. c. ECMO EC-CO2-R PE-CO 2-R
it is necessary to define, 1. 2. 3. the type of bypass bypass flow:CO ratio lung ventilatory mode - VV probably better than AV ~ 20-30% of CO adequate for EC-CO 2-R
clinical studies of EC-CO2-R include a total of 115 patients in 8 trials there were a total of 57, ~ 50% survivors improvement was usually rapid, within the first 48 hours the average duration of therapy was ~ 7 days when conventional ventilation → total static lung compliance ≤25 ml/cmH2O → survival ~ 0 this may improve to ~ 50% with EC-CO 2-R subsequent studies have shown no improvement in survival cf. conventional ventilation
ICU Respiratory
Complications of ECMO 1. 2. 3. anti-coagulation and bleeding complement activation cost - manpower & equipment ~ 1000 ml/d
Potential Advantages a. b. c. d. e. f. avoids lung hypoxia, maintains a high lung O2 supply avoids high airway pressures reduction in PA pressure correction of V/Q ratios - ↓ barotrauma - ↓ surfactant loss - ↓ HPV - reduced effects of PEEP/IPPV - all areas equally oxygenated - avoids regional alkalosis
? anticoagulation reduction of intrapulmonary thrombosis ? reduced incidence of septicaemia
ICU - Respiratory
Indications 1. 2. 3. prolonged intubation > 7-10 days > 2-3/24 in professional singer
early for condition where extended airway management highly likely upper airway obstruction i. failed intubation ii. elective for threatened impossible intubation iii. transport of critically ill patient iv. postsurgical where re-intubation is likely impossible laryngectomy, radical neck procedures maxillofacial procedures with jaw wiring v. traumatic upper airway disruption laryngeal fracture, tracheal disruption
Advantages 1. 2. 3. 4. reduced dead space improved patient tolerance removal of secretions reduced incidence of laryngeal injury → less sedation required
Complications 1. procedural - haemorrhage - misplacement - hypoxia - pneumothorax / pneumomediastinum
2. 3. 4.
decannulation, disconnection colonization, infection with tube - cuff herniation - obstruction - displacement - ulceration, erosion - fistula - tracheomalacia - granulomata, stenosis - haemorrhage
long term
ICU Respiratory
Clinical Studies
El Naggar 1976
56 patients with an early tracheostomy (day 3) showed an increase in colonisation rate but no increase in infections increased frequency of airway lesions but all resolved in time laryngeal trauma from ETT was progressive after day 11 → Stauffer therefore recommended tracheostomy at day 10 1981
large study with 150 patients suggested ETT safer than tracheostomy ≤ 3/52 however, a non-randomised study with bias, as the tracheostomy group, a. b. c. d. e. were sicker were intubated longer tracheostomised later different surgeons high complication rate i. infection ii. haemorrhage iii. wrong incision iv. cardiac arrest 36% 36% 8% !! 4%
stenosis criterion was too strict, only 10% narrowing, therefore, i. tracheostomy group ~ 65% ii. ETT group ~ 20% 1984
total of 74 trauma patients managed with either, a. b. ETT for 14 days, or tracheostomised on day 3 → no difference in laryngotracheal trauma, sepsis, or morbidity
ICU - Respiratory
Whited 1984
total of 200 patients with ETT, a. b. c. duration < 5 days 6-10 days > 11 days ~ 6% transient injury ~ 5% reversible laryngeal stenosis ~ 12% extensive laryngeal stenosis
conclusions, 1. 2. 3. 4. 5. Berlauk tracheostomy has many potential therapeutic advantages laryngeal injury after 6-10 days becomes significant tracheal stenosis is more easily treated than laryngeal stenosis the high incidence of infectious and laryngeal complications in part relates to the preceding prolonged ETT maintain on ETT for 7-10 days then tracheostomy if not contraindicated 1986
factors affecting laryngotracheal injury, 1. 2. 3. duration of intubation cuff shape and pressure tissue compatibility of tube & cuff
areas of damage from ETT, 1. 2. 3. 4. 5. posteromedial portion of true cords posteromedial surface of the arytenoid cartilages posterolateral surface of cricoid cartilage mucosa of 4-7 th tracheal cartilages anterior wall of the trachea
pathology of injury, a. b. c. d. ulceration, perforation ischaemia necrosis mucosal hypertrophy & granuloma formation adhesions, fibrosis, stenosis
ICU Respiratory
Kopp 1987
intubation injuries related to, 1. 2. 3. duration hypotension severity of underlying disease
no correlation found with hypoxia or steroids complications and overall incidence, a. b. c. d. e. f. g. h. i. j. k. glottic oedema glottic granuloma superficial ulceration of the arytenoids mucosal ulceration of the cricoid dilatation of the posterior commissure deep mucosal ulceration of the arytenoids cartilage ulceration of the arytenoids cartilage ulceration of the cricoid glottic maceration glottic synechia fracture of the arytenoids - 100% - 96% - 81% - 75% - 60% - 37% - 24% - 12% - 6% - 3% - 3%
higher incidence than previous studies severity of injury increased significantly after day 3 NB: concluded, "conversion to tracheostomy should be considered between day 4 & 7 of intubation" incidence of hoarse voice, a. b. c. d. on extubation at 1 week at 1 month permanent ~ 100% ~ 45% ~ 16% ~ 1.5%
ICU - Respiratory
Tracheostomy: Haemorrhage
tracheo-arterial fistula usually involves the, a. b. innominate artery common carotid artery ~ 70% ~ 4%
most common site is at the cuff, ∴ may be decreased by high volume/low pressure cuffs fistulas related to the stoma are more common if performed below the 4 th tracheal cartilage not yet reported as a complication of percutaneous tracheostomy overinflation of the balloon will tamponade bleeding in 80% of cases, ∴ first step Stenosis Summary a. tracheostomy i. strict criteria ii. ≥ 30% stenosis iii. ≥ 70% stenosis ETT ≥ 3 weeks
~ 98% ~ 36% ~ 11%
("30% in 30%") (symptomatic)
~ 19% ≤0.5% symptomatic
NB: but: less tracheal, more laryngeal injury, which is more difficult to treat Jones et al. Ann-Surg. 1989
5-year burn center experience with tracheostomies → 99 tracheostomies (n=3246) indications of prolonged respiratory failure or acute loss of airway sputum colonization was universal, however rates of pulmonary sepsis & mortality were not significantly increased 28 patients developed late upper airway sequelae, a. b. c. tracheal stenosis tracheoesophageal fistula tracheoarterial fistula - TS - TEF - TAF
duration of intubation correlated only with development of TAF TEF patients were significantly older and more likely to have evidence of tracheal necrosis at the time of tracheostomy the pathogenesis of upper airway sequelae in these patients → divergent responses to inhalation injury, infection, and intubation
NB: use of tracheostomies in burned patients with inhalation injuries is now reserved for specific indications, rather than as prophylactic airway management
ICU Respiratory
Mortality a. tracheostomy i. elective ii. emergency ETT > 3 weeks
~ 0.4-3% ~ 6-15% < 1%
Tube Characteristics
Type Tracheal Loading Force 1 Red Rubber 1000 g PVC, Silastic 200-500 g 100-250 g after 24 hrs (moulding) ≤20 cmH 2O
Cuff Pressure
~ 120 mmHg
force exerted in deformation of the tube to the anatomy of the upper airway
ICU - Respiratory
Def'n: the side effects of high airway pressures during IPPV → air outside the alveolar space
now probably inappropriate, trend toward "volutrauma" traditional risk factors during IPPV, 1. 2. 3. 4. 5. 6. large tidal volume high mean and peak inspiratory pressures high levels of PEEP volume cycled ventilators short expiratory time low lung compliance - especially with increased resistance *CAL, ARDS, ?asthma > 50 cmH2O
Clinical Features a. interstitial emphysema small parenchymal cysts linear air streaks radiating toward the hilum perivascular haloes intraseptal air pneumatoceles subpleural air pneumothorax i. simple ii. loculated iii. tension mediastinal emphysema subcutaneous emphysema pneumatoperitoneum deterioration in lung function 2° surfactant inhibition
- anterior, subpulmonic
c. d. e. f.
ICU Respiratory
Peak Airways Pressure and Ventilator Associated Lung Injury
Manning Chest 1994
2 forms of VALI, 1. barotrauma i. pulmonary interstitial emphysema ii. pneumothroax iii. pneumomediastinum iv. subcutaneous emphysema acute lung injury less well described, acute injury associated with IPPV
NB: growing evidence that lung volume, or more accurately lung overdistension, is the primary determinant of VALI
Airway Pressure vs Lung Volume P aw usually measured as ventilator generated pressure pressure acting to distend alveoli → transmural pressure therefore, 2 factors influence difference between Paw and Ptm, 1. 2. non-zeroflow states → δ aw - P alv) ∝ Q.Raw (P alteration of Ppl with Paw / lung volume i. pulmonary compliance ii. inspiratory / expiratory muscle activity iii. thoracic cage / abdominal compliance Palv - Ppl
Barotrauma multiple studies document correlation between peak Paw and barotrauma Petersen & Baier, CCM 1983, prospective study of 171 patients, 1. 2. 3. PpAW > 70 PpAW ~ 60-70 PpAW < 60 → → → 10/23 4/53 0/95 43% 8% 0%
ICU - Respiratory
however, conclusion that P pAW causes barotrauma is tenuous, 1. correlation of P pAW & barotrauma not always this strong Leatherman, ARRD '89, 42 asthmatic patients, no barotrauma despite, PpAW's as high as 110 cmH2O mean PAW ~ 68 cmH 2O barotrauma well documented at low levels of P pAW Rohlfing, Rad. '76, 6/38 patients with BT had P pAW < 25 ventilatory methods aimed at reducing P pAW of little benefit Mathru, CCM '83, CMV vs IMV → lower incidence with IMV despite higher PpAW Clevenger, Arc. Surg. '90, converted IPPV to HFJV for "Salvage" → ↓ mean PAW from 92 to 41 cmH 2O, ↑ BT from 0/15 to 7/15 within 21 hrs of conversion Tharratt, Chest '88, converted 31 pts with ARDS to PCIRV → ↓ mean PAW by 20 cmH2O, ↑ BT from 0/31 to 8/31 incidence of BT also associated with VL Bone, ARRD '75 / '76, 2 studies looking at BT and V T in ARDS i. 50 patients → mean VT ~ 22 ml/kg with BT (40%) mean VT ~ 17 ml/kg without BT ii. 106 pts → mean VT ~ 11 ml/kg with BT (3.8%) "large increases in PpAW are often associated with large increases in VL, but in most studies to date, no assessment of V L changes was made which would allow one to distinguish between the effects of high P pAW and those of lung overdistension", Manning Williams, ARRD '92, prospective study 22 asthmatics → risk factors for BT & CVS instability, "only variable predictive of BT was end-inspiratory lung volume, a measure of dynamic pulmonary hyperinflation" two animal studies looking at BT with / without thoracoabdominal binding : unbound group → lower mean tracheal pressure higher incidence of BT
2. 3.
ICU Respiratory
Acute Lung Injury studies looking at ventilator induced ALI limited to animals (obviously) various study end-points, 1. 2. 3. 4. macroscopic lung appearance histologic lung appearance alveolar permeability microvascular permeability
NB: studies separating P pAW and VL, ie bound versus unbound animals, support the concept that V L and not PpAW is associated with ALI
Patient Management
Low Thoraco-Abdominal Compliance P pl should increase in proportion to mean P AW, ∴ minimal increased risk of BT however, situations of predominately thoracic or abdominal compliance changes may result in regional overdistension High Airways Resistance potential problem, as P pAW may not correlate with hyperinflation Tuxen & Lane, ARRD '87, in severe asthmatics requiring mechanical ventilation, 1. 2. ↓ VT ↓ PIFR (VT const) → → ↓ both P pAW and hyperinflation ↓ PpAW but ↑ hyperinflation
NB: "management .... should focus on providing the minimum V T and VM consistent with acceptable (but not necessarily normal) gas exchange, and on using a sufficiently high inspiratory flow rate to allow adequate time for exhalation"
ICU - Respiratory
ARDS Maunder, JAMA '86, ARDS affects the lung in a "patchy" fashion, → areas of diseased and areas of near-normal lung
thus, V T will tend to be preferentially distributed to the areas of "normal" lung no specific ventilatory guidelines to ensure the absence of regional hyperinflation on the basis that static transpulmonary pressure ~ 35-40 cmH 2O inflates normal lung to VC, suggested peak Palv < 35-40 cmH 2O however, 1. 2. Marini, CCM '92 Egan, J.App.Phys → → P pAW may not correlate with peak P alv "normal" P pAW tolerated by whole lung inflation may result in BT with regional inflation
theoretical approach would be to scale V T in proportion to lung compliance 1. 2. ↓ normal lung → ↓ compliance → ↓ VT requirement monitor P plat & adjust VT, but ?? at what level
Questions 1. 2. 3. 4. 5. 6. what influence does PIFR, or more accurately dVL.dt, have upon BT? is patient-ventilator asynchrony a risk factor for BT? what are the relative roles of mean versus peak V L on VALI? what is the best approach for ventilation of ARDS patients? is there a difference between PCV and SIMV, providing both focus on avoidance of lung overdistension, with respect to VALI? does repetitive opening/closing of units result in higher BT? ie. should we ensure VT occurs above inflexion point
ICU Respiratory
Amato, Et Al AJRCCM 1995 overdistention and cyclic reopening of collapsed alveoli implicated in the lung damage found in animals submitted to artificial ventilation 28 patients with early ARDS were randomly assigned to 1. 2. new approach
- end-expiratory pressures > lower inflection point of the PV curve - VT < 6 ml/kg, PpAW < 40 cm H2O, permissive hypercapnia - volume-cycled ventilation, VT ~ 12 ml/kg - minimum PEEP guided by F IO2 and hemodynamics - 'normal' PaCO2 levels
NA exhibiting better, 1. 2. 3. 4. evolution of the PaO 2/FIO2 ratio compliance
(p < 0.0001) (p = 0.0018)
shorter periods under F IO2 > 50% (p = 0.001) lower FIO2 at the day of death (p = 0.0002)
(5/15 vs 7/13, p = 0.45)
NB: but no significant improvement in survival
concluded that "the NA ventilatory strategy can markedly improve the lung function in patients with ARDS, increasing the chances of early weaning and lung recovery during mechanical ventilation"
ICU - Respiratory
Definition Ashbaugh et al. (Lancet 1967) described a condition in adults which was similar to the respiratory distress syndrome of infants (1 of the 12 patients was 11 yrs old) the term ARDS was coined by Petty & Ashbaugh in 1971 previously no agreed diagnostic criteria, therefore difficulty in comparing studies of incidence, mortality and treatment efficacy actually represents a subset of acute lung injury the essential features include, a. b. c. d. e. f. acute respiratory failure, usually requiring mechanical ventilation severe hypoxaemia with a high PA-aO2 gradient bilateral diffuse infiltration on CXR stiff lungs with CT ≤50 ml/cmH2O pulmonary oedema should not be cardiogenic in origin, the PAOP should not be elevated, definitions PAOP ≤12-18 mmHg presence of a known predisposing condition - sepsis, trauma - aspiration
NB: Lloyd, Newman and Brigham (1984) objected to this as it precluded the diagnosis in patients with pre-existing conditions which raised LAP American-European Consensus Conference Def'n: acute lung injury is a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiologic, and physiologic abnormalities that cannot be explained by, but may coexist with, left atrial or pulmonary capillary hypertension: 1. 2. 3. 4. timing oxygenation CXR PAOP → → → → acute onset PaO2 / FIO2 ≤ 300 mmHg irrespective of PEEP bilateral infiltrates on frontal CXR ≤ 18 mmHg
Def'n: acute respiratory distress syndrome, is a subset of ALI, meeting the above criteria, where, 1. oxygenation → PaO2 / FIO2 ≤ 200 mmHg
NB: ALI/ARDS are a continuum and are not specific disease entities, therefore, any cut-off limit for definition purposes is strictly arbitrary
ICU Respiratory
studies of ARDS subgroups show that of those with PaO 2/FIO2 ≤200, 98% progress within 1 to 7 days to a ratio < 150 mmHg thus, the higher figure allows earlier 'diagnosis' for study purposes, however care must be taken to exclude other causes mechanical ventilation was not considered a requirement for definition, as when this is instituted is very institution/clinician dependent chronic lung diseases such as interstitial pulmonary fibrosis, sarcoidosis etc. would meet the criteria except for chronicity, and are thus excluded from the diagnosis CXR infiltrates should be bilateral, consistent with pulmonary oedema and importantly may sometimes be very mild PAOP measurement is not considered essential for diagnosis, but is clearly useful diffuse pulmonary infection, if meeting the above criterea, is included in the diagnosis however, this was not agreed upon by all members at the consensus Diagnostic Criteria Petty
NB: included for historical comparison 1. clinical setting i. catastrophic event ii. exclusions iii. 2. respiratory distress
- pulmonary or non-pulmonary - chronic respiratory disease - LV dysfunction - RR > 20 bpm - laboured breathing
CXR i. interstitial ii. alveolar
* diffuse / bilateral pulmonary infiltrates - early - late * with a F IO2 ≥ 0.6 * usually ~ 20-30 ml/cmH 2O
physiology i. PaO2 ≤ 50 mmHg ii. CT ≤ 50 ml/cmH 2O iii. QS/QT increased§ iv. VD/VT increased§
increased V/Q anomaly
pathology i. heavy lungs - usually ≥ 1000 g ii. congestive atelectasis iii. hyaline membranes & fibrosis
ICU - Respiratory
Murray ARRD 1988
Lung Injury Score
CXR Score:
alveolar consolidation none 1 quadrant 2 quadrants 3 quadrants 4 quadrants ≥ 300 225-299 175-224 100-174 < 100 ≤5 6-8 9-11 12-14 ≥ 15 ≥ 80 60-79 40-59 20-39 ≤ 19 cmH2O cmH2O cmH2O cmH2O cmH2O ml/cmH2O ml/cmH2O ml/cmH2O ml/cmH2O ml/cmH2O 0 1 2 3 4 0 1 2 3 4 0 1 2 3 4 0 1 2 3 4
Hypoxaemia Score: PaO2/FIO2
PEEP Score:
Compliance Score: CRS
No Lung Injury1 Mild to Moderate Lung Injury Severe Lung Injury (ARDS)
0 0.1-2.5 > 2.5
Final Score = aggregate sum / number of components used
useful to consider 2 distinct pathways, 1. 2. direct insult to lung cells indirect effects of systemic inflammatory response
despite effort, no consensus could be reached on the order of events leading to ALI many believe the pathogenesis is different for various precipitating causes NB: "current knowledge is neither sufficient to allow an intelligent conclusion about the precise sequence of events, nor sufficient to allow determination of which of these putative mechanisms are more important" Consensus Report, ICM 1994
ICU Respiratory
Risk Factors Direct injury1 1. apiration syndromes acid aspiration gastric aspiration near-drowning 2. infections bacterial, viral, PCP 3. pulmonary contusion 4. embolic syndromes amniotic fluid fat rarely air 5. radiation pneumonitis 6. drug toxicity bleomycin, salicylates, opioids paraquat, O 2 7. toxic gas / vapour inhalation NO2, NH3, SO2, Cl2 industrial solvents
Indirect injury 1. severe SIRS / sepsis 2. major non-thoracic trauma ISS, APACHE II, TISS clinical description 3. shock / prolonged hypotension reperfusion injury 4. massive blood transfusion 5. transfusion reaction 6. anaphylaxis / anaphylactoid reactions 7. rarely associated with pancreatitis DIC cardiopulmonary bypass head injury burns diabetic coma high altitude uraemia
modified from Nunn 3 rd Ed., LIGW & Consensus Report, ICM 1994
Pepe's group found the highest single risk factor was sepsis syndrome, with 38% of patients in this group developing ARDS 1. 2. 3. risk factor → risk factors → risk factors → ~ 25% ~ 42% ~ 85% risk of developing ARDS
Fowler's group found the highest incidence in aspiration (35.6%) followed by DIC (22.2%) and pneumonia (11.9%) the major predisposing factors are now agreed to be, 1. 2. 3. 4. 5. severe sepsis multiple trauma massive transfusion DIC ~ 25-42% - particularly gram (-)'ve - particularly with pulmonary contusion aspiration of gastric contents
NB: ICM 1994, highest incidence appears to be septic shock
ICU - Respiratory
it is extremely difficult, if not impossible to separate the toxic effects of a high F IO2 from the pathological conditions requiring their use however, it is unlikely that O 2 plays a significant role in pathogenesis there is considerable difference in the reported incidence, probably reflecting the different diagnostic criteria in different studies T.Oh: the true incidence is unknown and may only be ~ 7% of "at risk" patients there is, however, good agreement on the overall mortality, which is as high as 50% this tends to be higher in cases which follow septicaemia, being reported as a. b. Fein et al. (1983) Fowler et al. (1983) ~ 81% ~ 78%
multiple papers stating that mortality has remained relatively unchanged over the last 20 yrs Milberg et al. JAMA 1995 →
918 patients in 5 ICU's between 1983-1993, over 18 years age 1. 2. outcome measure major causes i. sepsis syndrome ii. trauma 30 day hospital mortality ~ 37% ~ 25%
3. 4.
crude mortality rates, adjusted for age, ARDS risk, sex were unchanged however, significant decrease in mortality in, i. sepsis related ARDS * 67% → 40% ii. patients < 60 years of age
ICU Respiratory
Infiltrative Phase earliest histological lesion is interstitial & alveolar oedema ~ 24-96 hrs post-injury this is characterized by damage to the integrity of the blood-gas barrier, both endothelial cells and alveolar type I cells → not visible by light microscopy EM shows extensive damage to type I alveolar epithelial cells, which may be totally destroyed the BM is usually preserved and the epithelial cells form a continuous layer, with cell junctions seemingly intact endothelial permeability is nevertheless increased interstitial oedema is found predominantly on the "service" side of the capillary, sparing the "active" side this pattern is similar to that observed with cardiogenic oedema pulmonary lymph drainage is capable of increasing ~ 8x without formation of oedema protein containing fluid leaks into the alveoli, together with rbc's and leukocytes bound in an amorphous material containing fibrous strands → triggers replication of alveolar type II cells this exudate may form sheets lining alveoli → hyaline membrane impaired surfactant production results from either alveolar epithelial injury or secondarily from the effects of therapy (IPPV / O 2) intravascular coagulation is common at this stage in patients with septicaemia, capillaries may be completely plugged with leukocytes and the underlying endothelium damaged Proliferation Phase cellular proliferation starts within 3-7 days of injury there is thickening of the endothelium, epithelium and interstitial space there is less oedema, but the spaces are filled with rbc's and inflammatory cells type I epithelial cells are destroyed and replaced by type II epithelial cells which proliferate but do not differentiate immediately to type I cells they remain cuboidal and ~ 10 times the thickness of normal type I cells this appears to be a non-specific response, as it also occurs in oxygen toxicity characterized clinically by worsening hypoxaemia and development of pulmonary hypertension pulmonary hypertension results from, a. b. c. vascular microthrombi platelet aggregation & release of vasoactive mediators impaired endothelial synthesis of nitric oxide
fibrosis commences after 7-10 days and ultimately fibrocytes predominate extensive fibrosis is seen in resolving cases within the alveoli, the protein rich exudate may organise to produce the characteristic 'hyaline membrane', which effectively destroys alveoli
ICU - Respiratory
Mechanisms of Causation due to the diverse aetiology several mechanisms of causation, at least in the early stages in all cases, initiation seems to occur following damage to the alveolar/capillary membrane with transudation often increased by pulmonary venoconstriction thereafter, the condition is accelerated by a number of positive feedback mechanisms the initial insult may be either direct or indirect (see table above) much of the interest is in the indirect causes, which may be mediated either by cellular or humoral elements cell types capable of damaging the membrane include, a. b. c. d. neutrophils basophils macrophages platelets - through arachidonic acid derivatives
humoral agents include, a. b. c. d. e. f. g. bacterial endotoxin O2 free radicals proteases thrombin, fibrin and FDP's histamine, bradykinin, and serotonin platelet activating factor (PAF) arachidonic acid metabolites
various chemotactic agents, especially C5a , play a major role in the direction of formed elements onto the pulmonary endothelium Malik, Selig and Burhop (1985) drew attention to the fact that many of the humoral agents are capable of producing pulmonary venoconstriction this facilitates transudation caused from increased permeability Seeger et al. noted that a number of proteins, including albumin but particularly fibrin monomer, antagonize the effects of surfactant T.Oh: two possible mechanisms of causation, 1. 2. C' activation fibrinolysis and platelet activation
NB: however, both suffer from sparse clinical evidence, C' has nopredictive value and is non-specific FDP-D 'antigen' identified in patients with ARDS and may be a marker of mediator injury
ICU Respiratory
Neutrophil Mediated Injury the postulated sequence begins with activation of C 5a , which results in margination of neutrophils on vascular endothelium this is known to be activated in sepsis and during cardiopulmonary bypass significant margination is seen in many cases of ARDS however, margination can occur without significant lung injury, as occurs during haemodialysis with a cellophane membrane the postulate is that the neutrophils are somehow primed prior to margination this may occur with endotoxin, which results in firm adherence of neutrophils to the endothelium C5a results in temporary adherence but more importantly triggers inappropriate release of lysosomal contents to the cell exterior, cf. into phagocytic vesicles four groups of substances released in this way may potentially damage the endothelium; 1. 2. O2 derived free radicals proteolytic enzymes (esp. elastase) → → lipid peroxidation inactivate α1-antitrypsin direct endothelial damage monocyte/macrophage chemotaxis (elastin fragments) vasoconstriction increased permeability neutrophil chemotaxis intravascular coagulation direct tissue damage
arachidonic acid metabolites →
platelet activating factors
the role of neutrophils has been studied in depleted animals with conflicting results ARDS does seem less severe in neutropaenic patients, however it still may develop while they possess the capability for tissue damage, it seems unlikely they are the sole agent Macrophages & Basophils these have been studied to a far lesser extent they contain a similar array of potentially tissue destructive factors and are already present within the alveoli there numbers are greatly increased in patients with ARDS Platelets these are also present in large numbers in the capillaries of patients with ARDS aggregation at that site is associated with an increase in capillary hydrostatic pressure, possibly due to a release of arachidonic acid metabolites they may also play a role in the normal integrity of the capillary endothelium (Malik, Selig & Burhop, 1985)
ICU - Respiratory
Mediators a. b. prostaglandins leukotrienes - TXA2 - PGI2 - chemotaxis - vasoconstriction - bronchoconstriction
lymphokines i. IL-1 & TNF
- widespread immune stimulation - activation of inflammatory response - septic syndrome, fever - vasodilatation - hyperdynamic circulation - systemic catabolism, hepatic anabolism - acute phase response ii. IL-1 & 2 - T-cell stimulation/activation iii. IL-3 & CSF's - marrow & specific colony stimulation iv. IL-4 & 6 - B-cell stimulation v. interferons - antiviral activity - T & NK cell stimulation IL-1, or endogenous pyrogen, acts on the pre-optic area of the hypothalamus with subsequent heat production d. complement - chemotaxis - vasodilatation - increased capillary permeability
others i. endotoxin ii. kallikrien / kinin system iii. histamine iv. serotonin v. FDP's
ICU Respiratory
Lung Mechanics
lung compliance CL is reduced (< 40 ml/cmH2O) and is adequately explained by histology there is impaired production of surfactant (Fein et al. 1982) Petty (1979) using BAL showed abnormally aggregated and inactive surfactant FRC is reduced below CC by collapse, tissue proliferation and increased elastic recoil alveolar/capillary permeability is increased as demonstrated by studies of transit times with inert tracer molecules the concept of "non-cardiogenic" capillary leak is oversimplified, possibilities being, a. b. C' activation fibrinolysis and platelet activation
Dankzer et al. (1979) found a bimodal distribution of perfusion → one range of near normal V/Q ratios, the other to areas of near zero V/Q this was sufficient to explain the PA-aO2 gradient without the need to evoke changes in the diffusing capacity DCO2 physiological shunt QS is usually so large (~ 40%) that a near normal PaO2 cannot be achieved even with a FIO2 = 1.0 the increase in VD , which may exceed 70%, would require a large VM to preserve normocapnia it may be argued that attempting normocapnia in these patients is inappropriate management gaseous exchange is further impaired, in that VO2 is usually increased, despite the patient being paralysed and artificially ventilated (Sibbald & Dredger, 1983) Changes in Respiratory Mechanics a. b. c. d. e. ↓ total pulmonary compliance ↓ FRC ↑ airways resistance ↑ work of breathing ↑ respiratory rate & decreased VT (Sibbald, 1983) (Start in Phase 1)
Changes in Haemodynamics a. ↑ PpAW
- ↑ RV afterload - ↑ RVEDV & RVEDP - ↓ RVEF ∝ 1/(mean PAW) - ↓ RV contractility
b. c. d.
normal LV function early ↑ PAOP, without ↑ LVEDV → ? ventricular interdependence / ? ↓ LV compliance LV dysfunction in later stages
ICU - Respiratory
Principals of Management
NB: → treatment of primary cause, other management is essentially supportive
no specific therapeutic measure has been shown to significantly reduce the development / progression of the disease there are four main objectives of management (Nunn) 1. 2. 3. 4. T.E. Oh 1. 2. 3. 4. 5. 6. ventilation fluid management cardiac support nutrition physiotherapy other therapies i. antibiotics ii. steroids iii. heparinisation iv. ECMO v. ultrafiltration * only by M,C&S, not prophylactic - late fibroproliferative phase, in absence of infection - not useful for ARDS - patients unresponsive to diuretics with H2O retention ? clearance of mediators of sepsis, medium MW ICM 1994 - PEEP, CPAP, PCV, IRV - permissive hypercapnoea, "open-lung" models maintenance of an adequate PaO2 minimize pulmonary transudation maintenance of an adequate circulation prevent complications, particularly sepsis
Concensus Conference
several therapeutic methods are so universally accepted that, although not formally tested, may be considered as standard, 1. 2. 3. 4. 5. suplemental O2 PEEP / CPAP mechanical ventilation avoidance of fluid overload delivery of care in an ICU setting
ICU Respiratory
Ventilation ventilation should be adjusted to maintain adequacy of oxygenation and to reduce peak and mean airway pressure PEEP is almost universally required to maintain an adequate P aO2 it is of no prophylactic benefit but does improve survival benefits of PEEP are, a. b. c. d. reduction in F IO2 improved DO2 increased compliance reduction in atelectasis
hazards of PEEP include, a. b. c. increase in total lung water inactivation / destruction of surfactant may produce a fall in CO and DO2
normocapnia becomes a lower priority as barotrauma becomes more likely HFJV & HFPPV provide no advantage over traditional ventilation they do result in a decrease in mean PIP, but there is no improvement in mortality ECMO has shown no proven benefit, mortality remains the same Morris et al. (AJRCCM '94) "Salt Lake City Trial", comparing, 1. 2. computer driven models of ventilation with SIMV PCIRV & EC-CO2R → no benefit in mortality
NB: maintaining similar mean PAW
Lessard et al. (Anaesth. '94 ) showed no benefit in terms of barotrauma, oxygenation, or survival with the use of PCIRV versus conventional ventilation when efforts to keep total PEEP and mean airway pressure the same were made the level of optimal PEEP is described using various end-points, 1. 2. 3. 4. maximal DO2 lowest QS PaO2 > 60 mmHg < 15% * with lowest F I O2 ≥ 30%
maximal improvement in CL i. dynamic V/P curves maximal volume recuitment for given P AW ii. static V/P curves inflexion point with recruitment
*above inflexion point
ICU - Respiratory
Pharmacotherapy fluid balance should be adjusted to lessen the formation of oedema Fein et al. recommend values of PAOP ~ 5-10 mmHg administration of NSA-C / 5% does not reduce the formation of oedema some early work suggested the administration of massive doses of steroids may halt the development of the disease, Sibbald et al. 1981 subsequent work has shown no benefit, or an increased incidence of sepsis and a higher mortality, thus the administration of steroids is not recommended for routine cases Meduri et al. (Chest '94) showed steroids may be of benefit for the subgroup of late proliferative ARDS providing underlying infection was meticulously ruled-out, 1. 2. 3. blood cultures, CUD urine specimen BAL + quantitative culture, or PSB no other septic foci - lines, GIT
other pharmacotherapy includes, 1. 2. 3. 4. 5. 6. 7. endotoxin Ab's free radical scavengers cyclo-oxygenase inhibitors thromboxane inhibition cytokine inhibition surfactant replacement PGE 1 - anti-LPS Ab - antioxidants, SOD, catalase, NAC - Indomethacin, Ibuprofen - ketoconazole - anti-TNF
NB: these are only of prophylactic benefit in animal studies, none has been shown to improve outcome in human studies, Ibuprofen improves early haemodynamic stability but not mortality
Outcome a. mortality ~ 50-70% unchanged over last decade ? small decrease depending upon criteria for diagnosis poor prognosis - elderly - severe disease, uncontrolled 1° cause - high PVR, RV dysfunction - impaired DO2
associated problems i. nosocomial pneumonia ~ 70% ii. high incidence of sepsis syndrome iii. MODS
ICU Respiratory
Fluid Management in ARDS / Pulmonary oedema
Simmons et al., ARRD Apr-1987
effect of fluid balance on survival in ARDS 213 patients in a prospective data collection study → 113 met criteria for ARDS multiple variables up to 14 days after intubation → CO, PAOP, MAP, I-O, ΣI-O, δ Wt significant differences in ΣI-O and δ between survivors and nonsurvivors on almost every day Wt → survivors lost weight and significantly lower ΣI-O cf. nonsurvivors logistic regression to determine if δ and ΣI-O could predict survival, Wt ↓ wt. ≥ 3 kg → 67% survival ↑ wt. ≥ 3 kg → 0% survival day 14 similar results obtained using comparably low and high values for ΣI-O NB: this does not establish a cause and effect relationship, likely means only that "sicker" patients needed more fluid resuscitation & developed "leakier" capillaries
Humphrey et al.,
Chest. May-1990
looked at survival and ICU length of stay of 40 ARDS patients analyzed to determine if a management strategy of lowering the PAOP was associated with an increased survival or a decreased ICU length of stay patients were divided into two groups: 1. 2. group 1 group 2 - reduction of PAOP ≥ 25% - reduction of PAOP ≤25%
survival to hospital discharge 1. 2. group 1 group 2 - 12/16 - 7/24 75% 29%
difference remained statistically significant stratifying patients by age & APACHE II NB: concluded that, "analysis supported the notion that treatment of low pressure pulmonary edema with reduction of PAOP is associated with an increased survival" similarly, this does not imply a causal relationship for therapy, patients in whom greater reductions in PAOP can be achieved are likely less severe and more likely to survive anyway
ICU - Respiratory
Eisenberg et al. ARRD Sep-1987
prospective evaluation of extravascular lung water (EVLW) instead of pulmonary artery wedge pressure measurements to guide the hemodynamic management of 48 critically ill patients randomized → protocol management, PM → routine management, RM groups RM group → EVLW measurements blinded groups similar for age, gender, and severity of illness of patients with initially high EVLW → EVLW decreased → PM ~ 18 ± 5% → RM ~ 4 ± 8% (p < 0.05) difference was greater in patients with CCF following the protocol, no adverse effects on mortality → 1. 2. not statistically different for entire groups significantly better (p < 0.05) for PM patients with initially high EVLW and normal PAOP (predominantly sepsis or ARDS patients)
- oxygenation - renal function
mortality for both groups of patients, 1. 2. initial EVLW initial EVLW > 14 ml/kg < 14 ml/kg → 13/15 → 13/32 87% 41% (p < 0.05)
NB: concluded that, "management based on a protocol using EVLW measurements is safe, may hasten the resolution of pulmonary edema, and may lead to improved outcome in some critically ill patients"
ICU Respiratory
Mitchell, Schuller, et al. ARRD 1992
randomised prospective trial to assess effect of management emphasising diuresis & fluid restriction on, 1. 2. 3. development or resolution of EVLW mechanical ventilation hours ICU duration
101 patients requiring PAC insertion, 1. 2. 52 patients → 49 patients → EVLW management PAOP management
89 patients with pulmonary oedema = EVLW > 7 ml/kg (ideal BW) no significant differences in baseline disease status (APACHE II, OSF), minor age difference
PAOP Group EVLWt : EVLW t=01 Cumulative I-O2 Median ICU Days3 Median MV ↑Creatinine4 ↑BUN Mortality5
EVLW Group ↓ t > 24 hrs ml ml 142 ± 3632 median = 754 7 days 9 days µmol/l mmol/l 35 ± 88 4.6 ± 9.6 35% (p = 0.05) (p = 0.047) µmol/l mmol/l (p = 0.21) (p < 0.05) ml ml
No change 2239 ± 3695 median = 1600 16 days 22 days 17.6 ± 79 2.1 ± 6.4 47%
only for the 89 patients with initial EVLW > 7 ml/kg No difference in - the number of patients requiring vasopressors/inotropes - the duration of use of vasopressors/inotropes
No difference in MV or ICU duration for the subset of patients with CCF / volume overload Small but statistically significant increase in plasma creatinine & BUN in EVLW group ICU plus within 48 hours of discharge if related to ICU admission pathology
ICU - Respiratory
Schuller, Mitchell et al. Chest 1991
aim to evaluate fluid balance and changes in extravascular lung water (EVLW) on survival in the ICU and short-term outcome in patients with pulmonary edema retrospective analysis of data, sorting by survival and "treatment received" taken from a randomized controlled trial of fluid restriction (Mitchell et al., ARRD 1991) 89 patients requiring PA catheterization with high EVLW > 7 ml/kg, 1. survival survivors had no significant fluid gain or change in EVLW but decreased wedge pressure and body weight, cf. nonsurvivors fluid balance < 1000 ml fluid gain at 36 hrs > 1000 ml fluid gain at 36 hrs median ventilation days ICU days hospital days → → survival ~ 74 % survival ~ 50 % (p < 0.05)
~ 50% for < 1000 ml fluid gain
NB: accounting for differences in the severity of illness, fluid balance was an independent predictor of survival
(p < 0.05)
NB: "These data support the concept that positive fluid balance per se is at least partially responsible for poor outcome in patients with pulmonary edema and defend the strategy of attempting to achieve a negative fluid balance if tolerated hemodynamically."
ICU Respiratory
there is a spectrum of presentations, a. acute massive aspiration i. acid aspiration pneumonitis ii. non-acid aspiration particulate non-particulate sub-acute aspiration chronic aspiration - Mendelsonn's syndrome - food, FB, non-acid vomitus - blood, water, near drowning - microaspiration - nosocomial pneumonia - nosocomial pneumonia - bronchopneumonia - bronchiectasis - lung abscess - ch. interstitial fibrosis - atypical mycobacterial fibrosis - late onset "asthma"
b. c.
Acute Acid Aspiration 1. 2. 3. 4. 5. acute pulmonary oedema ARDS acute "asthma" "atypical pneumonia" acute bronchopneumonia
often previously healthy person & rapid in onset, frequently preventable frequently non-infected acid aspirate antacids often useful Chronic Micro-Aspiration 1. 2. 3. nosocomial pneumonia recurrent bronchopneumonia chronic "asthma"
frequently in hospitalised patients and insidious in onset multiple risk factors and difficult to prevent the aspirate is frequently infected antacids may actually predispose → GIT colonisation ?? recent studies would not support his concept
ICU - Respiratory
Risk Factors a. altered conscious state - trauma - coma - ETOH, drugs (CNS depressants) - CVA - epilepsy - hypotension - drugs (CNS, NMJ) - intubation / extubation - tracheostomy - CVA - motor neurone disease, MS, GBS, CIP - elderly - pregnancy - hiatus hernia - obesity - bowel obstruction - NG tube - oesophageal disease - LOS dysfunction
impaired airway reflexes
Nature of Aspirate 1. 2. 3. 4. 5. gastric acid particulate infected fluid blood fresh vs. salt water
ICU Respiratory
Infected Aspiration differences for micro vs. macro-aspiration frequent colonization of the upper airways of hospitalized and critically-ill patients, a. pre-hospitalized aspiration → predominantly anaerobes - Bacteroides m. & f. - Fusobacterium - Peptostreptococcus - Pneumococcus - Micrococcus
& some aerobes
RX b.
Penicillin & Metronidazole
hospitalized patient + antacids → predominantly gram (-)'s - E. coli - Klebsiella - Proteus - Pseudomonas - Staphlococcus - Candida
& some gram (+)'s some fungi RX
Flucloxacillin & Gentamicin, or Cefotaxime + Flucloxacillin ± Metronidazole
1. prevention - sucralfate, antacids - topical antibiotics - cricoid pressure - ETT
2. 3. 4. 5. 6. 7. 8. 9.
protection of airway
tracheobronchial toilet - suction, lavage - flexible/rigid bronchoscopy oxygen & ventilatory support chest physiotherapy bronchodilator therapy antibiotics steroids - no proven benefit or harm - most would treat as above - no proven benefit or harm - may increase 2° infections
systemic support for ARDS, sepsis syndrome etc.
ICU - Respiratory
Def'n: a disease characterized by wheezing, dyspnoea and cough, resulting from airways hyperreactivity, and variable degrees of reversible airways obstruction
current emphasis is on airway inflammation in pathogenesis, in conjunction with smooth muscle mediated bronchoconstriction and intraluminal mucus a subgroup suffer sudden, unexpected increases in airflow obstruction, due mainly to bronchospasm, termed variously as, a. b. sudden asphyxic asthma hyperacute asthma - Wasserfallen, ARRD 1990 - ? Tuxen
characterized by, 1. 2. 3. 4. 5. minimal baseline airflow obstruction, but marked hyperreactivity innocuous or unrecognized stimulus very rapid severe onset, often fatal within 1 hr relatively rapid resolution comprise ~ 75% of ventilated asthmatics
this contrasts acute severe asthma, characterized by, 1. 2. 3. 4. 5. 6. persistent significant airflow obstruction → behaviour modification & denial attacks result from small deteriorations in function → 'apparent' sudden severe symptoms slow resolution, with large chronic component comprise ~ 25% of ventilated asthmatics FEV1 < 50% pred. relatively asymptomatic, with underperception of disease
studies of patients dying from SAA, cf. patients with chronic asthma, show, a. b. ↑ neutrophils / ↓ eosinophils in airways submucosa less intraluminal mucus
Kikuchi, et al., NEJM 1994, found patients with a history of near-fatal asthma have, a. b. a blunted hypoxic ventilatory response, and diminished dyspnoea during inspiratory resistive loading, cf. other asthmatics
NB: diminished patient perception increases the risk of future life-threatening or fatal asthma
ICU Respiratory
Assessment of Severity
NB: no single clinical measurement has been shown to reliably predict outcome Mild / Moderate1 loudness of wheeze2 forced expiratory time respiratory rate HR use of accessory muscles PEFR FEV1.0
1 2
Indications for IPPV conscious state inability to speak > 30 > 130 bpm
= most useful
pulsus paradoxus3 > 15 mmHg respiratory fatigue PaCO2 ≥ normal, or rising4 failure to respond to therapy
< 30% pred. < 30% pred.
generally not useful in severe failure poor correlation with degree of airflow limitation, Shim. et al., Arch.Int.Med.1983 may actually decrease with the onset of severe respiratory failure hypercapnoea usually only occurs with a FEV1 < 25%, but alone doesn't mandate IPPV; absence of hypercapnoea does not exclude severe obstruction & impending arrest
ICU Admission 1. 2. patients requiring IPPV severe airflow obstruction i. accessory mm., exhaustion, diaphoresis ii. p.paradox > 12 mmHg iii. PEFR < 25% poor response to initial therapy / deteriorate despite therapy altered mental status cardiac toxicity / complication
3. 4. 5.
ICU - Respiratory
Assessment During Ventilation a. b. c. expiratory time pulsus paradoxus autoPEEP i. static ii. dynamic alteration in P aCO2 pressure differential i. end-inspiratory occlusion P - P IP ii. peak-to-plateau gradient ~ 0.5-0.75s inspiratory pause δ / PIFR P → resistance but, with severe airflow obstruction 0.75s is inadequate for equilibration end-expiratory trapped gas volume = volume expired after prolonged expiration ( ≥ 1') ECG CXR - RAD, RVH & 'strain', acute TR - limited use, see over - end-expiratory occlusion pressure - δ IP prior to onset of airflow P
d. e.
f. g. h.
Indications for CXR 1. 2. 3. 4. any asthmatic post-intubation signs / symptoms of barotrauma clinical findings suggestive of pneumonia localizing signs on chest examination when the diagnosis is uncertain → exclusion
NB: Zieverink, Rad. 1982, 528 CXR's in 122 asthmatics → Factors to Exclude a. b. c. d. e. pneumothorax FB upper airway obstruction LVF & severe emphysema pulmonary emboli ± echocardiogram ± lower limb doppler, lung perfusion scan abnormalities in ~ 2.2%
ICU Respiratory
Investigations a. b. c. d. e. f. g. FBE, MBA serial AGA's CXR ECG microbiology paired serology PFT's during recovery - tracheal aspirate for MC&S - blood cultures if febrile - atypical pneumonia - serial PEFR - FEV 1/FVC
CVS Effects of Severe Asthma 1. pulmonary hypertension- HPV, 2° mediator release - acute ↑ RV afterload ± ↓ LV preload ∝ interdependence impaired venous return ↑ LV afterload 2° effects from 2° effects from drugs - SNS outflow - hypoxia, hypercarbia & acidosis - β-agonists, aminophylline
2. 3. 4. 5.
Mechanical Abnormality → a. b. c. d. e. increased airways resistance all airways involved but to differing degrees regional variation in time constants hyperinflation and obstruction rapid shallow respiration ↑ work of breathing
Pathology a. b. c. d. e. smooth muscle contraction inflammatory infiltrate & mucosal oedema mucus plugging & inspissation of secretions segmental/lobar obstruction or collapse barotrauma
ICU - Respiratory
Mediators a. b. c. d. e. f. g. histamine leukotrienes * LT-D 4 cholinergic nervous system neuropeptides from NANC nervous supply PG's IgE PAF
Complications a. b. hypoxia, hypotension - myocardial, cerebral hypoxic damage
respiratory i. barotrauma / volutrauma ii. iii. iv.
- pneumothorax, pneumomediastinum - pneumopericardium, subcutaneous emphysema mucus plugging, airway obstruction, atelectasis infection respiratory arrest
biochemical disturbances i. hypokalaemia, hypophosphataemia, hypomagnesaemia ii. hyperglycaemia iii. lactic acidosis - hypoxia / hypotension * β-agonists, aminophylline drug related i. theophylline toxicity ii. neuropathy / myopathy
? neuromuscular blockade & steroids
Long-Term Beta-2-Agonists 1. 2. 3. 4. heavy use (> 1 cannister/month) is a marker of severe asthma heavy or increased use warrants additional therapy with steroids use may make asthma worse patients currently using β2-agonists should slowly withdraw non-essential doses & use as rescue medication during "breakthrough" asthma
NB: position statement, American Academy of Allergy & Immunology, 1993
ICU Respiratory
Medical Treatment a. b. O2 therapy inhaled β2-agonists - continuous nebulized salbutamol in non-intubated patients MDI's + spacing devices are equally effective as nebulizers ~ 3% of radioactive aerosol delivered by small volume nebulizer reaches the lungs in mechanically ventilated patients (MacIntyre, CCM 1985) IV β2-agonists no proven advantage for - IV cf. inhaled route - selective agents cf. adrenaline result in hypokalaemia & tachyarrhythmias increase the VO2 , PaCO2 and lactic acidosis ∴ use in younger patients (preferrably < 40) not responding to inhaled RX aminophylline ~ 6 mg/kg/30 mins IV ~ 0.5 mg/kg/hr maintenance inferior to β2-agonists as monotherapy various studies have demonstrated addition of theophylline does not confer therapeutic benfit and increases tremor, N&V, arrhythmias, etc. other studies show opposite, AJRCCM '95 "inadequate evidence to support or reject the use of theophylline in this setting" ∴ use in patients with poor or incomplete response to β2-agonists/steroids NB: ↓ clearance ∝ CCF, liver failure, macrolides, ciprofloxacin
e. f.
ipratropium conflicting evidence but probably an additive effect, not first line agent steroids not useful via the nebulized route in the acute attack early IV administration useful, significant difference at 12 hours reduce the need/duration of hospitalisation & number of relapses "failure to treat with steroids contributes to asthma deaths" AJRCCM '95 others i. MgSO4 infusion benefit has been described in patients with normal plasma Mg++ levels ~ 50% of patients with SA have low plasma levels the 2 largest PRCT's failed to show any benefit "available data do not support the use of magnesium in SA" AJRCCM '95 ii. nitric oxide iii. heliox iv. ECMO
ICU - Respiratory
Effects of Steroids 1. 2. 3. 4. 5. 6. anti-inflammatory potentiate the effects of β-agonists receptor upgrading stabilisation of lysosomal membranes reduce capillary permeability inhibit histamine release
Indications for Antbiotics 1. 2. 3. fever & sputum containing polymorphs/bacteria clinical findings of pneumonia signs & symptoms of acute sinusitis
NB: majority are viral & there is no role for routine use Bronchioalveolar Lavage autopsy studies show marked mucus impaction of both large and small airways no benefit in SA has been demonstrated for chest physiotherapy, mucolytics or expectorants BAL using either saline or NAC may be useful in some patients in intubated patients, potential risk of an acute increase in V EI due to increased resistance NB: "should not be considered a part of routine management of ventilated asthmatics"
CPAP Ventilation a. potential advantages i. ↓ work of breathing ii. ↓ inspiratory muscle load & ↑ muscle efficiency iii. ↓ need for sedation / anaesthesia / intubation iv. ? ↓ incidence of - nosocomial pneumonia - otitis & sinusitis potential disadvantages i. gastric distension & risk of aspiration ii. less control over ventilatory pattern iii. exacerbation of gas-trapping & overexpansion iv. pressure necrosis
NB: "further studies involving large numbers of patients are needed"
ICU Respiratory
Paralysis 1. potential advantages i. ↓ VO2 & CO2 production ii. ↓ lactate production iii. may decrease risks of barotrauma *theoretical, not proven iv. ↓ expiratory muscle activity may ↓ airways resistance potential disadvantages i. difficulty assessing mental status / risks of awareness ii. ↑ risk of DVT iii. disuse muscle atrophy iv. ? causative role in myopathy in acute asthmatics with steroids other possible factors include hypokalaemia, hypophosphataemia & high dose beta-agonists the contention that the steroid molecule of vecuronium/pancuronium would potentiate this effect is not supported Fleugel, AJRCCM 1994
NB: concensus view, "until further data available, NMJ blockade should be reserved for patients unable to be ventilated with sedation alone" Ventilatory Parameters → low VT low rate high flow rate high FIO2 FIO2 → VT → rate → ≤ 10 ml/kg ≤ 10 bpm ≥ 80 l/min ≥ 0.5 ≤50 cmH 2O ≤30 mmHg (*not necessarily)
a. b. c. d. e.
adequate to prevent hypoxia limits peak PAW allows full expiration - ie. minimal auto-PEEP
pulse paradox
end-expiratory P Occ ≤10 mmHg measures of autoPEEP are only accurate in paralysed patients has not been shown to correlate with complications may significantly underestimate hyperinflation due to noncommunicating gas end-inspiratory volume < 20 ml/kg VEI > 20 ml/kg → ↑ barotrauma, hypotension (Tuxen et al., ARRD'92) however, not prospectively validated & doesn't measure all trapped gas end-inspiratory P Plat < 25 mmHg (30 cmH 2O) more easily determined than VEI but not a reliable predictor of complications like VEI, not prospectively validated, but complications rare at P Plat < 30 cmH2O this equates to ~ 1.6 l increase above FRC
ICU - Respiratory
Risks of Permissive Hypercapnia 1. 2. 3. 4. 5. cerebral vasodilatation cerebral oedema decreased myocardial contactility systemic vasodilation & hyperdynamic circulation pulmonary vasoconstriction
NB: most of these are not significant for otherwise healthy patients, hypoventilation is well tolerated with P aCO2 < 90 mmHg (Darioli, ARRD 1984) virtually all studies of permissive hypercapnia in SA report near-zero mortality rates, significantly less than studies where 'normal' AGA values are achieved, though there is no large RCT Prevention of Further Episodes 1. 2. 3. 4. 5. education - disease and drug administration
monitoring using a peak flow meter regular anti-inflammatory therapy use of a spacing device & mouth washing post-inhalation rescue use of β-agonists early presentation for medical assessment with deterioration
Causes of Death NB: a history of near-fatal asthma requiring mechanical ventilation is the single best predictor of subsequent asthma death 1. 2. 3. cerebral hypoxia barotrauma tension pneumothorax
ICU Respiratory
Common Causes 1. 2. 3. 4. 5. 6. viral pneumonia Mycoplasma pneumoniae - influenza A&B, parainfluenza - RSV, CMV, varicella ~ 5% community acquired
Legionella pneumophilia ~ 3% community acquired probably underdiagnosed to a significant degree Chlamydia psittaci pneumoniae Coxiella burnetti atypical mycobacteria * Q fever
Other Causes 1. infective i. atypical presentation of bacterial pneumonia ii. pulmonary TB iii. opportunistic infections in immunocompromised non-infective i. thromboembolic disease ii. collagen vascular disorders iii. malignancies aspiration pneumonitis
Slowly Resolving Pneumonia a. organism causes - antibiotic resistance - viral, fungal, parasitic - superinfection - inappropriate agent / dosage - bronchiectasis, empyema, lung abscess - bronchial obstruction - chronic aspiration - underlying malignancy - interstitial & other lung diseases - immunocompromised - LVF - malignancy, HIV *ESBL producers
b. c.
therapeutic causes host causes i. lung disease
other host diseases
ICU - Respiratory
from McLaws, MJA 1988, looking at general hospital populations → nosocomial infections occur in 6-7% of patients Chastre, , 15-35% of these are pneumonia with a mortality rate of 50-70% most are endogenous gram negative bacteria, many are polymicrobial a high proportion occur in ICU patients Daschner, ICM 1982, ICU patients → 1. 2. 3. the overall incidence of nosocomial infections in ICU patients ~ 12-20% UTI septicaemia pneumonia ~ 40% ~ 20% ~ 16%
NB: nosocomial infections in patients with ARDS ~ 70%
Aetiology a. gram negative bacilli ~ 70% - E. coli - Pseudomonas - Enterobacter - Klebsiella - Staphlococci - Enterococcus - Candida
b. c.
gram positive cocci fungal
~ 15-25% ~ 5%
Mortality a. gram negatives i. Pseudomonas ii. Klebsiella Serratia Enterobacter iii. E. coli gram positives viruses ~ 50-56% overall ~ 70% | | | ~ 40% ~ 30% ~ 5-25% ~ 7%
b. c.
ICU Respiratory
Risk Factors
Host Factors age newborn elderly > 60 multiple trauma severe 1° disease neutropaenia immunosuppression Therapeutic Factors ICU or SCN systemic antibiotics invasive catheters large transfusion need for haemodialysis corticosteroids
Meduri a. b. c. d. e. f. g. h.
Chest 1990 diagnosis of nosocomial pneumonia in an intubated patient is difficult tracheal aspirate in ventilated patients is often inaccurate & misleading colonisation rate > 60% risk factors for colonisation and infection are similar other conditions can simulate pneumonia and may go untreated recognition of a specific pathogen is important for effective treatment a large number of patients do not have pneumonia inappropriate antibiotics i. ↑ colonisation risk → ii. ↑ resistant bacterial strains iii. potential side effects iv. cost many diagnostic techniques superinfection
- histology = "gold standard"
Clinical Tracheal Aspirate LRS Bronchio-Alveolar Lavage Protected Sputum Brushings
64% 80-95% 95+% 75-100% 40-100%
80% 40-60% 40% 30-75% 40-100%
* these figures are from different studies, animal and patient, with different diagnostic criteria for pneumonia
ICU - Respiratory
Andrews Chest 1981 → sensitivity ~ 64% specificity ~ 80%
histology at PM versus clinical findings 1. 2. 3. 4. fever leukocytosis purulent tracheal aspirate new pulmonary infiltrate on CXR
NB: ARDS patients with a new infiltrate frequently do have pneumonia, non-ARDS patients with a new infiltrate frequently do not have pneumonia Fagon & Chastre ARRD 1989
looking for rate of development of nosocomial pneumonia in intubated ICU patients diagnosed with PSB with semiquantitative culture → sequential incidence, a. b. c. day 10 day 20 day 30 ~ 6.5% ~ 19% ~ 28% → overall incidence ~ 9%
40% of these were polymicrobial for the NCP group mortality was 71% cf. 29% in the non-pneumonia group the use of antibiotics selects out resistant Pseudomonas and MRSA Salata ARRD 1987
51 intubated ICU patients effectiveness of tracheal aspirate to distinguish colonisation from infective pneumonia
Nosocomial pneumonia
PMN's >1 > 10/hpf > 30,000/µl > 1+ > 1-10/oil field > 100,000 > 1-5% of PMNs +'ve 52% gram(-) < 10/hpf
< 2+
Bacteria CFU ICF organisms Elastin Fibres Squamous cells
< 2+ < 100,000 < 1% +'ve 9% > 10/hpf
ICU Respiratory
Johanson ARRD 1982
ventilated animal study of diagnostic tools
TA BAL PSB needle Bx
80% 74% 40% 50%
60% ?30% ?60% ?50%
1 1
100% 80% 70% 100%
40% 100% 100% 60%
1 2
Richard, ICM 1988, suction samples (LRS) versus PSB (< 10 CFU) Higuchi, ARRD 1982, primate model of acute lung injury ± pneumonia Chastre, ARRD 1984, PSB versus immediate post-mortem histology
Kirkpatrick, ARRD 1988, 8 "normal" subjects studied with BAL & PSB looking at the sterility of the samples, ie. contamination of the specimen 1. 2. PSB BAL = 7/8 = 1/8 but < 10 4 CFU
Gassorgues, ICM 1989, BAL vs PM in 13 intubated patients → BAL 100% sensitive but 75% specific
ICU - Respiratory
Chastre & Fagon AJM 1988
BAL vs. PSB in 21 intubated ICU patients, a. b. c. d. "both useful and complimentary" in diagnosis BAL → +'ve gram stain with intracellular bacteria > 25% PMN's rapid and useful WCC and semi-quantitative cultures (> 10 4 CFU) less useful PSB → > 103 CFU useful in diagnosis but results delayed 48 hrs - ie. lower sensitivity PSB gives higher false negatives supported by below AJRCCM 1995
prospective post-mortem study of diagnostic tool efficacy in diagnosis of VAP histology & culture performed within 30 min of death in 38 patients ventilated > 72 hrs a. b. histology (+) culture (+) - 18/38 patients - 12/18 patients ~ 47% ~ 32% definite VAP
Threshold1 CPIS mini-BAL BAL PSB BBS
Sensitivity % 72 67 58 42 83
Specificity % 85 80 95 95 80
>6 > 10 cfu/ml > 104 cfu/ml > 10 cfu/ml > 10 cfu/ml
4 3 3
Figures for definite VAP, ie histology & culture positive
conclusions, 1. 2. 3. as BBS is more sensitive & non-invasive, ∴ preferrable to PSB due to low sensitivity, results of a negative PSB should be viewed with caution overall diagnostic accuracy was greatest for BBS/BAL at 81%
(Clinical Pulmonary Infection Score)
CPIS, Pugin et al., ARRD 1991 1. 2. 3. 4. clinical biological radiographic microbiological
- temp., quantity & character of tracheal asp. - WCC, PaO2/FIO2 ratio - CXR
ICU Respiratory
Bonten et al. AJRCCM 1995
evidence for a causal relationship between gastric colonization and VAP based on studies relating colonisation to species causing pneumonia Torres et al., ARRD 1993 1. 2. 3. 4. VAP diagnosed by clinical criteria no chronological relationship established gastric pH values determined only once daily by indicator slide test no studies used double-blind PRCT study *poor sensitivity/specificity
PRCT of 141 patients, of whom 112 had continuous gastric pH monitoring a. b. group 1 group 2 58 54 - antacids, (Al/Mg-OH), 30 ml q4h - sucralfate 1g q4h
NB: no significant differences in median pH values stratifying patients by colonization, a. b. median pH values were higher in patients with gastric bacterial colonization no difference seen for oropharyngeal or tracheal colonization
ventilator associated pneumonia, a. b. c. diagnosed by BAL (> 104 CFU) / PSB (> 10 3 CFU) occurred in ~ 22% → same in both groups 51 isolates ~ 96% ~ 75% ~ 31% polymicrobial in 19/31 episodes → i. prior tracheal isolation ii. prior oropharyngeal isolation iii. prior gastric isolation
NB: in one case the organism resulting in VAP initially colonized the stomach, in five cases, colonization occurred simultaneously this is supported by Inglis et al., Lancet 1993, who showed chronological colonization from stomach to trachea in only 6/100 ventilated patients enteral feeding, a. b. c. d. did not alter gastric acidity increased gastric colonization with Enterobacteriaceae no change in oropharyngeal or tracheal colonization confounding factor of ↑ gastric volume controlled
NB: gastric acidity influenced gastric colonization, but not colonization of the upper respiratory tract or the incidence of VAP
ICU - Respiratory
ICU Pneumonias
1. 2. early onset ≤4 days nosocomial, or late onset
the incidence of ICU acquired pneumonia ~ 21% and ~ 54% of these occur within the first 4 days risk factors include, a. b. c. impaired airway reflexes severity of underlying pathology duration in ICU
Early Onset Pneumonia a. b. c. occurs within 4 days is very common is unrelated to - age - type of illness - immune suppression
d. e. f.
frequently oropharyngeal pathogens mainly in intubated patients little affected by antibiotic prophylaxis
Late Onset Pneumonia a. b. c. usually gram (-)'ve pathogen frequently impaired airway reflexes should (?) be influenced by antibiotic prophylaxis
ICU Respiratory
a. airways - trauma - tumour - infection - FB - trauma - tumour, 1° or 2° - infection, inflammation/vasculitis, infarction - LVF, MS - pulmonary emboli, infarction - pulmonary AVM
Def'n: massive haemoptysis, defined arbitrarily as blood loss, 1. 2. 3. between 200-600 ml expectorated per 24 hours, or resulting in acute airway obstruction, or resulting in acute hypotension
more than 90% of cases are due to chronic infection, as inflammation leads to profuse vascularisation of the high pressure bronchial circulation the most common causes are, 1. 2. 3. TB bronchiectasis / pulmonary abscess bronchial neoplasms ~ 15-20%
resections for haemoptysis > 600 ml/24 hrs carry a high mortality rate this is better than conservative management, which averages up to 75% surgery is probably indicated in those patients who, a. b. c. require multiple transfusion show progressive deterioration of pulmonary function continue to bleed despite adequate medical management
surgery is probably contra-indicated in those patients who, a. b. c. d. have inoperable bronchial carcinoma fail to have their bleeding site localised have severe bilateral pulmonary disease have severe debilitating systemic disease
ICU - Respiratory
most patients should have a rigid bronchoscopy, due to the greater ease of ventilation and suctioning upper lobe bleeding may require the use of a flexible scope moderate bleeding may be controlled through the bronchoscope prevention of soiling of the innocent lung may be achieved by the use of a bronchial blocker, such as a balloon-tipped Fogarty catheter, or DLT intubation if the patient is deemed inoperable, then bronchial embolisation may be attempted Anaesthesic Principals 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. preoxygenation and ventilation with 100% O 2 several large bore IV canulae should be inserted the patient should be cross-matched + baseline FBE the patients coagulation profile should be checked antibiotics should be commenced preoperatively adequate suctioning should be available on induction the bleeding lung should be dependent, and anti-aspiration measures should be employed alternatively, in the patient with massive haemoptysis, an awake, semi-upright intubation may be required separation of the two lungs, - DLT - SLT + bronchial blocker IPPV + PEEP - with regular intermittent suctioning
NB: after the airway is secured and the lungs separated, the bleeding lung should be in the non-dependent position patients are frequently hypovolaemic, therefore induction should follow adequate volume replacement and should be achieved with either a small dose of STP or ketamine, or alternatively use narcotics if a SLT is already in place, consideration should be given to, a. b. c. replacing it with a DLT the addition of a bronchial blocker endobronchial intubation
ICU Respiratory
Aetiology a. b. c. d. e. f. g. h. i. j. idiopathic infective circulatory inflammatory / autoimmune neoplastic industrial / occupational diseases iatrogenic metabolic congenital physical - drug induced, radiation, O2 toxicity
Differential Diagnosis a. infective pneumonias i. community acquired typical atypical uncommon
hospital acquired
- Streptococcal - Haemophilus - influenza, parainfluenza - mycoplasma, Legionella, Chlamydia - other viruses - Coxiella - TB - fungi - Pneumocystis - Brucella - Leptospirosis - Syphilis - MRSA - gram (-)'ves - staphylococcal, MRSA - anaerobes - fungi ± DIC
ICU - Respiratory
c. occupational diseases i. pneumoconioses - asbestosis, silicosis, berylosis, coal workers disease ii. zoonoses iii. chemical pneumonitis neoplasms - bronchogenic carcinoma - alveolar cell carcinoma - lymphomas, leukaemias - metastatic carcinomas, lymphangitic carcinomatosis - cystic fibrosis - α 1-antitrypsin deficiency - uraemia - hypercalcaemia - haemosiderosis - irradiation - heat, thermal - oxygen toxicity - blast injury - LVF - mitral stenosis - thromboembolic disease - bacterial endocarditis
e. f.
congenital metabolic
immunological i. hypersensitivity allergic alveolitis drugs ii. autoimmune
- farmer's lung, bird fancier's lung - SLE, RA, scleroderma, polyarteritis nodosa - Wegener's granulomatosis - dermatomyositis/polymyositis - Goodpasture's synd. - adriamycin, bleomycin, busulphan, cyclophosphamide - hydroxyurea, methotrexate, mitomycin - amiodarone, acetylsalicylic acid, chlorpropamide - carbamazepine, hydralazine, penicillamine - phenytoin, lignocaine, methadone, heroine - paraquat
drugs i. cytotoxic agents ii. non-cytotoxics
iii. k.
idiopathic idiopathic pulmonary fibrosis familial pulmonary fibrosis sarcoidosis alveolar proteinosis amyloid
ICU Respiratory
Causes of Infective Pneumonias
a. viruses - influenza A & B, parainfluenza - CMV, RSV, varicella - rhinoviruses, adenoviruses, enteroviruses - Staphlococci* *aerobic - Streptococci* - Micrococci - anaerobic - Branhamella, Acinetobacter - Bacillus, Lactobacillus - Clostridia - Nocardia - Haemophilus - Klebsiella - Legionella - E. coli - Enterobacter, Proteus, Serratia - Pasteurella, Yersinia, Citrobacter - Salmonella, Shigella - Bacteroides - Fusobacterium - Pseudomonas - Bordetella - Brucella - Mycobacterium tuberculosis, M. kansii * obligate intracellular parasites - Coxiella burnetti - Mycoplasma pneumoniae - Chlamydia psittaci - Aspergillus niger, Aspergillus fumigatus - Candida albicans, Cryptococcus - Histoplasma - Coccidioides - Sporotrichium - Blastomyces - Pneumocystis (rRNA ? fungal phylogeny) - Toxoplasma - Entamoeba - Strongyloides, Ascaris lumbricoides - Toxocara carnis (visceral larva migrans) - Echinococcus (hydatid disease) - Schistosomiasis (blood fluke) - Paragonomiasis (lung fluke)
bacteria i. gram (+)'ve cocci
ii. iii.
gram (-)'ve cocci gram (+)'ve rods
gram (-)'ve rods
v. c.
obligate anaerobes acid fast bacilli
cell wall deficient bacteria
fungi yeasts dimorphic
ICU - Respiratory
Environmental Factors
a. minerals - silicon, asbestos - beryllium - coal, bauxite - diatomaceous earth, talc - iron, barium, silver, tin - manganese, vanadium - nitrogen dioxide - chlorine, bromine - ammonia - phosgene, sulphur dioxide - acetylene, kerosene, carbon tetrachloride, hydrogen fluoride - hydrochloric, nitric, picric acids - Farmer's lung - pigeon fanciers lung - humidifiers, air-conditioners - maple bark, wood pulp, oak - mushroom, malt, sugar cane - furrier's - detergents, vineyard sprayers - fish, cheese, wheat weevil - hydrallazine - busulphan, bleomycin, methotrexate - nitrofurantoin, sulphas - methysergide - amiodarone - paraquat - petroleum derivatives
ICU Respiratory
Investigation Stage 1 a. history i. age, family history ii. drugs, smoking, allergies iii. occupation, pets / animals, hobbies, environment iv. personal contacts, friends / relatives v. overseas travel vi. nature, severity and time course of symptoms vii. past medical history - esp. CVS / RS examination i. upper & lower respiratory tracts amount & type of sputum presence/severity of respiratory failure ii. cardiac bruits/failure iii. vital signs iv. liver/spleen size, lymph nodes v. fundi vi. skin manifestations - purpura, erythema
Investigation Stage 2 a. b. FBE, ESR blood film i. RBC's: ii. WBC's: U,C&E's, LFTs blood cultures sputum - M, C & S - cytology - AFB micro and culture - M, C & S - sediment examination for active changes - haematuria anaemia, haemolysis, agglutination left shift, eosinophilia, blasts
c. d. e.
g. h. i.
CXR ECG Echo
ICU - Respiratory
Investigation Specialized 1. blood i. paired serology viruses, Legionella, Q fever, Chlamydia, Mycoplasma and fungi/parasites ii. cold agglutinins iii. HTLVIII / HIV Ab titre iv. autoantibodies - RF, SLE, cANCA, Goodpastures, ENA v. coagulation profile - INR, APTT, FDP's, fibrinogen vi. protein electrophoresis - immune complexes, myeloma - α1-antitrypsin deficiency sputum i. Ziehl-Neilson stain & culture for AFB's ii. immunofluorescence microscopy - Legionella - Influenza iii. silver stain - Pneumocystis * 3% saline induced sputum iv. wet preparation - parasites → - yeasts → nasopharyngeal washings mantoux skin test viral cultures faecal specimens (x3-6) PA catheter echocardiogram - throat swabs - faecal and sputum samples - micro - culture → → protozoan cysts, ova bacterial, viral - viruses
ova, cysts, larvae hyphae
3. 4. 5. 6. 7. 8.
- exclude / confirm LVF - SBE → low sensitivity, ∴ use TOE - atrial myxoma - LV function, valvular competence - liver / spleen / kidneys - fluid collections, abscesses - tumours - abscess, tumour - lymphadenopathy, mediastinal masses - CT directed biopsy - moderate ability to differentiate pathology
CT chest & abdomen
fine-cut CT chest
ICU Respiratory
11. bronchoscopy i. brushings
ii. iii. iv.
washings bronchiolar lavage biopsy
- MC&S - cytology - differential WCC - as above - MC&S - effector cell type & count - tumours - asthma - transbronchial lung biopsy
open lung biopsy, if i. diagnosis remains unclear after the above ii. the condition deteriorates despite empirical treatment iii. prior to a trial of immunosuppressives or steroids iv. no other (more accessible) organ is involved in the disease → - MC&S - M&C for AFB's - histopathology & frozen section - silver stain for Pneumocystis - immunoflorescence for Legionella - MC&S - cytology - biochemistry, pH, LDH, protein - autoimmune diseases - Goodpasture's - metastatic carcinoma - myeloma leukaemia, lymphoma - TB culture
pleural fluid
14. 15.
renal biopsy bone marrow biopsy
ICU - Respiratory
Interstitial Pneumonitis
a. b. c. idiopathic interstitial pneumonitis familial pulmonary fibrosis autoimmune diseases - rheumatoid arthritis, SLE - Wegener's granulomatosis, Goodpastures syndrome - scleroderma, polyarteritis nodosa, dermatomyositis
d. e. f. g.
sarcoidosis alveolar proteinosis congenital pneumoconioses - cystic fibrosis - α1-antitrypsin deficiency - silicon, asbestos - beryllium, coal, bauxite - diatomaceous earth, talc - iron, tin, barium, silver, manganese, vanadium - nitrogen dioxide, chlorine, bromine - phosgene, ammonia, sulphur dioxide - acetylene, kerosene, carbon tetrachloride, hydrogen fluoride - hydrochloric acid, nitric, picric acids - farmer's lung, bird fanciers lung - maple bark, wood pulp, oak - mushroom, malt, sugar-cane - furrier's, detergents, vineyard sprayers - humidifiers, airconditioners, etc. - hydrallazine, methotrexate - busulphan, bleomycin, nitrofurantoin - methysergide, amiodarone - sulphur derivatives
chemical pneumonitis
extrinsic allergic alveolitis
drug-induced intrinsic allergic alveolitis
Interstitial Pneumonitis 1. 2. 3. 4. 5. infective pneumonia atypical pneumonia malignancy
*Common Causes
lymphangitis carcinomatosis chronic LVF
ICU Respiratory
Upper Lobe 1. 2. 3. 4. 5. 6. S C H A R T → SCHART
- silicosis (progressive massive fibrosis) - sarcoidosis - coal workers pneumoconiosis - histiocytosis X - ankylosing spondylitis, aspergillosis - radiation - TB → RASIO
Lower Lobe 1. 2. 3. 4. 5. R A S I O
- rheumatoid arthritis - asbestosis - scleroderma - idiopathic - other - busulphan, bleomycin, amiodarone, methotrexate
ICU - Respiratory
Def'n: clinical syndrome of pulmonary & systemic embolic features, associated with a predisposing cause for bone marrow/fat emboli Aetiology a. b. c. pelvic, or long bone fractures orthopaedic surgical procedures hyperlipidaemic states ~ 100% have emboli ~ 5% develop FES ~ 60% have emboli - FES rare - pancreatitis - diabetes mellitus - lipid infusions - hepatic failure or trauma - SLE ? nephrotic syndrome - crush injury - bends - liposuction - lymphography - external cardiac massage - poisoning - sickle cell crisis - extracorporeal circulation
adipose trauma
NB: for (c-e) the majority of these, the finding is usually a post-mortem one, they rarely result in clinicaly significant FES
Massive Fat Embolism distinct from FES, with the clinical picture being that for any massive embolic syndrome this may be exaggerated by platelet aggregation and granule release lethal dose of fat for an average adult estimated at ~ 50-70 ml cf. the volume of fat contained in the femur ~ 70-100 ml
ICU Respiratory
Clinical Features NB: 1 major and 3 minor criteria are as sensitive & specific as any laboratory test a. major features i. petechial rash
ii. iii.
- chest, neck, palate, retina ~ 25-50% this is the only feature pathognomic of FES usually appears on 2nd-3rd days and lasts 2-3 days respiratory dysfunction arterial hypoxaemia & bilateral CXR infiltrates CNS dysfunction drowsiness, confusion, convulsions, coma * unrelated to head injury or other cause
minor features i. tachycardia ii. pyrexia - 38°-39°C ~ 60% iii. FBE - sudden fall in [Hb] - sudden thrombocytopaenia - high ESR iv. fundi - fat emboli, petechial haemorrhages v. urine - anuria, oliguria - fat globules vi. sputum - fat globules
Laboratory Investigations 1. 2. 3. 4. 5. 6. arterial hypoxaemia fat globules - blood, urine or sputum * nonspecific and may occur in other conditions
haemolytic anaemia thrombocytopaenia hypocalcaemia elevated serum lipase
Management heparin, aspirin, glucose, steroids & aprotinin do not alter incidence or mortality therapy is largely supportive once established all long bone fractures should be immobilized early
ICU - Respiratory
Def'n: Asthma: ≥ 15% δ 1 with FEV - bronchodilators - methacholine, histamine challenge
Chronic bronchitis: morning cough with sputum production for > 3 months of the year for 2 successive years, in the absence of any underlying disease which may account for these symptoms Emphysema: abnormal, permanent enlargement of the airways distal to the terminal bronchiole, with destruction of their walls and without obvious fibrosis (ATS), or diminished gas transfer interface (area), ↓ DLCO Smoking 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. produces both chronic bronchitis & emphysema, but little reversible airways disease impaired ciliary function & sputum clearance immunoparesis ↑ frequency of upper & lower respiratory tract infections ↑ COHb nicotine - chronic tissue hypoxia - polycythaemia - hypertension, ↑ SAP & DAP, ↑ PVR
accelerated atherosclerosis ↑ platelet adhesiveness major risk factor for ischaemic heart disease increased peripheral vascular disease increased bronchogenic carcinoma > 10 pkt/years (1 pkt/yr = 20/d)
ICU Respiratory
Exacerbation of CAL a. respiratory infection - bacterial, viral, fungal aspiration bronchospasm pneumothorax trauma, surgery neoplasm air pollutants cardiac AMI LVF, pulmonary oedema pulmonary emboli arrhythmia drugs sedatives, opioids anaesthetics muscle relaxants metabolic fever sepsis pancreatitis hyperthyroidism electrolytes low K+, Mg ++, PO 4= metabolic alkalosis other malnutrition high CHO intake depression of hypoxic drive
ICU - Respiratory
Acute Respiratory Failure
a. b. hypoxaemia pulmonary
- organ ischaemia / infarction - mental confusion, agitation - infection - aspiration - barotrauma - fibrosis - pulmonary emboli - hypertension, tachycardia, arrhythmias - late hypotension, bradycardia, QRS prolongation, EMD - altered organ perfusion - anxiety, distress - acute psychosis - obtundation, coma - ↑ ICP - acute renal failure - salt & water retention - pneumoperitoneum - ileus, gastric dilatation - acalculous cholecystitis - mucosal atrophy (TPN) - malnutrition - muscle wasting - nosocomial pneumonia - bacteraemia, septicaemia
e. f.
renal GIT
g. h. i.
nutritional microbiology
technical i. IV access ii. mask CPAP iii. intubation iv. mechanical ventilation v. PA catheter problems drug side effects i. steroids ii. antibiotics iii. aminophylline iv. β-agonists
ICU Respiratory
Clinical Presentation 1. pulmonary i. bronchial obstruction
- collapse - pneumonia, abscess, empyema - emphysema
ii. iii. iv. v. vi. vii. viii. 2.
pleural effusion bleeding / haemoptysis SVC obstruction Horner's syndrome brachial plexus or T1 lesion recurrent laryngeal nerve or phrenic nerve palsy incidental lesion on CXR
metastatic disease i. bone pain, pathological fracture, hypercalcaemia ii. hilar and cervical lymphadenopathy iii. cerebral iv. adrenal paraneoplastic i. cachexia ii. anaemia of chronic disease iii. hypertrophic osteoarthropathy iv. v. vi. neuropathy myopathy skin lesions
- finger clubbing - arthritis, periosteal new bone - carcinomatous myopathies - Eaton-Lambert syndrome - pigmentation, erythema - scleroderma, acanthosis nigrans - herpes zoster, herpes simplex
endocrine ectopic ADH ectopic PTH ectopic TSH ectopic ACTH carcinoid syndrome gynaecomastia viii. haematological
→ → → →
SIADH hypercalcaemia thyrotoxicosis Cushing's syndrome
- aplastic anaemia - thrombophlebitis - DVT's
ICU - Respiratory
CXR a. b. c. d. e. f. changes usually antedate symptoms by ~ 7 months symptoms → abnormal CXR ~ 98% further, the changes are suggestive of tumor in ~ 80% ~ 70% are centrally located at presentation, average size is ~ 3-4 cm other important diagnostic features include, i. tracheal deviation/obstruction ii. mediastinal mass - SCV, PA, main bronchi iii. pleural effusions iv. cardiac enlargement v. bullous cyst - rupture, compression vi. air-fluid levels ? abscess, soiling vii. parenchymal changes - V/Q inequality
Inoperability of Bronchial Carcinoma 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. distant metastases malignant pleural effusion recurrent laryngeal nerve involvement phrenic nerve involvement regional lymph nodes within 2 cm of the hilum high paratracheal, or contralateral hilar spread SVC syndrome PA involvement cardiac tamponade bilateral disease - brain, liver, adrenals & bone
NB: operability also depends upon cell type, unilateral or pleural spread may be operable with less invasive cell types
ICU Respiratory
Pneumonectomy Assessment
Test Type Whole-Lung Tests PFT AGB's Spirometry Risk Limits for Pneumonectomy hypercapnia on room air FEV1/FVC ≤ 50% FVC ≤ 2.0 l MBC ≤ 50% RV/TLC ≥ 50%
Lung volumes Single Lung Tests Simulated Pneumonectomy Split function tests (R&L) Balloon occlusion R/L PA
predicted FEV1 ≤ 0.85 l PBF > 70% diseased lung mean PAP PaCO2 PaO2 ≥ 40 mmHg ≥ 60 mmHg ≤ 45 mmHg
ICU - Respiratory
Def'n: RV enlargement 2° to thoracic, lung or pulmonary vascular disease, in the absence of congenital, or left sided heart disease; *RV failure is not required for the diagnosis right heart failure is defined as a chronic increase in the RV end-diastolic transmural pressure gradient, that is not expected from an increase in pulmonary blood flow (HPIM, 12th Ed) Aetiology 1. pulmonary vascular disease primary pulmonary hypertension chronic multiple emboli pulmonary vasculitis chronic parenchymal lung disease CAL diffuse interstitial lung diseases lung pump failure kyphoscoliosis neuromuscular diseases morbid obesity central drive failure obstructive sleep apnoea syndrome chronic mountain sickness
Pathogenesis NB: may be either - acute or chronic - episodic or progressive RV dilatation RV hypertrophy, later dilatation
a. b.
acute chronic
→ →
initially PAH occurs only during exercise or during stress this is accompanied by episodic RV dilatation with normal RVEDP and RV output later, persistent PAH leads to RV hypertrophy ± dilatation this is associated with sustained high RVEDP's and RVF, initially during exercise but later at rest
ICU Respiratory
Mechanisms a. b. loss of vascular bed irreversible pulmonary vasoconstriction i. chronic hypoxia ii. chronic acidosis pH < 7.2 iii. chronic hypercapnia
Exacerbating Factors 1. 2. 3. 4. 5. 6. 7. 8. progression of 1° lung disease intercurrent respiratory infection pulmonary emboli cardiac decompensation sedative & analgesic drugs ↑ work of breathing hypercatabolic states surgery - resistance (bronchospasm) - compliance - surgery, trauma - endocrine - pulmonary resection - upper abdominal/thoracic - arrhythmias - RV ischaemia
Signs a. stigmata of chronic lung disease - nicotine stains - dyspnoea, tachypnoea - central cyanosis - clubbing, skin changes - asterixis - RV thrust ± palpable P 2 - loud P 2 & wide split S2 - RV-S 4 - TI - recurrent SVT, MAT - high JVP - peripheral oedema - ascites, hepatomegaly
RV hypertrophy
RV failure
ICU - Respiratory
Symptoms a. b. c. d. e. f. those of chronic bronchitis / emphysema dyspnoea tiredness, fatigue, decreased exercise tolerance peripheral oedema palpitations daytime somnolence - AF - OSAS
Investigations a. b. c. FBE, ESR - polycythaemia, anaemia chronic disease - ↑ WCC, left shift
EC&U, LFT's, AGA ECG - P pulmonale - RVH (qv), RAD, RBBB - sinus tachycardia, AF, MAT RVH on ECG is rare except in primary pulmonary hypertension 'q'-waves in II, III, aVF may simulate AMI due to vertically placed heart - lung disease with large PA's - peripheral field oligaemia - usually no LVF or cardiomegaly - obstructive | restrictive components ± reversibility - dilated RV ± TI - to exclude chronic PE
e. f. g.
PFT's Echo V/Q Scan
Complications 1. 2. 3. 4. 5. 6. 7. 8. acute respiratory failure recurrent respiratory infections chronic hypoxia polycythaemia right heart failure arrhythmias sudden death cirrhosis (1° PAH)
ICU Respiratory
Treatment a. b. treat primary lung disease & cease smoking optimise remaining lung function i. lose weight ii. bronchodilators iii. steroids iv. diuretics v. antibiotics vi. physiotherapy prompt treatment of chest infections prevent pulmonary emboli respiratory stimulants (aminophylline) improve cardiac function i. digoxin ii. antiarrhythmics iii. diuretics pulmonary vasodilators i. nitric oxide ~ 10-40 ppm ii. PGI2 ~ 5-35 ng/kg/min expensive pulmonary & systemic vasodilator PA catheter required for monitoring noradrenaline 1 µg/min can be used to overcome the systemic vasodilation side effects include systemic vasodilatation, hypotension and nausea some units are now using this via the inhaled route iii. adenosine ~ 50-500 µg/kg/min iv. GTN v. ACEI vi. β2-agonists - isoprenaline ? dopexamine ++ vii. Ca entry blockers heart/lung transplantation
c. d. e. f.
ICU - Respiratory
Clinical Features 1. 2. 3. 4. 5. 6. marked obesity hypersomnolescence periodic breathing central and obstructive apnoea pulmonary hypertension cor pulmonale ± RF failure - especially daytime
Diagnostic Investigations 1. 2. 3. 4. hypercapnoea hypoxia polycythaemia depressed ventilatory response to CO2 & O2 - especially night-time / sleep studies
1974 ↓ FRC ↓ VC ↓ MBC (MVV) ↓ lung and chest wall compliance ↓ respiratory muscle efficiency - V to apices - Q to bases ~ 100-400%
common mechanical and circulatory factors in morbid obesity, a. b. lung volumes lung function
~ 30%
c. d. e. f.
↑ V/Q mismatch ↑ cardiac output pulmonary hypertension
↑ pulmonary and systemic blood volume
NB: these changes are proportional to the degree of obesity
ICU Respiratory
Leech 1987
multiple regression analysis of factors associated with hypercarbia and sleep apnoea, (p < 0.05) a. b. c. d. obesity ↓ FVC & FEV1 daytime hypoxia - height/weight ratio - absolute volume changes, cf. predicted PaO2 < 70 mmHg
severity of desaturation during sleep apnoeic periods
factors with poor, or no association, a. b. c. d. age FEV1/FVC ratio the P A-aO2 gradient - ie. airflow obstruction the number of sleep induced respiratory events
the syndrome is multifactorial, 1. 2. 3. chronic hypoxia ↑ work of breathing altered O2 / CO2 drives
Aetiology suggested factors include, a. b. c. d. e. f. ↑ weight → ↑ mechanical load *not supported by Leech above obstructive airways disease central sleep-apnoea ↑ V/Q mismatch, shunt and dead space impaired respiratory control mechanisms, ie. O2/CO2 drive
impaired respiratory mechanics & muscle function
ICU - Respiratory
Total compliance Lung compliance V/Q, Shunt
Simple Obesity
slight fall 25% fall increased mismatch
30% fall 40% fall large mismatch < 40% shunt 300% increase ↑↑ VO2 >> ↑ work 300-400% decrease
Work of breathing VO2 cost of breathing Diaphragm response to ↑ PaCO2
30% increase ↑ VO2 ~ ↑ work increases
Effects of weight-loss on the following variables
PaCO2 VC MBC Apnoeic periods Level of desaturation no change increase increase decrease improved decreases marked increase increase marked decrease markedly improved
ICU Respiratory
Sampson, Grassimo 1983
during quiet breathing there is little difference in the following parameters, a. b. c. d. VT, VC, TLC, FRC, RV, ERV, FEV 1/FVC, and RR ABG's mouth occlusion pressure age, sex, weight however, during hypercapnoeic rebreathing,
( l/min/mmHg-CO 2)
3.5 0.5-0.6 25%
1.83 0.91 23.8%
1.06 0.29 13.9% blunted
Mouth occlusion pressure
(cmH 2O/mmHg-CO 2)
Diaphragmatic EMG
(δ %/mmHg-CO 2)
normal or increased
Obesity Hypoventilation Syndrome lung volumes are similar in OHS/SO, ∴ it is unlikely that OHS relates solely to muscle weakness the slope of the CO 2-ventilation curve is altered, not shifted in a parallel fashion muscle diseases show a different pattern, with the diaphragmatic EMG showing the same pressure gradient the disease therefore, in summary, is a. b. multifactorial related to i. mechanical load ii. sleep apnoea iii. chronic hypoxia iv. altered central respiratory drive v. ? enhanced buffering of metabolic alkalosis
NB: represent a sub-group of obese patients, with probable pre-existing impaired central response to CO 2 and O2, in whom the added load of obesity results in chronic respiratory failure, ie. "non-fighters, unable to prevent CO2 retention"
ICU - Respiratory
NB: tension pneumothorax, from any cause but especially, 1. 2. 3. chest trauma barotrauma during mechanical ventilation obstructed pleural drains
Aetiology a. b. c. trauma surgery lung diseases - asthma - infections - emphysema - pulmonary infarction - bullous disease - CVC cannulation - tracheostomy - U-S/CT guided drainage/biopsy - bronchoscopy - thoracentesis - artificial ventilation - diving - aviation, training
ICU Respiratory
Def'n: an exudate is pleural fluid having one or more of the following 1. 2. 3. fluid:serum protein ratio fluid:serum LDH ratio absolute fluid LDH > 0.5 * protein > 30 g/l > 0.6 > 2/3 normal serum upper limit > 200 U/l
Transudative 1. 2. 3. 4. 5. 6. 7. CCF cirrhosis, ascites renal failure, nephrotic syndrome hypoproteinaemia peritoneal dialysis myxoedema Meig's syndrome + ascites & ovarian fibroma
Exudative 1. 2. 3. 4. 5. 6. 7. infectious inflammatory neoplastic pulmonary infarction traumatic drugs GIT - haemo/chylo-thorax - nitrofurantoin, methysergide - subphrenic abscess - oesophageal rupture - pancreatitis - collagen vascular disorders
8. 9. 10.
uraemia post-AMI other - asbestosis, DXRT
Management 1. 2. 3. full history and examination treat obvious cause thoracentesis ± pleural biopsy if suspected exudate
ICU - Respiratory
Appearance LDH absolute1 fluid:plasma Protein absolute fluid:plasma pH Glucose WCC (PMN's)
clear, cloudy, or bloody
clear < 200 < 0.6 < 30 < 0.5 > 7.2 > 2.2 mmol/l U/l
> 200 > 0.6 > 30 > 0.5 < 7.2 < 2.2
< 1,000 / ml
> 1,000 / ml
LIGW states < or > 1000 IU ??
Other Tests a. b. c. microbiology cytology "blood picture" i. eosinophilia ii. RBC's > 100,000 - M,C&S - stain & culture for AFB's - malignancy → ? drug induced - traumatic tap, trauma - malignancy - pulmonary emboli, infarction → - oesophageal rupture - pancreatitis - rarely in malignancy - high TG / low cholesterol ± high amylase + low C' & low glucose → collagen vascular disorder
amylase > 50-60 IU
e. f.
chylous ANA
NB: despite full evaluation, no cause will be found in ~ 25% of patients
ICU Respiratory
the thoracic duct starts as an extension of the cysterna chyli in the upper abdomen enters through the aortic hiatus and ascends extrapleurally between the aorta and azygous vein at the level of T5 , crosses to the left border of the oesophagous, ascending behind the aortic arch and subclavian artery it enters the venous system at the junction of the internal jugular and subclavian veins between 40-60% have anomalies of the course Aetiology a. b. c. d. e. congenital traumatic surgical infiltration or extrinsic compression thrombosis of the left subclavian vein - any thoracic procedure - rarely dissection of the neck *especially lymphoma
Biochemical Characteristics a. b. c. sterile, "milky" fluid amylase (+)'ve contents: - alkaline, pH ~ 7.4-7.8 - SG ~ 1012-1025 - pancreatic enzymes present total fat total protein albumin globulin glucose lymphocytes erythrocytes U&E's ~ ~ ~ ~ ~ ~ ~ ~ 4-60 g/l 20-60 g/l 12-41 g/l 11-30 g/l 3-11 mmol/l 400-6,000/µl 50-600/µl plasma
Treatment a. b. c. d. chest drain low fat diet TPN indications for surgical correction, i. drainage ≥ 1500 ml/d ii. failed conservative RX after 14 days iii. metabolic complications
ICU - Respiratory
Unilateral a. b. c. idiopathic congenital mediastinal mass - tumour, lymph nodes - thyroid, thymus - aortic dissection - cervical - surgical, post-CABG - interpleural, interscalene - stellate ganglion
d. e. f.
trauma local anaesthetics
features i. asymptomatic ii. small fall in VC iii. elevated hemidiaphragm on CXR iv. no movement on double-exposure CXR
Bilateral a. b. c. d. e. f. g. h. cervical cord damage motor neurone disease polyneuropathies poliomyelitis mediastinal tumour congenital "cryoanaesthesia" of phrenic nerves during open-heart surgery features i. paradoxical respiration ii. respiratory failure iii. large decrease in VC iv. failure to wean from IPPV after CABG
ICU Respiratory
Pulmonary Function Testing
reasons for performing PFT's include, 1. 2. 3. 4. identification of the type of lung disease quantification of the extent of lung disease determination of the response to therapy monitoring the rate of progression - obstructive vs. restrictive
the value of PFT's is most clearly demonstrated in those undergoing pulmonary resection for other surgery, there is little evidence of benefit as a routine screening technique, in the absence of clinical symptoms patients who may be considered for PFT's include, 1. 2. 3. 4. 5. 6. 7. patients with chronic pulmonary disease / symptoms heavy smokers with a history of chronic productive cough patients with chest wall or spinal deformities morbidy obese patients elderly > 70 years patients for thoracic surgery patients for major upper abdominal surgery
NB: the objective of testing is to predict the likelihood of postoperative complications, no single test is the best predictor of complications Hall et al. (Chest 1991) showed, 1. 2. 3. single best predictive factor was the ASA classification followed by site of incision - upper vs. lower abdominal age, smoking & obesity also ranked highly
NB: ASA grading may have in part been based on PFT's, but clinical assessment remains the best predictor a single spirometric study can provide FVC, FEV1/FVC, FEF25-75%, PEFR and VC "normal" limits are obtained from a sample population (Morris 1971) and the lower limit taken as 1.64 x SEE (SD of the regression line) below the same weight & height on the regression line this range should by definition include ~ 95% of the population the widely used practice of taking 80% of the predicted value should be avoided abnormalities on spirometry correlate with the incidence of postoperative complications however, the incidence and severity of postoperative complications do not correlate with the severity of the preoperative lung dysfunction
ICU - Respiratory
Clinical Spirometry 1. vital capacity VC effort independent, performed without concern for rapidity of exhalation decreases may be associated with restrictive lung disease, following excision, or from extrapulmonary factors, ie. chest wall disease forced vital capacity FVC during forced exhalation FVC < VC with significant dynamic airways closure principally disorders with increased airway resistance, or destruction of supporting architecture forced expiratory volume, 1 second FEV1 usually expressed as a percentage of FVC, where FEV 1/FVC > 80% largest observed FEV 1 and FVC from 3 readings are used, even if different curves reduced mainly by increased airways resistance, usually normal in restrictive defects forced expiratory flow, 200-1200 FEF200-1200 maximal expiratory flow rate MEFR peak flow can be measured by drawing a tangent to the steepest part of the curve more commonly the average flow over 1000 ml, after the initial 200 ml of exhalation is used this is slightly lower than the true peak flow, normal values > 500 l/min values < 200 l/min are associated with impaired cough & postoperative sputum retention, atelectasis and infection markedly impaired by obstruction of larger airways & responsive to bronchodilator therapy results are extremely effort dependent forced midexpiratory flow, 25-75% FEF25-75% maximal midexpiratory flow rate MMFR less effort dependent than PEFR, as avoids the initial highly effort dependent part of the expiratory curve however, still affected by patient effort and submaximal inspiration values in healthy young men ~ 4.5-5.0 l/s (300 l/min) abnormal values < 2 l/sec (120 l/min) initially thought to be more sensitive in detecting small airways disease cf. FEV1, but this has not been supported MBC
Maximum Breathing Capacity
patient is instructed to breath as hard & fast as possible for 12 seconds extrapolated to 1 minute, expressed as l/min, normal ~ 150-175 l/min predominantly affected by increased resistance & correlates well with FEV1 (MBC ~ FEV 1 x 35) 80% of MBC can be maintained for ~ 15 minutes affected by patient cooperation & effort
ICU Respiratory
Respiratory Muscle Strength 1. 2. PImax PEmax ~ -125 cmH 2O < -25 cmH 2O reflects inability to take an adequate inspiration ~ 200 cmH 2O < 40 cmH2O reflects inability to cough
Airway Resistance using a body plethysmograph, panting against a closed then open shutter, 1. 2. 3. shutter closed shutter open → → → Boyle's law & lung volume RAW calculated from δ and flow V GAW = 1/RAW
specific airway resistance and conductance are calculated for the given lung volume
NB: a mouthpiece is used to remove the effects of the upper airway, panting is used to keep the larynx dilated in ventilated patients, may use peak to plateau δ / instantaneous flow at P pAW P bi-exponential decay from PpAW to plateau, 1. 2. first phase due to airways resistance second phase due to "stress relaxation"
Alveolar-Arterial Oxygen Gradient normal gradient on room air ~ 8 mmHg → increasing with age ~ 25 mmHg at 70 yrs increased commonly in smokers & mild early chronic bronchitis Frequency Dependent Compliance Def'n: abnormal where CDyn < 80% of CStat decreases early with small airways obstruction both measurements require insertion of an oesophageal balloon, with flow measured by a pneumotachograph, 1. 2. CStat. - inspiratory slope of a static pressure volume curve at tidal volume CDyn - δ PIP V/δ
ICU - Respiratory
Flow Volume Loops differentiation of intrathoracic / extrathoracic obstruction the entire inspiratory, plus the immediate expiratory portions of the curve are highly effort dependent ratio of expiratory flow:inspiratory flow at 50% TLC ~ 1.0 upper airway obstruction inspiratory flow is reduced disproportionately & EF:IF 50% > 1.0 other patterns described on flow-volume loops, 1. fixed obstruction no significant change in airway diameter during inspiration/expiration EF:IF 50% ~ 1.0, with both curves showing a flattened plateau variable obstruction i. extrathoracic - vocal cord paralysis - chronic neuromuscular disorders - marked pharyngeal muscle weakness - obstructive sleep apnoea syndrome accompanied by inspiratory stridor & flow resistance EF:IF 50% > 2.0 intrathoracic - tracheal & bronchial tumours - tracheomalacia - vascular rings, thoracic aortic aneurysm accompanied by expiratory airway compression & ↑ flow resistance inspiration may be normal, with EF:IF 50% < 1.0
NB: differentiation is most accurate in the absence of diffuse airways disease
Multiple-Breath Nitrogen Washout normal lung behaves as a single compartment, with a single exponential washout curve for N 2 there is a direct correlation between abnormal N 2 washout and frequency dependent compliance uneven distribution of time constants is believed to be the basis of both curve analysis is tedious, requiring computer analysis
ICU Respiratory
Single-Breath Nitrogen Washout originally described by Fowler in 1949, but adapted to, 1. 2. 3. 4. full inspiration from RV to TLC with 100% O 2 expired N2 concentration measured line of best-fit drawn through the alveolar plateau increase in [N2]/l quantified → δ 2 % per litre N i. normal ~ 2% / l ii. smokers ~ 10% / l iii. abnormal in ~ 50% of asymptomatic smokers, therefore sensitive index of early lung dysfunction poor specificity due to large number of asymptomatics who do not progress to CAL
the original technique by Fowler involved only 1000 ml O2 from FRC and due to preferential ventilation of the bases resulted in a steeper plateau Forced Expiratory Flow Rates difficulty defining abnormal flows at low lung volumes during expiration early flow resistance is in the large airways, where flow is predominantly turbulent comparative curves using He/O 2 show increased flow in the early expiratory phase as expiration continues, the site of resistance moves proximally toward the alveoli, where flow is predominanlty laminar, and unaffected by altered gas density (He) therefore, at some point, the volume of isoflow, the two curves rejoin with small airways disease, flow becomes less density dependent and the difference between maximum flow rates decreases, and the VisoV increases normal values for V isoV ~ 10-15% of VC values > 25% are abnormal
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