Respiratory Flashcards
Indications for Mechanical Ventilation
- Airway Support - threatened airway, impaired airway reflexes
- Respiratory Support - high FiO2 required
- Ventilatory Support - deep sedation, regulate CO2
Delivery of non-invasive ventilation
- High flow nasal O2 - humidified O2, 40-60L/min FiO2 up to 1.0.
- CPAP
- BiPAP
Advantages of HFNO
- Humidification - prevent epithelial injury, help secretions
- PEEP
- Greater FiO2 - less entrainment of atmospheric gas
- Reduced CO2 dead space - washout
CPAP
- Continuous application of positive pressure throughout respiratory cycle
- Nasal, facemask, hood
- Better recruitment, improved V/Q
- Cheap, well tolerated
BiPAP
- Ventilatory support by difference between IPAP and EPAP
- Facmask
- ECOPD, prevent post-extubation respiratory failure.
PEEP
Pressure present in airway above atmospheric pressure at end expiration
Recruitment of alveoli and prevention of collapse (therefore reduced WOB)
Other physiological effects
- Improved pulmonary compliance
- Reduced venous return and preload
- Increased afterload and PVR
- Increased ICP by reduced venous drainage
Characteristics of ventilator modes
- Control - pressure or volume
- Cyclying - flow, time, pressure
- Trigger - patient, machine
- breath type - mandatory or spontaneous
- breath sequence - mandatory, intermittent mandatory, spontaneous
- synchronisation - synchronised, independent
- guarantee - TV, MV, pressure
PCV
- Pinsp, PEEP, Ti
- VT depends on compliance
- pressure rapidly delivered and held constant - square wave pattern
- flow decelerates
- pressure rapidly released in expiration
- gas equilibrates between varying alveolar time constants
VCV
- VT, PEEP, RR, flow pattern set
- constant inspiratory flow - gradual rise in Pinsp
Pressure support
Pinsp, PEEP, expiratory flow trigger set
Ventilator cycling
- Time - mandatory modes, insp and exp determined by time
- flow - insp and exp commenced after sensing change in flow (patient attempts breaths)
- pressure
Special modes
ASV - adjusts support based on patient requirements. support delivered in response to RR and effort
NAVA - neural assist - electronic activity from diaphragm, monitored via specialist NG tube
SIMV - time cycled mode mandatory breaths may be machine or patient triggered. pressure or volume controlled. spont ventilation permitted at varying parts of the cycle
APRV - Airway Pressure Release Ventilation
Advanced ventilatory mode
Maximises alveolar recruitment - used when alveolar recruitment felt to be possible
P-high, Thigh, Plow (0) and Tlow
CO2 release at Plow
breath spontaneously
extreme inverse ratio
Ads - recruitment, lung homogeneity, reducing in cyclical opening and closing of alveoli
disads - high local pressure, tachypnoea, rv dysfunction
Indications for proning
Critical care
- mod-severe ARDS Pf < 150 (< 48hrs into disease after IPPV optimised) PROSEVA trial
Theatre
- surgical access e.g. spine, posterior fossa
Contraindications
Absolute
- open chest, <24h post cardiac surgery, central ECMO cannulas, unstable spine
relative
- severe CVS instability, pregnancy, recent tracheostomy, significant trauma
Risks of proning
Instability
- airway dispalcement
- line displacement
- increased into abdominal pressure
- reflux and aspiration
Patient injury
- pressure sores
- brachial plexus
- periorbital oedema, chemises, blindness
Staff injury
How to prone
Pre-procedure
- MDT decision
- check with nurse in charge senior doctor re. timing
- ensure any procedures that require supine position carried out
- system assessment e.g. airway position, suction. 100% O2. stop non-essential infusions
- eye / nipple protection, remove anterior ecg stickers
- spigot and aspiration NG tube
Procedure
- minimum 1 airway and 2 each side
- pillows to chest, iliac crests, knees
- sheet over top and roll edges (Cornish pasty)
- slide away from ventilator
- turn to 90 degrees
- complete prone
post-procedure
- re-assess A-E
- check pressure areas
- complete positioning e.g. swimmers, revers trendelenburg
- 2-4 hourly head turn and arm change
- document
conscious proning
covid. if fio2 > 28% or more than basic resp support
position change every 1-2 hrs - fully prone, right recumbent, sitting up 30-60 degrees, left recumbent
Types of extra-corporeal life support
- VV-ECMO
- VA-ECMO
- AV-ECMO (rare)
- ECCO2R
- Cardiopulmonary bypass
- VAD
VV-ECMO concept
Gas exchange in native circulation failed
an oxygenator incorporated into extra-corporeal circuit
oxygenation determined by circuit flow rate and post-oxygenator oxygen content. increased by increasing flow rate
co2 diffuses out through oxygenator determined by sweep gas flow rate. CO2 more soluble, diffuses more readily and maintains diffusion gradient. clearance therefore related to sweep gas rather than blood flow
conventional ventilation reduced to rest settings and allow healing of pathology
VV oxygenator flows limited to 5-6l/min (cannula size)
VV-ECMO indications
despite optimum conventional management: including trial of proning:
- hypoxaemic resp failure PF < 80
- hypercapnia resp failure pH < 7.25
“potentially reversible severe resp failure”
- ventilatory support as bridge to lung transplant
specific clinical conditions include
- severe ARDS
- BPF
- severe asthma
- thoracic trauma
VV-ECMO contraindications
Absolute
- anticipated non-recovery without a viable plan to decannulate
relative
CNS - haemorrhage, severe debilitating pathology, significant njury
refractory or established MOF
Haem - bleeding, inability to anticoagulant
IPPV > 7 days with plat pressure > 30 and fio2 > 90
older age
O2 delivery in VV ECMO
O2 content minimum 240ml.min
O2 delivery minimum 300ml.min
Arterial O2 is mixture of venous blood removed and passed through oxygenator and blood passing through lungs and is typically 80-90%
increasing circuit flow increased circuit:native and therefore total O2 content
Issues on VV ECMO
recirculation - post oxygenator blood returning to oxygenator and not systemic circulation (high venous saturations) more common with single lumen dual cannula access
hypoxaemia - increased VO2 e.g. sepsis, recircualtion. DO2 / VO2 5:1 increase flow
CO2 removal - sweep gas 1-9l/min in 100% O2
Chatter - partial venous cannula occlusion e.g. rhythmic ventilation, cough, valsava
suck down - intravascular volume restriction or cannula misplacement abrupt reducing flow to 1l/min with full pump speed - haemolysis, air embolism
high Paco2 - may be increased metabolic state, circuit problem, monitoring problem. can increase sweep gas flow
ECMO emergencies
gas embolism - clamp return line, clamp drainage line, switch off pump, remove air using syringe at oxygenator port
accidental decannulation - turn off pump, compress site, major haemorrhage, emergency recannulation
circuit failure - change
VV-ECMO cannulas
Single lumen dual cannula - IJ - fem
bicaval dual lumen single cannula - RA / IVC
bifemoral
Dual lumen single cannula improved mobility, needs fluoroscopy / echo guidance
Haemodynamics on VV ecmo
hypoxia, hypercarbia, acidosis lead to elevated PA pressures, rv dysfunction. implication
- vv ECMO no direct haemodynamic support - need to manage conventionally
- improved oxygenation and co2 clearance improves PA pressures, rv function, lv function
- reduced thoracic pressures due to lower IPPV settings may also improve haemodynamics
Rest ventilator settings
recommended PEEP 10 Pinsp 25 rate 10 FiO2 as low as possible e.g. 30%
CESAR / EOLIA settings
weaning ecmo
reduced circuit flow or reduce sweep gas FiO2 from 1.0 - 0.21
over hours - days
assess ventilatory reserve
ECMO scoring systems
RESP - predicted survival on ecmo
Murray - predicted mortality without ecmo
RESP -22 to 16. Class I > 6 92% in-hospital survival. class V < -6 18% survival
Murray
- consolidation (quadrants on CXR)
- compliance
- P/F ratio
- PEEP
Severe > 2.5
ECMO trials
CESAR
- improved outcomes from severe potentially reversible resp failure in those transferred to ecmo centre (not with use of ecmo) vs conventional
- advocates transfer to specialist centre - Murray Score > 3 pH < 7.25 on optimum mx
EOLIA
- severe ARDS
- VV-ECMO vs VCV (28% crossover)
- no difference in 60d mortality.
What is ventilator weaning?
- slowly reducing ventilator support over time, increasing patients own ventilatory drive and extubation
- may be minutes - months
Simple: liberation from ventilator on first attempt (70%)
Difficult - 2-7 days after initial assessment
Prolonged - > 7 days
Clinical assessment of readiness to wean
- Initial pathology resolved
- Patient condition optimised
A: cough / reflexes satisfactory, secretions manageable, cuff leak present
B: FiO2 < 40%, spont breathing, adequate strength, min PEEP
C: stable
D: obeying commands
Objective assessment of weaning
- RR < 30
- TV > 5ml/kg
- FVC > 15ml/kg
- MV < 15l/min
Max inspiratory pressure < 30cmH20 (resp muscle strength)
Rapid shallow breathing index = f/Vt (L) - some evidence for extubation with RSBI < 105 spring SBT
P0.1/PImax > 0.3 = negative airway pressure from first 0.1s of occluded inspiration
Describe spontaneous breathing trial
- screen for readiness to wean
- sedation hold
- 30 min trial of T piece or minimal CPAP +/- PS
- assessment of success or failure
- if well tolerated consider extubation
Criteria for failure
B: RR > 35, SpO2 < 90%, high WOB
C: HR > 140 or change > 20%, SBP > 180 or < 90
D: agitation
Problems with weaning difficulty
increased LOS, VAP, ICU-AW, mortality
extubation failure and issues
Causes of failure to wean
Resp
- secretions
- poor cough
- inappropriate ventilator settings
- resistance from ETT
- VAP / unresolved infection
- Pulmonary oedema
CVS - High myocardial workload
- metabolic demand
- unresolved CVS failure
- fluid overload
- anaemia
CNS
- delirium
- weakness
- pain
Other pathology e.g. burns, malnutrition
Indications / advantages for tracheostomy
Indications
- prolonged wean
- longterm / home ventilation
- airway toilet
- upper airway obstruction e.g. laryngeal, VC
Advantages
- patient comfort
- reduce sedation
- improved mouth care
- reduced airway oedema
- ability to phonate / VC mobilisation
- improved larnyngeal sensation / swallowing
Tracheostomy timing
multifactorial
TRACMAN study early < 4d late > 10 days no difference in high risk prolonged ventilation
Percutaneous tracheostomy insertion
Pre-procedure
- CI e.g. coagulopathy, high FiO2
- consent, MDT decision, NIC
- team allocation - airway / bronch, sedation e.g. nurse, procedurist
- equipment prep
- positioning, USS
- 100% O2, aspirate NG
Procedure
- asepsis, clean skin
- xylocaine / adrenaline
- airway person retracts ETT until cuff seen at cords
- needle, with cannula, syringe, saline 1/2 or 2/3 tracheal rings
- midline insertion aspiration until air
- thread cannula, remove needle
- check cannula with bronc
- pass guide wire
- check with bronchiole
- scalpel incision then serial dilators
- rhino dilator and leave in situ for a minute or two
- remove and pass tracheostomy
- inflate cuff, ensure ETCO2, remove oral tube
- 2 x sutures and secure in place with tie
post-procedure
- CXR
- wean sedation
- document
Complications of tracheostomy
immediate
- bleeding / haemorrhage
- failure
- pneumothorax / submit emphysema
- aspiration
- damage to local structures e.g. thyroid, RLN
- loss of airway
short term
- deterioration in ventilation
- infection
- obstruction
- displacement
- tracheostomy’s-innominate artery fistula
long term
- granuloma
- VC dysfunction
- dysphagia, dysphonia
- stenosis
When can a patient be decannulated?
- improving trajectory
- MDT opinion, nursing, physio
- tolerating cuff deflation for prolonged period of time e.g. 24hrs
- secretion burden manageable
- minimal O2 requirement
Causes of restrictive lung diease
Pulmonary
- ILD
- ARDS
- TB
- Lobectomy
Extrapulmonary
- Resp centre = drugs, trauma
- Neurological - polio, GBS
- Neuromuscular = MG
- Muscular = dystrophies
- Thoracic wall = obesity, kyphoscoliosis, rib fracture
- pleural = plaques, effusions, PTX
Types of interstitial lung disease
300 + conditions
Known aetiology
- Iatrogenic e.g. radiation
- Extrinsic allergic alveolitis (hypersensitivity pneumonitis) e.g. farmers lung, pigeons lung
- pneumonconiosis (lung injury from dust particles) asbestosis, silicosis
- post-infectious
Unknown aetiology
- Idiopathic intersistial pneumonias
- sarcoidosis
- connective tissue disease
- lymphangioleiomyomatosis (LAM)
Classification of idiopathic interstitial pneumonias (ERS)
Major
- acute interstitial pneumonia (AIP)
- idiopathic pulmonary fibrosis (IPF) - worst mortality
- idiopathic non-specific interstitial pneumonia (NSIP)
- cryptogenic organising pneumonia (COP)
- respiratory bronchiolotisi ILD (RB-ILD)
Rare
- idiopathic lymphoid intersistial pneumonia
Unclassifiable
Acute interstitial pneumonia
progressive hypoxaemia
high mortality with no treatment
survivors have good outcomes
some might have recurrence or chronic disease
Sarcoidosis
systemic inflammatory condition commonly affecting lungs caused by collections of inflammatory cells forming granulomas.
can affect skin, CNS, liver, heart
CXR grading 1-4 - BL hilar lymphadenopathy, with infiltrate, infiltrates only, fibrosis
steroids, other immunosuppressants
Non-ICU management of ILD
- anti-inflammatory drugs
- anti-pulmonary hypertensives e.g. PDE-5 inhibitors
- Antifibrotic therapies e.g. nintedanib
Advanced - ILD - LTOT (symptomatic relief)
- Rehabilitation
- lung transplant
- palliative care
ILD referrals to critical care
Diagnosis crucial
Most commonly AIP, acute exacerbation of IPF, fulminant COP
Considerations
- aetiology / reversibility / response to treatment
- usual therapy e.g. LTOT
- complications - pulmHTN, cor pulmonale
- functional status
- Ix - PFTs, echo, BAL
- specialist opinion
Resp support - I+V usually inappropriate in IPF. NIV MDT decision
Steroid - pulsed MP - rapid progressive ILD with respiratory failure
cyclophosphamide
Sleep disordered breathing
several conditions causing hypoventilation during sleep
- snoring - partial airway obstruction without sleep disturbance
- OSA - intermittent complete airway obstruction
- OSA syndrome - OSA with daytime symptoms
- obesity hypoventilation syndrome - breathing reduced throughout sleep with or without airway obstruction. hypercapnia during day. (BMI > 30, PaCO2 > 6.5, SDB)
OSAS
daytime symptoms - headache, somnolescence, cognitive impairment
associated hypertension, cardiovascular dysfunction
contributory factors - male, smokers, obesity, reduced nasal patency
overnight polysomnography - AHI
- Mild < 5-15 / hr
- Mod 15-30
- severe > 30
Management
- conservative - lifestyle, weight loss
- CPAP
- mandibular re-positioning
- surgery - tonsillectomy, bariatric
Tuberculosis
Infectious disease caused by mycobacterium tuberculosis causing respiratory and/or multisystem disease
symptoms
- cough
- haemoptysis
- fever, weight loss, night sweats
Critical care and TB
- respiratory failure - often associated pneumonia, COPD or malignancy. significant comorbidity e.g. HIV
- Miliary TB - haematological dissemination - MODS, associated with immunosuppression
CNS TB - meningitis, tuberculomas.
other indications - TB related - pericardial effusion, massive haemoptysis, DIC (ciliary)
- treatment related - renal / liver failure
Challenges - difficult sampling
infectivity - multidrug resistance
TB diagnosis
- sputum acid fast bacilli (or PCR)
- bronchoscopy AFB (or PCR)
- alternative sites - LNs, CSF, pleural effusions
- overal clinical picture inc radiology
Culture - 2 x sputum for MC/S
- 2-4 weeks
- initial ZN stainig useful
- bronchoscopy high sensitivity
Radiology - upper lobe nodules, cavities, lymphadenopathy
critical care management
- MDT (resp, micro, ID, neuro)
- infection control - negative pressure, PPE
- Anti-TB drugs - 6-19mo
- co-infection - HIV, pneumonias
- complications - steroids for meningitis, hyponatraeumia, hydrocephalus, immun reconstitution
ARDS definition
Acute inflammatory lung disease causing respiratory failure manifested by hypoxaemia, consolidation, reduced compliance
Berlin definition
- Hypoxaemia P/F < 39.9kPA
- Bilateral infiltrates (CT / CXR)
- Within 1 week of trigger
- Not explained by cariogenic pulmonary oedema
Mild P/F 26.6 - 39.9 Kpa
Moderate P/f 13.3 - 26.6 Kpa
Severe P/f < 13.3 kPa
Pathophysiology of ARDS
- Epithelial and endothelial injury within alveolus
- inflammation of alveolar membrane - increased permeability, protein rich pulmonary oedema
- endothelial dysfunction and leakage of fluid and inflammatory cells into alveolus
- inactivation of surfactant
- consolidation, collapse, loss of gas exchange surface area
- loss of pulmonary vascular tone and hypoxic pulmonary vasoconstriction
- loss of gas exchange
histological phases of ARDS
- Exudative - 1st week - protein rich fluid flooding alveoli
- Proliferative - fibroproliferation and micro thrombi
- Fibrotic - widespread remodelling and scarring
Causes of ARDS
Pulmonary
- infection - bacterial, viral, fungal
- aspiration
- contusion
- Inhalational injury
- drowning
Extra-pulmonary
- Sepsis
- Major trauma
- Pancreatitis
- Burns
ARDS treatment
underlying cause and best supportive care
Mild - LPV, conservative fluid balance
Moderate - prone, NMB, higher PEEP
Severe - VV-ECMO if Murray score > 3 or pH < 7.2
general - nutrition, VTE prophylaxis, glycemic control
Steroids in ARDS
Equipoise
DEXA-ARDS - mortality benefit and ventilator free days. no proning.
recovery in covid-ards benefits
Hyperoxia
supernormal arterial partial pressure of O2
degree, duration and patient determine consequences. sometimes beneficial, sometimes harmful
harmful O2 therapy
patients at risk of hypercapnic respiratory failure
- COPD
- Bronchiectasis
- Neuromuscular disease
- Morbid obestiy
Hyperoxia recommended against in critical illness
- Acute MI
- Acute stroke
- Post ROSC
Others
- Neonatal - retinopathy, bronchopulmonary dysplasia
- bleomycin
- oxygen toxicity
Plus
- wastage
- energy consumpation
- fire risk
- cost
Pathophysiology of oxygen toxicity
- ROS generated by ETC
- increased imbalance between ROS and antioxidants due to hyperopia
- increased exposure of tissues to toxic interactions
- ROS cause harm by damaging DNA.RNA, damaging cell membrane, oxidant enzymes and impairing protein function
- Exposure time and PIO2 contribute
Effects of O2 toxicitt
Pulmonary
- epithelial damage
- chest pain, reduced VC
- inflammation
- stages similar to ARDSm permanent fibrosis possible
others
- impaired HPVC
- reduced CO2 elimination
- altered control of breathing
- absorption atelectasis
CNS
- nausea headache, dizziness, irritability seizures in hyperbaric conditions
Beneficial effects of high O2
Normobaric
- CO elimination
- PTX resorption
- cluster headache
- induction of anaesthesia
Hyperbaric
- decompression sickness
- wound healing
Oxygen target trials
ICU - ROX - 90-97% vs conventional. primary and secondary outcomes no difference
HOT ICU - 8 vs 12 kPA - no difference
UK ROX 88-92 vs conventional - ongoing
HAP
pulmonary infection contracted after 48 hr of admission to hospital
VAP
pulmonary infection contracted after 48 hr of mechanical ventilation
significance
- increase LOS, ventilator days, mortality
DDX
- HAP/CAP
- ARDS
- Pulmonary oedema
- contusion
- PE
VAP diagnosis
difficult - clinical, micro, radiological features
CPIS > 6 (MAX 12)
- increase pulmonary secretions
- fever
- leucocytosis
- P/F ratio
- new infiltrates
- +ve tracheal aspirate
VAP pathophysiology
Biofilm / aspiration
- ETT disrupts normal host defence
- secretions pool above cuff - colonised oropharyngeal
- slowly migrate through folds in cuff to trachea
- biofilm formation in tube - pushed in by ventilator
care bundle
group of evidence based interventions which together significantly improve outcomes
VAP prevention
care bundle
- head up 30 degrees
- daily sedation holds (reduce duration of intubation)
- mouth care
- subglottic suction
- tracheal tube pressure monitoring
- appropriate PPI (avoid unnecessary - bacterial overgrowth)
high impact intervention - reduce VAP, MRSA, ABX
other methods
- hygiene during handling airway euquipment
- tracheal tube design - cuff shape
- SDD
PE Risk factors
Strong
- lower limb fracture
- hospitalisation for HF or AF
- hip or knee replacement
- major trauma
- MI
- previous VTE
- spinal cord injury
Moderate
- AI disease
- CCF
- OCP
- post-partum
- cancer
-thrombophilia
weak
- 3 d bed rest
- immobility due to sitting
- obestity
- pregnancy
PE spiral of death
- increased RV afterload
- RV dilaation
- increased wall tension and RV O2 demand
- RV ischaemia,
- reduced RV contactility / output
- reduced LV preload / CO / systemic BP
- reduced coronary perfusion / RV O2 delivery
- obstructive shock
PE risk strtificiation
High risk
- cardiac arrest
- shock - sBP < 90 and end organ hypoperfusion ( GCS, oliguria, cold skin, lactate)
- persistent hypotension < 90 for 15 mins
- reperfusion tx, haemodynamic support
Intermediate high risk
- PESI III-V / RV dysfunction (TTE/CTPA) / elevated trop
- monitoring, rescue reperfusion
Intermediate low
- PESI III-V / RV dysfunction or troponin
- hospital mx
Low risk
- none or above
- early outpatient mx
PE Echo
Basal RV:LV ratio > 1
Mcconnells sign (RV free wall akinesia with sparing of the apex)
flattened septum
distended IVC
TAPSE < 16
mx acute RV failure in high risk PE
- volume optimisation - cautious 500ml bolus (normal / low CVP)
- NA 0.2-1mcg/kg/min - increases RV inotropy and systemic BP, restore CoPP beware excess vasoconstriction
- dobutamine 2-20mcg/kg/min - RV inotropy, may worsen arterial hypotension
- MCS- VA-ECMO
throbmolysis PE
- faster improvement in PAP, PVR vs LMWH / UFH
- greatest benefit in those within 48h symptom onset
- sig reduction in combined mortality and recurrence with 9.9% rate of severe bleeding, 1.7% rate of ICH
- PEITHO trial intermeidiate PE - reduced haemodynamic compriomise, worse major bleeding and stroke, no reduction in 30 d mortality
ABSOLUTE CI - active bleeding
- CNS malignancy
- haemorrhagic or ischaemic stroke last 6mo
- 3/52 - major trauma, surgery
relative CI - TIA
- anticoagulation
- advanced liver disease
PE scoring systems
PERC
wells score - low risk - d-dimer. high risk - ctpa
PESI (PE Severity index)
