Definitions, tables, Facts - Resp Flashcards
PO2 of inspired gas
PO2 = FiO2 x Patm
Eqns of PaO2 in trachea
PO2 = FiO2 (Patm-PH2O)
Alveloar gas eqn
PAO2 = (FiO2(Patm-PH2O) - (PACO2/RQ)
A-a gradient
PAO2 - PaO2
Oxygen content
Delivery
Content = (SpO2 x Hb x 1.34) + 0.023PaO2
Delivery = Content x CO
Types of hypoxia
Hypoxic - low arterial tension
Anaemic
Stagnant - low CO
Cyotoxic - poor utilisation by tissues
Compliance
Change in lung volume per unit change in pressure
Ml.cmH2O
Compliance eqn
1/total = 1/thorax + 1/lung
1/200 + 1/200 = 1/100 = 100
Driving pressure
Pplat - PEEP
Static compliance eqn
Cstat = Vt / (Pplat - PEEP)
Measured at absent flow
End inspiratory hold
Dynamic compliance eqn
Dyn = Vt / Ppeak - PEEP
Which is higher, peak or plateau pressure
Peak is higher
Peak is lung and chest wall compliance PLUS pressure to overcome airways
Which is lower Dynamic or Static
Dynamic is lower as peak is higher
Normal difference between static and dynamic compliance and why would it change
Dynamic is 2-3 ml.cmH2O lower
It will increase in obstructive disease when higher pressures needed
What would raise static compliance
Disease of parenchyma - ARDS, pneumonia
Chest wall - kyphoscoliosis, obesis, burns
Obesity
Pulse ox wavelengths
Isobestic points
660nm (absorbs de-oxy more) and 940nm (absorbs oxyHb more than de-oxy)
805nm (and 590nm)
What is an isobestic point
Point at which two substances absorb a certain wavelength of light to the same extent
Examples of oxygenation scores
P:F ratio
A-a gradient
Oxygenation index = (FiO2 x mean airwaypressure)/PaO2). X 100
Expresses the pressure needed to maintain a PF ratio
OI high - bad
Wavelength of IR for capnography
4.3um
Phases of capnograph
1 (flat line) inspiratory baseline. Inspiratroy gas with no CO2
2 - expiratory upstroke, deadspace gas turning to alveolar gas
3 - Alveloar plataeu
0 inspiratory downstorke
Role of capnograph
A - tube in right place
Remains in place
Tube patency and vent circuit
B - RR
Pathology - bronchospasm
Calculate dead space from increasing PeCO2 and PaCO2 (normally 0.7)
C - Presence of circulation —> CPR
Sudden fall - reduced CO
Peak pressure def
Max airway pressure in the cycle
Pressure applied to the large airways
Plateau pressure def
Pressure in airway during an inspiratory pause
Pressure applied to the alveoli
Describes types of ventilation
Describe in terms of CONTROL, CYCLE or TRIGGER
Control methods of ventilation
Volume or pressure
Vol - to be delivered, Paw determined by resistance and compliance
Pressure - we choose the pressure, resistance, compliance, and insp time determine volume
Describe cycling vent
Terminates the insp phase to allow expiration
Time - cycling by Tinsp
Flow - cycles when flow decreases by a designated % of peak insp flow
Volume - cycles when volume delivered
Limit - terminates insp if limits of pressure or volume reached
Describe trigger cycling
Variable that triggers insp
Time - after a designated period
Pressure - fall in pressure
Flow - decrease in flow
Neural activity
Flow patterns
Constant or decel
Constant - rapid increase then remains constant to target variable
Volume mode
Decel - Pressure controlled mode
Flow falls as alveolar pressure increases
Improves distribution of gas
Determinants of oxygenation
FiO2
Mean airway pressure - itself determined from PEEP and I:E (more time spent in insp = higher MAP)
Determinants of CO2 clearence
Frequency, tidal vol, volume of dead
Effects of MV
Anaesthetic - dose related hypotension, loss of drive, brady, reactions
AIrway - damage to structures, loss of airway
Haemo - PPV —> instability, decreased preload
VILI
Ways in which VILI can happen
Volutrauma - overdistention with excess Vt
Barotrauma - damage by excessive pressures
Atelectrauama - damage to sheer forces by repeated opening and closing
Biotrauma - alveloar membrane damagae
Oxygen toxicity
When to start NIV
PH<7.35 and PaCO2 > 6.5
Despite optimum medical therapy
When to intubate in AECOPD
Persitent or worsening acidosis despite NIV
Resp arrest/peri arrest
Contra indictation to NIV
Contra indictations to NIV
Severe facial deformity
Fixed upper airway obstruction
Burns
Excess secretions
Low GCS
Describe recruitment
Deliberate transient increase in intra thoraci pressure with improve oxygenation
Principle of reopening collapsed units by pressurising beyond critical opening pressure
Ways:
Sigh breath - Large Vt or high Pinsp for one breath
Sustained inflation 40cmH2O for 40 seconds
Extended sigh, increase in PEEP with same driving pressure
Incremental PEEP
Advantages/phsyiolgoy to proning
Homogenous distriubtion of ventilation
Improved thoraco-abdo compliance
Pressures evenly distributed
Heart/mediastinum moved off lung units
Drainage of secretions
Homogenous perfusion
Proning diverts blood to better aerated units
Reduces EVLW
Risk of proning
Turning and whilst prone
Turn Loss of airway/devices Spine, shoulder injury Increased sedation Transient hypoxia Instabiltiy
Prone Oedema and pressure areas Conjunctival oedema Retinal damage Airway obstruction Nerve damage Line damage
Types of weaning
Simple difficult and prolonged
Simple - extubated after first SBT
Difficult - upto 3 SBTs or 7 days
Prolonged - exceeds limits of difficult weaning
Long term - more than 21 days and more than 6 hours a day
Criteria for weaning
Airway - patent airway —> leak test
B - Minimal O2, low PEEP, low pressure support
Adequate vent drive
Good cough, secretion clearnece
C - haemodynamically stable
D - good GCS to protcet airway, no agitation
E - original pathology gone, no procedures needed
Weaning prediction tests
RSBI = Vt/F. (Aim less than 105)
(If peep=0 and ps=0)
P0.1 < -5
MIP
Failure of SBT
Physiology, gases, clinical
Phys: HR 20% above base or > 140 Sys BP >20%, or >180 or <90 Arrhythmia RR>50% baseline or >35 RSBI > 105
Gases
PaO2 <8 of 50%
PaCO2 > 6.5
PH < 7.32
Clinical
Cyanosis, pale, clammy, increased resp effort, agitation
Risk factors for extubation failure
Age>65 COPD Heart failure OSA/obsesity Neuromuscular disorders Postive balacne Vent>6 days
Indications for tracheostomy
Elective surgery, head and neck cancer
Emergency - loss of patent airway, pathology, neurological impairment
Prolonged wean
Excess secretions or no cough
Advantages of trache
Shorter - less dead space, less resistance to flow, reduced WOB, easy suction
Reduced sedation needs
Improved cough and secretions
Ability to communicate
Conduct physio
Avoid ETT - speech, ?eat, mouth care, comfort
Contra-indications to trache
Local - infection to site
Absnormal anatomy
Known difficult airway
Short neck / obesity (???)
C spine injury (no extension)
Systemic - Coagulopathy, haemodynbamic or resp comprimise, raised ICP
Complications of trache
Immediate, early and late
Im: Hypoxia/carbia Loss of airway Aspiration Haemorrage Damage to tracheal rings, bleeding, Ptx, exphysema Anaesthesia
Early Infection Displaced tube Ocllusion Tracheal ulcer, fistula, Bleeding via erosions
Late
Tracheal dilation, tracheomalacia, stenosis
Changes to voice
Why do a bronch
Diagnosis, therapeutic, assist
Diag: BAL for MC&S, cyto Biopsy Inhalational injury ETT position
Therapy -
Remove obstructions, sputum, blood, FB
Bronchial stent, BPF
Assist - fibreoptic tube
Perc trachy
DLT
Broncho blocker
Berlin Criteria
Timing, within 1 week of known clinical insult
Chest image - bilateral opacities, not explained by collapse, effusion or nodules
Origin - Resp failure not fully explained by cardiac failure or fluid overload
Hypoxia by PF ratio
39.9 to 26.6 mild
13.3 to 26.6 moderate
<13.3 severe
On a ventilator, with PEEP 5
Differential diagnosis of ARDS
Cardiogenic pulmonary oedema
Eosiniphilic pneumonia
Cryptogenic organising pneumonia
Diffuse alveloar haemorrhage
Aetiology of ARDS
Direct and indirect
Direct Pneumonia Viral pneumonitis, COVID Chemical Smoke Drowning Contusion Reperfusion Irrdation
Indirect Sepsis trauma pancreatitis Eclampsia, AFE TLE TRALI
Vent strategies in ARDS
Low Vt - 6ml/kg of IBW
Plateau < 30cmH20
PEEP - high or titrated by compliance curves
Recruitment manouvres —> improves O2, no effect on outcomes
Permissive hypercapnoea
Proning
HFOV
ECMO
Things not known to work in ARDS
Steroids - improve O2 but mort benefit??
Surfactant - no benefit
Statins - no benefit
iNO - improve O2 but no benefit
Mechanisms of inhalaltion injury
Heat —> oedema, erythema, ulceration
Toxins - sulphur, acids, damage by pH or free radicals
Environmental hypoxia
Pathophysiology
Exudative and fibrotic phase
Exudate - neutophil influx, increased permeability, type 2 pneumocyte loss and surfactant loss
Fibrotic - alveolitis
Treatments in burns via bronch
Salbutamol
Heparin
NAC
Carbon monoide
Binds Hb 250x more than O2, left shift of curve
Also - cytochrome oxidase inhibition
Therefore tissue hypoxia
Pulse ox cannot differentiate
Carboxy levels and treatment
> 10% is a problem
> 10% oxygen via high conc facemask
25% O2 and ventilation
40% or coma OR pregnant, OR non responding - HBO
100% O2 changes half life from 4 to 1 hour
HBO at 3atm reduces to 30 minutes
Cyanide mechanism
Binds to the ferric ion on cytochrome oxidase —> no aerobic cellular metabolism
Cytoxic hypoxia
Look out for unexplained lactic acidosis
Treatment of cyanide
Aim to induce a metHb - amyl nitrate, sodium nitrite
Bind cyanide - dicobalt edetate, hydroxycobalamin
Sulpur doneation - cyanide to thiocyanate —> sodium thiosulphate
Moderate asthma
PEFR 40-75%
Severe asthma
PEFR 33 to 50% predicted Resp Rate >35 HR 110 Low/Normal CO2 Cannot complete sentence
Life threatening asthma
PEFR <33% Reduced resp effort, Silent chest Arrhytmia Hypotension Brady Hypoxia - SpO2 <92% or <8kPa Hypercapnoea Altered GCS
Near fatal
Rising CO2
Need for MV
Risk factors for fatal asthma
Previous life threatening with need for ventilation
Hostpial admission in the last year
Three or more chronic meds
Use of salbutamol +++++
Brittle - type 1 - wide PEFR variability
Type 2 - sudden severe attacks when usually well controlled
Respiratory mechanics in asthma
Airflow limitation —> in small ariways. Flow limitation in exp.
Active exhalation increases intrathoracic pressures —> makes it worse
Dynamic hyperinflation - reduced exp time —> residual volume increases —> gas trapping
Hyperinflation moves you up the compliance curve, decreases compliances
Dynamic hyperinflation in mechanical ventilation
Identify - failrue of flow to return to baseline, before vent triggers, incomplete exp.
Measure by intrinsic/auto PEEP
Measured pressure on exp hold minus PEEP from vent is iPEEP
Under spontaneous breathing - measured by oesophageal balloon
Ways to make asthma better on a vent
NIV - limited role. Theoretical reducing WOB through IPAP, EPAP keeps airways open
Anaesthesia - use ketamine. BEWARE HYPOTENSION FROM PRELOAD LOSS
Sedation - ketamine, sevoflurane
Hyperinflation - prolong I:E ratio, short Tinsp, high flow rate, slow RR
PEEP -extrinsic PEEP usually at 80% of iPEEP.
Airway pressrues - plat 30.
Definie CAP and HAP
CAP - evolving in community of within 48 hours of admission
HAP - more than 48 hours after admission
Organisms in CAP/HAP
CAP - strep. Pneumonia,
H. Influenza
Legionella
Chlamydiea
Mycoplasma
HAP - gram negs
Pseudomonas
E.coli
Klebsiella
Acinebacter
Ways of reducing VAP
Reduce micro asp: 30 degree head up Prone vent Cuff pressures >30 Supraglottic suction Enteral feeding - no evidence of post pyloric feeding or prokinetics
Acid - PPI may increase risk
Colonisation - chlorhex. SDD
Extubate ASAP, sedation holds, SBT
Differential diagnosis of CAP in immunocomp
Diffuse or focal infiltrate
Diffuse -
CMV, PCP, Aspergilllius, cryptococcus,
Drugs, radiation, GvHD
Focal Gram negs S.aureus Aspergillus Cryptococcus
Investgiation for CAP
Blood culture
Sputum for gram stain and MC&S
Urine pneumococcal anitgens, legionalle
PCR mycoplasma, PCP
CURB 65 score
Confusion (AMTS<8) Urea >7 RR>30 BP<90 Age>65
Mortality of CURB
0 - 0.7% 1 - 3.2% 2 - 13% 3 - 17% 4 - 41% 5 - 57%
SMART COP system
Tool for if needing mechanical ventilation
Sys<90
Multilobe involement
Albumin
RR (age adjusted)
Tachycardia>125
Confusion
Oxygen
pH <7.35
5-6 points —> high risk
Complications of pneumonia
Parapneumonic effusion (50%) —> tap and drain if empyema
Abscess formation (worse in alcohol abuse, and aspriation)
Metastatic infection - S.aureus and pneumoniae.
Joints meninges and endocardium
Legionella specific - encephalitis, pericarditis, pancreatitis, hyponatraemia, deranged liver, low plts
Pleura effusions - catergories
Protein level - >30g - exudate, <30 transudate
Transudate: increased hydrostatic pressure OR reduced oncotic pressure
Heart, liver or kidney failure
Meigs
Hypothyroids
Small number of pituitary tumours
Exudative
Increased permability
Infection - TB, pneumonia, empyema
Malig - bronchial Ca, mesothel
Connective tissue - RA, SLE,
Inflammation - pancreatitis
Lights criteria
Exudate if:
Pleural to serum protein ratio >0.5
Pleural to serum LDH > 0.6
Pleural LDH > 2/3 upper limit of normal serum LDH
Features of an empyema
pH < 7.2 Glucose <3.3 Bacteria on microscopy Pus LDH >1000 in fluid
When to drain effusion
Diagnosis
Worsening resp failure
Infected
Options for organised effusion
Radiologically guided drainage
tPA instillation to break down
VATS
Types of Ptx
Primary - young tall men etc
SEcondary - empysema, cancer, TB, ARDS
Iatrogenic - pleural biospy, cental line, PPM
Traumatic
Ventilator assocaited
Management principles of Ptx
Small <2cm - conservative, high FIO2 may increased absorption
Larger - decompress and drain
Refractory - medical pleurodesis, VATS pleurectomy, open thoracotomy and pleurectomy
Aetiology of BPF
Post pulmonary surgery (pneumonectomy > lobectomy)
Post pneumonia
Cancer, bronchial, oesophageal
Trauma
ARDS
Radiation
Management of BPF
Chest drain without suction
Minimise airway pressures: Avoid PPV where possible, SBT ASAP Low pressures ?HFOV ?ECMO DLT/bronchial blocker
Closure:
Bronch - stent, glue, blocker
Lung surgery, stapling stump, lobectomy, segementectomy
Define massive haemoptysis
Blood loss within the airways at a rate that is an immediate risk to life
Could be as small as 200ml/24hr
Death from suffocation NOT haemorrhage
Sources of massive haemoptysis
Bronchial vessels 90%
Pulmonary 5%
Nonpulmonary systemic 5%
Causes of haemoptysis
Tb, lung absess, neoplasia
Inflammation - chronic bronchitis, fungal lung disease, vascullitis, CF, bronchiectasis
Coagulopathy, iatrogenic
Treatment of massive haemoptyiss
Large ETT for bronch
Place bleeding side down
Conisder DLT, bronchial blockers
Volume
Correct coagulopathy
TXA
Anti-tussive
Definitive: Bronch and find bleeding point
Balloon tampanade
Direct injection of haemostasis
Isolate bleeding lobe with blockers
CT angio and IR embolization
