Definitions, tables, Facts - Resp Flashcards

1
Q

PO2 of inspired gas

A

PO2 = FiO2 x Patm

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2
Q

Eqns of PaO2 in trachea

A

PO2 = FiO2 (Patm-PH2O)

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3
Q

Alveloar gas eqn

A

PAO2 = (FiO2(Patm-PH2O) - (PACO2/RQ)

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4
Q

A-a gradient

A

PAO2 - PaO2

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5
Q

Oxygen content

Delivery

A

Content = (SpO2 x Hb x 1.34) + 0.023PaO2

Delivery = Content x CO

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6
Q

Types of hypoxia

A

Hypoxic - low arterial tension
Anaemic
Stagnant - low CO
Cyotoxic - poor utilisation by tissues

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7
Q

Compliance

A

Change in lung volume per unit change in pressure

Ml.cmH2O

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8
Q

Compliance eqn

A

1/total = 1/thorax + 1/lung

1/200 + 1/200 = 1/100 = 100

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9
Q

Driving pressure

A

Pplat - PEEP

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10
Q

Static compliance eqn

A

Cstat = Vt / (Pplat - PEEP)

Measured at absent flow
End inspiratory hold

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11
Q

Dynamic compliance eqn

A

Dyn = Vt / Ppeak - PEEP

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12
Q

Which is higher, peak or plateau pressure

A

Peak is higher

Peak is lung and chest wall compliance PLUS pressure to overcome airways

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13
Q

Which is lower Dynamic or Static

A

Dynamic is lower as peak is higher

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14
Q

Normal difference between static and dynamic compliance and why would it change

A

Dynamic is 2-3 ml.cmH2O lower

It will increase in obstructive disease when higher pressures needed

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15
Q

What would raise static compliance

A

Disease of parenchyma - ARDS, pneumonia
Chest wall - kyphoscoliosis, obesis, burns
Obesity

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16
Q

Pulse ox wavelengths

Isobestic points

A

660nm (absorbs de-oxy more) and 940nm (absorbs oxyHb more than de-oxy)

805nm (and 590nm)

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17
Q

What is an isobestic point

A

Point at which two substances absorb a certain wavelength of light to the same extent

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18
Q

Examples of oxygenation scores

A

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

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19
Q

Wavelength of IR for capnography

A

4.3um

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20
Q

Phases of capnograph

A

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

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21
Q

Role of capnograph

A

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

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22
Q

Peak pressure def

A

Max airway pressure in the cycle

Pressure applied to the large airways

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23
Q

Plateau pressure def

A

Pressure in airway during an inspiratory pause

Pressure applied to the alveoli

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24
Q

Describes types of ventilation

A

Describe in terms of CONTROL, CYCLE or TRIGGER

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25
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
26
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
27
Describe trigger cycling
Variable that triggers insp Time - after a designated period Pressure - fall in pressure Flow - decrease in flow Neural activity
28
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
29
Determinants of oxygenation
FiO2 Mean airway pressure - itself determined from PEEP and I:E (more time spent in insp = higher MAP)
30
Determinants of CO2 clearence
Frequency, tidal vol, volume of dead
31
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
32
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
33
When to start NIV
PH<7.35 and PaCO2 > 6.5 Despite optimum medical therapy
34
When to intubate in AECOPD
Persitent or worsening acidosis despite NIV Resp arrest/peri arrest Contra indictation to NIV
35
Contra indictations to NIV
Severe facial deformity Fixed upper airway obstruction Burns Excess secretions Low GCS
36
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
37
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
38
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 ```
39
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
40
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
41
Weaning prediction tests
RSBI = Vt/F. (Aim less than 105) (If peep=0 and ps=0) P0.1 < -5 MIP
42
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
43
Risk factors for extubation failure
``` Age>65 COPD Heart failure OSA/obsesity Neuromuscular disorders Postive balacne Vent>6 days ```
44
Indications for tracheostomy
Elective surgery, head and neck cancer Emergency - loss of patent airway, pathology, neurological impairment Prolonged wean Excess secretions or no cough
45
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
46
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
47
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
48
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
49
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 ```
50
Differential diagnosis of ARDS
Cardiogenic pulmonary oedema Eosiniphilic pneumonia Cryptogenic organising pneumonia Diffuse alveloar haemorrhage
51
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 ```
52
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
53
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
54
Mechanisms of inhalaltion injury
Heat —> oedema, erythema, ulceration Toxins - sulphur, acids, damage by pH or free radicals Environmental hypoxia
55
Pathophysiology
Exudative and fibrotic phase Exudate - neutophil influx, increased permeability, type 2 pneumocyte loss and surfactant loss Fibrotic - alveolitis
56
Treatments in burns via bronch
Salbutamol Heparin NAC
57
Carbon monoide
Binds Hb 250x more than O2, left shift of curve Also - cytochrome oxidase inhibition Therefore tissue hypoxia Pulse ox cannot differentiate
58
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
59
Cyanide mechanism
Binds to the ferric ion on cytochrome oxidase —> no aerobic cellular metabolism Cytoxic hypoxia Look out for unexplained lactic acidosis
60
Treatment of cyanide
Aim to induce a metHb - amyl nitrate, sodium nitrite Bind cyanide - dicobalt edetate, hydroxycobalamin Sulpur doneation - cyanide to thiocyanate —> sodium thiosulphate
61
Moderate asthma
PEFR 40-75%
62
Severe asthma
``` PEFR 33 to 50% predicted Resp Rate >35 HR 110 Low/Normal CO2 Cannot complete sentence ```
63
Life threatening asthma
``` PEFR <33% Reduced resp effort, Silent chest Arrhytmia Hypotension Brady Hypoxia - SpO2 <92% or <8kPa Hypercapnoea Altered GCS ```
64
Near fatal
Rising CO2 | Need for MV
65
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
66
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
67
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
68
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.
69
Definie CAP and HAP
CAP - evolving in community of within 48 hours of admission HAP - more than 48 hours after admission
70
Organisms in CAP/HAP
``` CAP - strep. Pneumonia, H. Influenza Legionella Chlamydiea Mycoplasma ``` ``` HAP - gram negs Pseudomonas E.coli Klebsiella Acinebacter ```
71
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
72
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 ```
73
Investgiation for CAP
Blood culture Sputum for gram stain and MC&S Urine pneumococcal anitgens, legionalle PCR mycoplasma, PCP
74
CURB 65 score
``` Confusion (AMTS<8) Urea >7 RR>30 BP<90 Age>65 ```
75
Mortality of CURB
``` 0 - 0.7% 1 - 3.2% 2 - 13% 3 - 17% 4 - 41% 5 - 57% ```
76
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
77
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
78
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
79
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
80
Features of an empyema
``` pH < 7.2 Glucose <3.3 Bacteria on microscopy Pus LDH >1000 in fluid ```
81
When to drain effusion
Diagnosis Worsening resp failure Infected Options for organised effusion Radiologically guided drainage tPA instillation to break down VATS
82
Types of Ptx
Primary - young tall men etc SEcondary - empysema, cancer, TB, ARDS Iatrogenic - pleural biospy, cental line, PPM Traumatic Ventilator assocaited
83
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
84
Aetiology of BPF
Post pulmonary surgery (pneumonectomy > lobectomy) Post pneumonia Cancer, bronchial, oesophageal Trauma ARDS Radiation
85
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
86
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
87
Sources of massive haemoptysis
Bronchial vessels 90% Pulmonary 5% Nonpulmonary systemic 5%
88
Causes of haemoptysis
Tb, lung absess, neoplasia Inflammation - chronic bronchitis, fungal lung disease, vascullitis, CF, bronchiectasis Coagulopathy, iatrogenic
89
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