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FFICM > Definitions, tables, Facts - Resp > Flashcards

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
Q

Control methods of ventilation

A

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

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26
Q

Describe cycling vent

A

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

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27
Q

Describe trigger cycling

A

Variable that triggers insp

Time - after a designated period

Pressure - fall in pressure

Flow - decrease in flow

Neural activity

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28
Q

Flow patterns

A

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

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29
Q

Determinants of oxygenation

A

FiO2

Mean airway pressure - itself determined from PEEP and I:E (more time spent in insp = higher MAP)

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30
Q

Determinants of CO2 clearence

A

Frequency, tidal vol, volume of dead

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31
Q

Effects of MV

A

Anaesthetic - dose related hypotension, loss of drive, brady, reactions

AIrway - damage to structures, loss of airway

Haemo - PPV —> instability, decreased preload

VILI

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32
Q

Ways in which VILI can happen

A

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

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33
Q

When to start NIV

A

PH<7.35 and PaCO2 > 6.5

Despite optimum medical therapy

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34
Q

When to intubate in AECOPD

A

Persitent or worsening acidosis despite NIV

Resp arrest/peri arrest

Contra indictation to NIV

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35
Q

Contra indictations to NIV

A

Severe facial deformity

Fixed upper airway obstruction

Burns

Excess secretions

Low GCS

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36
Q

Describe recruitment

A

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
Q

Advantages/phsyiolgoy to proning

A

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
Q

Risk of proning

A

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
Q

Types of weaning

A

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
Q

Criteria for weaning

A

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
Q

Weaning prediction tests

A

RSBI = Vt/F. (Aim less than 105)
(If peep=0 and ps=0)

P0.1 < -5
MIP

42
Q

Failure of SBT

A

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
Q

Risk factors for extubation failure

A 
Age>65
COPD
Heart failure
OSA/obsesity
Neuromuscular disorders
Postive balacne
Vent>6 days
44
Q

Indications for tracheostomy

A

Elective surgery, head and neck cancer

Emergency - loss of patent airway, pathology, neurological impairment

Prolonged wean

Excess secretions or no cough

45
Q

Advantages of trache

A

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
Q

Contra-indications to trache

A 
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
Q

Complications of trache

A

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
Q

Why do a bronch

A

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
Q

Berlin Criteria

A

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
Q

Differential diagnosis of ARDS

A

Cardiogenic pulmonary oedema

Eosiniphilic pneumonia

Cryptogenic organising pneumonia

Diffuse alveloar haemorrhage

51
Q

Aetiology of ARDS

A

Direct and indirect

Direct
Pneumonia
Viral pneumonitis, COVID
Chemical
Smoke
Drowning
Contusion
Reperfusion
Irrdation
Indirect
Sepsis
trauma
pancreatitis
Eclampsia, AFE
TLE
TRALI
52
Q

Vent strategies in ARDS

A

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
Q

Things not known to work in ARDS

A

Steroids - improve O2 but mort benefit??

Surfactant - no benefit

Statins - no benefit

iNO - improve O2 but no benefit

54
Q

Mechanisms of inhalaltion injury

A

Heat —> oedema, erythema, ulceration

Toxins - sulphur, acids, damage by pH or free radicals

Environmental hypoxia

55
Q

Pathophysiology

A

Exudative and fibrotic phase

Exudate - neutophil influx, increased permeability, type 2 pneumocyte loss and surfactant loss

Fibrotic - alveolitis

56
Q

Treatments in burns via bronch

A

Salbutamol
Heparin
NAC

57
Q

Carbon monoide

A

Binds Hb 250x more than O2, left shift of curve
Also - cytochrome oxidase inhibition

Therefore tissue hypoxia

Pulse ox cannot differentiate

58
Q

Carboxy levels and treatment

A

> 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
Q

Cyanide mechanism

A

Binds to the ferric ion on cytochrome oxidase —> no aerobic cellular metabolism

Cytoxic hypoxia

Look out for unexplained lactic acidosis

60
Q

Treatment of cyanide

A

Aim to induce a metHb - amyl nitrate, sodium nitrite

Bind cyanide - dicobalt edetate, hydroxycobalamin

Sulpur doneation - cyanide to thiocyanate —> sodium thiosulphate

61
Q

Moderate asthma

A

PEFR 40-75%

62
Q

Severe asthma

A 
PEFR 33 to 50% predicted
Resp Rate >35 
HR 110
Low/Normal CO2
Cannot complete sentence
63
Q

Life threatening asthma

A 
PEFR <33%
Reduced resp effort,
Silent chest
Arrhytmia
Hypotension
Brady
Hypoxia - SpO2 <92% or <8kPa
Hypercapnoea
Altered GCS
64
Q

Near fatal

A

Rising CO2

Need for MV

65
Q

Risk factors for fatal asthma

A

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
Q

Respiratory mechanics in asthma

A

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
Q

Dynamic hyperinflation in mechanical ventilation

A

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
Q

Ways to make asthma better on a vent

A

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
Q

Definie CAP and HAP

A

CAP - evolving in community of within 48 hours of admission

HAP - more than 48 hours after admission

70
Q

Organisms in CAP/HAP

A 
CAP - strep. Pneumonia, 
          H. Influenza
          Legionella
          Chlamydiea
          Mycoplasma
HAP - gram negs
           Pseudomonas
           E.coli
           Klebsiella
           Acinebacter
71
Q

Ways of reducing VAP

A 
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
Q

Differential diagnosis of CAP in immunocomp

A

Diffuse or focal infiltrate

Diffuse -
CMV, PCP, Aspergilllius, cryptococcus,
Drugs, radiation, GvHD

Focal
Gram negs
S.aureus
Aspergillus
Cryptococcus
73
Q

Investgiation for CAP

A

Blood culture
Sputum for gram stain and MC&S
Urine pneumococcal anitgens, legionalle
PCR mycoplasma, PCP

74
Q

CURB 65 score

A 
Confusion (AMTS<8)
Urea >7
RR>30
BP<90
Age>65
75
Q

Mortality of CURB

A 
0 - 0.7%
1 - 3.2%
2 - 13%
3 - 17%
4 - 41%
5 - 57%
76
Q

SMART COP system

A

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
Q

Complications of pneumonia

A

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
Q

Pleura effusions - catergories

A

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
Q

Lights criteria

A

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
Q

Features of an empyema

A 
pH < 7.2
Glucose <3.3
Bacteria on microscopy
Pus
LDH >1000 in fluid
81
Q

When to drain effusion

A

Diagnosis
Worsening resp failure
Infected

Options for organised effusion
Radiologically guided drainage
tPA instillation to break down
VATS

82
Q

Types of Ptx

A

Primary - young tall men etc

SEcondary - empysema, cancer, TB, ARDS

Iatrogenic - pleural biospy, cental line, PPM

Traumatic

Ventilator assocaited

83
Q

Management principles of Ptx

A

Small <2cm - conservative, high FIO2 may increased absorption

Larger - decompress and drain

Refractory - medical pleurodesis, VATS pleurectomy, open thoracotomy and pleurectomy

84
Q

Aetiology of BPF

A

Post pulmonary surgery (pneumonectomy > lobectomy)

Post pneumonia

Cancer, bronchial, oesophageal

Trauma

ARDS
Radiation

85
Q

Management of BPF

A

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
Q

Define massive haemoptysis

A

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
Q

Sources of massive haemoptysis

A

Bronchial vessels 90%

Pulmonary 5%

Nonpulmonary systemic 5%

88
Q

Causes of haemoptysis

A

Tb, lung absess, neoplasia

Inflammation - chronic bronchitis, fungal lung disease, vascullitis, CF, bronchiectasis

Coagulopathy, iatrogenic

89
Q

Treatment of massive haemoptyiss

A

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

FFICM (59 decks)

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