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Pete FFICM SOE/OSCE > Resp > Flashcards

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

How do you calculate the A-a gradient

A

PAO2 - PaO2

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5
Q

Oxygen contentDelivery

A

Content = (SpO2 x Hb x 1.34) + 0.03 PaO2
Delivery = Content x CO

1.34 = Max 02 carrying capacity of blood
0.03 solubility constant for 02

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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/lung1/200 + 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. Why?

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 flowNeural 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 BiPAP

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 < -5MIP

42
Q

Failure of SBT

A

Physiology, gases, clinical

Phys:
HR 20% above base or > 140Sys BP >20%, or >180 or <90Arrhythmia
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
HFO
VECMO

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 of ARDS

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

Discuss Carbon monoxide

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>100% 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 donation - cyanide to thiocyanate —> sodium thiosulphate

61
Q

Moderate asthma

A

PEFR 40-75%

62
Q

Define 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
Altered GCS

64
Q

Define Near fatal Asthma

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 pressures - 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
BAL

74
Q

CURB 65 score

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

Mortality of CURB

A

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

76
Q

What is SMART-COP Score for Pneumonia Severity

A

Tool for if needing mechanical ventilation
Sys<90
Multilobe involement
Albumin
RR (age adjusted)
Tachycardia>125
Confusion
Oxygen
pH <7.355
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 permabilityInfection
- TB, pneumonia, empyema
- Malig - bronchial Ca, mesothel
- Connective tissue - RA, SLE,
- Inflammation - pancreatitis

79
Q

Descibe the Lights criteria for pleural effusion

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 drainaget
- PA 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
Iatrogenic
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

Pete FFICM SOE/OSCE (199 decks)

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