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Acute RespiratoryEmergencies
Acute RespiratoryEmergencies
Martin Johnson
Consultant PhysicianGartnavel / Western
Martin Johnson
Consultant PhysicianGartnavel / Western
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SummarySummary
What to expect - what are thecommon respiratory emergencies?
How to recognise the problem?
How to manage the problem?
What to expect - what are thecommon respiratory emergencies?
How to recognise the problem?
How to manage the problem?
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Relative Frequency of
Medical Emergencies
Relative Frequency of
Medical Emergencies
The burden of lung disease. 2nd Edition BTS 2006
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Relative Frequency of
Respiratory Emergencies
Relative Frequency of
Respiratory Emergencies
The burden of lung disease. 2nd Edition BTS 2006
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Immediate AssessmentImmediate Assessment
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How to recognise theproblem?
How to recognise theproblem?
HistoryImportance of the HPC
Examination
Investigation
HistoryImportance of the HPC
Examination
Investigation
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SymptomsSymptoms
DyspnoeaChest pain
Haemoptysis
DyspnoeaChest pain
Haemoptysis
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SymptomsSymptoms
DyspnoeaChest pain
Haemoptysis
DyspnoeaChest pain
Haemoptysis
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Dyspnoea: Pattern ofOnset
Dyspnoea: Pattern ofOnset
Sudden Pneumothorax
PTE
Aspiration
Cardiac event –arrhythmia, MI
Over hours / days Asthma Pneumonia
Pulmonary oedema
Sudden Pneumothorax
PTE
Aspiration
Cardiac event –arrhythmia, MI
Over hours / days Asthma Pneumonia
Pulmonary oedema
Intermittent
Asthma
Hyperventilation
Progressive COPD
IPF
Pleural effusion
Anaemia
LVF
Pulmonary hypertension
Intermittent
Asthma
Hyperventilation
Progressive COPD
IPF
Pleural effusion
Anaemia
LVF
Pulmonary hypertension
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Chest PainChest Pain
Myocardial ischaemiacentral
radiating to the jaw / arm(s)
squeezing / crushing / heavy weight
aggravated by exertion
relieved by rest / GTNassociated autonomic features
Myocardial ischaemiacentral
radiating to the jaw / arm(s)
squeezing / crushing / heavy weight
aggravated by exertion
relieved by rest / GTNassociated autonomic features
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Chest PainChest Pain
Myocardial ischaemiaPericardial pain
retrosternal
pleuritic
relieved by sitting forward
worse on swallowing, twisting andwith sternal pressure
Myocardial ischaemiaPericardial pain
retrosternal
pleuritic
relieved by sitting forward
worse on swallowing, twisting andwith sternal pressure
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Chest PainChest Pain
Myocardial ischaemiaPericardial pain
Respiratorytypically not central
pleuritic
Myocardial ischaemiaPericardial pain
Respiratorytypically not central
pleuritic
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Chest PainChest Pain
Myocardial ischaemiaPericardial pain
Respiratory
Oesophagealretrosternal
heart burncan be indistinguishable from cardiac
pain
Myocardial ischaemiaPericardial pain
Respiratory
Oesophagealretrosternal
heart burncan be indistinguishable from cardiac
pain
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Chest PainChest Pain
Myocardial ischaemiaPericardial pain
RespiratoryOesophageal
Musculoskeletallocalised
associated with tenderness
Myocardial ischaemiaPericardial pain
RespiratoryOesophageal
Musculoskeletallocalised
associated with tenderness
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SymptomsSymptoms
DyspnoeaChest pain
Haemoptysis
DyspnoeaChest pain
Haemoptysis
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HaemoptysisHaemoptysis
0
5
10
15
20
25
P e r c e n t a g e o f
c a s e s
Neoplasms
Bronchiectasis
Miscellaneous
Bronchitis
Bacterial
pneumoniaTuberculosis
Cryptogenic
Misc – PTE, LVF, aspergilloma, lung abscess, atypical mycobacteria
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Other Points from theHistory
Other Points from theHistory
Don’t overlook the rest of the historyPMH - e.g. previous DVT
Drug history - e.g. new medications
SmokingOccupation e.g. baker, asbestos exposure
Pets especially birds
FH
Don’t overlook the rest of the historyPMH - e.g. previous DVT
Drug history - e.g. new medications
SmokingOccupation e.g. baker, asbestos exposure
Pets especially birds
FH
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ExaminationExamination
Do not make the diagnosis from thehistory alone
It is negligent not to examine a patient
with new symptomsE.g. arrhythmia (esp AF / flutter)
pneumothorax
pericardial effusion
Do not make the diagnosis from thehistory alone
It is negligent not to examine a patient
with new symptomsE.g. arrhythmia (esp AF / flutter)
pneumothorax
pericardial effusion
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ObservationsObservations
HR
BP
Temp
HR
BP
Temp
SpO2
FIO2
RR
SpO2
FIO2
RR
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Examination
of the Chest
ExpansionPercussion
Auscultation
Air entry
Quality of breath sounds
Added sounds
Vocal resonance
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ExaminationExaminationWheeze
Asthma / COPD
Heart failure
Anaphylaxis
Foreign body
Stridor Foreign body
Epiglottitis
Anaphylaxis
Wheeze Asthma / COPD
Heart failure
Anaphylaxis
Foreign body
Stridor Foreign body
Epiglottitis
Anaphylaxis
Crackles
Pulmonary oedema Fibrosis
Pneumonia
Bronchiectasis
Clear chest PTE
Pneumothorax
Hyperventilation Metabolic acidosis
Anaemia
Drug overdose
Crackles
Pulmonary oedema Fibrosis
Pneumonia
Bronchiectasis
Clear chest PTE
Pneumothorax
Hyperventilation Metabolic acidosis
Anaemia
Drug overdose
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InvestigationsInvestigations
Blood – FBC, U&Es, (D-dimer, Tn,CRP)
ABGs
ECG
CXR
Blood – FBC, U&Es, (D-dimer, Tn,CRP)
ABGs
ECG
CXR
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Interpretation of Arterial Blood
Gases
Interpretation of Arterial Blood
Gases
PaCO2
PaCO2
H+
respiratory
acidosis metabolicacidosis
respiratoryalkalosis
metabolic
alkalosis
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ABGsABGs
PaO2 7.0
PaCO2 4.5
H+ 37
HCO3- 25
PaO2 7.0
PaCO2 4.5
H+ 37
HCO3- 25
Type 1 respiratoryfailure
Type 1 respiratoryfailure
What are the physiological mechanismsfor hypoxia?
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ABGsABGs
PaO2 7.0
PaCO2 8.0
H+ 55
HCO3- 26
PaO2 7.0
PaCO2 8.0
H+ 55
HCO3- 26
DecompensatedType 2respiratory failure
DecompensatedType 2respiratory failure
What is the physiological mechanismsfor hypercapnia?
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ABGsABGs
PaO2 7.0
PaCO2 8.0
H+ 41
HCO3- 34
PaO2 7.0
PaCO2 8.0
H+ 41
HCO3- 34
Compensated Type2 respiratoryfailure
Compensated Type2 respiratoryfailure
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ABGsABGs
PaO2 18.0
PaCO2 1.7
H+ 22
HCO3- 15
PaO2 18.0
PaCO2 1.7
H+ 22
HCO3- 15
HyperventilationHyperventilation
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ABGsABGs
PaO2 18.0
PaCO2 1.7
H+ 60
HCO3- 10
PaO2 18.0
PaCO2 1.7
H+ 60
HCO3- 10
Metabolic acidosisMetabolic acidosis
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ECGsECGsWhen can they be helpful?
Arrhythmia
Cardiac ischaemiaLVF
Pericardial effusion
P.E.
RVF / pulmonary hypertension
When can they be helpful?
Arrhythmia
Cardiac ischaemiaLVF
Pericardial effusion
P.E.
RVF / pulmonary hypertension
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CXRCXR
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Case 1Case 1
62♀
Ex-smoker Progressive SOB over 18 months
Now 4/7 SOB with productive cough
O/E S p
O2
85% on air RR 30/min
AE, minor wheeze, hyperinflated
62♀
Ex-smoker Progressive SOB over 18 months
Now 4/7 SOB with productive cough
O/E S p
O2
85% on air RR 30/min
AE, minor wheeze, hyperinflated
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Ix:
Bloods - WCC
ECG – normal
ABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3- 26
CXR -
Ix:
Bloods - WCC
ECG – normal
ABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3- 26
CXR -
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DiagnosisDiagnosis
Exacerbation of COPD
Decompensated type 2 respiratoryfailure
Exacerbation of COPD
Decompensated type 2 respiratoryfailure
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Outcome fromExacerbation of
COPD
Outcome fromExacerbation of
COPD
Uncomplicated exacerbation
79%
Immediate intubation
1%
Resolve with nebuliser,
controlled oxygen, etc4%
NIV16%
Acidotic20%
Exacerbation of COPD100%
Men: 75/100,000/yr
Women: 57/100,000/yr Plant 2000
T t tT t t
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TreatmentTreatment
O
N
A
P
O
N
A
P
www.nice.org.uk/CG012NICEguideline
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TreatmentTreatmentO Oxygen
N Nebulised bronchodilators
A Antibiotics
P Prednisolone
O Oxygen
N Nebulised bronchodilators
A Antibiotics
P Prednisolone
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TreatmentTreatmentNebulised Bronchodilators
Salbutamol 2.5 – 5mg as often as needed
Ipratropium bromide 500mcg 6 hourly
If patient is hypercapnic, the nebuliser should be driven bycompressed air, not oxygen (to avoid worsening
hypercapnia).
If oxygen therapy is needed during the nebuliser, it shouldbe administered simultaneously by nasal cannulae.
Nebulised Bronchodilators
Salbutamol 2.5 – 5mg as often as needed
Ipratropium bromide 500mcg 6 hourly
If patient is hypercapnic, the nebuliser should be driven bycompressed air, not oxygen (to avoid worsening
hypercapnia).
If oxygen therapy is needed during the nebuliser, it shouldbe administered simultaneously by nasal cannulae.
Evidence Level D
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TreatmentTreatmentAntibioticsshould be used in exacerbations with
purulent sputum
How many?
One – combination of amoxycillin / macrolide onlyused in pneumonia
First-line and second-line choicesdictated by likely organism
- S. pneumoniae, H. influenza, M. catarrhalis
aminopenicillin or macrolide or tetracycline(NICE)
(Coamoxiclav is a pretty safe first choice, Levofloxacin a
useful second choice)
Antibioticsshould be used in exacerbations with
purulent sputum
How many?
One – combination of amoxycillin / macrolide onlyused in pneumonia
First-line and second-line choicesdictated by likely organism
- S. pneumoniae, H. influenza, M. catarrhalis
aminopenicillin or macrolide or tetracycline(NICE)
(Coamoxiclav is a pretty safe first choice, Levofloxacin a
useful second choice)
T t tT t t
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TreatmentTreatmentPrednisolone consider in
patientsadmitted tohospital
Prednisolone consider in
patientsadmitted tohospital
Cochrane Review
2005
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TreatmentTreatmentPrednisolone
How much & for how long?
30mg for 7-14 days (NICE)
40 – 50 mg for 1/52 (local practice)
Should you taper?Not if course less than 2-3 weeks
Patients MUST be given clear instructions aboutwhy, when and how to stop their steroids
Prednisolone
How much & for how long?
30mg for 7-14 days (NICE)
40 – 50 mg for 1/52 (local practice)
Should you taper?Not if course less than 2-3 weeks
Patients MUST be given clear instructions aboutwhy, when and how to stop their steroids
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TreatmentTreatmentOther Options
IV aminophylline – no evidence but often usedin most severe cases
Doxapram – remarkably effective in short
term (hours) but mostly superseded by NIV
ITU – in this country rationed by limitedprovision of beds
Other Options
IV aminophylline – no evidence but often usedin most severe cases
Doxapram – remarkably effective in short
term (hours) but mostly superseded by NIV
ITU – in this country rationed by limitedprovision of beds
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Principles of Treatment of
Respiratory Failure
Principles of Treatment of
Respiratory Failure
1. Hypoxia will kill you first
2. Acidosis will kill you later
1. Hypoxia will kill you first
2. Acidosis will kill you later
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Principles of Treatment of
Respiratory Failure
Principles of Treatment of
Respiratory Failure
1. Correct Hypoxia to acceptable levelsO2 –
if Type 1 RF - aim for PaO2 > 10
if Type 2 RF – give controlled O2 - aim for PaO27-8
2. If respiratory acidosis develops, supportthe respiratory muscles
NIV (BiPAP) - on medical ward
intubation and IPPV - ICU
(respiratory stimulants e.g. doxapram)
1. Correct Hypoxia to acceptable levelsO2 –
if Type 1 RF - aim for PaO2 > 10
if Type 2 RF – give controlled O2 - aim for PaO27-8
2. If respiratory acidosis develops, supportthe respiratory muscles
NIV (BiPAP) - on medical ward
intubation and IPPV - ICU
(respiratory stimulants e.g. doxapram)
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Oxygen Toxicity in COPDOxygen Toxicity in COPD
O i i i COO i i i CO
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Oxygen Toxicity in COPDOxygen Toxicity in COPD
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OxygenOxygenNasal cannula
Standard maskMask with reservoir bag
Nasal cannula
Standard maskMask with reservoir bag
Inspired oxygen concentration depends on patient’s minute ventilation – patient also
breathes in an unknown amount of air
Inspired oxygen concentration depends on patient’s minute ventilation – patient also
breathes in an unknown amount of air
2-4L/min 25-40%
5-15L/min
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Controlled Oxygen
Therapy
Controlled Oxygen
TherapyVenturi (Valve) Masks
Deliver a high flow of amixture of oxygen andentrained air of knowncomposition provided
flow rate of oxygen is setcorrectly (specified onmask)
Venturi (Valve) Masks
Deliver a high flow of amixture of oxygen andentrained air of knowncomposition provided
flow rate of oxygen is setcorrectly (specified onmask)
Controlled OxygenControlled Oxygen
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Controlled Oxygen
Therapy
Controlled Oxygen
TherapyVenturi (Valve) Masks
Works by Bernoulli’sprinciple – if oxygenspeeds up its
pressure drops and alarge quantity of airis sucked in
Venturi (Valve) Masks
Works by Bernoulli’sprinciple – if oxygenspeeds up its
pressure drops and alarge quantity of airis sucked in
Controlled OxygenControlled Oxygen
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Controlled Oxygen
Therapy
Controlled Oxygen
TherapyVenturi (Valve) Masks
Works by Bernoulli’s principle –if oxygen speeds up itspressure drops and a largequantity of air is sucked in
The patient is surrounded by a
bubble of air/oxygen ofknown concentration
Venturi (Valve) Masks
Works by Bernoulli’s principle –if oxygen speeds up itspressure drops and a largequantity of air is sucked in
The patient is surrounded by a
bubble of air/oxygen ofknown concentration
40% O2
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Non-invasive VentilationNon-invasive Ventilation
= ventilation without an ET tube
avoids
ventilator associated pneumonia
need for an ITU bed
allows
intermittent support
normal eating, drinking, communication
= ventilation without an ET tube
avoids
ventilator associated pneumonia
need for an ITU bed
allows
intermittent support
normal eating, drinking, communication
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NIV/BiPAPNIV/BiPAPHow is it given?
NIV/BiPAPNIV/BiPAP
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NIV/BiPAP non-invasive ventilation/bilevel positive
airway pressure
NIV/BiPAP non-invasive ventilation/bilevel positive
airway pressure
What is it?
Pressure
Time
4cmH2O
Inspiration Expiration
12cmH2O
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NIV/BiPAPNIV/BiPAPHow is it given?
By a tight-fitting maskattached to an NIVmachine.
Typically an air compressorBiPAP with O2 supply
direct to mask (%O2would then be limited to~45-50%) but can be anICU type ventilator (up to100% O2)
How is it given?
By a tight-fitting maskattached to an NIVmachine.
Typically an air compressorBiPAP with O2 supply
direct to mask (%O2would then be limited to~45-50%) but can be anICU type ventilator (up to100% O2)
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Case 2Case 265 ♀ PMH: IPF
Sudden onset of left-sided pleuritic chest
pain
O/E Dyspnoeic at rest RR 30/min
Bibasal crackles R>L
65 ♀ PMH: IPF
Sudden onset of left-sided pleuritic chest
pain
O/E Dyspnoeic at rest RR 30/min
Bibasal crackles R>L
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Case 2Case 2Ix:
Bloods – Normal including D-dimer
ABGs PaO2 7, PaCO2 4.5,…
ECG – normal
CXR -
Ix:
Bloods – Normal including D-dimer
ABGs PaO2 7, PaCO2 4.5,…
ECG – normal
CXR -
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Case 1Case 1
PneumothoraxPneumothorax
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PneumothoraxPneumothorax
Defn: Air in the pleural space
Primary – no associated lung disease
(subpleural bleb) Secondary – associated lung disease
(typically fibrosis or emphysema)
No of hospital admissions:Men 16.7 / 100 000 / yr (approx 250 in Greater
Glasgow)
Women 5.8 / 100 000 /yr
Smoking is the greatest risk factor 12% lifetime risk in smokers (cf 0.1% in non-
smokers)
Half recur within 4 years
Defn: Air in the pleural space
Primary – no associated lung disease
(subpleural bleb) Secondary – associated lung disease
(typically fibrosis or emphysema)
No of hospital admissions:Men 16.7 / 100 000 / yr (approx 250 in Greater
Glasgow)
Women 5.8 / 100 000 /yr
Smoking is the greatest risk factor 12% lifetime risk in smokers (cf 0.1% in non-
smokers)
Half recur within 4 years
BTS Guidelines 2003
Volume of PneumothoraxVolume of Pneumothorax
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Volume of PneumothoraxVolume of Pneumothorax
Small – visible rim of < 2cm
Large – visible rim of ≥ 2cm
Small – visible rim of < 2cm
Large – visible rim of ≥ 2cm
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Treatment 1Treatment 1
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Treatment 2Treatment 2
AspirationAspiration
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pp
X
+ +
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Chest DrainChest Drain
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Chest DrainChest Drain
X
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Chest DrainChest Drain
Complications of ChestComplications of Chest
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DrainDrain
Penetration of lung, stomach, spleen,liver, heart, great vessels
Pleural infection (1%)Surgical emphysema (malpositioned
tube or kinked/blocked tube)
Penetration of lung, stomach, spleen,liver, heart, great vessels
Pleural infection (1%)Surgical emphysema (malpositioned
tube or kinked/blocked tube)
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Myths DebunkedMyths Debunked Are expiratory films useful?
Does high flow oxygen work? Should we clamp drains before
removal?
Are large drains better than smalldrains?
What is first-line management of a
tension pneumothorax?
Are expiratory films useful?
Does high flow oxygen work? Should we clamp drains before
removal?
Are large drains better than smalldrains?
What is first-line management of a
tension pneumothorax?
No
YesNo (?)
No
No
YesNo (?)
No
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Tension PneumothoraxTension PneumothoraxIntrapleural pressure exceeds
atmospheric due to one-way valveeffect – results in venous return,
cardiac output, BPPatient rapidly distressed –
sweating, cyanosis,
HR,
RR,EMD/PEA arrest
Intrapleural pressure exceeds
atmospheric due to one-way valveeffect – results in venous return,
cardiac output, BPPatient rapidly distressed –
sweating, cyanosis,
HR,
RR,EMD/PEA arrest
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Tension PneumothoraxTension Pneumothorax
Not dependenton the size of
the
pneumothorax
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Tension PneumothoraxTension PneumothoraxTreatment
Cannula of at least4.5cm length in 2nd
ICS MCL
Treatment
Cannula of at least4.5cm length in 2nd
ICS MCL
X
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Tension PneumothoraxTension PneumothoraxTreatment
Cannula of at least4.5cm length in 2nd
ICS MCL
then
Chest drain
Treatment
Cannula of at least4.5cm length in 2nd
ICS MCL
then
Chest drain
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Case 3Case 335 ♂ PMH: UC
Sudden onset of SOB 3/7 ago
Productive cough and left sided pleurisy for 2/7
O/E pyrexial
Left basal crackles and dullness
35 ♂ PMH: UC
Sudden onset of SOB 3/7 ago
Productive cough and left sided pleurisy for 2/7
O/E pyrexial
Left basal crackles and dullness
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Ix:
Bloods - WCC; D-dimer
ECG – normal
ABGs - PaO2 9.0, PaCO2 5.3, …
CXR –
Ix:
Bloods - WCC; D-dimer
ECG – normal
ABGs - PaO2 9.0, PaCO2 5.3, …
CXR –
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Diff Δ:-
PTE
Pneumonia
Diff Δ:-
PTE
Pneumonia
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Pulmonary EmbolismPulmonary EmbolismAnnual incidence – 60-70 / 100 000 / yr
1000 in Greater GlasgowTypically PTE is present in 15 – 40% of
cases where the diagnosis is considered
Modern diagnostic pathway uses:-
clinical probability
D-dimer assayCTPA
Annual incidence – 60-70 / 100 000 / yr
1000 in Greater GlasgowTypically PTE is present in 15 – 40% of
cases where the diagnosis is considered
Modern diagnostic pathway uses:-
clinical probability
D-dimer assayCTPA
Pulmonary EmbolismPulmonary Embolism
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Diagnostic Pathway
PIOPED II AJM 2006
ClinicalProbability
ClinicalProbability
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yy
Risk of PTE
BTS Guidelines 2003
Clinical Probability ScoresClinical Probability Scores
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PIOPED II AJM 2006
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Revised Geneva ScoreRevised Geneva Score
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D-dimer AssayD-dimer AssayQuantitative ELISA based assays (e.g. VIDAS)
have sensitivity of ~ 95% But specificity poor
The only useful D-dimer result is a negativeone
Chance of having had a PTE with negative D-dimer is low clinical probability 0.7 – 2%
moderate clinical probability 5%
high clinical probability >15%
Quantitative ELISA based assays (e.g. VIDAS)
have sensitivity of ~ 95% But specificity poor
The only useful D-dimer result is a negativeone
Chance of having had a PTE with negative D-dimer is low clinical probability 0.7 – 2%
moderate clinical probability 5%
high clinical probability >15%
PIOPED II AJM 2006
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D-dimer AssayD-dimer AssayIt should not be done:-
As a screening test on all generalmedical patients
In high probability cases
It should not be done:-
As a screening test on all generalmedical patients
In high probability cases
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ImagingImaging CTPA
rapidly becoming the first line test
sensitivity may be as low as 83% (PIOPED II NEJM 2006)
however, safe to withhold anticoagulation if CTPAnegative (prevalence of further event by 3/12 ~
1.5%) in low/moderate risk debate as to best practice in CTPA –ve / high risk
patients
very useful for revealing alternative diagnoses
V/Q a useful alternative where CT contraindicated (e.g.
iodine allergy) – generally only useful if CXR normal
and no chronic cardiorespiratory disease
CTPA
rapidly becoming the first line test sensitivity may be as low as 83% (PIOPED II NEJM 2006)
however, safe to withhold anticoagulation if CTPAnegative (prevalence of further event by 3/12 ~
1.5%) in low/moderate risk debate as to best practice in CTPA –ve / high risk
patients
very useful for revealing alternative diagnoses
V/Q a useful alternative where CT contraindicated (e.g.
iodine allergy) – generally only useful if CXR normal
and no chronic cardiorespiratory disease
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TreatmentTreatment LMW h i LMW h i
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LMW heparinDifficulties arise with
- obese patients
- renal failure- rapid reversal
Oral anticoagulation with warfarinAim for INR of 2 – 3
Duration of anticoagulationTemporary risk factors 4-6/52
Idiopathic 3-6/12
Risk of major bleeding≤ 3% at 3/12
mortality ≤ 0.5%
Investigation for cancer usually unnecessary
LMW heparinDifficulties arise with
- obese patients
- renal failure- rapid reversal
Oral anticoagulation with warfarinAim for INR of 2 – 3
Duration of anticoagulationTemporary risk factors 4-6/52
Idiopathic 3-6/12
Risk of major bleeding≤ 3% at 3/12
mortality ≤ 0.5%
Investigation for cancer usually unnecessaryBTS Guidelines 2003
M i PTEM i PTE
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Massive PTEMassive PTEA pulmonary embolism so large as
to cause circulatory collapseUsually the patient has presented
with clear acute event often withsyncope and is in extremis
Signs of right heart failure with
hypoxia i.e. BP, JVP, RV gallop,clear chest
A pulmonary embolism so large as
to cause circulatory collapseUsually the patient has presented
with clear acute event often withsyncope and is in extremis
Signs of right heart failure with
hypoxia i.e. BP, JVP, RV gallop,clear chest
Investigation of massive
PTE
Investigation of massive
PTE
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PTEPTEIf patient peri-arrest, do not delay
treatment for investigations
If patient unstable, consider a
cardiac echo (looking for RVdilatation) as first-line test
If patient stabilises, proceed toCTPA
If patient peri-arrest, do not delay
treatment for investigations
If patient unstable, consider a
cardiac echo (looking for RVdilatation) as first-line test
If patient stabilises, proceed toCTPA
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Treatment of Massive PTETreatment of Massive PTE
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Thrombolysis
BTS Guidelines 2003
Other Treatment OptionsOther Treatment Options
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Other Treatment OptionsOther Treatment Options
Clot fragmentation by pulmonaryartery catheter / interventional
radiology
Embolectomy
Clot fragmentation by pulmonaryartery catheter / interventional
radiology
Embolectomy
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How does a PE make you hypoxic?
When would you give iv heparin?
thrombolysis?
an IVC filter?
How long should you anticoagulate?
Should you investigate for cancer?
How does a PE make you hypoxic?
When would you give iv heparin?
thrombolysis?
an IVC filter?
How long should you anticoagulate?
Should you investigate for cancer?
D dimerD dimer
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D-dimerD-dimerSensitive but not specific test for VTE
Allows you to rule out PTE or DVT inpatients with low / moderate clinicalprobability (VIDAS assay)
It should not be done:-As a screening test on all general medical
patients
In high probability casesOnly useful if negative
Sensitive but not specific test for VTE
Allows you to rule out PTE or DVT inpatients with low / moderate clinicalprobability (VIDAS assay)
It should not be done:-As a screening test on all general medical
patients
In high probability casesOnly useful if negative
Clinical ProbabilityClinical Probability
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Clinical ProbabilityClinical ProbabilityIn a patient with clinical features of PTE
(sudden onset SOB, chest pain,haemoptysis…..)
a) Is there no other reasonable clinicalexplanation?
b) Is there a major risk factor?
a AND b HIGH
a OR b but not both MEDIUMneither a nor b LOW
In a patient with clinical features of PTE(sudden onset SOB, chest pain,haemoptysis…..)
a) Is there no other reasonable clinicalexplanation?
b) Is there a major risk factor?
a AND b HIGH
a OR b but not both MEDIUMneither a nor b LOW
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Case 2Case 2
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Case 2Case 2 45 ♀
SOB over several months
Worse at night, disturbing sleep
Wheezy at times with productive cough
Son recently acquired pet rat
O/E Speaking in short sentences
HR 120/min RR 30/min
PEF – not recorded Sp02 93% on air
Widespread wheeze
45 ♀
SOB over several months
Worse at night, disturbing sleep
Wheezy at times with productive cough
Son recently acquired pet rat
O/E Speaking in short sentences
HR 120/min RR 30/min
PEF – not recorded Sp02 93% on air
Widespread wheeze
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Ix:
Bloods – normal
ECG – normal
ABGs PaO2 8, PaCO2 3.9,…
CXR
Ix:
Bloods – normal
ECG – normal
ABGs PaO2 8, PaCO2 3.9,…
CXR
CXRCXR
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CXRCXR
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How severe?How severe?
Severity of Acute AsthmaSeverity of Acute Asthma
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Treatment of Acute
Asthma
Treatment of Acute
Asthma
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AsthmaAsthma
Treatment of Acute
Asthma
Treatment of Acute
Asthma
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AsthmaAsthma
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Anaphylaxis caseAnaphylaxis case
Correction of Hypoxia and
Hypercapnia
Correction of Hypoxia and
Hypercapnia
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yp pyp p Correct hypercapnia by increasing alveolar ventilation
Correct hypoxia by reducing shunt i.e. you need toimprove O2 delivery or decrease blood supply todiseased areas
Correct hypercapnia by increasing alveolar ventilation
Correct hypoxia by reducing shunt i.e. you need toimprove O2 delivery or decrease blood supply todiseased areas
Uncontrolled OxygenUncontrolled Oxygen
2L/min by nasal cannula does notnecesssarily give 28%
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2
20
2
10
Time
Flow
necesssarily give 28%
Uncontrolled OxygenUncontrolled Oxygen
2L/min by nasal cannula does notnecesssarily give 28%
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2
20
2
10
Time
Flow
necesssarily give 28%
24% 35%
Recommended