emergency respiratory gla uk

8/17/2019 Emergency Respiratory Gla UK

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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


Medical Emergencies

The burden of lung disease. 2nd Edition BTS 2006


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Respiratory Emergencies


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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Myocardial ischaemiaPericardial pain

retrosternal

pleuritic

relieved by sitting forward

worse on swallowing, twisting andwith sternal pressure


retrosternal

pleuritic

relieved by sitting forward

worse on swallowing, twisting andwith sternal pressure


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Respiratorytypically not central

pleuritic


Respiratorytypically not central

pleuritic


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Respiratory

Oesophagealretrosternal

heart burncan be indistinguishable from cardiac

pain


Respiratory

Oesophagealretrosternal

heart burncan be indistinguishable from cardiac

pain


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RespiratoryOesophageal

Musculoskeletallocalised

associated with tenderness


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


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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Respiratory Failure


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


Works by Bernoulli’sprinciple – if oxygenspeeds up its

pressure drops and alarge quantity of airis sucked in


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


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


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


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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X


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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


ICS MCL

X


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Tension PneumothoraxTension PneumothoraxTreatment


ICS MCL

then

Chest drain

Treatment


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


103/112

Ix:

Bloods – normal

ECG – normal


CXR

Ix:

Bloods – normal

ECG – normal


CXR

CXRCXR


104/112

CXRCXR


105/112

How severe?How severe?

Severity of Acute AsthmaSeverity of Acute Asthma


106/112

Treatment of Acute

Asthma

Treatment of Acute

Asthma


107/112

AsthmaAsthma

Treatment of Acute

Asthma

Treatment of Acute

Asthma


108/112

AsthmaAsthma


109/112

Anaphylaxis caseAnaphylaxis case

Correction of Hypoxia and

Hypercapnia

Correction of Hypoxia and

Hypercapnia


110/112

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%


111/112

2

20

2

10

Time

Flow

necesssarily give 28%

Uncontrolled OxygenUncontrolled Oxygen

2L/min by nasal cannula does notnecesssarily give 28%


112/112

2

20

2

10

Time

Flow

necesssarily give 28%

24% 35%

emergency respiratory gla uk

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