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Acute Respiratory Emergencies
Acute Respiratory Emergencies
Martin JohnsonConsultant PhysicianGartnavel / Western
Martin JohnsonConsultant PhysicianGartnavel / Western
SummarySummary
What to expect - what are the common respiratory emergencies?How to recognise the problem?How to manage the problem?
What to expect - what are the common respiratory emergencies?How to recognise the problem?How to manage the problem?
Relative Frequency of Medical EmergenciesRelative Frequency of Medical Emergencies
The burden of lung disease. 2nd Edition BTS 2006
Relative Frequency of Respiratory Emergencies
Relative Frequency of Respiratory Emergencies
The burden of lung disease. 2nd Edition BTS 2006
Immediate AssessmentImmediate Assessment
How to recognise the problem?
How to recognise the problem?
HistoryImportance of the HPC
Examination
Investigation
HistoryImportance of the HPC
Examination
Investigation
SymptomsSymptoms
DyspnoeaChest painHaemoptysis
DyspnoeaChest painHaemoptysis
SymptomsSymptoms
DyspnoeaChest painHaemoptysis
DyspnoeaChest painHaemoptysis
Dyspnoea: Pattern of Onset
Dyspnoea: Pattern of Onset
SuddenPneumothoraxPTEAspirationCardiac event –arrhythmia, MI
Over hours / daysAsthmaPneumoniaPulmonary oedema
SuddenPneumothoraxPTEAspirationCardiac event –arrhythmia, MI
Over hours / daysAsthmaPneumoniaPulmonary oedema
IntermittentAsthmaHyperventilation
ProgressiveCOPDIPFPleural effusionAnaemiaLVF Pulmonary hypertension
IntermittentAsthmaHyperventilation
ProgressiveCOPDIPFPleural effusionAnaemiaLVF Pulmonary hypertension
SymptomsSymptoms
DyspnoeaChest painHaemoptysis
DyspnoeaChest painHaemoptysis
Chest PainChest Pain
Myocardial ischaemiacentral radiating to the jaw / arm(s)squeezing / crushing / heavy weightaggravated by exertionrelieved by rest / GTNassociated autonomic features
Myocardial ischaemiacentral radiating to the jaw / arm(s)squeezing / crushing / heavy weightaggravated by exertionrelieved by rest / GTNassociated autonomic features
Chest PainChest Pain
Myocardial ischaemiaPericardial pain
retrosternalpleuriticrelieved by sitting forwardworse on swallowing, twisting and with sternal pressure
Myocardial ischaemiaPericardial pain
retrosternalpleuriticrelieved by sitting forwardworse on swallowing, twisting and with sternal pressure
Chest PainChest Pain
Myocardial ischaemiaPericardial painRespiratory
typically not centralpleuritic
Myocardial ischaemiaPericardial painRespiratory
typically not centralpleuritic
Chest PainChest Pain
Myocardial ischaemiaPericardial painRespiratoryOesophageal
retrosternalheart burncan be indistinguishable from cardiac pain
Myocardial ischaemiaPericardial painRespiratoryOesophageal
retrosternalheart burncan be indistinguishable from cardiac pain
Chest PainChest Pain
Myocardial ischaemiaPericardial painRespiratoryOesophagealMusculoskeletal
localisedassociated with tenderness
Myocardial ischaemiaPericardial painRespiratoryOesophagealMusculoskeletal
localisedassociated with tenderness
SymptomsSymptoms
DyspnoeaChest painHaemoptysis
DyspnoeaChest painHaemoptysis
HaemoptysisHaemoptysis
0
5
10
15
20
25
Perc
enta
ge o
f cas
es
Neoplasms
Bronchiectasis
Miscellaneous
Bronchitis
BacterialpneumoniaTuberculosis
Cryptogenic
Misc – PTE, LVF, aspergilloma, lung abscess, atypical mycobacteria
Other Points from the History
Other Points from the History
Don’t overlook the rest of the historyPMH - e.g. previous DVTDrug history - e.g. new medicationsSmokingOccupation e.g. baker, asbestos exposurePets especially birdsFH
Don’t overlook the rest of the historyPMH - e.g. previous DVTDrug history - e.g. new medicationsSmokingOccupation e.g. baker, asbestos exposurePets especially birdsFH
ExaminationExamination
Do not make the diagnosis from the history aloneIt is negligent not to examine a patient with new symptomsE.g. arrhythmia (esp AF / flutter)
pneumothoraxpericardial effusion
Do not make the diagnosis from the history aloneIt is negligent not to examine a patient with new symptomsE.g. arrhythmia (esp AF / flutter)
pneumothoraxpericardial effusion
ObservationsObservations
HR
BP
Temp
HR
BP
Temp
SpO2
FIO2
RR
SpO2
FIO2
RR
Examination of the Chest
ExpansionPercussionAuscultation
Air entryQuality of breath soundsAdded soundsVocal resonance
ExaminationExamination
WheezeAsthma / COPDHeart failureAnaphylaxisForeign body
StridorForeign bodyEpiglottitisAnaphylaxis
WheezeAsthma / COPDHeart failureAnaphylaxisForeign body
StridorForeign bodyEpiglottitisAnaphylaxis
CracklesPulmonary oedemaFibrosisPneumoniaBronchiectasis
Clear chestPTEPneumothoraxHyperventilationMetabolic acidosisAnaemiaDrug overdose
CracklesPulmonary oedemaFibrosisPneumoniaBronchiectasis
Clear chestPTEPneumothoraxHyperventilationMetabolic acidosisAnaemiaDrug overdose
InvestigationsInvestigations
Blood – FBC, U&Es, (D-dimer, Tn, CRP)ABGsECGCXR
Blood – FBC, U&Es, (D-dimer, Tn, CRP)ABGsECGCXR
ABGsABGs
Normal values
PaO2 10 – 13.3 kPaPaCO2 4.8 – 6.1 kPaH+ 35 – 45HCO3- 22 – 26 mmol/L
DoWrite the results in the notesDocument oxygen prescription
Normal values
PaO2 10 – 13.3 kPaPaCO2 4.8 – 6.1 kPaH+ 35 – 45HCO3- 22 – 26 mmol/L
DoWrite the results in the notesDocument oxygen prescription
Interpretation of Arterial Blood Gases
Interpretation of Arterial Blood Gases
PaCO2 PaCO2
H+
respiratory acidosis metabolic
acidosisrespiratory alkalosis
metabolic alkalosis
ABGsABGs
PaO2 7.0PaCO2 4.5 H+ 37HCO3- 25
PaO2 7.0PaCO2 4.5 H+ 37HCO3- 25
Type 1 respiratory failure
Type 1 respiratory failure
What are the physiological mechanisms for hypoxia?
ABGsABGs
PaO2 7.0PaCO2 8.0 H+ 55HCO3- 26
PaO2 7.0PaCO2 8.0 H+ 55HCO3- 26
Decompensated Type 2 respiratory failure
Decompensated Type 2 respiratory failure
What is the physiological mechanisms for hypercapnia?
ABGsABGs
PaO2 7.0PaCO2 8.0 H+ 41HCO3- 34
PaO2 7.0PaCO2 8.0 H+ 41HCO3- 34
Compensated Type 2 respiratory failure
Compensated Type 2 respiratory failure
ABGsABGs
PaO2 18.0PaCO2 1.7 H+ 22HCO3- 15
PaO2 18.0PaCO2 1.7 H+ 22HCO3- 15
HyperventilationHyperventilation
ABGsABGs
PaO2 18.0PaCO2 1.7 H+ 60HCO3- 10
PaO2 18.0PaCO2 1.7 H+ 60HCO3- 10
Metabolic acidosisMetabolic acidosis
ECGsECGs
When can they be helpful?
ArrhythmiaCardiac ischaemiaLVFPericardial effusionP.E.RVF / pulmonary hypertension
When can they be helpful?
ArrhythmiaCardiac ischaemiaLVFPericardial effusionP.E.RVF / pulmonary hypertension
CXRCXR
Case 1Case 1
62 ♀ Ex-smokerProgressive SOB over 18 monthsNow 4/7 SOB with productive cough
O/E SpO2 85% on air RR 30/minAE, minor wheeze, hyperinflated
62 ♀ Ex-smokerProgressive SOB over 18 monthsNow 4/7 SOB with productive cough
O/E SpO2 85% on air RR 30/minAE, minor wheeze, hyperinflated
Ix:
Bloods - WCCECG – normalABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3
- 26
CXR -
Ix:
Bloods - WCCECG – normalABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3
- 26
CXR -
DiagnosisDiagnosis
Exacerbation of COPD
Decompensated type 2 respiratory failure
Exacerbation of COPD
Decompensated type 2 respiratory failure
Outcome from Exacerbation of
COPD
Outcome from Exacerbation of
COPDUncomplicated exacerbation
79%Immediate intubation
1%
Resolve with nebuliser,controlled oxygen, etc
4%
NIV16%
Acidotic20%
Exacerbation of COPD100%
Men: 75/100,000/yrWomen: 57/100,000/yr Plant 2000
TreatmentTreatment
O
N
A
P
O
N
A
P
www.nice.org.uk/CG012NICEguideline
TreatmentTreatment
O Oxygen
N Nebulised bronchodilators
A Antibiotics
P Prednisolone
O Oxygen
N Nebulised bronchodilators
A Antibiotics
P Prednisolone
TreatmentTreatment
Nebulised Bronchodilators
Salbutamol 2.5 – 5mg as often as needed
Ipratropium bromide 500mcg 6 hourly
If patient is hypercapnic, the nebuliser should be driven by compressed air, not oxygen (to avoid worsening hypercapnia). If oxygen therapy is needed during the nebuliser, it should be 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 by compressed air, not oxygen (to avoid worsening hypercapnia). If oxygen therapy is needed during the nebuliser, it should be administered simultaneously by nasal cannulae.
Evidence Level D
TreatmentTreatment
Antibioticsshould be used in exacerbations with purulent sputumHow many?
One – combination of amoxycillin / macrolide only used in pneumonia
First-line and second-line choicesdictated by likely organism
- S. pneumoniae, H. influenza, M. catarrhalisaminopenicillin or macrolide or tetracycline (NICE)(Coamoxiclav is a pretty safe first choice, Levofloxacin a useful second choice)
Antibioticsshould be used in exacerbations with purulent sputumHow many?
One – combination of amoxycillin / macrolide only used in pneumonia
First-line and second-line choicesdictated by likely organism
- S. pneumoniae, H. influenza, M. catarrhalisaminopenicillin or macrolide or tetracycline (NICE)(Coamoxiclav is a pretty safe first choice, Levofloxacin a useful second choice)
TreatmentTreatmentPrednisoloneconsider in patients admitted to hospital
Prednisoloneconsider in patients admitted to hospital
Cochrane Review 2005
TreatmentTreatment
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 weeksPatients MUST be given clear instructions about why, 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 weeksPatients MUST be given clear instructions about why, when and how to stop their steroids
TreatmentTreatment
Other OptionsIV aminophylline – no evidence but often used in most severe casesDoxapram – remarkably effective in short term (hours) but mostly superseded by NIVITU – in this country rationed by limited provision of beds
Other OptionsIV aminophylline – no evidence but often used in most severe casesDoxapram – remarkably effective in short term (hours) but mostly superseded by NIVITU – in this country rationed by limited provision of beds
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
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 > 10if Type 2 RF – give controlled O2 - aim for PaO27-8
2. If respiratory acidosis develops, support the respiratory muscles
NIV (BiPAP) - on medical wardintubation and IPPV - ICU(respiratory stimulants e.g. doxapram)
1. Correct Hypoxia to acceptable levelsO2 –
if Type 1 RF - aim for PaO2 > 10if Type 2 RF – give controlled O2 - aim for PaO27-8
2. If respiratory acidosis develops, support the respiratory muscles
NIV (BiPAP) - on medical wardintubation and IPPV - ICU(respiratory stimulants e.g. doxapram)
Oxygen Toxicity in COPDOxygen Toxicity in COPD
Oxygen Toxicity in COPDOxygen Toxicity in COPD
OxygenOxygen
Nasal cannulaStandard maskMask with reservoir bag
Nasal cannulaStandard 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 <50%
15L/min <70%
Controlled Oxygen Therapy
Controlled Oxygen Therapy
Venturi (Valve) MasksDeliver a high flow of a
mixture of oxygen and entrained air of known composition provided flow rate of oxygen is set correctly (specified on mask)
Venturi (Valve) MasksDeliver a high flow of a
mixture of oxygen and entrained air of known composition provided flow rate of oxygen is set correctly (specified on mask)
Controlled Oxygen Therapy
Controlled Oxygen Therapy
Venturi (Valve) MasksWorks by Bernoulli’s
principle – if oxygen speeds up its pressure drops and a large quantity of air is sucked in
Venturi (Valve) MasksWorks by Bernoulli’s
principle – if oxygen speeds up its pressure drops and a large quantity of air is sucked in
Controlled Oxygen Therapy
Controlled Oxygen Therapy
Venturi (Valve) MasksWorks by Bernoulli’s principle –
if oxygen speeds up its pressure drops and a large quantity of air is sucked in
The patient is surrounded by a bubble of air/oxygen of known concentration
Venturi (Valve) MasksWorks by Bernoulli’s principle –
if oxygen speeds up its pressure drops and a large quantity of air is sucked in
The patient is surrounded by a bubble of air/oxygen of known concentration
40% O2
Non-invasive VentilationNon-invasive Ventilation
= ventilation without an ET tube
avoidsventilator associated pneumonianeed for an ITU bed
allowsintermittent supportnormal eating, drinking, communication
= ventilation without an ET tube
avoidsventilator associated pneumonianeed for an ITU bed
allowsintermittent supportnormal eating, drinking, communication
NIV/BiPAPNIV/BiPAPHow is it given?
NIV/BiPAPnon-invasive ventilation/bilevel positive
airway pressure
NIV/BiPAPnon-invasive ventilation/bilevel positive
airway pressure
What is it?
Pressure
Time
4cmH2O
Inspiration Expiration12cmH2O
NIV/BiPAPNIV/BiPAPHow is it given?By a tight-fitting mask
attached to an NIV machine.
Typically an air compressor BiPAP with O2 supply direct to mask (%O2would then be limited to ~45-50%) but can be an ICU type ventilator (up to 100% O2)
How is it given?By a tight-fitting mask
attached to an NIV machine.
Typically an air compressor BiPAP with O2 supply direct to mask (%O2would then be limited to ~45-50%) but can be an ICU type ventilator (up to 100% O2)
Case 2 Case 2
65 ♀ PMH: IPFSudden onset of left-sided pleuritic chest painO/E Dyspnoeic at rest RR 30/minBibasal crackles R>L
65 ♀ PMH: IPFSudden onset of left-sided pleuritic chest painO/E Dyspnoeic at rest RR 30/minBibasal crackles R>L
Case 2Case 2
Ix:
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 -
Case 1Case 1
PneumothoraxPneumothoraxDefn: Air in the pleural spacePrimary – 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 factor12% lifetime risk in smokers (cf 0.1% in non-smokers)
Half recur within 4 years
Defn: Air in the pleural spacePrimary – 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 factor12% lifetime risk in smokers (cf 0.1% in non-smokers)
Half recur within 4 years
BTS Guidelines 2003
Volume of PneumothoraxVolume of Pneumothorax
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
Treatment 1Treatment 1
Treatment 2Treatment 2
AspirationAspiration
X
+ +
Chest DrainChest Drain
Chest DrainChest Drain
X
Chest DrainChest Drain
Complications of Chest Drain
Complications of Chest Drain
Penetration of lung, stomach, spleen, liver, heart, great vesselsPleural infection (1%)Surgical emphysema (malpositionedtube or kinked/blocked tube)
Penetration of lung, stomach, spleen, liver, heart, great vesselsPleural infection (1%)Surgical emphysema (malpositionedtube or kinked/blocked tube)
Myths DebunkedMyths Debunked
Are expiratory films useful?Does high flow oxygen work?Should we clamp drains before removal?Are large drains better than small drains?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 small drains?What is first-line management of a tension pneumothorax?
NoYesNo (?)
No
NoYesNo (?)
No
Tension PneumothoraxTension Pneumothorax
Intrapleural pressure exceeds atmospheric due to one-way valve effect – results in venous return,
cardiac output, BPPatient rapidly distressed –sweating, cyanosis, HR, RR, EMD/PEA arrest
Intrapleural pressure exceeds atmospheric due to one-way valve effect – results in venous return,
cardiac output, BPPatient rapidly distressed –sweating, cyanosis, HR, RR, EMD/PEA arrest
Tension PneumothoraxTension Pneumothorax
Not dependent on the size of the pneumothorax
Tension PneumothoraxTension Pneumothorax
Treatment
Cannula of at least 4.5cm length in 2nd
ICS MCL
Treatment
Cannula of at least 4.5cm length in 2nd
ICS MCL
X
Tension PneumothoraxTension Pneumothorax
Treatment
Cannula of at least 4.5cm length in 2nd
ICS MCL
then
Chest drain
Treatment
Cannula of at least 4.5cm length in 2nd
ICS MCL
then
Chest drain
Case 3Case 3
35 ♂ PMH: UCSudden onset of SOB 3/7 agoProductive cough and left sided pleurisy for 2/7
O/E pyrexialLeft basal crackles and dullness
35 ♂ PMH: UCSudden onset of SOB 3/7 agoProductive cough and left sided pleurisy for 2/7
O/E pyrexialLeft basal crackles and dullness
Ix:
Bloods - WCC; D-dimerECG – normalABGs - PaO2 9.0, PaCO2 5.3, …
CXR –
Ix:
Bloods - WCC; D-dimerECG – normalABGs - PaO2 9.0, PaCO2 5.3, …
CXR –
Diff Δ:-PTEPneumonia
Diff Δ:-PTEPneumonia
Pulmonary EmbolismPulmonary Embolism
Annual incidence – 60-70 / 100 000 / yr 1000 in Greater Glasgow
Typically PTE is present in 15 – 40% of cases where the diagnosis is consideredModern diagnostic pathway uses:-
clinical probabilityD-dimer assayCTPA
Annual incidence – 60-70 / 100 000 / yr 1000 in Greater Glasgow
Typically PTE is present in 15 – 40% of cases where the diagnosis is consideredModern diagnostic pathway uses:-
clinical probabilityD-dimer assayCTPA
Pulmonary EmbolismPulmonary EmbolismDiagnostic Pathway
PIOPED II AJM 2006
Clinical Probability
Clinical Probability
Risk of PTE
BTS Guidelines 2003
Clinical Probability ScoresClinical Probability Scores
PIOPED II AJM 2006
Revised Geneva ScoreRevised Geneva Score
D-dimer AssayD-dimer Assay
Quantitative ELISA based assays (e.g. VIDAS) have sensitivity of ~ 95%But specificity poor
The only useful D-dimer result is a negative one
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 negative one
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
D-dimer AssayD-dimer Assay
It should not be done:-As a screening test on all general medical patientsIn high probability cases
It should not be done:-As a screening test on all general medical patientsIn high probability cases
ImagingImaging
CTPArapidly becoming the first line testsensitivity may be as low as 83% (PIOPED II NEJM 2006)
however, safe to withhold anticoagulation if CTPA negative (prevalence of further event by 3/12 ~ 1.5%) in low/moderate riskdebate as to best practice in CTPA –ve / high risk patientsvery useful for revealing alternative diagnoses
V/Qa useful alternative where CT contraindicated (e.g. iodine allergy) – generally only useful if CXR normal and no chronic cardiorespiratory disease
CTPArapidly becoming the first line testsensitivity may be as low as 83% (PIOPED II NEJM 2006)
however, safe to withhold anticoagulation if CTPA negative (prevalence of further event by 3/12 ~ 1.5%) in low/moderate riskdebate as to best practice in CTPA –ve / high risk patientsvery useful for revealing alternative diagnoses
V/Qa useful alternative where CT contraindicated (e.g. iodine allergy) – generally only useful if CXR normal and no chronic cardiorespiratory disease
TreatmentTreatmentLMW heparin
Difficulties arise with - obese patients- renal failure- rapid reversal
Oral anticoagulation with warfarinAim for INR of 2 – 3
Duration of anticoagulationTemporary risk factors 4-6/52Idiopathic 3-6/12
Risk of major bleeding≤ 3% at 3/12mortality ≤ 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 4-6/52Idiopathic 3-6/12
Risk of major bleeding≤ 3% at 3/12mortality ≤ 0.5%
Investigation for cancer usually unnecessaryBTS Guidelines 2003
Massive PTEMassive PTE
A pulmonary embolism so large as to cause circulatory collapseUsually the patient has presented with clear acute event often with syncope and is in extremisSigns 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 with syncope and is in extremisSigns of right heart failure with hypoxia i.e. BP, JVP, RV gallop, clear chest
Investigation of massive PTE
Investigation of massive PTE
If patient peri-arrest, do not delay treatment for investigationsIf patient unstable, consider a cardiac echo (looking for RV dilatation) as first-line testIf patient stabilises, proceed to CTPA
If patient peri-arrest, do not delay treatment for investigationsIf patient unstable, consider a cardiac echo (looking for RV dilatation) as first-line testIf patient stabilises, proceed to CTPA
Treatment of Massive PTETreatment of Massive PTE
Thrombolysis
BTS Guidelines 2003
Other Treatment OptionsOther Treatment Options
Clot fragmentation by pulmonary artery catheter / interventional radiology
Embolectomy
Clot fragmentation by pulmonary artery catheter / interventional radiology
Embolectomy
How does a PE make you hypoxic?
When would you giveiv 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 giveiv heparin?thrombolysis?an IVC filter?
How long should you anticoagulate?
Should you investigate for cancer?
D-dimerD-dimer
Sensitive but not specific test for VTEAllows you to rule out PTE or DVT in patients with low / moderate clinical probability (VIDAS assay)It should not be done:-
As a screening test on all general medical patientsIn high probability cases
Only useful if negative
Sensitive but not specific test for VTEAllows you to rule out PTE or DVT in patients with low / moderate clinical probability (VIDAS assay)It should not be done:-
As a screening test on all general medical patientsIn high probability cases
Only useful if negative
Clinical ProbabilityClinical Probability
In a patient with clinical features of PTE (sudden onset SOB, chest pain, haemoptysis…..)
a) Is there no other reasonable clinical explanation?
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 clinical explanation?
b) Is there a major risk factor?
a AND b HIGH a OR b but not both MEDIUMneither a nor b LOW
Case 2Case 2
45 ♀SOB over several months
Worse at night, disturbing sleepWheezy at times with productive coughSon recently acquired pet rat
O/E Speaking in short sentencesHR 120/min RR 30/minPEF – not recorded Sp02 93% on airWidespread wheeze
45 ♀SOB over several months
Worse at night, disturbing sleepWheezy at times with productive coughSon recently acquired pet rat
O/E Speaking in short sentencesHR 120/min RR 30/minPEF – not recorded Sp02 93% on airWidespread wheeze
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
How severe?How severe?
Severity of Acute AsthmaSeverity of Acute Asthma
Treatment of Acute Asthma
Treatment of Acute Asthma
Treatment of Acute Asthma
Treatment of Acute Asthma
Anaphylaxis caseAnaphylaxis case
Correction of Hypoxia and Hypercapnia
Correction of Hypoxia and Hypercapnia
Correct hypercapnia by increasing alveolar ventilationCorrect hypoxia by reducing shunt i.e. you need to improve O2 delivery or decrease blood supply to diseased areas
Correct hypercapnia by increasing alveolar ventilationCorrect hypoxia by reducing shunt i.e. you need to improve O2 delivery or decrease blood supply to diseased areas
Uncontrolled OxygenUncontrolled Oxygen
2
20
2
10
Time
Flow
2L/min by nasal cannula does not necesssarily give 28%
Uncontrolled OxygenUncontrolled Oxygen
2
20
2
10
Time
Flow
2L/min by nasal cannula does not necesssarily give 28%
24% 35%