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Acute Respiratory

Emergencies
Martin Johnson
Consultant Physician
Gartnavel / Western

Summary
What to expect - what are the
common respiratory emergencies?
How to recognise the problem?
How to manage the problem?

Relative Frequency of
Medical Emergencies

The burden of lung disease. 2nd Edition BTS 2006

Relative Frequency of
Respiratory Emergencies

The burden of lung disease. 2nd Edition BTS 2006

Immediate Assessment

How to recognise the


problem?
History
Importance of the HPC

Examination
Investigation

Symptoms
Dyspnoea
Chest pain
Haemoptysis

Symptoms
Dyspnoea
Chest pain
Haemoptysis

Dyspnoea: Pattern of
Onset
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

Symptoms
Dyspnoea
Chest pain
Haemoptysis

Chest Pain
Myocardial ischaemia
central
radiating to the jaw / arm(s)
squeezing / crushing / heavy weight
aggravated by exertion
relieved by rest / GTN
associated autonomic features

Chest Pain
Myocardial ischaemia
Pericardial pain
retrosternal
pleuritic
relieved by sitting forward
worse on swallowing, twisting and
with sternal pressure

Chest Pain
Myocardial ischaemia
Pericardial pain
Respiratory
typically not central
pleuritic

Chest Pain
Myocardial ischaemia
Pericardial pain
Respiratory
Oesophageal
retrosternal
heart burn
can be indistinguishable from cardiac
pain

Chest Pain
Myocardial ischaemia
Pericardial pain
Respiratory
Oesophageal
Musculoskeletal
localised
associated with tenderness

Symptoms
Dyspnoea
Chest pain
Haemoptysis

Haemoptysis
Neoplasms

Percentage of cases

25
20
15
10
5
0

Bronchiectasis
Miscellaneous
Bronchitis
Bacterial
pneumonia
Tuberculosis
Cryptogenic

Misc PTE, LVF, aspergilloma, lung abscess, atypical mycobacteria

Other Points from the


History
Dont overlook the rest of the history
PMH - e.g. previous DVT
Drug history - e.g. new medications
Smoking
Occupation e.g. baker, asbestos exposure
Pets especially birds
FH

Examination
Do not make the diagnosis from the
history alone
It is negligent not to examine a patient
with new symptoms
E.g.
arrhythmia (esp AF / flutter)
pneumothorax
pericardial effusion

Observations
HR

SpO2

BP

FIO2

Temp

RR

Examination
of the Chest
Expansion
Percussion
Auscultation
Air entry
Quality of breath sounds
Added sounds
Vocal resonance

Examination
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

Investigations
Blood FBC, U&Es, (D-dimer, Tn,
CRP)
ABGs
ECG
CXR

ABGs
Normal values
PaO2
PaCO2
H+
HCO3-

10 13.3 kPa
4.8 6.1 kPa
35 45
22 26 mmol/L

Do
Write the results in the notes
Document oxygen prescription

Interpretation of Arterial Blood


Gases
H+

respiratory
acidosis

PaCO2

PaCO2

metabolic
acidosis

K
respiratory
alkalosis

metabolic
alkalosis

ABGs
PaO2
PaCO2
H+
HCO3-

7.0
4.5
37
25

Type 1 respiratory
failure

What are the physiological mechanisms


for hypoxia?

ABGs
PaO2
PaCO2
H+
HCO3-

7.0
8.0
55
26

Decompensated
Type 2
respiratory failure

What is the physiological mechanisms


for hypercapnia?

ABGs
PaO2
PaCO2
H+
HCO3-

7.0
8.0
41
34

Compensated Type
2 respiratory
failure

ABGs
PaO2
PaCO2
H+
HCO3-

18.0
1.7
22
15

Hyperventilation

ABGs
PaO2
PaCO2
H+
HCO3-

18.0
1.7
60
10

Metabolic acidosis

ECGs
When can they be helpful?
Arrhythmia
Cardiac ischaemia
LVF
Pericardial effusion
P.E.
RVF / pulmonary hypertension

CXR

Case 1
62 Ex-smoker
Progressive SOB over 18 months
Now 4/7  SOB with productive cough
O/E SpO2 85% on air RR 30/min
AE, minor wheeze, hyperinflated

Ix:
Bloods -  WCC
ECG normal
ABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3- 26
CXR -

Diagnosis
Exacerbation of COPD
Decompensated type 2 respiratory
failure

Outcome from
Exacerbation of
COPD

Exacerbation of COPD
100%
Uncomplicated exacerbation
79%

Immediate intubation
1%

Acidotic
20%
Resolve with nebuliser,
controlled oxygen, etc
4%

NIV
16%

Men: 75/100,000/yr
Women: 57/100,000/yr

Plant 2000

Treatment
www.nice.org.uk/CG012NICEguideline

O
N
A
P

Treatment
O

Oxygen

Nebulised bronchodilators

Antibiotics

Prednisolone

Treatment
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

Treatment
Antibiotics
should be used in exacerbations with
purulent sputum
How many?
One combination of amoxycillin / macrolide only
used in pneumonia

First-line and second-line choices


dictated 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)

Treatment
Prednisolone
consider in
patients
admitted to
hospital

Cochrane Review
2005

Treatment
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 about
why, when and how to stop their steroids

Treatment
Other Options
IV aminophylline no evidence but often used
in most severe cases
Doxapram remarkably effective in short
term (hours) but mostly superseded by NIV
ITU in this country rationed by limited
provision of beds

Principles of Treatment of
Respiratory Failure
1. Hypoxia will kill you first
2. Acidosis will kill you later

Principles of Treatment of
Respiratory Failure
1. Correct Hypoxia to acceptable levels
O2
if Type 1 RF - aim for PaO2 > 10
if Type 2 RF give controlled O2 - aim for PaO2
7-8

2. If respiratory acidosis develops, support


the respiratory muscles
NIV (BiPAP) - on medical ward
intubation and IPPV - ICU
(respiratory stimulants e.g. doxapram)

Oxygen Toxicity in COPD

Oxygen Toxicity in COPD

Oxygen
Nasal cannula
Standard mask
Mask with reservoir bag

2-4L/min 25-40%
5-15L/min <50%
15L/min <70%

Inspired oxygen concentration depends on


patients minute ventilation patient also
breathes in an unknown amount of air

Controlled Oxygen
Therapy
Venturi (Valve) Masks
Deliver 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
Venturi (Valve) Masks
Works by Bernoullis
principle if oxygen
speeds up its
pressure drops and a
large quantity of air
is sucked in

Controlled Oxygen
Therapy
Venturi (Valve) Masks
Works by Bernoullis 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 Ventilation
= ventilation without an ET tube
avoids
ventilator associated pneumonia
need for an ITU bed
allows
intermittent support
normal eating, drinking, communication

NIV/BiPAP
How is it given?

NIV/BiPAP

non-invasive ventilation/bilevel positive


airway pressure
What is it?
Pressure
Inspiration

Expiration

12cmH2O
4cmH2O

Time

NIV/BiPAP
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 (%O2
would then be limited to
~45-50%) but can be an
ICU type ventilator (up to
100% O2)

Case 2
65 PMH: IPF
Sudden onset of left-sided pleuritic chest
pain
O/E Dyspnoeic at rest RR 30/min
Bibasal crackles R>L

Case 2
Ix:
Bloods Normal including D-dimer
ABGs PaO2 7, PaCO2 4.5,
ECG normal
CXR -

Case 1

Pneumothorax
BTS Guidelines 2003

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 nonsmokers)

Half recur within 4 years

Volume of Pneumothorax

Volume of Pneumothorax
Small visible rim of < 2cm
Large visible rim of 2cm

Treatment 1

Treatment 2

Aspiration
+

Chest Drain

Chest Drain

Chest Drain

Complications of Chest
Drain
Penetration of lung, stomach, spleen,
liver, heart, great vessels
Pleural infection (1%)
Surgical emphysema (malpositioned
tube or kinked/blocked tube)

Myths 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?

No
Yes
No (?)
No

Tension Pneumothorax
Intrapleural pressure exceeds
atmospheric due to one-way valve
effect results in  venous return,
 cardiac output,  BP
Patient rapidly distressed
sweating, cyanosis,  HR,  RR,
EMD/PEA arrest

Tension Pneumothorax
Not dependent
on the size of
the
pneumothorax

Tension Pneumothorax
Treatment
Cannula of at least
4.5cm length in 2nd
ICS MCL
X

Tension Pneumothorax
Treatment
Cannula of at least
4.5cm length in 2nd
ICS MCL
then
Chest drain

Case 3
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

Ix:
Bloods -  WCC;  D-dimer
ECG normal
ABGs - PaO2 9.0, PaCO2 5.3,
CXR

Diff :PTE
Pneumonia

Pulmonary Embolism
Annual incidence 60-70 / 100 000 / yr
B 1000 in Greater Glasgow
Typically PTE is present in 15 40% of
cases where the diagnosis is considered
Modern diagnostic pathway uses:clinical probability
D-dimer assay
CTPA

Pulmonary Embolism
Diagnostic Pathway

PIOPED II AJM 2006

Clinical
Probability
Risk of PTE

BTS Guidelines 2003

Clinical Probability Scores

PIOPED II AJM 2006

Revised Geneva Score

D-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 Ddimer is
low clinical probability
0.7 2%
moderate clinical probability 5%
high clinical probability
>15%
PIOPED II AJM 2006

D-dimer Assay
It should not be done:As a screening test on all general
medical patients
In high probability cases

Imaging
CTPA
rapidly becoming the first line test
sensitivity 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 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

Treatment
LMW heparin
Difficulties arise with
- obese patients
- renal failure
- rapid reversal

Oral anticoagulation with warfarin


Aim for INR of 2 3

Duration of anticoagulation
Temporary risk factors
Idiopathic

4-6/52
3-6/12

Risk of major bleeding


3% at 3/12
mortality 0.5%

Investigation for cancer usually unnecessary


BTS Guidelines 2003

Massive PTE
A pulmonary embolism so large as
to cause circulatory collapse
Usually the patient has presented
with clear acute event often with
syncope and is in extremis
Signs of right heart failure with
hypoxia i.e. BP, JVP, RV gallop,
clear chest

Investigation of massive
PTE
If patient peri-arrest, do not delay
treatment for investigations
If patient unstable, consider a
cardiac echo (looking for RV
dilatation) as first-line test
If patient stabilises, proceed to
CTPA

Treatment of Massive PTE


Thrombolysis

BTS Guidelines 2003

Other Treatment Options


Clot fragmentation by pulmonary
artery catheter / interventional
radiology
Embolectomy

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-dimer
Sensitive but not specific test for VTE
Allows 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
patients
In high probability cases

Only useful if negative

Clinical 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
a OR b but not both
neither a nor b

HIGH
MEDIUM

LOW

Case 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

Ix:
Bloods normal
ECG normal
ABGs PaO2 8, PaCO2 3.9,
CXR

CXR

How severe?

Severity of Acute Asthma

Treatment of Acute
Asthma

Treatment of Acute
Asthma

Anaphylaxis case

Correction of Hypoxia and


Hypercapnia
Correct hypercapnia by increasing alveolar ventilation
Correct hypoxia by reducing shunt i.e. you need to
improve O2 delivery or decrease blood supply to
diseased areas

Uncontrolled Oxygen
2L/min by nasal cannula does not
necesssarily give 28%
Flow

20
10
2

Time

Uncontrolled Oxygen
2L/min by nasal cannula does not
necesssarily give 28%
Flow

20

24%

35%
10

Time