Acidosis Respiratoria

Assessment of respiratory
acidosis
The right clinical information, right where it's needed
Last updated: Aug 21, 2015
Table of Contents
Summary
Overview
Aetiology
Emergencies
4
6
Urgent considerations
Red flags
Diagnosis
Step-by-step diagnostic approach
8
8
Differential diagnosis overview
12
Differential diagnosis
15
References
33
Disclaimer
35
Summary
Respiratory acidosis occurs when acute or chronic derangements of the respiratory system lead to inefficient
clearance of carbon dioxide. These derangements may involve primary disease of the lung parenchyma, problems
with the chest wall, neuromuscular failure, or a disorder of central control of ventilation.
In both cases, alveolar gas exchange units are unable to sufficiently excrete carbon dioxide, leading to an increase
in the arterial carbon dioxide levels above the normal range of 35 to 45 mmHg (4.7-6.0 kPa). With the increase
in carbon dioxide, hydrogen ions accumulate, causing the arterial pH to fall below the normal range (i.e., <7.35).
In acute respiratory failure, there is insufficient buffering capacity to handle the dramatic increase in arterial and
venous carbon dioxide. Over time, more and more carbon dioxide is processed by carbonic anhydrase to
bicarbonate (the Hamburger shift). This leads to chloride excretion by the kidney with ammonium, and the pH
gradually rises.[1]
Acute respiratory acidosis is usually secondary to acute respiratory failure. The consequences of failing to
recognise acute respiratory failure include marked hypoxaemia, hyperkalaemia, cardiovascular instability, and
cardiac arrest.
Assessment of respiratory acidosis
Overview
OVERVIEW
Aetiology
Respiratory acidosis is due either to an acute reduction in alveolar ventilation (cannot breathe or will not breathe) or a
dramatic increase in carbon dioxide production, or to a failure to increase alveolar ventilation in association with increased
production. While patients with COPD have chronic hypercarbia, their pH is usually between 7.35 and 7.4.
The causes of respiratory acidosis are diverse and may result from disorders of many different organ systems. The
differential diagnosis of respiratory acidosis can be formulated based on the acuity of the acidosis (acute or chronic) or
by organ system. Determination of the acuity of an acidosis can be complicated by other underlying acid-base disorders.
Because of this, an algorithm that approaches the differential diagnoses from an organ-based perspective is useful.
Parenchymal lung disease

Both intrinsic lung disease and pulmonary vascular pathology can impair carbon dioxide excretion.
Common causes are COPD and pneumonia.[2] Cardiogenic pulmonary oedema rarely causes hypercarbia, and it is
a late complication of ARDS due to a combination of the use of PEEP and increased dead space.
Acute lung injury is an uncommon but serious cause.
Airway obstruction
Often dramatic and acute, airway obstruction is a life-threatening emergency.
Causes include foreign body aspiration, laryngospasm, status asthmaticus, and angio-oedema.
Laryngospasm, status asthmaticus, and angio-oedema are uncommon causes of respiratory acidosis except in the
last stages when patients present with hypoxaemia or respiratory distress.
Central nervous system

CNS depression leads to alveolar hypoventilation.
Often associated with altered mental status.
Common causes include intentional or accidental drug ingestion.
Serious causes include CNS infarct, haemorrhage, and infection.
Oxygen therapy administered to patients with COPD, resulting in hyperoxia, has been associated with hypercarbia.
The mechanism is multifactorial but probably results from a combination of respiratory depression and increased
alveolar dead space consequent to reversal of hypoxic pulmonary vasoconstriction.[3]
Impaired chest wall mobility

Characterised by restriction of the normal chest wall excursion.
Pleural disease (effusion, empyema, pneumothorax, haemothorax, fibrothorax) may impair normal lung parenchymal
expansion.
Common causes include obesity, pleural effusions, and empyema.
Serious causes include flail chest, pneumothorax, haemothorax, and empyema.
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Overview
Skeletal disease such as kyphoscoliosis and ankylosing spondylitis minimises normal chest expansion.
OVERVIEW
Neuromuscular disorders
Neuromuscular disorders can affect any component of the nerve-muscle complex.
Other neuromuscular abnormalities are typically present.
Common causes include electrolyte derangements (hypokalaemia and hypophosphataemia).
Serious causes include progressive neurological diseases (Guillain-Barre syndrome, amyotrophic lateral sclerosis),
high cord trauma/lesion, organophosphate ingestion, tetanus, and botulism.
Systemic illnesses such as myasthenia gravis and hypothyroidism can be associated with hypoventilation, although
hypothyroidism is an uncommon cause of respiratory acidosis except in the last stages when patients present with
hypoxaemia.
Overproduction of carbon dioxide

Systemic illnesses can lead to increased carbon dioxide production sufficient to overwhelm the normal respiratory
system, but overproduction of carbon dioxide is a rare cause of respiratory acidosis.
Some causes are malignant hyperthermia, sepsis, heat exhaustion, thyrotoxicosis, and overfeeding with parenteral
nutrition.
Other
Inadequate mechanical ventilation and insufflation of carbon dioxide into a body cavity (laparoscopic surgery)
should be considered in the appropriate clinical setting.
The causes of respiratory acidosis associated with inadequate mechanical ventilation are diverse, and specific
testing should focus on the history and examination findings.
Low tidal volume ventilation will commonly cause respiratory acidosis due to intentional hypoventilation as part
of a lung-protective ventilation strategy.
Emergencies
Urgent considerations
(See Differential diagnosis for more details)
Nearly all causes of acute respiratory acidosis can develop into life-threatening situations. The primary concern in these
patients is impending respiratory failure. Initial emergent treatment for respiratory acidosis, irrespective of the underlying
cause, involves immediate assessment of the patient with basic stabilisation (airway, ventilatory, cardiovascular support)
and rapid identification of potential aetiologies via a thorough secondary survey.
Initial assessment
Once respiratory acidosis is identified, the first objective is to determine the stability of the patient and provide airway,
ventilatory, or cardiovascular support where necessary.
EMERGENCIES
For patients with obtundation, haemodynamic instability, or evidence of respiratory muscle fatigue (accessory muscle
use, dyspnoea, tachypnoea), consideration should be given to initiating mechanical ventilatory support and transfer to
a monitored setting (e.g., ICU) prior to further investigative studies.[4] [5]
Further assessment
Once the patient is stabilised, evaluation for serious causes of respiratory acidosis should be initiated to allow prompt
and specific treatment of the individual underlying cause.
Laboratory tests should include the following:
ABG
FBC to evaluate for polycythaemia or raised WBC count
Toxicology testing for possible drug ingestion, lumbar puncture to evaluate for CNS infection, and serum chemistries
for severe electrolyte derangements should be rapidly obtained.
Imaging would include the following depending on suspected causes:
Imaging of the chest (CXR or CT) is warranted to evaluate for serious parenchymal lung disease (pneumonia,
cardiogenic pulmonary oedema, pneumothorax).
Urgent evaluation with CT scanning of the brain should be undertaken to screen for CNS causes such as infarction,
haemorrhage, or trauma.
Management of respiratory acidosis may include ventilatory support (invasive or non-invasive) and further specific medical
therapies for treatment of the causative pathophysiology.[6] [2]
Red flags
COPD
Multilobar pneumonia
Cardiogenic pulmonary oedema
Acute lung injury/ARDS
Status asthmaticus
Foreign body aspiration
Emergencies
Laryngospasm
Angio-oedema
Drug use (narcotics, alcohol, sedatives, anaesthetics)
Oxygen therapy in COPD
CNS infarct or haemorrhage
Head trauma
CNS infection
Pleural effusion
Pneumothorax
EMERGENCIES
Empyema
Haemothorax
Flail chest
Hypokalaemia
Hypophosphataemia
Paralytic agents and organophosphates
High cord trauma/lesions (above C4)
Guillain-Barre syndrome
Myasthenia gravis
Amyotrophic lateral sclerosis
Phrenic nerve trauma
Tetanus
Botulism
Sepsis
Fever/malignant hyperthermia
Inadequate mechanical ventilation
Diagnosis
Step-by-step diagnostic approach

Once respiratory acidosis has been identified by ABG analysis, the approach to narrowing the differential diagnosis and
determining the severity of the patient's condition is aided by the identification of its acuity (acute or chronic). This is
done through the synthesis of information from the ABG itself, history, and physical examination.[7]
Historical findings may immediately point to the underlying cause, such as head trauma and drug ingestion, or provide
only limited information, as with the obtunded patient. The physical examination should focus on assessment of the
neurological and respiratory systems with careful examination of the lung fields, which can yield useful information
regarding the presence of underlying parenchymal disease.
Further laboratory studies are warranted when metabolic abnormalities or specific systemic diseases are suspected
aetiologies. Radiographic imaging is key to the evaluation of respiratory acidosis, as it can provide rapid screening for
head, cervical, or chest pathology.
ABG analysis
Once a diagnosis of respiratory acidosis has been established with ABG sampling by confirming the presence of an
abnormally low pH (<7.35) with concomitant elevation in the PaCO2 (>45 mmHg), further analysis of the ABG result is
required to determine the acuity of the condition. Knowledge of whether respiratory acidosis is acute or chronic is
extremely important, as it helps to identify the underlying cause of acidosis and evaluate the severity of the patient's
clinical condition. Acute respiratory acidosis tends to have a more serious (often life-threatening) clinical presentation
than that of chronic respiratory acidosis.
DIAGNOSIS
In acute respiratory acidosis, for every 10 mmHg increase in PaCO2, the pH will decrease by 0.08 and the serum bicarbonate
and base excess will be within normal range due to the acute nature of the underlying process. To calculate the anticipated
compensation in chronic respiratory acidosis, recall that the pH in chronic respiratory acidosis decrease by only 0.03
units for every 10 mmHg increase in PaCO2. For patients with compensated chronic respiratory acidosis (e.g., in COPD),
the pH will be normal despite an elevated PaCO2. Renal mechanisms of compensation can correct the respiratory acidosis
within 24 hours. Changes in pH outside these ranges suggest a superimposed metabolic abnormality (either acidosis or
alkalosis). The presence of hypoxaemia with respiratory acidosis can help to narrow down the differential diagnosis to
those processes that cause profound alveolar hypoventilation, such as sedative overdose and CNS infarction, or regional
ventilation-perfusion mismatch, such as multilobar pneumonia.
It is important to note that the degree of acidosis and the potential concerns are different depending on whether the
problem is respiratory or metabolic. An equivalent pH in metabolic acidosis (e.g., 7.0) is a much worse clinical sign, as the
body has dual buffering and compensatory mechanisms for metabolic acid (the carbamate-bicarbonate system
bicarbonate buffer, and carbon dioxide elimination), whereas elevated carbon dioxide causes a dramatic fall in pH, but
the patient is actually less sick, as there is little buffering capacity for carbon dioxide. Moreover, studies in critical illness
have demonstrated that patients tolerate hypercarbic acidosis very well.
Acute respiratory acidosis is commonly caused by:
Exacerbation of COPD (causes acute on chronic respiratory acidosis)
Hypokalaemia and hypophosphataemia
Status asthmaticus
Pleural effusion
Pneumothorax
Diagnosis

Head trauma
CNS infection.
Other important but uncommon causes of acute respiratory acidosis are:
Laryngospasm
Angio-oedema
Sepsis
Fever/malignant hyperthermia.
Chronic respiratory acidosis is commonly caused by:
Hypoventilation syndrome in obesity
Obesity
Hypothyroidism
COPD
Kyphoscoliosis.
Historical considerations
Onset of symptoms
COPD commonly presents with acute or chronic respiratory acidosis secondary to an exacerbation caused by a
lower respiratory tract infection, pulmonary embolism, pneumothorax (due to bullous rupture), or cor pulmonale.
Fever, cough, pleuritic chest pain, and hypoxia suggest an underlying parenchymal process such as pneumonia or
empyema.
Chronic conditions including obesity-hypoventilation syndrome, multiple sclerosis, myasthenia gravis, and
kyphoscoliosis may be associated with few or no symptoms.
Acute causes of respiratory acidosis often present with more overt symptoms such as rapidly progressive ascending
neurological weakness suggestive of Guillain-Barre syndrome.
Pre-existing medical conditions
The presence of chronic diseases associated with respiratory acidosis including COPD, myasthenia gravis, and
multiple sclerosis can assist in determining the underlying cause.
The presence of atherosclerotic disease or atrial fibrillation increases the likelihood of CNS pathology (i.e., infarction).
A history of depression may increase suspicion for toxic ingestion.
DIAGNOSIS
The degree of acuity and magnitude of symptoms aids in narrowing the differential diagnosis.
Diagnosis
Medication history
Narcotics and analgesics may lead to respiratory depression.
A recent increase in continuous oxygen flow rate in a COPD patient can cause hypoventilation.
Use of ACE inhibitors or angiotensin receptor blockers increases the risk of angio-oedema.
Excessive daytime sleepiness and headaches on wakening are seen in hypoventilation syndrome in obesity.
Physical examination findings

Pulmonary examination
Although non-specific, abnormal findings on pulmonary auscultation (egophony, crackles, wheeze, dullness to
percussion) can help localise chest pathology.
Obstructed breathing patterns include seesaw chest movements, nasal flaring, and supraclavicular and subcostal
recession.
Paradoxical movement of a portion of the chest wall with spontaneous breathing suggests flail chest.
Cardiac examination
A right ventricular heave and tricuspid regurgitation suggest chronic right ventricular failure (cor pulmonale)
associated with COPD and obesity hypoventilation syndrome.
An irregular cardiac rhythm, valvular murmurs, or carotid bruits may suggest an embolic source if a CNS event is
present.
Neurological examination
Obtundation, anisocoria, and abnormal unilateral papillary reflex signify a possible brainstem infarct.
DIAGNOSIS
Asterixis, myoclonus, seizures, or miosis may be present depending on the ingested substance.
Symmetrical hyporeflexia/areflexia of the lower extremities is a cardinal sign of Guillain-Barre syndrome.
Laboratory evaluation
Toxicology testing
Indicated in the obtunded patient to screen for pharmacological depressants.
Lumbar puncture
Useful to screen for CNS infection.
Serum electrolyte measurement
To assess potassium and phosphate levels.
Specific tests to screen for systemic diseases
TSH for hypothyroidism
10
Diagnosis
Anti-acetylcholine receptor antibody for myasthenia gravis

C1 esterase inhibitor functional assay for hereditary angio-oedema
Anti-nuclear antibodies for scleroderma
HLA-B27 antigen for ankylosing spondylitis.
Microbiological testing
Sputum microscopy, culture, and sensitivity for the assessment of pneumonia.
Muscle biopsy
Indicated if muscular dystrophy, malignant hyperthermia, polymyositis, or dermatomyositis is suspected.
Imaging studies
Imaging of the chest with CXR and chest CT is key to screening for underlying lung and chest wall disease. CXR is
the most rapid and readily available imaging modality to screen for causes of respiratory acidosis. CT scanning can
often add more information but may not be readily available.
Brain imaging with CT or MRI is indicated to screen for head trauma, stroke, or haemorrhage.
Overnight polysomnography is a useful screening tool for obesity-hypoventilation syndrome and primary alveolar
hypoventilation.
Dynamic fluoroscopy with deep inspiration (sniff test) can diagnose phrenic nerve damage.
EMG and nerve conduction testing demonstrates diffuse denervation and abnormal amplitude of compound muscle
action potentials with preserved conduction velocities in amyotrophic lateral sclerosis.
Pulmonary function testing
FVC and maximal inspiratory and expiratory pressures should be monitored in all patients with neuromuscular
disorders affecting the chest wall muscles and diaphragm.[8]
Reduced lung volumes are seen in kyphoscoliosis and obesity.
11
DIAGNOSIS
FVC and maximal inspiratory and expiratory pressures are used to evaluate the respiratory system integrity in
Guillain-Barre syndrome and myasthenia gravis.
Diagnosis
Differential diagnosis overview

Common
COPD
Head trauma
CNS infection
Pleural effusion
Pneumothorax
DIAGNOSIS
Obesity
Kyphoscoliosis
Hypokalaemia
Hypophosphataemia
Uncommon
Pulmonary fibrosis
Status asthmaticus
12
Diagnosis
Uncommon
Laryngospasm
Angio-oedema
Primary alveolar hypoventilation
Empyema
Haemothorax
Flail chest
Scleroderma
Ankylosing spondylitis
Fibrothorax
Hypothyroidism
DIAGNOSIS
Multiple sclerosis
Myasthenia gravis
Muscular dystrophy
Polymyositis and dermatomyositis
Tetanus
Botulism
Poliomyelitis
13
Diagnosis
Uncommon
Sepsis
DIAGNOSIS
Insufflation of CO2 into body cavity (e.g., laparoscopic surgery)
14
Diagnosis
Differential diagnosis
Common
COPD
History
Exam
1st Test
positive smoking history,

wheeze; recurrent
exacerbations with
dyspnoea and sputum
production are typical
tachypnoea, increased
work of breathing with
pursed lips, tripod
positioning (accessory
muscle use), tracheal tug,
and barrel chest on
inspection; prolonged
expiratory phase, wheeze,
and diminished breath
sounds on auscultation
CXR: hyperinflation,
reduced lung markings,
bullae, and flattened
diaphragms
CXR is useful to support
the diagnosis of COPD.
Additionally, it can exclude
other causes of wheeze or
triggers of exacerbation
(heart failure, pneumonia,
pneumothorax, pulmonary
embolism).
Other tests
Exam
1st Test
Other tests
fever, chills, cough with

productive sputum,
pleuritic chest pain,
dyspnoea, haemoptysis;
history of recent ill
contacts
examination over affected

lung region demonstrates
dullness to percussion;
coarse crackles, bronchial
breathing, and pleural rub
on auscultation; increased
vocal resonance and
whispered pectoriloquy,
and tactile fremitus
CXR: focal consolidation

in >1 lobe
CXR is the first diagnostic
test to confirm pneumonia.
CT chest: focal
consolidation in >1 lobe
CT of the chest is rarely
needed but may provide
better visualisation of the
extent of disease.
sputum Gram stain and
culture: evidence of
pathogenic bacteria
Microbiological cultures
should be taken before the
initiation of antibiotics if
the patient's clinical state
permits.

History
Exam
1st Test
Other tests
acute onset of respiratory

distress, dyspnoea,
coughing, wheeze, and
possibly aphonia related to
inhalation of a foreign body
stridor over the larynx,

fixed or localised wheeze,
cyanosis, localised
diminished breath sounds
CXR: foreign body or

evidence of unilateral
obstruction
CXR can serve to localise
foreign bodies if they have
passed below the carina.
laryngoscopy/bronchoscopy:
direct visualisation of
foreign body
Laryngoscopy and
bronchoscopy are useful
as diagnostic tests when
15
DIAGNOSIS
History
Diagnosis
Common
History
Exam
1st Test
Other tests
For supracarinal
obstruction, symptoms are
often severe enough to
require emergent
intervention (Heimlich
manoeuvre, intubation).
history of aspiration is
unclear and x-rays are
inconclusive (e.g.,
paediatric patients).
DIAGNOSIS

History
Exam
1st Test
known history of
psychiatric or substance
abuse disorders increases
the likelihood of
intentional or accidental
ingestion of CNS
depressants; history of
recent surgery requiring a
general anaesthetic
obtundation or coma with

diminished respiratory
effort; miosis, asterixis,
myoclonus, or seizures
may be present depending
on ingested substance
drug and toxicology

screen: drug or metabolite
on assay
Toxicology testing should
include screening for
opioids, barbiturates,
benzodiazepines, and
ethanol.
Other tests
osmolar gap: >12

mmol/L
An osmolar gap (between
measured and calculated
plasma osmolality) is useful
to screen for ethanol,
ethylene glycol, or
methanol ingestion.

History
Exam
1st Test
recent increase in or
addition of supplemental
oxygen for therapy of
COPD
hypersomnolence,
confusion, or obtundation;
effort; prolonged
expiratory phase with
associated wheeze on
auscultation
pulse oximeter: oxygen

saturation >92%
The chronic hypercapnia
associated with moderate
to severe COPD leads to a
change in the normal
stimulus for respiration
(from hypercapnia and
acidosis to hypoxaemia).
Excessive supplemental
oxygen can lead to both a
blunting of the hypoxic
vasoconstriction of the
16
Other tests
Diagnosis
Common
History
Exam
1st Test
Other tests
pulmonary vascular bed

and a diminished stimulus
for breathing.

Exam
1st Test
Other tests
headache or acute onset

of focal neurological
deficits; development of
respiratory acidosis from
this cause typically results
from a comatose state
obtundation, anisocoria,
and abnormal unilateral
papillary reflex signify
possible brainstem infarct;
irregular cardiac rhythm,
valvular murmurs, or
carotid bruits suggest an
embolic source
CT brain: evidence of
infarct or haemorrhage
CT scanning allows
exclusion of intracerebral
haemorrhage. Detection
of infarction on CT
depends on the timing of
the imaging relative to the
event. Characteristic
changes are of an area of
low attenuation with
surrounding oedema and
associated sulcal or
ventricular effacement.
MRI brain: evidence of

infarct or haemorrhage
CT scan is the initial
diagnostic test of choice
given its ease and rapidity.
However, acute or subtle
regions of infarct and
haemorrhage may not be
easily detected, and thus
MRI of the brain is a useful
secondary imaging
modality. MRI
characteristics depend on
the timing of the imaging
relative to the event.
However, the distribution
of abnormalities can offer
clues to the aetiology (i.e.,
wedge-shaped infarcts in
thromboembolic disease,
distal margin ischaemia in
watershed infarcts related
to hypoperfusion).
History
Exam
1st Test
Other tests
history of recent trauma or

inability to obtain aetiology
of impaired consciousness
level
overt evidence of trauma

(skull deformity,
laceration); Battle's sign
(post-auricular
ecchymoses) or raccoon
sign (periorbital
ecchymoses) signifies
basilar skull fracture
head trauma
CT findings include skull
fracture, subdural
haematoma, or
intraparenchymal
bleeding.
Head trauma
17
DIAGNOSIS
History
Diagnosis
Common
CNS infection
History
Exam
1st Test
Other tests
recent history of fever,

headache, nausea, or
photophobia may be
obtained; risk of
immunodeficiency (HIV,
organ transplant), missed
immunisations, and recent
travel should be assessed
fever, tachycardia, and

obtundation; meningism
including Kernig's (pain on
thigh flexion and knee
extension) and Brudzinski's
(hip and knee flexion
induced by neck flexion)
signs may be elicited;
presence of papilloedema
must be ruled out
LP: analysis of
cerebrospinal fluid
including glucose, total
protein, cell
count/differential, and
Gram stain/culture
While a CT scan of the brain
is not required prior to an
LP, it is often performed to
screen for elevated
intracranial pressure and
risk of herniation. A normal
CT scan does not
necessarily mean an LP is
safe, and therefore should
be used in conjunction
with the physical
examination to determine
risk of herniation.[10]
increased intracranial
pressure or herniation
Apart from screening for
evidence of increased
intracranial pressure prior
to performing an LP, a CT
scan may reveal an
alternative diagnosis for
the presenting signs and
symptoms (e.g., tumour,
abscess).
Other tests
CT features of increased
intracranial pressure
include sulcal effacement,
loss of grey-white matter
distinction, and
obliteration of the normal
ventricular space.
DIAGNOSIS

History
Exam
1st Test
history of disordered sleep

including excessive
daytime sleepiness,
headaches on wakening,
depression, and frequent
naps during the day
obesity and increased neck

circumference; signs of cor
pulmonale (jugular venous
distention, dyspnoea on
minimal exertion,
hepatomegaly, peripheral
oedema)
overnight
polysomnography:
abnormal frequency of
hypopnoeic and apnoeic
events
While obstructive sleep
apnoea (OSA) often
accompanies
hypoventilation syndrome
in obesity, the presence of
OSA is not an absolute
requirement in this
disorder.[11]
18
Diagnosis
Common
Pleural effusion
History
Exam
1st Test
Other tests
history of heart failure,

chest malignancy
(malignant pleural
effusion), or liver disease
(hepatic hydrothorax) may
be present with associated
dyspnoea
'stony' dull to percussion,

diminished breath sounds,
and reduced vocal
resonance on auscultation
in large effusions; smaller
effusions may not be
detectable on examination
CXR: blunting of
costophrenic angle or
effusion on affected side
There are no
differentiating signs on
CXR between pleural
effusion and haemothorax.
CT chest: effusion
CT scan aids in evaluating
the aetiology of the
effusion.
History
Exam
1st Test
Other tests
acute onset of dyspnoea

and unilateral pleuritic
chest pain; recent trauma
to the chest; history of
COPD or asthma
tachypnoea, unilateral
diminished breath sounds,
and reduced vocal
resonance on auscultation;
reduced expansion;
tracheal deviation away
from side of collapsed
lung, hypotension, and
central cyanosis in tension
pneumothorax
CXR: partial or total

collapse of lung
Tension pneumothorax
(presence of mediastinal
shift) is a medical
emergency, and its
treatment should be
initiated on the basis of a
clinical diagnosis and
should not be delayed in
order to undertake a CXR.
History
Exam
1st Test
history of obesity, snoring,

or daytime
hypersomnolence
elevated body mass index,

increased neck
circumference, and
minimal chest excursion
with deep inspiration
PFT: reduced lung

volumes
While vital capacity and
total lung capacity are
reduced in obesity, some
studies suggest that
reduction in functional
residual capacity better
correlates with the degree
of obesity.[12]
Pneumothorax
DIAGNOSIS
Obesity
Other tests
19
Diagnosis
Common
Kyphoscoliosis
History
Exam
1st Test
Other tests
many patients can be

asymptomatic but may
report shortening of
height; some report back
pain
obvious deformity of the

spine may be evident
CXR: distortion of the

spine and thorax
PFT: reduced lung

volumes
Total lung capacity,
functional residual
capacity, and residual
volume are reduced in
kyphoscoliosis.
History
Exam
1st Test
Other tests
palpitations, nausea,
abdominal cramping, or
constipation, skeletal
muscle weakness or
cramping, or psychosis;
detailed drug history
should be obtained for
medications causing
hypokalaemia (e.g.,
diuretics)
hypotension, cardiac
dysrhythmias, lethargy,
ileus, muscle
fasciculations, or tetany
serum potassium: <3.5

mmol/L (<3.5 mEq/L)
DIAGNOSIS
Hypokalaemia
serum magnesium:
<0.75 mmol/L (<1.5
mEq/L)
Other electrolytes, such as
magnesium, should also be
evaluated, as abnormalities
in these values may
provide clues as to the
primary cause of
hypokalaemia.
Hypophosphataemia
History
Exam
1st Test
weakness of large muscle

groups and diplopia or
dysarthria (secondary to
muscle weakness) are the
most common complaints;
numbness and tingling of
the extremities may also
be experienced
hypotension,
hypoventilation, mental
status changes, and
peripheral muscle
weakness
serum phosphate: <0.6

mmol/L (<2 mg/dL)
Other tests

History
Exam
1st Test
inappropriate ventilator
settings or change in
examination should focus

on ensuring appropriate
CXR: atelectasis of lung

parenchyma or
20
Other tests
Diagnosis
Common
History
Exam
1st Test
clinical status of an
intubated patient
(development of fever,
pulmonary embolism) can
lead to respiratory acidosis
ventilator settings and

functioning equipment
(endotracheal tube
placement), and evaluating
patient's clinical status
inappropriate endotracheal
tube placement
Other tests
Uncommon
Exam
1st Test
Other tests
patients may report

orthopnoea, paroxysmal
nocturnal dyspnoea, lower
extremity oedema,
dyspnoea on minimal
exertion, and weight gain
jugular venous distention,

fine bibasal crackles, S3
gallop rhythm,
hepatomegaly, and
peripheral oedema
CXR: cardiomegaly,
bilateral lower lobe
shadowing, pleural
effusion, enlarged hilar
vessels, upper lobe
diversion, fluid in
horizontal fissure, Kerley B
lines
Bilateral lower lobe
shadowing is due to
alveolar oedema, and
Kerley B lines are due to
interstitial oedema.
2-dimensional
echocardiography: left
ventricular dysfunction,
valvular heart disease
Other tests
DIAGNOSIS
History

History
Exam
1st Test
antecedent history of
ARDS aetiologies including
sepsis, pneumonia, chest
trauma, pancreatitis, fat
embolism, aspiration, near
drowning, blood
transfusion, and cardiac
bypass surgery
tachypnoea, tachycardia,
scattered crackles, and
agitation
CXR: diffuse, bilateral

alveolar infiltrates
21
Diagnosis
Uncommon
Pulmonary fibrosis
History
Exam
1st Test
patients classically present

with slowly progressive
dyspnoea, initially on
exertion, accompanied by
a non-productive cough
cyanosis, clubbing, and

accessory muscle use on
inspection; fine bibasal
end-inspiratory crackles on
auscultation; evidence of
pulmonary hypertension
(jugular venous distention,
peripheral oedema,
hepatomegaly, dyspnoea
on minimal exertion)
CXR: diffuse, bilateral

reticular infiltrates
While useful for the
diagnosis of pulmonary
fibrosis, CXR findings may
be non-specific.
Other tests
high-resolution CT
chest: peripheral, bibasal
honeycombing changes,
traction bronchiectasis
While a CXR can be useful
for the diagnosis of
pulmonary fibrosis,
high-resolution CT
scanning offers more
information regarding the
extent of disease and
staging for prognosis.[9]
DIAGNOSIS
Status asthmaticus
History
Exam
1st Test
Other tests
recent upper respiratory

infection and increased
bronchodilator use without
symptomatic relief; prior
history of intubation for
respiratory failure
accessory muscle use,

inability to speak in full
sentences, and
panexpiratory wheeze;
complete lack of wheeze
('silent chest') is a sign of
impending respiratory
failure
pulse oximeter: oxygen

saturation <92%
Development of
hypoxaemia indicates need
for consideration of
mechanical ventilation.
peak expiratory flow:

predicted values based on
age, height, and gender
Peak expiratory flow is
useful for monitoring
response to therapy and is
predicted based on the
patient's age, height, and
gender (charts available to
identify predicted value).
History
Exam
1st Test
Other tests
acute onset of wheeze or

dyspnoea after accidental
aspiration of liquids,
mucus, or food, or
immediately post
extubation
frequent coughing, stridor,

and increased work of
breathing are
characteristic; inability to
phonate may be present
none: clinical diagnosis

Condition presents with
acute onset of wheeze or
dyspnoea after accidental
aspiration of liquids, mucus
or food, or immediately
post extubation. Clinical
Laryngospasm
22
Diagnosis
Uncommon
Laryngospasm
History
Exam
1st Test
Other tests
examination reveals
frequent coughing, stridor,
and increased work of
breathing with or without
inability to phonate.
Angio-oedema
History
Exam
1st Test
possible history of
recurrent facial swelling,
recent exposure to ACE
inhibitors; may have known
history of allergies
marked oedema of the lips,

tongue, and periorbital
tissue are cardinal signs
C1 esterase inhibitor
functional assay: <70%
normal activity level
Hereditary angio-oedema
can be assessed by testing
the activity level of C1
esterase inhibitor.
Diagnosis of idiopathic
angio-oedema is based on
clinical grounds.
Other tests
Primary alveolar hypoventilation

Exam
1st Test
Other tests
predominantly men (aged

20-50 years) present with
lethargy, fatigue, dyspnoea
at rest, daytime
hypersomnolence, and
frequent night-time
awakening (Ondine's
curse)
hypersomnolence and
signs of cor pulmonale
(dyspnoea on minimal
exertion, hepatomegaly,
peripheral oedema, jugular
venous distention)
none: clinical suspicion

confirmed by further tests
Condition presents,
predominantly in men
aged 20 to 50 years, with
lethargy, fatigue, dyspnoea
at rest, daytime
hypersomnolence, and
frequent night-time
awakening. Clinical
examination reveals
hypersomnolence and
signs of cor pulmonale
(dyspnoea on minimal
exertion, hepatomegaly,
peripheral oedema, jugular
venous distention).
CXR: patchy
opacification, typically
centrally distributed
CXR findings are areas of
patchy atelectasis due to
hypoventilation.
PFT: reduced total lung
volume
overnight
polysomnography:
periods of central apnoea
and hypoxaemia
23
DIAGNOSIS
History
Diagnosis
Uncommon
Empyema
History
Exam
1st Test
Other tests
recent history of
pneumonia, fever,
aspiration, or chest pain;
pleuritic chest pain
dyspnoea, cough, fever,

and tachycardia;
diminished breath sounds
over affected area on
auscultation
CXR: loculated pleural

fluid collection
CT chest: fluid collection

the extent and location of
the empyema, which may
assist in guiding definitive
drainage procedures.
History
Exam
1st Test
Other tests
pleuritic chest pain; recent

history of blunt or
penetrating chest trauma;
symptoms of a bleeding
diathesis or ruptured aortic
aneurysm
(abdominal/back pain,
pulsatile abdominal mass)
tachypnoea, splinting,
fever, and diminished
breath sounds over the
affected lung region; signs
of haemodynamic
instability or collapse,
diminished, or differential
lower extremity pulses, and
abdominal bruit in
ruptured aortic aneurysm
CXR: blunting of
costophrenic angle or
effusion on affected side
There are no
differentiating signs on
CXR between haemothorax
and pleural effusion.
CT chest: localised
haemothorax
the extent and aetiology of
haemothorax.
History
Exam
1st Test
Other tests
recent history of severe

blunt force injury to the
chest or disease sufficient
to cause numerous rib
fractures (e.g., multiple
myeloma)
paradoxical movement of
a portion of the chest wall
with spontaneous
breathing; tachypnoea and
chest pain typically
accompany the injury
CXR: 3 ribs fractured in

at least 2 places
CXR is the most rapid way
to confirm the diagnosis.
Three or more rib fractures
are required to generate
instability of the thoracic
cage, leading to flail chest.
Respiratory acidosis is
more often due to the
underlying lung injury.
CT chest: damage to
underlying parenchyma
the possibility of damage
to the adjacent lung and
mediastinal structures.
Haemothorax
DIAGNOSIS
Flail chest
24
Diagnosis
Uncommon
Scleroderma
History
Exam
1st Test
Other tests
skin thickening, Raynaud's

phenomenon (finger pain,
pallor, or cyanosis in
response to cold), gastric
reflux, and symptoms of
right-sided heart failure
(lower extremity oedema,
dyspnoea on minimal
exertion)
thickened skin resulting in

taut-appearing face and
tapered fingers
(sclerodactyly); calcinosis
and telangiectasias; dry
crackles on auscultation
autoimmune antibody
panel: positive
Serological diagnosis of
scleroderma includes a
panel of autoimmune
antibodies including ANAs,
topoisomerase antibodies,
and anti-ribonucleoprotein
antibodies.[13]
high-resolution CT
chest: ground glass
infiltrates, honeycombing,
High-resolution CT is
useful for determining
presence and severity of
pulmonary involvement in
scleroderma. Early findings
include ground glass
infiltrates suggestive of
alveolitis. As the disease
progresses, fibrosis,
honeycombing, and
predominate.
Ankylosing spondylitis
Exam
1st Test
Other tests
lower back pain (worse at

night and in the morning)
is typical; repeated
episodes of pain are
common and, as disease
progresses, pain moves up
the spinal column
pain on palpation of the

sacroiliac joint, reduced
lateral flexion of the spine
and reduced chest
expansion with deep
inspiration
x-rays of pelvis and

lumbar spine: erosion or
sclerosis of the sacroiliac
joint
X-rays should be in the
anteroposterior plane.
HLA-B27 antigen:
positive
HLA-B27 antigen is not
required for the diagnosis
of ankylosing spondylitis.
It is positive in 92% of
white patients with the
disease but can have
variable presence in other
racial groups.
History
Exam
1st Test
Other tests
symptoms may be
non-specific; history of
previous injury to the
pleura (empyema, surgery,
haemothorax) increases
risk
dullness to percussion;
pleural rub and diminished
breath sounds on
auscultation
CT chest: thickened
pleura with trapped lung
Fibrothorax
25
DIAGNOSIS
History
Diagnosis
Uncommon
Hypothyroidism
History
Exam
1st Test
Other tests
fatigue, weakness,
constipation, cold
intolerance, depression,
and decreased libido are
characteristic
bradycardia, coarse dry

hair, pale dry skin, lateral
eyebrow sparing, and
thyroid goitre; in
myxoedema hypotension,
hypothermia, and coma
are characteristic signs
TSH: >4.2 mIU/L

TSH above the upper limit
of the laboratory reference
range is considered
elevated. If TSH is elevated,
free thyroxine (FT4) should
be assessed. Elevated TSH
associated with low FT4 is
consistent with primary
hypothyroidism.[14]
free thyroxine (FT4): <8

picomol/L (<0.6 ng/dL)
If TSH is elevated, FT4
should be assessed.
Elevated TSH associated
with low FT4 is consistent
with primary
hypothyroidism.[14]
DIAGNOSIS

History
Exam
1st Test
recent exposure to
paralytic agents (e.g.,
induction for anaesthesia)
or organophosphates (e.g.,
insecticides) is necessary
for this diagnosis;
organophosphate
exposure is associated with
increased secretions,
abdominal pain, fatigue,
and confusion depending
on the agent ingested
clinical findings include

ataxia, slurred speech,
coma, miosis, diaphoresis,
or fasciculations,
depending on exposure
none: history of exposure

Diagnosis made by prompt
recognition of potential
exposure to offending
agents and exclusion of
other causes for
presenting symptoms (e.g.,
infection). Condition
presents with history of
recent exposure to
paralytic agents (e.g.,
induction for anaesthesia)
or organophosphates (e.g.,
insecticides) and, with the
latter, is associated with
increased secretions,
abdominal pain, fatigue,
and confusion, depending
on the agent ingested.
Clinical examination may
reveal ataxia, slurred
speech, coma, miosis,
diaphoresis, or
fasciculations, depending
on the exposure.
26
Other tests
Diagnosis
Uncommon
History
Exam
1st Test
Other tests
recent history of trauma or

endotracheal intubation
(especially in patients with
rheumatoid arthritis)
neurogenic shock
(bradycardia, hypotension,
peripheral vasodilatation,
and hypothermia); partial
or complete paralysis
below the site of injury;
cough may be weak or
absent
CT of cervical spine:
fracture, displacement, or
mass
CT imaging of the cervical
spine is the standard of
care test in suspected high
cord trauma.
cervical spine x-rays:

visible fracture or
deformity
Three views of the cervical
spine should be obtained:
anterior-posterior, lateral,
and odontoid.
MRI of cervical spine:
fracture, displacement, or
mass; soft tissue and/or
ligamentous injury
Exam
1st Test
Other tests
ascending weakness
and/or tingling beginning
in the lower extremities,
which can spread to the
upper body and arms;
incontinence, back pain,
and difficulty speaking;
antecedent viral infection
or tick bite may be
reported
hyporeflexia or areflexia
combined with
symmetrical lower
extremity weakness is a
cardinal sign; cranial nerve
and sensory deficits, and
ileus, may also be present

ascending weakness
and/or tingling beginning
in the lower extremities,
which can spread to the
upper body and arms,
incontinence, back pain,
and difficulty speaking. An
antecedent viral infection
or tick bite may also be
reported. Clinical
examination reveals the
cardinal signs of
hyporeflexia or areflexia
combined with
symmetrical lower
extremity weakness, as
well as cranial nerve and
sensory deficits, and ileus.
LP: elevated
cerebrospinal fluid protein
(>400 mg/L)
While the diagnosis is
typically made on clinical
grounds, an LP may assist
in excluding other
aetiologies for the
presenting symptoms. A
normal LP does not
exclude this diagnosis.
FVC: <30 mL/kg
FVC <30 mL/kg should
prompt monitoring in an
ICU. If FVC is <15-20
mL/kg, prophylactic
intubation should be
considered.[15]
maximal inspiratory
and expiratory
pressures: inability to
generate negative
pressure of 30 cmH2O
and positive pressure of
40 cmH2O
Values below these
thresholds should be
considered an indication
for prophylactic intubation.
27
DIAGNOSIS
History
Diagnosis
Uncommon
Multiple sclerosis
History
Exam
1st Test
Other tests
various neurological
complaints typically
separated in space and
time including
paraesthesias, weakness,
ataxia, and diplopia
various abnormal
neurological findings may
be present depending on
site of multiple sclerosis
plaques
MRI brain: areas of

demyelination
Gadolinium contrast
administration allows
visualisation of active
plaques.
LP: oligoclonal bands

evoked potentials:
abnormal amplitude
and/or latency in response
to nerve stimulation
Visual or somatosensory
nerve stimulation
DIAGNOSIS
Myasthenia gravis
History
Exam
1st Test
Other tests
progressive muscle
weakness worsened by
activity and relieved with
rest; difficulty with vision,
chewing, and talking
while the screening

neurological examination
can be normal, muscle
fatigue (ocular, trunk
muscles) can be readily
elicited
FVC: <15 mL/kg

If myasthenia gravis is
suspected as the aetiology
of respiratory acidosis,
management of
impending respiratory
failure is key.[8] FVC should
be monitored every 4
hours and, if <15 mL/kg or
the patient is unable to
clear secretions, elective
intubation should be
considered.
anti-acetylcholine
receptor antibody:
positive
Muscular dystrophy
History
Exam
1st Test
Other tests
history of progressive
muscle weakness, difficulty
walking, and poor balance
are characteristic
examination of affected
children reveals signs of
proximal muscle weakness
leading to an abnormal,
waddling gait; calf
pseudohypertrophy,
absence of deep tendon
reflexes, and macroglossia
may also be present
muscle biopsy:
degeneration of muscle
fibres
Degree of degeneration
depends on stage of
disease.
CK: elevated
Elevation in CK is typically
seen in muscular
dystrophy.
28
Diagnosis
Uncommon
History
Exam
1st Test
Other tests
insidious onset of muscle

weakness, often beginning
distally and migrating to
include proximal muscle
groups
tongue and thigh

fasciculations,
hyper-reflexia, and
weakness of intrinsic hand
muscles
EMG: diffuse denervation,

abnormal amplitude of
compound muscle action
potential
nerve conduction
study: preserved
conduction velocities
Polymyositis and dermatomyositis

History
Exam
1st Test
Other tests
slow onset of painless

proximal muscle weakness
with difficulty rising from a
sitting position or raising
the arms
heliotrope periorbital rash,

Gottron's sign (purple
papular eruption over
dorsal interphalangeal
joints), and shawl sign
(violaceous rash across
deltoids and neck) in
dermatomyositis
CK: >5 times normal

upper limit
CK elevations are nearly
uniformly seen. Additional
tests of muscle
inflammation (aldolase,
ESR) can also be abnormal.
MRI of thighs: abnormal

signal intensity in inflamed
muscle
Imaging may be useful to
assist with site of potential
muscle biopsy.
muscle biopsy:
inflammatory infiltration of
muscle

Exam
1st Test
Other tests
dyspnoea, orthopnoea, and

chest pain in the setting of
trauma, chest surgery
(cardiac bypass,
thoracotomy), or known
malignancy within the
chest
diminished diaphragmatic
excursion with inspiration
(as assessed by
end-expiratory and
end-inspiratory percussion
of the posterior chest)
CXR: elevation of
unilateral diaphragm
fluoroscopy: paradoxical
movement of
hemidiaphragm with deep
inspiration
Also known as the 'sniff
test'.
History
Exam
1st Test
Other tests
painful muscle spasms and

stiffness, trismus (lockjaw),
and dysphagia in
unimmunised people
muscle spasms, rigidity,

autonomic instability, and
seizures

painful muscle spasms and
stiffness, trismus (lockjaw),
and dysphagia in
unimmunised people.
Clinical examination
reveals muscle spasms,
rigidity, autonomic
instability, and seizures.
Tetanus
29
DIAGNOSIS
History
Diagnosis
Uncommon
Botulism
History
Exam
1st Test
Other tests
botulism due to
food-borne aetiologies is
associated with GI
complaints and cranial
nerve paralysis;
wound-associated
botulism is associated with
trauma and fever
cranial nerve deficits and

symmetrical descending
paralysis are typical; signs
of autonomic involvement
(orthostatic hypotension,
dry eyes, dry mouth, and
ileus) may also be present

Condition presents with GI
complaints and cranial
nerve paralysis when due
to food-borne aetiologies,
and trauma and fever in
wound-associated
botulism. Clinical
examination reveals cranial
nerve deficits, symmetrical
descending paralysis, and
signs of autonomic
involvement (orthostatic
hypotension, dry eyes, dry
mouth, and ileus).
serum toxin levels:

positive
Serological types A, B, and
E of the botulinum toxin
cause the majority of
botulism cases in humans,
with type E typically found
in fish. Toxin levels may
also be measured in urine
and stomach contents.
bioassay: positive
Mouse injected with
suspected contaminated
sample (with and without
botulinum antitoxin) is
monitored for botulism.
DIAGNOSIS
EMG: muscle action

potential abnormalities
Reduced amplitude of
muscle action potential in
response to single or
low-frequency stimulation.
Increased muscle action
potential response
following high-frequency
or tetanic stimulation.
nerve conduction
study: preserved
conduction velocities
Distinguishes botulism
from Guillain-Barre
syndrome.
Poliomyelitis
History
Exam
1st Test
weakness associated with

history of self-limiting
nausea, vomiting and
anorexia, headache, and
neck stiffness
asymmetrical muscle
weakness and atrophy,
tachypnoea, and
muscle strength
poliovirus antibodies:
positive IgM titre
Positive during acute
phase. Serum should be
sent for acute and
convalescent titres of the
3 major polioviruses.
Appropriate interpretation
of antibodies depends on
30
Other tests
Diagnosis
Uncommon
Poliomyelitis
History
Exam
1st Test
Other tests
the timing of the infection

related to symptoms.[16]
Sepsis
History
Exam
1st Test
fever, dyspnoea, and

confusion; symptoms
related to site of primary
infection (e.g., cough,
dysuria)
examination findings are

non-specific and related to
the source of sepsis;
patients typically
tachypnoeic, tachycardic,
and possibly hypotensive
microbiological cultures
(blood, urine, sputum):
evidence of pathogenic
bacteria
Microbiological cultures
should be taken before the
initiation of antibiotics if
the patient's clinical state
permits.
Other tests
Exam
1st Test
recent exposure to general

anaesthesia or depolarising
agents is typically the
triggering event
fever, muscular rigidity,

tachycardia, tachypnoea,
and hypotension are
cardinal signs
muscle biopsy:
contractures
For malignant
hyperthermia.
Caffeine-halothane
contracture test: muscle
biopsies in malignant
hypothermia elicit
contractures at lower
levels than those from
standardised controls
when exposed to caffeine
and halothane.
Other tests
DIAGNOSIS
History

History
Exam
1st Test
history of recent
laparoscopic surgery
examination can be normal

or demonstrate a
distended abdomen or
postoperative changes

history of recent
laparoscopic surgery.
Clinical examination can be
Other tests
31
Diagnosis
Uncommon
Exam
1st Test
associated with recent

surgery
normal or demonstrate a
distended abdomen or
postoperative changes
associated with recent
surgery.
Other tests
DIAGNOSIS
History
32
References
Key articles
Alfaro V, Torras R, Ibez J, et al. A physical-chemical analysis of the acid-base response to chronic obstructive
pulmonary disease. Can J Physiol Pharmacol. 1996;74:1229-1235. Abstract
Ram FS, Picot J, Lightowler J, et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due
to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2004;(3):CD004104. Full
text Abstract
Royal College of Physicians, British Thoracic Society, Intensive Care Society. Non-invasive ventilation in chronic
obstructive pulmonary disease: management of acute type 2 respiratory failure. Concise Guidance to Good Practice
series, No 11. October 2008. http://www.brit-thoracic.org.uk/ (last accessed 6 August 2015). Full text
Epstein SK, Singh N. Respiratory acidosis. Respir Care. 2001;46:366-383. Abstract
Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med.
2014;371:1434-1445. Abstract
Joffe AR. Lumbar puncture and brain herniation in acute bacterial meningitis: a review. J Intensive Care Med.
2007;22:194-207. Abstract
Lawn ND, Fletcher DD, Henderson RD, et al. Anticipating mechanical ventilation in Guillain-Barr syndrome. Arch
Neurol. 2001;58:893-898. Full text Abstract
References
1.
Alfaro V, Torras R, Ibez J, et al. A physical-chemical analysis of the acid-base response to chronic obstructive
pulmonary disease. Can J Physiol Pharmacol. 1996;74:1229-1235. Abstract
2.
Ram FS, Picot J, Lightowler J, et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due
to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2004;(3):CD004104. Full
text Abstract
3.
Austin MA, Wills KE, Blizzard L, et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease
patients in prehospital setting: randomised controlled trial. BMJ. 2010;341:c5462. Full text Abstract
4.
Royal College of Physicians, British Thoracic Society, Intensive Care Society. Non-invasive ventilation in chronic
obstructive pulmonary disease: management of acute type 2 respiratory failure. Concise Guidance to Good Practice
series, No 11. October 2008. http://www.brit-thoracic.org.uk/ (last accessed 6 August 2015). Full text
5.
O'Driscoll BR, Howard LS, Davison AG; British Thoracic Society Collaborators. BTS guideline for emergency oxygen
use in adult patients. Thorax. 2008;63(suppl 6):vi1-vi68. Full text Abstract
6.
Epstein SK, Singh N. Respiratory acidosis. Respir Care. 2001;46:366-383. Abstract
7.
Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med.
2014;371:1434-1445. Abstract
8.
Cabrera Serrano M, Rabinstein AA. Usefulness of pulmonary function tests and blood gases in acute neuromuscular
respiratory failure. Eur J Neurol. 2012;19:452-456. Abstract
9.
Sung A, Swigris J, Saleh A, et al. High-resolution chest tomography in idiopathic pulmonary fibrosis and nonspecific
interstitial pneumonia: utility and challenges. Curr Opin Pulm Med. 2007;13:451-457. Abstract
33
REFERENCES
REFERENCES
References
10.
Joffe AR. Lumbar puncture and brain herniation in acute bacterial meningitis: a review. J Intensive Care Med.
2007;22:194-207. Abstract
11.
Olson AL, Zwillich C. The obesity hypoventilation syndrome. Am J Med. 2005;118:948-956. Abstract
12.
Jones RL, Nzekwu MM. The effects of body mass index on lung volumes. Chest. 2006;130:827-833. Full text Abstract
13.
Steen VD. Autoantibodies in systemic sclerosis. Semin Arthritis Rheum. 2005;35:35-42. Abstract
14.
Devdhar M, Ousman YH, Burman KD. Hypothyroidism. Endocrinol Metab Clin North Am. 2007;36:595-615. Abstract
15.
Lawn ND, Fletcher DD, Henderson RD, et al. Anticipating mechanical ventilation in Guillain-Barr syndrome. Arch
Neurol. 2001;58:893-898. Full text Abstract
16.
WHO. New approaches to poliovirus diagnosis using laboratory techniques: memorandum from a WHO meeting.
Bull World Health Organ. 1992;70:27-33. Full text Abstract
34
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DISCLAIMER
35
Contributors:
// Authors:
M. Bradley Drummond, MD
Assistant Professor
Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD
DISCLOSURES: MBD declares that he has no competing interests.
Eddy Fan, MD, PhD
Assistant Professor of Medicine
Interdepartmental Division of Critical Care Medicine, University of Toronto, Mount Sinai Hospital, Toronto, Canada
DISCLOSURES: EF declares that he has no competing interests.
// Peer Reviewers:
Guy Soo Hoo, MD, MPH
Director
Intensive Care Unit, West Los Angeles VA Healthcare Center, Clinical Professor of Medicine, Geffen School of Medicine, UCLA, Los
Angeles, CA
DISCLOSURES: GSH declares that he has no competing interests.
Harman Paintal, MBBS
Division of Pulmonary and Critical Care Medicine
Veterans Affairs Palo Alto Health Care System (VAPAHCS), Palo Alto, CA
DISCLOSURES: HP declares that he has no competing interests.
Patrick J. Neligan, MA, MB BcH, FCARCSI, FJFICM
Consultant in Anaesthesia and Intensive Care
Galway University Hospitals, Senior Lecturer in Anaesthesia, National University of Ireland, Galway Department of Anaesthesia
and Intensive Care, University College Hospitals, Galway, Ireland
DISCLOSURES: Not disclosed.

Acidosis Respiratoria

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Acidosis Respiratoria

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Assessment of respiratory

Last updated: Aug 21, 2015

Differential diagnosis overview

Assessment of respiratory acidosis

Parenchymal lung disease

Central nervous system

Impaired chest wall mobility

Assessment of respiratory acidosis

Overproduction of carbon dioxide

Assessment of respiratory acidosis

Assessment of respiratory acidosis

Assessment of respiratory acidosis

Step-by-step diagnostic approach

Assessment of respiratory acidosis

Inadequate mechanical ventilation

Assessment of respiratory acidosis

Physical examination findings

Assessment of respiratory acidosis

Anti-acetylcholine receptor antibody for myasthenia gravis

Pulmonary function testing

Assessment of respiratory acidosis

Differential diagnosis overview

Assessment of respiratory acidosis

Assessment of respiratory acidosis

Insufflation of CO2 into body cavity (e.g., laparoscopic surgery)

Assessment of respiratory acidosis

positive smoking history,

fever, chills, cough with

examination over affected

CXR: focal consolidation

Foreign body aspiration

acute onset of respiratory

stridor over the larynx,

CXR: foreign body or

Assessment of respiratory acidosis

Drug use (narcotics, alcohol, sedatives, anaesthetics)

obtundation or coma with

drug and toxicology

osmolar gap: >12

Oxygen therapy in COPD

pulse oximeter: oxygen

Assessment of respiratory acidosis

pulmonary vascular bed

CNS infarct or haemorrhage

headache or acute onset

MRI brain: evidence of

history of recent trauma or

overt evidence of trauma

Assessment of respiratory acidosis

recent history of fever,

fever, tachycardia, and

Hypoventilation syndrome in obesity

history of disordered sleep

obesity and increased neck

Assessment of respiratory acidosis

history of heart failure,

'stony' dull to percussion,

acute onset of dyspnoea

CXR: partial or total

history of obesity, snoring,

elevated body mass index,

PFT: reduced lung

Assessment of respiratory acidosis