Diagnose immediately a foreign body in the airways and anaphylaxis, and as emergencies spontaneous pneumothorax, pulmonary embolism, pulmonary oedema, asthma attack and acute exacerbation of COPD.
Identify asthma, COPD, heart failure and unstable angina as causes of recurrent or chronic dyspnoea.
Identify psychogenic hyperventilation syndrome and its important differential diagnoses.
Dyspnoea is a subjective feeling of difficulty breathing. Acute respiratory failure Respiratory Failure is a disturbance of blood gas exchange: arterial pO2< 8.0 kPa or pCO2> 6.0 kPa.
Atrial fibrillation, atrial flutter or supraventricular tachycardia Supraventricular Tachycardia (SVT) in a cardiac patient may lead to acute heart failure that is sometimes difficult to distinguish from the physiological sinus tachycardia caused by respiratory failure.
Carbon monoxide poisoning: pulse oximetry reading is normal even though the patient has severe hypoxaemia.
The patient is a young adult with a tendency for the condition.
The patient feels short of air; however, pO2 is high, pCO2 is low, and pH is high (respiratory alkalosis).
The patient has paraesthesia of the hands and dizziness.
Lung auscultation is normal.
The patient is often slightly tachycardic, and ECG often shows ST depressions.
The condition may be associated with preceding alcohol intake.
Secondary hyperventilation syndrome with a normal or only slightly lowered PO2 is often associated with pulmonary embolism, asthma, pneumothorax and metabolic acidosis
Vocal cord dysfunction (VCD)
The patient is often a relatively young woman.
Inspiration is laboured and stridor-like.
Wheezing is heard during exercise.
Dyspnoea that has lasted from a few hours to one day
Wheezing. Remember auscultation also during forced expiration.
Respiratory sounds are subdued in severe asthma or emphysema.
A respiratory tract infection (sinusitis!) or exposure to dust is often the cause of the exacerbation. The symptoms are aggravated by infection, allergen and/or physical exertion.
The onset of obstructive pulmonary disease is often slow.
In COPD patients dyspnoea does not always correlate with pulmonary function: "blue bloaters" adapt to CO2 retention dangerously well; "pink puffers" suffer from severe dyspnoea even when pCO2 is normal and pO2 only slightly lowered.
Aggravation of chronic heart failure
Even a mild heart failure may cause strong dyspnoeic symptoms in a patient with severe pulmonary disease.
Pneumonia; bacterial or viral
Particularly in cases with underlying severe pulmonary disease
Remember the possibility of aspiration in aged and neurological patients (impaired swallowing, decreased level of consciousness).
<92% is clearly abnormal; in patients with a chronic pulmonary disease, values < 90-88% are considered to be abnormally low
Does not measure hypoventilation.
Should be performed on all patients with dyspnoea in all emergency units.
CRP, basic blood count with platelet count
Blood gas analysis
Informative, but rarely available in primary care. Basic investigation in respiratory insufficiency. The patient has respiratory failure when pO2< 8.0 kPa and/or pCO2> 6.0 kPa Respiratory Failure.
Plasma N-peptide concentrations if heart failure is suspected Chronic Heart Failure. The concentration is increased also in other conditions than heart failure.
Negative plasma fibrin D-dimer test excludes pulmonary embolism Pulmonary Embolism with high probability if the pretest probability of embolism is low or moderate at most. If the probability of pulmonary embolism is moderate or high, a CT scan or a ventilation-perfusion lung scan is warranted.
Obesity and poor physical condition are often misdiagnosed as heart failure.
Slow pulmonary embolism gives initially few symptoms; remember thrombosis susceptibility.
Clinical signs of pneumothorax are not easily detected unless they are searched for intentionally, and pneumothorax may difficult to discern even on a chest x-ray (especially if the monitor is of low quality).
The main symptom of unstable angina pectoris is often dyspnoea on exertion; remember the risk factors.
The diagnosis of carbon monoxide poisoning is often missed; pulse oximetry does not reveal anoxia!
There is not always clear dyspnoea in hypoventilation. Oxygen therapy may worsen hypoventilation: be careful not to administer too much oxygen.
Physiological tachycardia resulting from respiratory failure is sometimes difficult to distinguish from primary arrhythmia.
The patient may simultaneously have several causes for dyspnoea (pneumonia and pulmonary embolism, asthma attack and pneumothorax, etc.).
Oxygen is administered as symptomatic treatment if the patient is hypoxaemic.
Patients with COPD or in whom hypoventilation is associated with obesity often have a tendency to carbon dioxide retention. In these patients, oxygen should be administered no more than 1-2 l/min or with the concentration of 24-28% through mask; SpO2 rise over 90-92% should be avoided.