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Shortness of Breath

Dyspnoea is a common problem that we see in the emergency department on a daily basis. It compromises of three main common complaints - increased work of breathing, the presence of chest tightness or the feeling of "air hunger" or the sensation of not getting enough oxygen.

When you are taking a history from a patient with shortness of breath, the cardinal symptoms that you need to ask about include;
  • Cough
  • Sputum Production
  • Haemoptysis
  • Wheeze
  • Chest Pain
  • Fever
  • Hoarseness or Stridor
  • Night Sweats


When you are assessing a patient with shortness of breath, you need to recognize the signs and symptoms consistent with severe respiratory distress. These include:
  • Inability to speak
  • Diaphoresis
  • Tripod positioning - this is where the patient stands or sits leaning forwards, supporting the upper body with the hands on the knees or another surface. This position optimises the mechanics of respiration by taking advantage of the accessory muscles of the neck and upper chest to get more air into the lungs.
  • Extreme tachypnoea (respiratory rate greater than 30 breaths per minute)
  • Hypoxaemia (Pulse Oximetry < 90%)
  • Accessory muscle use and intercostal recession
  • Tracheal tug
  • Stridor
  • Silent chest on ausculation - this is a particularly important finding in the patient with severe asthma.
  • Tachycardia or Bradycardia
  • Pulsus Paradoxus - this is an abnormally increased fall in the blood pressure of more than 10 mmHg on inspiration. The paradox is that you can detect heartbeats on auscultation of the chest that are not palpable at the radial pulse. This sign is seen in several conditions that include cardiac tamponade, pericarditis, croup and obstructive lung disease such as asthma and COPD

Watch the video below to see the signs of severe shortness of breath.
While most patients who present to the emergency department with shortness of breath will have a respiratory or cardiac cause for their presentation, you should have a comprehensive differential diagnosis for your patients presentation. You should consider the following conditions in your differential:
  • Asthma
  • COPD
  • Acute pulmonary oedema
  • Acute coronary syndrome
  • Valvular heart disease
  • Pneumothorax
  • Pneumonia
  • Pulmonary embolism
  • Airway obstruction
  • Trauma (chest wall injuries and smoke inhalation)
  • Neurological causes (spinal cord injury, muscular dystrophy, GBS and stroke)
  • Endocrine causes (DKA)
  • Metabolic causes (metabolic acidosis from sepsis)
  • Toxicological causes (salicylate toxicity)
  • Haematological causes (anaemia)
  • Gastrointestinal causes (massive ascites)
  • Psychiatric causes (anxiety)


In patients with shortness of breath, you will need to organise investigations to help you narrow your differential diagnosis. Investigations to consider should be dependent on your initial differential diagnosis and may include:

Chest X-Ray - this is an exceedingly important investigation as it will give you a lot of information such as:
  • Consolidation (seen in pneumonia)
  •  Hyperexpansion of the lungs which is seen in asthma and COPD
  • Interstitial oedema (acute pulmonary oedema and ARDS)
  • Pneumothorax
  • Rib fractures and lung contusions following a traumatic chest injury
  • Pleural effusions


Lung Ultrasound - this is a relatively new bedside assessment tool for the investigation of the patient with shortness of breath. It can be used to diagnose:
  • Pneumothorax - the sensitivity and specificity for pneumothorax using this test is much better than chest x-ray. The findings include loss of lung sliding and the abscence of the seashore pattern in B mode ultrasound.
  • Pulmonary oedema - the presence of multiple lung rockets and pleural effusions are highly suggestive of congestive cardiac failure.
  • Basic echocardiography; dilated RA/RV with right heart strain suggestive of pulmonary embolism; pericardial effusion suggestive of pericardial tamponade; basic contractility of the heart - useful in the diagnosis of heart failure.



 Pulse Oximetry - this is a very useful non-invasive test bedside test that gives you information about the oxygenation of the patient.


 Arterial Blood Gas - this gives you a lot of useful information such as:
  • Hypoxia
  • Hypercarbia seen in type 2 respiratory failure
  • The presence of a metabolic acidosis that may be driving the patients presentation of shortness of breath


Spirometry - while this is a useful test for determining causes of chronic shortness of breath, its usefulness is limited in the emergency department. Its main role is in the assessment of severity of asthma. In patients with a peak expiratory flow rate less than 50%, this is an independent predictor of the need for hospital admission.

Complete blood count - look for an elevated white cell count in patients with sepsis and a low haemoglobin in patients with anaemia. You need to be aware that some patients (in particular elderly and the immunosuppressed) may not present with an elevated WCC in the presence of sepsis. Immunosuppressed patients on chemotherapy may have evidence of significant neutropaenia in the presence of significant sepsis.

C-Reactive Protein (CRP) - can be a useful marker in patients with sepsis. It is slightly more sensitive than a WCC.

Blood Cultures - this should not be a routine test on patients who present with infection. Indications for taking a blood culture would include severe sepsis, septic shock and high-risk patients. High risk patients are nursing home patients, immunosuppressed patients, alcoholics, diabetics and intravenous drug users - this group of patients are at a higher risk of gram negative sepsis or sepsis related to atypical organisms.

D-dimer - this is a useful test in excluding the diagnosis of pulmonary embolism in patients who are low and intermediate risk for PE. We will talk about risk stratification a little later.

ECG - features to look for include evidence of ischaemia and infarction. You should also look for arryhthmia's such as atrial fibrillation that may present as shortness of breath.

Troponin - useful in the diagnosis of acute coronory syndrome.

CT Pulmonary Angiogram (CTPA) - used in the diagnosis of patients in whom pulmonary embolism is suspected. Indications are in patients who are low and intermediate risk with a positive d-dimer or in high risk patients.

Ventilation perfusion scan (V/Q Scan) - this is an alternative test to the CT pulmonary angiogram in the diagnosis of pulmonary embolism.


The management of patients with shortness of breath is dependent on their presentation. Interventions to consider include:
  • Supplemental oxygen - invariably most patients with shortness of breath will require oxygen therapy. This should be used in patients who are hypoxic. You need to be careful using oxygen in patients with COPD with type 2 respiratory failure and hypercarbia as it may depress their respiratory drive. In patients with type 2 respiratory failure, you should aim to achieve oxygen saturations between 88 and 92%.
  • The use of oral airways such as the guerdal airway and nasopharyngeal airway to open up the airway in patients with a depressed level of consciousness that are not able to maintain an airway.
  • High flow humidified oxygen therapy via nasal cannulae. This is a relatively new concept and can be used in patients with hypoxic respiratory failure to improve oxygenation. At higher flow rates, a small degree of positive airway pressure may be achieved. Studies suggest that this may be up to 10 cm H2O.
  • Non-invasive ventilation - CPAP and BiPAP. Both of these modalities can be used in patients with respiratory failure - both type 1 and type 2. BiPAP is commonly used in patients with exacerbations of COPD, asthma and pneumonia. CPAP is commonly used in patients with acute pulmonary oedema.
  • Invasive mechanical ventilation - this is used in patients with severe respiratory failure who are too sick for, or have failed non-invasive mechanical therapy.
  • ECMO - extracorporeal membrane oxygen therapy. This is an intervention that can be used for refractory cariogenic shock and severe respiratory failure in whom mechanical ventilation is failing. It is similar to placing a patient on cardiopulmonary bypass and is only used when all other interventions have failed. It is most commonly used in severe refractory ARDS.
  • Presumptive management of patients - in patients who present with severe respiratory distress, it may be difficult to initially work out exactly what the underlying pathology is. In these cases, it is not uncommon for us to start therapies for multiple conditions in the initial resuscitative phase. For example a patient in severe respiratory distress has a history of COPD and congestive cardiac failure, and the initial management of this patient may include therapies directed at both of these conditions.


Now that we have discussed the initial management of patients with respiratory distress, we should consider some of the common emergency department presentations for shortness of breath, how they present, what investigations to order and how to manage each of these problems.

Pneumonia

Pneumonia is an infection of the lungs characterised by exudation into the alveoli. The symptoms of pneumonia include fever, productive cough, SOB and pleuritic chest pain. There should be signs on clinical examiniation or radiological evidence of consolidation. The signs of consolidation include;
  • Reduced expansion
  • Increased vocal fremitus and resonance
  • Dull percussion
  • Bronchial breath sounds or crackles
  • Pleural rub
Investigations;
  • Routine bloods such as FBC, CRP and EUC are supportive, none of them are diagnostic.
  • Chest X-Ray (CXR) - the sensitivity for consolidation is 40-69%. This means that up to 1/3 of patients with pneumonia will have no changes on CXR.
  • Lung Ultrasound (USS) - this is a bedside test that has a sensitivity of up to 98% in experienced operators hands.
  • Consider Blood Cultures in patient with severe sepsis or in high risk patients (immunosuppressed, alcoholics, diabetics, nursing home patients)
  • Sputum Culture - not useful in the ED, but may guide antibiotic therapy later on.
  • Blood gas - a venous gas is a great screening tool for respiratory failure. A normal PCO2 will exclude type 2 respiratory failure.
  • Pulse Oximetry - excellent estimate of PaO2
Management;
  • Supportive management as described above
  • Antibiotic therapy - in severe pneumonia use a 3rd generation cephalosporin (ceftriaxone) with a macrolide (azithromycin). In patients with penicillin hypersensitivity (anaphylaxis), use a fluroquinolone (moxifloxacin) as a single agent. In patients with septic shock who are going to the intensive care unit, an antipseudomonal cephalosporin or gentamicin should be added. Patients with a severe pneumonia are also at risk for staphylococcal sepsis, and you should cover for MRSA with vancomycin.
Picture
RML Consolidation
Asthma
  • This is a chronic reversible inflammatory disease
  • It is characterised by decreased expiratory flow and airway obstruction.
  • There is air trapping and barotrauma
  • In severe cases, there is decreased venous return due to obstruction and lung hyperinflation resulting in hypotension.
  • Patients will present with muscle fatigue and respiratory failure resulting in hypoxia and hypercarbia.
  • Bedside spirometry can predict the need for hospital admission, with peak flow rates less than 50% highly indicative of the need for admission.
  • Risk factors for deterioration or severe episodes include: a past history of sudden, severe episodes, prior intubation, prior ICU admissions, 2 or more hospitalisations or 3 or more ED visits in the last year, hospitalization or ED visit in the last month.
  • Pulse oximetry is a useful indicator of hypoxia and type 1 respiratory failure.
  • Arterial blood gases should only be performed in patients with moderate to severe respiratory distress. In patients with mild respiratory distress, non-invasive monitoring with pulse oximetry is sufficient.
  • The chest x-ray usually just shows hyperinflated lungs consistent with chronic obstructive disease. It should be used to look for complications such as pneumonia or pneumothorax.
  • The cornerstone of management is with bronchodilator therapy and steroids. Bronchodilator therapy is with aerosolised salbutamol. The bioequivalence of oral versus intravenous steroids is similar, so oral prednisone is the preferred medication. Intravenous hydrocortisone should be used in patients who are unable to tolerate oral medication - usually patients who are critically unwell and ventilated (non-invasive or mechanically ventilated)
  • In severe cases of asthma, other interventions can include the use of ipratropium, intravenous salbutamol, magnesium, ketamine, adrenaline and inhalational anaesthesia.



COPD
  • This is also a chronic inflammatory disease. It differs to asthma in that it is a progressive disease that is not completely reversible.
  • There are 2 major types of presentation - the blue bloater and the pink puffer.
  • Acute exacerbations present with increased shortness of breath. Infective exacerbations present with increased sputum production and purulence.
  • Management of these patients is with aerosolised salbutamol and ipratropium and the use of steroids.
  • Antibiotics are indicated if there is evidence of an infective process such as fever, increased sputum production or purulence of the sputum.
  • Frequently patients with moderate to severe respiratory distress are placed on early BiPAP. This intervention has been effective at reducing intubation rates.
Picture
COPD - Hyperinflated Lungs

Pulmonary Embolism.

  • Patients with PE's present with pleuritic chest pain and shortness of breath. They may also present with syncope or haemoptysis.
  • Signs on clinical examination are usually non-specific and can include tachypnoea, tachycardia, fever, shock and right heart failure (elevated JVP, RV gallop and heave). They may also present with signs of a DVT.
  • The first thing to do in the work-up of a patient with PE is to risk stratify the patient using the Wells criteria for PE.
  • In low risk patients, you can also use the PERC rule to rule out the PE.
  • Patients who are low risk and PERC positive or intermediate risk should have a D-dimer performed. If the D-dimer is negative in this group of patients, then PE is ruled out.
  • Patients who are high risk or who have a positive D-dimer should have advanced imaging to rule out the diagnosis of PE. This can be with the use of CT pulmonary angiogram or a VQ scan.
  • The chest x-ray is usually normal, however rarely you may see a Hampton's hump or Westermark sign which is diagnostic for PE.
  • Treatment is largely supportive with oxygen therapy if they are hypoxaemic. Patients with hypotension should receive intravenous fluids and vasopressors if there is no response to fluids.
  • Patients with a PE should be commenced on anticoagulant therapy - either heparin or a low molecular weight heparin followed by the commencement of warfarin.
  • Haemodynamically unstable patients should be thrombolysed. If there is a contraindiaction to thrombolysis, the patient should be referred to cardiothoracic surgery for consideration of thrombectomy.
Picture
Hampton's Hump - Pleural based wedge shaped opacity (pulmonary infarction)
Picture
Westermark Sign - Relative oligaemia (focal loss of lung markings) from PE

Acute Pulmonary Oedema

  • This is the most common cardiac cause for shortness of breath.
  • Common causes include medication non-compliance, diet (excessive salt), arrhythmias, ACS, hypertensive crisis, volume overload (renal failure), PE, exacerbation of a co-morbidity (COPD) and infection.
  • Symptoms include orthopnoea, paroxysmal nocturnal dyspnoea and leg oedema.
  • Signs of congestive cardiac failure include tachypnoea, jugular venous distension, displaced apex beat, a gallop rhythm, third heart sound, pulmonary congestion (crackles on auscultation), RUQ abdominal tenderness (hepatic congestion) and pitting oedema to the lower limbs.
  • The chest x-ray will show cardiomegaly, a diffuse interstitial infiltrate with upper lobe diversion and the presence of Kerly B lines.
  • The ECG may show signs of ischaemia or infarction. It may also show a cardiac arrhythmia such as atrial fibrillation which may have precipitated the heart failure.
  • Troponins are useful for diagnosing acute coronary syndrome and NSTEMI. Mild elevations in the troponin may be seen in patients with heart failure with no evidence of myocardial ischaemia.
  • BNP (Brain Natriuretic Peptide) is a test which is not clinically useful in the emergency department setting. It is usually only positive in patients who are obviously in heart failure.
  • Acute pulmonary oedema is a symptom, and when present, one needs to look for an underlying cause and treat for this.
  • Symptomatic management is with supplemental oxygen and non-invasive ventilation such as CPAP.
  • Preload and afterload should be reduced with the use of nitrates, particularly when the patient is hypertensive.
  • Diuretic therapy is only useful once afterload reducation has been achieved.
  • Morphine is not beneficial in the treatment of acute pulmonary oedema and has been shown to increase mortality rates.
  • Patients with cardiogenic shock and pulmonary oedema should be treated with inotropes and PCI if clinically indicated.
Picture
APO - cardiomegaly, upper lobe diversion and interstitial infiltrate.

Pneumothorax

  • This is an abnormal collection of air in the pleural space.
  • It commonly presents with pleuritic chest pain and shortness of breath.
  • A tension pneumothorax is a pneumothorax that presents with cardiovascular collapse. It may also be diagnosed radiologically with evidence of mediastinal shift without cardiovascular collapse.
  • The common findings in a patient with pneumothorax include tachypnoea, hypoxaemia, tachycardia, tracheal deviation, hyper-resonance on percussion and jugular venous distension.
  • The management of a pneumothorax is dependent on its size and whether there is evidence of tension.
  • The treatment of a tension pneumothorax should be immediate decompression with either a needle thoracotomy or a finger thoracotomy for needle failures. Tension pneumothorax should always be treated with a formal chest drain.
  • Small pneumothoraces that have minimal symptoms can be managed expectantly.
  • Moderate and large pneumothoraces with no evidence of tension can be treated with mini-chest drains known as pleurocaths.

Picture
Left pneumothorax with mediastinal shift
Here is a podcast on "The Approach to the Patient with Shortness of Breath"