Most common aetiologies for acute dyspnoea in hospitalised patients:
Alveolar problem
Flash Pulmonary oedema (e.g. due to tachyarrhythmia, ischaemica/ACS, hypertensive emergency, TACO)
Aspiration pneumonitis
TRALI
Airway problem
Anaphylaxis
Angioedema
Mucous plug
Endotracheal tube dislodgement
Pulmonary embolism
Pneumothorax (post-procedure)
Tamponade (post-procedure, post-MI)
Overview of Assessment and Management
Always call for help
Give oxygen
Assess the patient
CXR/ABG/VBG
Consider adjuncts
Escalation of care
Assessment
Can remember as RATES (respiratory rate, auscultate, trachea position, effort of breathing and saturation)
Airway Patency
Assess airway function
Signs of partial airway obstruction:
Hoarse voice, inability to speak or cough
Stridor, snoring or gurgling secretions
Soft-tissue retraction-tracheal tug, rib or abdominal recession
Loss, or an uncoordinated rise and fall, of the chest and/or abdomen
βSee-sawβ pattern of chest and abdominal movement: the chest is drawn in and the abdomen expands on inspiration and the opposite occurs on expiration
Altered level of consciousness or mental status or agitation
GCS β€8
Features of partial airway obstruction
Tripod position
Reluctance to speak or cough
Increased work of breathing with nasal flaring accessory muscle use
Inspect
Upper airway for foreign material if possible or using laryngoscopy
Erythema or urticaria with lip, tongue or palatal swelling
Listen for bronchospasm and examine for circulatory features that suggest Anaphylaxis
Localised trauma, burns infection or tumour
Palpate the anterior neck, including the thyroid cartilage for pain, inflammation, crepitus, swelling or masses
Investigate for any cause of depressed consciousness (e.g. hypoglycaemia or opioid intoxication)
Signs and features of complete airway obstruction
No stridor, airway sounds or breath sounds on lung auscultation
Inability to ventilate the patient with a bag-mask
Do not neglect airway issues and place heavy importance of suctioning if relevant (e.g. aspiration, mucous plugging)
Use supplemental oxygen in all hypoxic patients with high-flow oxygen at 15 L/min through a mask with a reservoir, (target oxygen saturation > 90-92%)
High inspired oxygen concentrations do not depress ventilation in patients who are in respiratory distress
In patients with COPD who chronically retain COX2β titrate use of a venturi mask
Giving too much oxygen to patients who chronically retain COX2β causes a rise in PaCOX2β because:
Changes in pulmonary vasoconstriction, dead space and shunting (V/Q mistmatch)
Haldane effect (haemoglobin molecules release COX2β in the presence of oxygen)
Blunting of the hypoxic drive; these patients depend on mild hypoxia to stimulate their respiratory centre
If unsure if they are a chronic retainer, check any previous blood gas results
Begin empirical OX2β treatment under pulse oximetry monitoring
Increase/decrease oxygen delivery until OX2β saturation is 88-92% by using different oxygen mixers in a venturi mask or changing the flow rate in a simple mask
Recheck blood gases and watch for a change in PCOX2β:
Continue with current therapy if COX2β is normalising
Decrease oxygen deliver if COX2β is increasing but maintain OX2β saturation of 88-92%
If COX2β is increasing and you are unable to maintain oxygen saturation >88%, the patient requires assisted ventilation (BiPAP) see ventilation below
Blood gases are necessary to determine the adequacy of ventilation (can use either venous or arterial as it will likely not influence immediate management) - see ABG Interpretation
If wheezing, consider bronchodilators (see: COPD Exacerbation) perhaps nebulised
Rule out tachy-arrythmia or demand related ischaemia if you can prior