DYSPNOEA
Physiological mechanisms of dyspnea
Dyspnoea refers to the abnormal and uncomfortable awareness of
breathing.
• Its physiological mechanisms are poorly understood; possible
afferent sources for the sensation include receptors in respiratory
muscles, juxta-capillary (J) receptors (sense interstitial fluid), and
chemoreceptors (sensing increased CO2 and decreased O2).
Clinical assessment
All patients need a full history and examination. Key points in the
assessment are:
• Duration and onset of breathlessness.
Include speed of onset and the duration of symptoms—enquiring about
exercise tolerance over a period of time is a useful way of assessing
duration and progression.
• Severity of breathlessness. assess the level of handicap and disability by
asking about effects on lifestyle, work, and daily activities.
• Exacerbating factors.
• ask about rest and exertion, nocturnal symptoms, and body position.
• nocturnal breathlessness may provide clues to the likely cause:
left ventricular failure (LVF) causes breathlessness after a few hours of
sleep and resolves after about 45min.
asthma tends to occur later in night
Orthopnoea is suggestive of LVF or diaphragm paralysis, although it is
also common in many chronic lung diseases.
• Associated symptoms, such as cough, haemoptysis, chest pain, wheeze,
stridor, fever, loss of appetite and weight, ankle swelling, and voice change.
• Wheeze may occur with pulmonary oedema, pulmonary
embolism (PE), bronchiolitis, and anaphylaxis, in addition to asthma and
chronic obstructive pulmonary disease (COPD)
• Breathlessness during swimming is characteristic of bilateral diaphragm
paralysis.
Causes of breathlessness grouped by speed
of onset
Instantaneous
• Pneumothorax
• PE.
Acute (minutes to hours):
• airways disease (asthma, exacerbation of COPD, upper airways
obstruction)
Cardiac disease (e.g. acute myocardial infarction, arrhythmia, valvular
disease, tamponade, aortic dissection)
• parenchymal disease (pneumonia, pulmonary oedema, pulmonary
haemorrhage, acute hypersensitivity pneumonitis)
• metabolic acidosis
• hyperventilation syndrome.
Sub-acute (days):
• pleural effusion
• acute interstitial pneumonia
• Superior vena cava obstruction
• pulmonary vasculitis.
Chronic (months to years):
• Obstructive airways disease (COPD, asthma)
• Diffuse parenchymal disease (including idiopathic pulmonary
fibrosis, sarcoidosis)
• pulmonary vascular disease (chronic thromboembolic disease,
pulmonary hypertension)
• hypoventilation (chest wall deformity, neuromuscular weakness,
obesity)
• anaemia
• thyrotoxicosis.
Examination of the cardiovascular and respiratory systems to distinguish
cardiac and respiratory causes of breathlessness
Observe the pattern and rate of breathing.
Assess for signs of respiratory distress.
Look for paradoxical abdominal movement if the history suggests
diaphragmatic paralysis.
Investigations:
Initial investigations typically include resting oximetry, chest radiograph (CXR), and electrocardiogram
(ECG).
Further tests depend on clinical suspicion
Arterial blood gases ABGs
Computed tomographic pulmonary angiography (CTPA)
High-resolution Ct (HRCT)
Blood tests (full blood count (FBC) and thyroid-stimulating hormone (TSH))
Echocardiogram (echo), exercise ECG
Cardiac catheterization.
Full pulmonary function tests
• Assessing the severity of an acute asthma attack
• Severe attack:
• • Unable to complete sentences in one breath.
• • Respiratory rate ≥ 25/min.
• • Pulse rate ≥110 beats/min.
• • PEF 33–50% of predicted or best.
Life threatening attack
PEF <33% of predicted or best.
• • Silent chest, cyanosis, feeble respiratory eff ort.
• • Arrhythmia or hypotension.bradycardia
• • Exhaustion, confusion, or coma.
• • Arterial blood gases:
• • Normal/high PaCO2 >4.6kPa.
• • PaO2 <8kPa, or SaO2 <92%.
Thrombolysis
• Benefi t reduces steadily from onset of pain, target time is
• <30min from admission; use >12h from symptom onset
requires specialist advice.
• Do not thrombolyse ST depression alone, T-wave
inversion alone, or normal ECG.
• Thrombolysis is best achieved with tissue plasminogen
activators (eg tenecteplase as a single IV bolus)
• Previous intracranial haemorrhage. •Ischaemic
• stroke <6months. •Cerebral malignancy or AVM.
•Recent major trauma/surgery/
• head injury (<3wks). •GI bleeding (<1 month).
•Known bleeding disorder. •Aortic
• dissection. •Non-compressible punctures <24h,
eg liver biopsy, lumbar puncture.
• Relative CI: •TIA <6 months. •Anticoagulant
therapy. •Pregnancy/<1wk post partum.
•Refractory hypertension
(>180mmHg/110mmHg). •Advanced liver
disease.
• •Infective endocarditis. •Active peptic ulcer.
•Prolonged/traumatic resuscitation
Pneumothorax
• Spontaneous: In young thin men) due to rupture of a
subpleural bulla.
Chronic lung disease: Asthma; COPD; cystic fi brosis; lung fi
brosis; sarcoidosis.
• • Infection: TB; pneumonia; lung abscess.
Traumatic: Including iatrogenic (CVP line insertion, pleural
aspiration or biopsy,
• Percutaneous liver biopsy, positive pressure ventilation).
Carcinoma.
• Signs: Reduced expansion, hyper-resonance to
percussion, and diminished breath
• sounds on the aff
• ected side. With a tension pneumothorax, the
trachea will be deviated away from the aff ected
side and the patient will be very unwe
Management
Depends on whether it is a primary pneumothorax
or secondary (=underlying lung disease or smoker
>50yrs old), size, and symptoms.
• Size is measured from the visible lung margin to chest
wall at level of the hilum.
• Pneumothorax due to trauma or mechanical
ventilation requires a chest drain.
• Aspiration of a pneumothorax /chest drain
•Thanks you
