Shortness of breath must be taken seriously.

1. Dr. Bikal Lamichhane
NAMS, 1st year resident
APPROACH TO DYSPNEA

2. INTRODUCTION
 Dyspnea denotes the feeling of an ‘uncomfortable
need to breathe’ .
 The American Thoracic Society consensus
statement defines dyspnea as
 a “subjective experience of breathing discomfort that
consists of qualitatively distinct sensations that vary in
intensity. The experience derives from interactions
among multiple physiological, psychological, social,
and environmental factors and may induce secondary
physiological and behavioral responses.”
 Respiratory or cardiac dysfunction, or manifestation
of psychological distress , anaemia, thyrotoxicosis or
metabolic acidosis .

3. Descriptor &Pathophysiology of SOB

4.  Mechanisms:
- stimulation of intrapulmonary afferent nerves by
interstitial inflammation or thromboembolism.
- mechanical loading of respiratory muscles by
airflow obstruction or reduced lung compliance in
fibrosis.
- hypoxia due to ventilation/perfusion mismatch,
stimulating chemoreceptors.

5. MECHANISMS OF DYSPNEA

9. CAUSES

10. GRADING

14. APPROACH
HISTORY :
 Onset
- Instantaneous : pneumothorax, pulmonary embolus or
acute allergy.
- Over hours : asthma,acute pulmonary oedema or acute
infections.
- Insidious : Effusions, interstitial diseases and tumours.
- Acute, intermittent episodes :myocardial ischemia,
bronchospasm, or pulmonary embolism,
- Chronic persistent - COPD, interstitial lung disease, and
chronic thromboembolic disease.

15.  Variation:- Effect of position, infections, and
environmental stimuli
- Nocturnal dyspnea suggests CHF or asthma.
- Comfortable at rest and when asleep but struggle
with exertion – COPD.
- Breathlessness on lying down (orthopnoea) -
heart failure ,severe airflow obstruction or
diaphragmatic weakness , obesity, or asthma
triggered by esophageal reflux.
- Platypnea (dyspnea in the upright position with
relief in the supine position) - Left atrial myxoma
or hepatopulmonary syndrome

16. PND
 PND is the occurrence of dyspnea during
sleep where typically, a patient is woken
up few hours into sleep with transient
acute pulmonary edema.
 In contrast to orthopnea it can last up to half
an hour or so.
 PND is relieved by assuming upright position

17. MECHANISM
 Absorption of edema fluid with increase in Rt
ventricular output causing over filling the lungs
 Diminished sympathetic drive of sleep,
decreasing LV contractility
 Nocturnal arrhythmia
 Sleep apnea

18. ORTHOPNEA
 It refers to dyspnea on supine position
 It results from increase in hydrostatic pressure
in lung that occurs in assumption of supine
position.
 Sitting up leads to rapid relief of symptom.

19.  It is related to increase in venous return to the
heart in supine position.
 Increase in venous return which can not be
handled by failing left ventricle.
 It is a sign of LV dysfunction

20.  It is associated with cough which is called as
nocturnal cough.
 The transient rise in left ventricular pressure
results in transient lung stiffness and
consequent cough.
 The severity can be graded by the number of
pillow used at night, ex. Three pillow
orthopnea
 It can also be seen in COPD and condition

21. CAUSES
 Left heart failure
 COPD
 Constrictive pericarditis
 Severe ascites
 B/L Diaphragmatic paralysis

22. PHYSICAL EXAMINATION
 Vital signs
- Fever - infectious or inflammatory process
- Hypertension in the setting of a heart failure - diastolic dysfunction
- Tachycardia - fever, cardiac dysfunction, and deconditioning
- Resting hypoxemia - hypercapnia, ventilation-perfusion mismatch,
shunt, or impairment in diffusion capacity
 Pulsus paradoxus - COPD, acute asthma, or pericardial disease.
 Anemia
 Cyanosis
 Cirrhosis (spider angiomata, gynecomastia).
 Respiratory rate
 Clubbing - interstitial pulmonary fibrosis , bronchiectasis,
 Joint swelling or deformity - collagen-vascular disease.

23. RESPIRATORY SYSTEM EXAMINATION
 Chest - symmetry of movement
 Inability to speak in full sentences - impairment of the ventilatory
pump.
 Increased work of breathing (supraclavicular retractions; use of
accessory muscles of ventilation; and the tripod position) - increased
airway resistance or stiffness of the lungs and chest wall.
 Percussion :-
- Dullness - pleural effusion
- Hyperresonance - emphysema
 Auscultation :
- Wheezes, prolonged expiratory phase, and diminished breath
sounds - disorders of the airways
- Rales - interstitial edema or fibrosis

24. CARDIAC EXAMINATION
 Signs of elevated right heart pressures :
- jugular venous distention, edema, accentuated
pulmonic component to the second heart sound).
 left ventricular dysfunction (S3 and S4 gallops)
 Valvular disease (murmurs).

26. INVESTIGATIONS
CHEST IMAGING
 Lung volumes :
- Hyperinflation - obstructive lung disease,
- Low lung volumes - interstitial edema or fibrosis,
diaphragmatic dysfunction, or impaired chest wall motion.
 Evidence of interstitial disease, infiltrates, and emphysema.
 Prominent pulmonary vasculature in the upper zones -
pulmonary venous hypertension
 Enlarged central pulmonary arteries - pulmonary arterial
hypertension
 Enlarged cardiac silhouette - dilated cardiomyopathy or
valvular disease.
 Bilateral pleural effusions - CHF ,collagen-vascular disease.
 Unilateral effusions - carcinoma , pulmonary embolism ,heart
failure or parapneumonic effusion.

27. LABORATORY STUDIES
 Hematocrit - anemia
 Metabolic panel - metabolic acidosis
 Arterial blood gas
 Electrocardiography - ventricular hypertrophy , prior
myocardial infarction
 Spirometry - obstructive or restrictive ventilatory
defect
 Additional pulmonary function tests ( lung volumes,
diffusion capacity, tests of neuromuscular function).
 Echocardiography - systolic dysfunction, pulmonary
hypertension, valvular heart disease.
 Bronchoprovocation testing - asthma
 Brain natriuretic peptide - CHF ,right ventricular
strain .

28. Differentiating Cardiovascular and
respiratory cause :
 cardiopulmonary exercise test (CPET) - incremental
symptom-limited exercise (cycling or treadmill) with
measurements of ventilation , pulmonary gas exchange,
pulmonary vascular pressures and cardiac output.
 If, at peak exercise, the patient achieves predicted
maximal ventilation, demonstrates an increase in dead
space or hypoxemia, or develops bronchospasm -
respiratory system.
 If the heart rate is >85% of the predicted maximum, if the
anaerobic threshold occurs early, if the blood pressure
becomes excessively high or decreases during exercise,
if the O2 pulse (O2 consumption/heart rate) falls, or if
there are ischemic changes on the electrocardiogram -

31. REFERENCES
 HARRISON’S PRINCIPLES OF INTERNAL
MEDICINE -20TH EDITION
 DAVIDSON’S PRINCIPLE AND PRACTICE OF
MEDICINE -23RD EDITION

32. THANK YOU