APPROACH TO DYSPNEA
Dr. [Link]
MBBS DNB FAMILYMEDICINE
DEFINITION
• The American Thoracic Society consensus
statement de nes d spnea 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
MECHANISMS UNDERLYING DYSPNEA
• Dyspnea can arise from a variety of pathways,
including generation of a erent signals
from the respiratory system to the central nervous
system (CNS), e erent signals from the
CNS to the respiratory muscles, and particularly
when there is a mismatch in the integrative signaling
between these two pathways, termed
e erent-rea erent
mismatch
• A erent signals trigger the CNS (brainstem and/or cortex) and
include primarily
• (1) Peripheral chemoreceptors in the carotid body and aortic arch and central
chemoreceptors in the medulla that are activated by hypoxemia, hypercapnia, or
acidemia
• (2) Mechanoreceptors in the upper airways, lungs (including stretch receptors,
irritant receptors, and J receptors), and chest wall (including muscle spindles as
stretch receptors and tendon organs that monitor force generation)
• Activated in the setting of an increased work load from a disease state producing an
increase in airway resistance that may be associated with symptoms of chest tightness
(e.g., asthma or COPD) or decreased lung or chest wall compliance (e.g., pulmonary
brosis)
• Pulmonary vascular receptor responses to changes in pulmonary artery pressure and
skeletal muscle (termed metaboreceptors) that are believed to sense changes in the
biochemical environment
• E erent signals are sent from the CNS (motor
cortex and brainstem) to the respiratory muscles and are also
transmitted by corollary discharge to the sensory cortex
• They are believed to underlie sensations of respiratory e ort (or
“work of breathing”) and perhaps contribute to sensations of “air
hunger,” especially in response to an increased ventilatory load in a
disease state such as COPD
• In addition, fear or anxiety may heighten the sense of dyspnea by
exacerbating the underlying physiologic disturbance in response to an
increased respiratory rate or disordered breathing pattern
ASSESSING DYSPNEA
causes of acute dyspnea
Cardiovascular system
Acute myocardial ischemia
Heart failure
Cardiac tamponade
Respiratory system
Bronchospasm
Pulmonary embolism
Pneumothorax
Pulmonary infection - bronchitis, pneumonia
Upper airway obstruction - aspiration, anaphylaxis
Causes of chronic or recurrent dyspnea
Upper airway
Laryngeal mass
Vocal fold paralysis
Inducible laryngeal obstruction
(also known as paradoxical vocal fold motion)
Goiter
Neck mass compressing airway
Chest/abdominal wall
Diaphragmatic paralysis
Kyphoscoliosis
Late pregnancy
Massive obesity
Ventral hernia
Ascites
Intra-abdominal process
Causes of chronic or recurrent dyspnea
Pulmonary
Asthma
Bronchiectasis
Bronchiolitis
COPD/emphysema
Interstitial lung disease
Mass compressing or occluding airway
Pleural effusion
Previous major lung resection (eg, lobectomy, pneumonectomy)
Pulmonary right-to-left shunt
Pulmonary hypertension
Trapped lung
Venous thromboembolism (VTE)
Causes of chronic or recurrent dyspnea
Cardiac
Arrhythmia
Constrictive pericarditis, pericardial effusion
Coronary heart disease
Deconditioning
Heart failure (systolic or diastolic dysfunction)
Intracardiac shunt
Restrictive cardiomyopathy
Valvular dysfunction
Neuromuscular disease
Amyotrophic lateral sclerosis
Phrenic nerve disease/dysfunction
Glycolytic enzyme defects (eg, McArdle)
Mitochondrial diseases
Polymyositis/dermatomyositis
Causes of chronic or recurrent dyspnea
Toxic/metabolic/systemic
Anemia
Metabolic acidosis
Renal failure
Thyroid disease
Miscellaneous
Anxiety
Early pregnancy (effect of progesterone)
HISTORY
• The patient should be asked to describe in his or her own words
what the discomfort feels like as well as the e ect of position ,
infections, and environmental stimuli on the dyspnea
• Chest tightness – bronchoconstriction
• Sensation of inability to take a deep breath may correlate with
dynamic hyperin ation from COPD
• Orthopnea - congestive heart failure (CHF), mechanical
impairment of the diaphragm associated with obesity, or asthma
triggered by esophageal re ux
• Nocturnal dyspnea - CHF or asthma
• Acute, intermittent episodes of dyspnea - myocardial ischemia,
bronchospasm, or pulmonary embolism
• Chronic persistent dyspnea - COPD, interstitial lung disease, and
chronic thromboembolic disease
• Risk factors for drug-induced or occupational lung disease and for
coronary artery disease
• Platypnea - dyspnea in the upright position with relief in
the supine position
• Causes:Left atrial myxoma or hepatopulmonary syndrome
PHYSICAL EXAMINATION
• Fever -Infectious or in ammatory process
• Hypertension - Diastolic dysfunction
• Tachycardia - Fever, cardiac dysfunction, and deconditioning
• Resting hypoxemia suggests processes involving hypercapnia,
ventilation-perfusion mismatch, shunt, or impairment in
di usion capacity
• Inability of the patient to speak in full sentences before stopping
to get a deep breath suggests a condition that leads to stimulation
of the controller or impairment of the ventilatory pump with
reduced vital capacity
• Evidence of increased work of breathing (supraclavicular
retractions; use of accessory muscles of ventilation; and the
tripod position, characterized by sitting with the hands braced
on the knees) is indicative of increased airway resistance or
sti ness of the lungs and the chest wall
• Respiratory rate
• Pulsus paradoxus
• Systolic pressure decreases by >10 mmHg on inspiration-COPD, acute asthma,
or pericardial disease
• General examination
• signs of anemia (pale conjunctivae), cyanosis, and cirrhosis (spider angiomata,
gynecomastia)
• Examination of the chest
• Symmetry of movement
• Percussion
• Dullness - Pleural e usion
• Hyperresonance- Pneumothorax and emphysema
• Auscultation
• Wheezes,rhonchi, prolonged expiratory phase, and diminished breath sounds -
Disorders of the airways
• Rales - Interstitial edema or brosis
• Cardiac examination for
• 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
• Abdomen examination
• Paradoxical movement of the abdomen
• Presence of increased respiratory distress
• Inward motion during inspiration is a sign of diaphragmatic weakness
• Rounding of the abdomen during exhalation is suggestive of
pulmonary edema.
• Clubbing of the digits - interstitial pulmonary brosis or
bronchiectasis,
• Joint swelling or deformation as well as changes consistent with
Raynaud’s disease may be indicative of a collagen-vascular process that
can be associated with pulmonary disease
• Patients should be asked to walk under observation with oximetry in
order to reproduce the symptoms
• The patient should be examined during and at the end of exercise for
new ndings that were not present at rest (e.g., presence of wheezing)
and for changes in oxygen saturation
LABORATORY STUDIES
• CBC -Anemia
• BUN ,[Link] -Metabolic
• Sodium
• Potassium
• Chloride
• Calcium
• TSH,FT4,FT3
• Blood sugar-Metabolic
• ABG- Respiratory failure
• ECG – Ventricular hypertrophy and prior myocardial infarction
• Spirometry - Obstructive/restrictive ventilatory defect
• 2D ECHO - Systolic dysfunction,pulmonary hypertension,valvular
heart disease
• Bronchoprovocation testing- Asthma
• Home peak ow monitoring- Asthma
• Brain natriuretic peptide levels - CHF
CHEST IMAGING
• The lung volumes should be assessed
• Hyperin ation - Obstructive lung disease,
• Low lung volumes - Interstitial edema or brosis, diaphragmatic
dysfunction, or impaired chest wall motion
• The pulmonary parenchyma should be examined for evidence of
interstitial disease, in ltrates, and emphysema
• Prominent pulmonary vasculature in the upper zones - Pulmonary
venous hypertension
• Enlarged central pulmonary arteries- Pulmonary arterial
hypertension.
• An enlarged cardiac silhouette - Dilated cardiomyopathy or valvular
disease
• Bilateral pleural e usions - CHF and some forms of collagen
vascular disease
• Unilateral e usions - Carcinoma , pulmonary embolism, heart
failure, parapneumonic e usion
• CT of the chest is generally reserved for further evaluation of the
lung parenchyma (interstitial lung disease) and possible pulmonary
embolism if there remains diagnostic uncertainty
CARDIOPULMONARY EXERCISE TEST
• CPET includes incremental symptom limited exercise (cycling or
treadmill) with measurements of ventilation and pulmonary gas exchange
and, in some cases, includes Nnoninvasive and invasive measures of
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, the respiratory system may be the cause of the problem
• Alternatively, 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 O pulse (O consumption/heart
2 2
rate, an indicator of stroke volume) falls, or if there are ischemic changes
on the electrocardiogram, an abnormality of the cardiovascular system is
likely the explanation for the breathing discomfort
• Additionally, a CPET may also help point toward a peripheral extraction
de cit or metabolic/ neuromuscular disease as potential underlying
processes driving dyspnea.
