Skip to content
Download PDF

Dyspnea

Chapter 39 | Part 2 – Cardinal Manifestations & Presentation · Part 2 – Cardinal Manifestations & Presentation · Chapter 39

Key Clinical Points

  1. Dyspnea is a subjective experience of breathing discomfort; it must be self-reported.
  2. Signs of increased work of breathing (tachypnea, accessory muscle use) are measurable by clinicians.
  3. Prevalence increases significantly with age, reaching up to 37% in adults ≥70 years.
  4. Dyspnea often predicts outcomes in COPD better than FEV1.
  5. Supplemental O2 is indicated if resting O_2 saturation is ≤88% or drops to that level during activity/sleep.
  6. Platypnea (dyspnea when upright, relief when supine) suggests left atrial myxoma or hepatopulmonary syndrome.
  7. Pulsus paradoxus (>10 mmHg decrease in systolic pressure on inspiration) suggests COPD, acute asthma, or pericardial disease.
  8. Clubbing of digits indicates interstitial pulmonary fibrosis or bronchiectasis.
  9. Chronic breathlessness syndrome is defined as breathlessness persisting despite optimal treatment of underlying pathophysiology.
  10. Opioids may reduce air hunger but require individual risk-benefit assessment regarding respiratory depression.

DEFINITION & CLASSIFICATION

• Definition (Harrison's 29e): "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.'" • Symptom vs. Sign: ◦ Symptom: Subjective experience; must be self-reported. ◦ Sign: Measurable indicators of increased work of breathing (WOB) reported by clinicians. → Examples: Tachypnea, accessory muscle use, intercostal retraction.

EPIDEMIOLOGY

• Prevalence: ◦ Community: 9–13%. ◦ Elderly (≥70 years): Up to 37%. ◦ Inpatients/Ambulatory: Up to one-half of inpatients and one-quarter of ambulatory patients experience dyspnea. • Clinical Impact: ◦ Emergency Department: Frequent cause of ER visits (3–4 million per year). ◦ COPD: Dyspnea may predict outcomes better than FEV1; integrated into GOLD guidelines. ◦ Post-COVID: Increased incidence and persistent symptoms noted in the setting of SARS-CoV-2.

ETIOLOGY & PATHOPHYSIOLOGY

• Mechanism: Complex interaction of afferent signals (to CNS) and efferent signals (from CNS to muscles). ◦ Efferent-reafferent mismatch: A key driver of the sensation of dyspnea. • Afferent Signals (Sensory): ◦ Chemoreceptors: ◦ Peripheral: Carotid body and aortic arch. ◦ Central: Medulla. ◦ Triggered by: Hypoxemia, hypercapnia, or acidemia → produces 'air hunger'. ◦ Mechanoreceptors: ◦ Location: Upper airways, lungs (stretch, irritant, J receptors), and chest wall (muscle spindles, tendon organs). ◦ Triggered by: Increased airway resistance (chest tightness) or decreased lung/chest wall compliance. ◦ Metaboreceptors: Located in skeletal muscle; sense changes in the biochemical environment. ◦ Pulmonary Vascular Receptors: Respond to changes in pulmonary artery pressure. • Efferent Signals (Motor): ◦ Sent from CNS (motor cortex/brainstem) to respiratory muscles. ◦ Also transmitted via corollary discharge to sensory cortex → contributes to 'work of breathing' sensation. • Psychological Factors: Fear or anxiety can exacerbate the physiological disturbance and heighten the sense of dyspnea.

CLINICAL FEATURES

• Symptoms: Chest tightness, air hunger, inability to get a deep breath, tachypnea, increased WOB, exertional hypoxemia. • Signs: Wheezing, accessory muscle use, supraclavicular retractions, tripod position, wet crackles, dry end-inspiratory crackles, clubbing. • Temporal/Positional Patterns: ◦ Chronic: Duration >1 month. ◦ Acute: Suggests myocardial ischemia, bronchospasm, or pulmonary embolism. ◦ Orthopnea: Indicates CHF, mechanical impairment of diaphragm (obesity), or asthma triggered by GERD. ◦ Nocturnal: Suggests CHF or asthma. ◦ Platypnea: Dyspnea in upright position with relief in supine → suggests left atrial myxoma or hepatopulmonary syndrome. • Severity Grading (Table 39-1): ◦ Grade 0: Not troubled by breathlessness, except with strenuous exercise. ◦ Grade 1: Shortness of breath walking on level ground or with walking up a slight hill. ◦ Grade 2: Walks slower than people of similar age on level ground due to breathlessness, or has to stop to rest when walking at own pace on level ground. ◦ Grade 3: Stops to rest after walking 100 m or after walking a few minutes on level ground. ◦ Grade 4: Too breathless to leave the house, or breathless with activities of daily experience (e.g., dressing/undressing). → Integrated into GOLD guidelines.

DIFFERENTIAL DIAGNOSIS

• General Approach: Graded approach starting with H&P and initial testing; 85% of causes are pulmonary or cardiac. • Pulmonary Causes: ◦ Airways disease: Asthma, COPD, upper airway obstruction (Symptoms: chest tightness, tachypnea; Signs: wheezing, accessory muscle use). ◦ Parenchymal disease: Interstitial lung disease (Signs: dry end-inspiratory crackles, clubbing). ◦ Chest wall disease: Kyphoscoliosis, neuromuscular (NM) weakness (Sign: decreased diaphragm excursion). ◦ Pulmonary vasculature: Pulmonary hypertension (Sign: elevated right heart pressures). • Cardiac Causes: ◦ Left heart failure: Coronary artery disease, cardiomyopathy (Signs: wet crackles, pulsus paradoxus in pericardial disease). ◦ Pericardial disease: Constrictive pericarditis, cardiac tamponade. • Other Causes (Table 39-2): ◦ Anemia: Exertional breathlessness → check hematocrit. ◦ Deconditioning/Psychological: Poor fitness or anxiety. ◦ Metabolic: Anaerobic metabolism from poor fitness; check BMP. ◦ Gastrointestinal: GERD, aspiration pneumonitis (increased sensitivity to hypercapnia). ◦ Post-COVID syndrome: Persistent symptoms after infection.

DIAGNOSTIC APPROACH

  1. Initial Assessment: History and physical examination; assess ability to speak in full sentences.
  2. Immediate Testing: Walking oximetry (monitor O_2 during movement) and Peak flow assessment.
  3. Decision Point 1: If diagnosis obtained → Treat.
  4. Phase 1 Testing (if no diagnosis): Chest x-ray, initial vital signs, CBC, basic metabolic panel, ECG, Spirometry.
  5. Decision Point 2: If diagnosis obtained → Treat.
  6. Phase 2 Testing (if no diagnosis): Chest CT (with angiography for suspected embolism), Lung volumes, DLCO, tests of neuromuscular function, Echocardiogram, cardiac stress testing.
  7. Decision Point 3: If diagnosis obtained → Treat.
  8. Phase 3 Testing (if no diagnosis): Cardiopulmonary exercise testing (CPET) and subspecialty referral.

Clinical Findings & Interpretations: • Pulsus Paradoxus: Systolic pressure decrease >10 mmHg on inspiration → consider COPD, acute asthma, or pericardial disease. • Chest X-ray: Hyperinflation (obstructive); low volumes (restrictive/parenchymal); pulmonary vascular patterns; pleural effusions. • Spirometry: Identifies obstructive vs. restrictive defects; prompts further testing if needed. • CPET Criteria for Respiratory Cause: Peak exercise → achieved predicted maximal ventilation, increased dead space, hypoxemia, or bronchospasm. • CPET Criteria for Cardiovascular Cause: Heart rate >85% of predicted max, early anaerobic threshold, high/low blood pressure, falling O_2 pulse (indicator of stroke volume), or ischemic ECG changes.

MANAGEMENT & TREATMENT

  1. Primary Goal: Correct underlying condition and address reversible causes.
  2. Supplemental Oxygen: ◦ Indicated if resting O_2 saturation ≤88% or if it drops to this level during activity/sleep. ◦ In COPD: Proven to improve mortality in hypoxemic patients.
  3. Pulmonary Rehabilitation: Includes home/community programs (yoga, Tai Chi); improves exercise capacity and reduces hospitalizations; also effective for post-COVID conditions.
  4. Pharmacologic Therapy: ◦ Opioids: ◦ Purpose: Reduce air hunger by suppressing respiratory drive and influencing cortical activity. ◦ Caution: Risk of respiratory depression; must be evaluated individually based on risk-benefit profile. ◦ Anxiolytics: No consistent benefit shown for dyspnea.

KEY PEARLS & HIGH-YIELD POINTS

• Symptom vs. Sign: Dyspnea is a subjective symptom; tachypnea and accessory muscle use are objective signs. • Diagnostic Thresholds: O_2 saturation ≤88% is the critical threshold for supplemental oxygen. • Pulsus Paradoxus: >10 mmHg drop on inspiration is highly suggestive of pericardial disease, COPD, or asthma. • CPET Utility: Used when pulmonary and cardiac causes are both possible but not clearly distinguishable by standard tests. • Chronic Breathlessness Syndrome: Defined as breathlessness persisting despite optimal treatment of the underlying pathophysiology.

Reference Tables

TABLE 39-1 An Example of a Clinical Method for Rating Dyspnea: The Modified Medical Research Council Dyspnea Scale a

Harrison's 22e, p.268

GRADE OF
DYSPNEA		 DESCRIPTION
0 Not troubled by breathlessness, except with strenuous
exercise
2 Walks slower than people of similar age on level ground
due to breathlessness, or has to stop to rest when walking
at own pace on level ground
4 Too breathless to leave the house, or breathless with
activities of daily living (e.g., dressing/undressing)

TABLE 39-2 Differential Diagnosis of Disease Processes Underlying Dyspnea SYSTEM Pulmonary

Harrison's 22e, p.269

SYSTEM TYPE OF PROCESS EXAMPLE OF DISEASE
PROCESS		 POSSIBLE
PRESENTING
DYSPNEA
SYMPTOMS		 POSSIBLE PHYSICAL
FINDINGS		 POSSIBLE
MECHANISMS
UNDERLYING
DYSPNEA		 INITIAL DIAGNOSTIC STUDIES
(AND POSSIBLE FINDINGS)
Pulmonary Airways disease Asthma, COPD, upper
airway obstruction		 Chest tightness,
tachypnea,
increased WOB,
air hunger, inability
to get a deep
breath		 Wheezing, accessory
muscle use,
exertional hypoxemia
(especially with
COPD)		 Increased WOB,
hypoxemia,
hypercapnia,
stimulation of
pulmonary receptors		 Peak flow (reduced); spirometry
(OVD); CXR (hyperinflation; loss of
lung parenchyma in COPD), chest
CT and airway examination for
upper airway obstruction
Parenchymal
disease		 Interstitial lung
diseasea		 Air hunger, inability
to get a deep
breath		 Dry end-inspiratory
crackles, clubbing,
exertional hypoxemia		 Increased WOB,
increased respiratory
drive, hypoxemia,
hypercapnia,
stimulation of
pulmonary receptors		 Spirometry and lung volumes
(RVD); CXR and chest CT
(interstitial lung disease)
Chest wall disease Kyphoscoliosis,
neuromuscular (NM)
weakness		 Increased WOB,
inability to get a
deep breath		 Decreased diaphragm
excursion; atelectasis		 Increased WOB;
stimulation of
pulmonary receptors
(if atelectasis is
present)		 Spirometry and lung volumes
(RVD); MIP and MEPs (reduced in
NM weakness)
Pulmonary
vasculature		 Pulmonary
hypertension		 Tachypnea Elevated right heart
pressures, exertional
hypoxemia		 Increased respiratory
drive, hypoxemia,
stimulation of
vascular receptors
Cardiac Left heart failure
____
Pericardial disease		 Coronary
artery disease,
cardiomyopathyc
_______
Constrictive
pericarditis; cardiac
tamponade		 Chest tightness, air
hunger		 Elevated left
heart pressures;
wet crackles on
lung examination;
pulsus paradoxus
(pericardial disease)		 Increased WOB and
drive, hypoxemia,
stimulation of
vascular and
pulmonary receptorsd		 Consider BNP testing, especially
in the acute setting; ECG, ECHO,
may need stress testing and/
or LHC
Variable Anemia
Deconditioning
Psychological
Metabolic
disturbances
Gastrointestinal (e.g.,
gastroesophageal
reflux disease
[GERD], aspiration
pneumonitis)
Post-COVID syndrome		 Exertional
breathlessness
Poor fitness
Anxiety		 Variable Metaboreceptors
(anemia, poor fitness);
chemoreceptors
(anaerobic
metabolism from
poor fitness); some
subjects may have
increased sensitivity
to hypercapnia