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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.

Dyspnea on Exertion
Authors

Sandeep Sharma1; Muhammad F. Hashmi2; Madhu Badireddy3.

Affiliations
1 Mery Fitzgerald Hospital
2 Health service executive (HSE)
3 Christus Santa Rosa Hospitals

Last Update: September 10, 2020.

Introduction
Dyspnea, also known as shortness of breath, is a patient's perceived difficulty to breathe.
Sensations and intensity can vary and are subjective. It is a prevalent symptom impacting millions
of people. It may be the primary manifestation of respiratory, cardiac, neuromuscular,
psychogenic, or systemic illnesses, or a combination of these. Dyspnea on exertion is a similar
sensation. However, this shortness of breath is present with exercise and improves with
rest. Exercise is defined here as any physical exertion, which increases metabolic oxygen demand
above the body's ability to compensate. Oxygen is vital to the human body as it is used for oxidative
phosphorylation, and it is the last acceptor of an electron in the electron transport chain. The
sensation of dyspnea mostly comes when our body is lacking oxygen delivery.[1]

Oxygen Delivery:  Hb x 1.39 x SaO2 x Cardiac Output + 0.003 x Pao2

Hb is the concentration of hemoglobin in grams per liter

1.39- oxygen binding capacity of hemoglobin per gram

SaO2 is hemoglobin oxygen saturation expressed as a fraction (like- 98% will be 0.98)

Cardiac output is described as the amount of blood pumped by the heart in liter per minute

0.003 x pao2 is the amount of dissolved oxygen in the blood in milliliters

If a body has low Hb, hemoglobinopathies, some toxicities affecting Hb (like carbon monoxide
toxicity), low cardiac output (congestive heart failure [CHF], myocardial infarction [MI],
arrhythmia) a person will feel dyspneic.[2]

Etiology
Dyspnea on exertion is a symptom of various diseases rather than a disease itself. As such, its
etiology can be designated as arising from two primary organ systems: the respiratory system and
the cardiac system. Other systemic illnesses may by culprit as well as a combination of different
etiologies.

Respiratory causes may include asthma, acute exacerbation of chronic obstructive pulmonary
disorder (COPD), pneumonia, pulmonary embolism, lung malignancy, pneumothorax, or aspiration.
[1]

Cardiovascular causes may include congestive heart failure, pulmonary edema, acute coronary
syndrome, pericardial tamponade, valvular heart defect, pulmonary hypertension, cardiac
arrhythmia, or intracardiac shunting.

Other systemic illnesses, such as anemia, acute renal failure, metabolic acidosis, thyrotoxicosis,
cirrhosis of the liver, anaphylaxis, sepsis, angioedema, and epiglottitis, may also cause dyspnea on
exertion.

Epidemiology
The epidemiology of dyspnea on exertion is highly variable depending on etiology.[1]

Pathophysiology
Dyspnea on exertion is the sensation of running out of the air and of not being able to breathe fast
or deeply enough during physical activity. It results from multiple signal interactions with
receptors in the central nervous system (CNS), peripheral chemoreceptors, and mechanoreceptors
in the respiratory tract and chest wall.

The respiratory center is comprised of 3 neuron groupings in the brain: the dorsal and ventral
medullary groups and the pontine grouping. The pontine grouping further classifies into the
pneumotaxic and apneustic centers. Inhalation is managed by the dorsal group, and the ventral
medulla accounts for exhalation. The pontine groupings play their part in modulating the intensity
and frequency of the medullary signals where the pneumotaxic groups limit inhalation, and the
apneustic centers prolong and encourage inhalation. Each of these groups communicates with one
another to unify the efforts as the pace making potential of respiration.

Sensory information to the respiratory center regarding the volume of the lung space is provided
by mechanoreceptors located in the airways, trachea, lung, and pulmonary vessels. There are two
primary types of thoracic sensors: slow adapting stretch spindles and rapid adapting irritant
receptors. Slow-acting spindle sensors convey only volume information.

However, the rapid-acting receptors respond to both the volume of the lungs and chemical triggers,
such as foreign agents that may be harmful. Both kinds of mechanoreceptors signal through cranial
nerve X to the brain to escalate the rate of breathing, the volume of breaths, or to stimulate
coughing patterns of breathing because of irritants present in the airway.

Peripheral chemoreceptors comprise of the carotid and aortic bodies. Both receptors function to
monitor the partial pressure of oxygen in the arterial blood. However, hypercapnia and acidosis
enhance the sensitivity of these sensors and play a partial role in the functioning of receptors. Once
stimulated by hypoxia, carotid and aortic bodies send a signal via cranial nerve IX (the
glossopharyngeal nerve) to the nucleus tractus solitarius in the brain, which then, stimulates
excitatory neurons to increase the rate of ventilation. It has been postulated that the carotid bodies
comprise 15% of the total driving force of respiration.[3]

Central chemoreceptors manage the majority of control over the respiratory drive. They function
by sensing pH changes in the CNS. Prime locations within the brain include the ventral surface of
the medulla and the retrotrapezoid nucleus. pH changes within the brain, and surrounding
cerebrospinal fluid is derived primarily from increases or decreases in carbon dioxide levels.
Carbon dioxide is a lipid-soluble molecule that freely diffuses across the blood-brain barrier. This
characteristic proves to be useful in that rapid changes in pH within the cerebrospinal fluid are
possible. Chemoreceptors responsive to pH change are located on the ventral surface of the
medulla. As these areas become more acidic, sensory input is generated to stimulate
hyperventilation, and carbon dioxide within the body is reduced through the increased ventilation.
When pH rises to more alkalotic levels, hypoventilation occurs, and carbon dioxide levels decrease
secondary to decreased ventilation.
Respiratory centers located within the medulla oblongata and pons of the brainstem are
responsible for generating the baseline respiratory rhythm. However, the rate of respiration is
modified by allowing for aggregated sensory input from the peripheral sensory system, which
monitors oxygenation, and the central sensory system, which monitors pH and indirectly carbon
dioxide levels along with several other portions of the cerebellar brain modulate to create a unified
neural signal. The signal is then sent to the primary muscles of respiration, the diaphragm, external
intercostals, and scalene muscles along with other minor muscles of respiration.[4]

History and Physical

The history and physical exam should ascertain whether there are any chronic underlying
cardiovascular or pulmonary illnesses. Key components of history include onset, duration,
aggravating factors, and alleviating factors. The presence of cough may indicate the presence of
asthma, chronic obstructive pulmonary disease (COPD), or pneumonia. A severe sore throat could
indicate epiglottitis. Pleuritic quality chest pain may indicate pericarditis, pulmonary embolism,
pneumothorax, or pneumonia. Orthopnea, paroxysmal nocturnal dyspnea, and edema suggest a
possible diagnosis of congestive heart failure. Tobacco use is a common history finding that
increases the likelihood of COPD, congestive heart failure, and pulmonary embolism. If indigestion
or dysphagia is present, consider gastroesophageal reflux disease or gastric secretion aspiration in
the lungs. A barking quality cough, especially in children, may suggest croup. The presence of fever
strongly suggests an infectious etiology.

The physical exam should begin with a rapid assessment of the ABCs (airway, breathing, and
circulation). Once determined to be stable, a full physical exam can be done. To determine the
severity of dyspnea, one needs to observe respiratory effort, use of accessory muscles, mental
status, and ability to speak. Engorgement of the neck veins may imply cor pulmonale caused by
severe COPD, congestive heart failure, or cardiac tamponade. Thyromegaly may indicate
hyperthyroidism or hypothyroidism. Percussion of the lung lobes for dullness can determine the
presence or absence of consolidation and effusion. Hyperresonance on percussion is a worrisome
finding that indicates possible pneumothorax or severe bullous emphysema. Lung auscultation
may reveal absent breath sounds indicating the presence of region occupying mass, such as pleural
effusion or malignancy. The presence of wheezing is highly consistent with the diagnosis of
obstructive lung diseases such as asthma or COPD. However, wheezing may be associated with
pulmonary edema or pulmonary embolism. Pulmonary edema and pneumonia may present with
rales on auscultation. Auscultation of the heart may reveal the presence of dysrhythmia, cardiac
murmurs, or aberrant heart gallops. An S3 gallop indicates cardiac overfilling seen in left
ventricular systolic dysfunction and congestive heart failure (CHF). An S4 gallop suggests left
ventricular dysmotility and dysfunction. A loud P2 indicates possible pulmonary hypertension.
Murmurs may indicate valvular dysfunction. Diminished heart sounds may indicate cardiac
tamponade. Pericarditis may present with a rubbing cardiac sound on auscultation. On abdominal
examination, hepatomegaly, ascites, positive hepatojugular reflux may suggest a diagnosis of CHF.
Lower extremity edema is associated with CHF, and extreme swelling of the extremities suggests
possible deep venous thrombosis that can lead to a pulmonary embolism. Digital clubbing is
present in some forms of lung malignancy or severe chronic hypoxia. Cyanosis of the extremities
indicates hypoxia.[5]

Evaluation
Every evaluation should begin with a rapid assessment of the ABC status of the patient. Once these
are determined to be stable and no life-threatening status present, a complete history, and physical
exam can be collected. Vital signs should be assessed for heart rate, respiratory rate, body
temperature, body mass index (BMI), and oxygen saturation. Oxygen saturation may be normal at
rest, so oxygen saturation with physical exertion should be obtained. In normal physiological
conditions, the pulse oximetry improves as V/Q matching improves. Fever may indicate an
infectious etiology. A chest x-ray is the first diagnostic test that should be utilized in evaluating
dyspnea on exertion. If abnormal, the disease process is likely cardiac or a primary pulmonary
process. An echocardiogram is needed to evaluate cardiac function, pericardial space, and valvular
function.

Additionally, an electrocardiogram should be obtained to evaluate for myocardial infarction or

right-sided heart pattern strain. Elevated pro-brain natriuretic peptide (BNP) levels can further a
congestive heart disease diagnosis. Exercise stress testing is also beneficial to determine cardiac
function along with exercise oxygenation. If the chest x-ray is normal, then spirometry is needed to
determine lung function. Abnormal spirometry can indicate either an obstructive pathology such
as asthma, COPD, or physical airway obstruction or restrictive disease processes such as interstitial
fibrosis. Spirometry can also indicate the presence of respiratory muscle weakness from muscular
or neurological abnormalities. Normal spirometry indicates a need to evaluate for hypoxia as a
source of dyspnea. The restrictive pathology can be confirmed with lung volumes, which will show
reduced total lung capacity (TLC). In obstructive lung disease, the TLC is increased, and the RV/TLC
ratio is increased. Diffusion capacity is reduced in disease processes that affect the alveolar
membrane area and or thickness. For example, it will be reduced with interstitial lung disease
(ILD), emphysema, pulmonary embolism (PE), CHF, and obesity.

Arterial blood gas testing is used for this purpose as well as to calculate the A-a gradient and assess
for an acidotic state. If PaO2 is low with a normal chest x-ray, then pulmonary embolism should be
considered. The pH is mostly alkalotic in the setting of PE. This is to blow carbon dioxide to
relatively increase the partial pressure of oxygen. In a pregnant female, d-dimer with leg
ultrasound and V/Q scan should be ordered first. Detection of a mismatch in 2 or more areas
indicates pulmonary embolism. D-dimer testing has low specificity and high sensitivity. Spiral CT of
the chest is an alternative to V/Q scanning. In acute settings, the CT chest with PE protocol is the
gold standard. If the dyspnea on exertion is chronic, then chronic thromboembolic pulmonary
hypertension (CTEPH) should be considered, and the VQ scan is the test of choice and is considered
the gold standard. The VQ scan in this setting has a “moth-eaten” appearance.

A normal scan necessitates cardiac catheterization to determine pulmonary hypertension,

intracardiac shunting, or coronary artery disease. A normal cardiac catheterization diagnoses
idiopathic dyspnea. If hypoxia is not present with a PaO2 greater than 70 mm Hg, correlation with
oxygen saturation is needed. Abnormal oxygen saturation indicates possible carbon monoxide
poisoning, methemoglobinemia, or an abnormal hemoglobin molecule.

Normal oxygen saturation requires a complete blood count (CBC) to evaluate hemoglobin content
and hematocrit values. The white blood count also assesses for an immune response to possible
infection. Hematocrit less than 35% is anemia.

Oxygen Delivery:  Hb x 1.39 x SaO2 x Cardiac Output + 0.003 x Pao2

If one cannot determine the etiology of dyspnea, then we should order a cardiopulmonary exercise
test (CPET). If the CPET does not show any cardiac or pulmonary etiology, then the likely diagnosis
for dyspnea on exertion is physical deconditioning.

All testing modalities should target clinical suspicion and the history and physical exam to avoid
overtesting and minimize the cost to the patient.[6]

Treatment / Management
Treatment for dyspnea on exertion depends on its underlying etiology. The first intervention is to
determine that there are no life-threatening etiologies present on an acute presentation by
monitoring the ABCs (airway, breathing, and circulation) of the patient. Once determined to be
stable and that no immediate lifesaving interventions are necessary, assessment for further
treatment can be made. If a patient is a tobacco smoker, this should be discontinued. Various
inhaler therapies may be used in respiratory disease, including short-acting or long-acting
bronchodilators, inhaled antimuscarinics, and inhaled corticosteroids. Continuous supplemental
oxygen therapy is used to ease discomfort associated with dyspnea on exertion if oxygen saturation
is shown to decrease with exercise. [7] Cardiac function should be optimized when a cardiac illness
is identified. If myocardial infarction is suspected based on ST changes on electrocardiogram or
troponin marker evaluation, rapid percutaneous intervention should be performed by a
cardiologist. Therapy with aspirin, statin, ACE inhibitor, beta-blocker, heparin, and nitrates should
be initiated immediately if no contraindications. Occasionally, medications such as beta-blockers
and calcium-channel blockers can induce dyspnea on exertion by decreasing cardiac function,
which can be picked up on a CPET. These should be decreased or discontinued when possible. In
CHF, diuretic medications should be used to decrease vascular congestion from fluid overloading. If
the dyspnea on exertion is due to obesity or deconditioning physical therapy, an exercise regimen
should be pursued. If psychological problems are causing dyspnea on exertion, a selective
serotonin receptor inhibitor can be tried along with counseling sessions [8]. Weight loss in obese
patients, especially women, will improve outcomes.[9]

Differential Diagnosis
Acute dyspnea on exertion is most likely caused by:

Acute myocardial ischemia

Heart failure

Cardiac tamponade

Pulmonary embolism

Pneumothorax

Pulmonary infection in the form of bronchitis or pneumonia

Upper airway obstruction by aspiration or anaphylaxis

Chronic dyspnea is most likely caused by:

Asthma

Chronic obstructive pulmonary disease

Congestive heart failure

Interstitial lung disease

Myocardial dysfunction

Obesity

Deconditioning

The most common diagnosis underlying dyspnea on exertion is CHF.

Prognosis
In itself, dyspnea on exertion is harmless and a normal physiological finding; however, as it is a
symptom and not an illness, it may indicate an underlying disease. The prognosis is highly variable
and depends on the underlying etiology and comorbidities.

Complications
If left untreated, dyspnea on exertion can progress to acute respiratory failure with hypoxia and/or
hypercapnia, further leading to life-threatening respiratory or cardiac arrest or both.

Consultations
Based on possible underlying etiology after the initial evaluation, a cardiologist or a pulmonologist
needs to be consulted.

Deterrence and Patient Education

Patients need to be educated about the gravity of dyspnea on exertion. They need to be advised to
get immediate medical help for the recurrence of his symptoms, as this can be life-threatening.
Patients with CHF need to be educated about fluid restriction, dietary modifications, daily weights,
and compliance with medications, including diuretics, as advised. CHF management can be
overwhelming for patients and can lead to emotional lability and even depression[10][11]. Patients
need to be screened for mood disorders and referred to a psychiatrist if needed.

Enhancing Healthcare Team Outcomes

The most common cause of dyspnea on exertion is CHF. Management of CHF is complicated, and an
interprofessional approach is very important. The patient and his family need to be educated by a
specialty-trained nurse prior to discharge from the hospital. The patient needs close follow up with
their primary care physician, cardiologist, heart failure nurse, and dietician. The patient would also
benefit from home health services after discharge from the hospital to help monitor weight and
make sure they are taking all their medications. This would help reduce hospital readmission.

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