Shortness of breath — medically known as dyspnea — is one of the most common symptoms that bring people to seek medical attention. It’s also one of the most important to investigate because it can signal conditions ranging from easily treatable anemia to serious heart or lung disease.

While acute shortness of breath (sudden onset) requires immediate medical evaluation, chronic or gradually worsening breathlessness often has identifiable causes that blood tests can help uncover. Anemia, thyroid dysfunction, heart failure markers, kidney disease, and other conditions that affect oxygen delivery or utilization can all be detected through blood work.

Understanding what’s causing your breathlessness is the first step toward addressing it. This article explores the common causes of chronic shortness of breath and what blood tests can reveal about each.

Understanding Shortness of Breath

Shortness of breath is the subjective sensation of not being able to get enough air, or that breathing requires more effort than it should. Medically termed dyspnea (pronounced disp-NEE-uh), it’s one of the most common symptoms prompting people to seek medical care — and one of the most important to investigate thoroughly.

Dyspnea is a symptom, not a disease. It can arise from problems anywhere in the complex chain of oxygen delivery: the lungs (getting oxygen in), the blood (carrying oxygen), the heart (pumping oxygenated blood), or the tissues (using oxygen). Understanding this chain helps explain why so many different conditions can cause the same sensation of breathlessness.

How the body delivers oxygen:

To understand why shortness of breath occurs, it helps to understand the oxygen delivery system — a sophisticated chain where problems at any link can cause symptoms:

1. Ventilation: Air enters the lungs through the airways (nose, throat, trachea, bronchi). The respiratory muscles (primarily the diaphragm) expand the chest, creating negative pressure that draws air in. Problems here: airway obstruction (asthma, COPD), respiratory muscle weakness, chest wall restriction.
2. Gas exchange: In the lungs’ approximately 300 million tiny air sacs (alveoli), oxygen crosses a thin membrane into the blood while carbon dioxide crosses out to be exhaled. This requires the alveoli to be in contact with blood vessels (capillaries) and the membrane to be thin enough for gases to diffuse. Problems here: pneumonia (alveoli filled with fluid), pulmonary fibrosis (thickened membrane), pulmonary embolism (blood vessel blocked).
3. Oxygen transport: Hemoglobin molecules in red blood cells bind oxygen and carry it through the bloodstream. Each hemoglobin molecule can carry four oxygen molecules. Problems here: anemia (not enough hemoglobin), carbon monoxide poisoning (CO binds hemoglobin more tightly than oxygen).
4. Cardiac output: The heart pumps oxygenated blood to tissues throughout the body. The amount of oxygen delivered depends on both hemoglobin concentration and how much blood the heart pumps per minute. Problems here: heart failure (weak pump), arrhythmias (inefficient pumping), valvular disease.
5. Tissue delivery: Blood must reach the tissues that need oxygen. Once there, oxygen is released from hemoglobin to diffuse into cells. Problems here: peripheral vascular disease, shock states.
6. Cellular utilization: Cells use oxygen for energy production through cellular respiration. Problems here: metabolic disorders, mitochondrial dysfunction, cyanide poisoning (blocks cellular oxygen use).

Blood tests are particularly useful for identifying problems with steps 3-6 — oxygen transport, cardiac function, kidney disease affecting oxygen delivery, and metabolic issues. Lung problems (steps 1-2) typically require pulmonary function tests and imaging.

Types of shortness of breath:

The pattern of dyspnea provides important diagnostic clues:

Exertional dyspnea: Breathlessness that occurs with physical activity. Some degree is normal with vigorous exercise — everyone becomes breathless running up several flights of stairs. But becoming breathless with activities that previously were easy (walking across a room, climbing one flight of stairs, routine daily activities) suggests a problem. This is often the earliest symptom of cardiac or pulmonary disease.

Dyspnea at rest: Breathlessness even when sitting or lying still. This is more concerning and suggests more advanced disease or an acute problem requiring prompt evaluation.

Orthopnea: Shortness of breath when lying flat, relieved by sitting up or propping up with pillows. This is classic for heart failure — when you lie down, fluid redistributes from the legs into the central circulation, increasing blood return to the heart. A failing heart can’t handle this extra volume, and fluid backs up into the lungs. Clinicians often quantify orthopnea by asking how many pillows someone needs to sleep — “three-pillow orthopnea” indicates significant symptoms.

Paroxysmal nocturnal dyspnea (PND): Waking from sleep with sudden severe breathlessness, typically 1-2 hours after falling asleep, needing to sit up or stand (often going to a window for “fresh air”). Also classic for heart failure — fluid gradually redistributes during sleep until the lungs become congested enough to wake the person.

Platypnea: The opposite of orthopnea — shortness of breath when upright, relieved by lying down. This unusual pattern suggests specific conditions like hepatopulmonary syndrome or certain cardiac shunts.

Trepopnea: Breathlessness when lying on one side but not the other. Can occur with certain heart conditions or unilateral lung disease.

Acute versus chronic shortness of breath:

Acute shortness of breath (sudden onset over minutes to hours) is a medical emergency until proven otherwise. The differential diagnosis includes life-threatening conditions:

• Heart attack (myocardial infarction)
• Pulmonary embolism (blood clot in lung)
• Pneumothorax (collapsed lung)
• Severe asthma attack or COPD exacerbation
• Anaphylaxis (severe allergic reaction)
• Acute heart failure or flash pulmonary edema
• Cardiac tamponade (fluid compressing the heart)
• Pneumonia with respiratory failure

Acute dyspnea requires immediate evaluation — call emergency services. Don’t wait to see if it improves.

Chronic shortness of breath (developing gradually over weeks to months) is what this article primarily addresses. While still important to investigate, it usually allows time for systematic evaluation including blood tests and other diagnostic workup.

Warning signs requiring immediate medical attention:

• Sudden onset of severe breathlessness
• Chest pain, pressure, or tightness
• Fainting or near-fainting (syncope or presyncope)
• Confusion, altered mental status, or difficulty staying awake
• Blue or gray lips, fingertips, or skin (cyanosis) — indicates severe oxygen deprivation
• Coughing up blood (hemoptysis)
• High fever with breathing difficulty
• Severe swelling in legs that came on suddenly
• Inability to speak in full sentences due to breathlessness
• Breathing that’s getting rapidly worse
• Severe wheezing that doesn’t respond to rescue inhaler

Anemia: When Blood Can’t Carry Enough Oxygen

Anemia — a deficiency of red blood cells or hemoglobin — is one of the most common and most treatable causes of chronic shortness of breath. It’s also one of the most satisfying to treat because correcting anemia often produces dramatic improvement in symptoms.

Hemoglobin is the protein in red blood cells that carries oxygen. Each hemoglobin molecule can bind four oxygen molecules, and there are millions of hemoglobin molecules in each red blood cell. When there isn’t enough hemoglobin — either from too few red blood cells or inadequate hemoglobin in each cell — the blood simply can’t deliver adequate oxygen to tissues.

How anemia causes shortness of breath:

With insufficient hemoglobin, each heartbeat delivers less oxygen to tissues. The body has remarkable compensatory mechanisms that initially mask the problem:

• Increased heart rate: The heart beats faster to circulate blood more quickly. If each “trip” delivers less oxygen, making more trips can compensate.
• Increased stroke volume: The heart pumps more blood with each beat.
• Increased breathing rate and depth: Faster, deeper breathing maximizes oxygen uptake in the lungs.
• Increased cardiac output: The combination means more blood (carrying whatever oxygen it can) reaches tissues per minute.
• Redistribution of blood flow: Blood is directed away from less vital areas (skin, gut at rest) toward critical organs (brain, heart).
• Increased oxygen extraction: Tissues pull more oxygen from the blood passing through.
• Increased 2,3-DPG: A molecule that helps hemoglobin release oxygen to tissues more readily.

These compensatory mechanisms are remarkably effective at rest. Many people with moderate anemia feel fine sitting still. But during exertion — when oxygen demand increases — the compensatory mechanisms become inadequate. That’s why anemia typically causes exertional dyspnea first: you feel fine sitting but become breathless with activity.

As anemia worsens, compensatory mechanisms become insufficient even at rest, and dyspnea at rest develops.

Characteristics of anemia-related shortness of breath:

• Develops gradually as anemia worsens — the body adapts somewhat to slow changes
• Worse with exertion, improves with rest
• Often accompanied by fatigue — the most common symptom of anemia
• May notice rapid heartbeat (palpitations) with activity or even at rest
• Pale skin — particularly noticeable in nail beds, inner eyelids (conjunctivae), and palms
• Lightheadedness or dizziness, especially when standing up quickly
• Activities that were previously easy now cause breathlessness — “I used to climb these stairs without thinking about it”
• Headache, especially with activity
• Difficulty concentrating
• Cold hands and feet

Common causes of anemia:

Iron deficiency anemia: The most common type worldwide, affecting an estimated 1-2 billion people globally. Results from:

• Blood loss — heavy menstruation (most common in premenopausal women), GI bleeding (ulcers, colon polyps, cancer, hemorrhoids), frequent blood donation
• Inadequate dietary intake — rare in developed countries with varied diet but can occur with very restrictive diets
• Poor absorption — celiac disease, gastric bypass surgery, H. pylori infection, chronic antacid use
• Increased requirements — pregnancy, rapid growth in children

Vitamin B12 deficiency: Causes macrocytic anemia (large, dysfunctional red blood cells). Results from:

• Pernicious anemia — autoimmune destruction of cells needed for B12 absorption
• Inadequate intake — strict vegan diet without supplementation
• Malabsorption — gastric surgery, Crohn’s disease affecting terminal ileum, chronic pancreatitis
• Medications — metformin, proton pump inhibitors (long-term)

Folate deficiency: Also causes macrocytic anemia. Results from inadequate intake (especially in pregnancy), malabsorption, alcoholism, or certain medications.

Anemia of chronic disease (anemia of inflammation): Associated with chronic infections, inflammatory conditions (rheumatoid arthritis, inflammatory bowel disease), cancer, and kidney disease. The body sequesters iron as part of the immune/inflammatory response, making it unavailable for red blood cell production.

Chronic kidney disease: The kidneys produce erythropoietin (EPO), the hormone that stimulates the bone marrow to produce red blood cells. As kidney function declines, EPO production falls, and anemia develops. This is a major cause of anemia in older adults.

Hemolytic anemias: Red blood cells are destroyed faster than they’re produced. Can be inherited (sickle cell disease, thalassemia, hereditary spherocytosis) or acquired (autoimmune hemolytic anemia, mechanical destruction from artificial heart valves).

Bone marrow disorders: Aplastic anemia, myelodysplastic syndromes, leukemia, and other marrow disorders impair red blood cell production.

What to test:

Complete blood count (CBC) is the primary test for anemia. Key values include:

• Hemoglobin — the oxygen-carrying protein; low hemoglobin defines anemia
• Hematocrit — percentage of blood volume that is red blood cells
• MCV (Mean Corpuscular Volume) — average size of red blood cells; helps classify anemia:
  • Low MCV (microcytic) — suggests iron deficiency or thalassemia
  • Normal MCV (normocytic) — suggests anemia of chronic disease, kidney disease, or acute blood loss
  • High MCV (macrocytic) — suggests B12 or folate deficiency
• Red blood cell count
• RDW (Red cell distribution width) — variation in red cell size

If anemia is found, additional tests identify the cause:

• Ferritin — reflects iron stores; low ferritin confirms iron deficiency
• Serum iron — iron circulating in blood
• TIBC (Total Iron-Binding Capacity) — reflects transferrin availability; high in iron deficiency
• Transferrin saturation — calculated from iron and TIBC
• Vitamin B12 — for macrocytic anemia
• Folate — for macrocytic anemia
• Reticulocyte count — immature red blood cells; assesses bone marrow response
• Creatinine and eGFR — for kidney function

Heart Failure: When the Pump Weakens

Heart failure — when the heart can’t pump blood effectively enough to meet the body’s needs — is a major cause of shortness of breath and affects millions of people worldwide. Despite its name, heart failure doesn’t mean the heart has stopped; rather, it’s working less efficiently than it should.

As the heart’s pumping ability declines, two things happen: first, blood backs up into the lungs (causing pulmonary congestion and directly impairing breathing); second, tissues don’t receive adequate blood flow (causing fatigue and reduced exercise tolerance). Shortness of breath is often the symptom that brings heart failure to attention.

How heart failure causes shortness of breath:

Left-sided heart failure (the more common cause of dyspnea):

• The left ventricle — the heart’s main pumping chamber — can’t pump blood forward efficiently into the aorta and systemic circulation
• Blood backs up into the left atrium, then into the pulmonary veins, and finally into the lungs themselves
• Increased pressure in the pulmonary capillaries forces fluid to leak out into the lung tissue (pulmonary edema)
• This fluid interferes with gas exchange — oxygen can’t cross efficiently from the air sacs into the blood
• The fluid-filled lungs become stiff and harder to expand, increasing the work of breathing
• Receptors in the lungs sense the congestion and trigger the sensation of breathlessness
• In severe cases, fluid can actually fill the air sacs, causing severe respiratory distress

Right-sided heart failure:

• The right ventricle can’t pump blood forward efficiently into the pulmonary artery and lungs
• Blood backs up into the right atrium, then into the systemic veins
• This causes peripheral edema — swelling in the legs, ankles, and feet; abdominal fluid (ascites); and liver congestion
• Right-sided failure often results from left-sided failure (the backed-up blood increases pressure the right side must pump against) or from lung disease (cor pulmonale)
• Less directly causes dyspnea than left-sided failure, but contributes through fatigue, reduced exercise tolerance, and eventual impact on overall cardiac function

Heart failure with preserved ejection fraction (HFpEF): The heart muscle is stiff and doesn’t relax properly, even though it still contracts normally. Blood can’t fill the heart efficiently, leading to backup and congestion. This type is increasingly recognized and common in older adults, people with hypertension, and people with diabetes.

Heart failure with reduced ejection fraction (HFrEF): The heart muscle is weak and doesn’t contract forcefully enough. This is the “classic” heart failure, often resulting from heart attacks or dilated cardiomyopathy.

Characteristics of heart failure-related shortness of breath:

• Exertional dyspnea: Breathlessness with activities that were previously easy — often the earliest symptom. May be subtle at first: “I used to walk 18 holes, now I need a cart.”
• Orthopnea: Can’t lie flat without becoming breathless; needs to prop up with pillows. Clinicians ask “How many pillows do you sleep with?” — “two-pillow” or “three-pillow” orthopnea indicates severity.
• Paroxysmal nocturnal dyspnea (PND): Waking at night (typically 1-2 hours after falling asleep) gasping for air, needing to sit up or stand, often going to a window for “fresh air.” Very specific for heart failure.
• Bendopnea: Shortness of breath when bending forward (like tying shoes) — recently recognized as a heart failure symptom.
• Peripheral edema: Swelling in ankles and legs, worse at the end of the day, leaves indentations when pressed (“pitting edema”).
• Rapid weight gain: Several pounds gained over days from fluid retention — an important warning sign of worsening heart failure.
• Fatigue: Tiredness and reduced exercise tolerance, out of proportion to activity level.
• Cough: Especially when lying down; may produce frothy, pink-tinged sputum in severe cases.
• Nocturia: Needing to urinate frequently at night — when lying down, fluid returns from legs to circulation and is filtered by kidneys.
• Reduced appetite, nausea: From GI congestion.
• Confusion or difficulty thinking: From reduced brain perfusion.

What to test:

BNP (B-type natriuretic peptide) or NT-proBNP are the key blood tests for heart failure. These peptides are released by heart muscle cells when they’re stretched or under strain:

• Elevated levels strongly suggest heart failure is present
• Normal levels make heart failure very unlikely as a cause of dyspnea (high negative predictive value)
• Very useful for determining if breathlessness is cardiac or non-cardiac in origin
• Higher levels generally correlate with more severe heart failure and worse prognosis
• Can be used to monitor response to treatment — levels should fall as heart failure improves
• Some elevation can occur with kidney disease, atrial fibrillation, and other conditions, so interpretation requires clinical context

Additional tests assess heart failure causes, severity, and complications:

• CBC — anemia is common in heart failure and makes it worse; treating anemia can improve symptoms
• Creatinine, BUN, eGFR — kidney function is often impaired in heart failure (cardiorenal syndrome); kidney function affects medication choices
• Sodium, potassium — electrolytes affected by heart failure and its treatment (diuretics can cause abnormalities)
• TSH — thyroid dysfunction (both hypo- and hyperthyroidism) can cause or worsen heart failure
• Glucose, HbA1c — diabetes is a major heart failure risk factor
• Lipid panel — cardiovascular risk assessment
• Ferritin, iron — iron deficiency is common in heart failure even without anemia, and treating it improves symptoms
• Liver function tests — liver congestion can elevate liver enzymes

Thyroid Dysfunction

Both overactive and underactive thyroid can cause shortness of breath, though through different mechanisms. Thyroid disorders are common — affecting about 5% of the population — and often underdiagnosed, making thyroid testing an important part of evaluating unexplained dyspnea.

Hypothyroidism and breathlessness:

Hypothyroidism (underactive thyroid) can cause shortness of breath through multiple mechanisms:

• Respiratory muscle weakness: Low thyroid hormone reduces muscle strength throughout the body, including the diaphragm and intercostal muscles used for breathing. This increases the work of breathing and reduces exercise capacity.
• Reduced ventilatory drive: The brain’s respiratory center becomes less responsive to signals that normally stimulate breathing, potentially leading to shallow breathing and reduced oxygen levels, especially during sleep.
• Pleural effusion: Fluid can accumulate in the pleural space around the lungs, a condition called myxedema-related pleural effusion. This restricts lung expansion.
• Associated anemia: Hypothyroidism often causes mild normocytic anemia, compounding the sensation of breathlessness.
• Weight gain: Hypothyroidism frequently causes weight gain, which increases oxygen demand and mechanical restriction of breathing.
• Sleep apnea: Much more common in hypothyroidism due to upper airway changes and reduced respiratory drive. Sleep apnea causes daytime fatigue, reduced exercise tolerance, and can contribute to pulmonary hypertension.
• Reduced cardiac output: Hypothyroidism can cause bradycardia (slow heart rate) and reduced cardiac contractility, limiting oxygen delivery during exertion.
• Pericardial effusion: Fluid around the heart can occur in severe hypothyroidism, impairing cardiac function.

Other hypothyroidism symptoms typically accompany dyspnea: fatigue (often profound), weight gain, cold intolerance, constipation, dry skin, hair loss, brain fog, depression, muscle aches.

Hyperthyroidism and breathlessness:

Hyperthyroidism (overactive thyroid) increases metabolic rate and oxygen demand throughout the body, creating breathlessness through different mechanisms:

• Increased oxygen consumption: Every tissue is metabolizing faster, requiring more oxygen delivery. Even at rest, oxygen consumption is elevated; with exertion, the increased demand can exceed the body’s ability to supply.
• Cardiac effects: Hyperthyroidism causes rapid heart rate (tachycardia), often atrial fibrillation (irregular heart rhythm), and can eventually lead to heart failure if prolonged — all of which cause dyspnea. The heart is working harder but may become less efficient.
• Respiratory muscle weakness: Paradoxically, hyperthyroidism can also cause muscle weakness (thyrotoxic myopathy), affecting respiratory muscles.
• Anxiety component: Hyperthyroidism causes significant anxiety and a feeling of being “revved up.” Anxiety itself can cause the sensation of breathlessness and hyperventilation.
• Heat intolerance: The combination of heat intolerance and exertion can be particularly challenging for people with hyperthyroidism.

Other hyperthyroidism symptoms typically present: weight loss despite good appetite, rapid or irregular heartbeat, anxiety and nervousness, tremor, heat intolerance, excessive sweating, diarrhea, difficulty sleeping, bulging eyes (in Graves’ disease).

What to test:

TSH (Thyroid-Stimulating Hormone) is the primary screening test for both hypothyroidism and hyperthyroidism:

• Elevated TSH suggests hypothyroidism (the pituitary is trying to stimulate an underperforming thyroid)
• Suppressed (very low) TSH suggests hyperthyroidism (the pituitary is backing off because thyroid hormone is already too high)

Free T4 and Free T3 measure actual thyroid hormone levels and help confirm and characterize thyroid dysfunction.

TPO antibodies identify autoimmune thyroid disease (Hashimoto’s thyroiditis for hypothyroidism, sometimes present in Graves’ disease as well).

Kidney Disease

Chronic kidney disease (CKD) is strongly associated with shortness of breath, and dyspnea becomes increasingly common as kidney function declines. In advanced kidney disease, breathlessness is one of the most troublesome symptoms, affecting quality of life significantly.

How kidney disease causes breathlessness:

• Anemia: The kidneys produce erythropoietin (EPO), the hormone that stimulates the bone marrow to produce red blood cells. As kidney function declines, EPO production falls, leading to progressive anemia. This “anemia of CKD” is one of the most common causes of dyspnea in kidney disease and is often undertreated.
• Fluid overload: Failing kidneys can’t excrete fluid effectively. Fluid accumulates in the body, including in the lungs (pulmonary edema), directly impairing breathing. People with kidney disease may notice weight gain, leg swelling, and breathlessness that worsens between dialysis sessions (if on dialysis) or with dietary indiscretion (salt and fluid intake).
• Metabolic acidosis: The kidneys normally excrete acid and regenerate bicarbonate. Kidney failure leads to metabolic acidosis (acid buildup), which stimulates breathing — the body tries to “blow off” carbon dioxide to compensate for the acid load. This can cause increased respiratory rate and sensation of breathlessness.
• Uremic toxins: Accumulated waste products (uremia) affect multiple organs, including respiratory muscles (uremic myopathy), the lungs themselves, and the brain’s respiratory center.
• Associated heart disease: Kidney disease and heart disease share many risk factors and commonly occur together. Many people with CKD have underlying heart failure, coronary artery disease, or hypertensive heart disease contributing to their dyspnea.
• Pulmonary hypertension: More common in advanced CKD, possibly related to fluid overload, anemia, and vascular calcification.
• Sleep-disordered breathing: Sleep apnea is very common in kidney disease, contributing to daytime symptoms.

Characteristics of kidney disease-related dyspnea:

• Often progressive, worsening as kidney function declines
• May fluctuate with fluid status — worse when fluid-overloaded, better after dialysis or diuresis
• Accompanied by other uremic symptoms: fatigue, nausea, poor appetite, itching, trouble concentrating
• May have signs of fluid overload: leg swelling, elevated jugular venous pressure, rapid weight gain
• Often coexists with heart disease symptoms

What to test:

Creatinine and eGFR (estimated glomerular filtration rate) assess kidney function. eGFR is calculated from creatinine, age, sex, and race, and provides the best single measure of how well the kidneys are filtering blood.

BUN (Blood Urea Nitrogen) reflects kidney function and protein metabolism. The BUN/creatinine ratio can provide additional information.

CBC for anemia assessment — anemia is nearly universal in advanced CKD and contributes significantly to symptoms.

Bicarbonate (CO2) for acid-base status — low bicarbonate indicates metabolic acidosis.

Potassium — can be elevated in kidney disease, affecting heart and muscle function.

BNP/NT-proBNP — useful but must be interpreted carefully as levels are affected by kidney function.

Diabetes and Metabolic Conditions

Diabetes can contribute to shortness of breath through several pathways:

How diabetes affects breathing:

• Diabetic cardiomyopathy: Diabetes damages heart muscle independent of coronary artery disease
• Accelerated atherosclerosis: Increased risk of coronary artery disease and heart failure
• Diabetic nephropathy: Kidney disease from diabetes causes anemia and fluid overload
• Autonomic neuropathy: Can affect respiratory control
• Obesity: Often co-exists with diabetes; increases work of breathing
• Diabetic ketoacidosis: Severe complication causing characteristic deep, rapid breathing (Kussmaul breathing)

What to test:

Fasting glucose and HbA1c assess blood sugar control.

Creatinine and eGFR for kidney involvement.

BNP if heart failure suspected.

Obesity and Deconditioning

While not detected by standard blood tests, obesity and physical deconditioning are common causes of exertional dyspnea that should be considered — and importantly, they’re modifiable.

How obesity causes breathlessness:

• Increased metabolic demand: More body tissue requires more oxygen for basic metabolism. Even at rest, oxygen consumption is elevated. With exertion, the increased demand can exceed the body’s ability to supply.
• Mechanical restriction: Excess weight on the chest wall and abdomen physically restricts lung expansion. The diaphragm — the main breathing muscle — has less room to move downward when there’s abdominal fat pushing up against it.
• Reduced lung volumes: Functional residual capacity (the amount of air left in the lungs after a normal breath out) decreases. Total lung capacity may also be reduced. This means there’s less “reserve” for increased breathing demand.
• Increased work of breathing: More effort is required to move the chest wall against increased resistance. Breathing that should be effortless requires conscious effort.
• Ventilation-perfusion mismatch: Obesity can cause uneven distribution of air and blood in different parts of the lungs, reducing gas exchange efficiency.
• Sleep apnea: Very common in obesity. Obstructive sleep apnea causes repeated oxygen drops during sleep, disrupts sleep quality, and contributes to daytime symptoms including fatigue, reduced exercise tolerance, and sensation of not breathing well. It can also contribute to pulmonary hypertension over time.
• Associated conditions: Obesity increases risk of heart disease, diabetes, and other conditions that independently affect breathing. The metabolic syndrome associated with obesity has systemic inflammatory effects.
• Deconditioning: Obesity often coexists with physical inactivity, compounding the effect.

Deconditioning:

Physical inactivity leads to cardiovascular and muscular deconditioning — a real physiological state where:

• The heart becomes less efficient at pumping blood
• Cardiac output with exercise is reduced
• Muscles (including respiratory muscles) weaken
• Oxygen extraction by tissues decreases
• The anaerobic threshold (the point where you start breathing harder) occurs at lower exercise levels

The result is that activities that should be easy become difficult. Walking up stairs, walking across a parking lot, or other routine activities cause breathlessness.

While deconditioning is not a disease, it’s important to recognize for several reasons:

• It’s completely reversible with gradual, appropriate exercise
• It should be a diagnosis of exclusion — rule out other causes first
• It can coexist with other conditions, and addressing it can improve symptoms even when other causes are present

Important caveat: Don’t assume dyspnea is “just” deconditioning or “just” obesity without appropriate evaluation. These explanations are sometimes used to dismiss symptoms that actually have other, treatable causes.

Pulmonary Conditions

While lung diseases are primarily diagnosed with imaging and pulmonary function tests rather than blood tests, some blood markers can provide useful information.

COPD and asthma:

Chronic obstructive pulmonary disease (COPD) and asthma are leading causes of chronic dyspnea. Blood tests can identify:

• Polycythemia (elevated red blood cells) — the body’s response to chronic low oxygen
• Alpha-1 antitrypsin deficiency — a genetic cause of emphysema
• Eosinophilia — elevated eosinophils may indicate asthma or allergic component

Pulmonary embolism (blood clot):

While acute PE requires immediate evaluation, chronic thromboembolic disease can cause progressive dyspnea. D-dimer can help screen, though imaging is definitive.

Pulmonary hypertension:

High pressure in the pulmonary arteries causes progressive dyspnea. BNP/NT-proBNP may be elevated due to right heart strain.

Other Conditions Affecting Breathing

Anxiety and panic:

Anxiety can cause significant subjective breathlessness even when oxygen delivery is completely normal. Hyperventilation (rapid, shallow breathing) can cause its own symptoms including lightheadedness and tingling. While anxiety is a real condition requiring attention, it’s important to rule out physical causes of dyspnea first.

Neuromuscular disease:

Conditions affecting nerves or muscles (myasthenia gravis, ALS, muscular dystrophies) can weaken respiratory muscles. Progressive dyspnea, especially when lying down, may be an early sign.

Severe electrolyte abnormalities:

Profound abnormalities in potassium, magnesium, or phosphorus can affect muscle function including respiratory muscles.

The Testing Strategy for Shortness of Breath

A systematic approach to blood testing helps identify common causes of chronic dyspnea.

First-line tests for unexplained dyspnea:

Assessment for anemia:

• Complete blood count
• Ferritin
• Iron, TIBC
• Vitamin B12

Cardiac assessment:

• BNP or NT-proBNP

Thyroid function:

• TSH

Kidney function:

• Creatinine
• eGFR
• BUN

Metabolic assessment:

• Fasting glucose
• HbA1c

Additional tests based on findings:

• If anemia found: complete iron studies, B12, folate, reticulocyte count
• If BNP elevated: lipid panel, comprehensive metabolic panel, consider echocardiogram
• If kidney disease: electrolytes, bicarbonate, phosphorus
• If thyroid abnormal: Free T4, Free T3, thyroid antibodies
• If pulmonary embolism suspected: D-dimer (though imaging is usually needed)

What to Do With the Results

If anemia is found:

Treating anemia often dramatically improves shortness of breath. Iron supplementation for iron deficiency, B12 injections for B12 deficiency, or treatment of the underlying cause (stopping GI bleeding, treating kidney disease) can resolve symptoms. Many people don’t realize how breathless they were until their anemia is corrected and they feel the difference.

If heart failure markers are elevated:

Elevated BNP warrants cardiac evaluation, typically including echocardiogram. Heart failure is treatable with medications, lifestyle changes, and sometimes devices or procedures. Early identification and treatment significantly improve outcomes.

If thyroid dysfunction is found:

Treating hypothyroidism or hyperthyroidism typically improves breathing as part of overall symptom improvement. The time course depends on the severity and how long the dysfunction has been present.

If kidney disease is found:

Managing kidney disease (treating underlying causes, controlling blood pressure and diabetes, avoiding nephrotoxic medications) and treating associated anemia (erythropoiesis-stimulating agents if indicated) can improve symptoms.

If diabetes is found or poorly controlled:

Better blood sugar control reduces risk of diabetic complications affecting the heart and kidneys. If dyspnea is from diabetic cardiomyopathy or nephropathy, addressing diabetes is fundamental to management.

When Tests Are Normal

Normal blood tests provide valuable information — they rule out many important causes of dyspnea. But normal blood tests don’t mean nothing is wrong. They mean the conditions detectable by blood tests aren’t present, and the investigation should continue in other directions.

Consider these possibilities when blood work is unremarkable:

• Lung disease: COPD (chronic obstructive pulmonary disease), asthma, interstitial lung disease (pulmonary fibrosis), and other lung conditions are leading causes of chronic dyspnea but are diagnosed with pulmonary function tests (spirometry) and imaging (chest X-ray, CT scan), not blood tests. If you have chronic cough, wheezing, or a smoking history, pulmonary evaluation is essential.
• Deconditioning: Physical inactivity causes cardiovascular and muscular deconditioning — the heart becomes less efficient, respiratory muscles weaken, and activities that should be easy become difficult. This is a real phenomenon that blood tests won’t detect. The good news: it’s completely treatable with gradual, progressive exercise. However, deconditioning should be a diagnosis of exclusion — rule out other causes first.
• Obesity: Excess weight mechanically restricts lung expansion (the diaphragm has less room to move), increases oxygen demand (more tissue requires more oxygen), and is associated with conditions like sleep apnea. Weight loss can significantly improve dyspnea. Obesity can also coexist with other causes — don’t assume obesity is the only explanation without appropriate evaluation.
• Anxiety and panic disorder: Anxiety can cause very real, very distressing breathlessness without any abnormality in oxygen delivery. Hyperventilation (rapid, shallow breathing) can cause its own symptoms including lightheadedness, tingling, and chest tightness, which can worsen anxiety in a vicious cycle. Importantly, anxiety should not be assumed as the cause until physical causes are ruled out — but if physical evaluation is normal, anxiety may be the explanation and is treatable.
• Sleep apnea: Obstructive sleep apnea causes daytime symptoms including fatigue, reduced exercise tolerance, and a sensation of not breathing well, even though daytime oxygen levels may be normal. Sleep apnea requires a sleep study (polysomnography) for diagnosis, not blood tests. Risk factors include obesity, large neck circumference, snoring, and witnessed breathing pauses during sleep.
• Early or mild disease: Blood tests may be normal in early stages of conditions that later become apparent. Mild anemia, early kidney disease, or compensated heart failure may not yet produce abnormal laboratory values. If symptoms persist or worsen, repeat testing may be warranted.
• Pulmonary vascular disease: Pulmonary hypertension (elevated pressure in the pulmonary arteries) and chronic thromboembolic pulmonary hypertension (from old blood clots that didn’t fully dissolve) cause progressive dyspnea but often have normal basic laboratory tests. BNP may be elevated due to right heart strain, but diagnosis requires echocardiogram and potentially right heart catheterization.
• Coronary artery disease: Ischemic heart disease can cause dyspnea (especially with exertion) as an “anginal equivalent” even without typical chest pain. A normal BNP doesn’t rule this out — stress testing or coronary imaging may be needed.
• Vocal cord dysfunction: A condition where the vocal cords inappropriately close during breathing, causing episodic dyspnea often mistaken for asthma. Diagnosed by laryngoscopy during symptoms.

If blood tests are normal but dyspnea is significant and affecting quality of life, further evaluation is warranted. This might include pulmonary function tests, chest imaging, echocardiogram, cardiopulmonary exercise testing, or sleep study depending on the clinical picture. The goal is to identify and treat the cause, not just accept unexplained breathlessness.

The Bottom Line

Shortness of breath is your body telling you that something is affecting oxygen delivery or utilization — and it deserves to be taken seriously. While acute dyspnea requires immediate evaluation, chronic or gradually worsening breathlessness deserves systematic investigation to identify its cause.

Blood tests can identify many treatable causes of dyspnea:

• Anemia — perhaps the most treatable cause of chronic dyspnea. Correcting anemia through iron supplementation, B12 injections, or treatment of the underlying condition often produces dramatic improvement. Many people don’t realize how breathless they were until their anemia is corrected and they feel the difference.
• Heart failure — BNP/NT-proBNP testing can identify cardiac causes that require specific treatment. Heart failure is increasingly treatable with modern medications, and early identification significantly improves outcomes.
• Thyroid dysfunction — both hypothyroidism and hyperthyroidism can cause breathlessness through different mechanisms. Thyroid treatment typically improves symptoms as part of overall improvement.
• Kidney disease — causes anemia, fluid overload, and metabolic abnormalities that all contribute to dyspnea. Managing kidney disease addresses multiple mechanisms at once.
• Diabetes complications — diabetic heart disease and kidney disease affect breathing. Better diabetes control reduces risk of complications.

Don’t accept progressive breathlessness as inevitable aging or simply being “out of shape.” While deconditioning is real and common, it’s a diagnosis of exclusion — serious causes should be ruled out first. And even genuine deconditioning is treatable with gradual, appropriate exercise.

The pattern of your shortness of breath provides clues: exertional dyspnea that’s new or worsening, orthopnea (needing pillows to breathe at night), waking at night gasping for air, or dyspnea accompanied by chest pain, swelling, or other concerning symptoms all warrant evaluation.

Identifying the cause of your shortness of breath is the first step toward breathing easier. Simple blood tests — a CBC for anemia, BNP for heart failure, TSH for thyroid, creatinine for kidneys — can point toward or rule out many of the most important and most treatable causes. From there, appropriate treatment can help you get back to activities that breathlessness has limited.

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Key Takeaways

• Shortness of breath is a symptom that can arise from problems anywhere in oxygen delivery — lungs, blood, heart, or tissues
• Anemia is one of the most common and most treatable causes — a CBC can identify it; treating anemia often dramatically improves symptoms
• BNP/NT-proBNP testing helps identify heart failure — elevated levels indicate cardiac strain; normal levels make heart failure unlikely
• Thyroid dysfunction affects breathing — hypothyroidism through muscle weakness and metabolic effects; hyperthyroidism through increased oxygen demand
• Kidney disease causes dyspnea through anemia, fluid overload, and metabolic effects
• Acute shortness of breath requires immediate medical evaluation — don’t delay with sudden severe breathlessness
• Normal blood tests don’t rule out all causes — lung disease, deconditioning, obesity, and anxiety may require different evaluation
• Don’t accept chronic dyspnea as normal — investigate and identify treatable causes