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2. Acute and chronic dyspnoea
Indeed, dyspnea or shortness of breath, as a symptom, can be quite complex due to the variety of potential underlying causes. The body’s response to a perceived lack of oxygen involves multiple systems, primarily the respiratory and cardiovascular systems, and is regulated by both central and peripheral chemoreceptors.
Here's a deeper dive into the pathophysiology of dyspnea and how it can be triggered:
PATHOPHYSIOLOGY OF DYSPNEA
1. Imbalance in Oxygen Demand and Supply
Increased Oxygen Demand: During heavy exercise or in metabolic states such as hyperthyroidism, the body's demand for oxygen increases. If the increase cannot be met, it can lead to sensations of breathlessness.
Decreased Oxygen Delivery: This can happen due to respiratory issues (like asthma where airway constriction prevents adequate airflow) or cardiovascular problems (such as heart failure where the heart is unable to pump sufficient blood).
2. Role of Chemoreceptors
Central Chemoreceptors: Located in the medulla, these respond primarily to changes in the pH of the cerebrospinal fluid, which is influenced by carbon dioxide levels in the blood.
Peripheral Chemoreceptors: Found in the carotid bodies at the bifurcation of the carotid arteries and in the aortic arch, these react to decreases in blood oxygen levels, increases in carbon dioxide levels, and acidosis. They send signals to increase respiratory rate and depth to enhance oxygen intake and carbon dioxide expulsion.
3. Mechanical Factors
Restrictive Lung Disease: Diseases like pulmonary fibrosis decrease lung compliance, making it harder to expand the lungs, thereby increasing the work of breathing and causing dyspnea.
Obstructive Lung Disease: Conditions like COPD or asthma restrict airflow, making exhalation particularly difficult and leading to an increase in residual lung volume, which can cause a sensation of shortness of breath.
4. Cardiovascular Contributions
Inadequate cardiac output due to heart diseases can lead to poor oxygen delivery to tissues and resultant dyspnea.
5. Life-threatening Conditions
Conditions like pneumothorax (air in the pleural space) and pulmonary embolism (a clot in the pulmonary arteries) can acutely impair the ability to oxygenate blood and remove carbon dioxide, leading to sudden and severe dyspnea.
TYPES OF DYSPNEA
The types of dyspnea are categorized based on their timing, triggers, and associated conditions:
1. Exertional Dyspnea
Occurs during physical activity.
Common in heart and lung diseases and obesity, where the cardiovascular or respiratory system cannot meet the increased oxygen demand during exertion.
2. Resting Dyspnea
Present even at rest.
Typically seen in severe heart failure or advanced pneumonia, where even minimal exertion causes breathlessness.
3. Paroxysmal Dyspnea
Sudden, episodic occurrences.
Common in conditions like laryngitis, pertussis, asthma, and COPD, where inflammation or obstruction abruptly affects breathing.
4. Paroxysmal Nocturnal Dyspnea
Occurs suddenly during sleep.
Often in patients with asthma or early heart failure, related to fluid redistribution when lying flat.
5. Stenocardia
Dyspnea associated with chest pain, typically in diabetic patients where vascular issues are prevalent.
6. Orthopnea
Breathlessness that occurs when lying flat.
Common in heart failure, gastric ulcers, or pneumonia, where fluid in the lungs or abdominal pressure affects breathing.
7. Platypnea
Worsening dyspnea in the sitting position.
Rare and often associated with cardiovascular anomalies like left atrial myxoma, significant pulmonary embolism, or neuromuscular issues like intercostal muscle paralysis.
8. Trepopnea
Dyspnea that occurs when lying on one side but not the other.
Typically due to unilateral lung disease or pleural effusion affecting one lung more than the other.
9. Hyperacute Dyspnea
Develops within minutes.
Seen in emergencies such as pulmonary embolism, pneumothorax, anaphylaxis, angioedema, foreign body obstruction, or acute atrial fibrillation.
10. Acute Dyspnea
Onset within hours.
Examples include pulmonary edema or an acute asthma attack.
11. Subacute Dyspnea
Develops over days.
Associated with conditions like pleural effusion or anaemia.
12. Chronic Dyspnea
Develops over weeks to months.
Common in chronic conditions such as COPD, interstitial lung diseases (like sarcoidosis or lung fibrosis), or lung cancer.
13. Severe Dyspnea
Characterized by a significant increase in respiratory effort, fragmented speech, and often diaphoresis.
Indicates severe respiratory compromise requiring immediate intervention.
14. Imminent Respiratory Failure
Extreme fatigue, cyanosis, and impaired mental status are hallmarks.
This is a critical state, suggesting very poor oxygenation and impending respiratory collapse.
APPROACH
1. Support of Vital Functions
Immediate Care: Ensuring airway patency, monitoring vital signs, and providing supplemental oxygen. In severe cases, ventilatory support may be necessary if the patient is struggling to maintain adequate oxygenation or experiencing respiratory fatigue.
2. Supply Oxygen and Assess Need for Ventilator
Oxygen Therapy: Administering oxygen to relieve hypoxia. The decision to escalate to mechanical ventilation depends on the patient’s respiratory effort, blood gas values, and overall clinical condition.
3. Rule out Life-threatening Causes
Rapid Assessment: Identifying conditions like pneumothorax, pulmonary embolism, acute coronary syndrome, or severe asthma exacerbation that require immediate intervention.
4. Detailed Patient History
Key Information: Gathering details about the onset, duration, associated symptoms (like chest pain or fever), and any previous medical or family history relevant to respiratory or cardiac conditions.
5. Physical Examination
Inspection: Observing for signs like labored breathing, use of accessory muscles, skin color (cyanosis), and body position (e.g., sitting upright in orthopnea).
Palpation: Checking for any tenderness, masses, or thoracic deformities.
Percussion: Assessing for changes in lung sounds that might indicate fluid (dullness) or air (hyperresonance).
Auscultation: Listening for abnormal lung sounds such as crackles (indicative of fluid) or wheezing (airway narrowing), and heart murmurs which might suggest valvular issues.
6. Laboratory Tests
Arterial Blood Gas (ABG): Evaluates oxygenation, carbon dioxide levels, and blood acidity.
Cardiac Enzymes (e.g., Troponin): Helps in diagnosing myocardial infarction.
D-dimer: Used to rule out pulmonary embolism, though not specific.
BNP or pro-BNP: Indicates heart failure.
Complete Blood Count (CBC) and Basic Metabolic Panel: Provides insight into overall health, infection status, and kidney function.
7. Electrocardiogram (ECG)
Cardiac Function: Detects heart rhythm abnormalities, signs of heart strain or ischemia, particularly important in suspected cardiac causes of dyspnea.
8. Chest X-ray
Structural Abnormalities: Shows lung fields, heart size, and presence of fluid or air outside the lungs.
9. Computed Tomography (CT)
Detailed Imaging: Specifically valuable for diagnosing pulmonary embolism, assessing lung structure, and other thoracic pathology.
10. Transthoracic Echocardiography
Heart Structure and Function: Assesses cardiac chambers, wall motion, and valvular function which might contribute to dyspnea.
11. Spirometry
Lung Function: Measures the volume and flow of air during inhalation and exhalation, useful in diagnosing obstructive and restrictive lung diseases.
DIFFERENTIAL DIAGNOSES
1. Pneumonia
Symptoms: Common symptoms include fever, chills, cough (which can be productive), dyspnea, and in severe cases, hypoxemia.
Laboratory Findings: Elevated inflammatory markers (ESR, CRP, procalcitonin), leukocytosis indicating an immune response, and a positive sputum culture which helps identify the causative organism.
Imaging: Chest X-rays typically show consolidation and may also reveal pleural effusion, which indicates fluid accumulation due to inflammation.
2. COPD Exacerbation
Symptoms: Increased dyspnea, chronic cough with purulent sputum, which indicates infection.
Physical Examination Findings: Tachypnea (rapid breathing), diffuse wheezing, and decreased breath sounds, alongside an increased work of breathing.
Blood Gas Analysis: Often shows respiratory acidosis characterized by acidosis, hypercapnia (elevated CO2 levels), and hypoxia (low oxygen levels).
Imaging: X-rays may show hyperinflated lungs due to air trapping and could also reveal signs of concurrent pneumonia, pneumothorax, or pleural effusion.
3. Asthma Exacerbation
Symptoms and Signs: Similar to COPD in terms of increased dyspnea and wheezing but usually affects individuals with a history of asthma. Asthma exacerbations are often triggered by allergens, exercise, or stress.
Physical Examination: Emphasizes wheezing and difficulty in breathing.
Imaging and Lab Tests: Not as definitive as in COPD, often diagnosed based on clinical presentation and response to bronchodilators.
4. Tension Pneumothorax
Symptoms: Presents with severe, sharp chest pain and dyspnea. This condition is life-threatening and requires immediate attention.
Physical Examination: Hyperresonance on percussion, decreased or absent breath sounds on one side of the chest, tracheal deviation away from the affected side.
Clinical Signs: Tachycardia and hypotension due to reduced venous return to the heart.
Imaging: X-ray findings include absent lung markings on the affected side, tracheal and mediastinal shift to the opposite side, and possible pneumomediastinum.
5. Spontaneous Pneumothorax
Symptoms: Sudden onset of unilateral chest pain and dyspnea.
Imaging: X-ray or CT scan shows increased lucency with a visible rim of air between the lung and the chest wall (lung collapse), displaced lung markings, and possibly subcutaneous emphysema.
6. Pulmonary Embolism (PE)
Symptoms: Typically presents with pleuritic chest pain, acute onset of dyspnea, hypoxemia, cough, and sometimes hemoptysis.
Physical Findings: Hypotension or shock in cases of massive PE, and possible unilateral leg swelling or a history of deep vein thrombosis (DVT) which may be a source of the emboli.
Laboratory Tests: Elevated D-dimer is a common finding, which is a marker of clot degradation. Elevated troponins and BNP can indicate right ventricular strain due to the pulmonary obstruction.
ECG: Often shows normal or sinus tachycardia; in severe cases, signs of right ventricular strain such as a right bundle branch block may be present.
Imaging: CT angiography is the gold standard, showing filling defects in the pulmonary arteries. If CT is contraindicated, a perfusion-ventilation scan can be used to demonstrate areas of mismatch.
Echocardiography: Transthoracic echocardiography (TTE) may show right ventricle hypokinesis with preserved apical movement, indicating strain from pulmonary hypertension.
7. Acute Chest Syndrome in Sickle Cell Disease
Symptoms: Characterized by chest pain, fever, cough, dyspnea, and sometimes wheezing. It is a severe complication often triggered by infection or fat emboli.
Blood Tests: Anaemia and leukocytosis are common due to the underlying disease and inflammatory response.
Imaging: Chest X-ray often shows new pulmonary infiltrates which are a hallmark of this syndrome.
Management: Includes oxygenation, pain management, and possibly antibiotics and transfusions to manage the crisis and prevent further sickling and vascular occlusion.
8. Acute Respiratory Distress Syndrome (ARDS)
Symptoms: Acute onset of severe hypoxemic respiratory failure, usually within a week of a known clinical insult (e.g., sepsis, trauma, pneumonia).
Clinical Features: Patients exhibit diffuse, bilateral crackles due to non-cardiogenic pulmonary edema caused by increased vascular permeability.
Laboratory Tests: Arterial blood gases show marked hypoxemia.
Imaging: X-ray displays bilateral patchy, diffuse, or homogeneous lung infiltrates, which do not match the degree of cardiac failure (non-cardiogenic origin).
Echocardiography: TTE used to rule out cardiac causes by demonstrating preserved systolic function despite severe respiratory symptoms.
CARDIAC CAUSES OF DYSPNEA
1. Acute Coronary Syndrome (ACS)
Symptoms: ACS typically presents with heavy, dull, or squeezing chest pain that is substernal and may radiate to the left shoulder, jaw, or back. Accompanying symptoms often include nausea, vomiting, anxiety, dizziness, or even syncope, indicating a severe cardiac event.
ECG Findings: Key ECG changes include ST-segment elevation or depression, T-wave inversion, and the presence of new Q-waves, all indicative of myocardial injury or ischemia.
Laboratory Tests: Troponin levels are crucial, as they rise in response to myocardial cell death. Troponin can be elevated or at the high end of normal, depending on the stage of ACS upon presentation.
Echocardiography (TTE): TTE may show hypokinesis (reduced wall motion) and regional wall motion abnormalities, which indicate areas of the heart affected by ischemia or infarction.
2. Cardiac Tamponade
Symptoms: Characterized by the classical Beck's triad of hypotension, elevated jugular venous distention, and muffled heart sounds. Other symptoms include tachypnea (rapid breathing), dyspnea, and tachycardia. Pulsus paradoxus (a drop in blood pressure > 10 mmHg during inspiration) is a significant sign, and there is a risk of progression to cardiogenic shock.
ECG Findings: The ECG may show low voltage QRS complexes and electrical alternans, which is a phenomenon caused by the heart swinging in a large effusion.
X-ray Findings: Often shows an enlarged cardiac silhouette. Unlike in heart failure, pulmonary edema is typically absent, which can help differentiate tamponade from other causes of acute cardiac distress.
Echocardiography (TTE): The definitive diagnostic tool for tamponade, showing circumferential fluid accumulation around the heart. Other findings include collapsing cardiac chambers during diastole, exaggerated movements of the septa with respiration, and potentially a high ejection fraction due to the increased heart rate and initial compensatory mechanisms.
3. Heart Failure Exacerbation
Symptoms: Patients often report increased chest pressure, dyspnea, and cough.
Signs: Clinical examination may reveal hypoxemia, crackles in the lungs due to fluid overload, jugular venous distention, and peripheral edema.
Laboratory Tests: Elevated BNP (B-type Natriuretic Peptide) indicates heart stress, while increased troponins suggest myocardial strain. Hyponatremia (low sodium) is common due to fluid imbalance.
Imaging: Chest X-ray typically shows diffuse opacities consistent with pulmonary edema.
Echocardiography (TTE): Reveals wall motion abnormalities, and can assess for systolic or diastolic dysfunction, often showing decreased ejection fraction.
4. Atrial Fibrillation
Symptoms: Patients may experience dyspnea, palpitations, dizziness, and sometimes syncope due to irregular heart rhythm leading to variable cardiac output.
ECG Findings: Characteristic findings include an irregular rhythm and absent P-waves, replaced by erratic electrical activity at the atrial level.
Imaging: Chest X-ray may show signs of pulmonary edema and left atrial enlargement, which contribute to dyspnea.
Management: Includes rate or rhythm control, anticoagulation to prevent thromboembolic events, and addressing any underlying causes or contributing factors.
5. Acute Mitral Regurgitation
Symptoms: Presents with acute tachycardia, hypotension, signs of cardiogenic shock, and severe dyspnea.
Signs: A faint systolic decrescendo murmur may be heard, and patients may also report weakness, dizziness, and an altered mental state due to decreased cardiac output.
ECG: May show tachycardia with ST- and T-wave changes indicative of myocardial stress or ischemia.
Imaging: Chest X-ray can reveal pulmonary edema and sometimes cardiomegaly if the heart is strained over time.
Echocardiography (TTE): Shows the regurgitation of blood back into the left atrium during systole, normal or increased left ventricular size, and usually a normal ejection fraction unless the condition has progressed.
Diagnostic and Therapeutic Approaches
For these cardiac conditions, an integrated approach using clinical evaluation, lab tests, ECG, imaging, and TTE is crucial. Treatment strategies vary:
Heart Failure Exacerbation: Focuses on diuretics to manage fluid overload, ACE inhibitors or ARBs to reduce cardiac workload, and other supportive measures.
Atrial Fibrillation: Aims at controlling heart rate, managing rhythm, and preventing stroke.
Acute Mitral Regurgitation: Often requires urgent surgical intervention to repair or replace the mitral valve, alongside medical management to stabilize the patient.
UPPER AIRWAY CAUSES OF DYSPNEA
1. Angioedema
Symptoms: Swelling of the face, lips, tongue, and upper airway, often accompanied by urticaria (hives). Patients may also experience hypotension and bronchospasm, indicating a severe allergic reaction.
Laboratory Findings: Increased serum tryptase in histamine-mediated angioedema, suggesting an allergic reaction. In hereditary angioedema, there's typically a decrease in the C4 component due to complement consumption.
Management: Urgent treatment with antihistamines, corticosteroids, and epinephrine in severe cases. Patients with hereditary forms may require C1 inhibitor concentrate.
2. Foreign Body Aspiration
Symptoms: Initial choking event followed by coughing, respiratory distress, potential cyanosis, and altered mental status.
Clinical Signs: Wheezing, stridor, or localized absent breath sounds depending on the location of the obstruction.
Chronic Cases: May present with cough, recurrent pulmonary infections if the foreign body remains undetected.
Diagnostic Imaging: X-rays can reveal the presence of the foreign body in the trachea or bronchi.
Management: Immediate removal of the foreign body, typically by bronchoscopy.
3. Epiglottitis
Symptoms: Severe odynophagia (painful swallowing), pain over the larynx on palpation, and signs of significant respiratory distress such as hypoxia and a toxic appearance.
Other Signs: Dysphagia, stridor, drooling, and decreased voice volume are indicative of significant upper airway obstruction.
Laboratory Findings: Leukocytosis and increased C-reactive protein (CRP) suggesting infection.
Imaging: Lateral neck X-ray or endoscopy can show swollen epiglottis and surrounding tissues.
Management: Emergency management involves securing the airway, often under controlled conditions like in an operating room, followed by antibiotic therapy.
4. Deep Neck Infection
Symptoms: Fever, fatigue, dysphagia, dysphonia, and noticeable neck swelling, which can be unilateral or bilateral, with erythema over the affected area.
Respiratory Signs: Dyspnea and stridor if the infection causes significant swelling that impinges on the airway.
Laboratory Findings: Leukocytosis and elevated CRP, indicating an active infection.
Imaging: CT scans or MRI may show abscess formation, lymphadenitis, and decreased definition of anatomical spaces due to edema and inflammation.
Management: Treatment typically involves antibiotics, and in cases of abscess, surgical drainage may be necessary.
TOXIC METABOLIC CAUSES OF DYSPNEA
Salicylate Toxicity
Symptoms: Tachypnea, nausea, vomiting, dizziness, restlessness, and in severe cases, coma.
Lab Findings: Increased blood urea nitrogen, elevated anion gap reflecting metabolic acidosis.
Blood Gas: Respiratory alkalosis initially, which may transition to mixed respiratory alkalosis and metabolic acidosis as toxicity progresses.
Diabetic Ketoacidosis (DKA)
Symptoms: Polyuria, polydipsia, severe dehydration, nausea, vomiting, and altered mental status.
Blood Gas: Metabolic acidosis with an elevated anion gap due to the accumulation of ketone bodies.
Lab Findings: High blood glucose levels and ketonemia/ketonuria.
Carbon Monoxide (CO) Toxicity
Symptoms: Headache, dizziness, confusion, nausea, vomiting, dyspnea, chest pain, tachycardia, and hypotension.
Diagnosis: Based on history of exposure (e.g., smoke inhalation), symptoms, and increased carboxyhemoglobin levels in the blood.
Anemia
Symptoms: Postural hypotension, dizziness, tachycardia, and cool pale skin due to decreased oxygen-carrying capacity of the blood.
Lab Findings: Low hemoglobin and hematocrit levels.
OTHER CAUSES OF DYSPNEA
Other Causes
Pulmonary: Conditions like hemothorax, pleuritis, lung cancer, and pulmonary hypertension can directly affect lung function or the pleural space.
Gastrointestinal (GIT): Ascites and abdominal obesity can impede diaphragmatic movement, while gastro-esophageal reflux disease (GERD) can cause chronic cough and irritation.
Musculoskeletal: Rib fractures, diaphragmatic paralysis, severe kyphosis, and muscular dystrophy can all mechanically impair breathing.
Neurologic: Diseases like myasthenia gravis, Guillain-Barre syndrome, multiple sclerosis, and central nervous system events such as stroke or spinal cord injury can disrupt the neuromuscular control of breathing.
Endocrine: Conditions like metabolic acidosis and thyrotoxicosis can alter metabolic demands and respiratory drive.
Psychogenic: Panic attacks and anxiety can cause sensations of shortness of breath and hyperventilation, often without organic disease.
Iatrogenic: Some medications like non-selective beta-blockers, NSAIDs, and ticagrelor can exacerbate or trigger respiratory symptoms.