Approach

Once respiratory acidosis has been identified by arterial blood gas (ABG) analysis, the approach to narrowing the differential diagnosis and determining the severity of the patient's condition is aided by establishing its acuity (acute or chronic). This is done through the synthesis of information from the ABG, history, and physical exam.[9]

Historical findings may immediately point to the underlying cause, such as head trauma and drug ingestion, or provide only limited information, as with the obtunded patient.

The physical exam should focus on assessment of the neurologic and respiratory systems with careful examination of the lung fields, which can yield useful information regarding the presence of underlying parenchymal disease.

Further laboratory studies are warranted when metabolic abnormalities or specific systemic diseases are suspected etiologies. Radiographic imaging is key to the evaluation of respiratory acidosis, as it can provide rapid screening for head, cervical, or chest pathology.

Arterial blood gas analysis

Step 1: Is there acidosis?

  • Acidosis is indicated by an ABG pH below the normal range (i.e., <7.35)

Step 2: Respiratory or metabolic?

  • Respiratory acidosis is indicated by an increase in the arterial carbon dioxide levels above the normal range of 35 to 45 mmHg (4.7-6.0 kPa).

  • It is important to note that the degree of acidosis and the potential concerns are different depending on whether the problem is respiratory or metabolic.

  • An equivalent pH in metabolic acidosis (e.g., 7.0) is a much worse clinical sign, as the body has dual buffering and compensatory mechanisms for metabolic acid (the carbamate-bicarbonate system: bicarbonate buffer, and carbon dioxide elimination). Elevated carbon dioxide, on the other hand, causes a dramatic fall in pH, but the patient is actually less sick as there is little buffering capacity for carbon dioxide. Studies in critical illness have demonstrated that patients tolerate hypercapnic acidosis very well.

Step 3: Is the respiratory acidosis acute or chronic?

  • Knowledge of whether respiratory acidosis is acute or chronic is extremely important, as it helps to identify the underlying cause of acidosis and evaluate the severity of the patient's clinical condition.

  • Acute respiratory acidosis tends to have a more serious (often life-threatening) clinical presentation than that of chronic respiratory acidosis.

  • In acute respiratory acidosis, for every 10 mmHg increase in PaCO₂, the pH will decrease by 0.08 and the serum bicarbonate and base excess will be within normal range due to the acute nature of the underlying process.

  • To calculate the anticipated compensation in chronic respiratory acidosis, recall that the pH in chronic respiratory acidosis decreases by only 0.03 units for every 10 mmHg increase in PaCO₂. For patients with compensated chronic respiratory acidosis (e.g., in COPD), the pH will be normal despite an elevated PaCO₂.

  • Renal mechanisms of compensation can correct the respiratory acidosis within 24 hours.

  • Changes in pH outside these ranges suggest a superimposed metabolic abnormality (either acidosis or alkalosis).

Acute respiratory acidosis is commonly caused by:

  • Drug use (narcotics, alcohol, sedatives, anesthetics)

  • Oxygen therapy in COPD

  • Exacerbation of COPD (causes acute on chronic respiratory acidosis)

  • Hypokalemia and hypophosphatemia

  • Foreign body aspiration

  • Multilobar pneumonia

  • Pleural effusion

  • Pneumothorax

  • Inadequate mechanical ventilation

  • Central nervous system (CNS) infarct or hemorrhage

  • Head trauma

  • CNS infection.

Other important but uncommon causes of acute respiratory acidosis are:

  • Cardiogenic pulmonary edema

  • Status asthmaticus

  • Laryngospasm

  • Angioedema

  • Sepsis

  • Fever/malignant hyperthermia.

Chronic respiratory acidosis is commonly caused by:

  • COPD

  • Hypoventilation syndrome in obesity

  • Obesity

  • Hypothyroidism

  • Kyphoscoliosis.

Step 4: Is there hypoxemia?

  • The presence of hypoxemia with respiratory acidosis can help to narrow down the differential diagnosis.

  • Hypoxemia may occur with processes that cause profound alveolar hypoventilation, such as sedative overdose and CNS infarction, or regional ventilation-perfusion mismatch, such as multilobar pneumonia.

History

Onset of symptoms

  • The degree of acuity and magnitude of symptoms aids in narrowing the differential diagnosis.

  • COPD commonly presents with acute or chronic respiratory acidosis secondary to an exacerbation caused by a lower respiratory tract infection, pulmonary embolism, pneumothorax (due to bullous rupture), or cor pulmonale.

  • Fever, cough, pleuritic chest pain, and hypoxia suggest an underlying parenchymal process such as pneumonia or empyema.

  • Chronic conditions including obesity-hypoventilation syndrome, multiple sclerosis, myasthenia gravis, and kyphoscoliosis may be associated with few or no symptoms.

  • Acute causes of respiratory acidosis often present with more overt symptoms such as rapidly progressive ascending neurologic weakness suggestive of Guillain-Barre syndrome.

Pre-existing medical conditions

  • The presence of chronic diseases associated with respiratory acidosis including COPD, myasthenia gravis, and multiple sclerosis can assist in determining the underlying cause.

  • The presence of atherosclerotic disease or atrial fibrillation increases the likelihood of CNS pathology (i.e., infarction).

  • A history of depression may increase suspicion for toxic ingestion.

Medication history

  • Narcotics and analgesics may lead to respiratory depression.

  • A recent increase in continuous oxygen flow rate in a COPD patient can cause hypoventilation.

  • Use of ACE inhibitors or angiotensin receptor blockers increases the risk of angioedema.

Excessive daytime sleepiness and headaches on wakening are seen in hypoventilation syndrome in obesity.

Physical exam

Pulmonary exam

  • Abnormal findings on pulmonary auscultation (egophony, crackles, wheeze, dullness to percussion) can help localize chest pathology, but are nonspecific.

  • Obstructed breathing patterns include seesaw chest movements, nasal flaring, and supraclavicular and subcostal recession.

  • Paradoxical movement of a portion of the chest wall with spontaneous breathing suggests flail chest.

Cardiac exam

  • A right ventricular heave and tricuspid regurgitation suggest chronic right ventricular failure (cor pulmonale) associated with COPD and obesity hypoventilation syndrome.

  • An irregular cardiac rhythm, valvular murmurs, or carotid bruits may suggest an embolic source if a CNS event is present.

Neurologic exam

  • Obtundation, anisocoria, and abnormal unilateral pupillary reflex signify a possible brainstem infarct.

  • Asterixis, myoclonus, seizures, or miosis may be present depending on the ingested substance.

  • Symmetrical hyporeflexia/areflexia of the lower extremities is a cardinal sign of Guillain-Barre syndrome.

Laboratory evaluation

Serum electrolyte measurement

  • To assess potassium and phosphate levels.

Complete blood count

  • To evaluate for polycythemia or elevated white blood cell count

Toxicology testing

  • Indicated in the obtunded patient to screen for pharmacologic depressants.

Lumbar puncture

  • Useful to screen for CNS infection.

Specific tests to screen for systemic diseases

  • Thyroid-stimulating hormone for hypothyroidism

  • Antiacetylcholine receptor antibody for myasthenia gravis

  • C1 esterase inhibitor functional assay for hereditary angioedema

  • Antinuclear antibodies for scleroderma

  • HLA-B27 antigen for ankylosing spondylitis.

Microbiologic testing

  • Sputum microscopy, culture, and sensitivity for the assessment of pneumonia.

Muscle biopsy

  • Indicated if muscular dystrophy, malignant hyperthermia, polymyositis, or dermatomyositis is suspected.

Imaging studies

  • Chest x-ray (CXR) and chest computed tomography (CT) are key to screening for underlying lung and chest wall disease. CXR is the most rapid and readily available imaging modality to screen for causes of respiratory acidosis. CT scanning can often add more information.

  • Brain imaging with CT or magnetic resonance imaging is indicated to screen for head trauma, stroke, or hemorrhage.

  • Overnight polysomnography is a useful screening tool for obesity-hypoventilation syndrome and primary alveolar hypoventilation.

  • Dynamic fluoroscopy with deep inspiration (sniff test) can diagnose phrenic nerve damage.

  • Electromyography and nerve conduction testing demonstrates diffuse denervation and abnormal amplitude of compound muscle action potentials with preserved conduction velocities in amyotrophic lateral sclerosis.

Pulmonary function testing

  • Forced vital capacity (FVC) and maximal inspiratory and expiratory pressures are used to evaluate the respiratory system integrity in Guillain-Barre syndrome and myasthenia gravis.

  • FVC and maximal inspiratory and expiratory pressures should be monitored in all patients with neuromuscular disorders affecting the chest wall muscles and diaphragm.[10]

  • Reduced lung volumes are seen in kyphoscoliosis and obesity.

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