CONTENTS
- Symptoms
- Laboratory diagnosis of hypercapnia
- Causes of hypercapnia
- Evaluation
- Consequences of hypercapnia
- Management of hypercapnia
- Podcast
- Questions & discussion
- Pitfalls
symptoms of severe hypercapnia
- Delirium, somnolence, and eventually coma (“CO2 narcosis”).
- Coarse tremor, multifocal myoclonus, and asterixis.
- Headache (e.g., nocturnal hypoventilation may cause headache upon awakening).
acute-on-chronic hypercapnia can be insidious
- Patients with chronic hypercapnia (e.g., COPD or obesity hypoventilation syndrome) will adapt to this, including a blunting of their respiratory drive.
- Acute-on-chronic hypercapnia may present solely with an increase in somnolence.
- (In contrast, a patient with acute respiratory failure should respond to hypercapnia with robust tachypnea – which will tend to manifest with severe dyspnea rather than somnolence.)
diagnosis is based on VBG or ABG
- (1) Hypercapnia is defined as PaCO2 >45 mm. Hypercapnia may also be diagnosed from a venous blood gas (more on comparing VBG vs. ABG here).
- (2) Primary hypercapnia is hypercapnia that isn't a compensatory response to metabolic alkalosis.
acute, chronic, or acute-on-chronic?
- The patient's baseline bicarbonate level may help determine whether hypercapnia is acute or chronic (table above, right side). In chronic hypercapnia, there will be a greater degree of compensatory metabolic alkalosis.
- However, this analysis assumes the following:
- (1) The kidneys are working correctly.
- (2) There are no other factors affecting the bicarbonate level (i.e., no metabolic acidosis or metabolic alkalosis).
- ⚠️ In reality, there are often many other factors which can also affect the bicarbonate level. This prevents the bicarbonate level from being an accurate arbiter of whether the hypercapnia is acute or chronic (figure below).
Below are various potential causes of hypercapnia. A patient with substantial hypercapnia may have several factors promoting this simultaneously. For example, hypercapnia in asthma is generally due to a combination of bronchospasm and diaphragmatic muscle fatigue. Another example is that of a patient with chronic hypercapnia due to COPD, who may experience worsening hypercapnia due to any deterioration in lung function (e.g., pneumonia or cardiogenic pulmonary edema).
(1) respiratory drive problem (“won't breathe”)
- Respiratory suppressive medications, e.g.:
- Opioids.
- Benzodiazepines, barbiturates.
- Intoxicants (e.g., ethanol).
- Brainstem dysfunction (e.g., trauma, encephalitis, infarction, tumor).
- Hypothyroidism.
(2) neuromuscular/chest/airway problem (“can't breathe”)
- Spinal cord problem, e.g.:
- C-spine injury (C3-C5).
- Transverse myelitis (e.g., multiple sclerosis).
- Tumor.
- Neuromuscular weakness, e.g.:
- Neuropathy (e.g., Guillain-Barre syndrome, amyotrophic lateral sclerosis, phrenic nerve injury).
- Neuromuscular junction disorder (e.g., myasthenia gravis, botulism, tick paralysis).
- Myopathy (e.g., hypokalemia, hypophosphatemia, thyroid disease, polymyositis, dermatomyositis, muscular dystrophy, hypophosphatemia, critical illness myopathy, muscular fatigue).
- Restriction of lung inflation, e.g.:
- Abdominal distension, abdominal compartment syndrome.
- Obesity hypoventilation syndrome.
- Pleural effusion, pneumothorax.
- Kyphoscoliosis, ankylosing spondylitis.
- Upper airway problem, e.g.:
- Angioedema.
- Epiglottitis.
- Foreign body.
- Tracheal stenosis, tumor.
- Vocal cord paralysis or vocal cord dysfunction.
- Lower airway problem, e.g.:
- Small airway disease (e.g., COPD, asthma).
(3) increased dead space (“breathing isn't working”)
- Alveolar disease (e.g., pneumonia, ARDS, severe interstitial lung disease).
- Vascular disease (e.g., severe pulmonary embolism).
The causes of hypercapnia are very broad, so the evaluation will need to be tailored substantially depending on the clinical context. Below are some investigations which may be helpful:
physical examination
- Low respiratory rate suggests opioid intoxication or a central nervous system abnormality (consider a therapeutic trial of naloxone).
- Lack of distress suggests either:
- (1) Chronic or acute-on-chronic hypercapnia, with blunting of the respiratory drive.
- (2) Neurologic disease causing a respiratory drive problem.
- Neurological exam: Signs of brainstem or spinal cord pathology? Weakness?
- Auscultate over lungs & trachea: Bronchospasm? Stridor? How much air is the patient moving?
- For an intubated patient:
- Peak pressures may suggest airway obstruction below the level of the endotracheal tube. However, this may fail to detect an upper airway obstruction which is bypassed by the endotracheal tube.
- If the patient is hypercapnic despite a normal minute ventilation (e.g., ~7-8 liters/minute), this implies an increase in the dead space. An elevated gap between the ABG/VBG pCO2 versus the end tidal CO2 further supports an increase in dead space.
bedside pulmonary function tests (FVC, NIF)
- ⚠️ These tests aren't extremely sensitive or specific, but they can be helpful if extreme values are obtained. Since they are inexpensive and readily available, they may be worth obtaining. It's essential to ensure that patients are exerting themselves maximally during the test, because suboptimal effort will result in poor results.
- Negative inspiratory force (NIF) tests strength of diaphragm:
- Impaired NIF may suggest neuromuscular weakness.
- Preserved NIF largely exonerates the diaphragm and peripheral nerves.
- Forced Vital Capacity (FVC) is an integrated measurement of the diaphragmatic strength, restriction to lung inflation, and airway obstruction:
- Reduced FVC and reduced NIF suggests neuromuscular weakness.
- Reduced FVC with normal NIF suggests airway obstruction or restriction to lung inflation.
- Review of any prior pulmonary function tests (PFTs) may be helpful.
labs
- Electrolytes including Ca/Mg/Phos.
- Thyroid Stimulating Hormone (TSH).
- CBC (polycythemia suggests chronic hypoxemia, often seen with COPD).
- Creatinine kinase (may be elevated in myopathies, or hypothyroidism).
- Review of archival labs:
- Prior blood gas measurements are the most useful.
- If blood gas measurements aren't available, then chronically elevated bicarbonate levels support the possibility of chronic hypercapnia.
imaging
- Chest X-ray.
- MRI of brain/spine, if neurological examination suggests a lesion in those locations.
- CT scan of the neck & lungs (if evidence of upper airway pathology and/or pulmonary dysfunction). CT angiography of the thorax may be indicated if there is a concern for PE as a cause of hypercapnia.
electromyography (EMG)
- Among patients with neuromuscular weakness, this may facilitate diagnosis of neuropathies which require directed management (e.g., IVIG for management of Guillain-Barre syndrome).
hypercapnia is generally extremely well tolerated
- Permissive hypercapnia involves an intentional strategy of allowing the pCO2 to increase during mechanical ventilation (with a goal of avoiding barotrauma). The limits of safe hypercapnia are unclear. Specifically, there is no pCO2 level above which obvious harm is noted.
- Patients with COPD or obesity hypoventilation syndrome may live for years despite very substantial chronic hypercapnia. Although this isn't a desirable physiological state, its existence proves that hypercapnia itself isn't an immediate life-threat.
potential risks of hypercapnia
- Dyspneic agitation
- Acute hypercapnia may cause severe dyspnea with agitation. Among intubated patients, it may cause tachypnea and “bucking” the ventilator.
- Sedation (“CO2 narcosis”):
- Sedation is more likely to occur with more severe and/or chronic hypercapnia (since chronic hypercapnia causes a blunting of the respiratory drive).
- For patients who are not intubated, excessive sedation may be dangerous.
- For patients who are intubated, sedation is potentially beneficial (e.g., reducing the necessary dose of exogenous sedative).
- Pulmonary vasoconstriction:
- Global vasoconstriction of the pulmonary vasculature will increase the pulmonary vascular resistance.
- This may not be well tolerated among patients with substantial pulmonary hypertension, or with right ventricular failure.
- Increased intracranial pressure:
- Hypercapnia causes vasodilation of cerebral arteries, which will tend to increase intracranial pressure.
- For neurocritically ill patients who already have elevated intracranial pressure, hypercapnia could exacerbate this.
- Among patients without neurologic disease, this may cause headache.
There is no universal approach to treating hypercapnia, since this will vary widely depending on the clinical context. Among patients with chronic hypercapnia, the therapeutic goal is generally to return the patient to their baseline pCO2 level. Some examples of potential therapies are:
- Hypercapnia due to opioid intoxication may involve naloxone (depending on the severity; more on this here).
- Hypercapnia due to neuromuscular weakness may often be improved with noninvasive ventilation (e.g., BiPAP). Additionally, the underlying disorders may require specific management.
- Hypercapnia due to asthma or COPD requires specific treatment pathways for these disorders:
- Mild-moderate hypercapnia in an intubated patient may often be monitored without intervention (permissive hypercapnia).
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To keep this page small and fast, questions & discussion about this post can be found on another page here.
- When encountering hypercapnia, the first response is often to try to fix the hypercapnia (e.g., by using noninvasive ventilation or intubation). This often is not the correct approach (e.g., for patients with opioid intoxication). Thus, the treatment should always focus on identifying and treating the underlying disease.