Approach to respiratory acidosis: Clinical sciences

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Introduction 0:00–0:48

Respiratory acidosis refers to an increase in partial pressure of carbon dioxide or PCO2, with or without a compensatory increase in bicarbonate, resulting in increased hydrogen ion concentration in the blood.
This is almost always caused by hypoventilation, usually from the central nervous system, pulmonary or iatrogenic conditions.
Generally, respiratory acidosis is characterized by an arterial pH below 7.35 and a PCO2 above 45 millimeters of mercury.
As a reference, the normal PCO2 range is between 35 and 45 millimeters of mercury. If a patient presents with a chief concern suggesting respiratory acidosis, first perform an ABCDE assessment to determine if your patient is stable or unstable.

Unstable Patient 0:48–1:47

If your patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring.
Finally, provide supplemental oxygen if needed. Here is a clinical pearl.
Respiratory acidosis can be acute or chronic. The chronic form is asymptomatic.
However, if it worsens or if the patient has an acute case, they might present with headache, confusion, and altered mental status.
Their exam might show tremors, myoclonic jerks, and asterixis. These patients may require adequate ventilation by either endotracheal intubation or non-invasive positive pressure ventilation.
Now that unstable patients are taken care of, let's talk about stable ones. Your next step here is to obtain a focused history and physical examination and order labs, including an arterial blood gas analysis, or ABG and BMP.

Stable Patient 1:47–4:27

History findings depend on the specific cause, but most patients have shortness of breath. The physical exam might show abnormal breathing patterns such as a decreased respiratory rate, and signs of hypoxemia, like cyanosis.
As for the labs, ABG typically reveals an arterial pH below 7.35 and a PCO2 above 45 millimeters of mercury. BMP usually reveals normal or increased serum bicarbonate, depending on whether there is metabolic compensation, and possibly electrolyte imbalances, such as increased serum potassium.
If you see these findings, that's respiratory acidosis. Here's a clinical pearl to keep in mind.
After diagnosing respiratory acidosis, remember to assess for metabolic compensation by checking the serum bicarbonate level.
A compensated respiratory acidosis is characterized by a normal or slightly decreased arterial pH, increased PCO2, and increased serum bicarbonate level.
This occurs in chronic conditions where the kidneys have been able to reabsorb enough bicarbonate, restoring the acid-based balance.
Examples include interstitial lung diseases, restrictive chest wall disorders, and obesity. On the other hand, uncompensated respiratory acidosis will have a decreased arterial pH, increased PCO2, and normal serum bicarbonate level.
A simple way to know if there is metabolic compensation in respiratory acidosis and alkalosis is to use the 12345 rule. In the case of acidosis, for every 10 millimeters of mercury rise of PCO2 from the baseline of 40 millimeters of mercury, bicarbonates or HCO3 should increase by 1 in the acute or by 4 in the chronic respiratory acidosis from their baseline of 24 millimoles per liter.
When it comes to alkalosis, for every 10 millimeters of mercury decrease of PCO2 from the baseline, bicarbonate should decrease by 2 for the acute, or 5 for the chronic respiratory alkalosis from the baseline.
All right, let's talk about underlying causes, starting with iatrogenic ones. This is usually seen with hospitalized patients on respiratory support such as mechanical ventilation, so you'll need to check the ventilator settings.

Assess iatrogenic causes 4:27–5:20

If either the respiratory rate or tidal volume is too low, or if there's any evidence of equipment failure, your patient might not be exhaling enough carbon dioxide.
In this case, diagnose iatrogenic hypoventilation. Here's another clinical pearl.
Other major causes of iatrogenic respiratory acidosis include medications that primarily work by depressing the CNS activity.
Examples include anesthetic agents like propofol, sedatives like benzodiazepines, and opioids such as morphine. Let's move on to the central nervous system, or CNS related causes.

Assess CNS causes 5:20–7:21

These can lead to a decrease in the activity of the respiratory centers in the brain stem. Examples include intracranial pathologies such as brain stem stroke or trauma, substance abuse, and alcohol intoxication.
First up are intracranial pathologies. The history might reveal an acute onset of headache and risk factors for stroke such as high BP, smoking, or atrial fibrillation.
Also, don't forget to ask about any recent head trauma. The physical exam reveals a decreased respiratory rate and possibly altered mental status or focal neurological deficits like slurred speech.
With these findings, consider intracranial pathology and order a head CT scan or MRI. If imaging reveals ischemic changes or hemorrhage, your patient's respiratory acidosis is due to an intracranial pathology.
Next up is substance use or alcohol intoxication. In this case, history reveals the use of CNS depressants such as alcohol or opioids like morphine and heroin.
On a physical exam, you'll find a decreased respiratory rate and sometimes altered mental status. Be sure to check for pupil changes, particularly meiosis, which would suggest opioid use.
With these findings, consider substance use or alcohol intoxication and obtain a urine toxicology screen and serum alcohol level.
If the urine toxicology is positive for a relevant substance, diagnose substance use. On the other hand, if the serum alcohol level is elevated, then alcohol intoxication is the cause of respiratory acidosis.
Alright, let's move on to the causes related to airway obstruction. The key ones you should remember include severe asthma exacerbation and foreign body aspiration.

Assess airway obstruction 7:21–9:17

Patients with severe asthma exacerbation typically present with a cough, with or without chest tightness, and a known history of asthma.
The physical exam reveals bilateral wheezing with a rapid, shallow breathing pattern. In this case, consider severe asthma exacerbation.
Next, administer a bronchodilator. If there is clinical improvement, meaning improved breathing pattern and decreased wheezing, your patient's respiratory acidosis is due to asthma exacerbation.
Next up is foreign body aspiration. In these cases, history reveals choking and coughing with known or suspected foreign body aspiration.
The physical exam might reveal stridor, wheezing, or decreased breath sounds. With these findings, consider foreign body aspiration, then order a chest X-ray, and if a foreign body is identified, you can diagnose foreign body aspiration.
Here is a clinical pearl. Other forms of airway obstruction that can lead to respiratory acidosis include lung tumors and mucus plugging.
A patient with a lung tumor will likely have a history of weight loss, hemoptysis, and usually a smoking history. On the other hand, patients with mucus plugging typically report recurrent respiratory infections and may have COPD or cystic fibrosis.
In both cases, you will need a chest CT scan to confirm the diagnosis, which might show a tumor, or filling defects within the bronchi in the case of mucous plugging.
OK, let's talk about diseases affecting the lung parenchyma. Patients with pneumonia usually report productive cough, while the physical exam might reveal elevated body temperature, decreased oxygen saturation, and lung crackles.

Assess pulmonary parenchymal causes 9:17–10:35

With these findings, consider pneumonia and order a chest X-ray. If it reveals infiltrates, you can go ahead and diagnose pneumonia as the cause of respiratory acidosis.
Next up is ARDS. History typically reveals an acute onset of shortness of breath, often triggered by inhalation injury, pneumonia, or pancreatitis.
The physical exam might reveal accessory respiratory muscle use, decreased oxygen saturation, and diffuse lung crackles.
With these findings, consider ARDS. To confirm, order a chest X-ray and calculate the ratio of partial pressure of oxygen, or PAO2, to the estimated fraction of inspired oxygen, or FIO2.
If chest X-ray shows bilateral infiltrates and the PAO2 to FIO2 ratio is 300 millimeters of mercury or less, you can diagnose ARDS.
Lastly, let's have a look at the neuromuscular causes of respiratory acidosis. These patients usually have a known history of neuromuscular diseases such as myasthenia gravis, Guillain-Barre syndrome, or muscular dystrophy.

Assess neuromuscular causes 10:35–11:24

These diseases can cause weakness of the diaphragm and accessory respiratory muscles, leading to inefficient respiration and subsequent respiratory acidosis.
So along with neuromuscular disease, symptoms vary based on the condition and can include muscle weakness or ineffective coughing.
The physical exam might show dysarthria, symmetrical limb weakness, ascending paralysis, and ptosis. In this case, your patient's respiratory acidosis is due to a neuromuscular disease.
All right, as a quick recap, respiratory acidosis is confirmed when the arterial pH is below 7.35 and the PCO2 is above 45 millimeters of mercury.

Review 11:24–12:09

Causes of respiratory acidosis can be classified into several categories. There are iatrogenic causes such as inappropriate mechanical ventilator settings, CNS-related conditions including intracranial pathology or substance use.
Airway obstruction, like in severe asthma exacerbation or foreign body aspiration, lung parenchyma-related causes such as pneumonia and ARDS, and finally, neuromuscular causes which include conditions like myasthenia gravis.