Approach to respiratory alkalosis: Clinical sciences

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Introduction 0:00–0:56

Respiratory alkalosis refers to a decrease in the partial pressure of carbon dioxide or pCO2, resulting in a decrease in the concentration of hydrogen ions in the blood.
This is almost always caused by hyperventilation, which increases carbon dioxide removal relative to carbon dioxide production.
Hyperventilation typically occurs in response to triggers such as hypoxia, infection, metabolic acidosis, pain, anxiety, overdose of certain medications, or increased metabolic demand.
Respiratory alkalosis is characterized by a pH above 7.45, and a pCO2 below 35 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 alkalosis, perform an ABCDE assessment to determine if your patient is stable or unstable.

Unstable Patient 0:56–1:23

If they are unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring.
Lastly, provide supplemental oxygen, if needed. Let’s jump back to the ABCDE assessment and talk about stable patients.

Stable Patient 1:23–3:36

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.
The history will vary depending on the specific cause, but your patient may report shortness of breath, while the physical exam might show an increased rate and depth of breathing.
ABG typically shows an arterial pH above 7.45, and a pCO2 lower than 35 millimeters of mercury. Finally, BMP will show normal or decreased serum bicarbonate, depending on whether or not there is metabolic compensation; and might show electrolyte imbalances, such as hypokalemia.
With these findings, you can diagnose respiratory alkalosis. Here are some clinical pearls!
Once you’ve diagnosed respiratory alkalosis, remember to assess for metabolic compensation by checking the serum bicarbonate level.
A compensated respiratory alkalosis is characterized by a normal or slightly increased arterial pH, decreased pCO2, and decreased serum bicarbonate level.
This can be seen in chronic conditions in which the kidneys have had time to restore the acid-base balance, by excreting excess bicarbonate.
Examples include pregnancy, hyperthyroidism, and chronic liver disease. On the other hand, uncompensated respiratory alkalosis will have an increased arterial pH, a decreased pCO2, and a normal serum bicarbonate level.
A simple way to know if there is metabolic compensation in respiratory alkalosis and acidosis is to use the 1-2-3-4-5 rule.
When it comes to acidosis, for every 10 millimeters of mercury rise of pCO2 from the baseline, bicarbonates should increase by 1 in the acute, or by 4 in the chronic respiratory acidosis from their baseline.
On the flip side, in alkalosis, bicarbonate or HCO3 should decrease by 2 for the acute, or 5 for the chronic respiratory alkalosis from the baseline of 24 mmol/L.
Alright, let’s go over causes of respiratory alkalosis, starting with iatrogenic ones. This is often seen in hospitalized patients on respiratory support, like mechanical ventilation.

Assess iatrogenic causes 3:36–4:10

In this case, you should check the ventilator settings. If the respiratory rate or the tidal volume is too high, your patient might be removing excessive amounts of carbon dioxide, resulting in a low pCO2, and eventually alkalosis.
At this point, you can diagnose iatrogenic hyperventilation. Next, let’s take a look at the CNS-related causes.

Assess CNS causes 4:10–6:10

These are conditions that mainly lead to stimulation of the respiratory centers in the brainstem, leading to hyperventilation, then a low pCO2, and ultimately, respiratory alkalosis.
First up is psychogenic hyperventilation. These patients typically present with a sudden onset of shortness of breath and fear, often associated with an anxiety disorder.
The physical exam reveals an increased rate and depth of breathing but with no other signs of acute illness. If you see these findings, that’s psychogenic hyperventilation.
Next up are CNS infections. In this case, history reveals fever, headache, photophobia, and with or without neck stiffness, while the physical exam shows altered mental status and possibly nuchal rigidity.
If you see this, consider a CNS infection. This could be like meningitis or encephalitis.
Next, perform a lumbar puncture to collect cerebrospinal fluid and send it for analysis. If it shows any abnormalities, then the patient's respiratory alkalosis is due to a CNS infection.
Moving on to intracranial pathologies. Sometimes your patient might report a headache, a recent history of head trauma, or seizures.
The physical exam might reveal altered mental status; anisocoria, which refers to asymmetric pupils; and focal neurological deficits, such as hemiplegia.
With these findings, you should suspect an intracranial pathology, and then obtain a brain CT scan to confirm. If the CT reveals an intracranial tumor, diagnose your patient with respiratory alkalosis due to an intracranial tumor.
On the other hand, if the CT scan shows hemorrhage, diagnose respiratory alkalosis due to intracranial hemorrhage. Alright, let’s have a look at the pulmonary causes of respiratory alkalosis.

Assess pulmonary causes 6:10–8:19

These conditions cause hypoxemia, which triggers hyperventilation and eventually leads to a decreased pCO2. Let’s start with pulmonary embolism.
In this case, the history typically reveals an acute onset of pleuritic chest pain, shortness of breath, and sometimes hemoptysis.
The physical exam might reveal an increased respiratory rate, a low-grade fever, and/or unilateral calf pain and swelling.
With these findings, consider pulmonary embolism and obtain a CT angiogram of the chest. If it shows filling defects of pulmonary vessels, that's pulmonary embolism.
Moving on to pneumothorax. These patients present with an acute onset of chest pain and sometimes a recent history of chest trauma, although pneumothorax can result from ruptured blebs as well.
Some might have a history of chronic obstructive pulmonary disease or pulmonary fibrosis. The physical exam might show low blood pressure, jugular venous distention, and resonance on chest percussion.
In more severe cases, you can notice tracheal deviation. With these findings, consider pneumothorax and order a chest X-ray for confirmation.
If the X-ray shows a visible visceral pleural edge with no peripheral lung markings, you can diagnose respiratory alkalosis due to pneumothorax.
Next up is hemothorax. Your patient will typically report acute chest pain, with a history of chest trauma and possibly a preexisting coagulation disorder such as hemophilia.
The physical exam might reveal dullness on chest percussion and decreased tactile fremitus. In this case, consider hemothorax, and obtain a chest ultrasound.
If it shows a homogeneous and echogenic effusion, that’s hemothorax. Next up are hematological causes of respiratory alkalosis, which mainly involve severe anemia.

Assess hematological causes: Severe anemia 8:19–8:50

The history will reveal palpitations, and possibly acute blood loss. If the physical exam reveals conjunctival pallor, consider anemia and then obtain a CBC.
If there is a significant drop in hemoglobin from the patient’s baseline, their respiratory alkalosis is due to severe anemia.
Finally, let’s talk about drug toxicity and substance abuse. These are mainly CNS stimulants that lead to hyperventilation, by activating the respiratory centers in the brainstem.

Assess drug toxicity/substance use 8:50–10:23

Patients typically present with a history of changes in their medications or are taking salicylate-containing medications, most commonly aspirin.
They might also have a history of substance use with stimulant effects on the brain, such as amphetamines and cocaine. The physical exam might show altered mental status, needle marks, or nasal septal damage.
With these findings, consider drug toxicity or substance abuse. Next, order a serum salicylate level and a urine toxicology screen.
If the toxicology screen is positive for a substance that causes CNS stimulation, diagnose substance use as the cause of respiratory alkalosis.
On the flip side, if the serum salicylate level is elevated, you can make the diagnosis of salicylate toxicity. Here’s a high-yield fact!
Salicylate toxicity can cause both metabolic acidosis and respiratory alkalosis. Salicylates directly stimulate the medulla, which causes hyperventilation and subsequent respiratory alkalosis.
As salicylates get metabolized, keto acids and lactic acid build up, leading to metabolic acidosis. When these mechanisms are combined, they can result in a normal arterial pH.
Alright, as a quick recap… Respiratory alkalosis refers to a decrease in pCO2 and hydrogen ion concentration in the blood.

Review 10:23–11:08

It is confirmed once the blood pH is above 7.45, and pCO2 below 35 millimeters of mercury. Common causes of respiratory alkalosis include iatrogenic causes such as inappropriate mechanical ventilator settings; CNS causes like psychogenic hyperventilation, infections, and intracranial pathologies; pulmonary causes like pulmonary embolism, pneumothorax, and hemothorax; hematological causes such as severe anemia; and drug toxicity and substance abuse, such as salicylate toxicity and