Page created on December 17, 2018. Last updated on November 10, 2021 at 20:08

Respiratory acidosis

Definition

In respiratory acidosis we have:

• pH below 7.35
• Increased pCO₂
• Increased actual bicarbonate

When kidney compensation kicks in, after around 24 hours, will we also have:

• Increased standard bicarbonate
• Increased buffer base
• Positive base excess

Etiology

Because it is respiratory, it’s caused by a primary increase in pCO₂, due to inadequate ventilation. This decreases the pH. When pCO₂ increases will actual HCO₃^– also increase because they’re in an equilibrium. We’ll get to the compensation later.

Recall that CO₂ diffuses really easily in contrast to O₂, so diffusion disorders rarely lead to elevated pCO₂. Only hypoventilation will.

The only cause of respiratory acidosis is alveolar hypoventilation, which causes global respiratory failure,. We’ll repeat some causes here.

Common causes include:

• Airway obstruction
  • Asthma
  • COPD
  • Obstructive sleep apnoea syndrome
• CNS disturbances
  • Central sleep apnoea
  • Accidents
  • Tumors
  • CNS depressant drugs
    • Morphine
    • Sedatives
• Cardiac and pulmonary
  • Pulmonary oedema
  • Pulmonary embolism
  • Pulmonary fibrosis
  • Restrictive lung diseases
• Respiratory muscle weakness

Not all of these warrant an explanation, but some of them do.

CNS disturbances damage or depress the respiratory centre, which decreases the respiratory drive. Morphine is especially known for depressing the respiratory centre.

Consequences

• Hypercapnia causes brain vasodilation, which can increase the intracranial pressure
• Chronic hypercapnia is well tolerated, but it causes the respiratory centre to be less sensitive to CO₂, potentially causing breathing to be driven by hypoxia instead
• If the acidosis is severe the consequences will be similar as for metabolic acidosis.

Compensation

Intracellular buffers start working after 6 – 8 hours. However, they aren’t very effective. There will only be 1 mmol/L increase in serum bicarbonate for every 10 mmHg increase in pCO₂.

Because kidney compensation doesn’t kick in until after 24 hours can we distinguish two phases of respiratory acidosis, the acute phase and the chronic phase. In the chronic phase as the kidney started to retain more bicarbonate, in order to increase the bicarbonate:CO₂ ratio toward the normal 20:1.

When the kidney starts to retain bicarbonate will the standard bicarbonate also rise. In this phase will there be a 4 mmol/L increase in serum bicarbonate for every 10 mmHg pCO₂ increase, which is 4 times more efficient than in the acute phase.

The parameters change like this:

Parameter	Acute phase (no compensation)	Chronic phase (yes compensation)
pH	Decreased	Decreased less or normal
pCO2	Increased	Increased
Actual HCO3–	Increased	More increased
Standard HCO3–	Normal	Increased
Buffer base	Normal	Increased
Base excess	0	Positive

Treatment

Artificial ventilation may be used to wash out excess CO₂. The underlying cause should be treated.

Respiratory alkalosis

Definition

In respiratory alkalosis we have:

• pH above 7.45
• Decreased pCO₂
• Decreased actual bicarbonate

When kidney compensation kicks in, after around 24 hours, will we also have:

• Decreased standard bicarbonate
• Decreased buffer base
• Negative base excess

It’s basically the opposite of respiratory acidosis.

Etiology

The only way to have too low pCO₂ is by alveolar hyperventilation, the causes of which have already been discussed. Here are the most important:

• High altitude
• Anxiety
• Pain
• Pregnancy
• Hypoxaemia

Hypoxaemia causes hyperventilation as a compensatory reaction. If the arterial pO₂ falls below 60 mmHg the hypoxaemia start to stimulate ventilation.

Consequences

• Hypocapnia causes cerebral vasoconstriction, reducing the cerebral blood flow which can cause hypoperfusion, leading to unconsciousness and syncope
• Alkalosis causes:
  • Decrease in ionized Ca²⁺, just like in metabolic alkalosis. Neuromuscular excitability increases, potentially causing tetany, laryngospasm, and suffocation
  • → Extracellular K⁺ concentration decreases → hypokalaemia -> risk for arrhythmia increases
  • Haemoglobin-oxygen dissociation curve is shifted to the left, which decreases tissue oxygenation.
• In severe cases similar symptoms to metabolic alkalosis may occur.

When the blood becomes more alkaline will albumin become more ionized to its negative form. This causes it to bind more Ca²⁺, which reduces the ratio between ionized (free) Ca²⁺ and bound calcium in the blood. Only ionized calcium is physiologically active, so the active amount of calcium in the blood is effectively reduced. Calcium blocks sodium channels and inhibits depolarization. When calcium levels are reduced will the threshold for depolarization be lowered. This causes increased neuromuscular excitability, which can cause tetany that might affect the larynx, which can cause suffocation and death.

Alkalosis causes hypokalaemia by moving potassium out of the plasma and interstitial fluids into the urine. This is caused by the effects of intercalated cells in the collecting duct. The kidney wants to conserve H⁺ ions, but to do so it must excrete K⁺ ions to maintain electroneutrality. Hypokalaemia is arrhythmogenic through several mechanisms. Hypokalaemia makes the membrane potential more negative, making it harder to reach the threshold for depolarization.

Lastly will the alkalosis cause a left-shift of the oxygen-haemoglobin dissociation curve, meaning that oxygen now binds more strongly to haemoglobin. This causes the amount of oxygen released from haemoglobin into the tissues to be decreased.

Compensation

The situation is similar as for respiratory alkalosis. In the acute phase will only intracellular buffers work, but in the chronic phase will the kidneys excrete more bicarbonate.

In the acute phase will there be a cause a 2 mmol/L decrease in HCO₃^– for every 10 mmHg decrease in pCO₂.

In the chronic phase will there be a cause a 4 – 5 mmol/L decrease in HCO₃^– for every 10 mmHg decrease in pCO₂.

The parameters change like this:

Parameter	Acute phase (no compensation)	Chronic phase (yes compensation)
pH	Increased	Increased less or normal
pCO2	Decreased	Decreased
Actual HCO3–	Decreased	More decreased
Standard HCO3–	Normal	Decreased
Buffer base	Normal	Decreased
Base excess	0	Negative

Treatment

Treatment involves treating the underlying disorder. If caused by anxiety, breathing into a bag can also help.

If there is significant hypocalcaemia calcium may be administered.

Mixed acid-base disorders

What happens if there are multiple conditions present in the same person, where one would cause an alkalosis and the other an acidosis? The answer is that they could cancel each other out to some degree. pH may even become normal. That doesn’t mean that everything is fine – other components of the conditions could be dangerous.

We can also have respiratory alkalosis and metabolic alkalosis at the same time, where they worsen each other. The same goes for acidosis.

Some examples where there could be a mixed acid-base disorder:

Heart failure patient with pulmonary oedema. The patient may develop lactic acidosis because of hypoxaemia, and respiratory alkalosis or acidosis because of pulmonary oedema.

ICU patients with artificial ventilation and nasogastric suction. Respiratory alkalosis + metabolic alkalosis can occur.

Liver failure patient with ascites. The fluid loss into the abdomen causes secondary hyperaldosteronism. Liver failure causes type B lactic acidosis, and hyperaldosteronism causes metabolic alkalosis.