Causes of respiratory acidosis and alkalosis

By Alex Yartsev - Jul 12, 2015

Respiratory acidosis and alkalosis are featured in virtually every paper, and being able to identify a respiratory acid-base disturbance is a vital skill for the CICM fellowship candidate. The SAQs will frequently require the application of the usual rules of compensation to reveal a hidden acid-base disorder, eg. "this patient has a low CO2 but it is not low enough".

Questions which involve respiratory acid-base disturbances are too numerous to list. Some representative examples include the following:

Question 12.3 from the second paper of 2014
Question 3.4 from the first paper of 2013
Question 3.5 from the first paper of 2013
Question 8.3 from the first paper of 2012
Question 9.1 from the first paper of 2011
Question 7.2 from the first paper of 2009

Several CICM fellowship questions revolve around the core question, "what possible causes for this respiratory acid-base disturbance can you think of ?"

The causes can be split into aetiological categories, as below:

Causes of Respiratory Acidosis and Alkalosis
Respiratory Acidosis	Respiratory Alkalosis
Increased inspired fraction of CO₂ Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) Decreased alveolar ventilation CO₂ increases by 3mmg for every minute of apnoea central respiratory depression eg. by drugs or post-ictally neuromuscular disorders resulting in weakness lung or chest wall defects resulting in restriction airway obstruction, eg. after a seizure inadequate mechanical ventilation Increased metabolic CO₂ production Malignant hyperthermia Thyrotoxicosis Phaeochromocytoma Sepsis Liver failure Extremes of physical exertion Convulsive epilepsy	Respiratory control centre Head injury, stroke Anxiety, fear, stress, pain Salicylates Pregnancy Chronic liver disease Hypoxia Pulmonary receptors Pulmonary embolism Pneumonia Asthma Pulmonary oedema

Compensation for respiratory acid-base disorders

The general approach to the assessment of metabolic compensation for respiratory acid-base disturbances is discussed in greater detail in the apocryphal chapters devoted to blood gas analysis.

Specifically, the Bedside Rules section discusses a series of empirical formulae which can be used to assess the effectiveness of compensation:

The Boston rules: 1-4-2-5 rule:

The change in HCO₃ in response to a 10mHg change in PaCO₂

1mmol increase with acute respiratory acidosis
4mmol increase with chronic respiratory acidosis
2mmol decrease with acute respiratory alkalosis
5mmol decrease with chronic respiratory alkalosis

The 0.008 rule:

The pH change in response to an acute respiratory acid-base disturbance

pH = 7.40 - ((PaCO₂-40) x 0.008))

The 0.003 rule:

The pH change in response to a chronic respiratory acid-base disturbance

pH = 7.40 - ((PaCO₂-40) x 0.003))

The Copenhagen Rules: the 0-4-1-6 rules.

0: An acute change in PaCO₂ will not change the Standard Base Excess.

4: In chronic disorders, the expected change in SBE will be 0.4 times the change in PaCO₂ ... i.e. expected SBE = 0.4 × (40 - PaCO₂)

1: In compensation for metabolic acidosis, the compensatory change in PaCO₂ will be proportional to the SBE. ..i.e. expected CO₂ = 40 + (1.0 × SBE)

6: In compensation for metabolic alkalosis, the compensatory change in PaCO₂ will be proportional to 0.6 times the SBE, i.e CO₂ = 40 + (0.6 × SBE)

References

Bruno, Cosimo Marcello, and Maria Valenti. "Acid-base disorders in patients with chronic obstructive pulmonary disease: a pathophysiological review."BioMed Research International 2012 (2012).

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