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Maintaining the pH of blood is essential for normal bodily function. However, numerous clinical scenarios can result in disruption of the body’s acid-base balance. Monitoring of acid-base balance is done by testing patients’ arterial blood gases (ABGs). The results of ABG testing will often influence the treatment that patients receive. Therefore, a basic understanding of how to interpret ABG results can be useful for pharmacists to help them clarify the clinical picture.
The basics of acid-base balance
The optimal physiological pH of extracellular fluid is 7.35–7.45. A pH outside this range can cause protein denaturation and enzyme inactivation . Because pH is a logarithmic scale, a small change in pH reflects a large change in hydrogen ion (H+) concentration . The following equilibrium equation is crucial to understanding acid-base balance:
H2O + CO2↔H2CO3↔HCO3–+H+
This equation shows that carbon dioxide (CO2) in blood dissolves to form carbonic acid (H2CO3), which dissociates to form acidic H+ (which can then combine with physiological bicarbonate to push the equation back to the left). Blood pH depends on the balance of CO2 and HCO3 — a change in the amount of CO2 will not lead to a change in pH if it is accompanied by a change in the amount of HCO3 – that preserves the balance (and vice versa) . It is the renal and respiratory systems that are responsible for maintaining the pH of the blood.
One way that the body controls the pH of extracellular fluid is by increasing or decreasing the rate and depth of respiration and thereby the amount of CO2 expelled (ie, slow, shallow breathing retains more CO2 than fast, deep breathing).
Renal (metabolic) mechanisms
Another way that the body can control pH is via the kidneys, which occurs by either:
- Excretion of H+
- Renal tubular reabsorption of HCO3–
The kidneys can adjust the amount of H+ and HCO3– that is excreted in the
urine in response to metabolic acid production.
When acidosis or alkalosis occurs (either through respiratory or renal mechanisms), the opposite system will attempt to rectify this imbalance; this is termed “compensation”. For example, if the kidneys fail to excrete metabolic acids, ventilation is adjusted in order to eliminate more CO2.
It is important to note that compensatory changes in respiration can
occur over minutes to hours, whereas metabolic responses take hours or days to develop.
The body has three main buffers that minimise any changes in pH that occur when acids or bases are added, namely haemoglobin, HCO3– and proteins. Haemoglobin is six times more powerful as a buffer than proteins. However, HCO3– is the most important buffer in the blood and is the dominant buffer in the interstitial fluid. The intracellular fluid uses proteins and phosphate to buffer pH. At an intracellular
level buffering occurs instantly, but the effect is small.
Arterial blood gas sampling
Monitoring ABGs can be useful to:
- Assess the effectiveness of pulmonary gas exchange;
- Identify the presence of metabolic acidosis and alkalosis;
- Identify critically unwell patients requiring urgent intervention;
- Guide treatment and monitor response.
Some causes of acid-base disturbances can be found in Box 1.
Box 1: Some causes of acid-base disturbance[3,4]
The following are the commonly reported parameters of ABG results (see
Box 2 for the normal reference ranges):
- pH — to determine whether a patient’s blood pH is within physiological range;
- PaCO2 and PaO2 — the partial pressures of CO2 and oxygen in arterial blood, respectively HCO3– — indicates how much HCO3– is in the blood (and is therefore available as a buffer);
- Base excess (or deficit) — a measure of the excess or deficiency of base in the blood; by definition, it is the amount of base (in mmol) that would correct one litre of blood to a normal pH (if an excess, this is the amount of base needed to be removed for a normal pH, or if a deficit, the amount required to be added);
- Lactate — the end product of anaerobic glycosis (a rise indicates poor oxygenation and perfusion of tissues).
Other parameters commonly found on ABG reports are: haemoglobin, glucose and electrolytes (sodium, potassium, chloride and ionised calcium).
Interpreting the results
ABGs can be interpreted using a stepped approach:
Step 1 — check the pH
The pH should be assessed first. A pH of less than 7.35 indicates acidosis and a pH greater than 7.45 indicates alkalosis.
Step 2 — check the HCO3– and PaCO2
Having determined if the patient is acidotic or alkalotic, check the HCO3– and the PaCO2 to classify the results as follows:
- Metabolic acidosis: patients who are acidotic and have a HCO3– <22 (base excess <–2);
- Respiratory acidosis: patients who are acidotic with a PaCO2 >6;
- Metabolic alkalosis: patients who are alkalotic with a HCO3– >28 (base excess >+2);
- Respiratory alkalosis: patients who are alkalotic with a PaCO2 <4.7.
It is possible for patients to have a mixed respiratory and metabolic alkalosis or acidosis. This occurs when primary respiratory and primary metabolic disturbances exist simultaneously. If the two processes oppose each other, pH derangement will be minimised (see step 3). However, two processes that cause pH to move in the same direction may lead to profound acidosis or alkalosis.
Box 2: Normal results
Step 3 — Check for compensation
Check to see if the patient is compensating for his or her acid-base imbalance. Patients may partially or fully compensate for an acid-base imbalance by the “opposite” mechanism; for example metabolic acidosis
will be compensated for with respiratory alkalosis. This may create some apparently normal results amongst some deranged ones.
When interpreting acid-base status, it is important always to take the clinical context into account. For example, if presented with ABG results showing a normal pH, low PaCO2 and low HCO3– in a diabetic patient with high levels of ketones in urine the most likely primary disorder is metabolic acidosis (diabetic ketoacidosis), rather than respiratory alkalosis (see Box 3).
Step 4 — Calculate the anion gap
For a patient with metabolic acidosis it can be useful to calculate the anion gap because this can give some indication of the underlying cause of the acid-base imbalance.
The anion gap is the difference between the measured positively charged cations (sodium [Na+] and potassium [K+]) and the negatively charged anions (chloride [Cl–] and HCO3–). The following equation can be used to estimate the anion gap:
([Na+] + [K+]) – ([Cl–] + [HCO3–])
An increased anion gap indicates excess acid from the anions that are unmeasured (eg, ketones or lactate). It is also worth noting that a drop in a patient’s albumin lowers the anion gap. A deranged phosphate level can also affect the anion gap, but to a lesser extent[4,5].
Box 3: Classification[2,6]
If possible, the underlying cause of the acid-base derangement should be treated because without doing this the problem can recur. In some instances, it may not be possible to treat the underlying cause and drug treatment may be required to correct the acid-base imbalance.
Consider which blood gas disorderscould be affecting the following patients(for reference ranges see Box 2, p87).
PATIENT 1 A 68-year-old woman is admitted with abdominal pain, which is later found to be due to a pelvic abscess causing sepsis. Her arterial blood gases are as follows:
Base excess: –5.2
ANSWER This patient’s pH suggests that she is acidotic. Her PaCO2 is normal and her bicarbonate is low, suggesting a metabolic acidosis. This is supported by the increased base excess. Metabolic acidosis is commonly seen in septic patients as a result of tissue hypoxia causing a build-up of lactate.
PATIENT 2 A 33-year-old woman is admitted with H1N1 influenza and
multiple pulmonary emboli. Her arterial blood gases are as follows:
Base excess: 14.3
ANSWER This patient is highly alkalotic (a pH of 7.55 reflects a much greater change than if it had been, for example, 0.1 below normal because of the logarithmic nature of the pH scale). Her PaCO2 is normal but her bicarbonate is very high, which suggests a metabolic rather than respiratory process. The high base excess also supports this. This patient was also hypokalaemic, which was driving the metabolic alkalosis (this occurs by several mechanisms including renal retention of potassium ions at the expense of hydrogen ions).
- 1Baylis C, Till C. Interpretation of arterial blood gases. Surgery 2009;27:470–4.
- 2Hennessey I, Japp A. Arterial blood gases made easy. Philadelphia: : Elsevier Limited 2007.
- 3Atherton J. Acid-base balance: maintenance of plasma pH. Anaesthesia and Intensive Care Medicine 2009;10:557–61.
- 4Wargo K, Centor R. ABCs of ABGs: a guide to interpreting acid-base disorders. Hospital Pharmacy 2008;43:808–15.
- 5Kellum J. Disorders of acid-base balance. Critical Care Medicine 2007;35:2630–6.
- 6Drage S, Wilkinson D. Acid base balance. Update in Anaesthesia 2001;13.http://update.anaesthesiologists.org