Arterial Blood Gasses (ABGs) (Advanced)

Week 3

Context

Arterial blood gases or ABGs are often required in the assessment of a deteriorating patient. They are a good indicator of the severity of the patient's condition. They allow us to assess the oxygen delivery to tissues, the adequacy of ventilation and the acid-base balance. They assist in determining relevant treatment pathways.

Content

Chemical formulae used in this section:

H⁺ Hydrogen Ions
CO₂ Carbon Dioxide
O₂ Oxygen
H₂CO₃ Carbonic Acid
HCO₃^- Bicarbonate
H₂O Water

When and how to take ABGs

ABGs should be taken in patients suspected of respiratory failure, who are critically ill or patients who have deteriorated. ABGs should only be taken if they are going to be useful and affect the way that the patient is managed. A Venous Blood Gas is an alternative method of estimating systemic CO₂ and pH that does not require arterial blood sampling and can be utilised in the clinical area.

An ABG is taken in one of two ways: Either by an arterial stab, usually from the radial artery, but alternatively the femoral artery or brachial artery; or by taking blood from an indwelling arterial line (common in patients in critical care).

ABGs can only be taken by a qualified, competent and experienced health care worker. Please refer to your local guidelines for further information. Once the sample is taken, it is processed by a blood gas machine and results can be available within minutes, depending on the local circumstances.

ABG Parameters

Arterial Blood gases will provide information on the following parameters:

PaO₂ (Partial Pressue of Oxygen)
pH (acidity)
PaCO₂ (Partial Pressure of Carbon Dioxide)
HCO₃^- (bicarbonate)
Base excess / Base deficit
SaO₂ (Oxygen Saturation)
Serum Lactate

The physiology underpinning ABGs

pH

pH stands for Power of Hydrogen and is the term used for measuring acidity, therefore this determines the acidity of the blood. Hydrogen ions (H⁺⁾ are the product of normal cellular metabolism The more H⁺ in a solution, the more acidic it will be. H⁺ and pH have an inverse relationship on each other. If the H⁺ increases, the pH will decrease, making the blood more acidic. If H⁺ decreases, then the pH will increase, making the blood more alkalotic. Therefore acid-base balance is maintained by the H⁺ concentration in the blood.

Normal range for pH in the human body is 7.35 – 7.45.

Buffering

pH is maintained by both respiratory and renal systems, by several buffering systems. The main buffering system is the carbonic acid-bicarbonate system. The respiratory system controls the CO₂. In rapid and deep breathing, more CO₂will be expired. In shallow, slow breathing CO₂ is retained. CO₂ is acidic, so the more CO₂ present, the more acidic the blood will be. It is important to note that changes to respiration can have a rapid effect on the pH. Buffers are only a temporary means to regulate the acid-base balance as they are unable to excrete.

A buffer is a molecule that can either release or bind H⁺ to maintain pH. A buffer is used to resist changes to pH and is made up of a weak acid and a salt. So, the buffer can undergo a reaction to minimise the change to the pH. Buffers are only a temporary means to regulate the acid-base balance as they are unable to excrete. There are three individual buffers in the body:

Carbonic acid buffer
Phosphate buffer
Plasma protein buffer

Using the HCO₃^- buffering system, acid H⁺ can be eliminated via CO₂ in the expiratory gas. As CO₂ is expired, more carbonic acid can break down to release more CO₂. Hydrogen can be transported to the kidneys where HCO₃^- buffers transfer the acid to phosphate buffers in the renal filtrate, the phosphates carry the hydrogen out in the urine. As it is carried in circulation, HCO₃^- buffers reaches every cell in the body. The HCO₃^- buffering system is the major buffering system of the body system in terms of acid elimination.

When the number of hydrogen ions in the blood increases and the pH drops, the phosphate ions accept H⁺ in order to maintain equilibrium. When the H⁺ decrease, the phosphate ions release H⁺ and increase their number in the blood.

Protein buffers are either intracellular or extracellular, but are mainly intracellular and include haemoglobin. Protein molecules act as both H⁺ acceptors and H⁺ donors in the acid-base balance.

PaO₂/ PaCO2

Oxygenation is a common reason to take an ABG which helps to determine the amount of Oxygen required by the patient. Oxygen saturation measurement can be undertaken in a non-invasive way by the use of a oxygen saturations probe, however, it is also measured via ABG. In healthy adults there is approximately 20mls of oxygen per 100 mls of blood, with 97% of the oxygen binding to the haemoglobin and the other 3% dissolved in plasma.

PaO₂ measurement allows us to determine the amount of oxygen binding to haemoglobin. Normal PaO₂ is between 11.5 – 13 kPa. If the PaO₂ is high, it is indicative that there is too much oxygen bound to haemoglobin and the clinician needs to consider methods to reduce oxygen levels to normal and decrease the risk of oxygen toxicity. If the PaO₂ is low, a clinician needs to consider increasing oxygen levels.

HCO₃^-

Bicarbonate (HCO₃^-) is a weak base , regulated by the kidneys. 70% of CO₂ is carried in HCO₃^- in the blood from the tissues to the lungs for excretion. HCO₃^- reflects the renal component of the acid-base balance. The normal range is 20-24 mEq/L.

Base excess is the amount of alkaline that needs to be given to or taken away to adjust the pH back to the normal range. This represents how much the body is using the buffering systems to maintain pH, so if HCO₃^- is high, the base excess will be positive and if HCO₃^- is low there will be a deficit, and therefore a negative reading. So a high HCO₃^- reading demonstrates that the body is using the buffering systems to compensate for changes in the pH.

Responses to physiological changes

Remember that respiration is controlled by chemoreceptors, which are ultimately responsible for the following changes.

Increased CO₂ – the patient will experience increase Heart Rate (HR) and Respiratory rate (RR) to excrete CO₂
Decrease O₂ – you will notice an increase in RR to increase O₂
Decrease pH – the body will increase RR to decrease CO₂
Increase pH – will decrease RR to retain CO₂

Respiratory Acidosis

Respiratory acidosis is a condition caused by the lungs being unable to excrete excess CO₂, so it is retained in the body. The excess CO₂ combines with water to form a substance called Carbonic acid or H₂C0₃. Carbonic acid then dissociates to leave free H⁺, and these free H⁺ increase pH and therefore increase the acidity of the blood. Respiratory acidosis can be compensated by the kidney increasing HCO₃^- ions, but this process is not immediate and may take up to 2 days for the full effect.

The causes of respiratory acidosis are acute deterioration, chronic bronchitis, asthma, pneumonia, airway obstruction, drugs, head injury. Patients will experience a number of symptoms including difficult breathing, headache, drowsy, restless, tremor, hand flapping, confusion, tachycardia, cyanosis. Respiratory acidosis can be diagnosed quickly by an ABG analysis.

Respiratory Alkalosis

Respiratory alkalosis is rare and caused by a decreased CO₂ (often due to hyperventilation) which in turn cause the blood to become more alkalotic and the pH to be above 7.45. The likely causes of respiratory alkalosis include hyperventilation and high altitudes. The treatment for respiratory alkalosis is to increase CO₂ concentration.

Metabolic Acidosis

A patient with metabolic acidosis will have a pH below 7.35 and a plasma HCO₃^- less than 22 mEq/L. We know that the acidosis is metabolic because of the HCO₃^- being lower than the normal range. Causes of metabolic acidosis include severe diarrhoea, diabetic ketoacidosis, failure of kidneys to excrete H ions and shock. A patient experiencing metabolic acidosis will have some or all of the following symptoms tachypnoea, confusion, lethargy, decreasing consciousness and cardiac arrhythmias.

Metabolic Alkalosis

Metabolic alkalosis is identified by a pH higher than 7.45 and an increase inHCO₃^- more than 26 mEq/L. Metabolic alkalosis occurs as a consequence of a loss of H⁺ from the body or a gain in HCO₃^-. Causes of this include excessive vomiting, and diuretics. In metabolic alkalosis, HCO₃^- will be excreted by the kidneys and can be rapidly corrected.

Compensatory Mechanisms

Renal compensation is slow. In respiratory acidosis, the kidneys compensate for a fall in pH by excreting hydrogen and retaining HCO₃^-. Therefore the ABG may show a corrected (normal) pH but a high CO₂ and a high HCO₃^-, and positive base excess. This is more likely in patient with Chronic Obstructive Pulmonary Disease (COPD).
In a metabolic acidosis, chemoreceptors will stimulate hyperventilation in order to compensate for the increased hydrogen ions detected. Respiratory compensation is quick. Respiratory response to metabolic alkalosis is to decrease the respiratory rate. PCO₂ will rise. It is unlikely that a conscious patient will hyperventilate to compensate.

	pH	HCO₃^-	PaCO₂	Base excess/deficit
Respiratory Acidosis	< 7.35	Normal 22-26 mEq/L	>6.0 kPa	-
Respiratory Alkalosis	>7.45	Normal 22-26 mEq/L	< 4.5 kPa	-
Metabolic Acidosis	< 7.35	< 22 mEq/L	Normal 4.5-6.0 kPa	< -2
Metabolic Alkalosis	>7.45	> 26 mEq/L	Normal 4.5-6.0 kPa	at least +2

Task

So you can see if you understand other significance of ABGs try the Arterial Blood Gasses (ABGs) Analysis Test.

References and Further Reading

Coggan, J.M. (2008a) Arterial blood gas analysis 1. Understanding ABG reports. Nursing Times 104(18): 28–9.

Coggan, J.M. (2008b) Arterial blood gas analysis 2: Compensatory mechanisms. Nursing Times 104(19): 24–5.

Rogers, K. & McCutcheon, K. (2013) Understanding arterial blood gases Journal of Perioperative Practice 23.9 (September 2013): 191-197.

Simpson, H. (2004) Interpretation of arterial blood gases: a clinical guide for nurses. Links to an external site. British Journal of Nursing13.9; 522-528.

Williams, A. (1998) Assessing and interpreting arterial blood gases and acid-base balance. Links to an external site. BMJ (Clinical Research Edition) 317.7167: 1213-1216.

Woodrow, P. (2004) Arterial blood gas analysis. Nursing Standard 18(21), 45–52.