Advanced: A guide to regulation of blood gases: part two

  • Published: 02 December 2006 14:58
  • Last Updated: 24 April 2007 12:03

VOL: 102, ISSUE: 46, PAGE NO: 40

Liz Allibone, BSc, RGN, is nurse teacher, Nursing Development, Royal Brompton Hospital; Nicola Nation, BSc, RGN, is senior nurse, nursing development, Royal Brompton Hospital

Arterial blood gases (ABGs) provide information about a patient's respiratory and metabolic status. Equilibrium is achieved by a number of mechanisms including the respiratory and renal system. The degree to which blood gas results vary from normal limits helps the nurse to understand the effectiveness of organ function and the ability of the body to compensate for acute or chronic changes. To understand the significance of these changes it is necessary to look at the normal values and limits.

Arterial blood gases (ABGs) provide information about a patient's respiratory and metabolic status. Equilibrium is achieved by a number of mechanisms including the respiratory and renal system. The degree to which blood gas results vary from normal limits helps the nurse to understand the effectiveness of organ function and the ability of the body to compensate for acute or chronic changes. To understand the significance of these changes it is necessary to look at the normal values and limits.

ABGs provide information on a series of measured and calculated values (Table 1).

Interpretation of arterial blood gas results

A systematic approach to ABG interpretation is essential (Resuscitation Council, 2004; Jevon and Ewens, 2002; Shoulders-Odom, 2000). The step-by-step approach to ABG analysis devised by Simpson (2004) is described below:

Assess oxygenation

Examine partial pressure (PaO 2) of oxygen and oxygen saturation (SaO 2). Assess whether the value is normal, high or low. Consider this in the light of any supplementary oxygen that the patient is receiving (Simpson, 2004).

Determine the status of the pH

Note the pH value to determine the presence of acidosis or alkalosis. Normal pH is 7.35-7.45. Any value below 7.35 indicates acidosis and any value above 7.45 indicates alkalosis. A normal pH indicates one of two scenarios. Either the blood gas is normal in which case so will be the PaCO 2and HCO 3-. Alternatively, full compensation is present in which case the PaCO 2and HCO 3-will be deranged (outside normal values), as one parameter will be compensating for the deranged one (Tortora and Derrickson, 2005; Simpson, 2004).

Assess the respiratory component (PaCO 2)

PaCO 2values below 4.7kPa indicate a respiratory alkalosis (or respiratory compensation for a metabolic acidosis) and values above 6.0kPa indicate a respiratory acidosis (or respiratory compensation for a metabolic alkalosis) (Resuscitation Council UK, 2004). If the PaCO 2is deranged it is important to check whether it followsthe same direction (acidosis or alkalosis) as the pH. If so, this is the primary disorder (Simpson, 2004).

Assess the metabolic component (HCO 3-)

Values below 22mmol/L indicate metabolic acidosis (or renal compensation for respiratory alkalosis) and values above 26mmol/L indicate metabolic alkalosis (or renal compensation for a respiratory acidosis). If the HCO 3-value is abnormal, check whether it follows the same direction (acidosis or alkalosis) as the pH. If so this is the primary disorder (Simpson, 2004). Some clinicians prefer to use the base excess (or deficit) instead of the HCO 3-values. A base excess is defined as the amount of acid required to restore 1L of blood to a normal pH of 7.4. A base deficit is defined as the amount of alkali required to restore 1L of blood to a normal pH of 7.4 (Woodrow, 2004).

Assess for a mixture of disorders

A mixture of disorders may occur for two reasons: either a dual pathology is present or one disorder is compensating for the other. For example, if the PaCO 2and HCO 3-are both moving in the same direction (either indicating acidosis or alkalosis), a dual pathology must be present such as metabolic and respiratory acidosis. If one parameter is acidic and the other is alkaline, then one parameter is compensating for the other (Simpson, 2004; Heitz and Horne, 2001; Horne and Derrico, 1999).

Assess for compensation

This is the body's attempt to maintain a normal pH level. The respiratory system controls the carbon dioxide level and the renal system controls the bicarbonate level. The body uses these two systems to oppose each other in order to maintain a normal pH (Morton et al, 2005; Marieb, 2003).

Three types of compensation are possible:

  • In an uncompensated blood gas the pH is abnormal and either the CO 2or HCO 3-is abnormal. There is no indication that the opposite system has tried to correct for the other (Morton et al, 2005; Pruitt and Jacobs, 2004).
  • In a partially compensated blood gas, the pH is abnormal and both the CO 2and HCO 3-are also abnormal. One parameter will be deranged and following the same direction as the pH. This is the primary problem. The third parameter will be moving in the opposite direction in order to compensate for the primary disorder (Morton et al, 2005; Tortora and Derrickson, 2005; Pruitt and Jacobs, 2004) but it will not have changed enough to bring the pH back to the normal limits.
  • In a fully compensated state the pH is normal but is usually ?tending towards' alkalosis or acidosis (Morton et al, 2005). The two other parameters will be deranged and moving in opposite directions, one compensating for the other. The primary abnormality (metabolic or respiratory) is correlated with the abnormal pH (acidotic or alkalotic). Other clinical information will allow the clinician to interpret which parameter is compensating for which (Simpson, 2004). A typical example of a fully compensated status is a patient with COPD whose ABGs may show fully compensated respiratory acidosis (Pruitt and Jacobs, 2004; Bongard and Sue, 2003; Bourke, 2003).

The main causes of abnormal values are summarised in Tables 2 and 3.

Anion gap

Another measurement that may be used when interpreting blood gas results, particularly when the cause of a metabolic acidosis is not clinically obvious, is calculation of the ?anion gap' (Heitz and Horne, 2001; Hinds and Watson, 1999).

This is calculated as the difference between the sum of the bicarbonate and chloride concentrations and the sum of the sodium and potassium concentrations (Heitz and Horne, 2001; Hinds and Watson, 1999). The value normally ranges from 8-14mmol/L and represents the level of unmeasured anions in extracellular fluid (including sulphates, phosphates, plasma proteins, and organic acids such as lactates and ketones).

Table 1. Normal Values

Parameter

Normal values

Definition

pH

Measurement of H+ ion concentration

7.35-7.45

pH < 7.35 indicates acidosis

pH > 7.45 indicates alkalosis

PaCO 2

Partial pressure of carbon dioxide in arterial blood

4.7-6.0kPa

PaCO 2> 6.0kPa indicates acidosis

PaCO 2< 4.7kPa indicates alkalosis

HCO 3-

bicarbonate (buffer) in arterial blood

22-26mmol/L

< 22mmol/L indicates acidosis

> 26mmol/L indicates alkalosis

Base excess/deficit

Amount of acid or alkali required to restore 1L of blood to normal pH

-2 to +2mmol/L

> +2mmol/L indicates a base excess in the blood

< -2mmol/L indicates a base deficit in the blood

PaO 2

Partial pressure of oxygen in arterial blood

11.5-13.0kPa

PaO 2< 11.5kPa indicates insufficient oxygen
in blood (hypoxaemia)

PaO 2> 13.0kPa indicates more oxygen in blood
than necessary

SaO 2

The percentage of oxygen that is bound to haemoglobin

93-98%

< 93% indicates hypoxia

If metabolic acidosis is due to bicarbonate loss the ?anion gap' will be normal. Conversely, a metabolic acidosis will cause an increase in the ?anion gap', for example, in ketoacidosis, renal failure, and lactic acidosis (Heitz and Horne, 2001; Hinds and Watson, 1999).

Mixed respiratory and metabolic disturbances

Examples of mixed acid-base disorders include:

  • Diabetic ketoacidosis and vomiting;
  • Metabolic acidosis and metabolic alkalosis;
  • Pneumonia and COPD;
  • Acute and chronic respiratory acidosis;
  • Lactic acidosis and respiratory arrest - metabolic acidosis and respiratory acidosis;
  • Renal failure and opiate overdose - metabolic acidosis and respiratory acidosis.

A mixed acid-base disturbance occurs when two or more simple acid-base disorders are present at the same time. Some clinical conditions may lead to complex acid-base disturbances and therefore an accurate assessment of the clinical details is very important before making a diagnosis (Bourke, 2003). When two opposing disorders (alkalosis and acidosis) occur simultaneously, the pH is determined by the predominant disorder. In some cases the pH might be normal in the presence of a mixed acid-base disorder (Heitz and Horne, 2001).

This article has provided a systematic step-by-step approach in interpreting arterial blood gas results. In the next article in this series, common causes will be discussed as well as treatment for acute acid-base disturbances. Arterial blood gas interpretation is increasingly becoming an essential part of nursing practice. Therefore understanding the results can help the nurse to intervene safely, correctly and confidently and deliver better patient care. 

Table 2. Causes of abnormal respiratory values

Respiratory acidosis; inadequate alveolar ventilation, diffusion or perfusion or excess CO 2production

Lung disease, for example COPD,
pulmonary fibrosis

Pain

Central nervous system depression due to opiates, brainstem injury, anaesthesia

Pneumonia

Impaired respiratory muscle function, for example neuromuscular diseases, spinal
cord injury

Airway obstruction

Pulmonary embolus or severe pulmonary oedema

Chest wall injury/deformity

Cardiac arrest

Pneumothorax or haemothorax

Respiratory alkalosis; excessive ventilation or inadequate CO 2production

Hysteria, anxiety

Pyrexia, sepsis

Brainstem injury

Severe anaemia

Overmechanical ventilation, for example from setting the respiration rate too high

Increased basal metabolic rate

Hypoxia

Asthma

Table 3. Causes of abnormal metabolic values

Metabolic acidosis; excessive accumulation of H+ or excessive loss of HCO 3-

Diarrhoea

Renal disease

Following cardiorespiratory arrest

Diabetic ketoacidosis

Lactic acidosis

Intestinal fistulas

Drugs or chemicals such as methanol, salicylates

Metabolic alkalosis; excessive loss of H +or excessive gain of bases

Excessive vomiting

Excessive ingestion of antacids

Excessive naso-gastric tube aspiration

Diuretics

Liver failure

Hypokalaemia (low serum potassium levels)

Transfusion of large volumes of blood

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