Blood gases are frequently requested for seriously ill surgical patients. Apart from helping to establish a diagnosis, blood gases may also help to ascertain the severity of a particular condition (e.g. metabolic acidosis in sepsis), the direction that further interventions should take and the intensity of monitoring required. It is therefore essential that the surgical trainee not only appreciates the correct techniques involved in performing an arterial blood gas (ABG) analysis, but also has an understanding of the changes in the blood gas parameters in the commonly encountered clinical conditions. The following is an attempt to explain the indications and technique of performing an arterial blood gas sampling, the systematic analysis of a blood gas report and an understanding of its implications. The theoretical basis of respiratory pathophysiology and the biochemistry of acid base homoeostasis have not been dealt with in this article. Also, certain concepts have been explained in small print, only for the benefit of the curious reader.

Indications for an arterial blood gas analysis

Blood gas analyses are performed to evaluate the adequacy of ventilation, oxygenation, oxygen-carrying capacity of the blood and acid-base levels. ABGs are indicated in a number of clinical conditions to

1. Establish the diagnosis and severity of respiratory failure

2. Manage patients in intensive therapy units admitted for

· respiratory failure or dysfunction
· cardiac failure
· renal or hepatic failure
· poly trauma and multiorgan failure
· diabetic ketoacidosis
· sepsis and burns
· poisoning

3. Guide therapy in patients in the ITU, eg

· oxygen administration
· mechanical ventilation
· alkali treatment

4. Monitor patients during

· cardiopulmonary surgery
· cardiopulmonary exercise testing
· sleep studies

5. Determine prognosis in critically ill patients (5)

The aims of doing a blood gas analysis are to detect

1. the presence and severity of hypoxemia and hyper(hypo)capnia and the amount of metabolic compensation.

2. changes in acid-base homeostasis, which might need further investigation and intervention.

Arterial blood sampling

Blood can be drawn from an artery either via an indwelling arterial cannula or by direct arterial puncture. The commonest artery used is the radial followed by the dorsalis pedis; rarely the brachial and the femoral vessels (as they are the principal sources of blood supply to the limbs). Time should usually be allowed for the attainment of a steady state after alteration of ventilatory parameters or the FiO2; at least 5 minutes for any patient without obstructive lung disease and at least 30 minutes if he/she has obstructive lung disease (3).

Direct arterial puncture is usually done with a 21G or smaller needle. If the radial artery is to be used, the collaterality of blood flow to the hand must be checked by the Allen's test. The wrist is kept immobilized and if necessary extended with a support just below the dorsum of the wrist. Under aseptic precautions and with (out) local anaesthesia, the heparinised syringe with needle is introduced at an angle of 450 to the horizontal. The blood can then be aspirated in two ways. One is to penetrate the needle till it hits the bone and then withdrawing the needle while maintaining suction in the syringe till one sees bright red blood coming freely into the syringe. The other way is to penetrate the tissues while maintaining suction so that the artery is not pierced through and through. After drawing a sample, firm pressure must be applied at the site of arterial puncture for at least two minutes.

Click here for Precautions, Tips, alternatives to blood gas analysis

Reading of the report

Normal values in an ABG report. (Table 1)

Note: The arterial pO2 reduces with age. A rough guideline is that above the age of 40 years, paO2 = 105-age in years/2.

The pH of the blood is maintained within a normal range by a number of compensatory mechanisms, the most important being the body buffer mechanisms and the renal and respiratory systems. The degree of compensation varies between individuals and depends on the severity and duration of the primary problem and associated medical comorbidities. Respiratory compensation for metabolic problems is usually rapid and almost complete. The lungs respond quickly by increasing ventilation to blow off excessive carbon-dioxide (in metabolic acidosis) or decreasing ventilation to retain carbon-dioxide (in metabolic alkalosis). The latter compensation is less complete than the former for obvious reasons. The renal compensation for respiratory imbalances is slow and incomplete. The kidneys regulate extracellular fluid H+ ion concentration by secretion of H+ ions, reabsorption of filtered HCO3- ions, and the production of new HCO3- ions. Excess HCO3- is filtered into the renal tubules and eliminated in the urine. Depending on the need to excrete either an acid or a base load, the kidneys can excrete urine with a pH ranging from 4.5 to 8.0. A rough guide to the degree of compensation to primary changes in CO2 and HCO3 as a result of respiratory and metabolic imbalances respectively is shown in table 3.

Table 3. Respiratory and renal compensation in acid-base imbalance (5)

Algorithm for Blood Gas Analysis

Step 1 - Look at the PaO2 and PaCO2 levels

Note : if patient is on oxygen supplementation use PaO2/PiO2 instead of PaO2

Step II

To diagnoses associated respiratory abnormalities (if any) check if the PaCO2 values are similar to or grossly different from the expected values due to compensation by the lungs (Table 3)

Note : if the primary abnormality is in the PaCO2 and not in the standard bicarbonate values - go to Step 1

Abnormalities of gas exchange

Follow step I of the algorithm. A few concepts are explained further.

Hypoxia: The first step is to detect the presence of hypoxia (i.e., less than 60 mm Hg on room air). Patients with clinically evident respiratory problems who have been given oxygen supplementation before blood gas analysis must be assumed to be hypoxic at this stage. If a patient is being given oxygen supplementation, then the ratio of the paO2 (in mm Hg) to FiO2 (in %) is used to detect hypoxia. Usually, the oxygen saturation of the blood is also noted which correlates with the paO2 of the arterial blood and helps in establishing the diagnosis of hypoxia. The saturation as obtained by a blood gas analysis is more accurate than that obtained by a pulse oximetry, as it is not influenced by shock states and skin pigmentation.
Hypercapnia: The paCO2 level must then be noted, which will help in differentiating between type I and type II respiratory failure. In type I respiratory failure, the paCO2 will be normal or low (</=45) and in type II respiratory failure, the paCO2 will be high (>45).

Table 2. Causes of respiratory failure

Causes of type I respiratory failure include conditions with an impaired gas exchange and causes of type II respiratory failure include the causes of type I in an advanced state and conditions with impaired ventilation as shown in table II. Differentiation between types I and II failure is essential to determine the aetiology and institute further treatment. It may also rarely be used to restrict O2 supplementation in patients with type II disease because such patients are dependent on hypoxia for the respiratory drive and abolishing hypoxia might further suppress the CNS stimulation for respiration. Patients with persistent hypoxia, rising CO2 levels and respiratory acidosis require mechanical ventilation and are usually seen by the anaesthetist at this stage.
In patients on a ventilator, hypoxia might indicate one of several things, including

• accidental disconnection of the breathing circuit ( which should be evident by the alarms, fall in O2, fall in saturation on pulse oximetry, clinical evidence of respiratory distress, etc.)
  
• development of pneumothorax which could be detected clinically and might need confirmation by X-ray before intercostal tube drainage
• development or worsening of pre-existing chest problems (bronchopneumonia, ARDS, pulmonary contusion) might require changes in settings of the ventilator like increasing FiO2 levels, ventilatory rate or tidal volume, adding or increasing PEEP, or changing to other modes of ventilation.

A high CO2 level is always associated with hypoxia unless the patient is on oxygen supplementation. However, hypercarbia associated with a normal oxygen level should also be approached with the same urgency as the patient might deteriorate rapidly. The possibility of a venous sample as a cause of unexpected hypercarbia and hypoxia should be kept in mind. In patients on a ventilator, moderate rise in CO2 levels are currently considered acceptable and interventions to correct these might be associated with significant side effects including barotraumas and hypotension (permissive hypercarbia). Similarly, patients with COPD have adapted to higher levels of carbon-dioxide and might not require correction to normal levels.
Acute changes in paCO2 result in predictable changes in pH. For every increase in paCO2 of 20 mm Hg (2.6 kPa) above normal, the pH falls approximately by 0.1. For every decrease of paCO2 of 10 mm Hg (1.3 kPa) below normal, the pH rises by 0.1. Any change in pH outside these parameters is therefore metabolic in origin (1). The kidneys take time to compensate for the change in pH the amount of renal compensation indicates the chronicity of the problem and the need for urgent correction. Correction will usually involve a combination of treatment of the cause, initiation of mechanical ventilation or modification of the settings and reduction of CO2 production.

Alveolar-arterial oxygen gradient (A-a)PO2: This is the difference in the oxygen partial pressures between the alveolar and arterial sides. In patients with type II respiratory failure, it may help to determine whether the patient has associated lung disease or just reduced respiratory effort.

Click here for more details

The A-a gradient increases a little with age, but should be less than 2.6kPa (20mmHg). A normal gradient would imply conditions like CNS depression and neuromuscular disorders as the cause and a high gradient would imply some lung disease (1).

Abnormalities of acid base balance

Follow Step II of the algorithm. The concepts in the algorithm are explained further.

PH of the blood: The pH is usually maintained within a narrow range by a number of buffer systems in the body. A normal pH value may still be due to a well-compensated imbalance or a mixed acid base disorder and an abnormal value is definitely due to a poorly compensated acid base problem or due to both metabolic and respiratory derangements causing an imbalance in the same direction. A rough guide to the amount of compensation that can be expected for a given primary alteration in CO2 or HCO3 is given in table 3.
Serum bicarbonate: The actual bicarbonate is the value calculated from the blood gas sample. The standard/corrected bicarbonate is the value obtained after correction of CO2 levels to 40mm Hg and at room temperature. It gives a better estimate of the metabolic problem causing acid base imbalance. The base deficit/excess is the amount of deviation of the standard bicarbonate from the normal. The metabolic problem could either be a low (base deficit or metabolic acidosis) or high (base excess or metabolic alkalosis) standard bicarbonate.

Compensation: As discussed earlier, a primary metabolic derangement will be accompanied by some degree of respiratory compensation. The ability to detect the primary abnormality and the amount of compensation is hindered by other co-existing conditions causing respiratory acidosis and/or alkalosis. Also, coexisting medical problems can cause both metabolic acidosis and alkalosis. Step II of the algorithm gives a rough idea to determine the main features of the acid base imbalance.

Metabolic acidosis
Metabolic acidosis can be due to a variety of conditions. Treatment of metabolic acidosis is treatment of the cause. Direct administration of alkali (sodium bicarbonate) is reserved for severe cases. A number of conditions can result in metabolic acidosis, the most important among them being the under perfusion of tissues resulting in accumulation of lactic acid. Differentiation of the causes of metabolic acidosis requires the estimate of an entity called the 'anion gap'.

Anion gap

Body fluids including blood may contain a variable number of ions, but the total number of anions (negative ions) and cations (positive ions) are roughly the same. The ions that are usually measured in blood are cations like sodium and potassium and anions including chloride and bicarbonate. There are unmeasured ions in both groups (cations and anions), which also contribute to the ionic constitution of blood. The measured cations are usually greater than the measured anions by about 8-16mmol/L. This is because the unmeasured anions constitute a significant proportion of the total number of anions in blood. Proteins make this up predominantly, but also included are sulphates, phosphates, lactate and ketones.

Causes of a decreased anion gap include hypoalbuminaemia and severe haemodilution. Rarer causes include increase in minor cation concentrations like calcium and magnesium. Causes of a raised anion gap include dehydration and any cause of raised unmeasurable anions, like lactate, ketones and renal acids, along with treatment with drugs given as organic acids such as penicillin, salicylates and poisoning with methanol, ethanol and paraldehyde. Rarely it may be due to decreased minor cation concentrations such as calcium or magnesium.

Raised anion gap metabolic acidosis:

As documented above, accumulation of a number of acids can result in raised anion gap metabolic acidosis. In such cases, the reduction in serum HCO3- matches the anion gap. If not, a second acid base disorder should be kept in mind. When metabolic acidosis and alkalosis coexist, as in vomiting and ketoacidosis, the plasma HCO3- may be normal, and a raised anion gap may be the initial evidence of an underlying acid-base disturbance (2).

To differentiate between the many causes of 'increased anion gap metabolic acidosis', we measure the osmolar gap that is the difference between the measured osmolarity and the calculated osmolarity.

Click here for more detail

Normal anion gap (hyperchloraemic) metabolic acidosis

This usually results from conditions wherein there is a loss of alkali (i.e.HCO3-) or metabolic equivalent (eg, excretion of salts of organic anions in proportionate excess of chloride) or an accumulation of HCl or metabolic equivalent (eg, NH4Cl and chloride salts of amino acids) (2).
Loss of HCO3- can occur either due to GI causes or due to renal causes (renal excretion or insufficient generation). In many surgical conditions, the cause is usually obvious.

Click here for more detail

Examples of extrarenal causes are excessive diarrhoea or drainage of gastrointestinal secretions, NH4Cl administration, parenteral nutrition, rapid saline infusion and congestive cardiac failure. Generation of large amounts of organic anions can sometimes produce this type of metabolic acidosis (and not one with a raised anion gap), if the kidneys can prevent their accumulation by rapid excretion.
Examples of renal causes include the various types of renal tubular acidosis (type I, type II and type IV).

Metabolic acidosis (M Ac.)

Examples of different types of renal tubular acidosis (RTA)

Metabolic Alkalosis

Metabolic alkalosis can result from the loss of acid, addition of alkali or both in the kidneys or elsewhere. Extrarenal sites include stomach (loss of acid), redistribution of alkali from the intracellular stores to the ECF (as in potassium or chloride depletion), oral administration (antacids, ion-exchange resins, milk alkali syndrome, oral HCO3-) and parenteral administration of alkali (citrate in blood transfusions, bicarbonate in severe metabolic acidosis). Renal causes of alkali excess include mineralocorticoid excess, response to long-standing hypercapnia (persists even after correction of respiratory acidosis), hypokalemia (promotes H+ secretion in the distal nephron) and ECF volume depletion (impaired HCO3- excretion). Certain conditions can cause metabolic alkalosis by a number of mechanisms (eg diuretic use causes both ECF depletion and hypokalemia).

Respiratory Alkalosis

The principal cause of respiratory alkalosis (hypocapnia) is hypoxia and its causes (type I respiratory failure), further treatment of which has been detailed before. Other causes of acute respiratory alkalosis include anxiety, fever, pain, sepsis, hepatic failure, CNS disorders (stroke, infections), pulmonary disorders without hypoxia (infections and interstitial lung disease), delirium tremens and drugs (salicylate intoxication). Chronic causes include high altitude hypoxia, chronic hepatic failure, chronic pulmonary disease, CNS trauma, anaemia, hyperthyroidism, beriberi and pregnancy (2,4). Treatment should be directed towards the cause.

Problems with arterial blood gas analysis

ABG analysis is associated with a number of problems including 3

· Pain
· Preanalytical errors: air contamination, heparin dilution, storage, excessive delay before analysis
· Analytical errors: accurate differences between models of blood gas analysers
· Postanalytical errors: transcription errors, delays in reporting results
· Infection risk to patient (particularly with arterial catheter)
· Infection risk to clinician (particularly with arterial puncture)
· Thrombosis and distal embolization (particularly with arterial catheter) and ischemia
· Blood loss (particularly with arterial catheter), arterial spasm, hematoma
· Intermittent information
· Spontaneous variability of blood gas levels without clinical change in the patient
· Cost

Conclusion

Arterial blood gases can provide invaluable clinical information in critically ill surgical patients. It must however be remembered that they are static measurements and do not necessarily reflect the changing physiologic status of a sick patient. Therefore, any decision-making should be directed keeping in mind the overall condition of the patient and not the blood gas report alone. Picking up a major acid base disorder might not be as difficult as identifying other coexisting acid base imbalances which might be masked by the main disorder, but might also require active treatment.

Glossary

References for further reading

1. Williams AJ. ABC of oxygen. Assessing and interpreting arterial blood gases and acid-base balance. B M J 1998;317:1212-6.
2. Gluck SL. Acid-base. Electrolyte quintet. The Lancet 1998; 352: 474-9.
3. Hess D. Detection and monitoring of hypoxemia and oxygen therapy. Resp Care 2000;45:64-83.
4. Ventriglia WJ. Arterial blood gases. Emerg Med Clin N Am 1986; 4: 235-51.
5. DuBose Jr TD. Acidosis and alkalosis. Chapter 50. Section 7. Alteration in urinary function and electrolytes. In Fauci et al.     Harrison's Principles of Internal Medicine 14th edition. 1998; 277-86.