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A guide to regulation of blood gases: Part One

VOL: 102, ISSUE: 36, PAGE NO: 46

Liz Allibone, BSc, RGN, is nurse teacher, Nursing Development

Nicola Nation BSc, RGN, is senior nurse, Nursing Development; both at Royal Brompton Hospital

Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygen levels and aci…

 

Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygen levels and acid-base balance. Understanding the significance of the results and knowing when medical help is urgently required can improve patient care (Woodrow, 2004).

 

 

Indications for ABG measurement

 

ABG analysis is used to evaluate a number of clinical conditions and situations (Box 1). However, each patient must be judged individually, and ABG interpretation should not be considered in isolation. The clinician must be in possession of additional information to guide their diagnosis for example, past medical history and lung function tests (Simpson, 2004).

 

 

In many clinical situations blood gas analysis is preferable to pulse oximetry. Although pulse oximetry measures oxygen saturation and does not require an arterial puncture it does not measure levels of carbon dioxide. Pulse oximetry can also provide false readings caused by factors such as peripheral vasoconstriction, arrhythmias, shivering, anaemia, dyes, nail varnish and carbon monoxide (Bourke, 2003; Lynes, 2003; Fox, 2002; Casey, 2001; Dunn and Connelly, 2001; Woodrow, 1999). The procedure used to obtain a blood sample for ABG is described in Box 2.

 

 

Optimum cellular function depends upon adequate oxygenation and a balanced acid-base ratio. Hypoxaemia (decreased blood oxygen levels), if left uncorrected, will result in tissue hypoxia, cellular injury and death. Deviations in the acid-base balance or blood pH can also be life threatening (Horne and Derrico, 1999).

 

 

Parameters of blood gas measurement

 

Blood gas machines provide measurement of the following:

 

 

- pH;

 

 

- Respiratory function (oxygen and carbon dioxide saturation);

 

 

- Metabolic measures (bicarbonate, base excess). Not all gases present in the blood are routinely measured, for example, inert nitrogen that is dissolved in the arterial blood.

 

 

The standard unit of measurement of blood gases in the UK is the kilopascal (kPa) whereas in the USA (and therefore US textbooks) the more common unit of measurement is mmHg. If conversion is required nurses should be aware that 1 kPa is equivalent to approximately 7.5 mmHg (Woodrow, 2004).

 

 

Physiology of acid-base balance

 

Blood and extra-cellular fluid must be maintained at a fairly constant balance of acids and bases (homeostasis). A person’s well-being depends on her or his ability to maintain a normal pH and any deviation can compromise essential body processes and this can be life threatening (Woodrow, 2004).

 

 

An acid is a chemical that can release or donate hydrogen ions (H+). Strong acids ionise completely by releasing all of their H+ into a solution. Weak acids do not ionise completely, for example, carbonic acid is a weak acid occurring naturally in the body. A base is a chemical that can absorb, or receive H+: all bases are alkaline substances and may be strong or weak (Morton et al, 2005; Woodrow, 2004; Lynes, 2003). Bicarbonate (HCO3-) is one example of a base.

 

 

The more H+ that exist in solution the more acidic the solution becomes. The more HCO3- present the more alkaline the solution becomes (Marieb, 2003; Heitz and Horne, 2001). Hydrogen ions and bicarbonate ions are involved in practically all biochemical processes.

 

 

Normal body processes produce more acids than bases. For example, carbonic acid is made available from the carbon dioxide (C02) released during cellular respiration and hydrochloric acid is formed within the gastric tract and this acidifies the blood by contributing to the H+ concentration. Accordingly the body needs more HCO3- than it needs carbonic acid.

 

 

The basic function of cells is modified by any departure from the normal range of concentration of these ions. For this reason, the acids and bases that are constantly formed in the body must be kept in balance (Tortora and Derrickson, 2005) and problems arise when this delicate balancing act breaks down.

 

 

The overall acid-base balance is maintained by controlling the H+ concentration of body fluids. Homeostatic balance of pH relies on a narrow normal range of 7.35-7.45 and this is achieved by three mechanisms:

 

 

- Buffer systems;

 

 

- Respirations;

 

 

- Excretion by the kidneys (Tortora and Derrickson, 2005).

 

 

pH and hydrogen

 

 

The pH is defined as the concentration of H+ and arterial blood is normally slightly alkaline (7.35-7.45). A pH within this range represents a balance between the percentage of hydrogen ions and bicarbonate ions. Generally, pH is maintained in a ratio of 20 parts bicarbonate to one part carbonic acid (Tortora and Derrickson, 2005; Heitz and Horne, 2001). A pH below 6.8 or above 7.8 is usually fatal (Pruitt and Jacobs, 2004; Lynes, 2003). There is an inverse relationship between H+ concentration and pH value. As the concentration of H+ increases, pH decreases and as the concentration of H+ decreases the pH increases (Resuscitation Council (UK), 2004; Horne and Derrico, 1999).

 

 

Buffer systems

 

Chemical buffers in the blood, intracellular fluid and interstitial fluid act within seconds to protect tissues and cells by neutralising the harmful effects of any change in pH until other regulatory mechanisms take over. However, the effect is limited (Heitz and Horne, 2001).

 

 

The buffers prevent major changes in the pH of body fluids by removing or releasing H+ (Metheny, 2000) and they act like chemical sponges which soak up the problems of too much acid or can be wrung out to release acid when too much base is present (Simpson, 2004). The main chemical buffers are bicarbonate, phosphate and protein.

 

 

Carbonic acid-bicarbonate buffer system

 

 

The key buffering system for maintaining acid-base balance in the blood is the carbonic acid (H2C03) - bicarbonate (HCO3-) buffer. H2CO3 functions as a weak acid and sodium bicarbonate (NaHCO3) as a weak base (Tortora and Derrickson, 2005).

 

 

Strong acids combine with bicarbonate to make weak acids and strong bases combine with weak acids forming a neutral solution (Marieb, 2003). The kidneys assist the bicarbonate buffer system by regulating the production of bicarbonate. The lungs assist by regulating the production of carbonic acid.

 

 

Phosphate buffer system

 

 

This system acts in essentially the same way as the carbonic acid - bicarbonate system and depends on a series of chemical reactions to minimise pH changes. The phosphate buffer system is an important regulator of pH both in intracellular fluid and in the kidney tubules, where phosphates exist in greater concentrations. The phosphate buffer system aids in the excretion of H+ in the renal tubules. Released sodium ions form NaHCO3 that passes into the blood. The H+ that replace sodium are excreted in the urine. The kidneys help to maintain the pH by increasing the acidity of urine (Marieb, 2003).

 

 

Protein buffer system

 

 

Proteins in plasma and within cells are the body’s most plentiful and powerful source of buffers and make up the protein buffer system by binding with acids and bases to neutralise them (Tortora and Derrickson, 2005; Marieb, 2003). In the red blood cells haemoglobin functions as an intracellular buffer by combining with H+.

 

 

Haemoglobin - oxyhaemoglobin buffer system

 

 

This is an effective mechanism that buffers carbonic acid in red blood cells. When blood moves from the arterial end of the capillary to the venous end C02, from cellular respiration, enters the red cells and combines with H2O to form H2CO3.

 

 

Simultaneously, oxyhaemoglobin gives up its oxygen to the body cells and some becomes reduced haemoglobin carrying a negative charge. H+ are attracted to the haemoglobin from the H2C03 forming a weak acid (Tortora and Derrickson, 2005). This is the reason why haemoglobin gives up oxygen in the partial presence of C02.

 

 

Regulation by the respiratory system

 

Regulation of acid-base balance by the respiratory system has up to twice the buffering power of all the chemical buffers combined (Marieb, 2003). The system uses hypoventilation or hyperventilation as needed to regulate excretion and retention of acids within minutes of a change in pH (Morton et al, 2005; Woodrow, 2004; Marieb, 2003).

 

 

Chemoreceptors in the medulla of the brain sense pH changes and vary the rate and depth of breathing to compensate (Tortora and Derrickson, 2005). Breathing faster or deeper eliminates more C02 from the lungs. As C02 is lost less carbonic acid is produced and the pH rises. The body regulates this pH change by reducing C02 excretion, by slower and shallower breathing (Woodrow, 2004; Marieb, 2003).

 

 

It should be noted that the respiratory system cannot correct imbalances completely but with healthy lungs it is 50-70% effective (Heitz and Horne, 2001). The kidneys are responsible for long-term adjustments to pH.

 

 

Kidney excretion

 

The kidneys maintain acid-base balance in the body by reabsorbing acids and bases as needed or by excreting them in urine. Renal regulation can restore normal H+ concentration within hours or days (Simpson, 2004; Woodrow, 2004). To raise blood pH the renal tubules excrete H+ into the filtrate resulting in the urine becoming more acidic than normal. The kidneys also participate in the regulation of blood pH by increasing or decreasing HCO3- concentration in the blood (Tortora and Derrickson, 2005).The kidneys do this by regulating reabsorption of HCO3- and generating more HCO3- to replace that lost in the buffering of acids.

 

 

Conclusion

 

This article has reviewed why blood gases are taken and the physiological processes that maintain blood gases within normal ranges. The second part of this two-part series will outline how the results of blood gases can be interpreted in clinical practice.

 

 

Box 1. Indications for arterial blood gas analysis

 

- Establish the diagnosis and severity of respiratory failure

 

 

- Evaluate intervention, for example, oxygen therapy, respiratory support, alkali treatment

 

 

- Manage critical care patients with conditions such as cardiac failure, sepsis, burns

 

 

- Assess condition immediately following cardiorespiratory resuscitation

 

 

- Establish a baseline before surgery

 

 

- Monitor patients during or after cardiothoracic surgery, sleep studies, cardiorespiratory exercise testing

 

 

- Determine prognosis in critically ill patients

 

 

Box 2. The arterial blood sample

 

Taking the sample

 

 

- Arterial blood sample is obtained by a one-off arterial puncture (called an ‘arterial stab’) or is taken from an indwelling arterial catheter that enables blood to be sampled more frequently and painlessly.

 

 

- An arterial stab is performed with a needle (usually 21 gauge or smaller) attached to a syringe that is pre-filled with heparin (0.1-0.2ml of 1000iu heparin/ml) (Bourke, 2003; Docherty, 2002) to prevent the sample from clotting.

 

 

- The size of the syringe and the amount of blood drawn for arterial blood gas sampling ranges from 0.5ml, for children, to 3ml depending on local policy.

 

 

- The needle is usually inserted into the radial artery - but brachial or femoral arteries can be used in patients who have poor perfusion of blood.

 

 

- The blood should fill the syringe under its own pressure with a pulsatile action.

 

 

- Following an arterial puncture pressure should be applied to the arterial site for five minutes to prevent bleeding and reduce bruising (Woodrow, 2004; Docherty, 2002). This time period may need to be extended if the patient has prolonged clotting time or bleeding disorders.

 

 

- Capillary blood can also be taken from the earlobe for occasional ABG samples and this technique is considered by many to be less painful and less invasive than an arterial ‘stab’ (Dunn and Connelly, 2001).

 

 

Part two will be published in the 14 November 2006 issue.

 

 

This article has been double-blind peer-reviewed.

 

 

For related articles on this subject and links to relevant websites see www.nursingtimes.net

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