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Arterial Blood Gas Analysis 2: Compensatory mechanisms

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ABSTRACT

Coggon, J.M. (2008) Arterial blood gas analysis 2: compensatory mechanisms. Nursing Times; 104: 19, 24–25.
This is the second of a two-part unit discussing arterial blood gas (ABG) analysis. Part 1 outlined background information on ABG reports and focused on a systematic approach to ABG analysis. This part examines the physiology of the various lines of defence in the body and explores the concept of compensation. A step-by-step guide to interpretation and examples of uncomplicated ABGs are available in the Portfolio Pages for this unit at nursingtimes.net, as well as further practice examples relevant to this part of the unit.

AUTHOR
Jacqueline Mandy Coggon, MSc Critical Care, BSc Health Care Practice, Dip Nursing, ENB 100, RGN,
is clinical educator for critical care, integrated critical care unit, King’s Mill Hospital, Sherwood Forest Hospitals NHS Foundation Trust.

Learning objectives

  1. When interpreting an ABG result, be able to distinguish between the primary disorder and any evident compensatory action occurring.

  2. Understand what the ABG shows and be able to relate this to the patient, their clinical presentation and immediate needs.

Click here for PDFs of the articles and the Portfolio Pages corresponding to this unit

First line of defence

When the body suffers pH balance disturbances (whatever the cause), various mechanisms are set in motion to try to regain normality and ultimately preserve life. Metabolic control is the first line of defence and involves an extremely complex buffering system. Buffers are actually weak acids or weak bases, and can be imagined as being like sponges. They can bring about pH changes by either ‘soaking up’ excess hydrogen ions or ‘wringing themselves out’ to release hydrogen ions until the problem can be rectified. Buffers are only temporary holding measures and their actions cannot be sustained indefinitely. The buffers in the body include phosphate, the carbonic acid-bicarbonate system and plasma proteins such as albumin.

Carbonic acid-bicarbonate system
The equation CO2 + H2O H2CO3 H+ + HCO3 is fundamental to understanding acid base balance. Central to the equation is carbonic acid, a weak acid that can split to the ‘left’ to form carbon dioxide and water, or to the ‘right’ to form hydrogen and bicarbonate.

When carbonic acid splits to form carbon dioxide and water, it can be excreted via the lungs and the kidneys respectively. When it splits to the right it forms hydrogen and bicarbonate. Bicarbonate can be excreted through the kidneys and can be lowered when used to ‘soak up’ excess acid in the blood.

Hydrogen is only excreted through the urine in exchange for retention of other ions, mainly sodium. Nurses can check the extent of hydrogen excretion, as ‘normal blood’ with a pH of 7.4 produces urine with a pH of 5.0 (Woodrow, 2006).

Second line of defence

When the buffers’ capabilities are exceeded, the second line of defence comes into action, which can be recognised within 2–3 minutes of a problem occurring. The chemoreceptors in the body sense the build-up of acids, and messages are sent via the respiratory centre to the lungs to increase the volume and rate of respiration.

Acids can be converted to CO2 by the carbonic acid-bicarbonate buffering system, and then expired from the body. Conversely, if the chemoreceptors sense a reduced amount of hydrogen ions in the blood, the respiratory centre will send messages to the lungs to slow down the respiratory rate and reduce the volume of expiration in an attempt to retain acid. When using early-warning scores to assess patients who are at risk of becoming critically ill, the altered respiratory rate that is often noticed first. A PaCO2 level below 4kPa causes alkalosis while a level greater than 6kPa causes acidosis.

Third line of defence

The last is the renal control mechanism of defence. It may be the slowest to initiate but is the most powerful. It often takes hours or even days before any compensation is evident (Simpson, 2004). However, in the very young (when kidneys are immature) and older people (when kidneys may be impaired), this defence mechanism may be diminished or absent. The kidney tubules can influence the blood’s pH by selectively reabsorbing and eliminating chemicals.

The kidneys alter the pH of the blood in several ways, which includes their ability to:

  • Retain bicarbonate and phosphate, in favour of hydrogen and chloride. This occurs when the body is acidiotic;

  • Retain hydrogen and chloride in favour of bicarbonate and phosphate. This occurs when the body is alkalotic;

  • Generate more bicarbonate and phosphate.

Compensation

As far as possible, the body will compensate for pH imbalances until all reserve is lost and it can no longer do so.

The older patients are, the more co-morbidities they may be likely to have, thus making compensation more difficult. Similarly, the more serious their condition, the less likely it is that they will be able to compensate.

Compensation involves trying to create a state of ‘opposites’. For example, a patient suffering from respiratory acidosis will try to create the opposite state of metabolic alkalosis in order to compensate. Similarly, a patient in respiratory alkalosis will try to move to a state of metabolic acidosis. The principle of compensation is easy to remember as follows – the opposite of respiratory is metabolic and the opposite of acidosis is alkalosis.

Determining the problem
When compensatory mechanisms occur it can be confusing at first to ascertain which abnormal parameter is the primary problem or underlying condition, and which constitutes compensation.

Nurses can make use of the ‘golden rules’ (discussed in the Portfolio Pages for this unit) and ascertain which parameter is moving in accordance with the pH. If the PaCO2 is moving in the opposite direction from the pH, the patient will have a respiratory disorder. If the HCO3 is moving in the same direction as the pH, the patient will have a metabolic disorder. This should then make the compensatory mechanisms more evident.

Compensation will involve the three main lines of defence discussed above, and it is only a temporary holding measure until the problem can be rectified. Metabolic conditions will be primarily compensated for by the respiratory system and respiratory conditions will rely on the renal system for compensation.

Chemical buffering
Chemical buffering also plays an important role and compensation can be partial or complete (although very rare), bringing the pH into the normal range. This can be confusing for inexperienced practitioners, who might see the pH between 7.35 and 7.45 and think that the patient is well. For this reason it is imperative to take 7.4 as the absolute normal and neutral pH (Woodrow, 2006). Anything less than this should be treated as acidotic and anything higher than this should be treated as alkalotic.

[sub]Situations that may lead to overcompensation
It is impossible for patients to overcompensate without external influences. However, in critical care it may be evident that, for example, inappropriate ventilator settings can lead to overcompensation or another problem.

Conclusion

ABG interpretation takes practice. The more that nurses use this skill, the more competent they will become. Practitioners should allow a senior colleague to check their interpretation and remember that the result is never considered in isolation from other factors and clinical findings.

Although oxygen is very important, it is not used in the actual diagnosis of the condition. Nurses can always add extra oxygen or reduce it accordingly. It is important that practitioners never remove oxygen to obtain a baseline ABG result on air. It is better to titrate the oxygen according to subsequent ABG results (also refer to the ‘10 less rule’ discussed in part 1 of this unit).

While patients are ill it is imperative that practitioners endeavour to treat the underlying cause, as compensation alone will not provide a cure. It must be recognised as a temporary holding measure. Practitioners should act on their instincts and be aware that there may be more than one failing system.


Key references

Simpson, H. (2004) Interpretation of arterial blood gases: a clinical guide for nurses. British Journal of Nursing; 13: 9, 522–527.

Woodrow, P. (2006) Intensive Care Nursing: A Framework for Practice (2nd ed). Oxford: Routledge.

  • The full reference list for this unit is available in the corresponding Portfolio Pages

Portfolio pages online

Portfolio Pages can be filed in your professional portfolio as evidence of your learning and professional development. They contain learning activities that correspond to the learning objectives in this unit, presented in a convenient format for you to print out or work through on screen.

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