CLINICAL
systems of life
Potential hydrogen concentration (pH)
Blood pH is monitored to ensure that when it
deviates from the norm clinical care is adapted to
resolve the underlying issue (Docherty, 2002b). A pH
either less than 7.0 or above 7.8 is incompatible with
cellular metabolism and is therefore life-threatening
(Proehl, 1999). Low (acidic) pH is often considered to
be acute, while more serious high (alkalotic) pH is
often due to chronic medical conditions such as
chronic renal failure and is less easy to resolve in the
short term (Pruitt and Jacobs, 2004; Woodrow, 2004).
Johnny Zygo
Homeostatic control
There are two main components of acid-base
homeostatic control: respiratory and metabolic. Both
work to correct imbalance. As a general rule, a
respiratory abnormality will correct itself within
hours, whereas a metabolic abnormality may take up
24
u
Fig 1. Carbon
Dioxide Dissociation
CO2+H2O
Carbonic
anhydrase
tH CO
Plasma
3
t
HCO
tH
3
+
t
2
–
t
This article, the second in this series on homeostasis
and its role in maintaining stable bodily conditions,
discusses acid-base balance and explores blood gas
analysis, related conditions and nursing care.
Blood acid-base balance is under homeostatic
control through the nervous and endocrine systems,
which maintain normal levels of components in the
blood. This ensures that cellular processes are
optimised and not life-threatening (Tortora and
Grabowski, 2002). The normal components in the
blood are shown in Table 1.
The pH of blood reflects the number of hydrogen
ions in it – either too few or too many results in
cellular dysfunction and inadequate oxygen
transportation around the main body organs. This in
turn leads to tissue hypoxia and results in tissue
death if it is not reversed (Tortora and Grabowski,
2002; Adam and Osborne, 1997). Although carbon
dioxide (CO2) does not contain hydrogen ions it
rapidly reacts with water to form carbonic acid
(H2CO3), which further dissociates into hydrogen and
bicarbonate ions (HCO3–). This reaction is shown as
CO2 + H20 ⇔ H2CO3 ⇔ HCO3– + H+ (Proehl, 1999; Adam
and Osborne, 1997) (Fig 1).
CO2
t
Authors Brendan Docherty, MSc, PGCE, RN, is
patient access manager, executive director’s unit,
Prince of Wales Hospital, Sydney, Australia; Colette
Foudy, GradDip, RN, is clinical care coordinator,
intensive care unit, St George Private Hospital,
Sydney, Australia.
t
Homeostasis part 2: acid-base balance
-
HCO3
C1-
tH +HbDHHb
+
Carbon dioxide
transport in the
blood and
haemoglobin
buffering
Blood
brain
barrier
Chemoreceptors in medulla-sensitive to H+
u
Fig 2. Controlling
the acid-base balance
To respiratory centres
to 2–3 days to correct (Resuscitation Council (UK),
2000; Proehl, 1999). In respiratory dysfunction CO2
levels deviate from the norm. They are usually raised
as a result of inadequate breathing, which leads to
excess CO2 combining with water to form carbonic
acid. This in turn lowers the blood pH, resulting in
blood acidosis (Docherty, 2002b).
The respiratory system alters CO2 levels to
counteract changes in blood pH. In low pH (acidosis)
the medulla oblongata increases the respiration rate
and depth to correct the excessive CO2 level in the
NT 11 April 2006 Vol 102 No 15 www.nursingtimes.net
keywords n Homeostatic control n Acid-base balance n Acidosis n Alkalosis
Table 1. normal values of blood acid-base balance (1kPa = 7.5mmHg)
Item
Normal value
Notes
pH – potential hydrogen
concentration
7.35 to 7.45
<7.35=acidosis
>7.45=alkalosis
SaO2 – saturation of arterial
oxygen
10 to 14 kPa or
75 to 105 mmHg
Lower values are hypoxic. Ensure
haemoglobin is normalised
SaCO2 – saturation of arterial
carbon dioxide
4 to 6kPa or
30 to 45mmHg
Higher values are acidotic,
lower values are alkalotic
BE – base excess
-2 to +2
Negative values are acidotic,
positive values are alkalotic
Bicarbonate
22 to 26mmol/L
Lower values are acidotic,
higher values are alkalotic
(Pruitt and Jacobs, 2004; Woodrow, 2004; Docherty, 2002b)
blood (Tortora and Grabowski, 2002). In some
patients, especially those with underlying chronic
airway conditions or those who are neurologically
unstable, this change in respiratory function to correct
the acid-base imbalance (Fig 2) can make them tire
easily and respiratory support may be required, such
as continuous positive airway pressure or mechanical
ventilation (Docherty, 2002b). However, patients with
chronic airways disease are able to live normally with
a high CO2. In fact they require it as a stimulus to
breathe. In these patients restoration of CO2 should
be back to their usual level and not the normal
values listed in Table 1.
In high pH (alkalosis) the opposite will happen to
assist in retaining CO2 in the blood – resulting in more
hydrogen ions to counteract the alkaline effect.
In metabolic imbalance anaerobic processes
replace the normal oxidative metabolism, leading to
the formation of lactic acid in the blood (Tortora and
Grabowski, 2002). This lowers the pH, resulting in
blood acidosis. The metabolic (renal) system will
control bicarbonate levels to alter pH.
In low pH (acidosis) the base excess (alkali level)
will be negative indicating metabolic acidosis and the
acids must be neutralised (possibly by diluting with
additional fluid management), excreted by the
kidney or metabolised by increasing bicarbonate
levels (Woodrow, 2004; Adam and Osborne, 1997).
In high pH (alkalosis) the opposite will happen,
resulting in less bicarbonate production or reduced
renal clearance. Bicarbonate is an effective buffer but
should only be used in documented severe acidosis
(pH<7.1) as it releases more CO2 when it is
metabolised. It therefore improves the acidosis
initially but then worsens it if respiratory
compensations are not effective (RCUK, 2000).
NT 11 April 2006 Vol 102 No 15 www.nursingtimes.net
Other factors
In acid-base balance other factors are involved in the
homeostatic control of the vital components. These
have their own homeostatic mechanisms, which
should be considered when looking at the patient
holistically. They include:
1. Haemoglobin – The amount of haemoglobin in the
blood affects its oxygen-carrying capacity. When this
is identified, for example, through cyanosis, action
should be taken to restore the correct level, because
the body’s own homeostatic mechanisms take several
days to work. This may be too long in the acute
setting (Proehl, 1999).
Haemoglobin also acts as a buffer to hydrogen
ions in red blood cells, so in acidosis in low
haemoglobin states the cells are less able to buffer
the acidic effect as efficiently (Woodrow, 2004).
2. Temperature – Temperature will impact on the
amount of oxygen dissociation from oxyhaemoglobin
molecules in the circulating blood, and so this should
also be considered and corrected where possible
(Adam and Osborne, 1997).
3. Blood pressure – The cardiovascular system
should be sufficiently strong to circulate adequate
volumes of blood around the body and if there is
heart failure (for example low cardiac output) this will
impact on the delivery of oxygen to tissues and the
clearance of waste products such as carbon dioxide
(Proehl, 1999; Smith, 2000).
Where possible, support should be given if the body’s
own mechanisms are unable to cope with the demand.
This might be in the form of fluid management (for
example blood cells or crystalloid), drug therapy (for
example inotropic support) or mechanical support (for
example a pacemaker or intra-aortic balloon pump)
(Docherty, 2002a; Smith, 2000). n
References
Adam, S., Osborne, S. (1997).
Critical Care Nursing: science and
practice. Oxford: Oxford University
Press.
Docherty, B. (2002a)
Cardiorespiratory physical
assessment for the acutely ill: part
1. British Journal of Nursing; 11:
11, 750–758.
Docherty, B. (2002b)
Cardiorespiratory physical
assessment for the acutely ill: part
2. British Journal of Nursing; 11:
12, 800–807.
Proehl, J.A. (1999) Emergency
Nursing Procedures. Philadelphia,
PA: W.B. Saunders.
Pruitt, W.C., Jacobs M. (2004)
Interpreting arterial blood gases:
easy as ABC. Nursing; 34: 8, 50–53.
Resuscitation Council (UK) (2000)
Advanced Life Support. London:
RCUK.
Smith, G. (2000) Acute Lifethreatening Events Recognition
and Treatment Manual.
Portsmouth: Open Learning,
University of Portsmouth.
Tortora, G.J., Grabowski, S.R.
(2002) Principles of Anatomy and
Physiology. Chichester: John Wiley
& Sons.
Woodrow, P. (2004) Arterial blood
gas analysis. Nursing Standard; 18:
21, 45–55.
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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