Intensive and Critical Care Nursing (2008) 24, 28—40 ORIGINAL ARTICLE Pathophysiology of acid base balance: The theory practice relationship Sharon L. Edwards ∗ Buckinghamshire Chilterns University College, Chalfont Campus, Newland Park, Gorelands Lane, Chalfont St. Giles, Buckinghamshire HP8 4AD, United Kingdom Accepted 13 May 2007 KEYWORDS Summary There are many disorders/diseases that lead to changes in acid base Acid base balance; balance. These conditions are not rare or uncommon in clinical practice, but every- Arterial blood gases; day occurrences on the ward or in critical care. Conditions such as asthma, chronic Acidosis; obstructive pulmonary disease (bronchitis or emphasaemia), diabetic ketoacidosis, Alkalosis renal disease or failure, any type of shock (sepsis, anaphylaxsis, neurogenic, cardio- genic, hypovolaemia), stress or anxiety which can lead to hyperventilation, and some drugs (sedatives, opoids) leading to reduced ventilation. In addition, some symptoms of disease can cause vomiting and diarrhoea, which effects acid base balance. It is imperative that critical care nurses are aware of changes that occur in relation to altered physiology, leading to an understanding of the changes in patients’ condition that are observed, and why the administration of some immediate therapies such as oxygen is imperative. © 2007 Elsevier Ltd. All rights reserved. Introduction the essential concepts of acid base physiology is necessary so that quick and correct diagnosis can The implications for practice with regards to be determined and appropriate treatment imple- acid base physiology are separated into respi- mented. ratory acidosis and alkalosis, metabolic acidosis The homeostatic imbalances of acid base are and alkalosis, observed in patients with differing examined as the body attempts to maintain pH bal- aetiologies. By understanding normal physiological ance within normal parameters. principles and how they relate to clinical situations can enhance patient care. A good understanding of General principles of acid base balance ∗ Present address: Department of Pre-registration Nursing, Faculty of Health Studies, Buckinghamshire Chilterns Univer- sity College, United Kingdom. Tel.: +44 1494 522141x2123 The primary function of the respiratory system is to (Off.)/1442 876772 (Res.); fax: +44 1494 603182. supply an adequate amount of oxygen (O2) to tis- E-mail address: [email protected]. sues and remove carbon dioxide (CO2). The kidneys 0964-3397/$ — see front matter © 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.iccn.2007.05.003 Pathophysiology of acid base balance 29 Table 1 The major body buffer systems Site Buffer system Description Interstitial fluid (ISF) Bicarbonate For metabolic acids Phosphate and protein Not important because concentration is too low Blood Bicarbonate Important for metabolic acids + Haemoglobin Important for buffering CO2 and H Plasma proteins Minor buffer Phosphate Concentration too low Intracellular fluid Proteins Important buffer of extracellular H+ Phosphates Important buffer Urine Phosphate Responsible for most of titratable acidity + + Ammonia Important—–formation of NH4 and hence excretion of H Bone Calcium carbonate In prolonged metabolic acidosis will excrete any excess acids or alkali. The respi- Partial pressure of gases ratory and renal organs together with the buffering effects of blood maintain hydrogen ion (H+) con- Dalton’s law explains the partial pressure of a gas, centration. H+ concentration is one of the most which is the pressure exerted by a gas within a mix- important aspects of acid base homeostasis. When ture of gases independent of each gas in the mixture there is an increase or decrease in acid production, (Marieb, 2004). The partial pressure of each gas − blood bicarbonate (HCO3 ), proteins, and phos- is directly proportional to its percentage in the phate buffer body fluids (Table 1). However, there total mixture and in air is determined by atmo- comes a point in the disease process when these spheric pressure. Atmospheric pressure is 101 kPa buffers can no longer maintain appropriate concen- (760 mmHg), 21% of this air is oxygen, and the par- + trations of H . Patients admitted to hospital can tial pressure of oxygen (PO2) in atmospheric air is: have life threatening situations such as diabetic 21 ketoacidosis, asthma, severe vomiting, which alter × 101 = 21.2kPa pH balance and exacerbate their problems. 100 To maintain homeostasis during stress/strenuous exercise and/or illness/diseased states there is Within the alveoli the PO2 is different to air generally an increase in depth and rate of breathing because of enrichment in the air passages (dead due to stimulation of the sympathetic nervous sys- space) with CO2 and water vapour. Alveolar air con- tem (Richardson, 2003). High alveolar ventilation tains much more CO2 and water vapour and much less O and so makes a greater contribution to the brings more O2 into the alveoli, increasing O2, and 2 near-atmospheric pressure in the lungs, then they rapidly eliminating CO2 from the lungs (for chemical abbreviations see Table 2). do in air. This is due to: • gas exchanges occurring in the lungs, • humidification of air by the conducting passages, Table 2 Chemical abbreviations • mixing of gases in the dead space (contains air not involved in gaseous exchange) between the Abbreviation Interpretation nose and alveoli. O2 Oxygen CO2 Carbon dioxide In alveoli, PO2 averages only 13.2 kPa kPa Kilo pascals (100 mmHg). Continuous consumption of O2 PO2 Partial pressure of oxygen and production of CO2 in the cells means that PCO2 Partial pressure of carbon dioxide there is a partial pressure gradient both in the H+ Hydrogen ions lungs and at the tissue level ensuring diffusion of HCO − Bicarbonate ions 3 oxygen into the blood and CO2 from it (Waterhouse H2CO3 Carbonic acid and Campbell, 2002). Na+ Sodium + Changes in partial pressures of carbon dioxide K Potassium + − (PCO ) and H are sensed directly by the respira- Cl Chloride 2 + tory centre central chemoreceptors in the medulla NH4 Ammonium (Guyton and Hall, 2000). In contrast, a reduction 30 S.L. Edwards in PO2 is monitored by the peripheral chemorecep- blood cells) and breaks down into CO2 and water − tors located in the corotid and aortic bodies which (H2O) (Fig. 1). The CO2/HCO3 interaction is slow transmit nervous signals to the respiratory centre in plasma, but quicker in red blood cells due to the in the medulla for control of respiration (Schlichtig presence of carbonic anhydrase. et al., 1998; Williams, 1998). However, it is the CO ‘drive’ for breathing that dominates in health, 2 Respiratory disorders although the O2 ‘drive’ can be significant in some disordered states as an adaptation to chronic eval- Acid base disorders resulting from primary alter- uations of PC0 for example in chronic obstruction 2 ations in the PCO are termed respiratory disorders. lung conditions. 2 Any increase in concentration or retention of CO2 (considered a volatile source of acid which Metabolic generation of acids and alkali evaporates rapidly in body fluids) i.e. produc- tion > excretion will produce an increase in H+ Each day the body produces acids through normal through the generation of carbonic acid (H2CO3) metabolism, and acid or alkali is ingested in diet (Fig. 1). This lowers the pH and thus promotes the (Koeppen, 1998). The lungs release or strengthen development of a respiratory acidosis observed in the bond to acids as necessary and the kidneys also conditions where CO2 excretion is impaired such effectively eliminate or reabsorb acids, so there is as chronic obstructive pulmonary disease (COPD) no impact on whole body acid base status. If there (Koeppen, 1998). is an increase in production of acids, the body has Decreases in PCO2 concentration i.e. if excretion a number of buffers outlined in Table 1. If there is greater than production, will result in a decrease is a reduction in acids or loss of acids the excess in H+. The pH will rise and a respiratory alkalosis − + + bicarbonate (HCO3 ) is buffered by H to minimise results from a decreased concentration of free H . any change in pH. This is seen in conditions such as hyperventilation where CO2 excretion is excessive. The lungs there- fore play a major role in ensuring maintenance of Normal pH and hydrogen ion concentration H+ ion concentration (Guyton and Hall, 2000). of body fluids The pH is related to actual H+ concentration Metabolic disorders (Guyton and Hall, 2000). A low pH corresponds to a high H+ concentration and is evidence of an aci- Disorders of acid base physiology of non-respiratory dosis, and conversely a high pH corresponds to a origin are metabolic disorders and result from low H+ concentration known as an alkalosis. The abnormal metabolism (Holmes, 1993). Metabolic + − interrelationships between O2,H ,CO2 and HCO3 disorders may be due to excessive intake of acid are central to the understanding of acid base bal- or alkali or due to failure of renal function. If non- ance and reflect the physiological importance of the respiratory acid production exceeds the excretion − − − + CO2/HCO3 buffer system (Fig. 1). The CO2/HCO3 of acid from the body HCO3 decreases, and H buffer system largely takes up the majority of the concentration increases as in a metabolic acidosis + + − excess H . The H + HCO3 converts into H2C03 in (Koeppen, 1998). The CO2 yielded in a metabolic the presence of carbonic anhydrase (present in red acidosis is lost via the lungs. This is achieved, as an + − Figure 1 The interrelationship between H ,CO2 and HCO3 in acid base balance. Pathophysiology of acid base balance 31 increase in H+ will reduce pH, immediately stimu- respiratory or metabolic acid base disorder can be lating central chemoreceptors increasing rate and determined and whether the respiratory system or depth of respiration. This can be observed in condi- kidneys are compensating. tions such as diabetic ketoacidosis (due to elevated When attempting to analyse a person’s acid H+ production) and renal failure (due to inadequate base balance, scrutinise blood values in the fol- + H excretion), and is referred to as ‘respiratory lowing order (Table 4).