A complete history and physical ex- amination are essential to determine the cause of a discovered disorder. Acid-base The initial laboratory investigation of a suspected acid-base disturbance is assessment of arterial blood gases disturbances in and serum electrolytes. Further tests to differentiate the various causes of an identified disorder might then be the emergency indicated. Physiology department Fluctuations in the acidity of body fluids are resisted by several buffer systems. A buffer is a substance that Part 1: Piecing the clues together is able to absorb or donate hydrogen (H') ions. Equation I represents buff- TIMI E RUTLEDC1)E, MID, C1CP(EM) ering; the reaction can be driven ei- ther way, depending on whether there is a deficit or an excess of H+ ions. 1. HA H++A cid-base disorders reflect effects, including confusion and The pH of a solution containing this 4 * disturbances of hydrogen seizures.-' buffer system is determined by the ion homeostasis. Human An acidosis is a pathologic process Henderson-Hasselbalch equation: extracellular fluid pH (the that tends to push blood pH dow-n- negative logarithm ofthe hydrogen ion ward. An alkalosis, on the other hand, 2. pH = pKa + log[A ]/[HA] concentration) is normally maintained pushes the pH upward. An acidosis between 7.35 and 7.45. A plasma pH and an alkalosis can co-exist in a mixed In this equation Ka is the dissociation below 7.35 is termed acidemia, and a acid-base disorder; the pH then de- constant of the weak acid HA. The pH above 7.45 is termed alkalemia. pends on the dominant process. Respi- negative logarithm ofthis constant, or Numerous disease states can alter ex- ratory disorders result when either of pKa, is inversely proportional to the tracellular fluid pH significantly with these processes are caused by an accu- strength of the acid. The most effec- adverse physiologic effects. mulation or reduction of volatile acid tive buffers are those with pKas close Severe acidemia (pH < 7.20) has (CO*). An accumulation or a deficit of to physiologic pH. been shown to decrease myocardial non-volatile (or fixed) acid will result in The buffers in human blood in- contractility,' lower the threshold for metabolic disorders. These are con- clude bicarbonate, proteins, hemoglo- ventricular fibrillation,2 and diminish ventionally indicated by changes in the bin, phosphates, and sulfates. Bone the pressor response to catechola- blood bicarbonate concentration, or contains a large reservoir of fixed bi- mines.3 Hypotension and pulmonary [HCO, ]. carbonate and is capable of buffering edema can result, further complicat- Any patient with markedly abnor- a significant proportion of acute acid ing the patient's course. mal vital signs should be suspected of loads.) The isohydric principle stipu- Alkalemia causes a shift in the oxy- having an acid-base disturbance. Par- lates that all buffer pairs in a mixed sys- gen dissociation curve to the left (due ticular attention should be given to tem are in equilibrium with the same to an increased affinity ofhemoglobin the patient's respiratory rate, breath- H+ ion concentration, or [H+]. Mea- for oxygen) which impairs oxygen de- ing pattern, and breath odor (eg, the surements of one buffer system will livery to tissues. Severe alkalemia acetone smell of ketoacidosis or therefore reflect changes in the whole (pH > 7.55) can result in tissue hypo- tell-tale odors of certain intoxicants). acid-base system. xia, muscular irritability, cardiac ar- Patients with evidence of impaired The bicarbonate-carbonic acid rythmias, and central nervous system peripheral vascular perfusion or a di- buffer system is used clinically for the . e . * -. --*. O 0 0 O O 0 0 0 0 0 0 - 0 0 0 0 0 0 minished level of consciousness assessment of acid-base problems. It Dr Rudedge is a Iecturer in the Departenit should also have their acid-base status is the predominant extracellular fluid ofFamily and Commmuniy AIedicine, University determined. In general, the sicker pa- buffer system and is easily measured, of Tomnto, and is afull-time staff emegeny tients are, the more likely they are to providing information about both the physician at Alount Sinai Hospital, Towonto, Ont. have an acid-base disturbance. respiratory and metabolic factors de- 2254 Canadian Family Pyvsician \0I. 37(October 1991 termining acid-base status. The 1. FOR HYDROGEN IONS chemicalhermical equationeqationd fforisethissyus.Themsystem iS: Table RULES ESTIMATING FROM pH 3. HCO3 + H+ < H9CO1 =I11 _ H20 +C02I Carbon dioxide is produced daily Subtrat the last 2 digits of the pH pH [H+] in nmol/L by the complete metabolism of fat from 40. Then add the resul to 7.25 55 and carbohydrate; in solution it is hy- 40 = [HI in nmol/L drated by carbonic anhydrase, a 7.30 50 readily reversible reaction, to form 7.35 45 carbonic acid. The ventilatory system 7 under normal circumstances main- Rule 1 applies to pH values between 7.20 and 7.50 (in tihis 7.4040 tains the partial pressure of CO2 range the relationship between pH and [H ] is almost linear). 7.4535 (PC02) at 40 mmHg. Thus, carbonic acid has an open-ended ventilatory outlet (hence the term "volatile acid"). Non-volatile acid is produced dail by the metabolism of dietary precur- sors. These acids consume bicarbon- ate. Just as the lungs regulate carbon- When pH = 7.00, [H+I = 100 nmol/L pH [HI] in 1,1/Lam ic acid, the kidnieys are responsible for For each 0.10 incease in pH, HI is 80% 6.90 125 maintaining bicarbonate. Bicarbon- of the previous value (ie, multiply by 6 1 ate is generated in the kidney largely 0.8). Conversely, if the pH is < 7.00, 7.00 100 by metabolizing glutamine to ammo- divide by 0.8 (or multiply by 1.25) for 7.10 80 nium and bicarbonate, and excreting eac 0.10 unit decrease in pH. 7.20 64 ammonium ions in the urine." The Henderson-Hasselbalch 7_5 _ 32J_ erson-Hasselbequa- Rule 2 applies to pH values < 7.20 and pH volues > 7.50 (non- dlontionforforthethiss buffer system is: * Iinear ranges). Adjust value for each 0.10 unit decrease in pH. 7.6026 log[HCO1 4. pH = pK + [H2C03] [H2CO3j1 a[H+] = 40 nmol/L at pH of 7.40. Laboratories do not routinely measure [HCO3] or [H2COjd. Total At present, the acidity of body cess ofthat disorder. For example, the CO2 is a measure of blood HCO3, fluids is commonly measured and ex- compensation for a primary respira- H2CO3, and dissolved CO2. It is com- pressed as pH. Because the use ofpH tory acidosis is a metabolic alkalosis, monly substituted for [HCO3 ], as has some theoretical8 and practical and vice versa. HCO3 accounts for most of the total disadvantages, an increasing number Respiratory compensation for a CO2. The pCO2 is directly propor- of laboratories are now making avail- primary metabolic disorder occurs tional to [H2CO3] and therefore can able [H+] in nmol/L. The rules in relatively quickly by an appropri- be substituted for it as long as the dis- Table I allow one to quickly estimate ate ventilatory response. Metabolic sociation constant is adjusted. Kassir- [H+] from pH. The Henderson equa- compensation, however, occurs in two er and Bleich7 rearranged equation 4, tion should always be used to check phases. Acute metabolic compensation cancelling the logarithms and using lab results for sampling errors, lab er- occurs within the first 12 to 24 hours. the above substitutions. The result rors, or transcription errors. It is predominantly achieved through was an equation of great clinical util- buffering by hemoglobin and by buff- ity known as the Henderson equation: Compensation ers in bone and other tissues. Plasma When buffering is not enough to pre- [HCO3] changes only slightly. vent a change in pH due to a primary Chronic metabolic compensation 5. [H+] = 24pCO2 [HCO3 ] acid-base disturbance, compensation takes 1 to 5 days, which is the time it occurs. Compensation is a physiolog- takes for the kidneys to adjust the This equation emphasizes the inter- ic response to a primary disorder and plasma [HCO3]. dependence of the three main indices is not a second acid-base disturbance. Primary acid-base disturbances routinely measured to assess acid- The compensation for a primary dis- have been studied extensively to de- base status. order is the opposite physiologic pro- termine expected degrees ofcompen- Canadian Family Physician VOI 37: October 1991 2255 sation. Table 2 lists rules ofcompensa- Anesthesiologists who take part in tion that have been compiled from cardiac bypass surgery probably have previously published data.8-'2 If a the most experience with patients at compensatory process falls out of the hypothermic temperatures. Adult by- range of the expected response, then pass surgery is commonly done with a mixed acid-base disturbance exists. patients at 28°C and with neonates as low as 5°C. The trend among these Diagnosing acid-base anesthesiologists is to normalize the disturbances uncorrected arterial blood gases dur- A simple primary acid-base distur- ing these procedures. Corrected arte- bance always co-exists with a com- rial blood gas results in hypothermic pensatory process. The only compen- patients are difficult to interpret and satory process that is complete (ie, have little clinical relevance.'3 Until results in a normal pH) is the meta- proven otherwise, uncorrected arteri- bolic response to a sustained respira- al blood gas results should probably tory alkalosis.8 This requires at least be used to assess and manage 2 weeks and occurs at high altitudes acid-base disturbances in hypotherm- because of hypoxia-induced hyper- ic patients. ventilation. Therefore, with this ex- ception, the primary acid-base distur- The physiochemical approach bance is the process that is the furthest Within the last decade there has been from normal.