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ACID-BASE PROBLEMS

ACID-BASE PROBLEMS. G M Kellerman Hunter Area Pathology Service. GENERAL CONSIDERATIONS - 1.

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ACID-BASE PROBLEMS

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  1. ACID-BASE PROBLEMS G M Kellerman Hunter Area Pathology Service

  2. GENERAL CONSIDERATIONS - 1 • Enzymes, membrane carriers and other components of the cell are proteins and their amino acid side chains have a mixture of + and – charges. Each protein has its optimal activity with an appropriate constellation of these charges, which is pH dependent. • Accordingly, there is a narrow optimum pH for the entire body, as the numerous proteins all have their own personal optimum and overlap of all of them is limited. • Outside this optimum pH range, viability declines in both the direction of acidosis (limit in plasma pH about 6.7 in young patients, 6.8-6.9 in elderly patients with many comorbidities) and alkalosis (limit about pH 7.7-7.8). • We can assess the acid-base status by measuring any pair of buffer components, and the CO2/bicarbonate pair is the most convenient.

  3. GENERAL CONSIDERATIONS - 2 • Metabolic sources of acid: quantitatively the greatest is CO2, of which we produce some 15000 mmols per day or even more with exercise or hard work. This is all removed by respiration and a disturbance in this process leads to a respiratory acidosis (less effective removal = hypoventilation) or a respiratory alkalosis (more effective removal = hyperventilation) • Far less quantitatively are other non-volatile acids, but they must be buffered in the body until the kidney can excrete them. Normally these are sulphuric (from aminoacids cystine/methionine) and phosphoric (from phospholipids), and a variety of organic acids such as lactic, ketone bodies and a number of abnormal toxic substances (methanol, ethylene glycol) which are metabolised to acids. • Lactic and ketone acids are normally metabolised almost completely and their accumulation signifies metabolic derangement. • Several rare genetic errors can lead to metabolic acidosis.

  4. GENERAL CONSIDERATIONS - 3 • Disturbances in the handling of these metabolic acid products lead to metabolic acidosis (accumulation of too much acid) or metabolic alkalosis (excretion of too much acid) • On relatively uncommon occasions, patients consume too much base (sodium bicarbonate for indigestion, rarer with PPI drugs) or have an almost exclusively vegetarian diet and metabolise components of the diet to excess bicarbonate. • Acid can be lost by stomach (vomiting), while bicarbonate can be lost by colon. • The major adjustment is made by the kidney, so disturbances of acid base metabolism frequently follow disordered renal function, either from metabolic changes in otherwise normal cells (low K alkalosis, renal tubular acidosis) or from loss of nephrons in renal failure.

  5. RESPIRATORY ACIDOSIS - 1 Remember the Henderson-Hasselbalch equation pH = pK + log [Base]/[Acid], in this case [bicarbonate]/[CO2] Consider the consequences of an acute rise in pCO2 When the pCO2 increases, without a corresponding increase in BIC, this ratio decreases, and its log, and the pH will decrease or in other terms, the H+ ion concentration will increase In consequence, some of this increased H+ will bind to proteins especially haemoglobin, with consequent increase in BIC The amount of increase in BIC in normal blood is about 1 mmol/L for each 10 mmHg increase in pCO2 above its normal 40 mmHg. The blood gas machine compensates for this chemical adjustment in calculating the Base Excess.

  6. RESPIRATORY ACIDOSIS - 2 Because CO2 diffuses rapidly through cell membranes and fluids, there is essentially a complete equilibrium between its concentration in the blood capillary and alveolar air. So inequalities of perfusion in different parts of the lung average out and the plasma pCO2 depends only on the volume of air respired each minute and the rate of production. Thus a respiratory acidosis, with increase in pCO2, results from hypoventilation. (Compare the different behaviour of oxygen) Frequent causes of hypoventilation include: Respiratory centre depression from brain stem pathology or depressant drugs such as opiates, barbiturates, anaesthetics etc Respiratory muscle weakness or fatigue, or painful respiration Obstruction anywhere in tracheobronchial tree from a multitude of conditions, or loss of lung volume from pneumothorax or effusion Stiffness or deformity in chest wall or costovertebral joints

  7. RESPIRATORY ACIDOSIS - 3 • When the respiratory acidosis has been present for some time, the kidney begins to compensate. This is believed to result from the increased pCO2 enabling a greater production of carbonic acid in the tubules, which ionises to BIC- + H+. The BIC is transported back to the plasma, and the H+ is excreted into the urine, bound to urinary buffers such as phosphate or ammonia. The resulting ammonium cation needs a chloride anion to maintain electrical neutrality, so there is a net loss of Cl- which is replaced 1:1 by BIC in the blood. • A normal kidney completes this compensation in 2-3 days, and the increase in plasma BIC is about 3.5 mmol/L for each 10 mmHg increase in pCO2. Damaged kidneys are slower and less effective. • This increase in BIC restores the BIC/CO2 ratio towards normal, and the pH rises towards normal, but stays at least a little lower. • The blood gas machine does not compensate for this BIC increase, it records it as a positive Base Excess

  8. RESPIRATORY ALKALOSIS - 1 • A decrease in pCO2 from any cause, without a corresponding decrease in BIC, will increase the ratio of BIC/CO2 and its log, so the pH will rise, that is the H+ concentration will fall. • A decrease in CO2 can result only from an increase in respiratory volume without an increase in CO2 production = hyperventilation. • Common causes of hyperventilation • Voluntary – but usually self limited • Anxiety states – acute or chronic • Many types of lung disease, via receptors in lung and transmitted via the vagus nerve • Severe hypoxia from any cause, severe anaemia • Respiratory stimulant drugs • Normal pregnancy

  9. RESPIRATORY ALKALOSIS - 2 • When the pCO2 falls and the H+ concentration falls, haemoglobin acts as an acid (instead of acting as a base in acidosis) and the H+ that it releases reacts with BIC in plasma to form CO2 which is expired. • The fall in plasma BIC averages about 2 mmol/L for each 10 mmHg fall in pCO2 in an acute episode. • The kidney compensates over 2-3 days by not making as much H+ as normal, because it has less CO2 to make carbonic acid, so that BIC is lost in the urine due to incomplete reabsorption of filtered BIC. Cl- is retained in its place if it is available in the diet. • This compensation restores the BIC/CO2 ratio towards normal and the pH falls towards normal, but usually stays a little higher. • The usual compensation is about 4 mmol/L decrease in BIC per 10 mmHg drop in pCO2 • The blood gas machine compensates for the acute change but shows the renal compensation for the chronic condition as a negative Base Excess

  10. METABOLIC ACIDOSIS - 1 • Addition of any acid other than CO2 results in combination of its H+ with BIC to form CO2 (expired) and the anion from the acid remains in the plasma replacing the BIC whose concentration decreases. • Thus the ratio of BIC/CO2 decreases, as does its log, and the pH falls • This change rapidly penetrates into and stimulates the respiratory centre so that the respiratory excursion is increased and the pCO2 is consequently lowered. • In contrast to the renal compensation for respiratory disturbances, which takes 2-3 days to be complete, the respiratory compensation for metabolic acidosis (or alkalosis) is very rapid. • Very approximately a decrease in BIC of 1mmol/L results in a decrease in pH of 0.01-0.015 and a decrease in pCO2 of approximately 1-1.5 mmHg if all else is normal, but when the BIC falls much below 10 mmol/L the changes are greater. These numbers depend on a normal respiratory function.

  11. METABOLIC ACIDOSIS - 2 • Common causes of metabolic acidosis are: • Failure of the kidney to excrete H+ appropriately – either a specific tubular defect in H+ generation or transport with normal GFR, or a low GFR due to a variety of damaging conditions. • Loss of BIC from bowel • Abnormally high amount of formation of acids in the body or abnormally low rate of removal, including: • Lactic acid is made normally and in increased amount in exercise or tissue anoxia, removed by gluconeogenesis in liver and a little in kidney. Excess production, or slow removal (liver pathology, metformin) cause accumulation • Ketone bodies (betahydroxybutyric acid and acetoacetic acid) from fatty acid oxidation accumulate in starvation and diabetic ketosis, in amounts greater than heart, brain and muscle can use.

  12. METABOLIC ACIDOSIS - 3 • Many foreign substances either act as acids, or are converted into acids by metabolism. • Common substances are: • Methanol which forms formic acid • Ethylene glycol (antifreeze) – glycolic, glyoxylic and oxalic acids • Acidic antibiotics such as some synthetic penicillin analogues can accumulate • Paracetamol and several other drugs detoxicated by glutathione can cause “pyroglutamic” acidosis • Many inborn errors (genetic lack of catabolic enzymes) cause acidosis due to accumulation of the products they cannot remove • Severe tissue breakdown as in rhabdomyolysis can cause acidosis

  13. METABOLIC ACIDOSIS – 4INVESTIGATIONS • The blood gas machine will show the BIC, pCO2 and pH, and will record an appropriate negative base excess • On the usual laboratory electrolyte picture we can calculate the “anion gap” which is a representation of the amount of unmeasured anions in the normal grouping of Na, K, Cl and BIC. These unmeasured anions are predominantly on proteins, especially albumin, + small quantities of some organic acids such as citrate, lactate etc, none at more than about 1-2 mmol/L. This anion gap (Na + K) – (Cl + BIC) is normally about 12 (7-17 range). • When the acidosis results from failure of the kidney selectively to secrete enough H+ – as in proximal or distal renal tubular acidosis – the decrease in BIC is balanced by an excess of Cl- because nearly all the other functions of the kidney are preserved. In such a case the “anion gap” is normal.

  14. METABOLIC ACIDOSIS – 5INVESTIGATIONS • When there is the accumulation of any normally present anion other than chloride, or any abnormal anion, then the “anion gap” will be increased because this other anion is not represented in the calculation. In principle, and approximately, the excess of the “anion gap” above 12 should be equal to the amount of the unmeasured extra anion, but all the measurements are plus/minus and exact correspondence is not to be expected to better than about 5 mmol/L. • These extra anions can be sulphate + phosphate in renal failure when GFR is not enough to clear normal production, or any of the other anions mentioned or others in the textbooks. • Remember that as albumin is the major contributor to the “anion gap” with its many negative charges, the “gap” depends on the plasma albumin level and in hypoalbuminaemia (common in sick patients) the normal “anion gap” is proportionately lower.

  15. METABOLIC ALKALOSIS - 1 • Increase in BIC without corresponding increase in CO2 increases the BIC/CO2 ratio and the pH • The respiratory centre compensates rapidly by decreasing the respiratory volume, so that pCO2 rises and the pH comes back towards normal, usually not quite there. • Even large intakes of alkali such as Na bicarbonate have little effect on plasma BIC, as the kidney has a great capacity to excrete both of the ions when they are in excess (normal filtrate has 4500 mmol/day BIC, and even 100g NaBIC is only 1200 mmol BIC). A high Ca intake, as with milk, can impair this excretion. • Most patients with metabolic alkalosis have a degree of effective circulating volume depletion with deficits of Na, K and/or Cl, and therapy aims to replete the missing ion(s)

  16. METABOLIC ALKALOSIS - 2 • Common causes include: • Gastrointestinal losses – vomiting, suction, antacids, high Cl- diarrhoea (genetic error in carrier, villous adenoma) • Renal losses – especially diuretics, excess mineralocorticoids • Ion exchange across cell membranes – hypokalaemia • Excess BIC or citrate administration • Most of these result in the “contraction alkalosis” where there is insufficient Cl- available due to selective losses (gut, sweat, kidney) and the only way to get rid of the excess BIC- would require loss of Na+ to balance its charge. The resultant loss of extracellular and intravascular volume would make the patient worse. • Blood gas machine shows a positive Base Excess

  17. COMBINED ACID-BASE PROBLEMS • While it is true that a great number of patients have a single condition of respiratory or metabolic origin, in referral level hospitals quite a high proportion have more than one disturbance. If the results do not fit one of the simple pictures already described, then it is necessary to look for these combinations, and the patient’s history is an essential part of this diagnostic procedure. • The blood gas machine results also frequently point to clues, so now we take a look at such a readout and “how to read and interpret a blood gas report”. • The machine uses ion selective electrodes to measure H, Na, K, Cl, Ca, different types but equally selective electrodes to measure CO2, O2, glucose, lactate, and absorbance at multiple wavelengths to measure haemoglobin and some of its fractions such as metHb, COHb. It calculates BIC from CO2 and pH, and the base excess.

  18. BLOOD GAS REPORT - 1 • My routine is as follows – you may like to vary it but be careful! • Look at pH – is it normal, high (suggests alkalosis) or low (acidosis) • Look at pCO2 – is it high (hypoventilation) or low (hyperventilation) • Look as Base Excess – is it within normal limits (suggests normal or an acute respiratory disturbance) or abnormal – suggests a metabolic disorder or renal compensation for respiratory problem • Do these numbers add up to one of the previously described pictures? Are the deviations from normal of the expected order of magnitude for the compensations already described? • Look at the K – does this fit with a hypokalaemic alkalosis? • Look at the pO2 and calculate the “A-a gradient” from A-a gradient = Inspired pO2 – (arterial pO2 + arterial pCO2 x 1.25) Is this normal for age, or is there evidence for V/Q mismatch? Then I look at anything else – Ca, Na, Hb, Lac, COHb etc Check the FiO2 and whether it is arterial or venous – if there!

  19. BLOOD GAS REPORT - 2 • Different blood gas analysers have different combinations of electrodes (the more you have, the more expensive it is!) • Some electrodes do not have absolute specificity (which can lead to errors) and this depends on the manufacturer’s choice of enzyme. • Thus some (but not all) glucose electrodes also measure maltose • Some (but not all) lactate electrodes also measure glycolate and D-lactate as well as the physiological L-lactate • Venous blood normally has: • pH about 0.05 units less than arterial • pCO2 about 5 mmHg higher than arterial • Base Excess much the same as arterial • BIC about 2 mmol/L more than arterial • pO2 much less than arterial – range 15-40 mmHg

  20. COMBINED A-B PICTURES - 1 • I shall list and discuss those that are commonest in our community – you may like to add others as necessary for your community • 1. Acute on chronic respiratory acidosis. This occurs when a patient with a chronic compensated respiratory acidosis suffers from an acute respiratory problem that further impairs respiratory excursion – such as respiratory tract infection of any type, muscle fatigue, opiate administration, general sepsis etc. The most obvious feature is that the pCO2 is higher than expected for the BIC, and the pH is lower than in a normally compensated state. The history is most helpful. In principle, a pCO2 >55-60 mmHg is not really compatible with any comfort – or even long term survival – because most of these patients have a large V/Q inequality and at this pCO2 their pO2 is usually <40 mmHg unless they can afford domiciliary O2 therapy (which many in Australia do use)

  21. COMBINED A-B PICTURES - 2 • 2. Combined metabolic and respiratory acidosis This most often occurs when a patient with a metabolic acidosis cannot increase respiration enough to compensate. Common causes could be a patient with sepsis and lactic acidosis with pneumonia and poor ventilation, or too much sedative: diabetic ketoacidosis that has been complicated by, or resulted from, a serious lung problem, or inhalation of vomitus. Alternatively, a primary respiratory acidosis can be complicated by sepsis and hypotension, or by a myocardial infarct with shock. • Combined respiratory acidosis and metabolic alkalosis This occurs when a patient with a compensated respiratory acidosis, with high BIC, is given large doses of diuretics for the oedema of cor pulmonale and gets a low K alkalosis added on

  22. COMBINED A-B PICTURES - 3 • 4. Combined chronic respiratory acidosis with metabolic acidosis can present with a most confusing picture when the degree of lactic acidosis from the sepsis/decreased tissue perfusion etc just balances the increase in BIC resulting from the compensation for the high pCO2 . The resultant BIC can appear normal, as will the Base Excess, but the pCO2 will be high and the pH low. In such cases the patient is very ill and the history and clinical picture will be essential in sorting out this very dangerous combination • 5. Combined chronic respiratory acidosis with acute respiratory alkalosis. This combination is seen with COAD (CO2 retention) with superadded pulmonary embolus or infection, which stimulates respiration so that pCO2 may come back to normal for a time. You need the history to avoid missing this nasty combination

  23. COMBINED A-B PICTURES - 4 • There are other rarer combinations that we can discuss if you have examples. • The most complex problem (which we do not see any more since an overdose with aspirin is no longer a popular suicide attempt in Australia) is that of salicylate intoxication, with 3 simultaneous changes. 1. There is a raised anion gap metabolic acidosis from the salicylate anion, of 3-6 mmol/L or more 2. There is a further contribution from some lactate accumulation, as salicylate interferes with mitochondrial function 3. There is further lowering of pCO2 due to direct stimulation of the respiratory centre by salicylate The result is a low pCO2 ,a low BIC and a pH which may be normal or on either side of normal

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