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Acid-Base (Anesthesia Text)

NOTE: This content is currently being rewritten by our editors, but we have included the original article from OpenAnesthesia’s encyclopedia section before our March 2023 site update.

Buffering Systems

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 10.3, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer.

Arterial vs. Venous Gases

Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C.

A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more).

Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide toxicity will normalize mixed venous O2 in the face of inadequate oxygen delivery.

Concepts: Alpha and pH Stat

The pKa of buffer systems, and the pH of blood are inversely related to temperature (H+ is proportional to temperature). Thus, a pH of 7.4 at any temperature less than 37&degC actually represents acidosis (pH is inversely related with temperature, so if you add heat to a system, pH will drop). The “alpha stat” approach to acid-base management allows the measured pH to change based on the patient’s actual temperature, whereas the “pH stat” approach keeps the pH at 7.4 regardless of temperature. The importance of anion gap (normally 3-11 mEq/L) and delta-delta 1) Check validity of gas [H+] nEq/L = 24 x pCO2/[HCO3-] accurate to +/-3 2) Determine primary disorder 3) check to see if compensation is adequate. Compensation should never return pH to normal, if so a secondary process is occurring 4) Check the anion gap even if the pH is normal. Note that expected anion gap = 2.5 x [albumin]. Any anion gap > 20 is a primary metabolic acidosis regardless of pH or bicarb 5) If an anion gap is present, check the delta-delta regardless of pH. One can have hidden acidoses and/or alkaloses in the face of a normal pH, only detectable by looking at the gap and delta-delta. If delta-delta added to bicarbonate is > 30, an alkalotic process is occurring, if < 23 an acidotic process is occurring (i.e., original bicarb was < 23).

Base Excess: NON-respiratory component of an acid-base disturbance (blood sample is corrected to a pCO2 of 40 mm Hg and then titrated to a pH of 7.4, although in practice most blood gas analyzers simply calculate base excess).

Physiologic Effects of Acid-Base Disturbances:

In terms of myocardial contractility, acidemia is more problematic than alkalemia. Acidemia begins to affect contractility at a pH of 7.2 or less, however most of these changes are initially counteracted by an increased release of catecholamines (also stimulated by H+). When pH drops below 7.1, the heart becomes less responsive to catecholamines, and serious decompensation can occur. Also note that respiratory acidosis is worse than metabolic acidosis, as CO2 can more easily cross cell membranes

Traditional (Henderson-Hasselbach) vs. Physiochemical (Stewart) Approach to Acid-Base

The Stewart approach to acid base, first described in 1981, is an alternative to the Henderson-Hasselbach approach taught to most medical students. The Henderson-Hasselbach equation describes the associative relationship between pH, HCO3-, and pCO2, but is NOT a causal relationship. It was developed approximately 100 years ago in order to give clinicians an easy way ot estimate pH (which is relatively difficult to measure directly). The problem with the Henderson-Hasselbach equation is that, while mathematically correct, it is often misinterpreted to imply that pH is dependent on HCO3-. In fact, it can be proven (as Stewart did) that there are only three mathematically independent variables on which pH depends – the strong ion difference (SID), the total weak acid concentration, and pCO2. SID is equal to the difference between all completely associated cations (sodium, potassium, magnesium, calcium) and anions (chloride, lactate). The total weak acid is the sum of phosphate and albumin. There is a non-linear relationship between SID and pH. The reason that sodium bicarbonate increases pH is not because of the bicarbonate per se, but because the strong ion difference of sodium bicarbonate is positive (sodium is a strong cation, bicarbonate is a weak anion). Administration of any agent with a positive SID (e.g. calcium gluconate) will increase pH, whereas administration of any agent with an SID of zero or less (e.g. calcium chloride, sodium chloride) will decrease pH. The normal SID in a healthy person is 40-44 mEq/L

Acid Base Interpretation

Expected Compensation

Expected Compensatory Changes: remember that [H+] = 24 x PCO2 / [HCO3-], and also that while respiratory compensation is almost immediate, metabolic compensation takes 6-12 hours to appear and several days to maximize.

Metabolic Acidosis: As bicarbonate goes from 10 to 5, pCO2 will bottom out at 15.

pCO2 = 1.5 x [HCO3-] + 8 (or ↓ pCO2 = 1.25 x Δ[HCO3-])

Metabolic Alkalosis: compensation here is less because CO2 is driving force for respiration.

pCO2 = 0.7 x [HCO3-] + 21 (or ↑ pCO2 = 0.75 x Δ[HCO3-])

Respiratory Acidosis:

Acutely: ↑ [HCO3-] = 0.1 x Δ pCO2 or ↓ pH = 0.008 x Δ pCO2 Chronically: ↑ [HCO3-] = 0.4 x Δ pCO2 or ↓ pH = 0.003 x Δ pCO2

Respiratory Alkalosis: Metabolic compensation will automatically be retention of chloride (i.e., hyperchloremic, usually referred to as “loss of bicarb” although it is the strong ion difference that matters). If you have an anion gap, then you’ve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process.

Acutely: ↓ [HCO3-] = 0.2 x Δ pCO2 (or ↑ pH = 0.008 x Δ pCO2) Chronically: ↓ [HCO3-] = 0.4 x Δ pCO2 (or ↑ pH = 0.017 x Δ pCO2)

Acid Base Interpretation Algorithm

1. Determine the primary problem (normal values are: pH 7.36 – 7.44; pCO2 = 36 – 44 mm Hg; HCO3- = 22 – 26 mEq/L).

2. Check for compensation. Compensation should not be complete and should be in accordance with the above rules.

3. Check the anion gap. Note that the anion gap is mostly made of plasma proteins, and 50% reduction in plasma proteins can drop the anion gap by up to 75% [J Crit Care 8: 187, 1993]. The normal range for anion gap is 8 – 12 mEq/L but should probably be calculated as AG = 2 x [alb (g/dL)] + 0.5 x [PO4 (mg/dL)] [Crit Care 4: 6, 2000]. The anion gap in and of itself should not be used as evidence of acidosis unless it approaches 30 mEq/L [NEJM 303: 854, 1980]. In fact, an anion gap can sometimes be evidence of alkalosis, presumably because the alkalotic state increases the negative charge on albumin molecules [Medicine 56: 38, 1977; South Med J 81: 229, 1988]. In all, the anion gap is a useful adjunct to metabolic acidoses but it is very insensitive and the lack of a gap does not preclude the organic acidoses such as lactic acidosis [Heart Lung 25: 79, 1995] (Big Three: lactic acid, DKA, and renal failure. Non-gap acidosis = diarrhea, saline infusion, early renal failure, and RTA).

4. If there is an anion gap, add the delta gap to the bicarbonate to look for a hidden problem. Another way of thinking about the delta – in a pure anion gap acidosis, the increase in AG equals the HCO3- deficit (because AG = Na+ – [Cl- + HCO3-]), i.e., ΔAG/Δ[HCO3-] = 1.0. In a non-gap acidosis, by contrast, ΔAG/Δ[HCO3-] = 0. To get a sense of which acidosis predominates, look at the ΔAG/Δ[HCO3-] ratio.

The Questionable Value of the ABG

Arterial blood is not a sensitive marker for acid-base status in peripheral tissues, particularly during extreme situations – in cardiopulmonary resuscitations, the ABG may show normal pH and near-normal pCO2 while the venous blood gases show a pH of 7.15 and a pCO2 of 70, much closer to the actual tissue levels. [NEJM 315: 153, 1986]

Metabolic Acidoses

Organic Acidoses (lactic acid, ketones, renal failure)
(all of these are carbon-based acids and produce an anion gap)

Lactate and Lactic Acid (common in the neurosurgical population)

Lactate ≠ lactic acid (requires hydrogen ions from ATP hydrolysis to convert), and thus elevated lactate does not always signify lactic acidosis. In the lactate shuttle it can be used as an alternative fuel source – in fact, lactate’s role as an oxidative fuel has been described in exercise [Fed Proc 45: 2924, 1986], and it may be used as an oxidative fuel in the early stages of shock. It can be used by the heart and CNS as oxidative fuel, may be protective. Normal [lactate] < 2 mM at rest but up to 5 mM during exercise [Crit Care Med 20: 80, 1992] – it is important to know that levels as high as 4 mM may not be associated with acidosis, so hyperlactatemia ≠ acidosis. The most common causes of hyperlactatemia are 1) hypoxemia in shock (hypoxemia in anemia is rarely associated with hyperlactatemia) 2) endotoxin and 3) thiamine deficiency. In shock states, blood lactate levels have strong prognostic value [Circulation 16: 989, 1970] – if levels are 10 mM or above, survival is negligible. Endotoxin causes hyperlactatemia by inhibiting pyruvate dehydrogenase [Am Rev Respir Dis 145: 348, 1992] and not by producing oxygen deprivation. Similarly, thiamine is a cofactor for pyruvate dehydrogenase and thus can produce hyperlactatemia [Lancet 1: 446, 1984] – as thiamine deficiency is common in the ICU, this should always be a consideration. Another less common cause of hyperlactatemia is alkaline pH via alterations in enzyme kinetics of the glycolytic pathway [Am J Med 85: 867, 1987] – normally this is cleared by the liver and thus does not occur until pH ~ 7.6, but in patients with liver failure it can occur at lower pH. Rare causes include medications (propylene glycol used in IV benzos, phenytoin, nitroglycerine – causes lactatemia in 20-65% of patients on high dose benzos for 2 days or more [Chest 128: 1674, 2005]), hepatic insufficiency, seizures, epinephrine infusions, nitroprusside toxicity (cyanide, this is a bad sign), and acute asthma [Intensive Care Med 20: 27, 1994]. The anion gap should not be used to screen for lactic acidosis, as there are several reports of a normal gap with elevated lactate [Crit Care Med 18: 275, 1990] – immediate lactate measurements can be obtained at the bedside using 0.13 mL blood, all in under 2 minutes [JAMA 272: 1678, 1994]. If labs must be sent, be sure to place them on ice. D-lactate is produced by certain enteric bacteria [Lancet 336: 599, 1990] and via fermentation can produce metabolic acidosis and ecephalopathy [Am J Med 79: 717, 1985]. Humans only produce L-lactate, which is what the lab measures. Most D-LA cases follow small bowel resections, so if a post-op patient has an anion gap but no measurable lactate, and you suspect acidosis, ask for a specific D-lactate measurement. In the past, alkali therapy was used to treat lactic acidosis but this has been called into question for several reasons. In intact organisms, lactic acid can actually increase cardiac output [Crit Care Clin 3: 747, 1987] by stimulating catecholamine release and vasodilation. Also, extracellular acidosis has been shown to protect energy-depleted cells from death [Am J Physiol 255: C315, 1988]. Sodium bicarbonate has actually been shown to be relatively ineffective at lowering pH in patients with lactic acidosis [Intensive Care Med 12: 286, 1986], probably because the pK of carbonic acid is 6.1, making the pH range of effectiveness 5.1 – 7.1 for the bicarbonate buffer system. In other words, the bicarbonate buffer system does not work at physiologic pH! Bicarbonate is better described as a CO2 transport mechanism and not as a buffer [Marino]. Also, the pCO2 of standard bicarbonate solutions is 200 mm Hg (lung has to eliminate it) Undesirable attributes of bicarbonate include CO2 generation, increases in blood lactate levels [Chest 104: 93, 1993], and binding calcium with subsequent depression of myocardial contractility [Intensive Care Med 12: 286, 1986]. Carbicarb may be a superior buffer [Crit Care Med 22: 1616, 1994] as it is 50% disodium carbonate, which has a lower pCO2 than sodium bicarbonate. The amine tromethamine (THAM) can also provide buffering (range 6.8 – 8.8) without the production of CO2 [Ann Emerg Med 18: 341, 1989]. Neither of these alternatives has proven to be clinically better than bicarbonate. Marino’s recommendation is to give a trial bicarbonate infusion if pH drops below 7.1, otherwise avoid it, but this may not be supported in the literature as there does not seem to be any conclusive evidence that buffer agents are either beneficial or detrimental for cardiac resuscitation [Crit Care Med 27: 1009, 1999]. In cases of septic shock, there does not seem to be any utility of for pH > 7.15. [Crit Care Med 32: 858, 2004]

Ketones and Ketosis

The liver can convert fatty acids to both β-hydroxybutyrate and acetoacetate, but the ratio of BOHB:AcAc usually ranges from 3:1 to 8:1. Unfortunately, the nitroprusside detection method only reacts to AcAc and even then at levels above 3 Eq/L, which is rare – it is thus a very insensitive marker for ketoacidosis. [J Crit Illness 11: 428, 1996]

Diabetic Ketoacidosis

In 20% of cases there is no history of diabetes. 50% of patients have a concurrent illness, often infection [Postgrad Med 96: 75, 1994]. Blood glucose is > 250 mg/dL but may not be above 350. There is no correlation between glucose and the severity of ketoacidosis [Mayo Clin Proc 63: 1071, 1988]. Furthermore, the anion gap is variable and can sometimes even be normal. [Am J Med 80: 758, 1986]

Treatment of Diabetic Ketoacidosis

Fluids 1L/hr NS for 2 hours, then 1/2 NS @ 250-500 mL/hr Insulin 0.1U/kg IV push, then 0.1 U/hg/hr by continuous infusion. Decrease dose by 50% when HCO3- rises above 16 mEq/L Potassium For [K+] < 3 give 40 mEq over an hour, for 3-4 give 30, 4-5 = 20, and 5-6 = 10 Phosphate If [PO42+] < 1.0 mg/dL, give 7.7 mg/kg over 4 hours

If blood glucose does not fall within the first hour, the insulin dose should be doubled – measure glucose every 1-2 hours, but keep in mind that fingersticks cannot be used until levels fall below 500 mg/dL [Postgrad Med 96: 75, 1994]. Dextrose can be added to fluids when glucose approaches 250 mg/dL. If there is evidence of hypovolemic shock, one can consider replacing with albumin or hetastarch. Remember that while potassium stores are low, serum [K+] is normal in 74% and elevated in 22% – monitor [K+] qh for the first 4-6 hours. Phosphate, while low in most patients, does not seem to affect outcome so do not use routinely, only if depletion is severe i.e., < 1.0 mg/dL. Bicarbonate is ineffective [Postgrad Med 96: 75, 1994]. Note that aggressive volume resuscitation can lead to a replacement of anion gap acidosis with hyperchloremic acidosis, so a shift of the excess AG:bicarbonate deficit ratio is more informative than following the serum bicarbonate, which may not rise (AG:bicarb def. 1.0 for pure keto, 0.0 for hyperCl).

Alcoholic Ketoacidosis

Usually appears 1 to 3 days after a heavy binge of drinking [Am J Med 91: 119, 1991], caused by reduced nutrient intake, hepatic oxidation of ethanol (↑ NADH and BOHB production), and dehydration. These patients often have concurrent disorders (pancreatitis, UGI bleeds, seizures) and are hypo-electrolytic. They often have mixed acid-base disorders. Diagnose by clinical setting and history along with presence of ketones in blood or urine (if your test is sensitive). Treat with dextrose-containing saline solution and correct electrolyte abnormalities as needed.

Treatment of Metabolic Acidosis (in general)

Bicarbonate is sometimes given for pH < 7.1, but if given, must be accompanied by adequate ventilatory support (because it is converted to CO2). Because it has never been shown to be beneficial, it should be given only on a trial basis (ex. 1/2 the calculated dose, then repeat pH and hemodynamic measurements). To make an infusion of NaHCO3, mix 3 ampules (50 mEq/amp) in a 1L bag of D5, which gives 150 mEq Na (similar to NS), with 3 amps of bicarbonate. Carbicarb and THAM are newer agents that do not produce CO2, however they have not been shown to improve mortality.

Hyperchloremic Acidoses

(non-gap, often associated with hypokalemia)

NaCl infusion (consider switching from 0.9% NaCl to Lactated Ringers)
Posthypocapnea (common in the neurosurgical population)

Renal tubular acidosis

Assessing Renal Acid Excretion: the Urine Anion and Osmolar Gaps
When trying to understand the origin of a metabolic acidosis, it may be useful to know whether or not the kidney is contributing the derangement. The kidneys respond to metabolic acidosis by attempting to increase the strong ion difference (which will increase pH). This can be accomplished by retaining sodium bicarbonate as well as by excreting ammonium (NH4+) chloride. Traditionally we are taught that NaHCO3 retention is the primary mechanism for combatting a metabolic acidosis but this is limited by the important role that sodium plays in the regulation of intravascular volume (similarly, K+ is crucial from an electrophysiological standpoint, thus retention of KHCO3 is not an ideal means of maintaining pH). Chloride, by contrast, is a relatively unimportant ion and exists in large quantities, thus making it an ideal candidate to pair with a weak cation for the regulation of pH. The pKa of NH4+ is 9.25, thus it behaves as a weak cation.

In the setting of a metabolic acidosis, the kidneys will excrete NH4Cl as well as H+ paired with various anions, which increase the serum SID and increase the pH. The urine SID (also know as the urine anion gap [UAG]) is equal to urine sodium plus urine potassium minus urine chloride and urine and is an estimate of the amount of NH4+ excreted. Thus, in the setting of a metabolic acidosis with appropriate renal compensation, UAG will be negative (which reflects the NH4+ excreted). A positive UAG in the setting of metabolic acidosis suggests a renal component to the acid-base abnormality (e.g. renal tubular acidosis)

The amount of unmeasured anion can be estimated by calculating the urinary anion gap:

Urinary Anion Gap

  • UAG = [Na+] + [K+] – [Cl-]
  • Normal: zero
  • Appropriate renal response to acidosis: secretion of fixed acid (e.g., NH4+), thus UAG is negative
  • Inappropriate renal response to acidosis: UAG is zero or positive

In a properly functioning kidney, NH4+ will be excreted and because electroneutrality is maintained, high amounts of Cl- will also be excreted – since NH4+ is not measured, the UAG will be negative. A limitation of this technique is the presence of unmeasured anions (ex. β-hydroxybutyrate) [Gabrielli, Layon, Yu. Civetta, Taylor and Kirby’s Critical Care, 4th edition, LWW: p 632-3. 2008 (ISBN 0781768691)]. The concept of UAG was made widespread by Batlle et al., who showed that UAG in normal patients subjected to an acid load was ~ -20 mEq/L, whereas UAG in patients with altered renal function (RTA, aldosterone deficiency) was 20-40 mEq/L [Batlle DC et al. NEJM 318: 594, 1988]. A more recent study by Tapaneya-Olarn C et al. suggests that urine osmolal gap may be a better indicator of NH4+ excretion than UAG [Tapaneya-Olarn C et al. J Med Assoc Thai 82: S98, 1999]

Metabolic Alkalosis

The most common acid-base disturbance in hospitalized patients [Intensive Care Med 8: 725, 1980]. NG suction, diuretics, volume depletion, citrate in banked blood (requires 8 units transferred before HCO3- rises [Rose BD. Metabolic Acidosis: McGraw-Hill, 1994]), and post-hypercapnea (i.e., compensatory, then ventilation is increased an patient will temporarily be alkalotic). Note that volume repletion does not correct “contraction alkalosis” unless adequate Cl- is used, so give 0.9% NaCl.

Adverse Effects

The clinical significance of these effects is unclear, but they deserve mention – 1) Hypoventilation: variable, often minor, but has been reported as a contributing factor to failed weaning [J Intensive Care Med 5S: S22, 1995], but this does not kick in until serum HCO3- reaches the mid 30’s or higher [Marino]. Theoretically, alkalosis can reduce tissue oxygenation by two mechanisms – first, more free Ca2+ binds to albumin, reducing the amount of free Ca2+ and reducing contractility. Second, alkalosis shifts the hemoglobin curve left, impairing the release of oxygen. Furthermore, alkalosis can increase glycolysis which can increase tissue requirements [J Surg Res 26: 687, 1979]. Neurologic (depressed consciousness, seizures, carpopedal spasms) are almost always reserved to cases of respiratory alkalosis.


Often the cause is obvious (NG tube, diuretics) but when it’s not, the urine chloride can be quite helpful. Chloride-responsive alkalosis ([Cl-] < 15 mEq/L) is by far the most common variety (gastric acid loss, diuretics, volume depletion, renal compensation) and most of these patients are volume depleted. Chloride-resistant cases (mineralocorticoid excess, potassium depletion, or both) are more rare and most of these patients are usually volume overloaded.

Classification of Metabolic Alkalosis (measure urine [Cl-])
Chloride-Responsive [Cl-]urine < 15 mEq/L Chloride-Resistant [Cl-] urine > 25 mEq/L
Gastric acid loss (vomit, NG suction) Mineralocorticoid excess
Diuretics (most common form of metabolic alkalosis in neurosurgery patients)
Volume depletion
Exception: early diuretic therapy is chloride responsive despite an elevated [Cl-] urine


As the vast majority of non-neurosurgical ICU patients have a chloride-responsive alkalosis, replacement of Cl- (in the form of NaCl, KCl, or HCl) is the mainstay of therapy. To calculate the chloride deficit, use 0.2 x wt x (100 – [Cl-]) and to calculate the volume of NaCl needed divide this by 154 (mEq/L for NS) KCl is not very effective at repleting chloride because it can’t be administered faster than 40 mEq/h, however as potassium depletion is a cause of alkalosis (albeit chloride-resistant) it is indicated in and only in hypokalemic patients – it is important to note that replacing potassium will do nothing if magnesium also needs to be replace. [Arch Intern Med 145: 1686, 1985] HCl should only be used when rapid correction needed (ex. pH > 7.5) – the [H+] deficit = 0.5 x wt x ([HCO3-]measured – [HCO3-]desired), where [HCO3-]desired = 35 and rate of replacement = 0.2 mEq/kg/hr (for 1N solution, infuse at 0.2 x wt/100 L/hr). Beware, these solutions can extravasate and produce tissue necrosis even when given via central line [Crit Care Med 17: 963, 1989]. Nothing stronger than 0.1N should ever be used Ammonium chloride should not be used as it can produce encephalopathy, especially in patients who are renally or hepatically insufficient [Rose BD. Metabolic Acidosis: McGraw-Hill, 1994]. Arginine hydrochloride can lead to severe hyperkalemia and should also be avoided. [Rose BD. Metabolic Acidosis: McGraw-Hill, 1994] In the past, some have advocated H2-blockers in patients getting prolonged NG suction, but Marino disagrees because of the risk of GI tract colonization – this may be supported in the literature – in a study of ranitidine infusion in postoperative pediatric liver transplant patients, metabolic alkalosis did not develop in the study patients at 24 or 48 h postoperatively (p >= 0.05 versus controls). [Am J Ther 1:281, 1994] For chloride-resistant alkalosis due to mineralocorticoid excess in the NON-NEUROSURGICAL PATIENT, acetazolamide (5-10 mg/kg IV or PO) is ideal because it is both a diuretic and it inhibits carbonic anhydrase, blocking HCO3- resorption and thus encouraging excretion (watch K+ closely however, as acetazolamide encourages its excretion). In the neurosurgical patient, acetazolamide increases CBF and ICP [Neurochirurgia (Stuttg) 33: 29, 1990; Stroke 26: 1234, 1995], thus it should never be used. Potassium (and magnesium) depletion needs to be considered and addressed in the remainder of these rare patients.

Respiratory Alkalosis

PaCO2 < 20-25 mm Hg and pH > 7.55 should be avoided. Treat by decreasing minute ventilation if possible, or judicious use of narcotics if needed (in patients with an overactive respiratory drive, simply changing the ventilatory mode will not be helpful). Oftentimes the addition of dead space to the ventilatory circuit can be curative.

Respiratory Acidosis

PaCO2 > 45 mm Hg and pH < 7.36 can be a complication of 1) various intracranial insults and 2) high cervical injuries. Hypercapnia can increase ICP. Severe respiratory acidosis may even impair cardiac function and cause hypotension.

Acid-Base Considerations in the Neurosurgical Patient
Acid-Base Considerations in the Neurosurgical Patient

CBF changes approximately by 3% for each 1 mm Hg change in PaCO2 but the effect only lasts 4-6 hours. [Andrews]
The CNS is relatively impermeable to H+ and HCO3- (but is permeable to CO2), thus during respiratory compensation, brain pH can oppose systemic pH [Andrews]. Acute administration of bicarbonate or inorganic acid can produce the same effect.
NEVER give acetazolamide to a neurosurgical patient, because it can cause an acute cerebral acidosis, increased CBF and ICP. [Neurochirurgia (Stuttg) 33: 29, 1990; Stroke 26: 1234, 1995]