A bed side approach to acid

1
A bed side approach to acidbase fluid
physiology utilising classical and
physicochemical approachesExamples and Appendix

• Ryan Hughes MBBS
• Anaesthetic and Intensive Care Registrar,
  Launceston General Hospital, Tasmania.
• Matthew J. Brain MBBS, FCICM, FRACP
• Intensive Care Staff Specialist, Launceston
  General Hospital, Tasmania.
• Adjunct Clinical Lecturer, Monash University.

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In a little more detail
Approach Interpretation Explanatory Notes
Look at the patient or history Are the results current? Expectations and explanations of likely abnormalities can be sought from chronicity, shock, GIT losses, renal/hepatic dysfunction, diuretics, renal replacement therapy, head injury, sedation, mechanical ventilation settings, etc. Rapid administration of fluids or other resuscitation events (e.g. adrenaline induced lactic acidosis) may partially obscure underlying processes. Expectations and explanations of likely abnormalities can be sought from chronicity, shock, GIT losses, renal/hepatic dysfunction, diuretics, renal replacement therapy, head injury, sedation, mechanical ventilation settings, etc. Rapid administration of fluids or other resuscitation events (e.g. adrenaline induced lactic acidosis) may partially obscure underlying processes.
PaO2 Adage Trust No-one, Assume nothing, Give oxygen! Hypercapnoea is NEVER an indication to withhold oxygen. So called CO2 retainers require additional ventilatory support. An severe metabolic acidosis with a rising CO2 may also rapidly require additional ventilatory assistance. Adage Trust No-one, Assume nothing, Give oxygen! Hypercapnoea is NEVER an indication to withhold oxygen. So called CO2 retainers require additional ventilatory support. An severe metabolic acidosis with a rising CO2 may also rapidly require additional ventilatory assistance.
pH (Do NOT stop analysis if normal) pH lt 7.4 overall acidemia pH gt 7.45 overall alkalemia Normal pH is 7.4 for arterial blood. (7.35 for venous blood). Implications for disturbance severity and end organ, particularly cardiovascular, function.
pCO2   pCO2 elevated respiratory acidosis present. pCO2 low respiratory alkalosis present. Is pCO2 expected given pH?   Our focus remains on identifying all the processes that contribute to the overall pH however it is important to assess the adequacy of the ventilator response and whether it can be sustained. The Rules of Thumb can be applied here with arguably the most important the 1 HCO3- for 10 CO2 suggesting acute respiratory acidosis.
Standard Base Excess BE lt -2 there is a metabolic acidosis. BE gt 3 there is a metabolic alkalosis. Base Excess is the simplest sensitive marker for the detection of metabolic disturbances but contributes little to differentiating the aetiological mechanism. It is also prone to normalising in mixed metabolic disturbances.
Albumin Low albumin there is a metabolic alkalosis (severe if lt20 g/L). Occasionally a high albumin or abnormal proteins in high concentration may result in a metabolic acidosis, however hypoalbuminemia is significantly more common. A high phosphate similarly results in acidosis but the effect is rarely large enough on its own to be of major significance.
Is Lactate elevated? Subtract lactate from AGcorrected. Lactate gt 2 there is a metabolic acidosis.   Lactate gt 2 implies anaerobic metabolism. If AGcorrected remains raised after subtraction of lactate, other unmeasured anions are present.
Calculate Anion Gap (AG) Correct for albumin   AGcorrected gt 15 there is a metabolic acidosis. Unmeasured anions are contributing to an acidosis. Occasionally an abnormal cation (e.g. Lithium or severe hyperkalaemia) may widen the anion gap and potentially mask an unmeasured anion. See text discussion.
Sodium (Tonicity) Hyponatremia Water Excess / Hypernatremia Water Depletion All strong Ions and charge space are diluted / concentrated by same amount, thus dilution of SID leads to acidosis etc.
Correct Chloride for Tonicity Cl-corrected gt ref range there is a metabolic acidosis. Cl-corrected lt ref range there is a metabolic alkalosis. Identifies hypo / hyper chloremia relative to body water status. Note we use Corrected Cl-Measured Cl- x 140/measured Na. See text for discussion.

Blood pH is described as acidemic / alkalemic as
a summation of all contributing respiratory and
non-respiratory acidifying and alkalinising
processes. The entire sequence should be followed
whether or not pH is normal. Each step below pH
qualitatively implies an acidifying or
alkalinising process contributing to the overall
pH, the severity of an abnormality suggests the
size of its contribution. Missing from this
algorithm (for simplicity) is high or low
phosphate (high ? acidosis, low ?alkalosis) and
the contribution of extremes of haemoglobin which
is detected by the standard base excess but
otherwise may not be appreciated.
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Blood Gases

• For each gas work through the algorithm to
  identify acidifying/alkalinising processes and
  their contribution to acid base status

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Gas 1
pH 7.5 pCO2 24 pO2 134 Na 134 K 4.9 Cl- 110 Ca2
1.05 Glucose 8.4 Lactate 1.9 Hb 90 BE 3.5 A.G. 5
.3 AG (inc K) 10.2 HCO3- 18.7

• Brief history
• Clinical information
• 67 year old male day 1 in ICU post pushbike vs.
  truck collision. He has a large hemothorax,
  multiple rib fractures and multiple long bone
  injuries. Previously fit and well.
• Albumin 21g/L

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Clinical Approach

• Suggestions from history Trauma may result in an
  acidosis from ischemia, shock and large volume
  saline resuscitation. Ventilation may be
  increased (pain, mechanical ventilator settings)
  or decreased from chest wall injury / opiates
• pH 7.5 gtgt Overall alkalaemia
• pCO2 24 gtgt respiratory alkalosis
• Utilise 2 for 10 rule gtgt expect HCO3 to be 21 if
  pure disturbance
• The value on the ABG of 18 suggests other
  processes
• Base Excess 3.5 gtgt (upper limit 3) trend to
  mild metabolic alkalosis
• Albumin 21 gtgt there is a hypoalbuminaemic
  metabolic alkalosis (moderate)
• Lactate 1.9 gtgt not elevated
• Anion Gap 5.3 gtgt normal range
• Corrected for hypoalbuminaemia gtgt 9.5 (remains
  normal)
• Sodium 134 gtgt presence of dilutional acidosis
  (mild)
• Corrected Cl- 114 gtgt presence of hyperchloraemic
  metabolic acidosis (moderate)
• Measured Cl- 110 (110140/134 114) upper
  reference 108

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Discussion 1

• This example demonstrates hidden metabolic
  disturbances.
• On first glance the pH is raised and the CO2 is
  decreased suggesting primary respiratory
  alkalosis
• Applying the 2 for 10 rule of acute respiratory
  alkalosis is suggestive but not quite consistent
  with a pure respiratory disturbance.
• BE suggests overall metabolic processes also
  contribute to the alkalosis
• Rapid application of algorithm demonstrates that
  this patient has three simultaneous metabolic
  disturbances despite a near normal base excess
  and anion gap.
• There is a dilutional acidosis, a hyperchloraemic
  acidosis, and a pathologic low albumin
  (alkalosis).
• Each of these factors may be finessed in the
  fluid management of this patient.
• Please note if A.G. calculation includes
  potassium then A.G. reference range is higher 12
  20 mEq/L.

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Gas 2
pH 7.54 pCO2 36 pO2 72 Na 138 K 3.5 Cl- 103 Ca2
1.15 Glucose 10.1 Lactate 1.8 Hb 103 BE 7.8 A.G.
4.2 AG (inc K) 8 HCO3- 30.8

• Brief history
• Clinical information
• 67 year old female, multiple comorbidities, day 1
  in ICU after admission for an acute coronary
  syndrome complicated by congestive cardiac
  failure.
• Albumin 27 g/L

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Clinical Approach

• pH 7.54 gtgt overall alkalaemia
• pO2 72 gtgt borderline oxygenation
• pCO2 36 gtgt only decreased slightly (trivial
  respiratory alkalosis)
• Base Excess 7.8 gtgt there is an overall
  metabolic alkalosis
• Albumin 27 gtgt there is a hypoalbuminemic
  alkalosis (moderate)
• Lactate 1.8 gtgt not elevated
• Anion Gap (no K) 4.2 gtgt normal range
• Corrected for hypoalbuminaemia gtgt 7.5 (normal)
• Sodium 138 gtgt normal range
• Corrected Cl 106 gtgt normal range

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Discussion 2

• This example demonstrates alkalaemia of
  hypoalbuminaemia.
• There is very little in the way of other
  disturbances in this patient.
• The CO2 is slightly low, but not low enough to
  explain the alkalaemia.
• The base excess clearly indicates the presence of
  a metabolic alkalaemia.
• Note that bicarbonate is elevated while chloride
  is within the normal range. Over several days if
  renal compensation were to occur one might
  expect renal retention of chloride and
  normalisation of HCO3. The raised chloride would
  then be compensating for the hypoalbuminaemic
  acidaemia.

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Gas 3

• Brief History
• Clinical information
• 93 year old female with multiple comorbidities
  day 1 post fixation of fractured neck of femur.
  Developed rapid atrial fibrillation and
  subsequent left ventricular failure.
• Albumin 22

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Clinical Approach 3

• History suggests potential for tissue ischemia
  (lactic acidosis), renal failure (A.G. and non
  A.G. acidosis) and potential for hypercarbia
  (post-operative analgesia / high spinal),
  respiratory failure.
• pH 7.22 gtgt overall acidaemia
• pO2 70 gtgt borderline oxygenation (FiO2 known)
• pCO2 36 gtgt decreased slightly consistent with
  raised respiratory rate
• Likely metabolic acidosis gtgt according to rules
  of thumb for a metabolic acidaemia the CO2 should
  be roughly 22 thus inadequate respiratory
  compensation is occurring.
• Base Excess -12.1 gtgt there is a significant
  metabolic acidosis
• Albumin 22 gtgt a counter-acting metabolic
  alkalosis (moderate)
• Lactate 3.7 gtgt there is a metabolic acidosis
  (moderate)
• Anion Gap (no K) 11.3 gtgt slightly above normal
  range
• Corrected for hypoalbuminaemia gtgt 15.8 however
  normalises after subtracting lactate -gt no other
  unmeasured anion present
• Sodium 134 gtgt presence of dilutional acidosis
  (mild)
• Corrected Cl 113 gtgt presence of hyperchloraemic
  acidosis (moderate)

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Discussion 3

• This gas demonstrates several disturbances.
• There is clearly an overall acidaemia present.
• The CO2 is 36, utilising the rules of thumb
  there is only a mild and inadequate respiratory
  compensation for the degree of metabolic acidosis
  suggesting respiratory failure. This is
  consistent with the borderline oxygenation.
• Base excess clearly identifies the metabolic
  acidosis. The anion gap does not identify the
  high anion gap acidosis until corrected for
  hypoalbuminaemia. The unmeasured anion in this
  case is lactate and subtracting it from the anion
  gap yields a reading bordering on normal.
• Correcting the anion gap for albumin is
  recognising the metabolic alkalosis that results
  from the loss of negatively charged albumin.
• Sodium is low in this patient implying a mild
  dilutional acidosis while the corrected chloride
  is 113 suggesting a hyperchloraemic acidosis.
  This may have resulted from excessive
  administration of 0.9 saline or be a more
  chronic response to low albumin.

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Gas 4

• Brief History
• 62 year old man day 4 post ICU admission for an
  intracerebral haemorrhage and low GCS. He is
  intubated and ventilated. He has nil significant
  past history and normal renal function.
• Albumin 22

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Clinical Scenario 4

• History suggests possibilities of primary
  hyperventilation from brain insult and
  possibility of receiving significant volumes of
  saline to prevent secondary vasospasm (HHH
  therapy hypervolemia, hypertension,
  haemodilution)
• pH 7.42 normal range
• pCO2 25 gtgt there is a respiratory alkalosis
  (moderate)
• At this stage recall the 2 for 10 rule of acute
  respiratory alkalosis (despite the normal pH)
  that would suggest the bicarbonate should be
  roughly 21.
• Base Excess -6.5 gtgt there is a metabolic
  acidosis
• Albumin 22 gtgt presence of hypoalbuminaemic
  metabolic alkalosis (moderate)
• Lactate 0.9 gtgt normal range
• Anion Gap (no K) 8.8 gtgt normal range
• Corrected for hypoalbuminaemia gtgt 13.3
  borderline but not outside normal range
• Sodium 139 gtgt normal range
• Corrected Cl 115 gtgt presence of hyperchloraemic
  acidosis (moderate)

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Discussion 4

• In this example there is a normal pH with
  underlying disorders fully counteracting each
  other
• The CO2 of 25 implies respiratory alkalosis. We
  dont know if this is driven by the ventilator
  settings or his spontaneous respiratory rate.
• The overall metabolic acidaemia is identified
  by the BE of -6.5. BE is derived using the pH,
  bicarbonate and Hb to estimate whether acidosis
  is present.
• This patient has a significant hyperchloraemic
  metabolic acidosis (probably due to saline
  administration) with the normal pH resulting from
  a secondary hypocapnoea (respiratory alkalosis)
  and a pathologic hypoalbuminaemia (metabolic
  alkalosis).

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Gas 5

• Brief History
• 72 year old male day 1 post ICU admission for
  high speed MVA with severe chest injuries. He is
  intubated and ventilated. He has a past history
  of emphysema.
• Albumin 29
• BE -6.9

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Clinical Scenario 5

• Suggestions from history Trauma may result in an
  acidosis from ischemia, shock and large volume
  saline resuscitation. Ventilation may be
  increased (pain, mechanical ventilator settings)
  or decreased from chest wall injury / opiates
• pH 7.32 overall acidaemia
• pCO2 36 decreased slightly
• At this stage likely to be a metabolic problem
  gtgt according to the rules of thumb for a
  metabolic acidaemia the HCO3 should be roughly 32
• Base Excess -6.9 gtgt there is a metabolic
  acidosis
• Albumin 32 gtgt presence of hypoalbuminaemic
  metabolic alkalosis (mild)
• Lactate 1.4 gtgt normal range
• Anion Gap 7 gtgt normal range
• Corrected for hypoalbuminaemia gtgt 12 in the upper
  normal range
• Sodium 140 gtgt normal range
• Corrected Cl 113 gtgt presence of hyperchloraemic
  acidosis (moderate)

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Discussion 5

• A metabolic cause of acidaemia with the lowered
  CO2 consistent with respiratory compensation.
• BE identifies the metabolic acidaemia and anion
  gap is on the borderline of normal and
  subtracting the lactate of 1.4 makes it more
  unlikely that there are any other unmeasured
  anions.
• Albumin is once again low contributing a
  hypoalbuminaemic metabolic alkalosis and the main
  contributor is again a hyperchloraemic metabolic
  acidosis, most likely from large volume saline
  resuscitation.

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Gas 6

• Brief History
• Clinical information
• 32 year old female with a necrotic foot abscess
  and multiple comorbidities transferred to ICU in
  status asthmaticus. This gas is taken
  immediately on ICU admission where the patient is
  intubated and ventilated.
• Albumin 32

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Clinical Scenario 6

• Expectations from history Significant
  hypercarbia is likely while therapies such as
  salbutamol infusion may result in a lactic
  acidosis. History suggesting underlying sepsis
  may also result in acidosis.
• pH 7.01 overall severe acidaemia
• pCO2 112 severe respiratory acidosis
• Acute respiratory acidosis bedside rules for
  acute respiratory acidosis the 1 for 10 rule.
  Estimated bicarbonate is 31
• Base Excess -5.6 gtgt suggests coexistent
  metabolic acidosis
• Albumin 32 gtgt hypoalbuminaemic metabolic
  alkalosis (mild)
• Lactate 1.1 gtgt normal range, not a component of
  acidosis.
• Anion Gap 3.7 gtgt normal range
• Corrected for hypoalbuminaemia gtgt 5.7 (normal)
• Sodium 138 gtgt normal range
• Corrected Cl 107 gtgt high normal range (trend
  toward hyperchloraemic acidosis)

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Discussion 6

• This gas is relatively straight forward in the
  sense that there is one major disturbance.
• This patient has severe airway obstruction and
  significant hypercapnoeic respiratory acidosis.
• The 1 for 10 rule of acute respiratory acidosis
  predicts that bicarbonate should be roughly 31
  with a CO2 this high.
• Other aspects of this blood gas are unremarkable
  aside from a mild hypoalbuminaemic metabolic
  alkalosis and the cause of the BE is not apparent.

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Gas 7

• Brief History
• Clinical information
• 48 year old female brought to ED with a two day
  history of vomiting and lethargy on a background
  of type 1 diabetes mellitus. Hypotensive,
  tachycardic, cool and clammy
• Chloride 112
• Albumin 32

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Clinical Scenario 7

• The story suggests DKA however contributing
  sepsis or toxins must always be considered.
• pH 6.87 overall severe acidaemia
• pCO2 24 gtgt respiratory alkalosis contribution
• The pH is too low to use the last two digits to
  estimate the CO2. Alternatively one can use
  Winters rule pCO21.5x(HCO3) 8 rule which
  gives us an estimate of 14. This suggests the
  patient is unable to maintain an adequate minute
  ventilation to compensate and may soon require
  ventilatory support.
• Base Excess -28.3 gtgt there is a severe
  metabolic acidosis
• Albumin 32 gtgt presence of a mild hypoalbuminaemic
  metabolic alkalosis
• Lactate 4.0 gtgt there is a lactic acidosis
• Corrected A.G. 21.6 gtgt raised- suggests the
  presence of unmeasured anions in this case
  both keto-acids and lactate
• Corrected for Kgt4 (i.e. add 1.6) 23.2
• Subtract lactate of 4.0 19.2 -gt remains
  elevated confirming other anions
• Sodium (corrected) 136 gtgt normal range
• Note must be corrected for glucose when
  determining resuscitation fluid and rate of
  acceptable change of serum osmolality.
• Corrected Na Measured Na (serum glucose
  5.5)/3
• Corrected Cl 115 gtgt there is a hyperchloraemic
  acidosis (moderate)

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Discussion 7

• A severe metabolic acidosis with multiple
  components
• As the pH is extremely low the rules of thumb
  approximation of last two numbers of the pH
  CO2 for respiratory compensation in metabolic
  acidosis fails. Instead Winters rule of thumb
  pCO2 1.5x(HCO3) 8 yields a result of 14,
  consistent with significant metabolic acidosis.
  Here the pCO2 of 24 suggests inadequate minute
  ventilation.
• This case demonstrates the additive nature of the
  anion gap what we want to know is whether a
  significant ketoacidosis is present however the
  anion gap will include the lactic acidosis.
• The corrected anion gap is 21.6. The amount that
  potassium is above normal (i.e. 1.6) by must be
  added (not necessary if K is included in the
  anion gap calculation) and the lactate of 4.0
  must be subtracted. In this case A.G. remains
  widened consistent with diabetic ketoacidosis.
• In addition a mild dilutional acidosis (Na 136)
  is present and a significant hyperchloraemic
  acidosis (corrected chloride 115) is present.
• The acidaemia is contributed to by ketoacids,
  lactic acid, hyperchloraemia and dilution (water
  shift from ICF) it is partially compensated by a
  respiratory alkalosis and a mild pathologic
  hypoalbuminaemic alkalosis.
• Note In hyperglycaemic states a significant
  volume of intracellular water is osmotically draw
  into the ECF as the hyperglycaemia is treated
  the sodium corrected for glucose must be serially
  calculated Corrected Na Measured Na (serum
  glucose 5.5)/3 as well as calculated
  osmolality (2Nameasuredglucoseurea) so that
  change in corrected sodium does not exceed 12
  mEq/L/24 hours to avoid osmotic demyelination and
  cerebral oedema does not result from too rapid a
  return of water into the brain. (Note An osmolal
  gap should also be looked for with this
  presentation)
• It should be noted that for acid base purposes,
  the measured values of sodium and other strong
  electrolytes are used, not the values corrected
  for glucose as this is the measured values are
  the strong ion concentrations in the currently
  available ECF water.

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Gas 8

• Clinical History
• 37 year old male with intellectual disability and
  inherited thrombophilia brought to the ED for
  investigation after several days abdominal pain
  and vomiting.
• Respiratory rate 19/min
• Chloride 100 mmol/L
• Albumin 28 g/L
• Haemoglobin 186 g/L

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Clinical Scenario 8

• History suggests Vomiting metabolic alkalosis?
  Perforation / ischemic bowel lactic acidosis
• pH 7.41 normal range, any disturbances fully
  counteract each other
• pCO2 32 gtgt pCO2 low -gt a respiratory alkalosis
  exists
• Rules of Thumb suggest presence of metabolic
  alkalosis expected pCO2 0.7 HCO3 20 mmHg
  (range /- 5) result is expected pCO2 of 34.
  Note the 5 for 10 rule of respiratory alkalosis
  also fits so clinical history is essential.
• Base Excess -3.1 gtgt only just outside range,
  does not emphasise the significant
  abnormalities present
• Albumin 28 gtgt presence of a contributing
  hypoalbuminaemic metabolic alkalosis
  (moderate)
• Lactate 8.0 gtgt there is a lactic acidosis
  (severe)
• Corrected AG 20.7 gtgt elevated normalises after
  subtracting lactate, implying no other
  unmeasured anions contributing.
• Sodium 138 gtgt normal range
• Corrected Cl 101 gtgt normal range lower value
  expected considering vomiting
• Haemoglobin 186 gtgt haematocrit 60 highly
  abnormal and implies reduced plasma volume
  with increased buffering effect of
  haemoglobin, this will be included in BE
  calculation

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Discussion 8

• The gas is challenging in isolation however the
  history suggests a hypochloraemic metabolic
  alkalosis should be present, and the extremely
  elevated lactate suggests significant ischemia or
  severe sepsis. Such an elevated lactate in
  isolation would normally be associated with a
  very low pH and low pCO2.
• Both the 5 for 10 rule of chronic respiratory
  alkalosis or the metabolic alkalosis pattern of
  expected pCO2 0.7 HCO3 20 mmHg (range /-
  5) would fit the results. The history of vomiting
  suggests the latter while the elevated
  respiratory rate is more consistent with the
  former.
• Hypoalbuminaemia contributes to the metabolic
  alkalosis and the increased buffering power of
  erythrocytes at high haematocrits also
  contributes though the effect is small. Both
  these factors will trend the base excess toward
  the normal range, however neither is particularly
  severe.
• The corrected anion gap is raised, however once
  the lactate of 8 is subtracted a normal value is
  attained, so no additional anions are suggested
  by this. Of interest though if Equation 3 is
  utilised, with the remaining values Total
  Calcium 2.71 mmol/L, Mg 0.8 mmol/L, PO42-
  2.22 mmol/L then the two sides dont balance
• The sum of all cations is 151.8 and anions 140.5.
  This is the Strong Ion Gap i.e. a gap that the
  summary anion gap missed implying that other
  unmeasured anions are in fact present (though
  this would only worsen an acidosis)
• Overall then the detected abnormalities are a
  severe lactic metabolic acidosis, with a
  compensatory respiratory alkalosis and
  hypoalbuminaemic metabolic alkalosis combining to
  fully normalise the pH.
• The high haematocrit (acute) also suggests severe
  volume depletion however without abnormalities of
  Na or Cl- we cannot easily identify a
  concentration alkalosis or hypochloraemic
  alkalosis.
• The patient had 2m of ischemic intestine
  (secondary to thrombosis) and after fluid
  resuscitation and laparotomy the lactate fell to
  4.0 the haemoglobin 118, Albumin 19 with pH
  7.46, pCO2 39 HCO3- 27.7 BE 3.7, AGcorrected
  12.5, Na 141, Cl- 109. These abnormalities
  resolved over the next 48 hours.

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Appendix 1 Glossary

• Electrolytes An electrolyte is any substance
  that dissociates into charged ions in solution.
• Electrical neutrality A fundamental property of
  physiologic fluids is that net charge is zero,
  ions move across membranes sometimes against
  concentration gradients to maintain this and
  conjugate acid/bases may dissociate according to
  their dissociation constant.
• Strong electrolytes / ions are named because
  their dissociation is complete with none of the
  parent salt remaining in solution. Na, K and
  Cl- are examples of strong ions.
• Strong Ion Difference The net difference in
  concentration between strong cations and anions
  in solution is known as the strong ion difference
  (SID) - the units of which are mEq/L (charge).
  When a solution has a SID the net charge
  difference must be accounted for by a weak
  electrolyte in equilibrium with and if none
  exists then water changing its dissociation state
  (this will change the pH). Weak acids and bases
  also change their dissociation state depending on
  the SID of the surrounding solution and their
  propensity to dissociate.
• Low SID Fluid Any fluid where no or minimal
  charge difference exists between strong cations
  and strong anions such as sodium chloride or pure
  water is termed a low SID fluid, i.e. electrical
  neutrality is entirely accounted for by strong
  electrolytes.
• Weak electrolytes are variably dissociated
  depending on the properties of the solution they
  are dissolved in.

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Appendix 2 Classic acid base analysis

• Contemporary acid-base teaching has focussed on
  delineating a primary disorder as respiratory or
  metabolic followed by how well compensated the
  primary process is. Unfortunately in most
  critically ill patients, multiple factors
  contribute to the final pH with compensation
  being from both physiologic mechanisms but also
  from other pathologic mechanisms.
• Classically acid base has been taught utilising
  the Henderson Hasselbalch equation to delineate
  the primary disorder as respiratory or metabolic.
  The resulting bedside approach can be
  summarised
• 1. Look at the pH (acidaemia or alkalaemia)
• 2. Look at the CO2 (high/low/normal) to determine
  if a primary respiratory disorder is responsible
  (pH and CO2 change in opposite direction) or if a
  metabolic process is contributing (abnormal
  base excess / pH and CO2 fall or rise together).
• 3. Assess degree of compensation a normal pH
  with abnormal CO2 or base excess is fully
  compensated. The rules of thumb in the nomogram
  (Figure 1) assist in classifying the disorder.
• 4. If a metabolic component exists, calculate the
  anion gap to determine if pathologic weak acids
  are contributing and search for them if present.
  If anion gap not widened, interrogated history,
  renal function, GI loss etc. for aetiology.
• This rapid analysis doesnt differentiate between
  acute and chronic metabolic conditions as
  respiratory compensation is rapidly achieved
  being the time it takes for a new minute
  ventilation to achieve a new steady state pCO2.
  However a history of the illness will often
  identify acute changes. If only two rules of
  thumb were to be remembered we would recommend
  the 1 for 10 in acute respiratory acidosis, and
  the post-decimal of the pH equals the CO2 in
  metabolic acidosis. Acute conditions that result
  in these states usually require more urgent
  intervention.
• This technique for analysing blood acid-base
  chemistry is well known however several features
  need to be appreciated to not confuse the
  analysis with the pathology. First it is skewed
  toward identifying respiratory disturbances, the
  metabolic processes are anion gap or non-gap and
  does not easily encompass hyperchloraemic states
  or low albumin contributions.
• The rules of thumb utilising HCO3 change
  relative to CO2- need to be appreciated as
  patterns that are seen in various pathologies,
  not as representing the body directly changing
  the HCO3- to compensate for the CO2 it cant,
  the two are bound by the H.H. equation and the
  large volume of other species in the ECF that
  affect the H.
• This method is an established and tested way to
  identify many disorders, and particularly useful
  in identifying if a respiratory compensation is
  not adequate when a metabolic disorder is present.