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A bed side approach to acid

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Discussion 1. This example demonstrates hidden metabolic disturbances. On first glance the pH is raised and the CO2 is decreasedsuggesting primary respiratory alkalosis – PowerPoint PPT presentation

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Title: 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.

2
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.
3
Blood Gases
  • For each gas work through the algorithm to
    identify acidifying/alkalinising processes and
    their contribution to acid base status

4
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

5
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

6
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.

7
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

8
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

9
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.

10
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

11
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)

12
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.

13
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

14
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)

15
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).

16
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

17
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)

18
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.

19
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

20
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)

21
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.

22
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

23
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)

24
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.

25
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

26
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

27
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.

28
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.

29
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.
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