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Interpretation of Arterial Blood Gases

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Title: Interpretation of Arterial Blood Gases


1
Interpretation of Arterial Blood Gases
2
Contents
  • Introduction
  • Common terms and definitions
  • Oxygenation
  • Ventilation and acid base status
  • Interpretation of arterial blood gases

3
Introduction
  • Arterial blood gas analysis (ABG) is an integral
    part of the diagnosis of the critically ill
    patient. With the information gained from this
    procedure directing patient care, an awareness of
    how the body maintains acid-base balance and the
    disturbances that can occur is essential
  • The purpose of this presentation therefore is to
    outline the basic principles of acid base balance
    and to provide a systematic approach to the
    interpretation of arterial blood gases

4
Definition of Terms
5
Common Terms and Definitions
  • Acid-base balance
  • refers to the regulation of hydrogen ions (H) in
    the body fluids
  • Acid
  • a substance that yields H in solution
  • e.g. hydrochloric acid - HCl ? H Cl
  • Base
  • a substance that combines with H in solution
  • e.g. sodium hydroxide NaOH ? Na OH

6
  • pH
  • is a measure of the concentration of H in
    solution
  • is the negative logarithm of the hydrogen ion
    concentration
  • is inversely related to the number of hydrogen
    ions in solution
  • Acidaemia
  • pH less than 7.35
  • Alkalaemia
  • pH greater than 7.45
  • (acidaemia and alkalaemia reflect pH
    abnormalities in the blood, acidosis and
    alkalosis refer to the physiological process that
    causes such imbalances)

7
  • Buffer
  • substances which resist changes in pH by
  • absorbing H when acid is added to a solution
  • releasing H when a base is added to a solution

8
Physiology
9
Oxygenation
  • although not used in acid-base interpretation,
    oxygenation is an essential component of the ABG
    analysis
  • with no storage system, the cells must rely on a
    continuous supply of oxygen at a rate that
    precisely meets ever changing metabolic demands
    if tissue hypoxia is to be avoided
  • as a result, oxygenation has not only been
    considered separately in this presentation but
    also given priority in the recommended approach
    for blood gas analysis

10
The Carriage of Oxygen
  • Oxygen is transported by the blood in two ways
  • 3 dissolved in plasma
  • 97 bound to haemoglobin (Hb)
  • Availability to the tissues depends on
  • oxygen content
  • cardiac output and regional blood flow
  • oxygen dissociation curve

11
Oxygen Dissociation Curve
Arterial
97
Minimum saturation point
88
Venous
75
O2 Saturation
P50
50
13.3
5.3
6.7
3.5
PO2 (KPa)
12
Shifts in the Oxygen Dissociation Curve
  • Left shift
  • alkalosis
  • hypothermia
  • ? 2,3-DPG
  • variant Hb

Saturation
P50
50
  • Right shift
  • acidosis
  • hyperthermia
  • ? 2,3-DPG

2.4
5.3
3.5
PaO2 (KPa)
13
Oxygen Cascade

dry atmospheric gas 21 KPa dry atmospheric gas 21 KPa dry atmospheric gas 21 KPa dry atmospheric gas 21 KPa dry atmospheric gas 21 KPa dry atmospheric gas 21 KPa dry atmospheric gas 21 KPa
humidified tracheal gas 19.8 KPa humidified tracheal gas 19.8 KPa humidified tracheal gas 19.8 KPa humidified tracheal gas 19.8 KPa humidified tracheal gas 19.8 KPa humidified tracheal gas 19.8 KPa
alveolar gas 14 KPa alveolar gas 14 KPa alveolar gas 14 KPa alveolar gas 14 KPa alveolar gas 14 KPa
arterial blood 13.3 KPa arterial blood 13.3 KPa arterial blood 13.3 KPa arterial blood 13.3 KPa
capillary blood 6-7 KPa capillary blood 6-7 KPa capillary blood 6-7 KPa
mitochondria 1-5 KPa mitochondria 1-5 KPa

venous blood 5.3 KPa
14
Assessing the Patients Oxygenation
  • Information on oxygenation is obtained from
  • PaO2
  • measures the amount of oxygen dissolved in plasma
  • normal values on room air range from 10 13.3
    KPa
  • should increase when supplemental oxygen is given
  • SaO2
  • indicates the amount of oxygen bound to
    haemoglobin
  • is determined by blood gas analysis or pulse
    oximetry
  • a value of ? 95 is normal for a healthy adult

15
  • As with all assessment the PaO2 should not be
    considered in isolation, examination of the
    following will place this value in context for
    each patient and therefore result in accurate
    interpretation
  • medical history
  • clinical picture
  • the amount of oxygen the patient is receiving
    (fraction of inspired oxygen or FiO2)

16
  • should an ABG result show that the PaO2 is lower
    than expected for the given FiO2, then the
    calculating the alveolar to arterial gradient can
    help determine the cause of hypoxaemia
  • before this calculation can be performed however
    the partial pressure of oxygen in the alveolus
    must established
  • this is achieved be performing the alveolar gas
    equation

17
Alveolar Gas Equation
  • PAO2 FiO2 (Pb PAH2O) PaCO2
  • R
  • Where
  • PAO2 alveolar PO2
  • Pb barometric pressure (101 KPa)
  • PAH2O alveolar partial pressure of water (6.3
    KPa)
  • PaCO2 arterial PCO2
  • R respiratory exchange ratio (0.8)

18
pH 7.08 PaCO2 10.6 KPa PaO2 - 4.9 KPa SBC -
26 mmol/L SBE - 3 mmol/L SaO2 - 86
  • Using the results opposite, calculate the PAO2
    for a patient who is
  • on room air
  • receiving 50 oxygen

19
  • PAO2 FiO2 (Pb PAH2O) PaCO2
  • R
  • Room air
  • PAO2 .21 (101 6.3) 10.6 6.63 KPa
  • 0.8
  • 50 oxygen
  • PAO2 .5 (101 6.3) 10.6 34.1 KPa
  • 0.8

20
Alveolar to Arterial Oxygen Gradient
  • the PaO2 can never be greater than the partial
    pressure of oxygen that exists in the alveolar
    space
  • in young healthy individuals breathing ambient
    air the PaO2 is approximately 2 KPa less than the
    PAO2, this figure rises to 4 KPa in the elderly
  • this difference represents the alveolar to
    arterial oxygen gradient
  • the equation for calculating the A-a oxygen
    gradient (AaO2) is
  • AaO2 PAO2 PaO2

21
Significance of the A-a Oxygen Gradient
  • if the PAO2 is low but the transfer of oxygen
    from the alveolus to arterial blood is normal the
    AaO2 gradient will remain small
  • e.g. hypoventilation
  • if the PAO2 is normal but structural problems
    limit the transfer of oxygen from the alveolus to
    arterial blood the AaO2 gradient will increase
  • e.g. ARDS, pulmonary embolus

22
  • This ABG result is from a postoperative patient
    who is
  • self ventilating on room air
  • cyanosed with shallow breathing
  • Calculate the AaO2 gradient to establish if the
    hypoxaemia present results from
  • hypoventilation
  • damage to the lung parenchyma

pH 7.08 PaCO2 10.6 KPa PaO2 - 4.9 KPa SBC -
26 mmol/L SBE - 3 mmol/L SaO2 - 86
23
  • PAO2
  • .21 (101 6.3) 10.6 6.63 KPa
  • 0.8
  • AaO2 gradient
  • 6.63 4.9 1.73 KPa
  • This is normal AaO2 gradient which suggests the
    hypoxaemia is caused by hypoventilation - this is
    probably the result of residual anaesthetic gases

24
  • This ABG result is from a patient who has
    suffered a head injury, they are
  • self ventilating on room air
  • deeply unconscious and have vomited once
  • Calculate the AaO2 gradient to establish if the
    hypoxaemia present results from
  • hypoventilation
  • damage to the lung parenchyma

pH 7.23 PaCO2 8.1 KPa PaO2 - 4.9 KPa SBC -
26 mmol/L SBE - 3 mmol/L SaO2 - 86
25
  • PAO2
  • .21 (101 6.3) 8.1 9.78 KPa
  • 0.8
  • AaO2 gradient
  • 9.78 4.9 4.88 KPa
  • The higher than normal AaO2 gradient would
    suggest there is a primary lung problem and
    hypoxaemia is not related to hypoventilation - as
    the patient has vomited aspiration is a likely
    cause

26
Assessing the Patients Acid-Base Balance
  • having assessed the PaO2, the acid base status of
    the patient should now be considered
  • as acid-base balance is affected by both
    respiratory and metabolic function the PaCO2 and
    bicarbonate (SBC) measurements must therefore
    also be analysed
  • PaCO2
  • measures the amount of carbon dioxide dissolved
    in plasma
  • assesses the patients ventilatory function
  • normal values range from 4.6 6.0 KPa

27
  • Standard bicarbonate (SBC/HCO3-)
  • the actual bicarbonate value of the ABG is
    affected by both respiratory and metabolic
    processes
  • by determining the portion of bicarbonate
    resulting from respiratory dysfunction the blood
    gas analyser is able to calculate the standard
    bicarbonate level
  • this figure reflects dysfunction that is purely
    metabolic in origin
  • normal values range from 22 26 mmol/L

28
  • Standard base excess (SBE)
  • examination of the SBC will provide sufficient
    information to enable blood gas interpretation
  • some clinicians use this information as an
    indication of the amount of treatment or
    neutralisation required to overcome the metabolic
    acidosis (base deficit) or metabolic alkalosis
    (base excess) and return the pH to 7.4
  • normal values range from -2 to 2 mmol/L

29
The Importance of H Concentration
  • Fluctuations outside the normal blood pH 7.35
    7.45 affect
  • enzyme activity
  • the excitability of nerve and muscle cells
  • potassium levels in the body
  • oxygens affinity for haemoglobin
  • A blood pH of less than 7.0 and greater than 7.8
    is not compatible with life

30
Threats to Normal pH Level
  • H are constantly being added to the bodily
    fluids as a result of metabolic activities
  • Carbonic acids (volatile)
  • are derived from the metabolism of glucose and
    fats
  • produce CO2
  • are mostly handled by respiration
  • Non carbonic acids (non-volatile)
  • come from protein metabolism
  • are excreted by the kidneys

31
Threats to Normal pH Level
H flux
H excretion
H production
carbonic acid (volatile) 15,000
mmol/Day non-carbonic acids (non-volatile) 80
mmol/Day
15,000 mmol/Day
80 mmol/Day
extracellular fluid 40 nmol/L
32
Mechanisms of Acid-Base Regulation
  • The concentration of H in the blood is regulated
    sequentially by
  • chemical buffering by intracellular and
    extracellular buffers
  • the control of PaCO2 by the respiratory centre in
    the brain stem
  • the control of bicarbonate ions (HCO3) and H
    excretion by the kidney

33
Buffer Systems
  • Bicarbonate buffer system
  • the bicarbonate-carbonic acid buffer system is
    the primary buffer in extracellular fluid
  • carbonic acid is formed by the reaction of carbon
    dioxide and water, the product then dissociating
    to form hydrogen and bicarbonate ions
  • CO2 H2O ? H2CO3 ? H HCO3
  • the normal ratio of bicarbonate to carbonic acid
    in the plasma is 201

ca
34
Effects of an Unbuffered Solution
  • adding hydrochloric acid (HCL, strong acid) to an
    unbuffered solution increases the amount of free
    H and therefore the acidity of the solution

HCL
H
Na
Cl
35
Actions of a Buffer System
  • the basic member (HCO3) in the buffered solution
    binds with some of the H thus neutralising its
    effects giving rise to a less dramatic change
    in pH

HCL
H
Na
Cl
H2CO3
HCO3
36
Henderson-Hasselbalch Equation
  • pH 6.1 log HCO3
  • PaCO2 x 0.23
  • 6.1 log 24 mmol/L
  • 5.3 KPa x 0.23
  • 6.1 Log (201)
  • 6.1 1.3 7.4

37
Effect of Changes in HCO3/H2CO3 Ratio on pH
  • HCO3
  • PaCO2 x 0.23

ratio
20 1 normal acid-base balance
20 1 alkalosis
lt
gt
20 1 acidosis
38
  • Other chemical buffer systems include
  • proteins primary ICF buffer also buffers ECF
  • haemoglobin primary buffer against H2CO3
    changes
  • phosphate important urinary buffer also
    buffers ICF
  • although immediate in response, buffers cannot
    maintain acid-base balance unlike the lungs and
    kidneys they are unable to actively excrete acids
    and therefore the respiratory and renal systems
    are concurrently called into play

39
Respiratory Regulation
return to homeostasis
decreased blood pH
increased blood pH
? respiratory rate
eliminates more CO2 ? less H2CO3 H formed
stimulates the respiratory centre in the medulla
40
Renal Regulation
  • the kidneys are the most potent acid-base
    regulatory mechanism
  • unlike the respiratory system, they have the
    ability to return the pH almost exactly to normal
  • they control the pH of body fluids by adjusting 3
    interrelated factors
  • HCO3- reabsorption
  • HCO3- generation
  • HCO3- secretion

41
  • Bicarbonate
  • Bicarbonate reabsorption

renal tubular lumen
peritubular capillary
renal tubular cell
Na
Na
Na
HCO3-
HCO3- H
HCO3-
H
CA
H2CO3
H2CO3
H2O CO2
CO2 H2O
urine
blood
42
Bicarbonate generation
  • Bicarbonate generation
  • phosphate absorption of H

peritubular capillary
renal tubular cell
renal tubular lumen
Na
Na
Na
HPO42-
HCO3- H
HCO3-
H
CA
H2CO3
NaH2PO4-
H2O CO2
urine
blood
43
  • ammonia formation

peritubular capillary
renal tubular lumen
renal tubular cell



Na
Na
Na
Cl-
HCO3- H
HCO3-
H
CA
H2CO3
NH3
H2O CO2
Na4Cl-
NH3
urine
blood
44
  • Bicarbonate secretion
  • some tubule cells of the kidney have the
    capability to reabsorb chloride ions (Cl) into
    the blood and secrete HCO3 into renal tubular
    fluid
  • more active during conditions of alkalosis, this
    mechanism allows the body to decrease the total
    amount of base in extracellular fluid and restore
    homeostasis

45
Abnormalities of Acid-Base Balance
46
Classification of Acid Base Balance Disorders
  • the maintenance of pH is dependant on the ratio
    of HCO3H2CO3
  • acid base disturbances that occur as a result of
    a disruption to this ratio are classified by both
    cause (respiratory or metabolic) and direction
    (acidosis or alkalosis)

HCO3
24
1.2
201
H2CO3
HCO3
47
Respiratory Acidosis
24
H2CO3
131
1.84
HCO3
  • ABG indicators
  • pH below 7.35
  • PaCO2 above 6 KPa
  • Aetiology
  • Occurs with any condition that impedes
  • ventilation and the elimination of CO2
  • gaseous exchange at the capillary/alveolar level
  • chest wall expansion

48
Conditions that Cause Respiratory Acidosis
  • Central causes
  • brain injury
  • stroke
  • trauma
  • drugs
  • anaesthetic
  • sleep apnoea

Airway obstruction
  • Peripheral neurological causes
  • nerve injury spinal cord trauma,
  • phrenic nerve palsy
  • neuropathy Guillain-Barre syndrome, polio
  • motor neurone disease, epidural
  • Lung disease
  • COPD
  • asthma
  • pneumothorax
  • pulmonary
  • oedema
  • Chest wall causes
  • deformity scoliosis, flail chest, obesity
  • muscular weakness electrolyte imbalance
  • myaesthenia gravis, muscle relaxants

49
Acute Versus Chronic Respiratory Acidosis
  • Acute
  • sudden hypercapnia shifts the equilibrium of the
    bicarbonate buffer system to the right, thereby
    generating additional H
  • CO2 H2O ? H2CO3 ? H HCO3
  • with renal compensation not yet started there is
    little or no increase in HCO3 and so the pH will
    fall

shift
increase in HCO3 takes several days
hypoventilation ? CO2
50
  • Chronic
  • CO2 accumulates over a prolonged period
  • unlike acute respiratory acidosis, where clinical
    manifestations are linked to the retention of
    CO2, symptoms experienced are often related to
    the underlying disease process
  • compensatory changes have time to occur pH may
    be within normal limits despite an elevated PaCO2
  • the respiratory centre becomes insensitive to CO2
    leaving hypoxaemia as the major respiratory drive

51
Metabolic Compensation of Respiratory Acidosis
  • Acute conditions
  • the pH will fall by 0.06 and the HCO3 will rise
    by 0.8 mmol/L when the PaCO2 increases by 1 KPa
  • use the following formulas to determine if the pH
    and HCO3 fall within the predicted values
  • pH 7.4 (measured PaCO2 5.3) x 0.06
  • HCO3 24 (measured PaCO2 5.3) x 0.8

52
  • Chronic conditions
  • the pH will fall by 0.02 and the HCO3 will rise
    by 3.0 mmol/L when the PaCO2 increases by 1 KPa
  • use the following formulas to determine if the pH
    and HCO3 fall within the predicted values
  • pH 7.4 (measured PaCO2 5.3) x 0.02
  • HCO3 24 (measured PaCO2 5.3) x 3.0

53
  • using the results below, calculate the expected
    pH and HCO3 for both acute and chronic
    conditions

pH 7.28 PaCO2 7.46 KPa PaO2 - 9.33
KPa SBC - 26 mmol/L SBE - 2 mmol/L SaO2 - 89
54
  • Acute
  • pH 7.4 (7.46 5.3) x 0.06 6.1
  • HCO3 24 (7.46 5.3) x 0.8 25.73
  • Chronic
  • pH 7.4 (7.46 5.3) x 0.02 7.36
  • HCO3 24 (7.46 5.3) x 3.0 30.48

55
Respiratory Alkalosis
HCO3
0.6
401
24
H2CO3
  • ABG indicators
  • pH above 7.45
  • PaCO2 below 4.6 KPa
  • Aetiology
  • hyperventilation is the mechanism responsible for
    all cases of respiratory alkalosis

56
Conditions that Cause Respiratory Alkalosis
  • Central Causes
  • head injury
  • stroke
  • tumour
  • hyperventilation syndrome
  • pain
  • fever
  • stress
  • Pulmonary causes
  • pneumonia
  • asthma
  • fibrosis
  • pulmonary oedema
  • ARDS
  • pulmonary embolus

Hepatic failure
  • Cardiac causes
  • MI
  • heart failure
  • Other
  • thyrotoxicosis
  • hypoxaemia
  • drugs
  • sepsis
  • excessive mechanical ventilation
  • Pregnancy
  • progesterone

57
Metabolic Compensation of Respiratory Alkalosis
  • as with respiratory acidosis, it is possible to
    predict the degree of compensation that will
    occur in respiratory alkalosis
  • Acute conditions
  • pH 7.4 (5.3 - measured PaCO2 ) x 0.06
  • HCO3 24 - (5.3 - measured PaCO2 ) x 1.5
  • Chronic conditions
  • pH 7.4 (5.3 - measured PaCO2 ) x 0.02
  • HCO3 24 - (5.3 - measured PaCO2 ) x 3.8

58
Compensation of Respiratory Alkalosis
Directional Changes
Imbalance pH PaCO2 HCO3
Uncompensated ? ? normal
Partial compensation ? ? ?
Complete compensation normal ? ?
59
Metabolic Acidosis
12
H2CO3
101
1.2
HCO3
  • ABG indicators
  • pH below 7.35
  • SBC below 22 mmol/L
  • Aetiology
  • due to a gain in H or loss of HCO3
  • is differentiated by the presence or absence of
    an anion gap

60
Anion Gap
  • plasma, like all body fluids, is electrically
    neutral
  • the anion gap is the difference between the major
    cation and the major anions

Cations mmol/L Anions mmol/L
sodium 142 chloride 103
potassium 5 bicarbonate 26
calcium 5 albumin 17
magnesium 2 organic acids 5
phosphate 2
sulphate 1
Total 154 Total 154
61
Calculating the Anion Gap
  • Na - (Cl HCO3) anion gap
  • e.g. 142 (103 26) 13 mmol/L
  • (normal values range from 8 - 16 mmol/L)

62
Why Measure the Anion Gap?
  • the anion gap is reflective of the unmeasured
    anions in the plasma
  • its primary function is to allow the elimination
    of some of the possible causes of metabolic
    acidosis
  • it is classified as either high, normal or, in
    rare cases, low

63
High Anion Gap Acidosis
  • a high anion gap indicates that there is loss of
    HCO3 without a subsequent increase in Cl
  • electroneutrality is maintained through the
    increased production of ketones, lactate,
    phostates, and sulphates
  • as these anions do not form part of the anion gap
    calculation, the anion gap is greater than normal

64
Causes of High Anion Gap Acidosis
  • Endogenous sources of acid production
  • ketoacidosis (diabetic, alcoholic, starvation)
  • anaerobic metabolism (cardiopulmonary problems,
    sepsis, convulsions)
  • renal failure
  • Exogenous sources of acid production
  • drug and alcohol intoxication (salicylates,
    isoniazid, iron, ethylene glycol, methanol,
    paraldehyde)

65
Normal Anion Gap Acidosis
  • the balance between the measured positive and
    negative ions is not disturbed
  • with the loss of HCO3 being compensated for by
    an increase in Cl, the anion gap remains in
    normal range
  • normal anion gap acidosis is therefore also
    referred to as hyperchloraemic acidosis

66
Causes of Normal Anion Gap Acidosis
  • Gastrointestinal losses of HCO3
  • diarrhoea
  • drainage of pancreatic / biliary secretions
  • small bowel obstruction
  • urinary diversion
  • Renal losses of HCO3
  • renal tubular acidosis
  • carbonic anhydrase inhibitors e.g. acetazolamide

67
Respiratory Compensation of Metabolic Acidosis
  • by increasing alveolar ventilation the
    respiratory centre elicits a fall in PaCO2, the
    resultant rise in pH sees the HCO3H2CO3 ratio
    move back towards 201
  • the degree of respiratory compensation in
    metabolic disturbances can be predicted by
    Winters formula
  • expected PaCO2 (1.5 x HCO3) (8/-2) x
    0.133

68
Applying Winters Formula
  • by Winters formula the expected PaCO2 for a
    metabolic acidosis with an SBC of 14 mmol/L
    ranges from 3.6 4.1 KPa
  • expected PaCO2 (1.5 x 14) (6) x 0.133
    3.6
  • expected PaCO2 (1.5 x 14) (10) x 0.133
    4.1
  • an additional respiratory condition may co-exist
    if the PaCO2 falls outside of the predicted
    range

69
Corrected Bicarbonate
  • it is possible, by correcting the HCO3, to
    determine whether or not a second acid-base
    disturbance is being masked by a high anion gap
    acidosis
  • to correct the HCO3 for the effect of the high
    anion gap acidosis the measured HCO3 must be
    added to the missing HCO3
  • corrected HCO3 measured HCO3 (anion
    gap - 12)

70
  • the corrected bicarbonate for a high anion gap
    acidosis of 28mmol/L and a measured HCO3 of 8
    mmol/L 24 mmol/L
  • corrected HCO3 measured 8 (28 -12) 24
  • with the HCO3 in normal limits, no other
    metabolic disturbance exists
  • recalculating the corrected bicarbonate using a
    measured HCO3 of 18 mmol/L demonstrates a
    primary metabolic alkalosis co-exists
  • corrected HCO3 measured 18 (28 -12) 34

71
Metabolic Alkalosis
HCO3
1.2
301
36
H2CO3
  • ABG indicators
  • pH above 7.45
  • SBC above 26 mmol/L
  • Aetiology
  • produced by
  • an excessive gain of HCO3 in the ECF
  • a loss of H from the ECF

72
Causes of Metabolic Alkalosis
Addition of base to ECF excessive alkali ingestion massive blood transfusion volume depletion
Chloride depletion loss of acidic gastric juices diuretics
Potassium depletion hypokalaemia hyperaldosteronism Cushings syndrome Bartters syndrome
73
Respiratory Compensation of Metabolic Alkalosis
  • hypoventilation causes a compensatory rise in
    PaCO2
  • the level of compensatory change is less
    predictable than in metabolic acidosis
  • the expected elevation in PaCO2 is 0.8 KPa for
    every 10mmol/L increase in HCO3
  • this degree of respiratory compensation can be
    predicted by the following formula
  • PaCO2 5.3 (0.8 x (measured HCO3 - 24 /
    10)

74
  • the expected rise in PaCO2 for a metabolic
    alkalosis with a HCO3 of 34 mmol/L is 6.1 KPa
  • PaCO2 5.3 (0.8 x (34- 24 / 10) 6.1

75
Mixed Acid-Base Disturbances
  • more than one of the four primary disorders is
    occurring simultaneously
  • the separate disorders may have a neutralising or
    additive effect on the pH
  • apply the principles outlined to determine if
    compensation falls into predicted ranges
  • if not, there are a number of disorders
    independently co-existing

76
Examples of Mixed Disturbances
  • salicylate intoxication - metabolic acidosis and
    respiratory alkalosis
  • renal failure and vomiting metabolic acidosis
    and metabolic alkalosis
  • hyperemesis during pregnancy metabolic
    alkalosis and respiratory alkalosis
  • COPD and vomiting metabolic alkalosis and
    respiratory acidosis
  • respiratory acidosis and respiratory alkalosis
    cannot co-exist

77
Systematic Method of Arterial Blood Gas
Interpretation
  • assess oxygenation
  • determine pH status - ? ? 7.35, normal or ? 7.45
  • assess PCO2 - ? ? 4.5 KPa, normal or ? 6.0 KPa
  • assess SBC -? ? 22 mmol/L, normal or ? 26 mmol/L
  • assess for compensation

78
Interpretation of Arterial blood Gases
79
Interpretation of Arterial Blood Gases
  • Making use of the compensatory formulae in the
    presentation, examine following arterial blood
    gases to
  • identify the acid-base disturbance(s) present
  • assess if compensation has occurred

80
Example One
  • This ABG result is from a 60 year old patient
    with pneumonia. He is self ventilating on 35
    oxygen
  • is he hypoxic?
  • is there an acid-base or ventilation problem?

pH 7.20 PaCO2 8.0 KPa PaO2 - 8.85 KPa SBC -
26 mmol/L SBE - 2 mmol/L SaO2 - 89
81
Is He Hypoxic?
  • Yes
  • at 14.29 KPa, the alveolar to arterial oxygen
    gradient is high
  • PAO2 .35(101 6.3) 8.0 23.14 Kpa
  • 0.8
  • A-aO2 gradient 23.14 8.85 14.29 KPa
  • it is likely the pneumonia has resulted in
    inadequate ventilation and perfusion, thus
    affecting the transfer of oxygen from the
    alveolus to arterial blood

82
Is there an Acid-Base or Ventilation Problem?
  • Yes
  • the pH is low
  • the PaCO2 is high
  • the SBC is normal
  • respiratory acidosis

pH 7.20 PaCO2 8.0 KPa PaO2 - 8.85 KPa SBC -
26 mmol/L SBE - 2 mmol/L SaO2 - 89
83
Has Compensation Occurred?
  • No
  • calculating the predicted changes in pH and HCO3
    confirms that compensation has not yet taken
    place
  • predicted pH 7.4 (8.0 5.3) x 0.06 7.23
  • predicted HCO3 24 (8.0 5.3) x 0.8
    26.16
  • the results are consistent with acute respiratory
    acidosis, there is no additional disturbance
    present

84
Analysis
  • uncompensated respiratory acidosis with
    hypoxaemia most likely secondary to pneumonia

85
Example Two
  • This ABG result is from a 48 year old patient
    who has a 5 day history of severe vomiting. On
    examination she is tachycardic, hypotensive and
    dehydrated. The ABG is taken on room air
  • is she hypoxic?
  • is there an acid-base or ventilation problem?

pH 7.23 PaCO2 2.9 KPa PaO2 - 12.5 KPa SBC -
10 mmol/L SBE - -14 mmol/L SaO2 - 97 Na -
140 mmol/L Cl- - 77 mmol/L
86
Is She Hypoxic?
  • No
  • this is a normal PaO2 for a patient of this age
    breathing room air

87
Is there an Acid-Base or Ventilation Problem?
  • Yes
  • the pH is low
  • the PaCO2 is low
  • the SBC is low
  • metabolic acidosis

pH 7.23 PaCO2 2.9 KPa PaO2 - 12.5 KPa SBC -
10 mmol/L SBE - -14 mmol/L SaO2 - 97 Na -
140 mmol/L Cl- - 77 mmol/L
88
Has Compensation Occurred?
  • Yes
  • using Winter's formula, the expected PaCO2 for a
    metabolic acidosis with an SBC of 10mmol/L ranges
    from 2.79 3.32 KPa
  • predicted PaCO2 (1.5 x 10) 6 x 0.133 2.79
  • predicted PaCO2 (1.5 x 10) 10 x 0.133
    3.32
  • as the PaCO2 falls within this range,
    compensation is adequate and no separate
    respiratory disorder exists

89
Is the Anion Gap Normal or High?
  • High 53 mmol/L
  • anion gap 140 (77 10) 53
  • this elevated anion gap is secondary to
    hypovolaemia, this has occurred as a result of
    persistent vomiting, and the subsequent
    accumulation of lactic acid

90
Is the Corrected Bicarbonate in Normal Limits?
  • No
  • corrected HCO3 10 (53 - 12) 51 mmol/L
  • higher than normal, the corrected bicarbonate
    demonstrates the presence of a concurrent
    metabolic alkalosis - this is also the result of
    severe vomiting and the loss of acidic gastric
    juices

91
Analysis
  • mixed high anion gap metabolic acidosis (with
    adequate compensation) and metabolic alkalosis
    that is most likely the result of lactic acidosis
    and vomiting

92
Example Three
  • This ABG result is from a 23 year patient who
    has attended AE complaining of acute
    breathlessness. She is very anxious, has a
    respiratory rate of 35 and is self ventilating on
    room air
  • is she hypoxic?
  • is there an acid-base or ventilation problem?

pH 7.48 PaCO2 3.9 KPa PaO2 - 10.6 KPa SBC -
22 mmol/L SBE - -2.5 mmol/L SaO2 - 96
93
Is She Hypoxic?
  • No
  • this is a normal PaO2 for breathing on room air

94
Is there an Acid-Base or Ventilation Problem?
  • Yes
  • the pH is high
  • the PaCO2 is low
  • the SBC is normal
  • respiratory alkalosis

pH 7.48 PaCO2 3.9 KPa PaO2 - 10.6 KPa SBC -
22 mmol/L SBE - -2.5 mmol/L SaO2 - 96
95
Has Compensation Occurred?
  • No
  • calculating the expected changes in pH and HCO3
    confirms that compensation has not yet taken
    place
  • expected pH 7.4 (5.3 3.9) x 0.06 7.48
  • expected HCO3 24 (5.3 3.9) x 1.5 21.9
  • the results are consistent with acute respiratory
    alkalosis, there is no additional disturbance
    present

96
Analysis
  • uncompensated respiratory alkalosis most likely
    secondary to anxiety and hyperventilation

97
Example Four
  • This ABG result is from a 50 year old moderately
    dehydrated man admitted with a 2 day history of
    acute diarrhoea. He is self ventilating on room
    air
  • is he hypoxic?
  • is there an acid-base or ventilation problem?

pH 7.31 PaCO2 4.2 KPa PaO2 - 12.4 KPa SBC -
16 mmol/L SBE - -8 mmol/L SaO2 - 98 Na - 134
mmol/L Cl- - 108 mmol/L
98
Is He Hypoxic?
  • No
  • this is a normal PaO2 for breathing on room air

99
Is there an Acid-Base or Ventilation Problem?
  • Yes
  • the pH is low
  • the PaCO2 is low
  • the SBC is low
  • metabolic acidosis

pH 7.31 PaCO2 4.2 KPa PaO2 - 12.4 KPa SBC -
16 mmol/L SBE - -8 mmol/L SaO2 - 98 Na - 134
mmol/L Cl- - 108 mmol/L
100
Has Compensation Occurred?
  • Yes
  • using Winter's formula, the expected PaCO2 for a
    metabolic acidosis with an SBC of 16mmol/L ranges
    from 3.99 4.52 KPa
  • predicted PaCO2 (1.5 x 16) 6 x 0.133 3.99
  • predicted PaCO2 (1.5 x 16) 10 x 0.133
    4.52
  • as the PaCO2 falls within this range,
    compensation is adequate and no separate
    respiratory disorder exists

101
Is the Anion Gap Normal or High?
  • Normal 10 mmol/L
  • anion gap 134 (108 16) 10
  • this normal anion gap is most probably the result
    of the gastrointestinal loss of HCO3 that
    occurs with diarrhoea

102
Analysis
  • normal anion gap metabolic acidosis with adequate
    compensation most likely secondary to severe
    diarrheoa

103
Example Five
  • This ABG result is from a 63 year old patient
    admitted from the COPD clinic who is dyspnoeic,
    has a productive cough and a pyrexia of 37.9?C.
    She is self ventilating with a saturation of 89
    on an FiO2 of .28
  • is she hypoxic?
  • is there an acid-base or ventilation problem?

pH 7.35 PaCO2 8.5 KPa PaO2 - 7.3 KPa SBC -
34 mmol/L SBE - 10 mmol/L SaO2 - 88
104
Is She Hypoxic?
  • Yes
  • the SpO2 and calculated saturation agree
  • at 8.59 KPa, the alveolar to arterial oxygen
    gradient is high
  • PAO2 .28(101 6.3) 8.0 15.89 Kpa
  • 0.8
  • A-aO2 gradient 15.89 7.3 8.59 Kpa
  • it is likely that structural damage associated
    with COPD is affecting the transfer of oxygen
    from the alveolus to arterial blood

105
Is there an Acid-Base or Ventilation Problem?
  • Yes
  • the pH is normal
  • the PaCO2 is high
  • the SBC is high
  • respiratory acidosis

pH 7.35 PaCO2 8.5 KPa PaO2 - 7.3 KPa SBC -
34 mmol/L SBE - 10 mmol/L SaO2 - 88
106
Has Compensation Occurred?
  • yes
  • calculating the predicted changes in pH and HCO3
    confirms that compensation has taken place
  • predicted pH 7.4 (8.5 5.3) x 0.02 7.34
  • predicted HCO3 24 (8.5 5.3) x 3.0 33.6
  • the results are consistent with chronic
    respiratory acidosis, there is no additional
    disturbance present

107
Analysis
  • compensated respiratory acidosis with hypoxaemia
    most likely secondary to chronic respiratory
    disease

108
Example Six
  • This ABG result was taken from a 60 year old man
    admitted with lobar pneumonia. Self ventilating
    on room air, current medication is a thiazide
    diuretic which was prescribed 9 months ago
    during a previous admission with cardiac
    failure
  • is he hypoxic?
  • is there an acid-base or ventilation problem?

pH 7.64 PaCO2 4.26 KPa PaO2 - 10 KPa SBC -
33 mmol/L SBE - 9 mmol/L SaO2 - 95
109
Is He Hypoxic?
  • No
  • this is a normal PaO2 for breathing on room air

110
Is there an Acid-Base or Ventilation Problem?
  • Yes
  • the pH is high
  • the PaCO2 is low
  • the SBC is high
  • respiratory and metabolic alkalosis

pH 7.64 PaCO2 4.26 KPa PaO2 - 10 KPa SBC -
33 mmol/L SBE - 9 mmol/L SaO2 - 95
111
Has Compensation Occurred?
  • based on the recent clinical diagnosis of
    pneumonia, compensation for an acute respiratory
    alkalosis with a PaCO2 of 4.26 would predict a pH
    of 7.46 and a ?HCO3? of 22.4
  • expected pH 7.4 (5.3 4.26) x 0.06 7.46
  • expected HCO3 24 (5.3 3.9) x 1.5 22.44
  • the actual values are much higher than this and
    therefore indicate that metabolic alkalosis is
    also present

112
Analysis
  • mixed alkalosis, most likely related to the long
    term use of diuretics (chronic metabolic
    alkalosis) and hyperventilation (acute
    respiratory alkalosis) in response to decreased
    lung compliance seen with pneumonia

113
References
  • Drage, S. and Wilkinson, D. (2001) Acid Base
    Balance. World Anaesthesia Online.
    www.nda.ox.ac.uk,wfsa/html/u13/u1312_01.htm (last
    accessed 20th May 2009).
  • Hicks, G.H. (2000) Cardiopulmonary Anatomy and
    Physiology. W.B. Saunders Company Philadelphia.
  • Metheny, N.M. (2000) Fluid and Electrolyte
    Balance Nursing Considerations. Philadelphia
    Lippincott.
  • Ramsey and Gomersall (2004) Interpretation of
    Arterial Blood Gases.
  • Simpson, H. (2004) Interpretation of Arterial
    Blood Gases A Clinical Guide for Nurses. British
    Journal of Nursing, 13(9) pp 522-8.
  • Sherwood, L. (2001) Human Physiology From Cells
    to Systems. Pacific Grove Brooks/Cole.
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