Arterial blood gas analysis

INTRODUCTION

• Most common clinical problem encountered in ICU

• Today we will discuss about the approach to indentify this acid-base disorder based on a well-
defined rules that can be applied to arterial blood gas(ABG) and serum electrolyte measurement
 WHY TO ORDER AN ABG

• Aids in establishing a diagnosis

• Helps guide treatment plan
• Aids in ventilator management
• Improvement in acid/base management allows for optimal function of medications
• Acid/base status may alter electrolyte levels critical to patient status/care
• Follow up
 NORMAL VALUES

• PH- 7.35-7.45 In pregnant mother these values are:

• Ph- 7.43
• PO2- 95 mmHg- 100 mmHg
• Po2- 104 mm of Hg
• PCO2- 35 mmHg - 45mmHg
• PCO2- 32mmhg
• HCO3- 22 – 26Meq/L • HCO3- 20 – 21mEq/L
• AG – 10-12 • AG – 10-12

• OG- -10 - +10 • OG- -10 - +10

 BASIC CONCEPTS
• Acids are of two types : volatile – H2CO3, (respiratory acid, from CO2) and fixed (Metabolic, lactate: from incomplete
metabolism of glucose, ketones : from incomplete metabolism of fatty acids and phosphates & sulphates from incomplete
metabolism of protiens)
• Daily CO2 production = 0.2 X 60 X 24 L ( assuming O2 consumption is 250ml/min and RQ is 0.8) or about 12 mol per day
• Daily metabolic acid production per day : is way more than the CO2 production, therefore it is concluded that there are more
buffering systems to neutralise this acids other than bi-carbonate
• Outside the acceptable range of pH, cellular homeostasis will be hampered as changes in neuronal excitability, denaturation
of proteins and enzymes, cellular death
• To counter this our body has several defence mechanisms:
i. BUFFERS : EXTRACELLULAR: HCO3, NH4+, INTARCELLULAR : PROTEINS, PHOSPHATES
ii. RESPIRATORY CONTROLS : CONTROL OF CO2
iii. RENAL SYSTEM : CONTROL OF HCO3 AND NH4+
 Oxidation of Metabolism of Non-
CO2 HA
carbohydrates proteins volatile
and fatty acids
acids
Intracellular buffers ↔ H+ A-

CO2 + H2O
↔ H2CO3
↔ HCO3- H+ A-
+

Reabsoptio
n

HCO3- H+ A-
CO2 CO2 Components +
NH3
of acid-base
balance
NH4+ HA/A-
 CHECK FOR THE VALIDITY OF ABG
• Henderson equation : pH H+ conc pH H+ conc
[H+ ][HCO3-]/ PaCO2 =
6.75 178 7.40 40
24
6.80 151 7.45 35
• The hydrogen ion is 6.85 141 7.50 32
calculated by
6.90 126 7.55 28
subtracting the two
6.95 112 7.60 25
digits after the decimal
7.00 100 7.65 22
point of pH from 80,
e.g. If the pH is 7.23 7.05 89 7.70 20
then [H+] = 80 - 23 = 57 7.10 79 7.75 18
or [H+] = 10(9-pH) 7.15 71 7.80 16
• PH VALUE AND 7.20 63 7.85 14
CORRESPONDING H+ 7.25 56 7.90 13
ION CONCENTRATION 7.30 50 7.95 11
7.35 45 8.00 10
 VALIDITY OF ABG

pH 7.284
• From HH equation we can derive that
PaCO2 43.4 mmHg
PaO2 84.1 mmHg [H+] x HCO3- /PaCO2 = 24
HCO3- 20.6 mmol/L • From the ABG we can say that pH = 7.28 i.e, [H+] = 50
Na 147 mmol/L
• Then the equation will be 50 x 20.6/43.4 = 23.7
K 7.4 mmol/L
• Hence the ABG is a valid one
Ca 0.88 mmol/L
Cl 110 mmol/L
Lactate 2.28 mmol/L
Pct 44.2 %
SO2 94.9 %
CLASSIFICATION OF ACID-BASE DISORDER
• According to traditional concepts of acid-base physiology, the [H +] in extracellular fluid is determined by the balance
between the partial pressure of carbon dioxide (PCO 2) and the concentration of bicarbonate (HCO 3) in the fluid.

• The equation is [H+] = 24 x (PaCO 2/HCO3-)

Acid base disorder Primary Change Secondary Response

Respiratory acidosis ↑ PCO2 ↑ HCO3
Respiratory alkalosis ↓ PCO2 ↓ HCO3
Metabolic acidosis ↓ HCO3 ↓ PCO2
Metabolic alkalosis ↑ HCO3 ↑ PCO2

• Respiratory acid-base disorder: an increase in PCO2 is a respiratory acidosis, and a decrease in PCO2 is a respiratory
alkalosis
• Metabolic acid-base disorder: a decrease in HCO3 is a metabolic acidosis, and an increase in HCO3 is a metabolic
alkalosis.
 STAGE I
• In the first stage of the approach, the PaCO2 and pH are used to identify the primary acid-base
disorder.

• Rule 1: If thePaCO2and/or the pH is outside the normal range, there is an acid-base disorder.
• Rule 2: If the PaCO2 and pH are both abnormal, compare the directional change.

Rule 2a: Rule 2b:

If the PaCO2 and pH change in the same direction, If the PaCO2 and pH change in opposite directions,
there is a primary metabolic acid-base disorder. there is a primary respiratory acid-base disorder.
 STAGE I CONTD……
• Rule 3: If only the pH or PaCO2 is abnormal, the condition is a mixed metabolic and
respiratory disorder (i.e., Equal and opposite disorders).

Rule 3a Rule 3b
If the PaCO2 is abnormal, the directional change in If the pH is abnormal, the directional change in pH
PaCO2 identifies the type of respiratory disorder identifies the type of metabolic disorder (e.g., low pH
(e.g., high PaCO2 indicates a respiratory acidosis), indicates a metabolic acidosis) and the opposing
and the opposing metabolic disorder. respiratory disorder.
 STAGE II

• The second stage of the approach is for cases where a primary acid-base disorder has been
identified in stage I. The goal in stage II is to determine if there is an additional acid-base
disorder.
• If a mixed acid-base disorder was identified in stage I, go directly to stage III

• Rule 4: For primary metabolic disorder : if measured PaCO2 is higher than expected, there is a
secondary respiratory acidosis, if measured PaCO2 is lower than expected, there is a secondary
respiratory alkalosis
 RESPONSES TO METABOLIC ACID-BASE
DISORDER
• METABOLIC ACIDOSIS:
• The secondary response to metabolic acidosis is an increase in minute ventilation (tidal volume and respiratory
rate) and a subsequent decrease in PaCO2. This response appears in 30–120 minutes, and can take 12 to 24 hours
to complete
• The magnitude of this changes will be:
• PaCO2 = (1.5 X [HCO3-]) +8 ± 2 = (1.5 X 18) +8 ± 2 = 27 + 8 ± 2 = 35 ± 2

• METABOLIC ALKALOSIS:
• The secondary response to metabolic alkalosis is a decrease in minute ventilation and a subsequent increase in paco2.
• This response is not as vigorous as the response to metabolic acidosis because the peripheral chemoreceptors are not
very active under normal conditions, so they are easier to stimulate than inhibit
• The magnitude of these response will be

• ΔPaCO2 = 0.75 ΔHCO3-

 METABOLIC ACIDOSIS
• A post-operative 42 yrs, 55kg female patient with
partial gastrectomy on 2nd post-operative day pH 7.134
shows the following blood gas parameters:
PaO2 88 mmHg
• pH and PCO2 both change in same direction, so PaCO2 34 mmHg
the disorder is metabolic HCO3- 17 mmol/
• this is a case of metabolic acidoosis L
Na 145 mEq/L
• Expected PaCO2 = 1.5 x HCO3 + 8 (+/-) 2 K 6.2 mEq/L
= 1.5 x 17 + 8 (+/-) 2
= 25 + 8 (+/-) 2 Cl 110 mEq/L
= 33 (+/-) 2 Lactate 4.4 mmol/
• Bi-carbonate = 0.3 x Body Wt x Base Deficit L
= 0.3 x 55 x (24 - 17) mmol Ca++ 0.878 mmol/
= 115.5 mmol L
• Required NaHCO3 (7.5%) = [115.5/0.9] ml Hct 33 %
= 128.8 ml
SaO2 94 %
 METABOLIC ALKALOSIS

pH 7.536 • pH and PCO2 both change in same direction, so the disorder is

PCO2 45.2 mmHg metabolic
• This is a case of metabolic alkalosis
PO2 91.9 mmHg • HCO3- is 37.5
HCO3- 37.5 mmol/L • So expected ∆PaCO2 = 0.75 x ∆ HCO3-
Na 142 mmol/L = 0.75 x (37.5 – 24) = 0.75 x 13.5
= 10
K 2.1 mmol/L • Therefore expected PaCO2 will be (35 to 45) + 10 = 45 to 55
Ca NA
Cl 107 mmol/L
Lactate NA
Hct 27 %
SO2 97.7 %
• RULE 5:
For primary respiratory disorder: for a primary respiratory disorder, a normal
or near-normal HCO3 indicates that the disorder is acute.

• ACUTE RESPIRATORY DISORDERS

• Acute changes in PaCO2 have a small effect on the plasma HCO3, as indicated in
the following two equations
• ΔHCO3- = 0.1 X ΔPaCO2 (FOR ACUTE RESPIRATORY ACIDOSIS)
= 0.1 X (60-40) = 2 Meq/L INCREASE IN HCO3-
• ΔHCO3- = 0.2 X ΔPaCO2 (FOR ACUTE RESPIRATORY ALKALOSIS)
= 0.2 X (40-30) = 2 Meq/L DECREASE IN HCO3-
• 53 yr old smoker patient has been being operated for intestinal obstruction. During intra-operative period
he developed severe bronchospasm. His blood gas parameter are as follows:

pH 7.146 • pH and PaCO2 goes in opposite direction, so this is a

PaCO2 64.4 mmHg case of respiratory acidosis
PaO2 117 mmHg • Expected ∆HCO3- = ∆PaCO2 x 0.1
= 0.1 x (64.4 - 40) = 0.1 x 24.4
HCO3- 26.2 mmol/l
= 2.44
Na 139.5 mmol/l • So expected HCO3- will be = 24 + 2.44 = 26.44
K 4.2 mmol/l • Therefore we can say that this is a case of Acute
Ca 0.853 mmol/l respiratory acidosis
Cl 101.9 mmol/l
Lactate 1.1 mmol/l
Hct 35.3 %
SaO2 98.7 %
 STAGE II CONTD……
• RULE 6: FOR A PRIMARY RESPIRATORY DISORDER WHERE THE HCO 3 IS ABNORMAL,
DETERMINE THE EXPECTED HCO3 FOR A CHRONIC RESPIRATORY DISORDER.

Rule 6a Rule 6b
For a chronic respiratory acidosis, if the HCO3 is lower For a chronic respiratory alkalosis, if the HCO3 is higher
than expected, there is an incomplete renal response, than expected, there is an incomplete renal response, and
and if the HCO3 is higher than expected, there is a if the HCO3 is lower than expected, there is a secondary
secondary metabolic alkalosis. metabolic acidosis.
• CHRONIC RESPIRATORY DISORDERS
• The renal response to an increase in PaCO2 is an increase in HCO3
reabsorption in the proximal renal tubules, which raises the plasma HCO3
concentration. The response to a decrease in PaCO2 is a decrease in renal
HCO3 reabsorption, which lowers the plasma HCO3 concentration
• The magnitude of this response is similar, regardless of the directional
change in PaCO2, so the equation below applies to both chronic
respiratory acidosis and alkalosis
• ΔHCO3- = 0.4 X ΔPaCO2 (CHRONIC RESPIRATORY ALKALOSIS)
• ΔHCO3- = 0.4 X ΔPaCO2 (CHRONIC RESPIRATORY ACIDOSIS)
• A 52 YR OLD CHRONIC SMOKER HAS BEEN BROUGHT TO ER WITH SEVERE RESPIRATORY DISTRESS. ON
EXAMINATION HIS BLOOD GAS ANALYSIS IS AS BELOW:

pH 7.291 • pH and PaCO2 changes in opposite direction, so this is a

PaCO2 80.8 mmHg case of respiratory acidosis
PaO2 104.2 mmHg • As HCO3- is higher than normal, we can say that there is
some metabolic compensation for the respiratory change
HCO3- 38.1 mmol/L
• Expected ∆HCO3- = 0.4 x ∆PaCO2
Na 145.4 mmol/L = 0.4 x (80.8 - 40) = 0.4 x 40.8
K 3.8 mmol/L = 16.32
Ca 0.98 mmol/L • So expected HCO3- = (20 to 26) + 16.32 = 36.32 to 42.32
Cl 104 mmol/L
Lactate 1.8 mmol/L
Hct 44 %
SaO2 97.3 %
 STAGE III

• The final stage of this approach is for patients with a metabolic acidosis, where the use of
measurements called gaps can help to uncover the underlying cause of the acidosis.
• These are described in the next slides.
 THE GAPS
• ANION GAPS: The anion gap is a rough estimate of the relative abundance of unmeasured anions, and is
used to determine if a metabolic acidosis is due to an accumulation of non-volatile acids (e.g., Lactic acid)
or a primary loss of bicarbonate (e.g., Diarrhea)
• DETERMINANTS : To achieve electrochemical balance, the concentration of negatively charged anions
must equal the concentration of positively charged cations. This electrochemical balance is expressed in the
equation shown below using electrolytes that are routinely measured, including sodium (na), chloride (CL),
and bicarbonate (HCO3), as well as the unmeasured cations (UC) and unmeasured anions (UA).
• NA + UC = (CL + HCO3-) + UA, BY REARRANGING WE CAN GET
• NA – (CL + HCO3-) = UA – UC,
• The difference (UA – UC) is a measure of the relative abundance of unmeasured anions, and is called the
anion gap (AG).
 ANION GAP CONTD.

• SO AG = NA – (CL + HCO3-) , OR MAY BE CALLED SIMPLE OR TRADITIONAL

• AG (CONVENTIONAL) = (NA + K) – ( CL + HCO3-)
• AG (MODERN) = (NA + K) – ( CL + HCO3- + LACTATE)

• SO IF ALBUMIN IS REDUCED BY 50% AG WILL BECOME 4 MEQ/L

 INFLUENCE OF ALBUMIN OVER ANION GAP
• The unmeasured anions and cations that normally contribute to the anion gap
• Albumin is the principal unmeasured anion, and the principal determinant of the anion gap.
Albumin is a weak (i.E., Poorly dissociated) acid that contributes about 3 meq/L to the AG for
each 1 g/dl of albumin in plasma (at a normal ph)
• A low albumin level in plasma will lower the AG, and this could mask the presence of an
unmeasured anion (e.g., Lactate) that is contributing to a metabolic acidosis
• Since hypoalbuminemia is present in as many as 90% of ICU patients , the following formula for
the “corrected AG” (AGC) has been proposed to include the contribution of albumin
• ANION GAP CORRECTED (FOR ALBUMIN) = CALCULATED ANION GAP +
2.5 X (NORMAL ALBUMIN IN GM/DL – OBSERVED ALBUMIN GM/DL)
= 11 + 2.5 (4 – 2.1) = 11 + 4.75 = 15.75
 CLASSIFICATION OF METABOLIC ACIDOSIS

• High anion gap • Normal anion gap • Low anion gap acidosis
• Gastrointestinal • Addition to blood of
• Lactic acidosis
• Renal insufficiency with abnormal cations, like
• Ketoacidosis hyperkalaemia lithium in lithium toxicity

•Toxins (e.G, • Renal tubular acidosis • Increase in cationic

ethylene glycol. • Hyperalimentation immunoglobulin ( plasma

Methanol. Salicylates. • Ketosis with increased ketone cell dyscrasia)

Propylene glycol. excretion • Reduction in major plasma

• Hipppurate anion albumin conc. Like in
Pyroglutamic acid )
• Cation exchange resin nephrotic syndrome
•Renal failure
• Hyperviscocity
• Severe hyperlipidaemia
 LACTIC ACIDOSIS
• Lactic acidosis occurs when the production of lactate in the body is greater than the liver’s capacity to clear it.
Lactate can be converted to CO2 and H2O by the liver

• Lactic acid is produced physiologically as a degradation product of glucose metabolism. Its formation from
pyruvate is catalyzed by lactate dehydrogenase. Under normal conditions, the ratio of lactate to pyruvate is
less than 20:1
• In anaerobic conditions, for example following vigorous exercise, lactate levels increase dramatically
• Activation of β-adrenergic receptors in skeletal muscle by stress (increased circulating catecholamines) or
exogenous infusion (epinephrine or norepinephrine infusions) increases lactate, with resulting aerobic
glycolysis.
• Serum lactate and arterial pH should be measured early in any critically ill patient
• > 2MEQ/L INDICATES ACIDOSIS,
• >5 MEQ/L INDICATES SEVERE ACIDOSIS
 • Lactate as a fuel:
• lactate is classified as an
organic fuel, and has a
caloric density (3.62
kcal/g) equivalent to
glucose (3.74 kcal/g)
• 1,500 mmoles of lactate
are produced daily
under aerobic conditions
and the principal sites of
production are skeletal
muscle (25%), skin
(25%), red blood cells
(20%), brain (20%), and
intestine (10%).

Activated neutrophils are an additional source of lactate in inflammatory conditions like acute respiratory distress
syndrome (ARDS)
The concentration of lactate in plasma is usually ″2 mmol/L, with a lactate:pyruvate ratio of 10:1
Lactate is cleared from plasma by the liver (60%), kidneys (30%), and heart (10%).
 LACTIC ACIDOSIS CONTD…
• TWO TYPES OF LACTIC ACIDOSIS ARE RECOGNIZED.
• TYPE A (Global inadequate oxygen delivery) is seen in hypovolemic or hemorrhagic shock, the
presence of a low mixed venous oxygen saturation (SvO2) with a high lactate concentration,
coupled with an elevated lactate-to-pyruvate ratio (>20:1), is indicative of type A (hypoxia
associated) acidosis

• TYPE B Occurs despite normal global oxygen delivery and tissue perfusion. (Type B lactic
acidosis is associated with any state characterized by excess circulating catecholamines
(endogenous or exogenous). Examples include simple exercise and the hyperinflammatory state
of trauma or sepsis)
• TYPE B LACTIC ACIDOSIS May also be seen in cyanide poisoning (associated with sodium
nitroprusside), with biguanides (metformin), and in hypercatabolic diseases, such as lymphoma,
leukemia, acquired immunodeficiency syndrome (AIDS), or diabetic ketoacidosis
 LACTIC ACIDOSIS CONTD…

• Presence of normal systemic indices does not exclude regional hypoperfusion or mitochondrial failure.
• Dynamic measurements of lactate over time are better predictors of outcome than are static measures.
• Lactate clearance has been proposed as an end point of resuscitation in sepsis, because lactate
concentration should decrease with adequate resuscitation
• A failure of lactate clearance in response to resuscitation suggests that global perfusion is not the
underlying problem and should prompt a search for a more sinister etiology
• Most cases of lactic acidosis involve the l -isomer. By comparison, d -lactic acidosis, a disorder
observed most commonly in patients with abnormal bowel anatomy, results in a rise in the AG, but the
lactate level is normal. D -lactate is not detected by the usual lactate assay, which measures only l –
lactate and a specific assay must be requested to diagnose this disorder.
 CAUSES OF LACTIC ACIDOSIS
• CLINICAL SHOCK SYNDROMES
• SYSTEMIC INFLAMMATORY RESPONSE SYNDROME
• THIAMINE DEFICIENCY
• PHARMACEUTICAL AGENTS : METFORMIN, ANTI-RETRO VIRAL AGENTS, EPINEPHRINE,
NITRO-PRUSSIDE, LINEZOLID
• NON-PHARMACEUTICAL TOXIDROMES : PROPYLENE ALCOHOL
• OTHER CAUSES : Other possible causes of hyperlactatemia in ICU patients include generalized seizures
(from hypermetabolism) , hepatic insufficiency (from reduced lactate clearance) , acute asthma (from
enhanced lactate production by the respiratory muscles) , and hematologic malignancies (rare)
• Most cases of d-lactic acidosis have been reported after extensive small bowel resection or after jejunoileal
bypass for morbid obesity
 METABOLIC ALKALOSIS
• PRIMARY METABOLIC ALKALOSIS IS CHARACTERIZED BY AN ELEVATED PLASMA HCO
−3 CONCENTRATION IN THE PRESENCE OF AN ARTERIAL PH ABOVE 7.40.
• PATHOPHYSIOLOGY: THERE ARE TWO STEPS INVOLVED IN THE DEVELOPMENT OF
METABOLIC ALKALOSIS. THE FACTORS THAT MEDIATE THE GENERATION PHASE MAY
DIFFER FROM THOSE THAT ENABLE ITS MAINTENANCE.
• A PRIMARY RISE IN THE PLASMA HCO −3 CONCENTRATION CAN BE INDUCED BY ONE OR MORE OF
THREE MECHANISMS:
• (A) LOSS OF ACID FROM THE GASTROINTESTINAL TRACT OR IN THE URINE,
• (B) ADMINISTRATION OF HCO −3 OR A PRECURSOR SUCH AS CITRATE, OR
• (C) LOSS OF FLUID WITH A CL− -TO-HCO −3 RATIO THAT IS HIGHER THAN THAT OF PLASMA
• THE THIRD CONDITION IS SOMETIMES REFERRED TO AS CONTRACTION ALKALOSIS BECAUSE THE
TOTAL HCO −3 CONTENT REMAINS RELATIVELY UNCHANGED WHILE THE EXTRACELLULAR FLUID
VOLUME “CONTRACTS AROUND IT,” THEREBY ELEVATING THE HCO −3 CONCENTRATION
 TYPES OF METABOLIC ALKALOSIS
• Chloride responsive Chloride resistant:
(urinary chloride >20mEq/L)
(URINARY CHLORIDE <15
MEQ/L)
• Mineralocorticoid excess
• Vomiting
• Nasogastric suction • Alkali loading
• Postdiuretic administration • During diuretic administration
• Posthypercapnia • Severe hypokalemia
• High-dose penicillin therapy
• Bartter’s and Gitelman’s syndromes
• Alkali loading a
Since the maintenance of metabolic alkalosis requires impairment of renal bicarbonate excretion, the pathophysiology of the renal
limitation determines the urinary chloride concentration. If, for example, there is underlying hypovolemia, the urinary chloride
concentration is low (< 15 mEq/L); in comparison, the urinary chloride concentration is > 20 mEq/L when the cause of renal bicarbonate
retention is a reduction in glomerular ltration rate, as in the milk-alkali syndrome, or in patients with acute tubular necrosis who received
large alkali loads.
• A hyperchloremic state may be associated with nephrotoxicity: saline infusion has been
associated with reduced renal blood flow, renal vasoconstricton, reduced glomerular filtration,
splanchnic hypoperfusion, and perhaps an increased risk of contrast nephropathy
• Critically ill patients with sepsis frequently develop hyperchloraemic acidosis that appears to be
associated with worse outcomes. The use of Cl−-rich fluids was associated with a 3.7% absolute
increase in the risk for need of renal replacement therapy relative to balanced salt solution
• The presence of a significant base deficit and low pH in a patient with diabetic ketoacidosis or
lactic acidosis usually prompts continued fluid resuscitation. However, this strategy may be
inappropriate if the cause of acidosis is hyperchloremia
• Use of plasma-lyte 148 shows more rapid resolution of acidosis, improved hemodynamics and better
urine output when compared with 0.9% NaHCO3.
 MANAGEMENT OF METABOLIC ALKALOSIS

• CHLORIDE SENSITIVE:
• Cl- deficit should be calculated = 0.6 x body wt x (expected chloride – measured chloride)
= 0.5 x 55 x (103 - 90) meq
= 27.5 x 13 meq = 357.5 meq
• Cl deficit will be managed with Normal Saline (0.9%) = 1 litre NS contains 154 meq Cl
• So required volume of NS will be = (357/154) l = 2.3 litre (Approx.)
 METABOLIC ALKALOSIS CONTD

• CHLORIDE RESISTANT
• USUALLY RESPONSIVE TO POTASSIUM AND MAGNESIUM
SPPLEMENT
• 0.1 N HCL IS ANOTHEROPTIONN, TOO MUCH COMPLICATIONS
• ACETAZOLAMIDE CAN BE EMPLOYED
RESPIRATORY ACIDOSIS
• Respiratory acidosis complicates a wide variety of pathologic processes.
• Neurologic injury (stroke, spinal cord injury, botulism, tetanus)
• Toxic suppression of the respiratory center (opioids, barbiturates, benzodiazepines)
• Neuromuscular disorders (guillain-barré syndrome, myasthenia gravis)
• Abdominal hypertension, flail chest, hydro-hemo-pneumothorax, pulmonary edema, and pneumonia

• It also complicates anesthesia with excessive sedation, partial neuromuscular

blockade, and intraoperative hypoventilation
• Frequently, mechanical ventilation is required to reverse the acidosis
 RESPIRATORY ALKALOSIS

• Caused by hyperventilation, in response to anxiety or pain, central respiratory stimulation (as

occurs early in salicylate poisoning), or excessive artificial ventilation
• Acute respiratory alkalosis usually accompanies acute metabolic acidosis, in which case the
reduction in pco2 from baseline (usually 40 mm hg) is equal to the magnitude of the base deficit
 MEASUREMENT OF OXYGEN
• ARTERIAL BLOOD GAS ANALYSIS IS USED TO ASSESS OXYGENATION, VENTILATION
• OXYGENATION IS REFLECTED IN THE PAO2, WHICH IS A FUNCTION OF THE ALVEOLAR PARTIAL
PRESSURE OF O2 (PAO2) AND THE EFFICIENCY OF O2 TRANSFER FROM ALVEOLI TO THE PULMONARY
CAPILLARY BLOOD
• IN HEALTHY ADULTS BREATHING ROOM AIR AT SEA LEVEL, PAO2 RANGES BETWEEN 80 AND 100 MM HG.
THE NORMAL VALUE OF PAO2 DECREASES WITH INCREASING AGE AND INCREASING ALTITUDE
• HYPOXEMIA IS DEFINED AS A PaO2 LESS THAN 80 MM HG. HYPOXEMIA HAS FIVE PHYSIOLOGIC CAUSES
• 1. HYPOVENTILATION
• 2. V˙ /Q˙ MISMATCHING
• 3. RIGHT-TO-LEFT SHUNT
• 4. DIFFUSION LIMITATION
• 5. DIFFUSION-PERFUSION MISMATCH

• THE FIRST THREE CAUSES EXPLAIN MOST CASES OF HYPOXEMIA IN THE PERIOPERATIVE SETTING.
 OTHER INDICES OF OXYGENATION
• PaO2 : it is limited in providing a measure of the magnitude of the O2 exchange deficiency because
of its dependence on the FiO2 & nonlinear relationship between PaO2 and blood O2 content
• Several indices based on the PaO2 that account for the FiO2 or the PaO2 have been developed
1. THE ALVEOLAR-ARTERIAL PARTIAL PRESSURE GRADIENT OF O2 ([A-a]PO2), [ = 0.21 × (AGE + 2.5) ]
2. THE RESPIRATORY INDEX ([A-a]PO2)/PaO2),
3. THE ARTERIAL-ALVEOLAR RATIO OF O2 PARTIAL PRESSURES (PaO2/PAO2),
4. THE RATIO BETWEEN PaO2 AND FiO2 (PaO2/FiO2).
• LIMITATIONS : A) THESE INDICES ARE DEPENDANT ON Fio2*, Hb, PaCO2* AND O2 CONSUMPTION, ANY VARIATION
WILL CHANGE THE VALUE WITH OUT SIGNIFICANT ALTERATION IN LUNG FUNCTION
B) THESE INDICES FAILED TO SHOW THE CHANGE IN V/Q MATCHING WITH CHANGE IN FIO2
C) INDICES THAT USE PAO 2 RELY ON THE ASSUMPTIONS OF THE ALVEOLAR GAS EQUATION,
INCLUDING PA =
PAO2, WHICH MAY NOT HOLD TRUE IN PATHOLOGIC CONDITIONS.
*
PAO2 = [713 X FIO2] – [ PaCO2 X 1.25]
• OXYGENATION INDEX:
The oxygenation index is a calculation used in intensive care medicine to measure the fraction of inspired
oxygen (FiO2) and its usage within the body. A lower oxygenation index is better - this can be inferred by
the equation itself.

Oxygenation index (OI) is routinely used as an indicator of severity of HRF in neonates, with
an arbitrary cutoff of 15 or less for mild HRF, between 16 and 25 for moderate HRF, between 26
and 40 for severe HRF, and more than 40 for very severe HRF

• (MAP X FIO2 X100)/POST DUCTAL O2

• 40 = MORTALITY >80 – 90%
• 25 – 40 = MORTALITY RISK 50 – 60%
• IF OXYGENATION INDEX IS >40%, IT IS AN INDICATION FOR ECMO
 TIPS
• Use of heparin:
• Liquid or crystalloid heparin, used in standard ABG sampling syringes contains na-heparin. So
whenever ABG is measured from a leftover sample na+ content may be spuriously high and due
to binding of K+ & ca++ with negatively charged heparin their conc may be spuriously low
• Lithium or electrolyte balanced heparin may counter this problem
• Temperature correction:
• If blood drawn at temp above 39*C, values should be corrected for temp.
• For each degree of temp change greater than 37*c PaO2 increases 7.2%, PaCO2 increases 4.4%,
pH decreased by 0.015
• Air bubble:
• An ABG specimen to the laboratory via a pneumatic tube system can result in alterations in PaO2
secondary to contamination with room air.
• If a pneumatic tube system is to be used, one must be sure that all air bubbles are carefully
expelled from the abg specimen and that a pressure-tight transport container is used
 TIPS

• The sample should be processed immediately, otherwise a slush of ice (not cubes) should be used
to carry the sample
• Changes in ABG every 10 min in vitro
 TIPS
• SPURIOUS HYPOXAEMIA:
• Or leucocyte larceny , extreme leukocytosis secondary to leukemia can cause spurious
hypoxemia and spurious lowering of the mixed venous PO2 due to oxygen consumption by
leukocytes. The decay in PO2 in the first 2 minutes for blood with leukocyte counts of between
55.2 X 10(3)/mm3 and 490.0 X 10(3)/mm3 ranged from 13 to 72 mmhg. The degree of PO2
decay was blunted by placing the blood on ice and was obliterated by adding potassium cyanide.
• ALTERNATIVES OF ARTERIAL BLOOD: Severe peripheral vascular disease makes radial arterial
puncture difficult, or the patient refuses arterial blood sampling or cannulation.
• Hemodynamically stable patients, pHa is, on average, 0.03 units higher than central venous
phH(pHcv) and PaCO2 is lower than central venous carbon dioxide (PcvCO2 ) by 5 mm hg
• pHA = (1.027 × pHCV) − 0.156
• PaCO2 = (0.754 ×PcvCO2 ) + 2.75
 TIPS

• Progress has been made in the area of noninvasive measurement of gas

exchange. This includes oximetry, transcutaneous PO2 and PCO2 (PtcCO2 )
measurement, end-tidal CO2, and indwelling intravascular electrode systems.
• Improvement in the ability of transcutaneous systems to accurately assess SPO2
and PtcCO2 in critically ill patients as long as the PaCO2 is less than 56 mm hg
Thank
you