arterial blood gases interpretation11111

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BLOOD GASES INTERPRETATIO N Mahmoud El Said Neonatal fellowship Herra general Hospital Mecca 2015

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Page 1: Arterial blood gases interpretation11111

BLOOD GASES INTERPRETATION

Mahmoud El SaidNeonatal fellowship

Herra general HospitalMecca 2015

Page 2: Arterial blood gases interpretation11111

What is ABG • Arterial Blood Gas (ABG) is an

investigation which plays an important role in therapeutic decision making

• And requires proper interpretation. • So a proper understanding of

various components that are analyzed is vital.

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Why measuring Blood Gases?

For evaluation of:• 1-Adequacy of Ventilation• 2-Oxygenation• 3-Acid Base status• 4-Assess the response to an

intervention

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Drawing arterial blood for ABG:• A plastic (15 min) / glass (1 h)

syringe is used.• 0.1ml of Heparin is used for 1ml of

blood drawn, as an anticoagulant. (Heparin is withdrawn into the syringe and pushed back, thus allowing heparin to just coat the syringe)

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• The safest place to draw blood for ABG is radial artery at the wrist.

• Allen s test should be done before arterial sampling to test the circulation of the hand.

• After the blood is drawn, pressure applied to the puncture site for 5-10 minutes to stop the bleeding.

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• The syringe should be sealed immediately with cap (or needle tip inserted to a cork) to avoid air bubbles.

• Blood drawn should be analyzed within 10 minutes. Otherwise it should be cooled to 4 C with ice slush when a delay of up to one hour is acceptable. (Usually the syringe is sent in a flask with ice).

• Routine practice of temperature correction for blood gas measurements is not required.

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• Commonly used in newborn

• Good in stable babies• Underestimate PaO2

• Replaced by noninvasive monitors tcPaO2 and pulse oximetery

Capillary Sampling

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•Technique:–Choose an outer portion of the infant’s heel, avoiding the antero-medial aspect.–Consider wrapping the foot in a warm cloth for five minutes to increase the blood flow.–Cleanse the area with alcohol. –Be sure to allow the area to dry, because alcohol may alter the reading.

Capillary Sampling

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–Grasp the heel firmly at the arch and ankle.–Avoid excessive squeezing of the foot, which may cause hemolysis.–Puncture the heel perpendicular to the skin with one continuous, deliberate motion to a depth not to exceed 2.5 mm.–Remove the first drop of blood with a gauze pad and collect the subsequent large drop of blood on the capillary tube.–Once the blood has been obtained, apply pressure to the puncture site and consider use of an adhesive bandage if necessary.

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Unreliable Capillary Blood Gases

• Seriously ill patients• Shock, hypotension• Peripheral vasoconstriction. • In the first day of life, poor perfusion

to the hands and feet ("acrocyanosis").

=Use arterial blood gases.

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•Technique:

–Same as routine daily sampling

–Same precautions for air bubbles, heparin content and timing

Venous Sampling

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ABG parameters• Measured values:• pH• PaCO2

• PaO2

Calculated values: • HCO3 • Base Excess• O2 saturation• ctO2 • P (A-a) O2

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Normal Neonatal A B G Values

• pH 7.4 ± 0.05.• PaCO2 40 ± 5 mm Hg.• PaO2 60 ± 10 mm Hg (term infant). 55 ± 10 mm Hg (preterm infant).• HCO3 24 ± 4 mEq/liter.• Base Excess 0 ± 4 mEq/liter.• O2 saturation 92 ± 1%.• ctO2 15 ± 7 mL / dL.• P (A-a) O2 < 15 mmHg.

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Stepwise approach to ABG Analysis

1-Determine whether patient is alkalemic or acidemic using the arterial pH measurement.

2-Determine whether the acid-base disorder is a primary respiratory or metabolic disturbance based on the PH,pCO2 and serum HCO3

- level.

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3-If a primary respiratory disorder is present, determine whether it is acute or chronic.

4-In respiratory disorders, determine if there is adequate compensation of the metabolic system.

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5-In metabolic disorders, determine if there is adequate compensation of the respiratory system.

6-If a metabolic acidosis is present, determine the anion gap.

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7-In normal (non) anion gap acidosis, determine the urinary anion gap - helpful to distinguish renal from non renal causes.

8-Determine patient oxygenation status (PaO2, ctO2, P (A-a) O2 & SaO2) – hypoxemic or not.

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Step one: Are the available data consistent or not

• You must able to establish that the available data (PH, pCO2 and HCO3) are consistent.

• Subtract the calculated H+ from 80; this give the last two digit of a PH beginning with 7.

• PH= 7. (80-H+).

»PH= 7. (80- 24 x pCO2) HCO 3

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Step two: Evaluate pHpH acidemia if ˂ 7.35.pH alkalemia if ˃7.45.

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Step three: Evaluate the Primary Acid-Base Disorder

• In the 2nd stage of the approach, the

measured pH &PaCO2 are used to determine if an acid-base disturbance is present and, if so, to identify the primary acid-base disorder.

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Rule 1 • An acid-base abnormality is

present if either the PaCO2 or the pH is outside the normal range.

A normal pH or PaCO2 does not exclude the presence of an acid-base abnormality.

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Rule 2

• If the pH and PaCO2 are both abnormal, compare the directional change.

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Rule 2•A-If both change in the same direction (both increase or decrease), the primary acid-base disorder is metabolic.

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Rule 2•B-And if both change in opposite directions, the primary acid-base disorder is respiratory.

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Example•Consider a patient with an arterial pH of 7.23 and a PaCO2 of 23 mm Hg.

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Example• The pH and PaCO2 are both

reduced (indicating a primary metabolic problem) and the pH is low (indicating acidemia), so the problem is a primary metabolic acidosis.

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Rule 3:• If the pH or PaCO2 one is normal and the other is abnormal, there is a mixed metabolic and respiratory disorder.

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Rule 3:• A-If the pH is normal and PCO2

is abnormal, the direction of change in PaCO2

identifies the respiratory disorder. And the metabolic disorder will be in the opposite direction.

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Rule 3:• B-And if the PaCO2 is normal

and PH is abnormal, there is double disorder, acidosis or alkalosis according to the direction of PH.

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Example:• Consider a patient with an arterial pH of

7.37 and a PaCO2 of 55 mm Hg. • The pH is normal and PCO2 is abnormal, so

there is a mixed metabolic and respiratory acid-base disorder.

• The PaCO2 is elevated, so the respiratory disorder is an acidosis, and thus the metabolic disorder must be an alkalosis.

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Example:• Therefore, this is a combined

respiratory acidosis and metabolic alkalosis.

• There is no primary acid-base disorder in this situation; both disorders are equivalent in severity that is why the pH is normal.

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• Remember that the compensatory responses to a primary acid-base disturbance are never strong enough to correct the pH, but act to reduce the severity of the change in pH.

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• Therefore, a normal pH in the presence of an acid-base disorder always signifies a mixed respiratory and metabolic acid-base disorder.

• (It is sometimes easier to think of this situation as a condition of overcompensation for one of the acid-base disorders.)

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Step four: Compensated, Uncompensated, or Partially

Compensated• The step four of the approach is for cases

where a primary acid-base disorder has been identified in Step three.

• The goal in Step four is to determine if the compensatory responses are adequate and if there are additional acid-base derangements.

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Rule 4:• If there is a primary metabolic acidosis or

alkalosis, use the measured serum bicarbonate concentration in Equations;

• Acidosis: Expected pCO2 = (1.5 × HCO3 ) + 8 ± 2. • Alkalosis: Expected pCO2 = (0.7 × HCO3 ) + 21 ±

2. to identify the expected PaCO2 and

respiratory compensation.

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Rule 4:• If the measured and expected PaCO2 are

equivalent, the condition is fully compensated.

• If the measured PaCO2 is higher than the expected PaCO2, there is a superimposed respiratory acidosis(uncompensated).

• If the measured PCO2 is less than the expected PCO2, there is a superimposed respiratory alkalosis.

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Example:• Consider a patient with a PaCO2 of

23 mm Hg, an arterial pH of 7.32, and a serum HCO3 of 15 mEq/L.

• The pH is acidemic and the pH and

PCO2 change in the same direction, so there is a primary metabolic acidosis.

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Example:• Equation should be used to calculate the

expected PCO2: (1.5 × 15) + (8 ±2) = 30.5 ± 2 mm Hg.

• The measured PaCO2 (23 mm Hg) is lower than the expected PaCO2, so there is an additional respiratory alkalosis.

• Therefore, this condition can be described as a primary metabolic acidosis with a superimposed respiratory alkalosis.

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expected PaCO2 28.5 32.5 40 50

Compensated metabolic acidosis.

a primary metabolic acidosis with a superimposed respiratory acidosis

a primary metabolic acidosis with a superimposed respiratory alkalosis

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Rule 5:• If there is a respiratory acidosis or alkalosis, use the

PaCO2 to calculate the expected pH using Equations for respiratory acidosis:

• Acute: Expected PH = 7.4 - 0.008 × (CO2-40 ). • Chronic: Expected PH = 7.4 - 0.003 × (CO2-40)

Or Equations for respiratory alkalosis:• Acute: Expected PH = 7.4 + 0.008 × (40-CO2). • Chronic: Expected PH = 7.4 + 0.003 × (40-

CO2).

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• Compare the measured pH to the expected pH to determine if the condition is acute, partially compensated, or fully compensated.

• For respiratory acidosis, if the measured pH is lower than the expected pH for the acute, uncompensated condition, there is a superimposed metabolic acidosis, and if the measured pH is higher than the expected pH for the chronic, compensated condition, there is a superimposed metabolic alkalosis.

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pH scale 7.24 7.34 7.4 7.5

partially Compensated

a primary respiratory acidosis with a superimposed Metabolic alkalosis

a primary respiratory acidosis with a superimposed metabolic acidosis

acute chronic

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• For respiratory alkalosis, if the measured pH is higher than the expected pH for the acute, uncompensated condition, there is a superimposed metabolic alkalosis, and if the measured pH is below the expected pH for the chronic, compensated condition, there is a superimposed metabolic acidosis.

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Example• Consider a patient with a PaCO2 of

23 mm Hg and a pH of 7.54. • The PaCO2 and pH change in

opposite directions so the primary problem is respiratory and, since the pH is alkalemic, this is a primary respiratory alkalosis.

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• The expected pH for an acute respiratory alkalosis is 7.40 + [0.008 × (40 - 23)] = 7.54.

• This is the same as the measured pH, so this is an acute, uncompensated respiratory alkalosis.

• If the measured pH was higher than 7.55, this would be evidence of a superimposed metabolic alkalosis.

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Step five : Anion gap• AG is a measure of the relative abundance of

unmeasured anions.• Used to evaluate patients with metabolic

acidosis.• Determinants of the Anion Gap:

AG= UA - UC = [Na+]-([Cl-] + [HCO3-])

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Unmeasured Anions

Proteins (15 mEq/L)Organic Acids (5

mEq/L)Phosphates (2

mEq/L)Sulfates (1mEq/L)UA = 23 mEq/L

Unmeasured Cations

Calcium (5 mEq/L)Potassium (4.5

mEq/L)Magnesium (1.5

mEq/L)

UC = 11 mEq/L

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The anion gapMg+ 2mEq/L

Ca+ 5 mEq/LK+ 4 mEq/L

Na+ (135-145) mEq/L

Other- 3mEq/L

Proteins –n 16mEq/L

Lactate- 2mEq/L

SO4 2- 2mEq/L

HPO4 2-, 2mEq/L

HCO3-(22-26)

Cl- (70-110)

Normal ABG

Unmeasured Cations

Unmeasured Anions

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• High AG metabolic acidosis is due to the accumulation of [H+] plus an unmeasured anion in the ECF.–Most likely caused by organic acid

accumulation or renal failure with impaired [H+] excretion.

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The anion gap ↑H+

K+ (3.5-4.5)

Na+ (135-145)

Anion Gap

HCO3-(22-26)

Cl- (70-110)

Anion Gap

HCO3-(<22)Cl- (70-110)

K+ (3.5-4.5)

Na+ (135-145)

Normal ABG Metabolic Acidosis +Wide Anion Gap

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• Normal AG metabolic acidosis is caused by the loss of HCO3

- which is counterbalanced by the gain of Cl- (measured cation) to maintain electrical neutrality.–Most likely caused by HCO3

- wasting from diarrhea or urinary losses.

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The anion gap ↓HCO3

K+ (3.5-4.5)

Na+ (135-145)

Anion Gap

HCO3-(22-26)

Cl- (70-110)

Anion Gap

HCO3-(<22)Cl- (>110)

K+ (3.5-4.5)

Na+ (135-145)

Normal ABG Metabolic Acidosis +Normal Anion Gap

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The anion gap H ↑ HCO3↓

K+ (3.5-4.5)

Na+ (135-145)

Anion Gap

HCO3-(22-26)

Cl- (70-110)

Anion Gap

HCO3-(<22)Cl- (>110)

Anion Gap

HCO3-(<22)Cl- (70-110)

K+ (3.5-4.5)

Na+ (135-145)

K+ (3.5-4.5)

Na+ (135-145)

Normal ABG Metabolic Acidosis +Wide Anion Gap

Metabolic Acidosis +Normal Anion Gap

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• Normal anion gap: 12± 4 mEq/L• Increased anion gap:

1. >14 mEq/L in children2. >16 mEq/L in LBW infants

(<2,500 g)3. >18 mEq/L in ELBW infants

(<1,000 g)

The anion gap

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•The cations and anions normally present in urine are Na+, K+, NH4+, Ca++,Mg++ and Cl-, HCO3-, sulphate, phosphate and some organic anions.•Only Na+, K+ and Cl- are commonly measured.•Cl- + UA = Na+ + K+ + UC•UAG = ( UA - UC ) = [Na+]+ [K+] - [Cl-]

Urinary anion gap

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•The Urinary Anion gap differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.•Urinary Anion Gap (UAG) provides a rough index of Urinary ammonium excretion. •Ammonium is positively charged so a rise in its Urinary concentration will cause a fall in UAG .

Urinary anion gap

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Urinary anion gap•If the acidosis is due to loss of base via the bowel the kidneys can respond by increasing ammonium excretion decreased UAG.•If the acidosis is due to loss of base via the kidney not able to increase ammonium excretion UAG will not be increased.•In a patient with a hyperchloraemic metabolic acidosis:

• Negative UAG GIT loss of bicarbonate• Positive UAG impaired renal distal

acidification.

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Interpretation of Anion GapAnion Gap

High anion Gap Normal or Low anion Gap

Lactic acidosisKetoacidosis

• Diabetes• Alcohol• Starvation

Toxins • Salicylate,• Methanol• Ethylglycol

Renal failure

Urinary Anion Gap

Positive Negative

Renal (RTA) GIT (Diarrheal)Fistula

Page 60: Arterial blood gases interpretation11111

PIO2 ( Pressure of Inspired Oxygen) = (Bp – H2O p) X FIO2 = (760 – 48) X 0.21 = 150 mmgh

PAO2 ( Pressure of alveolar Oxygen) = PIO2 – (PaCO2/R) = 150 – ( 45/0.8) = 100 mmgh

PaO2 ( Pressure of arterial Oxygen) = 60 – 90 mmgh

Step six : Oxygenation

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Arterial oxygen content is the sum of

hemoglobin bound oxygen in 100 ml blood

oxygen dissolved in plasma

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Oxygen content (ml/100 ml of blood)

= (1.37 x Hb )x SaO2) + (0.003 x PaO2)Where:      1.37    = Milliliters of oxygen bound to 1 g of hemoglobin at 100 percent saturation(%)

0.03  = Solubility factor of oxygen in plasma (ml/mm Hg)

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Ratio between the concentrations of O2Hb and HHb+ O2Hb

sO2(a) is the percentage of oxygenated Hb in relation to the amount of Hb capable of carrying oxygen.

Reference ranges: 90 –95 %

Arterial oxygen saturation

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Clinical interpretation of sO2

• Normal sO2 Sufficient utilization of actual oxygen transport capacity.

• Low sO2 Impaired oxygen uptake Right shift of ODC

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The situation in tissues

The situation in lung

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Several factors can affect the affinity of hemoglobin for oxygen• Alkalosis,

hypothermia, hypocapnia, and decreased levels of 2, 3-diphosphoglycerate (2, 3 DPG)

• increase the affinity of hemoglobin for oxygen.

• Shift to left

• Acidosis, hyperthermia, hypercapnia and increased 2, 3 DPG have the opposite effect.

• decreasing the affinity of hemoglobin for oxygen.

• shifting to the right.

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• This characteristic of hemoglobin facilitates oxygen loading in the lung and unloading in the tissue where the pH is lower and the PaCO2 is higher

• Fetal hemoglobin, which has a higher affinity for oxygen than adult hemoglobin, is more fully oxygenated at lower PaO2 values, This is important in utero.

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ctO2 Arterial concentration of total oxygen tO2 ctO2 = sO2 × 1.37 × ctHb + 0.003 × pO2 ml / dl.

Reference ranges : 8.8-22.3 mL / dL

Normal ctO2 adequate oxygen content of the arterial blood.

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Clinical interpretation of ctO2 High ctO2:•High pO2 Over oxygenation•Normal pO2 high ctHb (i.e.

hemoconcentration, polycytemia).Low ctO2: • low pO2 hypoxemia•Normal pO2 low ctHb and/or

dyshemoglobinemia

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• Cao2= (1.37 x 14g\dl )x 92%) + (0.003 x 60mmhg)•Cao2= (17.6 ml) + (0.1 ml)•Cao2= (99%) + (1%)

In premature

In the same infant with IVH & Hb content. Drops to 10.5 g/dl

• Cao2= (1.37 x 10.5g\dl )x 92%) + (0.003 x 60mmhg)•Cao2= (13.3 ml) + (0.1 ml) =13.4•Thus without change in PaO2 & SaO2 a 25% drop in Hb concent. reduces the O2 content by 24%

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• This concept is important to remember when taking care of infant with respiratory disease.

• Hb level should be monitored & if low rapid correction to keep adequate level of oxygenation.

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Hb type& quantity,Hb%,Meth,Oxy,

Cardiac output& tissue perfusionLung function&

Breathing O2 delivery to tissue

O2 content in blood

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The key concept is that when assessing a patient’s oxygenation, more information than just PaO2 and SaO2 should be considered.

PaO2 and SaO2 may be normal, but if hemoglobin concentration is low or cardiac output is decreased, oxygen delivery to the tissue is decreased.

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•The force that loads hemoglobin with oxygen in the lungs and unloads it in the tissues is the difference in partial pressure of oxygen.

•In the lungs alveolar oxygen partial pressure is higher than capillary oxygen partial pressure so that oxygen moves to the capillaries and binds to the hemoglobin. •In tissue partial pressure of oxygen is lower than that of the blood, so oxygen moves from hemoglobin to the tissue.

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Oxygen Parameters definitions

• Hypoxemia refers to a lower than normal arterial PO2.

• hypoxia refers to inadequate oxygen supply to the body tissue.

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P (A-a) O2Difference between the measured pressure of oxygen in the blood stream and the calculated oxygen in the alveolus. N < 15 mmHgIndicates whether hypoxia is a reflection of hypoventilation or due to deficiency in oxygenationP (A- a) O2 = 150 - (1.25 x PaCO2) - PaO2 mm Hg

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Alveolar-arterial DifferenceInspired O2 = 21 % piO2 = (760-45) x . 21 = 150 mmHg

O2

CO2

palvO2 = piO2 – pCO2 / RQ= 150 – 40 / 0.8= 150 – 50 = 100 mm Hg

PaO2 = 90 mmHg

palvO2 – partO2 = 10 mmHg

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P (A-a) O2A normal A-a gradient in the face of hypoxemia suggests the hypoxemia is due to hypoventilation and not due to underlying lung disorders.

An increased A-a gradient identifies decreased oxygen in the arterial blood compared to the oxygen in the alveolus.

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Alveolar- arterial Difference

O2

CO2

Oxygenation Failure WIDE GAPpiO2 = 150pCO2 = 40

palvO2= 150 – 40/.8=150-50 =100

PaO2 = 45

D = 100 - 45 = 55

Ventilation Failure NORMAL GAPpiO2 = 150

pCO2 = 80

palvO2= 150-80/.8 =150-100= 50PaO2 = 45D = 50 - 45 = 5

PAO2 (partial pres. of O2. in the alveolus.) = 150 - ( PaCO2 / .8 )760 – 45 = 715 : 21 % of 715 = 150

No click

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Other Oxygen parameters• p50a - oxygen tension at 50% saturation on

Oxygen Dissociation Curve. This is used to reflect affinity of Hb for oxygen. 25-29mmhg

• FMetHb - This is the fraction of methaemoglobin. Think of methaemoglobin like haemoglobin, but we carry less than 1% of it in our blood. As it is unable to combine with oxygen and it also decreases the oxygen carrying capacity of blood. Exposure to certain drugs and chemicals can dangerously elevate levels(iNO).

• 0.2-0.6%

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• FCOHb - Fraction of carboxyhaemoglobin. Much similar to FMetHb in its actions. Affinity of Hb for carbon monoxide is 200 times greater than that of oxygen and impairs oxygen transport and release (ODC shift to left, alkolosis). This level can be high in heavy smokers.

• 0.0-8.0%

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• Fshunte - Relative physiological shunt. Basically the amount of venous (de-oxygenated) blood that did not receive oxygen whilst travelling through the lungs. This can be caused by atelectasis, a pulmonary embolism (PE), mucous plugs and pulmonary oedema, all of which reduces oxygen transport into the blood.

• 1.0-10%

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Blood Gas Arterial Sample Venous Sample Capillary sample(Arterialized)

PaCO2 36-44 mmHg 42-50 mmHg 35-45 mmHg

pH 7.37-7.43 7.32- 7.38 7.35-7.45

PaO2 60-110 mmHg 37-42 mmHg 50-70 mmHg

HCO3 22-26 mEq/liter 23-27 mEq/liter 22-26 mEq/liter

Normal Ranges for Blood Gases in Healthy Newborns

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Errors in Blood Gas Measurement

• During collection and analysis of blood gases, the clinician should be aware of the following potential sources of error:

• 1-       Temperature – blood gas machines report results for 37° C. Hypo or hyperthermia can alter true arterial gas values.

 • 2-       Hemoglobin – calculated oxygen

saturations are based on adult hemoglobin, not on fetal or mixed hemoglobins.

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• 3-    Dilution – heparin in a gas sample will lower the PCO2 and increase the base deficit without altering the pH.

• 4-       Air bubbles – room air has a PCO2 close to 0 and a partial pressure of oxygen of 150. Therefore, air bubbles in the sample will decrease the PCO2 and increase the PO2 unless the PO2 is greater than 150.

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• Steady state. Ideally, blood gases should measure the infant’s condition in a state of equilibrium.

• After changing ventilator settings or disturbing the infant, a period of 20 to 30 minutes should be allowed for arterial blood chemistry to reach a steady state. This period will vary from infant to infant.

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• 5-DELAYED ANALYSIS Consumptiom of O2 & Production of CO2 continues after blood drawn into syringe.Iced Sample maintains values for 1 hour Uniced sample quickly becomes invalid PaCO2 3-10 mmHg/hour PaO2 at a rate related to initial value & dependant on Hb Saturation.

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• 6-TYPE OF SYRINGEpH & PCO2 values unaffectedPO2 values drop more rapidly in plastic syringes

(ONLY if PO2 > 400 mm Hg) Other advantage of glass syringes:

Minimal friction of barrel with syringe wall

Usually no need to ‘pull back’ barrel – less chance of air bubbles entering syringe

Small air bubbles adhere to sides of plastic syringes – difficult to expelThough glass syringes preferred, differences usually not of clinical significance plastic syringes can be and continue to be used

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Example3ds old is admitted to the hospital. He was diagnosed as severe ♂

anoxia. His arterial blood gas values are reported as follows:

pH 7.32PaCO2 32HCO3- 18

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• pH 7.32 PaCO2 32 HCO3- 18

• 1. Assess the pH. It is low (normal 7.35-7.45); therefore we have acidemia.

• 2. Assess the PaCO2. It is low. Normally we would expect the pH and PaCO2 to move in

opposite directions, but this is not the case.

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• pH 7.32 PaCO2 32 HCO3- 18

• Because the pH and PaCO2 are moving in the same direction, it indicates that the acid-base disorder is primarily metabolic.

• In this case, the lungs, acting as the primary acid-base buffer, are now attempting to compensate by “blowing off excessive C02”, and therefore increasing the pH.

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• pH 7.32 PaCO2 32 HCO3- 18

• 3. Assess the HCO3. It is low (normal 22-26). We would expect the pH and the HCO3 - to move in the same direction, confirming that the primary problem is metabolic.

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• pH 7.32 PaCO2 32 HCO3- 18

• What is your interpretation? Because there is evidence of compensation (pH and PaCO2 moving in the same direction) and because the pH remains below the normal range, we would

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interpret this ABG result as a• partially compensated metabolic acidosis.-

•pH ↓ PaCO2 ↓ HCO3 ↓

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Assessment of Acid–Base Status

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http://www.medcalc.com/acidbase.html

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Take home message:• Do not take decision on single ABG

result especially if there is major change than the previous ABG.

• Correlate the ABG result with the clinical condition of the case.

• PH &PCo2 both normal = normal ABG.

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Take home message:• PH& PCo2 both change in same

direction= the 1ry disorder is metabolic.• PH& PCo2 both change in opposite

direction= the 1ry disorder is respiratory.• PH normal & PCo2 abnormal = mixed

disorder respiratory disorder according to the direction of PCo2 and metabolic in the opposite direction.

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Take home message:• PH abnormal & PCO2 normal=

Double acidosis or double alkalosis according to the direction of PH.

• In metabolic acidosis you must calculate anion gap.

• Do not forget to comment on oxygenation.

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ThanksMahmoud el said2014