abg by faruk cfh

IN THE NAME OF ALLAAH,THE BENEFICENT,THE MERCIFUL IN THE NAME OF ALLAAH,THE BENEFICENT,THE MERCIFUL

A PRESENTATION BY

DR FAROOQUECHEST & FEVER HOSPITAL NAJRAN KSA

drfarooq_malik@yahoo.com

Taking Arterial Blood Taking Arterial Blood GasesGases

Dr MUHAMMAD FAROOQUE M.B;B.S D.T.C.D.

MEMBER EXECUTIVE COUNCIL PAKISTAN CHEST SOCIETY

Information Obtained from an ABG:

• Acid base status

• Oxygenation– Dissolved O2 (pO2)

– Saturation of hemoglobin

• CO2 elimination

• Levels of carboxyhemoglobin and methemoglobin

Indications:

• Assess the ventilatory status, oxygenation and acid base status

• Assess the response to an intervention

Contraindications:

• Bleeding diathesis

• AV fistula

• Severe peripheral vascular disease, absence of an arterial pulse

• Infection over site

PULSEOXIMETER VS ABGVS

Why an ABG instead of Pulse oximetry?

• Pulse oximetry uses light absorption at two wavelengths to determine hemoglobin saturation.

• Pulse oximetry is non-invasive and provides immediate and continuous data.

Why an ABG instead of Pulse oximetry?

• Pulse oximetry does not assess ventilation (pCO2) or acid base status.

• Pulse oximetry becomes unreliable when saturations fall below 70-80%.

• Technical sources of error (ambient or fluorescent light, hypoperfusion, nail polish, skin pigmentation)

• Pulse oximetry cannot interpret methemoglobin or carboxyhemoglobin.

Which Artery to Choose?

• The radial artery is superficial, has collaterals and is easily compressed. It should almost always be the first choice.

• Other arteries (femoral, dorsalis pedis, brachial) can be used in emergencies.

IS THERE AN ALTERNATIVE TO ARTERIAL IS THERE AN ALTERNATIVE TO ARTERIAL SAMPLE?SAMPLE?

USE A CAPILLARY SAMPLE FROM

EAR-LOBE OR

A HEEL PRICK IN INFANTS.

ANATOMY OF RADIAL ARTERY

Preparing to perform the Procedure:

• Make sure you and the patient are comfortable.

• Assess the patency of the radial and ulnar arteries.

MODIFIED ALLEN`s TEST

Collection Problems:

• Type of syringe– Plastic vs. glass

• Use of heparin

• Air bubbles

• Specimen handling and transport

Type of Syringe

• Glass-– Impermeable to gases

– Expensive and impractical

• Plastic-– Somewhat permeable to gases

– Disposable and inexpensive

The Kit

Heparin

• Liquid– Dilutional effect if <2-3 ml of blood

collected

• Preloaded dry heparin powder– Eliminates dilution problem

– Mixing becomes more important

– May alter sodium or potassium levels

Air bubbles• Gas equilibration between ambient air

(pO2 ~ 150, pCO2~0) and arterial blood.

• pO2 will begin to rise, pCO2 will fall• Effect is a function of duration of

exposure and surface area of air bubble.

• Effect is amplified by pneumatic tube transport.

Transport

• After specimen collected and air bubble removed, gently mix and invert syringe.

• Because the wbcs are metabolically active, they will consume oxygen.

• Plastic syringes are gas permeable.

• Key: Minimize time from sample acquisition to analysis.

Transport

• Placing the AGB on ice may help minimize changes, depending on the type of syringe, pO2 and white blood cell count.

• Its probably not as important if the specimen is delivered immediately.

Performing the Procedure:

• Put on gloves• Prepare the site

– Drape the bed– Cleanse the radial area with a alcohol

• Position the wrist (hyper-extended, using a rolled up towel if necessary)

• Palpate the arterial pulse and visualize the course of the artery.

Performing the Procedure:

• If you are going to use local anesthetic, infiltrate the skin with 2% xylocaine.

• Open the ABG kit

• Line the needle up with the artery, bevel side up.

• Enter the artery and allow the syringe to fill spontaneously.

Performing the Procedure:

• Withdraw the needle and hold pressure on the site.

• Protect needle• Remove any air bubbles• Gently mix the specimen by rolling it

between your palms• Place the specimen on ice and transport

to lab immediately.

ABG ANALYZER

SUMMARY

• BLOOD--------ARTERIAL• ARTERIES-RADIAL BRACHIAL FEMORAL• SYRINGE---HEPARINIZED• TOO MUCH HEPARIN----REDUCES PH• HEPARIN---O.1mL(1000i.u./Ml) to

Anticoagulate 2mL BLOOD• DISPOSIBLE PRE-HEPRANIZED

SYRINGES ARE AVAILABLE

The Blood Gas Report: normals…

pH 7.40 + 0.05

PaCO2 40 + 5 mm Hg

PaO2 80 - 100 mm Hg

HCO3 24 + 4 mmol/L

O2 Sat >95

Always mention and see FIO2

AN APPROACH TO BLOOD GAS EVALUATIONAN APPROACH TO BLOOD GAS EVALUATION

Pts history Clinical condition Assess adequacy of alveolar ventilation Calculate alveolar-to-arterial oxygen tension

gradient Calculate anion gap Measure plasma electrolytes Determine acid-base status of body

ABG REPORT COMPONENTSABG REPORT COMPONENTS Patients data---Name ,Age ,Sex ,# Clinical status----Fio2 ,RR ,Vent settings Arterial oxygen tension(paO2) Art;Co2 tension(paCO2) PH HCO3 Base excess Hb. O2 content O2 saturation Temperature Serum K+ value

DEFINING SOME COMPONENTSDEFINING SOME COMPONENTS

PH: POWER OF HYDROGEN ION. OR NEGATIVE LOGARITHM OF THE HYDROGEN ION

CO2: A GAS A RESPIRATORY ACID

THE ONLY ACID WHICH CAN BE EXHALED CARBONIC ACID IS ONLY FORMED

WHEN COMBINED WITH WATER

DEFINING SOME COMPONENTSDEFINING SOME COMPONENTS

BICARBONATE: IN ACID-BASE

DETERMINATION,THE CONCENTRATION(IN mEq/L)OF THE HCO3- ION IS CALCULATED FROM PCO2 & PH.

DEFINING SOME COMPONENTSDEFINING SOME COMPONENTS

Base excess: it is a measure of Metabolic Acid levelthe total Blood Base is About 48mmol/l

depending on Hb. Conc.Defined as amount of of fully-

ionized acid which would be required to return the pts blood to ph 7.4 when the co2 has been adjusted to 40mmhg. Use of BE: to estimate amount of treatment required to overcome the metabolic acidosis or alkalosis

Positive BE indicates Metabolic Alkalosis Negative BE indicates Metabolic Acidosis

Effect of TemperatureEffect of Temperature

When blood is cooled CO2 becomes more soluble reducing its pCO2 by about 4.5%/`C fall in temperature

PH rises by about 0.015/`C fall in temperature

HCO3 remain unchanged

The Key to Blood Gas Interpretation:The Key to Blood Gas Interpretation:4 Equations, 3 Physiologic Processes4 Equations, 3 Physiologic Processes

Equation Physiologic Process1) PaCO2 equation Alveolar

ventilation2) Alveolar gas equation Oxygenation3) Oxygen content equation Oxygenation

4) Henderson-Hasselbalch equation Acid-base balance

These 4 equations, crucial to understanding and interpreting arterial blood gas data,

PaCOPaCO2 2 equation: PaCOequation: PaCO22 reflects ratio of metabolic CO reflects ratio of metabolic CO22 production to alveolar ventilationproduction to alveolar ventilation

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------ VA = VE – VD

VA VE = minute (total) ventilation

VD = dead space ventilation 0.863 converts units to mm Hg

Condition State of

PaCO2 in blood alveolar ventilation

>45 mm Hg Hypercapnia Hypoventilation35 - 45 mm Hg Eucapnia Normal

ventilation<35 mm Hg Hypocapnia Hyperventilation

HypercapniaHypercapnia VCO2 x 0.863

PaCO2 = ------------------ VA

Hypercapnia (elevated PaCO2) is a serious respiratory problem. The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation (VA) for the amount of the body’s CO2 production (VCO2). Since alveolar ventilation (VA) equals total or minute ventilation (VE) minus dead space ventilation (VD), hypercapnia can arise from insufficient VE, increased VD, or a combination.

Hypercapnia Hypercapnia (continued)(continued)

VCO2 x 0.863

PaCO2 = ------------------

VA VA = VE – VD

Examples of inadequate VE leading to decreased VA and increased PaCO2: sedative drug overdose; respiratory muscle paralysis; central hypoventilation

Examples of increased VD leading to decreased VA and increased PaCO2: chronic obstructive pulmonary disease; severe restrictive lung disease (with shallow, rapid breathing)

Clinical assessment of hypercapnia is Clinical assessment of hypercapnia is unreliableunreliable

The PaCO2 equation shows why PaCO2 cannot reliably be assessed clinically. Since we never know the patient's VCO2 or VA, you cannot determine the VCO2/VA, which is what PaCO2 provides. (Even if tidal volume is measured, you can’t determine the amount of air going to dead space.)

There is no predictable correlation between PaCO2 and the clinical picture. In a patient with possible respiratory disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional change in PaCO2. A patient in respiratory distress can have a high, normal, or low PaCO2. A patient without respiratory distress can have a high, normal, or low PaCO2.

Dangers of hypercapniaDangers of hypercapnia

Besides indicating a serious derangement in the respiratory system, elevated PaCO2 poses a threat for three reasons:– 1) An elevated PaCO2 will lower the PAO2 (Alveolar gas

equation PAO2=PIO2-1.2(PaCO2)), and as a result lower the PaO2.

– 2) An elevated PaCO2 will lower the pH (Henderson-Hasselbalch equation PH=Pk+log HCO3/0.03(PaCO2)).

– 3) The higher the baseline PaCO2, the greater it will rise for a given fall in alveolar ventilation, e.g., a 1 L/min decrease in VA will raise PaCO2 a greater amount when the baseline PaCO2 is 50 mm Hg than when it is 40 mm Hg. (See next slide)

PCOPCO22 vs. Alveolar Ventilation vs. Alveolar Ventilation

The relationship is shown for metabolic carbon dioxide production rates of 200 ml/min and 300 ml/min (curved lines). A fixed decrease in alveolar ventilation (x-axis) in the hypercapnic patient will result in a greater rise in PaCO2 (y-axis) than the same VA change when PaCO2 is low or normal. (This situation is analogous to the progressively steeper rise in BUN as glomerular filtration rate declines.)

This graph also shows that, if alveolar ventilation is fixed, an increase in carbon dioxide production will result in an increase in PaCO2.

Alveolar Gas EquationAlveolar Gas Equation

PAO2 = PIO2 - 1.2 (PaCO2)where

PIO2 = FIO2 (PB - 47).

PAO2 = PIO2 - 1.2 (PaCO2)PAO2 = PIO2 - 1.2 (PaCO2)

PAO2 = PIO2 - 1.2 (PaCO2)*

where PAO2 is the average alveolar PO2, and PIO2 is the partial pressure of inspired oxygen in the trachea.

PIO2 = FIO2 (PB – 47 mm Hg)

FIO2 is fraction of inspired oxygen and PB is the barometric pressure. 47 mm Hg is the water vapor pressure at normal body temperature.

*Note: This is the ‘abbreviated version’ of the AG equation, suitable for most clinical purposes. In the longer version, the multiplication factor “1.2” declines with increasing FIO2, reaching zero when 100% oxygen is inhaled. In these exercises “1.2” is dropped when FIO2 is above 60%.

Alveolar Gas EquationAlveolar Gas EquationPAOPAO22 = PIO = PIO22 - 1.2 (PaCO - 1.2 (PaCO22))

where PIOwhere PIO22 = FIO = FIO22 (P (PB B – 47 mm Hg)– 47 mm Hg)

Except in a temporary unsteady state, alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). As a result, whenever PAO2 decreases, PaO2 does as well. Thus, from the AG equation:

If FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia).

If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease (suffocation causes hypoxemia).

If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease (mountain climbing causes hypoxemia).

P(A-a)OP(A-a)O22

P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the “A-a gradient,” though it does not actually result from an O2 pressure gradient in the lungs. Instead, it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance).

PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure.

PaO2 is always measured, on an arterial blood sample in a ‘blood gas machine’.

Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age). A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries. Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs.

Physiologic causes of low PaOPhysiologic causes of low PaO22

NON-RESPIRATORY P(A-a)O2

Cardiac right to left shunt IncreasedDecreased PIO2 NormalLow mixed venous oxygen content*Increased

RESPIRATORYPulmonary right to left shuntIncreasedVentilation-perfusion imbalance IncreasedDiffusion barrier IncreasedHypoventilation (increased PaCO2) Normal

*Unlikely to be clinically significant unless there is right to left shunting or ventilation-perfusion imbalance

Ventilation-Perfusion imbalanceVentilation-Perfusion imbalance

A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O2.

By far the most common cause of low PaO2 is an abnormal degree of ventilation-perfusion imbalance within the hundreds of millions of alveolar-capillary units. Virtually all lung disease lowers PaO2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary edema, COPD.

Diffusion barrier is seldom a major cause of low PaO2 (it can lead to a low PaO2 during exercise).

SaOSaO22 and oxygen content and oxygen content Tissues need a requisite amount of oxygen molecules for metabolism.

Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood. How much is provided by the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as:

CaO2 = quantity O2 bound + quantity O2 dissolved to hemoglobin in plasma

CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)

Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.

Oxygen dissociation curve: SaOOxygen dissociation curve: SaO22 vs. PaO vs. PaO22

Also shown are CaOAlso shown are CaO2 2 vs. PaOvs. PaO22 for two different hemoglobin contents: 15 gm% and 10 gm for two different hemoglobin contents: 15 gm% and 10 gm

%. CaO%. CaO22 units are ml O units are ml O22/dl. P/dl. P5050 is the PaO is the PaO22 at which SaO at which SaO22 is 50%. is 50%.

Point ‘X’ is discussed on later slide.Point ‘X’ is discussed on later slide.

SaOSaO22 – is it calculated or – is it calculated or measured?measured?

Always need to know this when confronted with blood gas data. SaO2 is measured in a ‘co-oximeter’. The traditional ‘blood gas

machine’ measures only pH, PaCO2 and PaO2,, whereas the co-oximeter measures SaO2, carboxyhemoglobin, methemoglobin and hemoglobin content. Newer ‘blood gas’ consoles incorporate a co-oximeter, and so offer the latter group of measurements as well as pH, PaCO2 and PaO2.

Always make sure the SaO2 is measured, not calculated. If it is calculated from the PaO2 and the O2-dissociation curve, it provides no new information, and could be inaccurate -- especially in states of CO intoxication or excess methemoglobin. CO and metHb do not affect PaO2, but do lower the SaO2.

Carbon monoxide – an important cause of hypoxemiaCarbon monoxide – an important cause of hypoxemia

Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO (higher in traffic-congested areas)

CO is colorless, odorless gas, a product of combustion; all smokers have excess CO in their blood, typically 5-10%.

CO binds @ 200x more avidly to hemoglobin than O2, effectively displacing O2

from the heme binding sites. CO is a major cause of poisoning deaths world-wide. CO has a ‘double-whammy’ effect on oxygenation: 1) decreases SaO2 by the

amount of %COHb present, and 2) shifts the O2-dissociation curve to the left, retarding unloading of oxygen to the tissues.

CO does not affect PaO2, only SaO2. To detect CO poisoning, SaO2 and/or COHb must be measured (requires co-oximeter). In the presence of excess CO, SaO2 (when measured) will be lower than expected from the PaO2.

CO does not affect PaOCO does not affect PaO22 – be aware! – be aware!

Review the O2 dissociation curve shown on a previous slide. ‘X’ represents the 2nd set of blood gases for a patient who presented to the ER with headache and dyspnea.

His first blood gases showed PaO2 80 mm Hg, PaCO2 38 mm Hg, pH 7.43. SaO2 on this first set was calculated from the O2-dissociation curve at 97%, and oxygenation was judged normal.

He was sent out from the ER and returned a few hours later with mental confusion; this time both SaO2 and COHb were measured (SaO2 shown by ‘X’): PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2 53%, carboxyhemoglobin 46%.

CO poisoning was missed on the first set of blood gases because SaO2 was not measured!

Causes of Hypoxia A General Causes of Hypoxia A General Classification Classification

1. Hypoxemia (=low PaO2 and/or low CaO2)– a. reduced PaO2 – usually from lung disease (most common

physiologic mechanism: V-Q imbalance) – b. reduced SaO2 -- most commonly from reduced PaO2; other

causes include carbon monoxide poisoning, methemoglobinemia, or rightward shift of the O2-dissociation curve

– c. reduced hemoglobin content -- anemia

2. Reduced oxygen delivery to the tissues– a. reduced cardiac output -- shock, congestive heart failure

– b. left to right systemic shunt (as may be seen in septic shock)

3. Decreased tissue oxygen uptake– a. mitochondrial poisoning (e.g., cyanide poisoning)– b. left-shifted hemoglobin dissociation curve (e.g., from

acute alkalosis, excess CO, or abnormal hemoglobin structure)

How much oxygen is in the blood, and How much oxygen is in the blood, and is it adequate for the patient?is it adequate for the patient?

PaOPaO2 2 vs. SaOvs. SaO22 vs. CaO vs. CaO22

The answer must be based on some oxygen value, but which one? Blood gases give us three different oxygen values: PaO2, SaO2, and CaO2 (oxygen content).

Of these three values, PaO2, or oxygen pressure, is the least helpful to answer the question about oxygen adequacy in the blood. The other two values -- SaO2 and CaO2 -- are more useful for this purpose.

How much oxygen is in the blood?How much oxygen is in the blood?PaOPaO2 2 vs. SaOvs. SaO22 vs. CaO vs. CaO22

OXYGEN PRESSURE: PaO2

Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin, PaO2 cannot tell us “how much” oxygen is in the blood; for that you need to know how much oxygen is also bound to hemoglobin, information given by the SaO2 and hemoglobin content.

OXYGEN SATURATION: SaO2

The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn’t reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content.

OXYGEN CONTENT: CaO2

Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2 provide information on the number of oxygen molecules, i.e., how much oxygen is in the blood. (Neither PaO2 nor SaO2 have units that denote any quantity.) Only CaO2 (units ml O2/dl) tells us how much oxygen is in the blood; this is because CaO2 is the only value that incorporates the hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen content equation:

CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)

Acid-Base Balance Acid-Base Balance Henderson Hasselbalch EquationHenderson Hasselbalch Equation

[HCO3

-] pH = pK + log___________

0.03 [PaCO2]

For teaching purposes the H_H equation can be shortened to its basic relationships:

ph=HCO3/paO2

pH is inversely related to pH is inversely related to [H[H++]; a pH change of 1.00 ]; a pH change of 1.00

represents a represents a 10-fold change in [H10-fold change in [H++]]

pH [H+] in nanomoles/L 7.00 1007.10 807.30 50 7.40 40 7.52 30 7.70 208.00 10

Acid base terminologyAcid base terminology

Acidemia: blood pH < 7.35 Acidosis: a primary physiologic process that,

occurring alone, tends to cause acidemia, e.g.: metabolic acidosis from decreased perfusion (lactic acidosis); respiratory acidosis from hypoventilation. If the patient also has an alkalosis at the same time, the resulting blood pH may be low, normal or high.

Alkalemia: blood pH > 7.45 Alkalosis: a primary physiologic process that,

occurring alone, tends to cause alkalemia. Examples: metabolic alkalosis from excessive diuretic therapy; respiratory alkalosis from acute hyperventilation. If the patient also has an acidosis at the same time, the resulting blood pH may be high, normal or low.

Acid base terminology (cont.)Acid base terminology (cont.)

Primary acid-base disorder: One of the four acid-base disturbances that is manifested by an initial change in HCO3

- or PaCO2. They are: metabolic acidosis (MAc), metabolic alkalosis (MAlk), respiratory acidosis (RAc), and respiratory alkalosis (RAlk). If HCO3

- changes first, the disorder is either MAc (reduced HCO3

- and acidemia) or MAlk (elevated HCO3-

and alkalemia). If PaCO2 changes first, the problem is either RAlk (reduced PaCO2 and alkalemia) or RAc (elevated PaCO2 and acidemia).

Compensation: The change in HCO3- or PaCO2 that results

from the primary event. Compensatory changes are not classified by the terms used for the four primary acid-base disturbances. For example, a patient who hyperventilates (lowers PaCO2) solely as compensation for MAc does not have a RAlk, the latter being a primary disorder that, alone, would lead to alkalemia. In simple, uncomplicated MAc the patient will never develop alkalemia.

Primary acid-base Primary acid-base disordersdisorders

- Respiratory alkalosis - Respiratory alkalosis -- Respiratory alkalosis - A primary disorder

where the first change is a lowering of PaCO2, resulting in an elevated pH. Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO3) by the kidneys; this reduction in HCO3

- is not metabolic acidosis, since it is not a primary process.

Primary Event Compensatory Event

HCO3- HCO3

- low pH high – ))))) pH high – )))))PaCO2 low PaCO2 low

Primary acid-base disordersPrimary acid-base disorders- Respiratory acidosis -- Respiratory acidosis -

Respiratory acidosis - A primary disorder where the first change is an elevation of PaCO2, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO3

- is not metabolic alkalosis, since it is not a primary process.

Primary Event Compensatory Event

HCO3- HCO3

- high pH low – ))))) pH low– )))))PaCO2 high PaCO2 high

Primary Acid-Base Primary Acid-Base Disorders Disorders

- Metabolic acidosis -- Metabolic acidosis - Metabolic Acidosis - A primary acid-base

disorder where the first change is a lowering of HCO3

-, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary hyperventilation; this lowering of PaCO2 is not respiratory alkalosis, since it is not a primary process.

Primary Event Compensatory Event

HCO3-low HCO3

-low pH low– ))))) pH low– ))))) PaCO2 PaCO2 low

Primary Acid-Base Primary Acid-Base Disorders Disorders

- Metabolic alkalosis -- Metabolic alkalosis - Metabolic alkalosis - A primary acid-base disorder where the

first change is an elevation of HCO3-, resulting in increased pH.

Compensation is a secondary hypoventilation (increased PaCO2) which is not respiratory acidosis, since it is not a primary process. Compensation for metabolic alkalosis (attempting to bring pH back down toward normal) is less predictable than for the other three acid-base disorders.

Primary Event Compensatory Event

HCO3-high HCO3

- highpH high – ))))) pH high– ))))) PaCO2 PaCO2 high

Anion GapAnion GapMetabolic acidosis is conveniently divided

into elevated and normal anion gap (AG) acidosis. AG is calculated as

AG = Na+ - (Cl- + CO2)

Note: CO2 in this equation is the “total CO2” measured in the chemistry lab as part of routine serum electrolytes, and consists mostly of bicarbonate. Normal AG is typically 12 ± 4 mEq/L. If AG is calculated using K+, the normal AG is 16 ± 4 mEq/L. Normal values for AG may vary among labs, so one should always refer to local normal values before making clinical decisions based on the AG.

Metabolic Acid-Base Disorders Metabolic Acid-Base Disorders -- Some clinical causes ---- Some clinical causes --

METABOLIC ACIDOSIS low HCO3- & low pH

– Increased anion gap• lactic acidosis; ketoacidosis; drug poisonings (e.g.,

aspirin, ethyelene glycol, methanol)– Normal anion gap

• diarrhea; some kidney problems, e.g., renal tubular acidosis, intersititial nephritis

METABOLIC ALKALOSISHCO3- HIGH & pH HIGH

Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis, diuretics; corticosteroids; gastric suctioning; vomiting

Chloride resistant: any hyperaldosterone state, e.g., Cushings’s syndrome; Bartter’s syndrome; severe K+ depletion

Respiratory Acid-Base Disorders Respiratory Acid-Base Disorders

-- Some clinical causes ---- Some clinical causes --

RESPIRATORY ACIDOSISPaCO2 HIGH & LOW pH Central nervous system depression (e.g., drug overdose)Chest bellows dysfunction (e.g., Guillain-Barré

syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema)

RESPIRATORY ALKALOSIS LOW PaCO2 & HIGH pH

Hypoxemia (includes altitude)AnxietySepsisAny acute pulmonary insult, e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism

Mixed Acid-base disorders are commonMixed Acid-base disorders are common

In chronically ill respiratory patients, mixed disorders are probably more common than single disorders, e.g., RAc + MAlk, RAc + Mac, Ralk + MAlk.

In renal failure (and other patients) combined MAlk + MAc is also encountered.

Always be on lookout for mixed acid-base disorders. They can be missed!

TTipsips to to diagnosingdiagnosing mixed acid-basemixed acid-base disorders disorders

TIP 1. Don’t interpret any blood gas data for acid-base diagnosis without closely examining the serum electrolytes: Na+, K+, Cl- and CO2.

A serum CO2 out of the normal range always represents some type of acid-base disorder (barring lab or transcription error).

High serum CO2 indicates metabolic alkalosis &/or bicarbonate retention as compensation for respiratory acidosis

Low serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis

Note that serum CO2 may be normal in the presence of two or more acid-base disorders.

Tips to diagnosing mixed acid-base disorders (cont.)Tips to diagnosing mixed acid-base disorders (cont.)

TIP 2 . Single acid-base disorders do not lead to normal blood pH. Although pH can end up in the normal range (7.35 - 7.45) with a mild single disorder, a truly normal pH with distinctly abnormal HCO3

- and PaCO2 invariably suggests two or more primary disorders.

Example: pH 7.40, PaCO2 20 mm Hg, HCO3- 12

mEq/L, in a patient with sepsis. Normal pH results from two co-existing and unstable acid-base disorders: acute respiratory alkalosis and metabolic acidosis.

Tips to diagnosing mixed acid-base disorders (cont.)Tips to diagnosing mixed acid-base disorders (cont.)

TIP 3. Simplified rules predict the pH and HCO3

- for a given change in PaCO2. If the pH or HCO3

- is higher or lower than expected for the change in PaCO2, the patient probably has a metabolic acid-base disorder as well.

The next slide shows expected changes in pH and HCO3

- (in mEq/L) for a 10 mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis).

Expected changes in pH and HCOExpected changes in pH and HCO33-- for for a 10 mm Hg changea 10 mm Hg change in PaCO in PaCO22

resulting from either primary hypoventilation (respiratory acidosis) or resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis).primary hyperventilation (respiratory alkalosis).

ACUTE CHRONIC Resp Acidosis

– pH LOW by 0.07 pH LOW by 0.03– HCO3

- HIGH by 1* HCO3- HIGH by 3-4

Resp Alkalosis

– pH HIGH by 0.08 pH HIGH by 0.03

– HCO3- LOW by 2 HCO3

- LOW by 5

*Units for HCO3- are mEq/L

Predicted changes in HCOPredicted changes in HCO33-- for a directional change in for a directional change in

PaCOPaCO22 can help uncover mixed acid-base disorders. can help uncover mixed acid-base disorders.

a) A normal or slightly low HCO3- in the presence of

hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO2 50 mm Hg, HCO3

- 22 mEq/L. Based on the rule for increase in HCO3

- with hypercapnia, it should be at least 25 mEq/L in this example; that it is only 22 mEq/L suggests a concomitant metabolic acidosis.

b) A normal or slightly elevated HCO3- in the presence of

hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30 mm Hg, HCO3

- 26 mEq/L. Based on the rule for decrease in HCO3 with hypocapnia, it should be at least 23 mEq/L in this example; that it is 26 mEq/L suggests a concomitant metabolic alkalosis.

Tips to diagnosing mixed acid-base disorders (cont.)Tips to diagnosing mixed acid-base disorders (cont.)

TIP 4. In maximally-compensated metabolic acidosis, the numerical value of PaCO2 should be the same (or close to) the last two digits of arterial pH. This observation reflects the formula for expected respiratory compensation in metabolic acidosis:

Expected PaCO2 = [1.5 x serum CO2] + (8 ± 2)

In contrast, compensation for metabolic alkalosis (by increase in PaCO2) is highly variable, and in some cases there may be no or minimal compensation.

(Summary (Summary )) Clinical and laboratory approach to Clinical and laboratory approach to acid-base diagnosisacid-base diagnosis

Determine existence of acid-base disorder from arterial blood gas and/or serum electrolyte measurements. Check serum CO2; if abnormal there is an acid-base disorder. If the anion gap is significantly increased there is a metabolic acidosis.

Examine pH, PaCO2 and HCO3- for the

obvious primary acid-base disorder, and for deviations that indicate mixed acid-base disorders (TIPS 2 through 4).

(Summary (Summary )) Clinical and laboratory approach to acid- Clinical and laboratory approach to acid-base diagnosis (cont.)base diagnosis (cont.)

Use a full clinical assessment (history, physical exam, other lab data including previous arterial blood gases and serum electrolytes) to explain each acid-base disorder. Remember that co-existing clinical conditions may lead to opposing acid-disorders, so that pH can be high when there is an obvious acidosis, or low when there is an obvious alkalosis.

Treat the underlying clinical condition(s); this will usually suffice to correct most acid-base disorders. If there is concern that acidemia or alkalemia is life-threatening, aim toward correcting pH into the range of 7.30-7.52 ([H+] = 50-30 nM/L).

Clinical judgment should always apply

The Blood Gas Report: normals…

pH 7.40 + 0.05PaCO2 40 + 5 mm HgPaO2 80 - 100 mm Hg

HCO3 24 + 4 mmol/L

O2 Sat >95Always mention and see FIO2

The essentials

HCO3

5The

Steps forSuccessfulBlood Gas

Analysis

SUMMARY OF INTERPRETATION

Step 2 Who is responsible for this change in pH ( culprit )? CO2 will change pH in opposite direction Bicarb. will change pH in same direction

Acidemia: With HCO3 < 20 mmol/L = metabolicWith PCO2 >45 mm hg = respiratory

Alkalemia:With HCO3 >28 mmol/L = metabolicWith PCO2 <35 mm Hg = respiratory

Step 1Look at the pH

Is the patient acidemic pH < 7.35or alkalemic pH > 7.45

Step 3If there is a primary respiratory disturbance, is it acute ?

.08 change in pH ( Acute )

.03 change in pH ( Chronic )

10 mm Change PaCO2

=

Step 4If the disturbance is metabolic is the respiratorycompensation appropriate?For metabolic acidosis:Expected PaCO2 = (1.5 x [HCO3]) + 8 ) + 2 or simply…expected PaCO2 = last two digits of pH

For metabolic alkalosis:Expected PaCO2 = 6 mm for 10 mEq. rise in Bicarb.

Suspect if ............. actual PaCO2 is more than expected :

additional …respiratory acidosis actual PaCO2 is less than expected :

additional …respiratory alkalosis

Step 4 cont.If there is metabolic acidosis, is there a wide anion gap ?

Na - (Cl-+ HCO3-) = Anion Gap usually <12

If >12, Anion Gap Acidosis : M ethanolU remiaD iabetic KetoacidosisP araldehydeI nfection (lactic acid)E thylene GlycolS alicylate

Common causes1) Lactic acidosis2) Metabolic disorders3) Renal failure

th step

Clinical correlation5

SUMMARYSUMMARY

PH<7.34

ACIDOSIS

HCO3<20 mEq/L

METABOLIC

RESP COMPN

pCO2<40mmHg

pCO2>45mmHg

RESPIRATORY

RENAL COMP

HCO3>24mEq/L

>7.45

ALKALOSIS

HCO3>28mEq/L PCO2<35mmHg

METABOLIC RESPIRATORY

RESP COMPN RENAL CMPN

pCO2>40mmHg HCO3<24mmHg

ABG

Resiratory acidosisResiratory acidosis

Ph decreased Pco2 increased

Stroke Drug over dose Aspirin ARD Hypoventilation

Chest physiotherapy Suction Increase R/R Increase Tidal Volume

Secondary retention of HCO3 by the kidneys

CAUSESABG

TREATMENT compensation

Metabolic acidosisMetabolic acidosis

PH Decreased HCO3 Decreased

Renal failure Diarrhoea Cardiogenic/septic shock Ketoacidosis Lacticacidosis

Sev hypoxia

Treat underlying cause Monitor I/O Protect against infection

Bringing the PH back upward normal by lowering of PaCO2

ABG CAUSES

TREATMENT COMPENSATION

Respiratory alkalosisRespiratory alkalosis

Anxiety, Head trauma Brain tumor, Fever Hepatic insufficiency Thyrotoxicosis pEmbolism altitude hypoxia

Sedation Support Decrease r/r Decrease tidal vol

Bringing the ph back down toward normal

Secondary lowering of HCO3 by kidneys

pH increased pCO2 decreased

ABG

causes

TREATMENT COMPENSATION

Metabolic alkalosisMetabolic alkalosis

PH INCREASED HCO3 INCREASED

VOL LOSS DIARRHOEA GASTRIC SUCTION STEROIDS DIURETIC THERAPY

MASSIVE BLOOD TRANSFUSION(citrate metabolized to HCO3)

Treat underlying cause Monitor I/O K+ replacement

LESS PREDICTABLE TO BRING DOWN PH TOWARD

NORMAL BY INCREASE IN PaCO2 IS HIGHLY VARIABLE

IN SOME CASES MAY BE NO OR MINIMAL COMPENSATION

ABG CAUSES

TREATMENT COMPENSATION

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