Abg By Faruk Cfh

IN THE NAME OF ALLAAH,THE BENEFICENT,THE MERCIFUL A PRESENTATION BY DR FAROOQUE CHEST & FEVER HOSPITAL NAJRAN KSA [email_address]

Taking Arterial Blood Gases Dr MUHAMMAD FAROOQUE M.B;B.S D.T.C.D. MEMBER EXECUTIVE COUNCIL PAKISTAN CHEST SOCIETY

IS THERE AN ALTERNATIVE TO ARTERIAL SAMPLE? USE A CAPILLARY SAMPLE FROM EAR-LOBE OR A HEEL PRICK IN INFANTS.

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 PaCO 2 40 + 5 mm Hg PaO 2 80 - 100 mm Hg HCO 3 24 + 4 mmol/L O2 Sat >95 Always mention and see FIO2

AN 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 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 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 COMPONENTS BICARBONATE: IN ACID-BASE DETERMINATION,THE CONCENTRATION(IN mEq/L)OF THE HCO3- ION IS CALCULATED FROM PCO2 & PH.

DEFINING SOME COMPONENTS Base excess: it is a measure of Metabolic Acid level the 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 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: 4 Equations, 3 Physiologic Processes Equation Physiologic Process 1) PaCO 2 equation Alveolar ventilation 2) Alveolar gas equation Oxygenation 3) Oxygen content equation Oxygenation 4) Henderson-Hasselbalch equation Acid-base balance These 4 equations, crucial to understanding and interpreting arterial blood gas data,

PaCO 2 equation: PaCO 2 reflects ratio of metabolic CO 2 production to alveolar ventilation VCO 2 x 0.863 VCO 2 = CO 2 production PaCO 2 = ------------------ VA = VE – VD VA VE = minute (total) ventilation VD = dead space ventilation 0.863 converts units to mm Hg Condition State of PaCO 2 in blood alveolar ventilation >45 mm Hg Hypercapnia Hypoventilation 35 - 45 mm Hg Eucapnia Normal ventilation <35 mm Hg Hypocapnia Hyperventilation

Hypercapnia VCO 2 x 0.863 PaCO 2 = ------------------ VA Hypercapnia (elevated PaCO 2 ) is a serious respiratory problem. The PaCO 2 equation shows that the only physiologic reason for elevated PaCO 2 is inadequate alveolar ventilation (VA) for the amount of the body’s CO 2 production (VCO 2 ). 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 (continued) VCO 2 x 0.863 PaCO 2 = ------------------ VA VA = VE – VD Examples of inadequate VE leading to decreased VA and increased PaCO 2 : sedative drug overdose; respiratory muscle paralysis; central hypoventilation Examples of increased VD leading to decreased VA and increased PaCO 2 : chronic obstructive pulmonary disease; severe restrictive lung disease (with shallow, rapid breathing)

Clinical assessment of hypercapnia is unreliable The PaCO 2 equation shows why PaCO 2 cannot reliably be assessed clinically. Since we never know the patient's VCO 2 or VA, you cannot determine the VCO 2 /VA, which is what PaCO 2 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 PaCO 2 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 PaCO 2 . A patient in respiratory distress can have a high, normal, or low PaCO 2 . A patient without respiratory distress can have a high, normal, or low PaCO 2 .

Dangers of hypercapnia Besides indicating a serious derangement in the respiratory system, elevated PaCO 2 poses a threat for three reasons: 1) An elevated PaCO 2 will lower the PAO 2 (Alveolar gas equation PAO2=PIO2-1.2(PaCO2)), and as a result lower the PaO 2 . 2) An elevated PaCO 2 will lower the pH (Henderson-Hasselbalch equation PH=Pk+log HCO3/0.03(PaCO2)). 3) The higher the baseline PaCO 2 , the greater it will rise for a given fall in alveolar ventilation, e.g., a 1 L/min decrease in VA will raise PaCO 2 a greater amount when the baseline PaCO 2 is 50 mm Hg than when it is 40 mm Hg. (See next slide)

PCO 2 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 PaCO 2 (y-axis) than the same VA change when PaCO 2 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 PaCO 2 .

Alveolar Gas Equation PAO 2 = PIO 2 - 1.2 (PaCO 2 )* where PAO 2 is the average alveolar PO 2 , and PIO 2 is the partial pressure of inspired oxygen in the trachea. PIO 2 = FIO 2 (P B – 47 mm Hg) FIO 2 is fraction of inspired oxygen and P B 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 FIO 2 , reaching zero when 100% oxygen is inhaled. In these exercises “1.2” is dropped when FIO 2 is above 60%.

Alveolar Gas Equation PAO 2 = PIO 2 - 1.2 (PaCO 2 ) where PIO 2 = FIO 2 (P B – 47 mm Hg) Except in a temporary unsteady state, alveolar PO 2 (PAO 2 ) is always higher than arterial PO 2 (PaO 2 ). As a result, whenever PAO 2 decreases, PaO 2 does as well. Thus, from the AG equation: If FIO 2 and P B are constant, then as PaCO 2 increases both PAO 2 and PaO 2 will decrease (hypercapnia causes hypoxemia). If FIO 2 decreases and P B and PaCO 2 are constant, both PAO 2 and PaO 2 will decrease (suffocation causes hypoxemia). If P B decreases (e.g., with altitude), and PaCO 2 and FIO 2 are constant, both PAO 2 and PaO 2 will decrease (mountain climbing causes hypoxemia).

P(A-a)O 2 P(A-a)O 2 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 O 2 pressure gradient in the lungs. Instead, it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance). PAO 2 is always calculated , based on FIO 2 , PaCO 2 and barometric pressure. PaO 2 is always measured , on an arterial blood sample in a ‘blood gas machine’. Normal P(A-a)O 2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age). A higher than normal P(A-a)O 2 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)O 2 signifies some sort of problem within the lungs.

Physiologic causes of low PaO 2 NON-RESPIRATORY P(A-a)O 2 Cardiac right to left shunt Increased Decreased PIO 2 Normal Low mixed venous oxygen content* Increased RESPIRATORY Pulmonary right to left shunt Increased Ventilation-perfusion imbalance Increased Diffusion barrier Increased Hypoventilation (increased PaCO 2 ) Normal *Unlikely to be clinically significant unless there is right to left shunting or ventilation-perfusion imbalance

Ventilation-Perfusion imbalance A normal amount of ventilation-perfusion (V-Q) imbalance accounts for the normal P(A-a)O 2 . By far the most common cause of low PaO 2 is an abnormal degree of ventilation-perfusion imbalance within the hundreds of millions of alveolar-capillary units. Virtually all lung disease lowers PaO 2 via V-Q imbalance, e.g., asthma, pneumonia, atelectasis, pulmonary edema, COPD. Diffusion barrier is seldom a major cause of low PaO 2 (it can lead to a low PaO 2 during exercise).

SaO 2 and oxygen content Tissues need a requisite amount of oxygen molecules for metabolism. Neither the PaO 2 nor the SaO 2 tells how much oxygen is in the blood. How much is provided by the oxygen content, CaO 2 (units = ml O 2 /dl). CaO 2 is calculated as: CaO 2 = quantity O 2 bound + quantity O 2 dissolved to hemoglobin in plasma CaO 2 = (Hb x 1.34 x SaO 2 ) + (.003 x PaO 2 ) Hb = hemoglobin in gm%; 1.34 = ml O 2 that can be bound to each gm of Hb; SaO 2 is percent saturation of hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O 2 /mm Hg PO 2 .

Oxygen dissociation curve: SaO 2 vs. PaO 2 Also shown are CaO 2 vs. PaO 2 for two different hemoglobin contents: 15 gm% and 10 gm%. CaO 2 units are ml O 2 /dl. P 50 is the PaO 2 at which SaO 2 is 50%. Point ‘X’ is discussed on later slide.

SaO 2 – is it calculated or measured? Always need to know this when confronted with blood gas data. SaO 2 is measured in a ‘co-oximeter’. The traditional ‘blood gas machine’ measures only pH, PaCO 2 and PaO 2, , whereas the co-oximeter measures SaO 2 , 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, PaCO 2 and PaO 2 . Always make sure the SaO 2 is measured, not calculated. If it is calculated from the PaO 2 and the O 2 -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 PaO 2 , but do lower the SaO 2 .

Carbon 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 O 2 , effectively displacing O 2 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 SaO 2 by the amount of %COHb present, and 2) shifts the O 2 -dissociation curve to the left, retarding unloading of oxygen to the tissues. CO does not affect PaO 2 , only SaO 2 . To detect CO poisoning, SaO 2 and/or COHb must be measured (requires co-oximeter). In the presence of excess CO, SaO 2 (when measured) will be lower than expected from the PaO 2 .

CO does not affect PaO 2 – be aware! Review the O 2 dissociation curve shown on a previous slide. ‘X’ represents the 2 nd set of blood gases for a patient who presented to the ER with headache and dyspnea. His first blood gases showed PaO 2 80 mm Hg, PaCO 2 38 mm Hg, pH 7.43. SaO 2 on this first set was calculated from the O 2 -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 SaO 2 and COHb were measured (SaO 2 shown by ‘X’): PaO 2 79 mm Hg, PaCO 2 31 mm Hg, pH 7.36, SaO 2 53%, carboxyhemoglobin 46%. CO poisoning w as missed on the first set of blood gases because SaO 2 was not measured!

Causes of Hypoxia A General Classification 1. Hypoxemia (=low PaO 2 and/or low CaO 2 ) a. reduced PaO 2 – usually from lung disease (most common physiologic mechanism: V-Q imbalance) b. reduced SaO 2 -- most commonly from reduced PaO 2 ; other causes include carbon monoxide poisoning, methemoglobinemia, or rightward shift of the O 2 -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 is it adequate for the patient? PaO 2 vs. SaO 2 vs. CaO 2 The answer must be based on some oxygen value, but which one? Blood gases give us three different oxygen values: PaO 2 , SaO 2 , and CaO 2 (oxygen content). Of these three values, PaO 2 , or oxygen pressure , is the least helpful to answer the question about oxygen adequacy in the blood. The other two values -- SaO 2 and CaO 2 -- are more useful for this purpose.

How much oxygen is in the blood? PaO 2 vs. SaO 2 vs. CaO 2 OXYGEN PRESSURE: PaO 2 Since PaO 2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin, PaO 2 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 SaO 2 and hemoglobin content. OXYGEN SATURATION: SaO 2 The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation (in arterial blood, the SaO 2 ). Note that SaO 2 alone doesn’t reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content. OXYGEN CONTENT: CaO 2 Tissues need a requisite amount of O 2 molecules for metabolism. Neither the PaO 2 nor the SaO 2 provide information on the number of oxygen molecules, i.e., how much oxygen is in the blood. (Neither PaO 2 nor SaO 2 have units that denote any quantity.) Only CaO 2 (units ml O 2 /dl) tells us how much oxygen is in the blood; this is because CaO 2 is the only value that incorporates the hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen content equation: CaO 2 = (Hb x 1.34 x SaO 2 ) + (.003 x PaO 2 )

Acid-Base Balance Henderson Hasselbalch Equation [HCO 3 - ] pH = pK + log___________ 0.03 [PaCO 2 ] For teaching purposes the H_H equation can be shortened to its basic relationships: ph=HCO3/paO2

pH is inversely related to [H + ]; a pH change of 1.00 represents a 10-fold change in [H + ] pH [H + ] in nanomoles/L 7.00 100 7.10 80 7.30 50 7.40 40 7.52 30 7.70 20 8.00 10

Acid 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.) Primary acid-base disorder : One of the four acid-base disturbances that is manifested by an initial change in HCO 3 - or PaCO 2 . They are: metabolic acidosis (MAc), metabolic alkalosis (MAlk), respiratory acidosis (RAc), and respiratory alkalosis (RAlk). If HCO 3 - changes first, the disorder is either MAc (reduced HCO 3 - and acidemia) or MAlk (elevated HCO 3 - and alkalemia). If PaCO 2 changes first, the problem is either RAlk (reduced PaCO 2 and alkalemia) or RAc (elevated PaCO 2 and acidemia). Compensation : The change in HCO 3 - or PaCO 2 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 PaCO 2 ) 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 disorders - Respiratory alkalosis - Respiratory alkalosis - A primary disorder where the first change is a lowering of PaCO 2 , resulting in an elevated pH. Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO 3 ) by the kidneys; this reduction in HCO 3 - is not metabolic acidosis, since it is not a primary process. Primary Event Compensatory Event HCO 3 - HCO 3 - low pH high – ))))) pH high – ))))) PaCO 2 low PaCO 2 low

Primary acid-base disorders - Respiratory acidosis - Respiratory acidosis - A primary disorder where the first change is an elevation of PaCO 2 , resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO 3 - is not metabolic alkalosis, since it is not a primary process. Primary Event Compensatory Event HCO 3 - HCO 3 - high pH low – ))))) pH low – ))))) PaCO 2 high PaCO 2 high

Primary Acid-Base Disorders - Metabolic acidosis - Metabolic Acidosis - A primary acid-base disorder where the first change is a lowering of HCO 3 - , resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary hyperventilation; this lowering of PaCO 2 is not respiratory alkalosis, since it is not a primary process. Primary Event Compensatory Event HCO 3 -low HCO 3 -low pH low – ))))) pH low – ))))) PaCO 2 PaCO 2 low

Primary Acid-Base Disorders - Metabolic alkalosis - Metabolic alkalosis - A primary acid-base disorder where the first change is an elevation of HCO 3 - , resulting in increased pH. Compensation is a secondary hypoventilation (increased PaCO 2 ) 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 HCO 3 -high HCO 3 - high pH high – ))))) pH high – )))))  PaCO 2 PaCO 2 high

Anion Gap Metabolic acidosis is conveniently divided into elevated and normal anion gap (AG) acidosis. AG is calculated as AG = Na + - (Cl - + CO 2 ) Note: CO 2 in this equation is the “total CO 2 ” 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 -- Some clinical causes -- METABOLIC ACIDOSIS low HCO 3 - & 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 ALKALOSIS  HCO 3 - 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 -- Some clinical causes -- RESPIRATORY ACIDOSIS  PaCO 2 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 PaCO 2 & HIGH pH Hypoxemia (includes altitude) Anxiety Sepsis Any acute pulmonary insult, e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism

Mixed 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!

T ips to diagnosing mixed acid-base disorders TIP 1 . Don’t interpret any blood gas data for acid-base diagnosis without closely examining the serum electrolytes: Na + , K + , Cl - and CO 2 . A serum CO 2 out of the normal range always represents some type of acid-base disorder (barring lab or transcription error). High serum CO 2 indicates metabolic alkalosis &/or bicarbonate retention as compensation for respiratory acidosis Low serum CO 2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis Note that serum CO 2 may be normal in the presence of two or more acid-base disorders.

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 HCO 3 - and PaCO 2 invariably suggests two or more primary disorders. Example: pH 7.40, PaCO 2 20 mm Hg, HCO 3 - 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.) TIP 3 . Simplified rules predict the pH and HCO 3 - for a given change in PaCO 2 . If the pH or HCO 3 - is higher or lower than expected for the change in PaCO 2 , the patient probably has a metabolic acid-base disorder as well. The next slide shows expected changes in pH and HCO 3 - (in mEq/L) for a 10 mm Hg change in PaCO 2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis).

Expected changes in pH and HCO 3 - for a 10 mm Hg change in PaCO 2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis). ACUTE CHRONIC Resp Acidosis pH LOW by 0.07 pH LOW by 0.03 HCO 3 - HIGH by 1* HCO 3 - HIGH by 3-4 Resp Alkalosis pH HIGH by 0.08 pH HIGH by 0.03 HCO 3 - LOW by 2 HCO 3 - LOW by 5 *Units for HCO 3 - are mEq/L

Predicted changes in HCO 3 - for a directional change in PaCO 2 can help uncover mixed acid-base disorders. a) A normal or slightly low HCO 3 - in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO 2 50 mm Hg, HCO 3 - 22 mEq/L. Based on the rule for increase in HCO 3 - 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 HCO 3 - in the presence of hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO 2 30 mm Hg, HCO 3 - 26 mEq/L. Based on the rule for decrease in HCO 3 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.) TIP 4 . In maximally-compensated metabolic acidosis, the numerical value of PaCO 2 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 PaCO 2 = [1.5 x serum CO 2 ] + (8 ± 2) In contrast, compensation for metabolic alkalosis (by increase in PaCO 2 ) is highly variable, and in some cases there may be no or minimal compensation.

(Summary ) Clinical and laboratory approach to acid-base diagnosis Determine existence of acid-base disorder from arterial blood gas and/or serum electrolyte measurements. Check serum CO 2 ; if abnormal there is an acid-base disorder. If the anion gap is significantly increased there is a metabolic acidosis. Examine pH, PaCO 2 and HCO 3 - for the obvious primary acid-base disorder, and for deviations that indicate mixed acid-base disorders (TIPS 2 through 4).

(Summary ) Clinical and laboratory approach to acid-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 + 0.05 PaCO 2 40 + 5 mm Hg PaO 2 80 - 100 mm Hg HCO 3 24 + 4 mmol/L O2 Sat >95 Always mention and see FIO2 The essentials HCO3

5 The Steps for Successful Blood Gas Analysis SUMMARY OF INTERPRETATION

Step 2 Who is responsible for this change in pH ( culprit )? CO 2 will change pH in opposite direction Bicarb. will change pH in same direction Acidemia: With HCO 3 < 20 mmol/L = metabolic With PCO 2 >45 mm hg = respiratory Alkalemia: With HCO 3 >28 mmol/L = metabolic With PCO 2 <35 mm Hg = respiratory Step 1 Look at the pH Is the patient acidemic pH < 7.35 or alkalemic pH > 7.45

Step 3 If there is a primary respiratory disturbance, is it acute ? .08 change in pH ( Acute ) .03 change in pH ( Chronic ) 10 mm Change PaCO 2 =

Step 4 If the disturbance is metabolic is the respiratory compensation appropriate? For metabolic acidosis: Expected PaCO 2 = (1.5 x [HCO 3 ]) + 8 ) + 2 or simply… expected PaCO 2 = last two digits of pH For metabolic alkalosis: Expected PaCO 2 = 6 mm for 10 mEq. rise in Bicarb. Suspect if ............. actual PaCO 2 is more than expected : additional … respiratory acidosis actual PaCO 2 is less than expected : additional … respiratory alkalosis

Step 4 cont. If there is metabolic acidosis, is there a wide anion gap ? Na - (Cl - + HCO 3 - ) = Anion Gap usually <12 If >12, Anion Gap Acidosis : M ethanol U remia D iabetic Ketoacidosis P araldehyde I nfection (lactic acid) E thylene Glycol S alicylate Common causes Lactic acidosis 2) Metabolic disorders 3) Renal failure

th step Clinical correlation 5

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 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 CAUSES ABG TREATMENT compensation

Metabolic 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 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 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

Abg By Faruk Cfh

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