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ABG

An arterial blood gas (ABG) analysis measures pH, oxygen, and carbon dioxide levels in arterial blood. It is used to assess respiratory and metabolic function. The document outlines how to perform an ABG, including using a syringe to draw blood from the radial, brachial, or femoral artery. It discusses components measured in an ABG and their normal ranges, as well as factors that can affect results. Common acid-base imbalances like respiratory acidosis and metabolic alkalosis are also summarized, along with their primary and compensatory responses.

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ARTERIAL BLOOD GAS ANALYSIS DR.SUBODH KUMAR MAHTO PGIMER,DR.RML HOSPITAL NEW DELHI
What is an ABG? • Arterial Blood Gas • Drawn from artery- Radial, Brachial, Femoral • It is an invasive procedure
Why to order an ABG? • Assess adequacy of ventilation and oxygenation • Aids in establishing a diagnosis and severity of respiratory failure • Assess changes in acid- base homeostasis • Helps to guide treatment plan • Helps in management of ICU patients.
Components of an ABG – pH – PaCO2 – PaO2 – HCO3 – O2saturation – BE
Others include • Haemoglobin • Hematocrit • Na • K • Glucose • Standard bicarbonate • Buffer base • Standard base excess • TCO2
• Base Excess: It indicates increase in the amount of buffer base. • It is the number of mmol of strong acid needed to adjust pH to 7.4 at PCO2 40 mm Hg. • Base Deficit: It indicates decrease in the amount of buffer base.
• Standard bicarbonate It is the bicarbonate conc. In plasma in a completely oxygenated blood sample at Pco2 of 40 mm Hg at 370C . SBC > 24 mmol/l indicates metabolic alkalosis SBC<24 mmol/l indicates metabolic acidosis Buffer base It is the total equivalent conc. of all anion buffer components of blood . Normal value =48 mmol/L
• Standard base excess • It gives a view of the base excess of the entire extracellular fluid. • It indicates average Hb of the fluid space through which bicarbonate distributes. • standard base excess is the value when the hemoglobin is at 5 g/dl. Total plasma CO2 (T-CO2) Total content of the CO2 normal value= 27 meq/L
Normal Values – pH - 7.35 - 7.45 – PaCO2 - 35-45 mmHg – PaO2 - 80-100 mmHg – HCO3 - 22-26 – O2sat - 95-100% – Base Excess - +/-2 m Eq/L
HOW TO DRAW AN ABG..??? • Equipments • Site Selection • Contraindication • Puncture procedure • Post puncture procedure • Sample handling
Equipments 1. One 1 cc to 5 cc vented, pre-heparinized, plastic syringe 2. One 20 - 25 gauge 1 –1 1/2” needle Longer needles for brachial and femoral artery puncture 3. One Biohazard labelled plastic bag 4. . Two 1 x 1 inch sterile gauze
• 5. Alcohol prep pad • 6. Specimen/Patient label • 7. Iodine pad • 8. One adhesive bandage • 9. Lab Form • 10. Ice
Site Selection • Radial Artery - 45 insertion angle • Brachial Artery - 60 - 90 insertion angle • Femoral Artery - 90 insertion angle • Dorsalis Pedis Artery • Posterior Tibial artery
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Contraindication • No absolute contraindications • Dialysis shunt – choose another site • Mastectomy – use opposite side • Patient on anticoagulant/aspirin therapy – may have to hold pressure on puncture site longer than normal
Site specific contraindication Radial : Buergers disease Raynauds Absent Ulnar collateral circulation AV dialysis shunt Femoral: Local infection
Puncture procedure 1. Check for orders 2.Explain the patient about compression of puncture site 3. Make positive patient I.D. 4. Put on gloves 5. Assemble needle to syringe a. keep needle sterile b. eject excess heparin and air bubbles c. pull back syringe plunger to at least 1 cc
4 things that “hurt” 1. Needle through skin (sharp) 2. Needle through arterial wall (blunt) 3. Miss & catch nerve (shooting) 4. Miss & hit periostium (sharp)
Site selection 1. Radial artery is always the first choice because it provides collateral circulation. • A. Palpate the right and left radials arterial pulse and visualize the course of the artery. • B. Pick strongest pulse i. if radial pulse weak on right, move to left ii. if pulse on left weak, then try brachial • 2. Brachial used as alternative site • 3. Femoral is the last choice in normal situations Highest complication rate
Check for: • a. Bleeding • b. movement of fingers and tingling sensation • c. pulse distal to puncture
Post puncture procedure 1. Remove any air bubbles from sample and cap syringe • Dispose of needle in sharps container 2. Roll syringe to mix heparin with sample 3. Immerse in ice 4. On lab slip indicate: a. FIO2 b. Patient temperature c. Ventilator parameters 5. Deliver to lab
Sample handling Sample should be analyzed as soon as possible – If iced sample can be stored » Glass syringe – 1 hour » Plastic syringe – 15 minutes Remember: Blood is living tissue that continues to consume O2 and produce CO2
ABG Specimen Collection/Handling • Transport specimen to laboratory in a biohazard container • Analyze specimen on an instrument that has been recently calibrated • Temperature correction specimen in analyzer • Increase in patient temp: PO2, PCO2, pH • Decrease in patient temp: PO2, PCO2, pH
Blood Gas Analyzer
Technical Causes of Abnormal Results • 1. Room air mixed with sample • a. PaO2 will equilibrate to above 160 • 2. CO2 will be lower due to equilibration • 3. Delay in running sample • O2 consumption will continue as will CO2 production – pH decreases • Iced, sample will last an hour without a change in the result • un-iced, ABG's can be significantly changed after 10 minutes
• 4. Venous sample drawn • a. Usually this in patients with shock • b. Should doubt when PO2 is significantly lower than expected • i. draw venous blood to check comparison or • ii. redraw sample
• 5. Heparin • a. Sodium Heparin 1% solution should be used • b. ammonium heparin will alter pH • c. dry lithium heparin is OK • • All unnecessary heparin should be ejected from syringe, excess can effect results
• 6. Patient pain • a. Can cause hyperventilation or breath holding • b. An anaesthetic may be injected prior to stick for pain • • Usually 2% lidocaine • • CAUTION – some people allergic to “caines” • 7. Machine errors • a. Improper calibration • b. Air bubbles in electrode
Acid-Base Physiology • pH is the negative logarithm to the base 10 of the hydrogen ion concentration in mmol/L • pH = - log10[H+] • An increase in pH indicates a proportionate decrease in the [H+] and a decrease in the pH indicates a proportionate increase in the [H+]. • H2CO3 generates 12,500 mmol H+ per day. • Normal metabolism of proteins and nucleotides generates about 100 mmol H+ per day in the form of sulphuric and phosphoric acids.
Calculation of pH • pH is calculated from Henderson-Hasselbalch equation . • pH = pK + log acid/bas • pH = 6.1 + log HCO3- H2CO3 Kassirer and Bliech modified equation • H+ = 24 x PCO2/HCO3-
Regulation of pH pH is maintained in narrow range by • 1) In seconds: buffer systems • 2)In minutes: CO2 excretion by the lungs • 3)In hours to days: renal excretion of H+, reabsorption of HCO3
Regulation of arterial pH • 1.BUFFERS –Buffer systems minimize the change in pH resulting from production of acid . • Main buffer system in humans is HCO3- in ECF and protein and phosphate buffers in ICF. 2.ROLE OF THE RESPIRATORY SYSTEM–Elimination of volatile acid CO2. • a. Respiratory centers in the brain respond to changes in pH of CSF and blood to affect ventilatory rate. • b. Ventilation directly controls the elimination of CO2.
ROLE OF KIDNEY It retains and regenerate HCO3- thereby regenerating the body buffer with the net effect of eliminating the non- volatile acid load a. H+ secretion 1. Free urinary H+ - minimal contribution 2. Ammonia 3. Phosphorus b. HCO3- reabsorption 1. Proximal tubule – 90% 2. Distal tubule -10%
Carbon dioxide transport • In Dissolved form : Carbon dioxide is twenty times more soluble in water than oxygen. • 100 ml of plasma with a PCO2 of 40 mmHg carries about 2.4 mlCO2 in solution. 5% of total CO2 carriage. • As carbamino compounds : 5 -10% of CO2 carriage • Bicarbonate: The remaining 85 -90% of carbon dioxide is carried by blood in the form of bicarbonate ions.
Acid base disorders • Acidemia –pH less than 7.35 • Acidosis – A process that would cause acidemia, if not compensated • Alkalemia–pH greater than 7.45 • Alkalosis – A process that would cause alkalemia if not compensated
Four primary acid-base disorders • Metabolic acidosis • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis
SIMPLE VS. MIXED ACID-BASE DISORDER Simple acid-base disorder – a single primary process of acidosis or alkalosis. Mixed acid-base disorder – presence of more than one acid base disorder simultaneously
COMPENSATION The normal response of the respiratory system or kidneys to change in pH induced by a primary acid-base disorder
Compensation • In the presence of acidosis or alkalosis, regulatory mechanisms occur which try to maintain arterial pH. • Disturbances in HCO3- result in respiratory compensation • Changes in CO2 are counteracted by renal compensation
a. Renal compensation – kidneys adapt to alterations in pH by changing the amount of HCO3- generated/excreted. Full renal compensation takes 2-5 days b. Respiratory compensation – alteration in ventilation allow immediate compensation for metabolic acid- base disorders
Characteristics of  acid-base disorders DISORDER PRIMARY RESPONSES COMPENSATORY RESPONSE Metabolic acidosis  [H+]  PH  HCO3 -  pCO2 Metabolic alkalosis  [H+]  PH  HCO3 -  pCO2 Respiratory acidosis  [H+]  PH  pCO2  HCO3 - Respiratory alkalosis  [H+]  PH  pCO2  HCO3 -
Prediction of compensation Metabolic acidosis PaCO2= (1.5 x HCO3 -) + 8 ± 2 Metabolic alkalosis PaCO2 will↑ 0.75 mmHg per mmol/L ↑ in [HCO3 -] Respiratory acidosis Acute [HCO3 -] will ↑ 0.1 mmol/L per mmHg in PaCO2 Chronic [HCO3 -] will ↑ 0.4 mmol/L per mmHg in PaCO2 Respiratory alkalosis Acute [HCO3 -] will ↑ 0.2 mmol/L per mmHg in PaCO2 Chronic [HCO3 -] will ↑ 0.4 mmol/L per mmHg in PaCO2
Anion Gap • Anion gap used to assess acid-base status in D/D of meabolic acidosis Anion gap based on principle of electro neutrality: • Total Serum Cations = Total Serum Anions • Na – (HCO3 + Cl) = Anion gap • Normal Anion gap – 10 +/- 2meq/L
• Albumin is the major unmeasured anion • The anion gap should be corrected if there are gross changes in serum albumin levels. AG (CORRECTED) = AG + { (4 – [ALBUMIN]) × 2.5}
Delta gap • Difference between – Change in anion gap ( AG) – Change in bicarbonate ( HCO3 - ) • Based on assumption that for each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L , to maintain a stable anion content. • Usual range: -6 to +6 meq/L ; should be 0
 AG =  HCO3 -  Pure High AG Met Acidosis  AG > HCO3 - ( Gap >6)  HCO3- does not decrease as expected. Associated Metabolic Alkalosis or respiratory acidosis  AG <  HCO3 - ( Gap < -6)  HCO3- does not increase as expected Associated N AG Met Acidosis or rarely respiratory alkalosis Delta ratio may also be calculated
PLASMA OSMOLAR GAP  Calculated Plasma Osmolarity = 2[Na+] + [Gluc]/18 + [BUN]/2.8 Normal Measured Plasma Osmolarity > Calculated Plasma Osmolarity (upto 10 mOsm/L)  Measured Plasma Osmolarity - Calculated Plasma Osmolarity > 10 mOsm/kg indicates presence of abnormal osmotically active substance Ethanol Methanol Ethylene glycol
URINARY ANION GAP • Urinary NH4 + levels can be estimated by calculating the urine anion gap (UAG) • UAG = [Na+ + K+]u – [Cl–]u • [Cl–]u > [Na+ + K+], the urine gap is negative by definition • Helps to distinguish GI from renal causes of loss of HCO3 by estimating Urinary NH4+ (elevated in GI HCO3 loss but low in distal RTA). • Hence a -ve UAG (av -20 meq/L) seen in former while +ve value (av +23 meq/L) seen in latter.
Urine PH • Non AG metabolic acidosis: – If urine pH > 5.5 : Type 1 RTA – If urine pH < 5.5 : Type 2 or Type 4 RTA • Type 2 or Type 4 RTA can be later differentiated using serum K+ level
METABOLIC ACIDOSIS
Causes of High AG Met Acidosis 1. Ketoacidosis: Diabetic Alcoholic Starvation 2. Lactic Acidosis: Type A (Inadequate O2 Delivery to Cells) Type B (Inability of Cells to utilise O2) Type D (Abn bowel anatomy) 3. Toxicity: Salicylates Paraldehyde Methanol Toluene Ethylene Glycol 4. Renal Failure 5. Rhabdomyolsis
CAUSES OF NORMAL ANION GAP METABOLIC ACIDOSIS 1. HCO3 loss: GIT Diarrhoea Pancreatic or biliary drainage Urinary diversions (ureterosigmoidostomy) Renal Proximal (type 2) RTA Ketoacidosis (during therapy) Post-chronic hypocapnia
2. Impaired renal acid excretion: Distal (type 1) RTA Hyperkalemia (type 4) RTA Hypoaldosteronism 3. Misc: Acid Administration (NH4Cl) Hyperalimentation Cholestyramine Cl HCl therapy (Rx of severe met alkalosis)
METABOLIC ALKALOSIS
CAUSES OF METABOLIC ALKALOSIS 1. EXOGENOUS HCO3- LOADS Acute alkali administration Milk – alkali syndrome 2. Effective ECFV contraction, normotention, K+ deficiency and secondary Hyperreninemic hyperaldosteronism: GI LOSS: Vomiting Gastric Aspiration Villous adenoma
RENAL LOSS : Diuretics Post hypercapnic state Hypercalcaemia Recovery from LA/KA Mg2+ deficiency Bartters/Gitelmans syndr Nonreabs anions – penicill 3. ECFV expansion, hypertension,K+ deficiency, and mineralocorticoid excess: HIGH RENIN : RAS Accelerated hypertension Renin sec tumor
LOW RENIN : PRIMARY ALDOSTERONISM – Adenoma, hyperplasia , carcinoma ADRENAL ENZYME DEFECTS – 11 b Hydroxylase, 17 alfa Hydr def CUSHINGS SYNDROME OR DIS. OTHERS- licorice, carbenoxolone 4. Gain of function mutation of renal sodium channel with ECF expansion , hypertension , K+ deficiency and hyporeninemic hypoaldosteronism : LIDDLES SYNDROME
RESPIRATORY ACIDOSIS
Causes of Respiratory Acidosis 1. CENTRAL : Drugs( anesthetics, morphine , sedatives) Stroke Infection 2. AIRWAY : Obstruction Asthma 3. PARENCHYMA : Emphysema Pneumoconiosis Bronchitis ARDS Barotrauma
• 4. NEUROMUSCULAR : • Poliomyelitis • Kyphoscoliosis • Myasthenia • Muscular dystrophies 5. MISCELLANEOUS • Obesity • Hypoventilation • Permissive Hypercapnia
Respiratory Alkalosis
Causes of Respiratory Alkalosis 1.CENTRAL NERVOUS SYSTEM STIMULATION Structural Causes Non Structural Causes Head trauma Pain Brain tumor Anxiety CVA Fever Meningitis, encephalitis Psychosis 2. HYPOXEMIA OR TISSUE HYPOXIA Pneumonia, pulm oedema Aspiration High Altitude
3. STIMULATION OF CHEST RECEPTORS : • Hemothorax • Flail chest • Cardiac failure • Pulmonary embolism 4. MIXED/UNKNOWN MECHANISMS: Drugs – Salicylates Nicotine Progesterone Thyroid hormone Catecholamines Xanthines (Aminophylline & related compounds) Cirrhosis Gram –ve Sepsis Pregnancy Heat exposure Mechanical Ventilation
A Stepwise Approach to Solving Acid-Base Disorders
Step – 1 : Check for ERRORS Have the required parameters been correctly fed..???  Patient’s Temperature  Fi O₂ : specially if patient is in ventilator  Hemoglobin : some machines may not measure it  Barometric pressure : some machines may not measure it
Effect of temperature
Effect of barometric pressure (Pb)
Sampling error..?? Arterial, veinous or mixed…???
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 Relation b/w pH & H+ conc. Assessment of validity of test results
Assessment of validity of test results • H+ in nmol/L = 24 × PCO₂/HCO₃ • If there is a discripancy between the 2 results, the blood should be reanalyzed.
Analyse the adequacy of oxygenation..
 STEP -2 : Comprehensive history and physical examination.  STEP -3 : Acidosis or alkalosis..??? See the pH (<7.35 or >7.45)  STEP -4 : Identify the primary disorder See the change in PCo2 & HCO3  STEP -5 : Calculate the compensatory response Is adequately compensated???
 STEP -6 : Calculate anion gap STEP -7 : Calculate the delta gap (unmask hidden mixed disorders) STEP -8 : Calculate the osmolar gap (for high AG acidosis)  STEP -9 : Calculate the urinary anion gap (Non AG metabolic acidosis)  STEP -10 : Formulate differential diagnosis
Lets try…..
Case-1 • 60 years old M, presents to the ED with rapid breathing and less responsive than usual. No other history available. ABG results pH 7.31 PCO₂ 10 HCO₃ 5 Na 123 K 5 Cl 99
Stepwise interpretation 1. At pH 7.3 H+ conc. Should be ≈50nmol/L – Calculated H+ = 24 × 10/5 = 24 × 2 = 48 – Both values corroborate, hence result is valid. 2. pH is 7.3 i.e Acidosis 3. HCO₃ value has gone down, primary process is metabolic 4. Respiratory compensation: – Calculated PCO₂ = (1.5 × 5)+8 ± 2 = 13.5 to 17.5 – Over compensated ; mixed disorder – a/w respiratory alkalosis
5. Anion gap: (123+5) – (99 + 5) = 19 – High anion gap metabolic acidosis 6. Delta gap : – Change in AG = (19-10) = 9 – Change in HCO₃ = (24-5) = 19 – Delta gap = 9-19 = -10 Presence of non anion gap metabolic acidosis also.!! 7. Osmolar gap: data not provided.
Finally … • Mixed acid base disorder, with presence of both high AG & normal AG metabolic acidosis and respiratory alkalosis.
Case-2 • A k/c/o COPD with cor pulmonale on treatment presented with progressive breathlessness. ABG results pH 7.42 PCO₂ 67 HCO₃ 42 Na 140 K 3.5 Cl 88
• pH is normal; but PCO₂ & HCO₃ both are increased. • Change in PCO₂ is 67-40 = 27 • Expected rise in HCO₃ should be 27 × 0.4 = 10.8 • Expected HCO₃ = 24+10.8 ≈ 35 • Actual HCO₃ = 42 • AG = 12 (N) • Mixed disorder, both respiratory acidosis & metabolic alkalosis.
Case -3 • A known case of case of chronic kidney disease, discontinued MHD & presented to the emergency in an altered state of sensorium. Attendants gave history of repeated episodes of vomiting at home. ABG results pH 7.42 PCO₂ 40 HCO₃ 25 Na 140 K 3.0 Cl 95
• pH, PCO₂, HCO₃ all WNL • AG = 23 (↑) • Delta gap = 13 – 1 = 12 (↑) • AG >> HCO3 – • Mixed disorder with presence of both high AG metabolic acidosis and metabolic alkalosis.
Case-4 • 65 yrs old M, past h/o AMI on medication, presented with high grade fever with, cough & yellowish expectoration for 5 days. Acute increase in shortness of breath. ABG results pH 7.3 PCO₂ 38 HCO₃ 16 Na 136 K 4 Cl 102
• pH 7.3 = Acidosis • HCO₃ is low ; primary disorder is metabolic acidosis • Expected PCO₂ = (1.5 × 16) + 8 = 32 • Calculated PCO₂ < estimated PCO₂ • AG = 22 • Delta gap = (10-8) = 2 • Mixed disorder with metabolic acidosis & respiratory acidosis
Take home messages…
• ABG is a very useful diagnostic tool for our day to day practice. • Approach to interpret should be step wise & in a systematic manner. • Any abnormal result should be analyzed cautiously in light of clinical context. • Appropriate use of this tool using clinical judgment is of paramount importance
ABG

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ABG

  • 1.
    ARTERIAL BLOOD GAS ANALYSIS DR.SUBODHKUMAR MAHTO PGIMER,DR.RML HOSPITAL NEW DELHI
  • 2.
    What is anABG? • Arterial Blood Gas • Drawn from artery- Radial, Brachial, Femoral • It is an invasive procedure
  • 3.
    Why to orderan ABG? • Assess adequacy of ventilation and oxygenation • Aids in establishing a diagnosis and severity of respiratory failure • Assess changes in acid- base homeostasis • Helps to guide treatment plan • Helps in management of ICU patients.
  • 4.
    Components of anABG – pH – PaCO2 – PaO2 – HCO3 – O2saturation – BE
  • 5.
    Others include • Haemoglobin •Hematocrit • Na • K • Glucose • Standard bicarbonate • Buffer base • Standard base excess • TCO2
  • 6.
    • Base Excess:It indicates increase in the amount of buffer base. • It is the number of mmol of strong acid needed to adjust pH to 7.4 at PCO2 40 mm Hg. • Base Deficit: It indicates decrease in the amount of buffer base.
  • 7.
    • Standard bicarbonate Itis the bicarbonate conc. In plasma in a completely oxygenated blood sample at Pco2 of 40 mm Hg at 370C . SBC > 24 mmol/l indicates metabolic alkalosis SBC<24 mmol/l indicates metabolic acidosis Buffer base It is the total equivalent conc. of all anion buffer components of blood . Normal value =48 mmol/L
  • 8.
    • Standard baseexcess • It gives a view of the base excess of the entire extracellular fluid. • It indicates average Hb of the fluid space through which bicarbonate distributes. • standard base excess is the value when the hemoglobin is at 5 g/dl. Total plasma CO2 (T-CO2) Total content of the CO2 normal value= 27 meq/L
  • 9.
    Normal Values – pH- 7.35 - 7.45 – PaCO2 - 35-45 mmHg – PaO2 - 80-100 mmHg – HCO3 - 22-26 – O2sat - 95-100% – Base Excess - +/-2 m Eq/L
  • 10.
    HOW TO DRAWAN ABG..??? • Equipments • Site Selection • Contraindication • Puncture procedure • Post puncture procedure • Sample handling
  • 11.
    Equipments 1. One 1cc to 5 cc vented, pre-heparinized, plastic syringe 2. One 20 - 25 gauge 1 –1 1/2” needle Longer needles for brachial and femoral artery puncture 3. One Biohazard labelled plastic bag 4. . Two 1 x 1 inch sterile gauze
  • 12.
    • 5. Alcoholprep pad • 6. Specimen/Patient label • 7. Iodine pad • 8. One adhesive bandage • 9. Lab Form • 10. Ice
  • 13.
    Site Selection • RadialArtery - 45 insertion angle • Brachial Artery - 60 - 90 insertion angle • Femoral Artery - 90 insertion angle • Dorsalis Pedis Artery • Posterior Tibial artery
  • 14.
  • 15.
    Contraindication • No absolutecontraindications • Dialysis shunt – choose another site • Mastectomy – use opposite side • Patient on anticoagulant/aspirin therapy – may have to hold pressure on puncture site longer than normal
  • 16.
    Site specific contraindication Radial: Buergers disease Raynauds Absent Ulnar collateral circulation AV dialysis shunt Femoral: Local infection
  • 17.
    Puncture procedure 1. Checkfor orders 2.Explain the patient about compression of puncture site 3. Make positive patient I.D. 4. Put on gloves 5. Assemble needle to syringe a. keep needle sterile b. eject excess heparin and air bubbles c. pull back syringe plunger to at least 1 cc
  • 18.
    4 things that“hurt” 1. Needle through skin (sharp) 2. Needle through arterial wall (blunt) 3. Miss & catch nerve (shooting) 4. Miss & hit periostium (sharp)
  • 19.
    Site selection 1. Radialartery is always the first choice because it provides collateral circulation. • A. Palpate the right and left radials arterial pulse and visualize the course of the artery. • B. Pick strongest pulse i. if radial pulse weak on right, move to left ii. if pulse on left weak, then try brachial • 2. Brachial used as alternative site • 3. Femoral is the last choice in normal situations Highest complication rate
  • 28.
    Check for: • a.Bleeding • b. movement of fingers and tingling sensation • c. pulse distal to puncture
  • 29.
    Post puncture procedure 1.Remove any air bubbles from sample and cap syringe • Dispose of needle in sharps container 2. Roll syringe to mix heparin with sample 3. Immerse in ice 4. On lab slip indicate: a. FIO2 b. Patient temperature c. Ventilator parameters 5. Deliver to lab
  • 30.
    Sample handling Sample shouldbe analyzed as soon as possible – If iced sample can be stored » Glass syringe – 1 hour » Plastic syringe – 15 minutes Remember: Blood is living tissue that continues to consume O2 and produce CO2
  • 31.
    ABG Specimen Collection/Handling •Transport specimen to laboratory in a biohazard container • Analyze specimen on an instrument that has been recently calibrated • Temperature correction specimen in analyzer • Increase in patient temp: PO2, PCO2, pH • Decrease in patient temp: PO2, PCO2, pH
  • 32.
  • 34.
    Technical Causes ofAbnormal Results • 1. Room air mixed with sample • a. PaO2 will equilibrate to above 160 • 2. CO2 will be lower due to equilibration • 3. Delay in running sample • O2 consumption will continue as will CO2 production – pH decreases • Iced, sample will last an hour without a change in the result • un-iced, ABG's can be significantly changed after 10 minutes
  • 35.
    • 4. Venoussample drawn • a. Usually this in patients with shock • b. Should doubt when PO2 is significantly lower than expected • i. draw venous blood to check comparison or • ii. redraw sample
  • 36.
    • 5. Heparin •a. Sodium Heparin 1% solution should be used • b. ammonium heparin will alter pH • c. dry lithium heparin is OK • • All unnecessary heparin should be ejected from syringe, excess can effect results
  • 37.
    • 6. Patientpain • a. Can cause hyperventilation or breath holding • b. An anaesthetic may be injected prior to stick for pain • • Usually 2% lidocaine • • CAUTION – some people allergic to “caines” • 7. Machine errors • a. Improper calibration • b. Air bubbles in electrode
  • 38.
    Acid-Base Physiology • pHis the negative logarithm to the base 10 of the hydrogen ion concentration in mmol/L • pH = - log10[H+] • An increase in pH indicates a proportionate decrease in the [H+] and a decrease in the pH indicates a proportionate increase in the [H+]. • H2CO3 generates 12,500 mmol H+ per day. • Normal metabolism of proteins and nucleotides generates about 100 mmol H+ per day in the form of sulphuric and phosphoric acids.
  • 39.
    Calculation of pH •pH is calculated from Henderson-Hasselbalch equation . • pH = pK + log acid/bas • pH = 6.1 + log HCO3- H2CO3 Kassirer and Bliech modified equation • H+ = 24 x PCO2/HCO3-
  • 40.
    Regulation of pH pHis maintained in narrow range by • 1) In seconds: buffer systems • 2)In minutes: CO2 excretion by the lungs • 3)In hours to days: renal excretion of H+, reabsorption of HCO3
  • 41.
    Regulation of arterialpH • 1.BUFFERS –Buffer systems minimize the change in pH resulting from production of acid . • Main buffer system in humans is HCO3- in ECF and protein and phosphate buffers in ICF. 2.ROLE OF THE RESPIRATORY SYSTEM–Elimination of volatile acid CO2. • a. Respiratory centers in the brain respond to changes in pH of CSF and blood to affect ventilatory rate. • b. Ventilation directly controls the elimination of CO2.
  • 42.
    ROLE OF KIDNEY Itretains and regenerate HCO3- thereby regenerating the body buffer with the net effect of eliminating the non- volatile acid load a. H+ secretion 1. Free urinary H+ - minimal contribution 2. Ammonia 3. Phosphorus b. HCO3- reabsorption 1. Proximal tubule – 90% 2. Distal tubule -10%
  • 43.
    Carbon dioxide transport •In Dissolved form : Carbon dioxide is twenty times more soluble in water than oxygen. • 100 ml of plasma with a PCO2 of 40 mmHg carries about 2.4 mlCO2 in solution. 5% of total CO2 carriage. • As carbamino compounds : 5 -10% of CO2 carriage • Bicarbonate: The remaining 85 -90% of carbon dioxide is carried by blood in the form of bicarbonate ions.
  • 44.
    Acid base disorders •Acidemia –pH less than 7.35 • Acidosis – A process that would cause acidemia, if not compensated • Alkalemia–pH greater than 7.45 • Alkalosis – A process that would cause alkalemia if not compensated
  • 45.
    Four primary acid-basedisorders • Metabolic acidosis • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis
  • 46.
    SIMPLE VS. MIXEDACID-BASE DISORDER Simple acid-base disorder – a single primary process of acidosis or alkalosis. Mixed acid-base disorder – presence of more than one acid base disorder simultaneously
  • 47.
    COMPENSATION The normal responseof the respiratory system or kidneys to change in pH induced by a primary acid-base disorder
  • 48.
    Compensation • In thepresence of acidosis or alkalosis, regulatory mechanisms occur which try to maintain arterial pH. • Disturbances in HCO3- result in respiratory compensation • Changes in CO2 are counteracted by renal compensation
  • 49.
    a. Renal compensation– kidneys adapt to alterations in pH by changing the amount of HCO3- generated/excreted. Full renal compensation takes 2-5 days b. Respiratory compensation – alteration in ventilation allow immediate compensation for metabolic acid- base disorders
  • 50.
    Characteristics of acid-base disorders DISORDER PRIMARY RESPONSES COMPENSATORY RESPONSE Metabolic acidosis  [H+]  PH  HCO3 -  pCO2 Metabolic alkalosis  [H+]  PH  HCO3 -  pCO2 Respiratory acidosis  [H+]  PH  pCO2  HCO3 - Respiratory alkalosis  [H+]  PH  pCO2  HCO3 -
  • 51.
    Prediction of compensation Metabolicacidosis PaCO2= (1.5 x HCO3 -) + 8 ± 2 Metabolic alkalosis PaCO2 will↑ 0.75 mmHg per mmol/L ↑ in [HCO3 -] Respiratory acidosis Acute [HCO3 -] will ↑ 0.1 mmol/L per mmHg in PaCO2 Chronic [HCO3 -] will ↑ 0.4 mmol/L per mmHg in PaCO2 Respiratory alkalosis Acute [HCO3 -] will ↑ 0.2 mmol/L per mmHg in PaCO2 Chronic [HCO3 -] will ↑ 0.4 mmol/L per mmHg in PaCO2
  • 52.
    Anion Gap • Aniongap used to assess acid-base status in D/D of meabolic acidosis Anion gap based on principle of electro neutrality: • Total Serum Cations = Total Serum Anions • Na – (HCO3 + Cl) = Anion gap • Normal Anion gap – 10 +/- 2meq/L
  • 53.
    • Albumin isthe major unmeasured anion • The anion gap should be corrected if there are gross changes in serum albumin levels. AG (CORRECTED) = AG + { (4 – [ALBUMIN]) × 2.5}
  • 54.
    Delta gap • Differencebetween – Change in anion gap ( AG) – Change in bicarbonate ( HCO3 - ) • Based on assumption that for each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L , to maintain a stable anion content. • Usual range: -6 to +6 meq/L ; should be 0
  • 55.
     AG = HCO3 -  Pure High AG Met Acidosis  AG > HCO3 - ( Gap >6)  HCO3- does not decrease as expected. Associated Metabolic Alkalosis or respiratory acidosis  AG <  HCO3 - ( Gap < -6)  HCO3- does not increase as expected Associated N AG Met Acidosis or rarely respiratory alkalosis Delta ratio may also be calculated
  • 56.
    PLASMA OSMOLAR GAP Calculated Plasma Osmolarity = 2[Na+] + [Gluc]/18 + [BUN]/2.8 Normal Measured Plasma Osmolarity > Calculated Plasma Osmolarity (upto 10 mOsm/L)  Measured Plasma Osmolarity - Calculated Plasma Osmolarity > 10 mOsm/kg indicates presence of abnormal osmotically active substance Ethanol Methanol Ethylene glycol
  • 57.
    URINARY ANION GAP •Urinary NH4 + levels can be estimated by calculating the urine anion gap (UAG) • UAG = [Na+ + K+]u – [Cl–]u • [Cl–]u > [Na+ + K+], the urine gap is negative by definition • Helps to distinguish GI from renal causes of loss of HCO3 by estimating Urinary NH4+ (elevated in GI HCO3 loss but low in distal RTA). • Hence a -ve UAG (av -20 meq/L) seen in former while +ve value (av +23 meq/L) seen in latter.
  • 58.
    Urine PH • NonAG metabolic acidosis: – If urine pH > 5.5 : Type 1 RTA – If urine pH < 5.5 : Type 2 or Type 4 RTA • Type 2 or Type 4 RTA can be later differentiated using serum K+ level
  • 59.
  • 60.
    Causes of HighAG Met Acidosis 1. Ketoacidosis: Diabetic Alcoholic Starvation 2. Lactic Acidosis: Type A (Inadequate O2 Delivery to Cells) Type B (Inability of Cells to utilise O2) Type D (Abn bowel anatomy) 3. Toxicity: Salicylates Paraldehyde Methanol Toluene Ethylene Glycol 4. Renal Failure 5. Rhabdomyolsis
  • 61.
    CAUSES OF NORMALANION GAP METABOLIC ACIDOSIS 1. HCO3 loss: GIT Diarrhoea Pancreatic or biliary drainage Urinary diversions (ureterosigmoidostomy) Renal Proximal (type 2) RTA Ketoacidosis (during therapy) Post-chronic hypocapnia
  • 62.
    2. Impaired renalacid excretion: Distal (type 1) RTA Hyperkalemia (type 4) RTA Hypoaldosteronism 3. Misc: Acid Administration (NH4Cl) Hyperalimentation Cholestyramine Cl HCl therapy (Rx of severe met alkalosis)
  • 63.
  • 64.
    CAUSES OF METABOLIC ALKALOSIS 1.EXOGENOUS HCO3- LOADS Acute alkali administration Milk – alkali syndrome 2. Effective ECFV contraction, normotention, K+ deficiency and secondary Hyperreninemic hyperaldosteronism: GI LOSS: Vomiting Gastric Aspiration Villous adenoma
  • 65.
    RENAL LOSS :Diuretics Post hypercapnic state Hypercalcaemia Recovery from LA/KA Mg2+ deficiency Bartters/Gitelmans syndr Nonreabs anions – penicill 3. ECFV expansion, hypertension,K+ deficiency, and mineralocorticoid excess: HIGH RENIN : RAS Accelerated hypertension Renin sec tumor
  • 66.
    LOW RENIN : PRIMARYALDOSTERONISM – Adenoma, hyperplasia , carcinoma ADRENAL ENZYME DEFECTS – 11 b Hydroxylase, 17 alfa Hydr def CUSHINGS SYNDROME OR DIS. OTHERS- licorice, carbenoxolone 4. Gain of function mutation of renal sodium channel with ECF expansion , hypertension , K+ deficiency and hyporeninemic hypoaldosteronism : LIDDLES SYNDROME
  • 67.
  • 68.
    Causes of RespiratoryAcidosis 1. CENTRAL : Drugs( anesthetics, morphine , sedatives) Stroke Infection 2. AIRWAY : Obstruction Asthma 3. PARENCHYMA : Emphysema Pneumoconiosis Bronchitis ARDS Barotrauma
  • 69.
    • 4. NEUROMUSCULAR: • Poliomyelitis • Kyphoscoliosis • Myasthenia • Muscular dystrophies 5. MISCELLANEOUS • Obesity • Hypoventilation • Permissive Hypercapnia
  • 70.
  • 71.
    Causes of RespiratoryAlkalosis 1.CENTRAL NERVOUS SYSTEM STIMULATION Structural Causes Non Structural Causes Head trauma Pain Brain tumor Anxiety CVA Fever Meningitis, encephalitis Psychosis 2. HYPOXEMIA OR TISSUE HYPOXIA Pneumonia, pulm oedema Aspiration High Altitude
  • 72.
    3. STIMULATION OFCHEST RECEPTORS : • Hemothorax • Flail chest • Cardiac failure • Pulmonary embolism 4. MIXED/UNKNOWN MECHANISMS: Drugs – Salicylates Nicotine Progesterone Thyroid hormone Catecholamines Xanthines (Aminophylline & related compounds) Cirrhosis Gram –ve Sepsis Pregnancy Heat exposure Mechanical Ventilation
  • 73.
  • 74.
    Step – 1: Check for ERRORS Have the required parameters been correctly fed..???  Patient’s Temperature  Fi O₂ : specially if patient is in ventilator  Hemoglobin : some machines may not measure it  Barometric pressure : some machines may not measure it
  • 75.
  • 77.
    Effect of barometricpressure (Pb)
  • 78.
  • 79.
    pH is inverselyrelated 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 Relation b/w pH & H+ conc. Assessment of validity of test results
  • 80.
    Assessment of validityof test results • H+ in nmol/L = 24 × PCO₂/HCO₃ • If there is a discripancy between the 2 results, the blood should be reanalyzed.
  • 81.
    Analyse the adequacyof oxygenation..
  • 82.
     STEP -2: Comprehensive history and physical examination.  STEP -3 : Acidosis or alkalosis..??? See the pH (<7.35 or >7.45)  STEP -4 : Identify the primary disorder See the change in PCo2 & HCO3  STEP -5 : Calculate the compensatory response Is adequately compensated???
  • 83.
     STEP -6: Calculate anion gap STEP -7 : Calculate the delta gap (unmask hidden mixed disorders) STEP -8 : Calculate the osmolar gap (for high AG acidosis)  STEP -9 : Calculate the urinary anion gap (Non AG metabolic acidosis)  STEP -10 : Formulate differential diagnosis
  • 84.
  • 85.
    Case-1 • 60 yearsold M, presents to the ED with rapid breathing and less responsive than usual. No other history available. ABG results pH 7.31 PCO₂ 10 HCO₃ 5 Na 123 K 5 Cl 99
  • 86.
    Stepwise interpretation 1. AtpH 7.3 H+ conc. Should be ≈50nmol/L – Calculated H+ = 24 × 10/5 = 24 × 2 = 48 – Both values corroborate, hence result is valid. 2. pH is 7.3 i.e Acidosis 3. HCO₃ value has gone down, primary process is metabolic 4. Respiratory compensation: – Calculated PCO₂ = (1.5 × 5)+8 ± 2 = 13.5 to 17.5 – Over compensated ; mixed disorder – a/w respiratory alkalosis
  • 87.
    5. Anion gap:(123+5) – (99 + 5) = 19 – High anion gap metabolic acidosis 6. Delta gap : – Change in AG = (19-10) = 9 – Change in HCO₃ = (24-5) = 19 – Delta gap = 9-19 = -10 Presence of non anion gap metabolic acidosis also.!! 7. Osmolar gap: data not provided.
  • 88.
    Finally … • Mixedacid base disorder, with presence of both high AG & normal AG metabolic acidosis and respiratory alkalosis.
  • 89.
    Case-2 • A k/c/oCOPD with cor pulmonale on treatment presented with progressive breathlessness. ABG results pH 7.42 PCO₂ 67 HCO₃ 42 Na 140 K 3.5 Cl 88
  • 90.
    • pH isnormal; but PCO₂ & HCO₃ both are increased. • Change in PCO₂ is 67-40 = 27 • Expected rise in HCO₃ should be 27 × 0.4 = 10.8 • Expected HCO₃ = 24+10.8 ≈ 35 • Actual HCO₃ = 42 • AG = 12 (N) • Mixed disorder, both respiratory acidosis & metabolic alkalosis.
  • 91.
    Case -3 • Aknown case of case of chronic kidney disease, discontinued MHD & presented to the emergency in an altered state of sensorium. Attendants gave history of repeated episodes of vomiting at home. ABG results pH 7.42 PCO₂ 40 HCO₃ 25 Na 140 K 3.0 Cl 95
  • 92.
    • pH, PCO₂,HCO₃ all WNL • AG = 23 (↑) • Delta gap = 13 – 1 = 12 (↑) • AG >> HCO3 – • Mixed disorder with presence of both high AG metabolic acidosis and metabolic alkalosis.
  • 93.
    Case-4 • 65 yrsold M, past h/o AMI on medication, presented with high grade fever with, cough & yellowish expectoration for 5 days. Acute increase in shortness of breath. ABG results pH 7.3 PCO₂ 38 HCO₃ 16 Na 136 K 4 Cl 102
  • 94.
    • pH 7.3= Acidosis • HCO₃ is low ; primary disorder is metabolic acidosis • Expected PCO₂ = (1.5 × 16) + 8 = 32 • Calculated PCO₂ < estimated PCO₂ • AG = 22 • Delta gap = (10-8) = 2 • Mixed disorder with metabolic acidosis & respiratory acidosis
  • 95.
  • 96.
    • ABG isa very useful diagnostic tool for our day to day practice. • Approach to interpret should be step wise & in a systematic manner. • Any abnormal result should be analyzed cautiously in light of clinical context. • Appropriate use of this tool using clinical judgment is of paramount importance