1. ARTERIAL BLOOD GASES ANALYSIS
Presenter: Dr. SUMAN NANDI
Moderator:Dr. APURBA BORAH

2. Introduction: -One of the main factors determining oxygen delivery to the cells is the oxygen content of the blood. ABG analysis is the gold standard for measurement of oxygenation. -Most frequent test in ICU -Particularly valuable in the setting of low flow states or abnormal Hb when SpO2 do not correlate with PaO2 -Clinical changes like resp. distress, shock, deterioration in mental status are clear indications for ABG analysis. Procedure: -Site: -Most commonly radial artery -Adv: presence of ulnar collateral (confirmed by allen’s test) & easy to palpate and stabilize -Femoral & Brachial artery ; arterialised ear lobe

3. Contraindications: -Anticoagulant therapy -H/o Clotting disorder -H/o arterial spasm following previous puncture -Severe PVD -Infection at the site -Arterial grafts

4. Complications: -Rare with proper positioning and procedure -Hematoma, vasospam, arterial aneurysm, fibrosis, infection, iatrogenic anemia due to repeated ABG analysis -Arterial line placement associated with increased ABG analysis, the catheter size & material (Teflon > Polyethylene) may cause arterial thrombosis esp. in decreased perfusion

5. Normal values: -pH : 7.35 to PaO2 : 80 to 100 mm Hg (10 to 13 kPa) -PaCO2 : 35 to 45 mm Hg (4.7 to 6.0 kPa) -HCO3- & SBC : 22 to 26 mEq/L -Anion Gap : 8 to 16 mEq/L -Hct : 35 to 45 -BE ecf & BE b : + 2 to -2 mmol/L -TCO2 : 40 mm Hg -SO2 : 95 to 100 % -PAO2 : 105 mm Hg -A-a gradient : < 20 mm Hg (2.6 kPa) -PaO2/FiO2 : >300 -Na+ :135 to 145 mEq/L -K+ :3.5 to 5.1 mEq/L

6. Algorithmic approach to ABG interpretation: (Text Book Of Critical Care) 1). Is the data internally consistent with Kassir’s modification of Henderson Hasselbalch Equation? 2). What is the underlying acid base abnormality? 3). Is the primary problem an acidosis? If yes Met. Or Resp.? 4). If Metabolic acidosis present, calculate Anion Gap. 5). See if additional disturbance present by calculating the delta (∆) gap. It is the difference between normal AG (8-16) with observed AG. Delta gap when added to measured HCO3- should equal 24. If it is <24 → non AG acidosis, if >24 → Metabolic alkalosis exists 6) Is resp. process purely compensatory, or is there an underlying resp. acidosis or alkalosis? Use Winter’s formula to calculate the expected PaCO2 in setting of pure compensation:

7. Checking ABG analysis validity:
-Winter’s formula: PaCo2 = 1.5 [HCO3-] + 8 +/- 2
-PaCo2 > expected → underlying resp. acidosis
-PaCO2< expected → underlying resp. alkalosis
7). Is primary problem an alkalosis? If so, resp. or
metabolic? The BE is helpful. Is it acute or chronic?
8). Determine underlying causes for metabolic or
respiratory derangement.
Checking ABG analysis validity:
-Kassir’s modification of H-H equation:
[H+] = 24 x {[PCO2 ] / [HCO3-]}
24 is combination of solubility coefficient of CO2 & pK.
-A divergence of [H+] by 1 nmol/L from baseline of 40 will
cause pH to change reciprocally by approximately 0.01 unit
within the range of 7.1 to 7.5
-ABG results are correct if it correlates with the above rule.

8. Summary of changes in pH, PaCO2 and HCO3- in Acid-Base disorders: Acid-base disorder pH PaCO2 HCO3- -Respiratory acidosis   N -Metabolic acidosis  N  -Respiratory alkalosis   N -Metabolic alkalosis  N  -Respiratory acidosis with renal compensation *  

9. Acid-base disorder pH PaCO2 HCO3- -Metabolic acidosis with respiratory compensation *   -Respiratory alkalosis with renal compensation  *   -Metabolic alkalosis with respiratory compensation  *   -Mixed metabolic and respiratory acidosis    respiratory alkalosis    * If the compensation is virtually complete the pH may be in the normal range-over compensation doesnot occur Those marked in bold are particularly common after cardiac arrest

10. Acid Base Balance: -Nearly all biochemical reactions in the body are dependent on maintaining physiological [H+]. -The regulation of [H+] is called Acid Base balance. That [H+] varies by only 18 nEq/L is a testament Acid Base control. -Concept of [H+] is explained Henderson Hasselbalch Equation: pH = log[HCO3-] /{ [PCO2 ] x 0.03} -Best explanation for Acid Base balance: -Strong Ion Difference (SID) -PCO2 -Total Weak Acid Concentration (ATOT) -Strong Ion Difference: -It is the sum of all the strong completely or almost completely dissociated cations (Na+, K+, Ca+, Mg2+) minus the strong anions (Cl-, lactate- etc)

11. -Although we can calculate SID as the Laws of Electroneutrality must be observed, if there is an SID other unmeasured ions must be present. -[H+] is not a strong ion as water doesnot completely dissociate but it can, does and must change in response to any change in SID, [PCO2 ] and ATOT to comply with the above law of electroneutrality -Strong ions cannot be made to achieve electroneutrality but [H+] are created or consumed based on changes in the dissociation of water.

12. -Other approaches for understanding Acid Base disorder 1) Boston Approach 2) Copenhagen Approach Boston Approach: a) If pH & PaCO2 are both abnormal, compare the directional change -If both change in the same direction the primary acid base disorder is metabolic -↓pH & ↓PaCO2 → Primary metabolic acidosis -↑pH & ↑PaCO2 → Primary metabolic alkalosis -If both change in opposite direction the primary acid base disorder is respiratory

13. -↓pH & ↑PaCO2 → Primary respiratory acidosis -↑pH & ↓PaCO2 → Primary respiratory alkalosis b) If either pH or PCO2 is normal, there is a mixed metabolic & respiratory disorder (one metabolic & other alkalosis) -If PaCO2 is normal, the directional change of pH identifies the metabolic disorder -↑pH → mixed met alkalosis & resp. acidosis -↓pH → mixed met acidosis & resp. alkalosis -If the pH is normal, the directional change of PaCO2 identifies the respiratory disorder -↑PaCO2 → mixed resp. acidosis & met. alkalosis -↓PaCO2 → mixed resp. alkalosis & met. acidosis c) If there is a primary acid base disorder proceed as directed below. If there is a mixed disorder skip this stage 1) If there is primary metabolic acidosis or alkalosis use the

14. following equations to calculate expected PaCO2 -Primary metabolic acidosis Expected PaCO2 = (1.5 x HCO3-) + (8 +/- 2) -Primary metabolic alkalosis Expected PaCO2 = (0.7 x HCO3-) + (21 +/- 2) -If PaCO2 higher than expected there is additional (2˚) respiratory acidosis -If PaCO2 lower than expected there is additional (2˚) respiratory alkalosis 2) If there is primary respiratory acidosis or alkalosis use following equations to predict pH -In acute respiratory acidosis : Expected pH =7.4 – [0.008 x(PaCO2 – 40)] -In acute respiratory alkalosis : Expected pH =7.4 + [0.008 x(40 -PaCO2)]

15. -In chronic respiratory acidosis: Expected pH = 7. 4 – [0
-In chronic respiratory acidosis: Expected pH = 7.4 – [0.003 x(PaCO2 – 40)] -In chronic respiratory alkalosis: Expected pH =7.4 + [0.003 x(40 -PaCO2 )] -If the calculated change in pH is between above mentioned range ( to x change in PaCO2 ) the disorder is partially compensated resp acidosis or alkalosis -For respiratory acidosis, if the pH is lower than expected for the acute condition, there is (2˚) met. acidosis & if pH is higher than expected for the chronic form, there is (2˚) metabolic alkalosis -For resp. alkalosis, if the pH is higher than expected for the acute form, there is (2˚) met. alkalosis & if pH is lower than expected for the chronic form, there is (2˚) met. acidosis

16. d) Evaluation of metabolic acidosis: -calculate the Anion gap Normal AG = 8 – 16 mEq/L -In presence of high AG met acidosis calculate gap-gap -Gap gap ratio = (AG excess) / (HCO3- def) -If GG < 1 → a normal AG met. acidosis coexists -If GG > 1 → a metabolic alkalosis coexists

17. Copenhagen approach: -It uses base excess as the assessment of the metabolic component. -Siggard-Anderson defined BE as the amount of acid or base required to return pH to 7.4 assuming PCO2 40 at 38ºC - Normal BE is +2 to -2 mmol/L -If BE > +2 → Metabolic Alkalosis -If BE < -2 → Metabolic Acidosis

18. Compensatory mechanisms in Acid Base disorders:
1). Immediate chemical buffering:
-Bicarbonate: most imp. In ECF
-Haemoglobin
-Phosphate & ammonium ions: Urinary buffers
-Other intracellular proteins
2) Pulmonary Compensation:
-By raising or lowering PaCO2
3) Renal Compensation:
-Increased filtration of HCO3-
-Increased excretion of titratable acids
-Increased production of ammonia

19. Respiratory Acidosis:
-These effects are generally not apprciable for hrs
and may not be maximal for upto 5 days.
Respiratory Acidosis:
-A) D/t Alveolar hypoventilation:
-CNS depression- drugs, sleep disorders, cerebral trauma
-NM disorders- Myopathies, Neuropathies
-Chest wall- flail chest, kyphoscoliosis
-Pleural- pneumothorax, pleural effusion
-Airway obstruction
-Upper- FB, tumour, laryngospasm
-Lower- Asthma, COPD, tumour
-Parenchymal lung disease- pulm. Odema, emboli,
pneumonia, aspiration, ILD
-Ventilator malfunction

20. -B) D/t Increased CO2 production: -Malignant hyperthermia -Intense shivering -Prolonged seizure activity -Burns Treatment of Respiratory Acidosis: -Treated by reversing the imbalance between CO2 production and alveolar ventilation -In most cases accomplished just by ↑ alveolar ventilation -Specific measures- Dantrolene for malignant hyperthermia - Muscle paralysis for tetanus - Anti thyroid drugs for thyroid storm -Other temporary measures: -Bronchodilation -Reversal of narcosis

21. -Respiratory stimulant: Doxapram
-Diuresis for ↑ lung compliance
-Indications for mechanical ventilation
-Mod. To severe acidosis (pH < 7.2)
-CO2 narcosis
-Impending respiratory muscle fatigue
-If pH < 7.1 and HCO3- < 15 mEq/L then IV NaHCO3-
Metabolic Acidosis:
-A) Increased AG:
-D/t increased endogenous nonvolatile acids
-Renal failure
-Ketoacidosis- Diabetic, Starvation, Alcoholic
-Lactic acidosis
-Inborn errors of metabolism

22. -Ingestion of toxins: Salicylates, methanol, sulfur
ethylene glycol, paraldehyde, toluene
-Rhabdomyolysis
-B) Normal AG
-↑ GI losses of HCO3-: diarrhoea, fistulas
ureterosigmoidostomy, ingestion of CaCl2, MgCl2
-↑ renal losses of HCO3-: RTA, carbonic anhydrase
inhibitors
-Large amounts of HCO3- free fluids
-↑ intake of –NH4Cl, Lysine & agrinine hydrochloride
-Plasma albumin accounts for the largest fraction of AG (about 11
mEq/L). AG decreases by 2.5 mEq/L for every 1 g/dl ↓ in albumin.
Treatment of Metabolic Acidosis:
-Any respiratory component should be corrected (PaCO2 <40)

23. Respiratory Alkalosis:
-If pH remains < 7.2 → IV 7.5% NaHCO3- (1mEq/L empirically)
-Raise pH to > 7.25 to avoid adverse effects of acidemia
-Profound or refractory acidemia → Hemodialysis
-Routine use of NaHCO3 in cardiac arrest or low flow states →
no longer recommended
-Specific Therapy
-Diabetic ketoacidosis: Fluids, insulin, K+, PO4-, Mg2+
-Salicylate poisoning: Alkalinization of urine with NaHCO3
-Methanol or Ethylene glycol poisoning: Ethanol infusions
Respiratory Alkalosis:
-Central stimulation: Pain, fever, anxiety, infection, drugs
-Peripheral stimulation: Hypoxemia, high altitude, CCF, asthma
-Iatrogenic: Ventilator induced

24. Metabolic Alkalosis: Treatment of Respiratory Alkalosis:
-Correction of underlying abnormality is the only way
-For severe alkalemia (pH>7.6) IV HCl, Arginine chloride,
Ammonium chloride may be indicated
Metabolic Alkalosis:
-Chloride sensitive:
-GI: Vomiting, gastric drainage, villous adenoma
-Renal: Diuretics
-Chloride resistant: Increased mineralocorticoid activity
-Misc: Massive blood transfusion, Na Penicillins etc
Treatment of Metabolic Alkalosis:
-Correct any respiratory component
-Chloride sensitive Met. Alk.: IV NaCl & KCl, PPI for GI losses
-Chloride resistant Met. Alk.: Aldosterone antagonists-
Spironolactone
-If pH>7.6 → IV HCl, NH4Cl or Arginine Cl or hemodialysis

25. Other parameters measured by an ABG analyser: 1) Hct
Other parameters measured by an ABG analyser: 1) Hct.: -Primary determinant of blood viscosity that bears a non linear relationship with DO2 (O2 delivery). -At low volumes Hct predictably adds to O2 content -At an Hct of 55 to 57% DO2 reaches its maximum in normal subjects, falling sharply with further rise. -Above 65% phlebotomy may to reqd. to avert hemo- dynamic crisis as ↑ Hct is associated with intravascular volume contraction

26. 2) A-a gradient: Normal < 20 mm Hg -Used to estimate pulmonary pathophysiology and to rule out hypoxemia d/t low alveolar PO2 as the cause of arterial hypoxemia -A person with low PAO2 (high altitude) will have a normal A-a gradient. -But a person with V/Q mismatch will have a widened A-a gradient -A-a gradient increases with age making it an unreliable predictor of degree of pulmonary dysfunction. 3) Respiratory index: -RI = P[ A-a] O2 / PaO2 -incorporates the effect of PaCO2 by including PAO2 (it is minimal but becomes imp. In the setting of permissive hypercapnia if FiO2 is not adequate)

27. 4). Sodium: -Normal: 135 – 145 mEq/L A) Hypernatremia: -Major causes: -Impaired thirst: Coma, essential hypernatremia -Osmotic diuresis: Diabetic ketoacidosis, non ketotic hyperosmolar coma, mannitol administration -Water loss: Neurogenic & Nephrogenic D.Insipidus -Excessive sweating -Coma with hypertonic NG feeding -S/S: -Restlessness, lethargy, hyperreflexia, seizures, coma and ultimately death -chronic better tolerated than acute form -Treatment: -a: Associated with water & Na+ loss  Replace isotonic loss  replace water deficit

28. -b: Only water loss  Replace water deficit eg
-b: Only water loss  Replace water deficit eg. D5 -c: With ↑ Na+  Loop diuretic  replace water def. B) Hyponatermia: -↓ Na+: diuretics, mineralcorticoid def., osmotic diuresis (glucose, mannitol), RTA, Vomiting, diarrhoea, sweating, burns -↑ Na+: SIADH, hypothyroidism, drug induced -n Na+: CCF, nephrotic syndrome, cirrhosis -S/S: -Early  Non sp. Anorexia, nausea, weakness -Cerebral oedema  lethargy, confusion, seizures, coma and death -Treatment: -↓Na+: Isotonic saline -n or ↑Na+: Water restriction -Acute cases:Na+ def =TBW x (desired Na+ - present Na+)

29. 5) Potassium: -Normal: 3. 5 to 5
5) Potassium: -Normal: 3.5 to 5.1 mEq/L A) Hypokalemia: -↑renal loss: RTA, drugs, diuresis, renin excess -↑GI loss: Vomiting, diarrhoea -ECFICF shifts: Insulin, acute alkalosis, barium ingestion -S/S: Cardiac- abnormal ECG (T wave flattening and inversion, prominent U wave, ST depression, ↑P wave amplitude, prolongation of P-R interval), arrhythmias, labile BP -NM: weakness, tetany, ileus -Treatment: -Best: Oral KCl (60-80mEq/d) -IV KCl for pts with risk for cardiac manifestations -If Met. Alk present  KCl -If Met. Acidosis present  Pot. bicarbonate

30. B) Hyperkalemia: -Acidosis, ↑ exercise, Succinylcholine -↓renal excretion: renal failure, drugs -↑ intake of K+ salts -S/S: ->8 mEq/L  skeletal muscle weakness >7mEq/LCardiac-ECG changes (peaked T waves, widening of QRS, prolongation of PR interval, loss of P wave), Ventricular fibrillation and asystole -Treatment: Should start if > 6mEq/L -Stop offending drugs (ACE I, NSAIDS etc) - 10% Cal. Gluconate for cardiac effects -If Met. Acidosis present: IV NaHCO3- -IV infusion of glucose + insulin -Hemodialysis

31. Venous Blood Gases Analysis: -Normal SvO2= 65% -Decreased in aberrant O2 delivery or uptake -Superior to ABG analysis in diagnosis of early haem. shock as the early ↓ pH seen in mixed venous blood may not be apparent in arterial blood -In cardiac arrest ↑ PaCO2 seen earlier than ABG -Continuous SvO2 for monitoring O2 delivery

32. Thank you