ABG interpretation.

1. Arterial Blood Gases & Interpretation Dr. Malak Amid General Practitioner at Abu setta Hospital

2. Contents Overview. Indications of ABG. Contraindication. Parameters and reference ranges. Other useful information from arterial blood gases. Factors influencing blood gas results. Primary acid-base disturbances. Mixed acid–base disorders Interpretation of ABG.

3. Overview An arterial blood gas (ABG) test measures the acidity (pH) and the levels of oxygen and carbon dioxide in the blood from an artery. Blood may be collected from one of the following arteries: •Radial artery in the wrist •Femoral artery in the groin •Brachial artery in the arm

4. Overview ABGs provide the following information: •Oxygenation •Adequacy of ventilation •Acid-base levels

5. Indications Respiratory failure - in acute and chronic states. Any severe illness which may lead to a metabolic acidosis - for example: Cardiac failure. Liver failure. Renal failure. Hyperglycaemic states associated with diabetes mellitus. Multiorgan failure.

6. Indications Sepsis. Burns. Poisons/toxins. Ventilated patients. Sleep studies

7. Contraindication An abnormal modified Allen test ( Assessment of collateral circulation ). Local infection or distorted anatomy at the potential puncture site ( eg , from previous surgical interventions, congenital or acquired malformations, or burns ). The presence of arteriovenous fistulas or vascular grafts. Known or suspected severe peripheral vascular disease of the limb involved.

8. Contraindication s evere coagulopathy. Anticoagulation therapy with warfarin, heparin and derivatives, aspirin is not a contraindication for arterial vascular sampling in most cases. Use of thrombolytic agents, such as streptokinase or tissue plasminogen activator .

9. Modified Allen Test digital occlusion of radial and ulnar artery

10. Modified Allen Test clenching of hand About 30 sec

11. Modified Allen Test ulnar artery occlusion released.

12. Modified Allen Test The test is then repeated, but this time the radial artery is released while the ulnar artery remains compressed .

13. Modified Allen Test Positive Modified Allen Test (Normal) : if the hands flushing within 5-15 sec it indicate that the ulnar artery has good blood flow. Negative Modified Allen Test (Abnormal) : if the hands does not flushing within 5-15 sec it indicate that the ulnar circulation is inadequate , in this situation the radial artery supplying arterial blood to that hand should not be punctured.

14. Parameters and reference ranges Analyte arterial blood gases venous blood gases pH 7.35 - 7.45 7.32 – 7.43 PaCO2 35-45 mmHg 4.7- 6.0 kPa 41 – 50 mmHg PaO2 75-100 mmHg 11-13 kPa 25 – 40 mmHg Base excess (BE) −2 to +2 mmol /L total CO2 (tCO2 ) 23-30 mmol /L 100-132 mg/Dl HCO3 22–26 mEq /L 23 – 27 mmol /L

15. How to differentiate between arterial and venous blood The venous oxygen is lower than the arterial oxygen. The PCO2 will be higher in venous than arterial blood. Arterial blood is bright red colour, but venous blood is dark maroon in colour. Arterial blood gases more painful and have more complication.

16. Notes : age and altitude dependent Kilopascals: to convert pressures to kPa , divide mmHg by 7.5 mmHg change in PaCO2 above or below 40 mmHg results in 0.008 unit change in pH in the opposite direction change in [HCO3-] of 10 mEq /L will result in a change in pH of approximately 0.15 pH units in the same direction

17. The Base E xcess The metabolic component of the acid–base balance is reflected in the base excess. This is a calculated value derived from blood pH and PaCO2. It is defined as the amount of acid required to restore a litre of blood to its normal pH at a PaCO2 of 40 mmHg . The base excess increases in metabolic alkalosis and decreases (or becomes more negative) in metabolic acidosis. While the base excess may give some idea of the metabolic nature of a disorder,

18. Interpreting acidemia on an ABG

19. Interpreting alkalaemia on an ABG

20. Other useful information from arterial blood gases Alveolar-arterial oxygen gradient : is a measure of the difference between the alveolar concentration of oxygen (A) and the arterial concentration of oxygen(a) . It is used in diagnosing the source of hypoxemia

21. Other useful information from arterial blood gases The alveolar–arterial oxygen gradient : P(A–a)O2 = PAO2 – PaO2 PaO2 = arterial oxygen tension PAO2 = alveolar oxygen tension PAO2 = FiO2(PB – PH2O) – (PaCO2 / 0.8)

22. Other useful information from arterial blood gases FiO2 = fraction of inspired oxygen PB = barometric pressure (760 mmHg at sea level) PH2O = water vapour pressure (47 mmHg at 37° C) *R = Respiratory quotient = 0.8 (usual) Normal value <15 mmHg

23. Other useful information from arterial blood gases Estimating A-a gradient: Normal A-a gradient = (Age+10) / 4 A-a increases 5 to 7 mmHg for every 10% increase in FiO2

24. Hypoxia (PaO2)< 95 mm Hg A-a gradient A-a gradient > 15 mmHg < 15 mmHg (Lung disease ) (Normal lungs) *( V/Q) imbalance High PaCO2 Low PaCO2 * Shunting * Hypoventilation * Low FiO2 Give 100% O2 PaO2 does not improve * Shunt   PaO2 increases   : * V/Q imbalance  

25. Other useful information from arterial blood gases Anion gap : The anion gap is the difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum. Its used to identify the cause of metabolic acidosis

26. Other useful information from arterial blood gases Calculation: With potassium : = ([Na+] + [K+]) − ([Cl−] + [HCO3−]) Without potassium (daily practice ): = Na+ − (Cl- + HCO3−) The reference range of the anion gap is 3-11 mEq /L

27. Factors influencing blood gas results Delayed processing of the sample may yield a falsely low PaO2, as the delay allows leucocytes to consume oxygen. This can be avoided by prompt transport of the sample on ice . Air bubbles introduced when performing the arterial puncture can also cause a falsely high PaO2 and a falsely low PaCO2 . This can be avoided by gently removing air bubbles within the specimen immediately after collection without agitating the sample.

28. Factors influencing blood gas results Body temperature can also affect arterial blood gas tensions. This is relevant in febrile or hypothermic patients, so body temperature should be recorded at the time of collection.

29. Primary Acid-Base D isturbances

30. Primary Acid-Base Disturbances Metabolic : change in HCO3 and pH in the same direction . Respiratory : change in HCO3 and pH in the opposie direction . . One Way To Remember This Relationship Is To Use The Acronym ROME : R espiratory O pposite M etabolic E qual

31. Respiratory Acidosis Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) causes increased blood carbon dioxide concentration and decreased pH. Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) causes increased blood carbon dioxide concentration and decreased pH.

32. Types of Respiratory A cidosis : acute respiratory acidosis : the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36 ). chronic respiratory acidosis : the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg).

33. Causes of Respiratory Acidosis : Respiratory centre depression (↓RR ). drugs (anaesthesia, sedative, narcotics ) Trauma Increasing ICP Stroke Encephalitis Central apnea Supplemental O2 in chronic Co2 retention ( i.e COPD)

34. Causes of Respiratory Acidosis : Neuromascular disorders (↓TV ): Myasthenia gravis Gullain-Barre syndrome Poliomyelitis Muscular dystrophies Myopathies Chest wall disease (obesity, kyphoscoliosis )

35. Causes of Respiratory Acidosis : Airway obstruction (↓FEV ). Mechanical hypoventilation (inadequate mechanical ventilation ).

36. Symptoms of Respiratory acidosis Symptoms of Respiratory Acidosis

37. Treatment of Respiratory Acidosis Treatment is aimed at the underlying disease, and may include : Bronchodilator drugs to reverse some types of airway obstruction Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP ) or a breathing machine, if needed Oxygen if the blood oxygen level is low Treatment to stop smoking

38. Respiratory Alkalosis Respiratory alkalosis is a condition marked by low levels of carbon dioxide in the blood due to breathing excessively

39. Types of respiratory alkalosis Acute respiratory alkalosis : occurs rapidly. For every 10 mmHg drop in PCO2 in arterial blood, there is a corresponding 2 mEq /L drop in bicarbonate ion due to acute compensation. During acute respiratory alkalosis, the person may lose consciousness where the rate of ventilation will resume to normal . Chronic respiratory alkalosis : is a more long-standing condition. For every 10 mmHg drop in PCO2 in arterial blood, there is a corresponding 5 mEq /L drop in bicarbonate ion. The drop of 5 mEq /L of bicarbonate ion is a compensation effect which reduces the alkalosis effect of the drop in PCO2 in blood. This is termed metabolic compensation.

40. Causes of Respiratory Alkalosis : Respiratory centre stimulation : CNS disorders Hepatic failure Gram negative sepsis Drugs (theophylline, catecholamine, psychotropic ) Pregnancy Anxiety Pain Mechanical hyperventilation (excessive mechanical ventilation)

41. Causes of Respiratory Alkalosis : Hypoxemia : Pulmonary disease (pneumonia, oedema, PE, ILD) Sever anaemia Heart failure High altitude

42. Symptoms of Respiratory Alkalosis

43. Treatment of Respiratory A lkalosis : Treatment is aimed at the condition that causes respiratory alkalosis . Breathing into a paper bag -- or using a mask that causes you to re-breathe carbon dioxide -- sometimes helps reduce symptoms .

44. Metabolic Acidosis metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney

45. Causes of Metabolic Acidosis Raised anion gap Normal anion gap ( hyperchloraemia ) Accumulation of acids : • Ketoacids in diabetic ketoacidosis (DKA). •Lactic acid, eg shock, infection. •Drugs/toxins, eg salicylates, ethylene glycol, methanol, paracetamol chronic renal failure (accumulation of sulfates , phosphates, urea Loss of bicarbonate or ingestion of acid : •Gastrointestinal tract (GIT) causes, eg longstanding diarrhoea, pancreatic fistula. •Renal tubular acidosis. •Addison's disease. •Drugs, eg carbonic anhydrase inhibitors.

46. Symptoms of Metabolic Acidosis

47. Management of Metabolic A cidosis General measures: Put the patient in the resuscitation area, or transfer to a high-dependency area as soon as feasible . Put the patient on an ECG monitor, SaO2 monitor and BP/HR monitor . In patients who are clinically unwell and have deteriorating SaO2 levels or conscious levels, consider intubation and assisted ventilation, after taking senior A&E/medical/anaesthetic advice . Get large-bore IV access (a central venous line may be needed) and rehydrate aggressively. Use colloids if necessary.

48. Management of Metabolic A cidosis Consider catheterisation to monitor urine output and obtain urine for analysis . If there is any possibility of drug or toxin ingestion, give initial therapies such as activated charcoal/chelating agents/emetics, dependent on the specific compound ingested and latest local guidelines for poisoning . Liaise with local or national toxicology/poisoning services if there has been ingestion of a potentially dangerous substance . Obtain specialist input (usually the on-call general medical team initially) as soon as possible .

49. Management of Metabolic A cidosis Correction of acidosis Treatment of the underlying cause is the aim. Use of bicarbonate infusions is not recommended, as it can lead to a fatal outcome. It should be used only where advised in cases of poisoning. Specific therapy for the underlying cause This is the most important and efficient way to correct the acidosis and improve the patient's outlook. Toxicological/general medicine/renal medicine expertise should be engaged to offer specific therapy for the identified underlying problem.

50. Complications of Metabolic A cidosis The major problem is suppression of myocardial contractility and unresponsiveness to catecholamines caused by the acidaemic state. This may lead to a vicious cycle of hypoperfusion , worsening lactic acidosis and further cardiac suppression, causing multi-organ failure. If pH is <7.1-7.2 then cardiac arrhythmias are likely .

51. Metabolic alkalosis Metabolic alkalosis is primary increase in HCO3− with or without compensatory increase in Pco2; pH may be high or nearly normal is a relatively frequent clinical problem that is most commonly due to the loss of hydrogen ions from the gastrointestinal tract or in the urine

52. Causes of Metabolic alkalosis most common causes: * Vomiting. * diuretics . * mineralocorticoid excess. To differentiate between these conditions, it is usually helpful to measure the urinary chloride concentration

53. Causes of Metabolic alkalosis In causes of metabolic alkalosis associated with a reduction in the ECV, there will be a stimulus for avid Na and Cl reabsorption to replenish extracellular volume. In these setting urinary Cl should be expected to be very low, < 25 meq /L.

54. Causes of Metabolic alkalosis If the urinary Cl is low, indicating a hypovolemic state, then administration of NaCl and water to replenish the extracellular volume should stop the stimulus for aldosterone production and in turn should lead to appropriate excretion of excess HCO3- and improvement of hypokalemia . Thus, leading to correction of the metabolic alkalosis. Such causes of metabolic alkalosis are said to be saline responsive

55. Causes of Metabolic alkalosis In contrast, states of mineralocorticoid excess are associated with an expanded volume and sometimes hypertension. The urinary Cl will be high (> 40 meq /L). In these patients, administration of saline would further expand the extracellular volume and worsen hypertension. It would not correct the alkalosis which is primarily due to hypokalemia . Such causes of metabolic alkalosis are said to be saline resistant.

56. Causes of Metabolic alkalosis Urine Cl < 25 meq /L Saline Responsive Urine Cl > 40 meq /L Saline Unresponsive Vomiting or nasogastric suction Diuretics Posthypercapnia Cystic Fibrosis Low chloride intake Primary mineralocorticoid excess Exogenous Alkali load Barrter's or Gitelman's syndrome Severe Hypokalemia (K< 2.0)

57. Causes of Metabolic alkalosis Causes of saline resistant metabolic alkalosis can further be distinguished based on whether or not the patient is hypertensive. Mineralocorticoid excess states tend to be associated with hypertension while exogenous alkali load, Barrters and Gitelman's syndrome are associated with normal blood pressure.

58. Symptoms of Metabolic A lkalosis

59. Treatment of Respiratory Alkalosis Saline - Responsive metabolic alkalosis: Re-expand volume with Normal Saline ( Primary Therapy). Supplement with Potassium to treat hypokalemia (alkalosis associated with severe hypokalemia will be resistant to volume resuscitation until K is repleted ) . H+ blockers or PPIs if vomiting/NG suction to prevent further losses in H+ ions. Discontinue diuretics.

60. Treatment of Respiratory Alkalosis Acetazolamide if NS contraindicated due to CHF. (Monitor for hypokalemia ). HCl or NH4Cl in emergency. ( HCl can cause hemolysis , NH4Cl should not be used in liver disease) Hemodialysis in patients with marked renal failure

61. Treatment of Respiratory Alkalosis Saline – Unresponsive metabolic alkalosis ( Mineraldocorticoid excess ). Surgical removal of mineralocorticoid producing tumor . Aldosterone inhibitor. ACE inhibitor. Discontinue steroids. Potassium repletion (only intervention needed to treat the alkalosis ).

62. Compensation When a patient develops an acid-base imbalance, the body attempts to compensate. the lungs and the kidneys are the primary buffer response systems in the body . The body tries to overcome either a respiratory or metabolic dysfunction in an attempt to return the pH into the normal range.

63. Compensation Metabolic compensation occurs over 2-3 days reflecting altered renal HCO3 production l secretion . Respiratory compensation through ventilation control of PaCo2 occurs immediately

64. Compensation A patient can be uncompensated, partially compensated, or fully compensated If the pH is between 7.35-7.45, the condition is fully compensated . If the pH is outside the range of 7.35-7.45, the condition is only partially compensated

65. Correlating arterial blood gas results with clinical features Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis pH ↓ ↑ ↓ ↑ PaCO2 N (uncompensated) ↓ (compensated) N (uncompensated) ↑ (compensated) ↑ ↓ HCO3ˉ ↓ ↑ N (uncompensated) ↑ (compensated) N (uncompensated) ↓ (compensated) BE ↓ ↑ N/↑ N/↓ Clinical features Kussmaul -type breathing shock, coma Paraesthesia, tetany, weakness Acute: air hunger, disorientation Chronic: hypoventilation, hypoxia, cyanosis Acute: hyperventilation, paraesthesia, light-headedness Chronic: hyperventilation, latent tetany

66. Mixed acid–base disorders It is possible to have a mixed respiratory and metabolic disorder that makes interpretation of an arterial blood gas result difficult . As a general rule, when a normal pH is accompanied by an abnormal PaCO2 or HCO3ˉ then a mixed metabolic-respiratory disorder exists .

67. Clinical examples of mixed respiratory and metabolic disturbances Respiratory acidosis and metabolic acidosis : A patient with acute pulmonary oedema after an acute myocardial infarct Respiratory alkalosis and metabolic alkalosis: A patient with hepatic cirrhosis who is given diuretics .

68. Clinical examples of mixed respiratory and metabolic disturbances Respiratory acidosis and metabolic alkalosis : A patient with long-standing chronic obstructive pulmonary disease who is given diuretics for concomitant heart failure. Respiratory alkalosis and metabolic acidosis . A patient with chronic renal failure who begins to hyperventilate secondary to anxiety

69. Interpretation of ABG Step 1 : Is The p H normal? pH Alkalemia > 7.45

70. Interpretation of ABG Step 2 : Is the disturbance respiratory or metabolic ? Match The CO2 Or The HCO3 With The pH ROME : R espiratory O pposite M etabolic E qual

71. Interpretation of ABG Step 3 : Is there appropriate compensation for the primary disturbance ? pH is between 7.35-7.45 fully compensated pH is outside 7.35-7.45 partially compensated .

72. Interpretation of ABG Step 4 : Are The pO2 And The O2 Saturation normal ? pO2 (<80 mmHg) Hypoxia SO2 (<95 %)

73. Interpretation of ABG Hypoxaemic respiratory failure (type I respiratory failure): PaO2 is less than 60 mm Hg (8 kPa ) with a normal or low PaCO2 Hypercapnic respiratory failure (type II respiratory failure): PaCO2 is more than 50 mm Hg (6.5 kPa ) and indicates inadequate alveolar ventilation.

74. Interpretation of ABG Respiratory failure may be acute or chronic : Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually therefore less than 7.3 . Chronic respiratory failure develops over several days or longer. There is sufficient time for renal compensation and an increase in bicarbonate so the pH is usually only slightly decreased. Clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale .

75. Question If the pH 7.30 , the PaCo2 is 50 , and the HCO3 is 24 , what is likely diagnosis ?

76. Question If the pH 7.30 , the PaCo2 is 50 , and the HCO3 is 24 , what is likely diagnosis ? Uncompensated Respiratory Acidosis

77. Question If the pH 7.49 , the PaCo2 is 25 , and the HCO3 is 22 , what is likely diagnosis ?

78. Question If the pH 7.49 , the PaCo2 is 25 , and the HCO3 is 22 , what is likely diagnosis ? Acute Respiratory Alkalosis

79. Question If the pH 7.35 , the PaCo2 is 25 , and the HCO3 is 9 , what is likely diagnosis ?

80. Question If the pH 7.35 , the PaCo2 is 25 , and the HCO3 is 9 , what is likely diagnosis ? Compensated Metabolic Acidosis

81. Question If the pH 7.29 , the PaCo2 is 30 , and the HCO3 is 18 , what is likely diagnosis ?

82. Question If the pH 7.29 , the PaCo2 is 30 , and the HCO3 is 18 , what is likely diagnosis ? Partially Compensated Metabolic Acidosis.

83. Question If the pH 7.45 , the PaCo2 is 48 , and the HCO3 is 28 , what is likely diagnosis ?

84. Question If the pH 7.45 , the PaCo2 is 48 , and the HCO3 is 28 , what is likely diagnosis ? Compensated Metabolic Alkalosis

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