Slide 1 ARTERIAL BLOOD GAS INTERPRETATION David O Neill MSc BSc RN NMP FHEA Associate Lecturer (Non Medical Prescribing) Cardiff University Advanced Nurse Practitioner Respiratory Medicine Slide 2 Learning Outcomes Understand Acidbase balance physiology Understand Buffer systems in acid base balance Basic understanding of Oxygen dissociation Know normal ABG parameters To systematically analyse and interpret ABG results Review Anion gap and its use Slide 3 Acid base terminology Acids are substances which have a high concentration of Hydrogen ions [H + ] Which two bodily substances have high concentration of hydrogen ions? (i.e. very acidic) Bases (or alkalis) are substances with low concentration of hydrogen ions and high concentration of bicarbonate ions [HCO 3 ] Which bodily substance has a high concentration of bicarbonate ions (i.e. very alkaline)
Slide 4 ph of body fluids Body Fluid ph Gastric juices 1.03.0 Urine 5.06.0 Arterial blood 7.4 Venous blood 7.36 CSF 7.32 Pancreatic fluid 7.88.0 Slide 5 ph scale Hydrogen ion concentration is expressed as the ph scale (range 1 to 14) Logarithmic scale If ph changes by 1 unit (7.0 to 6.0) Hydrogen ions increase by tenfold Greater [H + ] lower ph and vice versa Slide 6 Source of acids About 100mmols/day is formed as result of end products of cellular metabolism of protein, carbohydrates and fats It must be neutralised or excreted There are three main systems involved in acid base balance what are they?
Slide 7 Acid base balance Lungs Kidneys Bones Slide 8 Acid base balance Systems interrelated Acid exists in two forms VOLATILE Eliminated as CO2 gas NON VOLATILE Are eliminated by the renal tubules and regulated by HCO 3 Lungs & Kidneys (assisted by buffers) are main regulators of acidbase balance Slide 9 Carbonic acid Carbonic acid (H 2 CO 3 ) is a weak acid (Volatile) In presence of CARBONIC ANHYDRASE (an enzyme) It easily breaks down into carbon dioxide and water
Slide 10 Respiratory equation LUNGS KIDNEYS CO 2 + H 2 0 H 2 CO 3 HCO 3 + H + This is a reversible reaction and can go both ways Slide 11 Bicarbonate in the blood Slide 12 Oxygen dissociation curve
Slide 13 Buffer systems 1 Buffers: Absorb excessive H + ions (Acids) or OH ions (Bases) Exist in ICF and ECF compartments FUNCTION AT DIFFERENT RATES Exist as buffer pairs of weak acid and conjugate base Can associate and dissociate Slide 14 Buffer systems 2 The most important PLASMA buffer systems are: CARBONIC ACIDBICARBONATE and HAEMOGLOBIN Slide 15 Buffer systems 3 The most important INTRACELLULAR buffer systems are: PHOSPHATE AND PROTEIN
Slide 16 Buffer systems Buffer pair Buffer system Reaction Rate HCO 3 Bicarbonate H + + HCO 3 = H 2O + CO 2 INSTANT /H 2CO 3 Hb /HHb Haemoglobin HHb = H + + Hb INSTANT HPO 4 2 /H 2PO 4 Pr /HPr Phosphate H 2PO 4 Plasma proteins HPO 4 = H + + INSTANT HPr = H + + Pr INSTANT Slide 17 ORGAN SYSTEMS ORGANS MECHANISM RATE Lungs Regulates retention/elimination of CO 2 and hence H 2CO 3 Minuteshours Ionic shifts Kidneys Bone Exchange intracellular potassium and sodium for hydrogen Bicarbonate reabsorption and regeneration, ammonia formation, phosphate buffering Exchange calcium, phosphate and release of carbonate 24 hours Hours to days Hours to days Slide 18 Carbonic acidbicarbonate buffering The most important buffer. Operates in lungs AND kidney Lungs get rid of CO 2 and retain H 2 O Kidneys reabsorb H 2 CO 3 and water. Both systems work well together with the lungs quickly adjusting acid concentration and kidneys reabsorb or regenerate H 2 CO 3
Slide 19 Why is this important? All systems work together to maintain a NORMAL ph (7.357.45) Outside these parameters enzyme systems start to fail Deficit in any of these can affect acid base balance Adjustment of abnormal ph is called COMPENSATION but it can leave some abnormal values Slide 20 Renal buffering 1 Distal tubules: Secrete H + into urine and reabsorbs HCO 3 Phosphate (HPO 4 2 ) and ammonia (NH 3 ) HPO 4 2 (in tubule) combines with H + to create H 2 PO 4 which is lipid insoluble and hence excreted in urine Slide 21 Renal buffering 2 H + combines with NH 3 to form ammonium ions (NH 4 + ) which are excreted in urine Buffering H + requires use of CO 2 and H 2 O to form H 2 CO 3 New H 2 CO 3 is added to plasma and H + are excreted in urine resulting in more alkaline plasma
Slide 22 Normal ABG ph 7.357.45 PaCO2 4.6 6 kpa (3545mmHg*) PaO2 10.6 14.6 kpa (80110mmHg) HCO3 2426mmols/l Base Excess 3 to + 3 *To convert kpa to mmhg multiply by 7.5 Slide 23 Base excess Derived variable Indicates acidity/alkalinity Highly NEGATIVE numbers are very ACIDIC (eg 15) Highly POSITIVE numbers are very ALKALINE (eg +15) It is calculated from how much acid or alkaline is required to return ph to normal at standard temperature and pressure It is an alternative to looking at the HCO 3 value Slide 24 ABG Interpretation Step 1. Look at the ph Is it Low (equals ACIDIC) Is it High (equals ALKALINE) Is it Normal
Slide 25 ABG Interpretation Step 2 Look at the PaCO2 Is it HIGH (equals ACIDIC) Is it LOW (equals ALKALINE) Is it NORMAL Slide 26 ABG Interpretation Step 3 Look at PaO2 Is it HIGH Is it LOW Is it NORMAL Does Oxygen have a direct impact on acid base balance? Slide 27 ABG Interpretation Step 4 Look at the HCO3 OR Base Excess Is it LOW (EQUALS ACIDIC) Is it HIGH (EQUALS ALKALINE) Is it NORMAL
Slide 28 Examples ph 7.30 ACIDIC PaCO2 7.3kPa (55mmHg) ACIDIC PaO2 12kPa (85mmHg) NORMAL HCO3 24mmols/l NORMAL Base Excess +1 NORMAL Slide 29 Interpretation Its an ACIDOSIS The system causing the acidosis is RESPIRATORY (high CO2 causes acidosis) The ph is still deranged so its ACUTE The HCO3 and BE are still NORMAL so there is NO COMPENSATION So its an ACUTE RESPIRATORY ACIDOSIS (acute type II respiratory failure) Slide 30 Example 2 ph 7.37 PaCO2 7.3kPa (55mmHg) PaO2 8.0kPa (60mmHg) HCO3 30mmols/l Base Excess +7
Slide 31 Interpretation ph is NORMAL PaCO2 is HIGH (ACID) PaO2 is LOW (no effect on ph at this level) HCO3 is HIGH (ALKALINE) Base excess is HIGH (ALKALINE) Original disturbance was respiratory COMPENSATION has occurred returning ph to normal range Chronic Type II respiratory failure Slide 32 Example 3 ph 7.25 PaCO2 10kPa (75mmHg) PaO2 7kPa (52.5mmHg) HCO3 30mmols/l Base Excess +6 Slide 33 Interpretation ph is deranged (Acidotic) Therefore ACUTE PaCO2 is HIGH therefore ACID PaO2 is LOW (no effect) HCO3 and Base Excess are HIGH and therefore ALKALINE AND CHRONIC ACUTE ON CHRONIC TYPE II RESPIRATORY FAILURE
Slide 34 Example 4 ph 7.10 PaCO2 3kPa (22.5mmHg) PaO2 HCO3 20kPa (150mmHg) 14mmols/l Base Excess 12 Blood Glucose 30mmols/l Urine Ketones +++ Glucose +++ Slide 35 Interpretation ph is low therefore ACIDIC It is still deranged, therefore ACUTE PaCO2 is LOW (ALKALINE) PaO2 is high (probably too much O2) HCO3 is LOW therefore ACIDIC Base Excess is LOW therefore ACIDIC So its ACUTE METABOLIC ACIDOSIS with respiratory alkalosis (compensation) Given blood glucose and ketones in urine Diabetic Ketoacidosis Slide 36 Example 5 ph 7.50 PaCO2 6.6 kpa (50mmHg) PaO2 10kPa (75mmHg) HCO3 35mmols/l Base Excess +10
Slide 37 Interpretation ph is HIGH therefore ALKALINE It is still deranged therefore ACUTE PaCO2 is slightly High (ACIDOTIC) BUT it WON T get any higher, WHY? HCO3 is HIGH (ALKALINE) as is the Base Excess (ALKALINE) Therefore its an ACUTE METABOLIC ALKALOSIS with respiratory acidosis as compensation Slide 38 Example 6 ph 7.10 PaCO2 8kPa (60mmHg) PaO2 10kPa (75mmHg) HCO3 15mmols/l Base Excess 10 Slide 39 Interpretation 1 ph is LOW therefore ACID ph is still deranged, therefore ACUTE PaCO2 is HIGH therefore ACID PaO2 is? Normal HCO3 is LOW therefore ACID Base Excess is LOW, therefore ACID So what s going on?
Slide 40 Interpretation 2 It s a MIXED ACIDOSIS, Predominantly METABOLIC IN ORIGIN Action would be to CORRECT THE UNDERLYING METABOLIC COMPONENT (DKA, renal Failure, Cardiac failure leading to lactic acidosis) Then review the Pa CO2 which will probably then have little effect on the ph Slide 41 Anion gap Is an estimate of unmeasured Anions It is the difference between: Cations (Na and K) and Anions (Cl and HCO 3 ) NORMAL RANGE 1018mols/l Eg Na + K Cl + HCO 3 (135 + 4.0) (100 + 24) = 139 124 = 15 Slide 42 Metabolic Acidosis with increased anion gap Increased production of fixed or organic acids causes: HCO 3 to fall Unmeasured anions associated with the acids accumulate Caused by Increased Lactic acid (shock infection, hypoxia) Urea (renal failure) Ketones (diabetes, alcohol Drugs/toxins (salicylates, biguanides, ethylene glycol, methanol)
Slide 43 Metabolic Acidosis with normal anion gap Due to loss of bicarbonate or ingestion of hydrogen ions (Cl ) retained Caused by renal tubular acidosis Profuse diarrhoea Drugs (acetazolamide) Addisons disease Pancreatic fistula Ammonium chloride ingestion Slide 44 Questions Slide 45 References Longmore, M, Wilkinson, I, Torok, E (2001) Oxford Hnadbook of Clinical Medicine Oxford Oxford University Press. McCance KL, Heuther, SE. (2006). PathophysiologyThe biologic basis for disease in adults and children. St Louis. ElsevierMosby Parson PE Heffner JE. (2002) Pulmonary/Respiratory Therapy Secrets (2 nd Ed.) Philadelphia. Hanley & Belfus
Slide 46 Example 1 ph 7.494 PaCO2 (kpa) 3.2 (24mmHg) PaO2 (kpa) 21.6 (162.5) HCO3 (mmols/l) 21 BE 3.2 ALKALOSIS RESPIRATORY CAUSE ACUTE (ph still deranged) Minimal compensation hyperventilation, anxiety Slide 47 Example 2 ph 7.28 PaCO 2 10.6 (79.8) PaO2 6.9 (51.8) HCO 3 32 BE 7 ACIDOSIS RESPIRATORY CAUSE ACUTE COMPENSATION Acute respiratory acidosis with partial compensation Acute on chronic Type II respiratory failure Slide 48 Examples ph PaCO2 kpa 7.494 3.2 (24mmHg) 7.28 10.6 79.8 7.274 11.1 (83.3) 7.17 3.9 (29.5) PaO2 kpa 21.6 (162.5) 6.9 51.8 6.48 (48.6) 53 (400.5) HCO3 (mmols/l) BE 21 3.2 32 7 35 10.4 8 16.6
Slide 49 Examples ph PaCO2 kpa 7.278 5.2 (39.2) PaO2 kpa 8.1 (61.2) HCO3 (mmols/l) BE 16 7.9 6.867 105.1 60.3 8 16.6 7.335 12.2 (91.8) 7.365 10.1 (76.9) 10.5 (78.8) 14.6 (110) 16.7 9 40 15.4