Why and how to measure an ABG

Control of blood pH The normal pH range of blood is slightly alkaline (7.35 to 7.45) To function properly, the body maintains the pH of blood close to 7.4 There are three mechanisms by which the body controls the blood’s acid-base balance within this narrow range: • Intracellular and extracellular buffers • Regulation by the kidneys • Regulation by the lungs The most important pH buffer systems involve haemoglobin, carbonic acid (a weak acid formed from the dissolved CO2), and bicarbonate (its corresponding weak base) The bicarbonate buffer is effective because the concentrations of its components can be independently regulated Its key components are CO and HCO3- • The lungs regulate the partial pressure of CO in the blood (pCO2) by adjusting the rate of alveolar ventilation • The kidneys regulate the concentration of HCO 3- by adjusting the renal excretion of carbonic acid and the reabsorption of bicarbonate The Henderson-Hasselbalch equation Blood gas analysers directly measure pH and pCO2 HCO3- is calculated from the Henderson-Hasselbalch equation This equation shows that the pH is determined by the ratio of HCO3- concentration to pCO2, not by the value of either one alone The simplified version of the equation shown below expresses the relationships between the three values If you remember this version it will help you understand compensatory changes that are described later in the module Definitions Acidaemia This occurs when the blood pH is below 7.35 Alkalaemia This occurs when the blood pH is above 7.45 Acidosis • This is a process that causes acid to accumulate in the blood • It does not necessarily result in an abnormal pH • From the Henderson-Hasselbalch equation you can see that acidosis can be induced by a fall in HCO3- concentration or a rise in pCO2: • Occurring alone, it tends to cause acidaemia • Occurring at the same time as an alkalosis, the resulting blood pH may be normal, high, or low Alkalosis • This is a process that causes alkali to accumulate in the blood • It does not necessarily result in an abnormal pH • From the Henderson-Hasselbalch equation you can see that alkalosis can be induced by a rise in HCO3- concentration or a fall in pCO2: • When it occurs alone, it tends to cause alkalaemia • When it occurs at the same time as an acidosis, the resulting blood pH may be normal, high, or low Base excess The base excess is the quantity of base or acid needed to titrate one litre of blood to pH 7.4 with the pCO2 held constant at 5.3 kPa In the context of an acidosis a negative base excess indicates there is a metabolic component Why and how to measure an ABG Why measure an arterial blood gas? You should measure arterial blood gases to: • Determine acid-base balance • Determine oxygenation (arterial pO2 gives information about the efficiency of gas exchange and is more accurate than the peripheral oxygen saturation recording) • Diagnose and establish the severity of respiratory failure (pCO gives information about ventilation) • Guide therapy, for example oxygen or non-invasive ventilation in patients with chronic obstructive pulmonary disease (COPD) or therapy in patients with diabetic ketoacidosis The four primary acid-base disorders are: Respiratory acidosis Metabolic acidosis Respiratory alkalosis Metabolic alkalosis How you take an arterial blood gas? The following animation demonstrates the procedure for taking an arterial blood gas via a radial artery approach: Interpreting ABG results A stepwise approach to interpreting arterial blood gas results The following approach is a systematic way of helping you correctly interpret an arterial blood gas result (table 1) Table Five steps to interpreting arterial blood gas results Step Is there an acidaemia or an alkalaemia? Step Is the primary disturbance respiratory or metabolic? Step For a metabolic acidosis, is there a high anion gap? Step Is there compensation? If there is, is it appropriate? Step What is the alveolar-arterial gradient? Look at the arterial pO2 in the context of the inspired oxygen concentration and the arterial pCO2 First, you need to be familiar with normal values (table 2) Note that these values vary slightly from hospital to hospital, so always use your own hospital’s normal values Table 2: Normal arterial blood gas values Arterial pCO2 4.5-6.0 kPa Arterial pO2 11.0-13.0 kPa HCO3- 22.0-28.0 mmol/l Base excess -2.0 to +2.0 Anion gap 8.0-16.0 mmol/l Chloride 98.0-107.0 mmol/l Step 1: Acidaemia or alkalaemia? Look at the pH If it is: • Below 7.35, the patient is acidaemic • Above 7.45, the patient is alkalaemic If the pH is normal, look at the pCO2 and the concentration of HCO3- If either one or both are abnormal the patient may have a mixed disorder Step 2: Respiratory or metabolic? Is the primary disturbance respiratory or metabolic? Look at the pH, pCO2, and the concentration of HCO3- • • If the pH is below 7.35, an acidosis is causing acidaemia, and: o If the pCO2 is increased, there is a primary respiratory acidosis o If the concentration of HCO3- is decreased, there is a primary metabolic acidosis If the pH is above 7.45, an alkalosis is causing alkalaemia, and: o If the pCO2 is decreased, there is a primary respiratory alkalosis o If the concentration of HCO3- is increased, there is a primary metabolic alkalosis You are called to see a 60 year old woman on the orthopaedic unit who had a right hip replacement two weeks ago She has become breathless Her arterial blood gas results are as follows: • pH: 7.48 • pO2: 8.0 kPa • pCO2: 3.2 kPa • HCO3-: 25 mmol/l What is her acid-base disturbance? Step 1: There is an alkalaemia Step 2: Her pCO2 is reduced, so this is a primary respiratory alkalosis This patient has a primary respiratory alkalosis The differential diagnosis would include pulmonary embolus and hospital acquired pneumonia You see an 18 year old man in the accident and emergency department He has been vomiting for the last 24 hours and feels unwell His arterial blood gas results are as follows: What is his acid-base disturbance? • Na+: 138 mmol/l • K+: 3.0 mmol/l • Urea: 7.8 mmol/l • Creatinine: 130 àmol/l ã pH: 7.49 ã pO2: 12.7 kPa ã pCO2: 5.0 kPa • HCO3-: 31 mmol/l Step 1: There is an alkalaemia Step 2: His concentration of HCO3- is increased, so this is a primary metabolic alkalosis This patient has a primary metabolic alkalosis due to gastrointestinal loss of hydrogen ions from vomiting The hypokalaemia may also be contributing to the metabolic alkalosis Step 3: Causes of acidosis For a metabolic acidosis, is there a high anion gap? Identifying the type of acidosis will help you to narrow down the possible underlying causes What is the anion gap? In the body, the number of cations and anions are equal Blood tests measure most cations but only a few anions Therefore, adding all the measured anions and cations together leaves a gap that reflects unmeasured anions such as the plasma protein albumin Because Na+ is the primary measured cation and Cl- and HCO3- are the primary measured anions, the anion gap is calculated using the following formula: Na+ - (HCO3- +Cl-) The normal anion gap is 8-16 mmol/l Some hospital laboratories include K + when calculating the anion gap When K + is included the normal range is 12-20 mmol/l The main causes of a high anion gap acidosis (above 16 mmol/l) are given in table Table Main causes of a high anion gap acidosis (above 16 mmol/l) Increased endogenous acid production • Ketoacidosis (eg alcohol, starvation, diabetes) • Lactic acidosis o Type A: tissue oxygenation impaired  o Type B: tissue oxygenation not impaired:  Increased exogenous acids • Methanol Increased lactate from anaerobic tissue metabolism in states of hypoperfusion, eg shock Eg reduced lactate metabolism in liver failure Inability to excrete acid • Ethylene glycol (antifreeze) • Aspirin • Chronic renal failure The main causes of acidosis with a normal anion gap (8-16 mmol/l) typically associated with an increase in plasma Cl- are given in table Table Main causes of acidosis with a normal anion gap (8-16 mmol/l) Loss of bicarbonate • • • Impaired renal acid excretion Gastrointestinal tract: o Diarrhoea o Ileostomy o Pancreatic, biliary, intestinal fistula o Type (proximal) renal tubular acidosis Renal: • Carbonic anhydrase inhibitors • Type (distal) renal tubular acidosis • Type renal tubular acidosis (hypoaldosteronism) How to correct the anion gap for patients with a low albumin concentration Of the 8-16 mmol/l anion gap, 11 mmol/l is typically due to albumin A reduction in albumin concentration can therefore reduce the baseline anion gap A patient with a low albumin concentration may have a normal anion gap in the presence of a disorder that usually produces a high anion gap The anion gap is reduced by about 2.5 mmol/l for every 10 g/l fall in albumin concentration A 61 year old man with alcoholic liver disease is admitted following an upper gastrointestinal bleed His blood pressure is 90/40 mm Hg His arterial blood gas results are as follows: • Albumin: 20 g/l (n = 40 g/l) • Na+: 135 mmol/l • K+: 3.5 mmol/l • Cl-: 100 mmol/l • pH: 7.30 • pCO2: 3.3 kPa • HCO3-: 20 mmol/l • Lactate: IU/l What is the anion gap and what acid-base disturbance does he have? First calculate the anion gap: Na+ - (HCO3- + Cl-) = 135 - (100 + 20) = 15 mmol/l This is within the normal range of 8-16 mmol/l Next, correct the anion gap for the low albumin: • Anion gap = 15 mmol/l • Albumin is reduced by 20 g/l • For every 10 g/l fall in albumin, the anion gap is reduced by about 2.5 mmol/l • Therefore the anion gap has been reduced by mmol/l • When you correct it, the anion gap is 15 + = 20 mmol/l This patient therefore has a high anion gap metabolic acidosis In view of the high lactate and the hypotension this is likely to be secondary to type A lactic acidosis (see table 3) A 20 year old man feels unwell He is thirsty and drinking lots of fluids His arterial blood gas results are as follows: • Glucose: 30 mmol/l • pH: 7.32 • pO2 : 11.5 kPa • pCO2: 3.0 kPa • HCO3-:18 mmol/l • Na+: 148 mmol/l • K+: 3.5 mmol/l • Cl-: 100 mmol/l What acid-base disturbance does he have? Step 1: There is acidaemia Step 2: His concentration of HCO3- is decreased, so this is a primary metabolic acidosis Step 3: The anion gap = Na+ - (Cl- + HCO3-) 148 - 118 = 30 mmol/l This is increased This patient has a high anion gap metabolic acidosis, most likely due to diabetic ketoacidosis A 44 year old man with ulcerative colitis has had severe diarrhoea for the past two days His arterial blood gas results are as follows: • Creatinine: 200 àmol/l ã Urea: 17 mmol/l ã pH: 7.31 ã pO2 : 12.5 kPa • pCO2: 4.0 kPa • HCO3-:14 mmol/l • Na+: 135 mmol/l • K+: 3.1 mmol/l • Cl-: 113 mmol/l What acid-base disturbance does he have? Step 1: There is acidaemia Step 2: His concentration of HCO3- is decreased, so this is a primary metabolic acidosis Step 3: The anion gap = Na+ - (Cl- + HCO3-) 135 - (113 + 14) = mmol/l This is normal This patient has a normal anion gap metabolic acidosis, most likely secondary to loss of HCO3- from severe diarrhoea Step 4: Is there compensation? Compensation refers to the action taken by the body to restore the correct acid-base balance The normal compensatory measures are: • Buffers, which include haemoglobin, plasma proteins, bicarbonate, and phosphate This response occurs in minutes • Ventilatory response, which occurs in minutes to hours • Renal response, which may take up to several days Why is recognising compensation important? Recognising compensation will help you to separate primary disorders from derangements in arterial blood gases that exist only because of the primary disorder For example, a patient who hyperventilates and lowers their pCO solely as compensation for a metabolic acidosis is likely to have a partially compensated metabolic acidosis rather than a primary metabolic acidosis and primary respiratory alkalosis Although the pH can end up in the normal range (7.35-7.45) in patients with single disorders of a mild degree when fully compensated, a normal pH with an abnormal HCO3- and pCO2 should make you think of a mixed acid-base disorder You may find it difficult to decide whether an acid-base abnormality is caused by a mixed disorder or by compensation alone A useful aid is to be aware of the expected degree of compensation for the primary disorder If the change in one parameter is outside these expected changes, the disturbance is likely to be a mixed disorder (see table 5) Compensatory responses for metabolic disorders are not as predictable as those that occur for respiratory disorders Table Summary: compensatory responses Acid-base disorder Respiratory acidosis Initial chemical change pCO2 Compensatory response HCO3- Magnitude of compensation For every 1.3 kPa increase in pCO2 above 5.3 kPa in acute respiratory acidosis: • The HCO3- increases by 1.0 mmol/l What acid-base disturbance does he have? Step 1: There is acidaemia Step 2: His pCO2 and concentration of HCO3- are both raised Is this: a Chronic respiratory acidosis with appropriate metabolic compensation? b A metabolic alkalosis with respiratory compensation? c A mixed respiratory acidosis and metabolic alkalosis? Step 4: a The pCO2 is 2.6 kPa above normal Compensatory changes always occur in the same direction In a chronic respiratory acidosis, the expected compensatory change would be for the pH to decrease by 0.06 and the HCO 3- to increase by 7.0 (a pH of 7.34 and an HCO3- of 32 mmol/l) b The respiratory system rarely retains pCO2 to above 7.5 kPa Also the pH is less than 7.35 and the history is not consistent with a metabolic alkalosis as the primary disorder c The pH is acidotic and the metabolic compensation is appropriate for the change in pCO2 He has a chronic respiratory acidosis secondary to severe COPD A 20 year old man with Duchenne muscular dystrophy is admitted with a urinary tract infection He has a temperature of 39ºC He feels warm and is peripherally vasodilated with a blood pressure of 90/60 mm Hg Since being catheterised one hour ago he has passed ml urine His arterial blood gas results are as follows: • pH: 7.28 • pO2: 10.8 kPa • pCO2: 6.0 kPa • HCO3-: 18 mmol/l • Na+: 146 mmol/l • K+: 4.5 mmol/l • Cl-: 101 mmol/l What acid-base disturbance does he have? Step 1: There is acidaemia Step 2: His pCO2 is at the upper limit of normal and his concentration of HCO 3- is decreased Step 3: The anion gap is raised 146 - (101 + 18) = 27 mmol/l Step 4: For a metabolic acidosis you would expect the pCO to be reduced For a respiratory acidosis you would expect the HCO concentration to be increased He therefore has a mixed acid-base disorder He has a high anion gap metabolic acidosis, most likely from septic shock and a respiratory acidosis from Duchenne muscular dystrophy Step 5: The A-a gradient What is the alveolar-arterial gradient? The A-a gradient is the difference between the calculated alveolar pO and the measured arterial pO2 Arterial pO2 is a function of gas exchange and fractional inspired concentration of O2 in air (FiO2) The normal range therefore varies Calculating the A-a gradient allows you to determine whether a measured arterial oxygen value is normal for a patient’s: • Altitude • Inspired oxygen percentage • Rate of respiration It provides a means of assessing gas exchange at the bedside It enables you to calculate the efficiency with which oxygen goes from the alveoli into the arterial circulation The alveolar pO is always higher than the arterial pO2 In normal people the gradient is 2-4 kPa A raised gradient implies impaired gas exchange, so values greater than kPa are abnormal Deriving the A-a gradient When breathing air at sea level the partial pressure of inspired oxygen is 21 kPa This falls to 20 kPa when saturated with water vapour from the upper airways (the PiO2) In the alveolus O2 is taken up and replaced with CO2, which further reduces the alveolar pO2 to ~13-14 kPa The ratio of pCO2 produced to pO2 consumed is governed by the respiratory quotient Its value is estimated to be 0.8 Therefore, the alveolar pO is calculated by subtracting the pCO2 in the alveoli from the PiO2 The pCO2 value is slightly increased by the respiratory quotient Alveolar pO2 = inspired pO2 - alveolar pCO2 / 0.8 = inspired pO2 - alveolar pCO2 x 1.2 Because alveolar pCO2 is approximately equal to arterial pCO2, then: Alveolar pO2 = inspired pO2 - arterial pCO2 x 1.2 Because the A-a gradient is the difference between the calculated alveolar pO and the measured arterial pO2, you can calculate the gradient in kPa by subtracting the arterial pO2 from the calculated alveolar pO2: • Alveolar pO2 = PiO2 - arterial pCO2 x 1.2 • A-a gradient = alveolar pO2 - arterial pO2 • PiO2 = effective inspired pO2 A 21 year old woman who is known to have anxiety attends the accident and emergency department with shortness of breath Her chest x ray is normal Her respiratory rate is 20 breaths per minute Her arterial blood gas results on air are as follows: • pH: 7.46 • pO2 : 10.4 kPa • pCO2: 3.7 kPa • HCO3-: 25 mmol/l Is this patient having a panic attack or is there a more serious cause? Calculated alveolar pO2 = PiO2 - 1.2 x pCO2 = 20 - (1.2 x 3.7) = 20 - 4.44 = 15.56 kPa A-a gradient = 15.56 - 10.4 = 5.16 kPa (n = 2-4 kPa) This is raised This implies there is impaired gas exchange Oxygen has not diffused from the alveoli to the arterial circulation efficiently It means the measured arterial oxygen value is too low for the patient's rate of respiration A pulmonary embolism is in the differential diagnosis for this patient Common acid-base disorders Causes of the four primary acid-base disorders (click the names to expand) Respiratory acidosis Respiratory acidosis is a clinical disturbance that is due to alveolar hypoventilation (ie ventilatory failure) Failure of ventilation quickly increases the arterial pCO The main causes are given in table Table Main causes of respiratory acidosis Central depression of respiratory drive Neuromuscular disorders causing respiratory muscle weakness • Drugs, eg opioids and benzodiazepines • Central nervous system lesions • Oxygen in patients with chronic hypercapnia • Motor neurone disease • Bilateral diaphragmatic paralysis (eg following polio) Chest wall or thoracic cage abnormality Disorders affecting gas exchange • Guillain-Barré syndrome • Muscular dystrophy • Multiple sclerosis • Obesity hypoventilation syndrome • Kyphoscoliosis • Flail chest • Scleroderma • COPD • Pneumonia • Severe asthma • Acute pulmonary oedema • Obstructive sleep apnoea Airway obstruction Respiratory alkalosis Respiratory alkalosis is a clinical disturbance due to alveolar hyperventilation Respiratory alkalosis can be acute or chronic The main causes are given in Table Table Main causes of respiratory alkalosis Central nervous system stimulation • Hyperventilation (eg due to pain or anxiety) • Cerebrovascular accident • Meningitis Hypoxaemia or tissue hypoxia • Encephalitis • Tumour • Head trauma • High altitude • Severe anaemia • Ventilation/perfusion abnormality • Asthma • Pulmonary embolism • Pneumonia • Pulmonary oedema • Interstitial lung disease • Pneumothorax • Salicylates • Aminophyllines • Progesterone Pulmonary disease Drugs (respiratory stimulants) Metabolic acidosis Metabolic acidosis is a clinical disturbance characterised by a relative increase in total body acid You should consider the condition to be a sign of an underlying disease process affecting the body Identifying this underlying condition is essential for initiating appropriate therapy There are two types of metabolic acidosis: An increased anion gap A normal anion gap Metabolic alkalosis Metabolic alkalosis is a relatively common clinical problem It is characterised by high bicarbonate The main causes are given in table Table Main causes of metabolic alkalosis • Hydrogen ion loss • • Intracellular shift of hydrogen Gastrointestinal: o Vomiting o Nasogastric suction o Primary mineralocorticoid excess ( eg secondary to Conn’s or Cushing’s disease) o Loop or thiazide diuretics o Posthypercapni Renal: • Hypokalaemia • Diuretics • Body HCO3- concentration is normal • Extracellular volume contraction around a relatively constant amount of extracellular bicarbonate leads to increased plasma HCO3- Contraction alkalosis Note: Final assessment Question A 65 year old man who has a long standing kyphoscoliosis attends your clinic He reports intermittent shortness of breath on exertion His lung fields are clear His arterial blood gas results are as follows: • pH: 7.33 • pO2: 7.5 kPa • pCO2: 7.9 kPa • HCO3-: 33 mmol/l What is his acid-base disturbance? Acute respiratory acidosis Chronic respiratory acidosis Mixed acute respiratory acidosis and metabolic alkalosis Step 1: His pH is acidotic Step 2: His pCO2 is raised, so this is a respiratory acidosis Step 4: His concentration of HCO3- is raised This shows an attempt at compensation which is appropriate for a chronic respiratory acidosis rather than an acute respiratory acidosis Remember, in a chronic disorder the magnitude of compensation is greater, with subsequent better protection of the pH If it were an acute respiratory acidosis you would expect the pH to be closer to 7.26 and the concentration of HCO 3- to be 28 mmol/l Question You see a 20 year old woman with acute severe asthma in the accident and emergency department She is unable to speak in full sentences She has been given oxygen (15 l/min) via a reservoir bag mask Her arterial blood gas results are as follows: • pH: 7.47 • pO2: 11.2 kPa • pCO2: 3.7 kPa • HCO3-: 25 mmol/l What is her acid-base disturbance? Acute respiratory alkalosis Chronic respiratory alkalosis Compensated metabolic acidosis Step 1: There is an alkalosis Step 2: Her pCO2 is decreased, so this is a respiratory alkalosis Step 4: Her concentration of HCO3- is normal There is no compensation This is compatible with the acute history She has an acute respiratory alkalosis Question The same woman receives back to back nebulisers and intravenous aminophylline, but 30 minutes later she is not getting better Her repeat arterial blood gas results on the reservoir bag mask are as follows: • pH: 7.32 • pO2: 8.8 kPa • pCO2: 6.2 kPa • HCO3-: 25 mmol/l What is her acid-base disturbance now? Acute respiratory acidosis Chronic respiratory acidosis Acute metabolic acidosis Submit Step 1: There is an acidaemia Step 2: Her pCO2 is increased, so this is a respiratory acidosis Step 4: Her concentration of HCO3- is normal There is no compensation She has an acute respiratory acidosis A pO2 below kPa and a normal or rising pCO2 are blood gas markers of a life threatening asthma attack Question A 30 year old man with type diabetes has abdominal pain and vomiting His arterial blood gas results are as follows: • pH: 7.32 • pO2: 12.1 kPa • pCO2: 3.2 kPa • HCO3-: 18 mmol/l • Na+: 134 mmol/l • K+: 5.8 mmol/l • Cl-: 96 mmol/l What is his acid-base disturbance? Mixed metabolic acidosis and respiratory alkalosis Partially compensated metabolic acidosis Partially compensated respiratory alkalosis Step 1: There is acidaemia Step 2: His concentration of HCO3- is decreased, so this is a metabolic acidosis Step 3: Na+ - (HCO3- + Cl-) = 134 - 114 = 20 mmol/l There is a high anion gap Step 4: His pCO2 is decreased This is alveolar hyperventilation occurring as compensation Remember, respiratory compensation occurs in minutes to hours The pH is acidaemic This is therefore a partially compensated high anion gap metabolic acidosis Question A 30 year old man has had prolonged seizures He has been given 20 mg of intravenous diazepam and started on a phenytoin infusion Arterial blood gas results on 15 l/min oxygen via a reservoir bag mask are as follows: • pH: 7.28 • pO2: 15.0 kPa • pCO2: 8.0 kPa • HCO3-: 16 mmol/l • Na+: 140 mmol/l • K+: 4.0 mmol/l • Cl-: 98 mmol/l • Lactate: 5.0 IU/l What is his acid-base disturbance? Compensated metabolic acidosis Compensated respiratory acidosis Mixed metabolic and respiratory acidosis Step 1: There is acidaemia Step 2: His pCO2 is high, so this is a respiratory acidosis His concentration of HCO3- is low, so this is a metabolic acidosis Step 3: Anion gap = Na+ - (Cl- + HCO3-) = 140 - (98 + 16) = 26 mmol/l This is raised He has a high anion gap metabolic acidosis Step 4: Compensation for a metabolic acidosis would normally result in a low pCO Compensation for a respiratory acidosis would normally result in a high HCO 3- Remember: • Compensation always occurs in the same direction as the initial chemical change • The respiratory system rarely retains pCO2 to greater than 7.5 kPa and a value greater than this suggests a mixed disorder He has a mixed acid-base disorder He has a: • High anion gap metabolic acidosis, most likely a type A lactic acidosis from prolonged fitting Excessive muscular activity can lead to anaerobic metabolism and lactic acidosis • A respiratory acidosis, most likely from intravenous diazepam Question A 45 year old woman with previous peptic ulcer disease is admitted with persistent vomiting She looks dehydrated Her arterial blood gas results are as follows: • pH: 7.5 • pO : 14.0 kPa • pCO : 6.1 kPa • HCO : 40 mmol/l • Na : 140 mmol/l • K : 2.7 mmol/l • Urea: 8.3 mmol/l • Creatinine: 135 µmol/l 2 - + + What is her acid-base disturbance? Mixed respiratory acidosis and metabolic alkalosis Partially compensated respiratory acidosis Partially compensated metabolic alkalosis Step 1: There is an alkalosis Step 2: Her concentration of HCO3- is raised, so this is a metabolic alkalosis Step 4: Her pCO2 is slightly raised and therefore the compensation is appropriate Because there is an alkalosis she has a partially compensated metabolic alkalosis Question A 25 year old man attends the accident and emergency department because he has been breathless for five days His chest x ray shows a pneumothorax His arterial blood gas results on air are as follows: • pH: 7.43 • pO2: 10.5 kPa • pCO2: 3.8 kPa • HCO3-: 19 mmol/l What is his acid-base disturbance? Chronic respiratory alkalosis Compensated metabolic acidosis Mixed metabolic acidosis and respiratory alkalosis Step 1: The pH is normal although towards the alkalotic side Step 2: His pCO2 and concentration of HCO3- are both reduced This is either a compensated respiratory alkalosis or a compensated metabolic acidosis Step 4: Compensation is always in the same direction as the initial chemical change For every 1.3 kPa decrease in pCO2 from 5.3 kPa: • The HCO3- concentration decreases by 5.0 mmol/l in a chronic disorder and by 2.0 mmol/l in an acute disorder • The pH increases by 0.03 in a chronic disorder and by 0.08 in an acute disorder The compensatory response here is therefore appropriate for the change in pCO2 and in keeping with a chronic rather than an acute respiratory alkalosis Because the pH is on the alkalotic side and the patient has a five day history of breathlessness, he has a chronic respiratory alkalosis Remember metabolic compensation takes days Question A 44 year old man is on the high dependency unit following an ileostomy for Crohn’s disease His arterial blood gas results are as follows: • pH: 7.33 • pO2: 11.7 kPa • pCO2: 4.5 kPa • HCO3-: 18 mmol/l • Na+: 135 mmol/l • K+: 3.5 mmol/l • Cl-: 110 mmol/l • Urea: 6.8 mmol/l • Creatinine: 125 µmol/l • Albumin: 30 g/l What is his acid-base disturbance? Increased anion gap metabolic acidosis Normal anion gap metabolic acidosis Step 1: There is an acidaemia Step 2: His concentration of HCO3- is decreased, so this is a metabolic acidosis Step 3: The anion gap is Na+ - (HCO3- + Cl-) = 135 - (18 + 110) = mmol/l Correcting for albumin: • Albumin is reduced by 10 g/l • For every 10 g/l fall in albumin, the anion gap is reduced by about 2.5 mmol/l • Therefore, when you correct the anion gap for his low albumin the anion gap is + 2.5 = 9.5 mmol/l This is normal He has a normal anion gap acidosis most likely secondary to bicarbonate loss from his ileostomy Co Question The respiratory team admit a 78 year old man with severe chronic obstructive disease with congestive cardiac failure to hospital He is treated with nebulisers, steroids, and intravenous frusemide The doctors are aware from his previous notes that this man usually has a chronic respiratory acidosis After three days, his symptoms have improved The team check an arterial blood gas so that they know what his arterial blood gases are on discharge: • pH: 7.4 • pO2: 8.5 kPa • pCO2: 7.9 kPa • HCO3-: 44 mmol/l What is his acid base balance? A mixed respiratory acidosis and metabolic alkalosis A metabolic alkalosis with appropriate respiratory compensation A respiratory acidosis with appropriate metabolic compensation Step 1: His pH is normal When the pH is normal but the pCO or HCO3- concentration is abnormal then you should suspect a mixed disorder Step 2: His pCO2 is raised, so there is a respiratory acidosis His concentration of HCO3- is also raised, so there is a metabolic alkalosis Step 4: Compensation for a respiratory acidosis normally results in a high HCO 3-: The respiratory system rarely retains pCO to above 7.5 kPa as compensation for a metabolic alkalosis and a value greater than this suggests a mixed disorder So it is unlikely that this is a metabolic alkalosis with appropriate respiratory compensation The pCO is 2.6 kPa above normal This patient is known to have a chronic respiratory acidosis secondary to his severe chronic obstructive airways disease Remember that for a chronic respiratory acidosis, for every 1.3 kPa increase in pCO2 above 5.3 kPa, HCO3- increases by 3.5 mmol/l and pH decreases by 0.03 So in a chronic respiratory acidosis, the expected compensatory change would be for the pH to decrease by 0.06 and the HCO 3- to increase by mmol/l (so if this was a chronic respiratory acidosis with appropriate metabolic compensation, you would expect the pH to be 7.34 and the HCO3- 32 mmol/l) Remember that you should suspect a mixed acid-base disorder when the compensatory response occurs but the level of compensation is inadequate or too extreme In this patient, as you can see from these calculations, the compensatory response is too extreme (The HCO3- is 44 mmol/l rather than 32 mmol/l) So he has a mixed acid-base disorder He has a: Chronic respiratory acidosis secondary to severe chronic obstructive disease and A metabolic alkalosis, most likely secondary to his treatment with intravenous frusemide Question 10 A 35 year old woman is admitted following a mixed overdose of ibuprofen and paracetamol She currently appears well, sitting up in bed and conversing normally Her observations are: heart rate 79 bpm, respiratory rate 16 bpm, blood pressure 112/71 mmHg, saturations 98% on room air, and temperature 36.5oC Her arterial blood gas was performed by an emergency doctor and shows the following: • pH: 7.37 • pO2: 6.7 kPa • pCO2: 6.2 kPa • HCO3-: 28 mmol/l • Saturations 76% What does this show? A fully compensated respiratory acidosis Acute hypoxia (type respiratory failure) A venous blood gas A fully compensated metabolic alkalosis The saturations taken at the bedside not match the saturations on the blood gas (98% to 76% respectively) Although the peripheral pulse oximeter is less reliable than an arterial blood gas, it is unlikely for the pulse oximeter to over-estimate the oxygen saturations unless there is suspected carbon monoxide poisoning (which is not suggested in the history of this case) In addition, the patient is clinically well, with no evidence of respiratory distress Therefore, the sample is likely to be venous A venous sample is also likely to have a slightly raised pCO level and a low pO , as a result of cellular respiration 2 ... there is a metabolic component Why and how to measure an ABG Why measure an arterial blood gas? You should measure arterial blood gases to: • Determine acid-base balance • Determine oxygenation... respiratory acidosis, the expected compensatory change would be for the pH to decrease by 0.06 and the HCO 3- to increase by 7.0 (a pH of 7.34 and an HCO3- of 32 mmol/l) b The respiratory system... chronic disorder and by 0.08 in an acute disorder The compensatory response here is therefore appropriate for the change in pCO2 and in keeping with a chronic rather than an acute respiratory alkalosis