Interpreting an arterial blood gas report

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Arterial blood gas analysis can be performed quickly and gives useful information about A (oxygenation), B (ventilation) and C (perfusion) - which is why it is one of the first tests (with bedside glucose measurement) performed in critical illness. However, many clinicians fail to carry out a full analysis and benefit from information that could influence therapy.

The box below describes the 6 steps in arterial blood gas analysis:

1. Is the data consistent?

2. What is the primary acid-base abnormality? An abnormal pH always indicates the primary acid-base disturbance - the body never overcompensates

3. Check the appropriateness of compensation - there may be more than one acid-base disturbance

4. Measure the anion gap in any metabolic acidosis

5. Look at PaO2 - the A-a gradient may reveal disorders of oxygenation (see chapter 4)

6. Finally, consider the clinical situation - does the analysis fit with the clinical picture?

For example, in the following arterial blood gas: pH 725, PaCO2 4 5 kPa (35 mmHg) bicarbonate 14 8 mmol/l, PaO2 8 0 kPa (61 mmHg), there is a metabolic acidosis. pH 725 = [H+] 55 nmol/l. From the law of mass action we can see that the data is consistent - that is, there is no lab error.

Metabolic acidosis is the primary diagnosis. But although the PaCO2 is "normal" in this example, it is possible to estimate what the PaCO2 should be from compensatory responses empirically derived from human studies (see Table 3.4).

In this example there should be a 015 kPa (12 mmHg) fall in PaCO2 for every 1 mmol/l fall in HCO3. Assuming the lower limit of normal for HCO3 is 22 mmol/l, there has been a 7 mmol/l fall in HCO3 which should cause a 11 kPa (84 mmHg) fall in PaCO2. The PaCO2 in this example should be 3 4 kPa. It is "normal" because there is also a respiratory acidosis. This alerts you to the fact that the patient may be sicker than at first thought. Mixed acid-base disorders are common in clinical practice.

Normal arterial blood values are: pH 7-35-7-45, PaCO2 45-60 (35-46 mmHg), PaO2 11-145 kPa (83-108 mmHg), BE -2 to +2, bicarbonate 22-28 mmol/l. Useful information on acid-base balance can easily be gained from venous blood; oxygenation, however, cannot be interpreted.

Table 3.4 Compensatory responses

Disorder

Primary change

Compensatory response

Metabolic

Reduction in

0-15 kPa (1-2 mmHg)

acidosis

HCO3

fall in PaCO2 for

every 1 mmol/l fall

in HCO3

Metabolic

Increase in

0-01 kPa (0-7 mmHg)

alkalosis

HCO3

increase in PaCO2

for every 1 mmol/l

rise in HCO3

Acute respiratory

Increase in

1 mmol/l increase in

acidosis

PaCO2

HCO3 for every 1-3

kPa (10 mmHg)

rise in PaCO2

Chronic respiratory

Increase in

3-5 mmol/l increase

acidosis

PaCO2

in HCO3 for every

1-3 kPa (10 mmHg)

rise in PaCO2

Acute respiratory

Reduction in

2-0 mmol/l reduction

alkalosis

PaCO2

in HCO3 for every

1-3 kPa (10 mmHg)

fall in PaCO2

Chronic respiratory

Reduction in

5-0 mmol/l reduction

alkalosis

PaCO2

in HCO3 for every

1-3 kPa (10 mmHg)

fall in PaCO2

Self-assessment -

case histories

1. A 65-year-old man with COPD comes to the Emergency Department with shortness of breath. His arterial blood gases on air show: pH 7-29, PaCO2 8-5 (65-3 mmHg), standard bicarbonate 30-5 mmol/l, BE +4, PaO2 8-0 kPa (62 mmHg). What is the acid-base disturbance and what is your management?

2. A 60-year-old ex-miner with COPD is admitted with shortness of breath. His arterial blood gases on air show: pH 7-36, PaCO2 9-0 (65-3 mmHg), standard bicarbonate 35 mmol/l, BE +6, PaO2 6-0 (46-1 mmHg). What is the acid-base disturbance and what is your management?

3. A 24-year-old man with epilepsy comes to hospital in status epilepticus. He is given intravenous diazepam. Arterial blood gases on 10 l/min oxygen via reservoir bag mask show: pH 7-05, PaCO2 8-0 (61-5 mmHg), standard bicarbonate 16 mmol/l,

BE -8, PaO2 15 kPa (115 mmHg). His other results are sodium 140 mmol/l, potassium 4-0 mmol/l and chloride 98 mmol/l. What is his acid-base status and why?

4. A patient is admitted in a coma from a drug overdose and responds only to painful stimuli. Arterial blood gases on air show: pH 7-24, PaCO2 8-32 (64 mmHg), standard bicarbonate 29 mmol/l, BE +2, PaO2 7-8 kPa (60 mmHg). The Emergency Department doctor diagnoses drug intoxication with aspiration pneumonia because of the hypoxaemia. What is your assessment?

5. Twenty-four hours later you are asked to assess the same patient for discharge. She has woken up and the arterial blood gases have improved: pH 7-60, PaCO2 3-1 (24 mmHg), standard bicarbonate 22 mmol/l, BE -2, PaO2 9-1 kPa (70 mmHg). The hospital is in need of beds. Should you discharge this patient?

6. An 80-year-old lady is admitted with abdominal pain. Her vital signs are normal, apart from cold peripheries and a tachycardia. Her arterial blood gases on air show: pH 7-1, PaCO2 3-5 (30 mmHg), PaO2 9-5 kPa (73 mmHg), standard bicarbonate 8 mmol/l, BE -15. You review the clinical situation again - she has generalised tenderness in the abdomen but it is soft. Her blood glucose is 6-0 mmol/l (100 mg/dl), sodium 140 mmol/l, potassium 3-7 mmol/l, chloride 89 mmol/l, urea 6-5 mmol/l (BUN 18 mg/dl). There are reduced bowel sounds. The chest x ray is normal. The ECG shows atrial fibrillation. What is the reason for the acid-base disturbance?

7. A 44-year-old man comes to the Emergency Department with pleuritic chest pain and shortness of breath which he has had for five days. A moderately sized pneumothorax is seen on the chest x ray. His arterial blood gases on 10 l/min oxygen via simple face mask show: pH 7-44, PaCO2 3-0 (23 mmHg), standard bicarbonate 16-0 mmol/l, BE -4, PaO2 30-5 (234-6 mmHg). Is there a problem with acid-base balance?

8. A patient is admitted to hospital with breathlessness and arterial blood gases on air show: pH 7-2, PaCO2 4-1 (31-5 mmHg), standard bicarbonate 36 mmol/l, BE +10, PaO2 7-8 (60 mmHg). Can you explain this?

9. A 45-year-old woman with a history of peptic ulcer disease reports six days of persistent vomiting. On examination she has a blood pressure of 100/60 mmHg and looks dehydrated. Her blood results are as follows: sodium 140 mmol/l, potassium 2.2 mmol/l, chloride 86 mmol/l, bicarbonate 40 mmol/l, urea

29 mmol/l (BUN 80 mg/dl), pH 7-5, PaCO2 6-2 kPa (53 mmHg), PaO2 14 (107 mmHg), urine pH 5-0, urine sodium 2 mmol/l, urine potassium 21 mmol/l and urine chloride 3 mmol/l. What is the acid-base disturbance? How would you treat this patient? Twenty-four hours after appropriate therapy the HCO3 level is

30 mmol/l. The following urine values are obtained: pH 7-8, sodium 100 mmol/l, potassium 20 mmol/l and chloride

3 mmol/l. How do you account for the high urine sodium but low chloride concentration?

10. A 50-year-old alcoholic is brought in to the Emergency Department unconscious. He had appeared drunk beforehand with ataxia and slurred speech and has slowly lapsed into a coma. On examination he is unresponsive and has nystagmus. His vital signs are: respiratory rate 30/min, blood pressure 190/100 mmHg, pulse 110/min, temperature 360C. His bedside glucose measurement is 5 mmol/l (83 mg/dl). His arterial blood gases on 10 litres oxygen via reservoir bag mask show: pH 7-15, PaCO2 3-0 (23 mmHg), standard bicarbonate 7-6 mmol/l, BE -20, PaO2 40 (308 mmHg). His full blood count, liver enzymes and clotting are normal. Other results are: sodium 145 mmol/l, potassium 5 mmol/l, urea 3 mmol/l, creatinine 100 |imol/l, chloride 80 mmol/l. What do these arterial blood gases show? What is the cause of his unconsciousness?

11. Match the clinical history with the appropriate arterial blood gas values:

pH

paco2

HCO3 (mmol/l)

a

7-39

8-45 kPa (65 mmHg)

37

b

7-27

7-8 kPa (60 mmHg)

26

c

7-35

7-8 kPa (60 mmHg)

32

• A severely obese 24-year-old man

• A 56-year-old woman with COPD who is started on diuretic therapy for peripheral oedema resulting in 3 kg weight loss

• A 14-year-old girl with a severe asthma attack

12. A 50-year-old man is recovering on the surgical ward ten days after a total colectomy for bowel obstruction. He has type 1 diabetes and is on an intravenous insulin sliding scale and his ileostomy is working normally. His vital signs are: BP 150/70, respiratory rate 16/min, SaO2 98% on air, urine output 1500 ml/day, temperature normal and he is alert. Abdominal examination is normal and he is well perfused. The surgical team are concerned about his persistently high potassium level (which was noted before surgery) and metabolic acidosis. His blood results are: sodium 130 mmol/l, potassium 6-5 mmol/l, urea 14 mmol/l (BUN 39 mg/dl), creatinine 180 ^mol/l (2-16 mg/dl), chloride 109 mmol/l, 8am cortisol 500 nmol/l (18 ^g/dl). He is known to have diabetic nephropathy and is on Ramipril. His arterial blood gases on air show: pH 7-29, PaCO2 3-5 kPa (27 mmHg), PaO2 14 kPa (108 mmHg), bicarbonate 12 mmol/l. What is his acid-base disturbance and why? Should the surgeons request a CT scan of the abdomen to look for a cause for his acidosis?

Self-assessment - discussion

1. Is the data consistent? Yes - [H+] = 181 x 8-5/30-5 = 50 nmol/l which is pH 7-3. There is an acidaemia (low pH) with a high PaCO2 - a primary respiratory acidosis. The fact that the pH is abnormal indicates an acute change (or "decompensation"). There should be a 1 mmol/l increase in HCO3 for every 1-3 kPa (10 mmHg) rise in PaCO2 in an acute respiratory acidosis. The PaCO2 has risen by 2-5 kPa above the upper limit of normal so HCO3 should rise by around 2 mmol/l - as in this case. Management starts with assessment/treatment of the airway, breathing and circulation, followed by a quick assessment of disability (neurology), bedside glucose measurement, arterial blood gases, further information gathering and definitive treatment. Non-invasive ventilation is appropriate in this case if simple measures fail to improve the respiratory acidosis quickly.

2. Is the data consistent? Yes - [H+] = 181 x 9-0/35 = 46-5 nmol/l which is pH 7-36. There is a normal pH (euphaemia) despite a high PaCO2 (respiratory acidosis). This is due to compensation. There should be a 3-5 mmol/l increase in HCO3 for every 1-3 kPa (10 mmHg) rise in PaCO2. The PaCO2 has risen by 3-0 kPa above the upper limit of normal, so HCO3 should rise by around 8 mmol/l. The measured HCO3 is consistent at 35 mmol/l. Management includes assessment/treatment of airway, breathing, circulation and disability (neurology). A 28% Venturi mask is appropriate oxygen therapy, titrated to arterial PaO2 and PaCO2 plus treatment for his exacerbation of COPD.

3. Is the data consistent? Yes - [H+] = 181 x 8-0/16 = 90-5 nmol/l which is pH 7-05. There is both a raised PaCO2 and a reduced HCO3 suggesting mixed respiratory and metabolic acidosis. The anion gap is 26 mmol/l which is raised. The change in anion gap is 10 (upper limit of normal is 16) versus a change in HCO3 of 6 (lower limit of normal is 22). This ratio is raised and is suggestive of lactic acidosis. This interpretation is consistent with the clinical scenario - the patient has a lactic acidosis from fitting and a respiratory acidosis due to intravenous diazepam. This acid-base disturbance should spontaneously return to normal with supportive measures.

4. Is the data consistent? Yes - [H+] = 181 x 8-32/27 = 56 nmol/l which is pH 7-24. There is an acidaemia with a raised PaCO2 -the primary disturbance is a respiratory acidosis. In acute respiratory acidosis there should be a 1 mmol/l increase in HCO3 for every 1-3 kPa (10 mmHg) rise in PaCO2. The PaCO2 has risen by 2-3 kPa above the upper limit of normal so HCO3 should be around 29 mmol/l, which it is. The anion gap cannot be measured in this case without further information. The A-a gradient (see chapter 4) is normal in this case - suggesting that the hypoxaemia is due to alveolar hypoventilation rather than pneumonia.

5. Is the data consistent? Yes - [H+] = 181 x 3-1/22 = 26 nmol/l which is pH 7-6. There is alkalaemia with a low PaCO2 - a primary respiratory alkalosis. The fall in PaCO2 from 4-5 kPa (lower limit of normal) to 3-1 kPa should result in a reduction in HCO3 by nearly 4 mmol/l. The measured bicarbonate of 22 mmol/l is consistent. The A-a gradient (see chapter 4) is now raised which indicates that the respiratory alkalosis is due to intrinsic lung disease, for example, aspiration pneumonia. This analysis fits with the clinical picture. The patient should not be discharged.

6. Is the data consistent? Yes - [H+] = 181 x 3-5/8 = 80 nmol/l which is pH 7-1. There is acidaemia with a low HCO3 and low PaCO2 - a primary metabolic acidosis. There should be a 0-15 kPa (1-2 mmHg) fall in PaCO2 for every 1 mmol/l fall in HCO3. HCO3 has fallen from 22 (the lower limit of normal) to 8 mmol/l so PaCO2 should fall by 14 x 0-15 which is 2-1 kPa. The PaCO2 should be 2-4 kPa. The measured PaCO2 of 3-5 kPa indicates an accompanying respiratory acidosis. The anion gap is (140 + 3-7) -(89 + 8) = 46-7 mmol/l which is high. The change in anion gap versus the change in bicarbonate is 30-7/14 and this suggests lactic acidosis. The A-a gradient is slightly elevated which could indicate developing SIRS (see chapter 7). Is this analysis in keeping with the clinical picture? Yes - the combination of abdominal pain and a lactic acidosis should alert you to the possibility of intra-abdominal ischaemia. The elderly show few signs of an inflammatory response because of their less active immune system. The presence of atrial fibrillation is a clue to this diagnosis. Priorities in the management of this case are: assessment and treatment of the airway, breathing, circulation and disability followed by analgesia, further information gathering and definitive treatment.

7. Is the data consistent? Yes - [H+] = 181 x 3-0/15-1 = 36 nmol/l which is pH 7-44. Although the pH is normal, acid-base status is not. How can we tell which acid-base disturbance occurred first -the low PaCO2 or the low bicarbonate? By considering the clinical picture. Given the history of breathlessness for a few days, we can say the low PaCO2 due to hyperventilation occurred first. This is a compensated respiratory alkalosis. In a chronic respiratory alkalosis, there should be a 5-0 mmol/l reduction in HCO3 for every 1-3 kPa (10 mmHg) fall in PaCO2. The PaCO2 has fallen by 1-5 kPa below the lower limit of normal so the HCO3 should have fallen by just over 5-0 mmol/l - which it has in this case. Increased minute ventilation in normal pregnancy also causes a compensated respiratory alkalosis. This can cause confusion if the patient is being investigated for possible pulmonary embolism. The A-a gradient is not affected.

8. Is the data consistent? No - [H+] = 181 x 4-1/36 = 20 nmol/l which is pH 7-7. As you may have guessed, this is an impossible blood gas - the answer is lab error!

9. Is the data consistent? Yes - [H+] = 181 x 6-9/40 = 31 nmol/l which is pH 7-5. The results show an alkalaemia with a raised HCO3 and PaCO2 is a primary metabolic alkalosis. There should be a 0-01 kPa (0-7 mmHg) increase in PaCO2 for every 1 mmol/l rise in HCO3. The HCO3 has risen by 12 mmol/l above the upper limit of normal so PaCO2 should rise by 12 x 0-01 = 0-12 kPa. The expected PaCO2 is 6-12 kPa which is roughly the measured level. The physical findings and low urinary sodium levels point to volume depletion. The patient should be treated with both intravenous sodium chloride and potassium chloride. During therapy, volume expansion reduces sodium reabsorption in order to correct the metabolic alkalosis by excreting excess HCO3. The discrepancy between urinary sodium and chloride is primarily due to urinary HCO3 excretion. Urinary PaCO2 is similar to renal venous PaCO2 so from the law of mass action: Urinary [H+] 16 nmol/l = 181 x 6-2/urinary bicarbonate Urinary bicarbonate may be calculated as 70 mmol/l Further chloride replacement is necessary for as long as chloride depletion exists. Low urinary chloride may be seen as a marker of continuing volume depletion.

10. Is the data consistent? Yes - [H+] = 181 x 3-0/7-6 = 72 nmol/l which is pH 7-15. These results show a primary metabolic acidosis. There should be a 0-15 kPa (1-2 mmHg) fall in PaCO2 for every 1 mmol/l fall in HCO3. The HCO3 has fallen by 14-4 so PaCO2 should fall by 14-4 x 0-15 or 2-16 kPa. The expected PaCO2 level is 2-3 kPa. There is an accompanying respiratory acidosis, probably due to fatigue. The anion gap is (145 + 5) -(80 + 5) = 65 mmol/l which is very large. Poisoning, lactic/keto acidosis or renal failure are candidates. In this case poisoning is the most likely cause, given the normal liver tests, glucose and creatinine levels. Certain poisons characteristically cause a huge anion gap and are more commonly ingested by alcoholics - ethylene glycol (antifreeze) and methanol. These can be measured in the serum to confirm the diagnosis. Alternatively, the osmolal gap can be calculated. This is the difference between the calculated and actual osmolality of the serum. The calculated osmolality is as follows:

1-86 x sodium + urea + glucose 093

In normal individuals the osmolal gap is less than 10 mosmol/kg H20. In ethylene glycol poisoning it is raised, reflecting the unmeasured presence of ethylene glycol in the serum. Specific treatment consists of alcohol dehydrogenase inhibitors - either alcohol or 4-methylpyrazole (4-MP). Intravenous ethanol (alcohol) therapy requires frequent monitoring of blood alcohol levels, aiming for 100-150 mg/dl.

4-MP is more expensive but easier to administer, does not cause central nervous system depression and has more predictable pharmacokinetics. Management in this case is to secure the airway and give oxygen, assist ventilation and assess/treat circulatory abnormalities before moving on to a full examination, information gathering and definitive treatment.

11. From the history:

• Severe obesity suggests chronic hypercapnia (c)

• COPD and diuretic therapy suggests chronic hypercapnia with superimposed metabolic alkalosis (a)

• A severe asthma attack suggests acute respiratory acidosis (b)

12. Is the data consistent? Yes - [H+] = 181 x 3-5/14 = 53 nmol/l which is pH 7-29. The results show a primary metabolic acidosis. The expected PaCO2 is 3-1 kPa. The anion gap is (130 + 6-5) - (14 + 109) = 13-5 mmol/l which is normal. The PaO2 is normal on air. In a normal anion gap metabolic acidosis, bicarbonate is lost via the gastrointestinal tract (diarrhoea, fistula or uterosigmoidostomy) or the kidneys (tubular damage or acetazolamide therapy). Sometimes there is reduced renal H+ excretion. In this case there are no excess gastrointestinal losses, leaving the possibility of a renal problem, which fits with the clinical setting of diabetic nephropathy. Renal tubular acidosis is a collection of disorders where the kidneys either cannot excrete H+ or generate HCO3-. Serum potassium can help differentiate the types (see Table 3.5).

Table 3.5 Renal tubular acidosis

Problem

GFR

Serum potassium

Type 1

Distal H+

Normal

Low

(distal)

secretion

Type 2

Proximal H+

Normal

Low

(proximal)

secretion

Type 3

NH3 production

Reduced

Normal

(glomerular

(hence HCO3

insufficiency)

generation)

Type 4

Distal sodium

Reduced

High

(hyporeninaemic

reabsorption,

hypoaldosteronism

potassium secretion and H+ secretion

GFR = glomerular filtration rate

GFR = glomerular filtration rate

Hyporeninaemic hypoaldosteronism is commonly found in diabetic nephropathy and hypertensive renal disease. ACE inhibitors, spironolactone and NSAIDs (which further reduce aldosterone levels) worsen the hyperkalemia. Treatment consists of restricting dietary potassium and using fludrocortisone or bicarbonate supplements. Based on these findings and the clinical examination the surgeons do not need to request a CT scan of the abdomen.

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    How to interprete normal arterial blood gases report?
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