Richard Stretton Respiratory Registrar Arterial Blood Gases Richard Stretton Respiratory Registrar

Arterial Blood Gases Seen as complicated Misunderstood Important An easy way and a hard way

Objectives Develop an organised system for looking at blood gases Be able to comment on the arterial pO2 in relation to the FiO2 Interpret acid base disturbance and it’s significance in the acutely unwell

What Are We Measuring? pH pO2 pCO2 HCO3 Base Excess

Acid Base Balance BICARBONATE pH is carefully controlled Enzymatic Function relies on pH control Buffers Haemoglobin BICARBONATE Ammonium Phosphate

Striking the Balance H+ + HCO3-  H2CO3  CO2 + H2O When you’ve got too much H+, lungs blow off CO2 When you can’t blow off CO2, kidneys try to get rid of H+

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

5-step approach pO2 = 10 -13 kPa on air Assess Oxygenation Is the patient hypoxic? Is there a significant A-a Gradient? A-a Gradient is the difference in concentration of oxygen between the Alveolus (A) and the artery (a) Normal <3 A-a Gradient = PAO2 – (PaO2 + PaCO2/0.8)

I shouldn’t say this but… v.v.v.v. rough guide Inspired O2 - (pO2 + pCO2) Add together pO2 and pCO2 from your blood gas Take this away from the concentration of Oxygen the patient is breathing With an upper limit of normal of about 5

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

5-step approach Determine Acid-Base Deficit pH>7.45 alkalaemia pH<7.35 acidaemia Acidosis - a process causing excess acid to be present in the blood. Acidosis does not necessarily produce acidaemia Alkalosis - a process causing excess base to be present in the blood. Alkalosis does not necessarily produce alkalaemia.

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

5-step approach Determine the respiratory component Does this explain the acid-base deficit? PaCO2: >6.0 kPa - respiratory acidosis <4.7kPa - respiratory alkalosis

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

5-step approach Determine the metabolic component. Does this explain the acid-base deficit? HCO3 <22 mmols/l - metabolic acidosis >26 mmols/l - metabolic alkalosis

Remember…… H+ + HCO3-  H2CO3  CO2 + H2O When you’ve got too much H+, lungs blow off CO2 When you can’t blow off CO2, kidneys try to get rid of H+

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

5-step approach Which is primary and which is secondary? Remember Compensation doesn’t always completely restore pH to the normal range A mixed picture may be present

5-step approach Assess Oxygenation Determine Acid-Base Deficit Determine the respiratory component Determine the metabolic component Which is primary and which is secondary

Assumptions CO2 changes are related to respiratory changes HCO3 changes relate to metabolic changes Overcompensation does not occur Respiratory compensation is rapid Metabolic compensation is slow

Respiratory Acidosis Any cause of hypoventilation CNS depression Neuromuscular disease Acute or chronic lung disease Cardiac arrest Ventilator malfunction

Respiratory Alkalosis Any cause of hyperventilation Hypoxia Acute lung conditions Anxiety Fever Pregnancy Hepatic failure Some central CNS lesions

Metabolic Acidosis Added Acid Loss of Bicarbonate Renal failure Ketoacidosis Lactic acidosis Salicylate/Tricyclic overdose Renal tubular acidosis Diarrhoea Carbonic anhydrase inhibitors Ureteral diversion Chloride administration

Metabolic Alkalosis Loss of acid or gaining alkali Vomiting Diarrhoea Diuretics (and hypokalaemia generally) Ingestion of alkali

Reminder of normal values pH 7.35 – 7.45 (H+ = 35 -45) pO2 10 - 13 kPa on air pCO2 4.6 - 6.0 kPa HCO3 25 - 35 mmols/l Base excess ± 2.0

Lets get going…….. Working out acidosis/alkalosis and compensation is usually the bit people struggle with So…..

Outcome codes Outcome Code pH High Alkali Low Acid pCO2 HCO3

Translate Uncompensated Metabolic Acidosis Value Code Translate Opinion pH 7.1 Low Acid Acidaemia pCO2 5.3 Normal HCO3 16 Primary Uncompensated Metabolic Acidosis

Translate Uncompensated Respiratory Acidosis Value Code Translate Opinion pH 7.1 Low Acid Acidaemia pCO2 8.3 High Primary HCO3 26 Normal Uncompensated Respiratory Acidosis

Translate Uncompensated Respiratory Alkalosis Value Code Translate Opinion pH 7.56 High Alkali Alkalaemia pCO2 2.3 Low Primary HCO3 25 Normal Uncompensated Respiratory Alkalosis

Translate Compensated Metabolic Acidosis or Value Code Translate Opinion pH 7.37 Normal pCO2 2.1 Low Alkali ???? HCO3 14 Acid Compensated Metabolic Acidosis or Compensated Respiratory Alkalosis

Translate Compensated Respiratory Acidosis or Value Code Translate Opinion pH 7.40 Normal pCO2 8 High Acid ???? HCO3 35 HIgh Alkali Compensated Respiratory Acidosis or Compensated Metabolic Alkalosis

Translate Decompensated Respiratory Acidosis Value Code Translate Opinion pH 7.21 Low Acid Acidaemia pCO2 12 High Primary HCO3 32 Alkali Secondary Decompensated Respiratory Acidosis

What Now? Now you can determine any acid base pattern Convert the numbers into high/low/normal Convert that into acid/alkali What is primary, what is compensation? Distinguish between uncompensated, compensated, and decompensated

Nomenclature Uncompensated Respiratory Acidosis Acute Type 2 Respiratory Failure Compensated Respiratory Acidosis Chronic Type 2 Respiratory Failure Decompensated Respiratory Acidosis Acute on Chronic Type 2 Respiratory Failure

Case 1 Young female admitted with overdose of unknown tablets and smelling of alcohol pO2 12 kPa on air pH 7.24 PaCO2 2.5 HCO3 8 Metabolic Acidosis with respiratory compensation Metabolic Acidosis with respiratory compensation and increased anion gap e.g. TCA overdose A-a gradient 1.8

Case 2 Elderly male admitted from nursing home with one week history of fever and vomiting pO2 12 kPa on 4l by mask pH 7.49 PaCO2 6.3 HCO3 35 Metabolic alkalosis with respiratory compensation Metabolic alkalosis with respiratory compensation A-a gradient 18 assuming FiO2 is 0.4 Possibilities include vomiting alone or atypical pneumonia with vomiting to account for increased A-a gradient and metabolic derangement

Case 3a Middle aged man admitted with cough sputum and haemoptysis. Life-long smoker pO2 4 on air pH 7.19 PaCO2 9.7 HCO3 28 Acute respiratory acidosis with no time for metabolic compensation Acute respiratory acidosis with no time for metabolic compensation A-a gradient 6.7 Candidates should say that the patient should receive a higher FiO2 and consider NIV.

Case 3b Middle aged man admitted with cough sputum and haemoptysis. Life-long smoker pO2 6 on air SpO2 92% pH 7.32 PaCO2 10.0 HCO3 39 Acute respiratory acidosis with no time for metabolic compensation Practically fully compensated respiratory acidosis with hypoxia, but A-a gradient only 1.5 Increased FiO2 may not be necessary in this patient, AFTER the ABGs are known as this may be normal for them The two cases can be used to highlight the difference between acute life-threatening hypoxia with hypoventilation and chronic type II respiratory failure

Case 4 Middle aged man post cardiac arrest. Breathing spontaneously on endotracheal tube pO2 35 on 15l via reservoir mask pH 6.9 PaCO2 8.9 HCO3 13 Mixed metabolic and respiratory acidosis Mixed metabolic and respiratory acidosis probably lactic, following cardiac arrest A-a gradient 39.4 Candidate should recognise that gas exchange is not perfect despite that fact that the PaO2 is high Patient needs to remain ventilated despite the good PaO2, to optimise Acid-base balance before extubation

Case 5 Elderly lady with congestive cardiac failure pO2 9 on 40% oxygen pH 7.64 PaCO2 3.5 HCO3 29 Respiratory alkalosis secondary to pulmonary oedema. Acute as no metabolic compensation Respiratory alkalosis secondary to pulmonary oedema. Acute as no metabolic compensation A-a gradient 24.6

Case 6 Young diabetic male admitted with chest infection, vomiting and drowsiness pO2 12 on air pH 7.31 PaCO2 1.6 HCO3 6.0 Acute metabolic acidosis with respiratory compensation Acute metabolic acidosis with respiratory compensation, presumable DKA, although lactic acidosis secondary to sepsis might be an alternative thought, or TCA overdose with the drowsiness A-a gradient 3

Case 7 54 yr-old lady post MI. Acutely unwell, cold, clammy, hypotensive and oliguric pO2 10 on 60% oxygen pH 6.99 PaCO2 7.8 HCO3 14 Mixed pattern of respiratory and metabolic acidosis Mixed pattern of respiratory and metabolic acidosis due to cardiogenic shock A-a gradient 37.3

Case 8 50 yr-old man admitted with exacerbation of long-standing bronchial asthma. Respiratory rate of 18 pO2 5.1 on 60% oxygen pH 7.39 PaCO2 5.8 HCO3 26 Severe type I respiratory failure Could be venous sample! Severe type I respiratory failure. A-a gradient 44.7 Presence of normal CO2 potentially very worrying if this all due to asthma. Is there something else contributing to this degree of hypoxia at the same time? PE for example Candidates should be aware that a normal blood gas in acute severe asthma is either reassuring if the other features suggest that the asthma is not life-threatening. In the presence of other life-threatening features, this is a worrying blood gas

Questions ?

The 6th step… If an acidosis is present work out the anion gap to help determine cause. Anion Gap is the difference between the measured positive and negatively charged ions. It gives an estimate of the unmeasured ions in the serum Unmeasured – proteins, sulphates

Anion Gap Anion Gap = [Na+K] –[CL+HCO3] Normal anion gap 10-18

Metabolic Acidosis Increased anion gap (added acid) Renal failure Ketoacidosis Lactic acidosis Salicylate/Tricyclic overdose

Metabolic Acidosis Decreased anion gap (loss of bicarbonate) Renal tubular acidosis Diarrhoea Carbonic anhydrase inhibitors Ureteral diversion Chloride administration

High Anion Gap A M U D P I L E S

High Anion Gap Alcohol (Alcohol dissociates to become a week acid) M U

High Anion Gap Alcohol (Alcohol dissociates to become a week acid) Methanol (See alcohol. Causes blindness) U D P I L E S

High Anion Gap Alcohol (Alcohol dissociates to become a week acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) D P I L E S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) P I L E S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) Paraquat (Very nasty poison, universally lethal) I L E S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) Paraquat (Very nasty poison, universally lethal) Infection (Commonest cause. Localised tissue hypoxia leads to...) L E S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) Paraquat (Very nasty poison, universally lethal) Infection (Commonest cause. Localised tissue hypoxia leads to...) Lactic Acid (Product of anaerobic respiration, and tissue necrosis) E S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) Paraquat (Very nasty poison, universally lethal) Infection (Commonest cause. Localised tissue hypoxia leads to...) Lactic Acid (Product of anaerobic respiration, and tissue necrosis) Ethylene Gylcol (Antifreeze. Quite a potent acid, no longer sold in UK) S

High Anion Gap Alcohol (Alcohol dissociates to become a weak acid) Methanol (See alcohol. Causes blindness) Uraemia (Failure to reabsorb HCO3- and excrete H+) DKA (Ketones are dehydrogenated alcohols, and dissociate to acid) Paraquat (Very nasty poison, universally lethal) Infection (Commonest cause. Localised tissue hypoxia leads to...) Lactic Acid (Product of anaerobic respiration, and tissue necrosis) Ethylene Gylcol (Antifreeze. Quite a potent acid, no longer sold in UK) Salicylates (Aspirin causes resp alkalosis, then metabolic acidosis)

Normal Anion Gap Addison’s Disease High Output Fistulas RTA I, II, IV Acetazolamide Therapy Diarrhoea

Any more Questions?