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Richard Stretton Respiratory Registrar. Arterial Blood Gases. 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 pO 2 in relation to the FiO 2
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Richard Stretton Respiratory Registrar Arterial Blood Gases
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 • 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 • Assess Oxygenation pO2 = 10 -13 kPa on air • 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 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…..
Translate Uncompensated Metabolic Acidosis
Translate Uncompensated Respiratory Acidosis
Translate Uncompensated Respiratory Alkalosis
Translate Compensated Metabolic Acidosis or Compensated Respiratory Alkalosis
Translate Compensated Respiratory Acidosis or Compensated Metabolic Alkalosis
Translate 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
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
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
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
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
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
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
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
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
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