blood gas analysis

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ABG analysis “Nothing in life is to be feared, it is only to be understood. Now is the time to understand more, so that we may fear less.” – Marie Curie

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Blood Gas Analysis

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Page 1: Blood Gas Analysis

ABG analysis

“Nothing in life is to be feared, it is only to be understood. Now is the time to understand more, so

that we may fear less.”– Marie Curie

Page 2: Blood Gas Analysis

ABG analysis

• Approach to blood gas analysis

• Examples

• Information overload

• Homework

Page 3: Blood Gas Analysis

ABG analysis

Page 4: Blood Gas Analysis

Stepwise approach

• Examine the pH and compare it to the normal range

• Identify the primary process that led to the change in pH

• Calculate the serum anion gap

• Identify the compensatory process (if one is present)

• Identify if any other disorders are present or there is a mixed acid-base process.

• Give a summary statement

Page 5: Blood Gas Analysis

Normal Values

Page 6: Blood Gas Analysis

Step 1:

• Examine the pH and compare it to the normal range

– pH low – acidaemia– pH high – alkalaemia

Page 7: Blood Gas Analysis

Step 2:

• Determine the primary process that led to the change in the pH:– If acidaemia

• PCO2 is high – Resp Acidosis

• HCO3 is low – Metab Acidosis

– If Alkalaemia• PCO2 is low – Resp Alkalosis

• HCO3 is high – Metab Alkalosis

Page 8: Blood Gas Analysis
Page 9: Blood Gas Analysis

Identifing Primary Disorder

• Post-op on a PCA– ABG pH 7.25, PCO2 55, PO2 60, HCO3 25

• Cough fevers and dyspnoea– ABG pH 7.55, PCO2 30, PO2 63 HCO3 22

• Type 1 DM feels unwell– ABG pH 7.25, PCO2 28, PO2 95, HCO3 15

Page 10: Blood Gas Analysis

Step 3: Calculate the serum anion gap (SAG)

(Na+ + K+) - (Cl- + HCO3-) = SAG

normal < 16

Na – Cl + HCO3 = SAG

normal < 12

• Should be done on all gases – why?• Affected by serum albumin

– Low albumin = lower upper limit of normal AG– For every 10g/L reduction in albumin – upper limit of normal AG

is reduced by 2.5

Page 11: Blood Gas Analysis

? Mixed Disorder

• 30 F altered mental status. Tachypnoeic. Found with empty aspirin beside bed.

• ABG– pH 7.56 – PCO2 22 – PO2 110– HCO3 17 – Na 137 – Cl 99

Page 12: Blood Gas Analysis

Step 4: Identify the compensatory process (if present)

– The body will attempt to bring the pH back towards the normal range

Page 13: Blood Gas Analysis

Compensation

• The body never overcompensates for the primary process.

• The pace of compensation varies depending on whether it is respiratory or metabolic compensation.

• Despite the compensatory mechanisms, the pH may not return all the way to normal

• What may appear to be a compensatory process may not actually represent true compensation

• BASE EXCESS/BASE DEFICIT

Page 14: Blood Gas Analysis

Compensatory Process

1. 40 M mountain researcher ascends to 15000 ft. After 3 weeks has an ABG

– ABG pH 7.44, PCO2 24, PO2 55, HCO3 16, AG 11

2. 65 M severe COPD workup for home O2– ABG pH 7.36, PCO2 60, PO2 60, HCO 34, AG 8

3. 40 F severe diarrhoea with multiple episodes over a 24 hour period

– ABG pH 7.37, PCO2 32, PO2 75, HCO3 18, AG 10

Page 15: Blood Gas Analysis

Step 5: Determine if a Mixed Acid-Base Disorder is Present 1. Use compensation rules to see if expected response is present

– If not then there may be an additional process

2. Calculate Delta Gap

AG – 1224 – HCO3

Delta Ratio Suggests< 0.4 Hyperchloremic normal anion gap acidosis< 1 High AG & normal AG acidosis1 to 2 Pure Anion Gap Acidosis Lactic acidosis: average value 1.6 DKA more likely to

have a ratio closer to 1 due to urine ketone loss> 2 High AG acidosis and a concurrent metabolic alkalosis or a pre-

existing compensated respiratory acidosis

Page 16: Blood Gas Analysis

Compensation RulesCompensation rules for

ExpectedPCO2

Metabolic acidosis Metabolic alkalosis

1.5 x [HCO3] + 8 (+/- 2) 0.7 x [HCO3] + 20 (+/- 5)0.9 x [HCO3] + 9 (+/- 5)

Expected

HCO3

Respiratory acidosis Respiratory alkalosis

Acute Chronic Acute Chronic

24 + pCO2 – 40 X 1

1024 + pCO2 – 40 X 4

1024 - 40- pCO2 X 2

10

24 – 40 – pCO2 X 5

10

For every 10mmHg change in pCO2 from normal (40mmHg), there is an expected change in HCO3 as follows

Acute Chronic

In Resp Acidosis, HCO3 goes up by

1 4

Resp Alkalosis, HCO3 goes down by

2 5

Page 17: Blood Gas Analysis

Other Considerations

• Osmolar gap• Osmolar Gap = Measured Osm – Calculated Osm

(Calc Osm = 2 x Na + Urea + Glucose)

• Correction for Hyperglycaemia• Corrected Na+ = Measured Na+ + Glucose – 5

3

Page 18: Blood Gas Analysis

Other Considerations

• Oxygenation– Hypoxia

• A-a Gradient

– Gas Exchange• P/F ratio

• A-a gradient

• Causes of hypoxaemia– Low inspired partial pressure

of oxygen (eg. high altitude)– Hypoventilation – Shunt – V/Q mismatch

– Diffusion limitation (rarely an

issue at sea-level)

Page 19: Blood Gas Analysis

Differential Diagnosis

• High Anion Gap Metabolic Acidosis

• Normal Anion Gap Metabolic Acidosis (non-gap acidosis)

• Metabolic Alkalosis

• Respiratory Acidosis

• Respiratory Alkalosis

Page 20: Blood Gas Analysis

Examples

1. 45 m, found drowsy, vomit on shirt. Hypotensive and tachycardic

– ABG: pH 7.22, PCO2 29, PO2 78, HCO3 11, Na 131, Cl 90

2. 60 m, recent hospitalisation for pneumonia. Presents 1 week later with severe diarrhoea, abdo pain and hypotension

– ABG: pH 7.29, PCO2 25, PO2 89, HCO3 10, Na 129, Cl 99

3. 56 F chronic renal failure presents with dyspnoea, tachypnoea. Normal lung exam and CXR

– ABG: pH 7.28, PCO2 29, PO2 85, HCO3 15, Na 131, Cl 105

Page 21: Blood Gas Analysis

High Anion Gap Metabolic Acidosis

• CAT MUDPILES– Carbon monoxide/cyanide– Alcoholic Ketoacidosis– Toluene– Methanol/Metformin – Uremia – DKA/Alcoholic KA – Paraldehyde/propylene

glycol– Isoniazid/Iron– Lactic Acidosis – Ethanol/Ethylene Glycol – Salicylates

• Pathological Processes

• Ketoacids• Ingestions• Lactate• Renal Faliure/uraemia

• KILR• KILU

Page 22: Blood Gas Analysis

Normal Anion Gap Metabolic Acidosis

• USED CARP– Ureteroenterostomy– Saline hydration– Endocrinopathies (hyperparathyroid, hyperthyroid, Addison's)– Diarrhea/ DKA/ Drugs– Carbonic anhydrase inhibitors– Ammonium chloride– Renal tubular acidosis– Parenteral nutrition/Pancreatic fistula

• Losing HCO3 (GI or Renal)• Gaining Cl-

Page 23: Blood Gas Analysis

Metabolic Alkalosis

• Losing Acid (H+)– GI or renal

• Gain HCO3

• CLEVER– Contraction– Licorice – Endo: (Conn's, Cushings,

Bartter's) – Vomiting – Excess Alkali – Refeeding Alkalosis

• Chloride responsive– Vomiting– Nasogastric suction– Diurtetics

• Chloride unresponsive– Hyperaldosteroneism– Cushings– Bartters– Excess alkali– Licorice ingestion

Page 24: Blood Gas Analysis

Respiratory Acidosis

• Acute Respiratory Acidosis – CNS Depression

(drugs/CVA) – Airway Obstruction – Pneumonia – Pulmonary Edema – Hemo/Pneumothorax – Myopathy

• Chronic Respiratory Acidosis – COPD– Restrictive lung – Any hypoventilation

state

Page 25: Blood Gas Analysis

Respiratory Alkalosis

• Hyperventilation

• CNS disease

• Hypoxia

• Anxiety

• Mech Ventilators

• Progesterone

• Salicylates/Sepsis

Page 26: Blood Gas Analysis

Approach to ABG’s

• Examine the pH and compare it to the normal range

• Identify the primary process that led to the change in pH

• Calculate the serum anion gap

• Identify the compensatory process (if one is present)

• Identify if any other disorders are present or there is a mixed acid-base process.

• Give a summary statement