Transcript Surviving Sepsis

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Unexpected deterioration of sick patient
Hypoxaemia on sats monitoring
Reduced conscious level
Exacerbation of COPD
Monitoring of ventilated patient
Sepsis
Metabolic or electrolyte problem e.g. DKA
Drug Overdose
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Normal PaO2 11.5-13.5 kPa ON AIR
› Correct hypoxaemia immediately (target SpO2)
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Respiratory failure defined as PaO2 <8kPa (SpO2 <93%)
› Type I – normal PaCO2
› Type 2 – elevated PaCO2 (ventilatory failure)
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Significant respiratory failure may be present despite
‘normal’ or high PaO2
› Predicted PaO2 normally ~10kPa below FiO2
› e.g. 40% venturi, PaO2 should be ~30kPa
› Document oxygen use on ABG result!
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Look at the pH (normal range 7.35-7.45)
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pH <7.35 = acidaemia/acidosis
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pH >7.45 = alkaemia/alkalosis
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Acidosis or alkalosis may still be present with a ‘normal’ pH if
the body has already buffered = compensation
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CO2 is acidic and HCO3- is alkaline
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Normal compensation for acidosis is to decrease CO2 (rapid)
and increase HCO3- (takes longer)
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Normal compensation for alkalosis is to decrease HCO3- (and
increase CO2)
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Normal range for PaCO2 is 4.5-6.0kPa
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Acidosis (pH <7.35)
› PaCO2 >6.0kPa = respiratory acidosis
› PaCO2 <6.0kPa = metabolic acidosis
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Alkalosis (pH >7.45)
› PaCO2 >4.5kPa = metabolic alkalosis
› PaCO2 <4.5kPa = respiratory alkalosis
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Normal range for HCO3- is 22-26mmol/L
› Normal range for base excess (BE) is -2 to +2
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Acidosis (pH <7.35)
› HCO3- <22mmol/L (BE < -2) = metabolic acidosis
› HCO3- >22mmol/L (BE > -2) = respiratory acidosis
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Alkalosis (pH >7.45)
› HCO3- >26mmol/L (BE > +2) = metabolic alkalosis
› HCO3- <26mmol/L (BE < +2) = respiratory alkalosis
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What is the primary disturbance?
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Is there any compensation?
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Is there a mixed picture?
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e.g. in acidosis (pH <7.35)
› PaCO2 >6.0kPa with HCO3- >26mmol/L =
› Respiratory acidosis with partial metabolic compensation
› PaCO2 >6.0kPa with HCO3- <22mmol/L =
› Mixed respiratory and metabolic acidosis
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Lactate (normal range 0-2mmol/L)
› Elevated levels often associated with acidosis
› tissue hypoperfusion/anaerobic metabolism, liver/renal
failure or drugs (e.g. metformin)
› Degree of elevation correlates directly with mortality in sepsis
› Response to fluids also important
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Haemoglobin (Hb)
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Potassium (K+) and Sodium (Na+)
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Glucose (not on AMU analyzer)
78-year-old male admitted with IECOPD
becomes more drowsy and confused
whilst on AMU. Oxygen is being delivered
via a non-rebreathe bag and mask.
FiO2
pH
PaO2
PaCO2
HCO3BE
Lactate
0.4 (40%)
7.21
15.7kPa
8.9kPa
31mmol/L
+8
1.8mmol/L
0.21 (air)
7.35-7.45
11.5-13.5kPa
4.5-6.0kPa
22-26mmol/L
-2 to +2
<2.0mmol/L
Relative hypoxaemia (PaO2 should be ~30kPa)
 Respiratory failure = type 2 (elevated PaCO2)
 Acidosis (pH <7.35)
 High PaCO2 = respiratory acidosis
 High HCO3- = partial metabolic compensation
(likely chronic)
 Acute-on-chronic type 2 respiratory failure with
respiratory acidosis and partial metabolic
compensation
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29-year-old female with type 1 diabetes.
Admitted with 48h history of diarrhoea and
vomiting. Rapid respiratory rate. CBG
27mmol/L and blood ketones 4.9mmol/L.
FiO2
pH
PaO2
PaCO2
HCO3BE
Lactate
0.21 (21%)
7.36
13.7kPa
3.2kPa
14mmol/L
-12
2.8mmol/L
0.21 (air)
7.35-7.45
11.5-13.5kPa
4.5-6.0kPa
22-26mmol/L
-2 to +2
<2.0mmol/L
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Normal PaO2 on air i.e. no respiratory failure
Normal pH however;
Low HCO3- and BE with high lactate and ketones =
metabolic acidosis
Low PaCO2 = respiratory compensation (Kussmaul
respiration)
Fully compensated metabolic acidosis due to DKA
36-year-old male with alcohol
dependence and ALD. Admitted to AMU
following a staggered co-codamol
overdose. GCS 8/15 with small pupils and
respiratory rate of 10/min.
FiO2
pH
PaO2
PaCO2
HCO3BE
Lactate
0.35 (35%)
7.19
11.7kPa
7.5kPa
17mmol/L
-8
4.2mmol/L
0.21 (air)
7.35-7.45
11.5-13.5kPa
4.5-6.0kPa
22-26mmol/L
-2 to +2
<2.0mmol/L
Relative hypoxaemia (PaO2 should be ~25kPa)
 Respiratory failure = type 2 (elevated PaCO2)
 Acidosis (pH <7.35)
 High PaCO2 = respiratory acidosis
 Low HCO3- and BE = metabolic acidosis
 Mixed respiratory and metabolic (lactic) acidosis
 Hypoventilation due to reduced GCS (hepatic
encephalopathy) and opiate overdose
 Lactic acidosis due to liver failure/drug overdose
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56-year-old female admitted with acute
breathlessness. Recent marital stress. Heart
rate 120/min, respiratory rate 28/min, SpO2
96% on air. Chest clear. Looks anxious ++
FiO2
pH
PaO2
PaCO2
HCO3BE
Lactate
0.21 (40%)
7.49
10.1kPa
3.8kPa
25mmol/L
+2
0.7mmol/L
0.21 (air)
7.35-7.45
11.5-13.5kPa
4.5-6.0kPa
22-26mmol/L
-2 to +2
<2.0mmol/L
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Hyperventilation with respiratory alkalosis
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No metabolic compensation
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May be due to anxiety/panic attack but relative
hypoxaemia in this case suggests alternative cause
e.g. PE, pneumonia, acute asthma
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Cannot be used to assess pO2 or pCO2
› Normal pCO2 on VBG excludes hypercapnia
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Good correlation with ABG for other parameters
› pH, lactate, BE, HCO3-, electrolytes, Hb
› except if patient shocked/peri-arrest
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VBG usually adequate in all other situations
› Obtain VBG in all acutely unwell patients
› Especially sepsis, DKA, UGIB, AKI, overdose
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Sample must not be shaken and should be analysed
immediately (<10min) to prevent haemolysis
› lowers pH and increases K+
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K+ up to 0.5mmol lower than lab value
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Na+ up to 6mmol lower than lab value
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Hb 5g/L higher than lab value on average
Acid Base Disorder
pH
pCO2
HCO3-
Examples
Metabolic Acidosis
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Sepsis, shock,
AKI, drugs,
DKA
Metabolic Acidosis with
Respiratory Compensation
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DKA with
Kussmaul’s
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COPD, LVF,
reduced GCS
Respiratory Acidosis with
Metabolic Compensation
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COPD with
chronic T2RF
Metabolic Alkalosis
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Prolonged
vomiting
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Anxiety, PE,
pneumonia,
asthma
Respiratory Acidosis
Respiratory Alkalosis
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