Acid Base Calculations Quiz Rohit SOI
Acid Base CalculationsQuiz
Rohit SOI
Why do we do blood gasPoint of care test [ part of primary survey with Circulation Resuscitation].Instant information about
ph Paco2 Pao2 lactate Hb CoHb Na/ K/ Hco3 Glucose i Ca.
CORRELATION BETWEEN VBG AND ABG pH - Good Correlation
pooled mean difference: +0.035 pH units
pCO2 -Good Correlation in normocapnia non-correlative in severe shoc 100% sensitive in detecting arterial hypercarbia in COPD exac using cutoff of PaCO245 mmHg Mean difference pCO2 +5.7 mmHg (wide range in 95%CIs +/-20 mmHg in different studies)
HCO3 -Good Correlation
Mean difference −1.41 mmol/L (−5.8 to +5.3 mmol/L 95%CI)
CORRELATION BETWEEN VBG AND ABG (ctd)
Lactate- Dissociation above 2 mmol/L Mean difference 0.08 (-0.27 – 0.42 95%CI)
Base excess – Good Correlation Mean difference 0.089 mmol/L (–0.974 to +0.552 95%CI)
PO2 - Values compare poorlyPaO2 =36.9 mm Hg > venous,significant variability (95% CI from 27.2-46.6mmHg) (Byrne et al, 2014)
Calculations in clinical contextAcidemia or Alkalemia Others with lab testMetabolic or Respiratory calculated osmolality [osm gap]
Compensations anion gap corrected to albumin
Acute or Chronic urea creatinine ratio
Anion gap
Delta Ratio
Corrected Na and K
A-a gradient to Fio2
Serial testing.
Correction formulasMetabolic Acidosis expected PaCO2 = (1.5 × HCO3-) + 8
Metabolic Alkalosis expected PaCO2 = (0.7 × HCO3-) + 20
Acute Respiratory AcidosisFor every 10 mmHg increase in PaCO2, the HCO3- will rise by 1 mmol/L
In other words, expected HCO3 = 24 + ((PaCO2-40) / 10)
Chronic Respiratory AcidosisFor every 10 mmHg increase in PaCO2, the HCO3- will rise by 4 mmol/L
In other words, expected HCO3 = 24 + (4 × (PaCO2-40) / 10)
Acute Respiratory AlkalosisFor every 10 mmHg decrease in PaCO2, the HCO3- will fall by 2 mmol/L
In other words, expected HCO3 = 24 - (2 ×(PaCO2-40) / 10)
Chronic Respiratory AlkalosisFor every 10 mmHg decrease in PaCO2, the HCO3- will fall by 5 mmol/L
In other words, expected HCO3 = 24 - (5 ×(PaCO2-40) / 10)
Anion gap
Delta ratio - Hyperglycemia-- Corrected K--- Ionized CaDelta ratio= (change in anion gap) / (change in bicarbonate)
Applied to metabolic acidosis to determine the contribution to acidosis from the unmeasured anions, the delta ratio suggests the following distinctions:
• Less than 0.4 = pure normal anion gap acidosis
• 0.4-0.8 = mixed high and normal anion gap acidosis
• 0.8-2.0 = pure high anion gap acidosis
• More than 2.0= high anion gap acidosis and a pre-existing metabolic alkalosis
Corrected Na= Na + { glucose- 5}/ 3 For DKA
For each pH fall below 7.4, K should rise by 0.5 mmol/l above 5.0 mmol/l Concept of relative potassium change.
An increase in pH, alkalosis, promotes increased protein binding, which decreases free calcium level. Acidosis, on the other hand, decreases protein binding, resulting in increased free calcium levels.
A-a gradient
The equation for calculating the A–a gradient is
Where:
PAO2 = alveolar PO2 (calculated from the alveolar gas equation
PaO2 = arterial PO2 (measured in arterial blood)
In its expanded form, the A–a gradient can be calculated by:On room air ( FiO2 = 0.21, or 21% ), at sea level ( Patm = 760 mmHg ) assuming 100% humidity in the alveoli.
1- 86 yr f from home lives with partner arrived with AMS with background history of epilepsy VBG
Ph 7.067
Pco2 23.8
Po2 48
Hco3 6.7
Glu 10.9
Lac 14.25
Hb 128
Na 130.1
K 3.62
Cl 99
iCa 1.12
CoHb 0.3
So2 66
Temp 37
Acidemia
Met (1.5* 6.7)+8= 18.05
ag= 130- 99= 31- 6.7= 24.3
dr = ( 24-12) / ( 24-6.7)= 0.7
Mixed nagma / hagma
Relative Hypokalemia
2- 56 y m v/d for 2/7- pmx renal tubular acidosis and diabetes
VBG
Ph 7.31
Pco2 30
Po2 45
Hco3 15
Glu 25
Lac 1.9
Hb 110
Na 140
K 3
Cl 115
iCa 1.1
CoHb 0.3
So2 66
Temp 37
Acidemia
Met 1.5* 15=22.5+8= 30.5
Ag 140- 115=25-15= 10
Dr 12-10/24-15= 0.22 nagma
Na 140+( 25-5)/3=147
Hyperchloremic metabolic acidosis
3 26 m afebrile atraumatic with 3hrs onset AMS with vomit, on Fio2 0.6Abg
Ph 7.5
Pco2 20
Po2 80
Hco3 15
Glu 4.9
Lac 1.9
Hb 131
Na 143
K 4
Cl 100
iCa 1.1
CoHb 0.9
So2 78
Temp 37
Alkalemia
Resp 24- {(40-20)/10 * 2}= 20, but hco3 is 15
Resp 24-{ (40-20)/10*5}= 14
Ag 143-100=43-15= 28 high
Dr 28-12/ 24-16= 16/8= 2
Metabolic alkalosis with HAGMA
Resp alkalosis
PAo2 ( 713* 0.6= 428)- ( 20*1.25=25)= 403
Aa = 403-80=323.
4 86 male febrile nursing home resident abg
Ph 7.21
Pco2 54.2
Po2 74
Hco3 33.1
Glu 6.8
Lac 2.1
Hb 111
Na 146
K 5.4
Cl 96
iCa 1.2
CoHb 0.3
So2 86
Temp 37
Acidemia
Resp 24+{(54-40)/10*1}=25.4
Resp 24+{(54-40)/10*4}= 30
Ag 146-96=50-33= 17 metabolic acidosis
Metabolic alkalosis
Mild hyperlactemia.
5 30 yr male interhospital transfer after closed head injury, sedated and ventilated.
Ph 7.10 Na 146
Pco2 35 K 3.2
Po2 169 Cl 129
Hco3 11 iCa 0.89
Glu 7.9 CoHb 0.3
Lac 4.9 So2 99
Hb 110 Temp 37
Acidemia
Metabolic 1.5*11=16.5+8= 24.5.
Ag 146-129= 17-11= 6
Dr 12-6/ 24-11= 6/13= 0.5 ( nagma+ hagma)
hypernatremia/ hyperchloremia.
hypokalemia/ hypocalcemia
hyperlactemia
6 70 yr male with ccf with resp distress on non rebreather mask
Ph 7.58
Pco2 21
Po2 154
Hco3 19
Glu 8.9
Lac 2.1
Hb 100
Na 127
K 5.2
Cl 79
iCa 1.0
CoHb 0.3
So2 86
Temp 37
Alkalemia
Resp 24- {( 40-21)/10*2}= 20
Ag 127-79=48-19= 29 high
Dr 29-12/ 24-19= 17/5= more than 2
Met acidosis/metabolic alkalosis
Mild hyperlactemia.
7 50 y f iddm, unwell with vomiting.
Ph 7.41
Pco2 32
Po2 78
Hco3 19
Glu 35
Lac 1.6
Hb 101
Na 132
K 2.7
Cl 79
iCa 1.0
CoHb 0.3
So2 80
Temp 37
Near normal ph
Ag 132-79=53-19=34 high agma
Dr 34-12/24-19= 22/5= more than 2, concurrent metabolic alkalosis.
Corrected Na= 132+( 35-5)/3= 142.
hypokalemia
8 46 m from burndown plastic bottle factory
Ph 7.25
Pco2 46
Po2 78
Hco3 22
Glu 8.0
Lac 13
Hb 101
Na 135
K 3.5
Cl 90
iCa 1.0
CoHb 20
So2 90
Temp 37
Acidemia
Metabolic /resp
Met 1.5*22=33+ 8= 41
Resp 24+ {( 46-40)/10*1}= 25
Ag = 135-90= 45-22=23
Dr 23-12/24-22= 11/2= more than 2
Concurrent m alk
Hyperlactemia- cyanide poisoning
Co poisoning
9 57 y f unknown overdose, history of af,depression- hypotension and brady.
ABG f.21
Ph 7.11
Pco2 35
Po2 86
Hco3 17
Glu 24
Lac 8.7
Hb 101
Na 140
K 3.3
Cl 90
iCa 0.75
CoHb 3
So2 89
Temp 37
Acidemia
Metabolic 1.5*17=25.5+8= 33.5
Ag 140-90=50-17=33
Dr 33-12/24-17=21/7= more than 2
Metabolic alkalosis
Hyperglycemia
Hyperlactemia
Aa g 150-( 35*1.25)= 150-44= 106
106-86= 20
10 45 y m with had seizure b4 arrival to ed, took headache tablets as partner, initial ℅ nausea/vomiting. tachypnea.
ABG Fio2- 0.3
Ph 7.32
Pco2 20
Po2 125
Hco3 10
Glu 2.9
Lac 2.2
Hb 111
Na 138
K 3.2
Cl 108
iCa 1.0
CoHb 3
So2 92
Temp 37
Acidemia
Metabolic- 1.5*10+8= 23
Ag 138-108-10=20
Dr 20-12/24-10= 0.57
Hypoglycemia
Aa grad 713*0.3= 214-( 20X1.25 ) =189
189-125=64
Age/4+4= 45/4+4 = 15
Causes of Metabolic Acidosis (classified by Anion Gap)
A: High Anion-Gap Acidosis 1. Ketoacidosis
Diabetic ketoacidosis Alcoholic ketoacidosis Starvation ketoacidosis
2. Lactic Acidosis Type A Lactic acidosis (Impaired perfusion) Type B Lactic acidosis (Impaired carbohydrate metabolism)
3. Renal Failure Uraemic acidosis Acidosis with acute renal failure
4. Toxins Ethylene glycol Methanol Salicylates, metformin, iron, CO, CYANIDE
B : Normal Anion-Gap Acidosis (or Hyperchloremic acidosis)
1. Renal Causes Renal tubular acidosis Carbonic anhydrase inhibitors
2. GIT Causes Severe diarrhoea Uretero-enterostomy or Obstructed ileal conduit Drainage of pancreatic or biliary secretions Small bowel fistula
3. Other Causes Recovery from ketoacidosis Addition of HCl, NH4Cl
Causes of Resp AcidosisA: Inadequate Alveolar Ventilation
Central Respiratory Depression & Other CNS Problems
Drug depression of resp. center (eg by opiates, sedatives, anaesthetics)
CNS trauma, infarct, haemorrhage or tumour
Hypoventilation of obesity (eg Pickwickian syndrome)
Cervical cord trauma or lesions (at or above C4 level)
High central neural blockade
Poliomyelitis
Tetanus
Cardiac arrest with cerebral hypoxia
Nerve or Muscle Disorders
Guillain-Barre syndrome
Myasthenia gravis
Muscle relaxant drugs
Toxins eg organophosphates, snake venom
Various myopathies
Lung or Chest Wall Defects
Acute on COAD
Chest trauma -flail chest, contusion, haemothorax
Pneumothorax
Diaphragmatic paralysis or splinting
Pulmonary oedema
Adult respiratory distress syndrome
Restrictive lung disease
Aspiration
Airway Disorders
Upper Airway obstruction
Laryngospasm
Bronchospasm/Asthma
External Factors
Inadequate mechanical ventilation
Causes of Resp Acidosis (ctd)B: Over-production of Carbon Dioxide
Hypercatabolic Disorders
Malignant Hyperthermia
C: Increased Intake of Carbon Dioxide
Rebreathing of CO2-containing expired gas
Addition of CO2 to inspired gas
Insufflation of CO2 into body cavity (eg for laparoscopic surgery)
A rise in arterial pCO2 is a potent stimulus to ventilation so a respiratory acidosis will rapidly correct
unless some abnormal factor is maintaining the hypoventilation.
Causes of Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre) Head Injury Stroke Anxiety-hyperventilation syndrome (psychogenic) Other 'supra-tentorial' causes (pain, fear, stress, voluntary) Various drugs (eg analeptics, propanidid, salicylate intoxication) Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease)
Causes of Respiratory Alkalosis2. Hypoxaemia (act via peripheral chemoreceptors)
Respiratory stimulation via peripheral chemoreceptors3. Pulmonary Causes (act via intrapulmonary receptors)
Pulmonary Embolism Pneumonia Asthma Pulmonary oedema (all types)
4. Iatrogenic (act directly on ventilation) Excessive controlled ventilation
Causes of Met AlkalosisA: Addition of Base to ECF
Milk-alkali syndromeExcessive NaHCO3 intakeRecovery phase from organic acidosis (excess
regeneration of HCO3)Massive blood transfusion (due metabolism of
citrate)B: Chloride Depletion
Loss of acidic gastric juiceDiureticsPost-hypercapniaExcess faecal loss (eg villous adenoma)
C: Potassium DepletionPrimary hyperaldosteronismCushing’s syndromeSecondary hyperaldosteronismSome drugs (eg carbenoxolone)Kaliuretic diureticsExcessive licorice intake (glycyrrhizic acid)Bartter's syndrome Severe potassium depletion
D: Other DisordersLaxative abuse Severe hypoalbuminaemia
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