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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