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Acid Base
Fakhir
Acidemia and Acidosis
• Acidemia is a low pH or a high concentration of H+ in plasma.
• Acidosis is a process that adds H+ to or removes HCO3– from the
body.
High H+ ions
• Metabolic Acidosis means addition of H+ to the body or loss of HCO3
from the body. The physiological response is low CO2
• Respiratory Acidosis means increased arterial CO2 and H+ . The
expected clinical response is increase HCO3
Six Step approach of ABGs interpretation
1. Assess the internal consistency of the values using the Henderseon-
Hasselbach equation
2. Is there alkalemia or acidemia present?
3. Is the disturbance respiratory or metabolic?
4. Is there appropriate compensation for the primary disturbance?
5. Calculate the anion gap (if a metabolic acidosis exists)
6. If an increased anion gap is present, assess the relationship
between the increase in the anion gap and the decrease in [HCO3-]
1. Assess the internal consistency of the values
using the Henderseon-Hasselbach equation
[H+] = 24(PaCO2)
[HCO3-]
7.55 28
7.60 25
7.65 22
If the pH and
the [H+] are
inconsistent,
the ABG is
probably not
valid.
pH Approximate [H+]
(nmol/L)
7.00 100
7.05 89
7.10 79
7.15 71
7.20 63
7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
2. Is there alkalemia or acidemia present?
• pH < 7.35 acidemia
• pH > 7.45 alkalemia
3. Is the disturbance respiratory or
metabolic?
Acidosis Respiratory pH ↓ PaCO2 ↑
Acidosis Metabolic& pH ↓ PaCO2 ↓
Alkalosis Respiratory pH ↑ PaCO2 ↓
Alkalosis Metabolic pH ↑ PaCO2 ↑
4. Is there appropriate compensation for the
primary disturbance?
Disorder Expected compensation Correction factor
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ± 2
Acute respiratory acidosis Increase in [HCO3-]= ∆ PaCO2/10 ± 3
Chronic respiratory acidosis (3-5 days) Increase in [HCO3-]= 3.5(∆ PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-)
Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆ PaCO2/10)
Chronic respiratory alkalosis Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆
PaCO2/10)
5. Calculate the anion gap (if a metabolic
acidosis exists)
AG= [Na+]-( [Cl-] + [HCO3-] )-12 ± 2
• A normal anion gap is approximately 12 meq/L.
• In patients with hypoalbuminemia, the normal anion gap is lower
than 12 meq/L; the “normal” anion gap in patients with
hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL
decrease in the plasma albumin concentration (for example, a patient
with a plasma albumin of 2.0 gm/dL would be approximately 7
meq/L.)
If anion gap is raised
• If the anion gap is elevated, consider calculating the osmolal gap in
compatible clinical situations.
• Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal
failure
• Toxic ingestion is suspected
• OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8
• The OSM gap should be < 10
6. If an increased anion gap is present, assess the
relationship between the increase in the anion gap
and the decrease in [HCO3-]
Assess the ratio of the change in the anion gap (∆AG ) to the change
in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]
This ratio should be between 1.0 and 2.0 if an uncomplicated anion
uncomplicated anion gap metabolic acidosis is present.
What is the basis of delta delta
• If HCO3 would be 24 – the anion gap is 12
• If HCO3 drops to 23 – the anion gap will increase to 13
• And so on
Buffer system
Disorder pH Primary problem Compensation
Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2
Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2
Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-]
Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]
Selected etiologies of respiratory acidosis
• Airway obstruction
Upper
Lower
• COPD
• Asthma
• Other obstructive lung disease
• CNS depression
• Sleep disordered breathing (OSA or OHS)
• Neuromuscular impairment
• Ventilatory restriction
• Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia,
hypermetabolism, increased intake of carbohydrates
• Incorrect mechanical ventilation settings
Selected etiologies of respiratory alkalosis
• CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain
trauma, brain tumor, CNS infection
• Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2
• Stimulation of chest receptors: pulmonary edema, pleural effusion,
pneumonia, pneumothorax, pulmonary embolus
• Drugs, hormones: salicylates, catecholamines, medroxyprogesterone,
progestins
• Pregnancy, liver disease, sepsis, hyperthyroidism
• Incorrect mechanical ventilation settings
Selected causes of metabolic alkalosis
oHypovolemia with Cl- depletion
o GI loss of H+
o Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid
o Renal loss H+
o Loop and thiazide diuretics, post-hypercapnia (especially after institution of mechanical ventilation)
oHypervolemia, Cl- expansion
o Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome),
hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids,
hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate
administration
Selected etiologies of metabolic acidosis
oElevated anion gap:
o Methanol intoxication
o Uremia
o Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation
o Paraldehyde toxicity
o Isoniazid
o Lactic acidosisa
oType A: tissue ischemia
oType B: Altered cellular metabolism
o Ethanolb or ethylene glycolb intoxication
o Salicylate intoxication
Normal anion gap: will have increase in [Cl-]
o GI loss of HCO3-
oDiarrhea, ileostomy, proximal colostomy, ureteral diversion
o Renal loss of HCO3-
oproximal RTA
ocarbonic anhydrase inhibitor (acetazolamide)
o Renal tubular disease
oATN
oChronic renal disease
oDistal RTA
oAldosterone inhibitors or absence
oNaCl infusion, TPN, NH4+ administration
What happens in Cardiac Arrest
• Mixed disorder
Selected mixed and complex acid-base disturbances
Disorder Characteristics Selected situations
Respiratory acidosis with
metabolic acidosis
↓in pH
↓ in HCO3
↑ in PaCO2
•Cardiac arrest
•Intoxications
•Multi-organ failure
Respiratory alkalosis with
metabolic alkalosis
↑in pH
↑ in HCO3-
↓ in PaCO2
•Cirrhosis with diuretics
•Pregnancy with vomiting
•Over ventilation of COPD
Respiratory acidosis with
metabolic alkalosis
pH in normal range
↑ in PaCO2,
↑ in HCO3-
•COPD with diuretics, vomiting, NG suction
•Severe hypokalemia
Respiratory alkalosis with
metabolic acidosis
pH in normal range
↓ in PaCO2
↓ in HCO3
•Sepsis
•Salicylate toxicity
•Renal failure with CHF or pneumonia
•Advanced liver disease
Metabolic acidosis with
metabolic alkalosis
pH in normal range
HCO3- normal
•Uremia or ketoacidosis with vomiting, NG
suction, diuretics, etc.
Examples

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Acid base assessment 6 steps

  • 2. Acidemia and Acidosis • Acidemia is a low pH or a high concentration of H+ in plasma. • Acidosis is a process that adds H+ to or removes HCO3– from the body.
  • 3. High H+ ions • Metabolic Acidosis means addition of H+ to the body or loss of HCO3 from the body. The physiological response is low CO2 • Respiratory Acidosis means increased arterial CO2 and H+ . The expected clinical response is increase HCO3
  • 4.
  • 5. Six Step approach of ABGs interpretation 1. Assess the internal consistency of the values using the Henderseon- Hasselbach equation 2. Is there alkalemia or acidemia present? 3. Is the disturbance respiratory or metabolic? 4. Is there appropriate compensation for the primary disturbance? 5. Calculate the anion gap (if a metabolic acidosis exists) 6. If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO3-]
  • 6. 1. Assess the internal consistency of the values using the Henderseon-Hasselbach equation [H+] = 24(PaCO2) [HCO3-]
  • 7. 7.55 28 7.60 25 7.65 22 If the pH and the [H+] are inconsistent, the ABG is probably not valid. pH Approximate [H+] (nmol/L) 7.00 100 7.05 89 7.10 79 7.15 71 7.20 63 7.25 56 7.30 50 7.35 45 7.40 40 7.45 35 7.50 32
  • 8. 2. Is there alkalemia or acidemia present? • pH < 7.35 acidemia • pH > 7.45 alkalemia
  • 9. 3. Is the disturbance respiratory or metabolic? Acidosis Respiratory pH ↓ PaCO2 ↑ Acidosis Metabolic& pH ↓ PaCO2 ↓ Alkalosis Respiratory pH ↑ PaCO2 ↓ Alkalosis Metabolic pH ↑ PaCO2 ↑
  • 10. 4. Is there appropriate compensation for the primary disturbance? Disorder Expected compensation Correction factor Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ± 2 Acute respiratory acidosis Increase in [HCO3-]= ∆ PaCO2/10 ± 3 Chronic respiratory acidosis (3-5 days) Increase in [HCO3-]= 3.5(∆ PaCO2/10) Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-) Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆ PaCO2/10) Chronic respiratory alkalosis Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)
  • 11. 5. Calculate the anion gap (if a metabolic acidosis exists) AG= [Na+]-( [Cl-] + [HCO3-] )-12 ± 2 • A normal anion gap is approximately 12 meq/L. • In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the “normal” anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration (for example, a patient with a plasma albumin of 2.0 gm/dL would be approximately 7 meq/L.)
  • 12. If anion gap is raised • If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations. • Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure • Toxic ingestion is suspected • OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8 • The OSM gap should be < 10
  • 13. 6. If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO3-] Assess the ratio of the change in the anion gap (∆AG ) to the change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-] This ratio should be between 1.0 and 2.0 if an uncomplicated anion uncomplicated anion gap metabolic acidosis is present.
  • 14. What is the basis of delta delta • If HCO3 would be 24 – the anion gap is 12 • If HCO3 drops to 23 – the anion gap will increase to 13 • And so on
  • 15. Buffer system Disorder pH Primary problem Compensation Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2 Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2 Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-] Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]
  • 16. Selected etiologies of respiratory acidosis • Airway obstruction Upper Lower • COPD • Asthma • Other obstructive lung disease • CNS depression • Sleep disordered breathing (OSA or OHS) • Neuromuscular impairment • Ventilatory restriction • Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased intake of carbohydrates • Incorrect mechanical ventilation settings
  • 17. Selected etiologies of respiratory alkalosis • CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection • Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2 • Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus • Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins • Pregnancy, liver disease, sepsis, hyperthyroidism • Incorrect mechanical ventilation settings
  • 18. Selected causes of metabolic alkalosis oHypovolemia with Cl- depletion o GI loss of H+ o Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid o Renal loss H+ o Loop and thiazide diuretics, post-hypercapnia (especially after institution of mechanical ventilation) oHypervolemia, Cl- expansion o Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome), hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate administration
  • 19. Selected etiologies of metabolic acidosis oElevated anion gap: o Methanol intoxication o Uremia o Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation o Paraldehyde toxicity o Isoniazid o Lactic acidosisa oType A: tissue ischemia oType B: Altered cellular metabolism o Ethanolb or ethylene glycolb intoxication o Salicylate intoxication
  • 20. Normal anion gap: will have increase in [Cl-] o GI loss of HCO3- oDiarrhea, ileostomy, proximal colostomy, ureteral diversion o Renal loss of HCO3- oproximal RTA ocarbonic anhydrase inhibitor (acetazolamide) o Renal tubular disease oATN oChronic renal disease oDistal RTA oAldosterone inhibitors or absence oNaCl infusion, TPN, NH4+ administration
  • 21. What happens in Cardiac Arrest • Mixed disorder
  • 22. Selected mixed and complex acid-base disturbances Disorder Characteristics Selected situations Respiratory acidosis with metabolic acidosis ↓in pH ↓ in HCO3 ↑ in PaCO2 •Cardiac arrest •Intoxications •Multi-organ failure Respiratory alkalosis with metabolic alkalosis ↑in pH ↑ in HCO3- ↓ in PaCO2 •Cirrhosis with diuretics •Pregnancy with vomiting •Over ventilation of COPD Respiratory acidosis with metabolic alkalosis pH in normal range ↑ in PaCO2, ↑ in HCO3- •COPD with diuretics, vomiting, NG suction •Severe hypokalemia Respiratory alkalosis with metabolic acidosis pH in normal range ↓ in PaCO2 ↓ in HCO3 •Sepsis •Salicylate toxicity •Renal failure with CHF or pneumonia •Advanced liver disease Metabolic acidosis with metabolic alkalosis pH in normal range HCO3- normal •Uremia or ketoacidosis with vomiting, NG suction, diuretics, etc.

Editor's Notes

  1. This is usually the primary disorder Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 – 7.45) You will need to check the PaCO2, HCO3- and anion gap
  2. What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction
  3.  Usually, compensation does not return the pH to normal (7.35 – 7.45).
  4. If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present.
  5. It is important to remember what the expected “normal” anion gap for your patient should be, by adjusting for hypoalbuminemia 
  6. Buffer system does not compensate 100% CO2 is rapidly compensated as compared to HCO3