abg (emergency medicine)

Arterial blood gas analysis

DR. SHABBIRPOSTGRADUATE STUDENTDEPARTMENT OF EMERGENCY MEDICINE KIMS, BANGALORE

• CHEMICAL BUFFEREING • RENAL REGULATION• PULMONARY REGULATION

Chemical buffering• Chemical buffers are solutions that resist changes

in pH.• Intracellular and extracellular buffers provide an

immediate response to acid-base disturbances.• A buffer is made up of a weak acid and its

conjugate base. • A buffer system works best to minimize changes

in pH near its equilibrium constant (pKa).

• The relationship between the pH of a buffer system and the concentration of its components is described by the Henderson-Hasselbalch equation:

• The most important extracellular buffer is the HCO3−/CO2 system,

Pulmonary regulation

• CO2 concentration is finely regulated by changes in tidal volume and respiratory rate (minute ventilation) .

• A decrease in pH is sensed by arterial chemoreceptors and leads to increases in tidal volume or respiratory rate , CO2 is exhaled and blood pH increases.

• It is about 50 to 75% effective and does not completely normalize pH.

Renal regulation

• The kidneys control pH by adjusting the amount of HCO3

− that is excreted or reabsorbed.

• Reabsorption of HCO3− is equivalent to

removing free H+. Changes in renal acid-base handling occur hours to days after changes in acid-base status.

• HCO3− reabsorption occurs mostly in the

proximal tubule and, to a lesser degree, in the collecting tubule

• The H2O within the distal tubular cell dissociates into H+ and hydroxide (OH−); in the presence of carbonic anhydrase, the OH− combines with CO2 to form HCO3

−, which is transported back into the peritubular capillary.

• the H+ is secreted into the tubular lumen and joins with freely filtered HCO3

− to form CO2 and H2O, which are also reabsorbed.

Indications for ABG

• Assess ventilation & acid-base balance• Assess oxygenation status

Nomenclature & Criteria for Clinical Interpretation

Clinical Terminology Criteria

Ventilatory failure (respiratory acidosis) PaCO2 > 45 mm HgAcute ventilatory failure (respiratory acidosis) PaCO2 > 45

mmHg pH < 7.35Chronic ventilatory failure (respiratory acidosis) PaCO2 > 45

mmHgpH 7.36- 7.44

Alveolar hyperventilation (respiratory alkalosis) PaCO2 < 35 mmHg

Acute alveolar hyperventilation (respiratory PaCO2 < 35 mmHgalkalosis) pH > 7.45

Chronic alveolar hyperventilation (respiratory PaCO2 < 35 mmHg alkalosis) pH 7.36-7.44

Nomenclature & Criteria for Clinical Interpretation

Clinical Terminology Criteria

Acidemia pH < 7.35Alkalemia pH > 7.45Acidosis HCO3

- < 22 mmol/LBD > 5 mmol/L

Alkalosis HCO3- > 26 mmol/L

BE > 5 mmol/LMixed Respiratory Acidosis & Metabolic Acidosis

Respiratory Alkalosis & Metabolic AlkalosisCompensated Respiratory Acidosis & Metabolic Alkalosis

Respiratory Alkalosis & Metabolic Acidosis

ARTERIAL VENOUS

pH 7.38-7.42 7.36-7.39

PaO2 80-100 38-42

PaCO2 36-44 44-48

HCO3 22-26 20-24

SaO2 95-100 75

Henderson-Hasselbach pH= [HCO3]p

PC02

pH PCO2(mmHg)

[HCO3]p(mmol/L)

Normal 7.35-7.45 35-45 22-26

Acidotic < 7.35 > 45 < 22

Alkalotic > 7.45 < 35 > 26

Serum bicarbonate• In males, ranges are as

follows:• Age 12-24 months: 17-

25mmol/L• Age 3 years: 18-

26mmol/L• Age 4-5years: 19-



29mmol/L• Age 18 years or older:

22-29mmol/L

• In females, ranges are as follows:• Age 1-3years: 18-




28mmol/L• Age 10 years or older: 22-

29mmol/L

The primary disorders

Characteristics of compensatory disorders

DISORDER PRIMARY RESPONSES

COMPENSATORY RESPONSE

Metabolic acidosis

PH HCO3- pCO2

Metabolic alkalosis

PH HCO3- pCO2

Respiratory acidosis

PH pCO2 HCO3-

Respiratory alkalosis

PH pCO2 HCO3-

THE ANION GAP

• The anion gap is defined as serum Na concentration minus the sum of Cl− and HCO3

−concentrations; Na+− (Cl−+ HCO3−). The

term “gap” is misleading, because the law of electroneutrality requires the same number of positive and negative charges in an open system; the gap appears on laboratory testing because certain cations (+) and anions (−) are not measured on routine laboratory chemistry panels.

• The predominant "unmeasured" anions are PO4

3−, sulfate (SO4−), various negatively

charged proteins, and some organic acids, accounting for 20 to 24 mEq/L. The predominant "unmeasured" extracellular cations are K+, Ca++, and Mg++ and account for about 11 mEq/L. Thus the typical anion gap is 23 − 11 = 12 mEq/L. The anion gap can be affected by increases or decreases in the UC or UA.

• Increased anion gap is most commonly caused by metabolic acidosis in which negatively charged acids—mostly ketones, lactate, sulfates, or metabolites of methanol, ethylene glycol,or salicylate—consume (are buffered by) HCO3

−. Other causes of increased anion gap include hyperalbuminemia and uremia (increased anions) and hypocalcemia or hypomagnesemia (decreased cations).

• Decreased anion gap is unrelated to metabolic acidosis but is caused by hypoalbuminemia (decreased anions); hypercalcemia, hypermagnesemia, lithium intoxication, and hypergammaglobulinemia as occurs in myeloma (increased cations); or hyperviscosity or halide (bromide or iodide) intoxication. The effect of low albumin can be accounted for by adjusting the normal range for the anion gap 2.5 mEq/L upward for every 1-g/dL fall in albumin.

• Negative anion gap occurs rarely as a laboratory artefact in severe cases of hypernatremia, hyperlipidaemia, and bromide intoxication.

• The delta gap: The difference between the patient’s anion gap and the normal anion gap is termed the delta gap. This amount is considered an HCO3

− equivalent, because for every unit rise in the anion gap, the HCO3

− should lower by 1 (by buffering). Thus, if the delta gap is added to the measured HCO3

−, the result should be in the normal range for HCO3

−; elevation indicates the additional presence of a metabolic alkalosis.

Base Excess/ Deficit• Blood with large buffering capacity:

significant changes in acid content with little change in free H+ concentrations (pH)

• Academia or alkalemia: i buffering capacity, > potential for pH change from any given change in H+ content

• Buffering capacity depends on:[HCO3

-]RBC mass

• Base excess/deficit= (measured pH – predicted pH) x 100 x 2/3

Normal metabolic acid-base status: + 3 mmol/L

Relatively balanced metabolic acid-base status:+ 5 mmol/LClinically significant imbalance: +

10 mmol/L

Respiratory AcidosisAcute

r pH = 0.08 x (PCO2 – 40) 10ex. PCO2 = 60r pH = 0.08 x (60 - 40) = 0.16 10expected pH = 7.40 – 0.16 = 7.24

HCO3- increases 0.1 – 1 meq/L per 10 mmHg PCO2 increase

Compensation: cellular buffering: HCO3

renal adaptation: H+ secretion, Cl- reabsorption, net acid excretion

Respiratory acidosisChronic

r pH = 0.03 x (PCO2 – 40)10

ex. PCO2 = 60r pH = 0.03 x (60 – 40) = 0.06

10expected pH = 7.40 – 0.06 = 7.34

HCO3- increases 1-3.5 meq/L per 10 mmHg PCO2

increase

Respiratory Acidosis• COPD• O2 excess in COPD• Drugs• Barbiturates• Anesthetics• Narcotics• Sedatives

• Extreme ventilation-perfusion mismatch

• Exhaustion • Inadequate MV• Neurologic disorders

• Neuromuscular disease• Poliomyelitis• ALL• G-B syndrome• Electrolyte

deficiencies (K+, PO4-)

• Myasthenia gravis• Excessive CO2

production• TPN• Sepsis• Severe burns• NaHCO3

administration

Respiratory AlkalosisAcute

r pH = 0.08 x (40 – PCO2) 10

ex. PCO2 = 20r pH = 0.08 x (40 – 20) = 0.16

10expected pH = 7.40 + 0.16 = 7.56

HCO3- decreases 0-2 meq/L per 10 mmHg PCO2

decreaseCompensation: cellular buffering

renal response: retention of endogenous acids, excretion of HCO3

Respiratory AlkalosisChronic

r pH = 0.03 x (40 – PCO2)10

ex. PCO2 = 20r pH = 0.03 x (40 – 20) = 0.06

10expected pH = 7.40 + 0.06 = 7.46

HCO3- decreases 2-5 meq/L per 10 mmHg PCO2

decrease

Respiratory AlkalosisPrimary central

disorders• Hyperventilation

syndrome, anxiety• Cerebrovascular

disease• Meningitis,

encephalitisPulmonary disease• Interstitial fibrosis• Pneumonia• Pulmonary embolism• Pulmonary edema

(some patients)

HypoxiaSepticemia,

hypotensionHepatic failureDrugs• Salicylates• Nicotine• Xanthine's• Progestational

hormonesHigh altitudeMechanical ventilators

Metabolic AcidosisAnion Gap • artificial disparity between major plasma cations

& anions that are routinely measured• major plasma cations – major plasma anions• [Na+] – ([Cl-] + [HCO3-])• 12 + 2 (normal)• Minor cations: K+, Ca++

• Minor anions: phosphates, sulfates, organic anions

Metabolic Acidosis• Anion gap acidosis

~ process increases “minor anions”~ ex. lactatemia, ketonemia, renal failure, excessive

organic salt treatment, dehydration, ingestion (salicylates, methanol, ethylene glycol,

paraldehyde)~ process which decreases “minor cations” rare!

• Non-anion gap acidosis~ associated with increased plasma Cl- that has replaced HCO3

-

~ ex. GI loss of HCO3- (diarrhea), renal wasting of HCO3

- (RTA), ingestion of acids, parenteral hyperalimentation, carbonic anhydrase inhibitors

Metabolic AcidosisAbnormalities:• Overproduction of acids• Loss of buffer stores• Underexcretion of acids

Metabolic Acidosis

Expected PCO2 = ( [HCO3-] x 1.5) + 8 + 2(winters

formula)

ex. [HCO3-] = 11

expected PCO2 = (11 x 1.5) + 8 + 2 = 22.5- 26.5

PCO2 decreases 1- 1.5 mmHg per 1 meq/L HCO3-

decrease

Corrected [HCO3-] for Anion

Gap Metabolic Acidosis

Measured serum [HCO3-] + (anion gap – 12)

LACTIC ACIDOSIS

• Lactic acidosis results from overproduction of lactate, decreased metabolism of lactate, or both.

• Lactate is a normal byproduct of glucose and amino acid metabolism. There are 2 main types of lactic acidosis, A and B, and an unusual form,D-lactic acidosis.

• Type A lactic acidosis, the most serious form, occurs when lactic acid is overproduced in ischemic tissue to generate ATP during O2 deficit. Overproduction typically occurs during tissue hypoperfusion in hypovolemic, cardiac, or septic shock and is worsened by decreased lactate metabolism in the poorly perfused liver. It may also occur with primary hypoxia due to lung disease and with various hemoglobinopathies

• Type B lactic acidosis occurs in states of normal global tissue perfusion (and hence ATP production) and is less ominous. Lactate production may be increased from local relative hypoxia as with vigorous muscle use (eg, exertion, seizures, hypothermic shivering) and with cancer and ingestion of certain drugs or toxins . Drugs include the nucleoside reverse transcriptase inhibitors and the biguanides phenformin and, less so, metformin;Metabolism may be decreased due to hepatic insufficiency or thiamin deficiency.

Metabolic Alkalosis

Expected PCO2 = ( [HCO3-] x 0.75 ) + 20 + 5

ex. [HCO3-] = 34

expected PCO2 = (34 x 0.75) + 20 + 5 = 40.5- 50.5

PCO2 increases 0.5- 1 mmHg per 1 meq/L HCO3-

increase

Causes of Metabolic AlkalosisHypokalemia*Ingestion of large amounts of alkali or licoriceGastric fluid loss: Vomiting, NG suctioning*Hyperaldosteronism 20 to nonadrenal factors Bartter’s syndrome Inadequate renal perfusion diuretics (inhibiting NaCl reabsorption)*Bicarbonate administration Sodium bicarbonate overcorrection Blood transfusionAdrenocortical hypersecretion (e.g tumor)Steroids*Eucapnic ventilation posthypercapnia

* Common in the ICU

Limits of CompensationImbalance [HCO3

-] meq/L PCO2 mmHgRespiratory AcidosisAcute h0.1- 1/ 10 mmHg

PCO2hChronic h1- 3.5/ 10 mmHg

PCO2hRespiratory AlkalosisAcute i0- 2/ 10 mmHg PCO2iChronic i2- 5/ 10 mmHg PCO2iMetabolic Acidosis i1- 1.5/ 1 meq/L

[HCO3-] i

Metabolic Alkalosis h0.5- 1/ 1 meq/L [HCO3

-] h

Thank you !

abg (emergency medicine)

Health & Medicine