Upload
kalyan-ram
View
35
Download
0
Embed Size (px)
Citation preview
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-
27mmol/L• Age 6-7years: 20-
28mmol/L• Age 8-17years: 21-
29mmol/L• Age 18 years or older:
22-29mmol/L
• In females, ranges are as follows:• Age 1-3years: 18-
25mmol/L• Age 4-5years: 19-
26mmol/L• Age 6-7years: 20-
27mmol/L• Age 8-9years: 21-
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 !