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Mohammad A. Alfuhaily, PhD د. محمد عبدالمحسن الفحيلي

Associate Professor

College of Applied Medical Sciences, Department of Clinical Laboratory Sciences

كلية العلوم الطبية التطبيقية
Building 24, Office 2299
مدونة

Arterial Blood Gases (ABGs)

*Physiology:

-Acid-base balance is essential for oxygen uptake and release, enzyme activity, and use of minerals and metabolites. 

-Most cells have a pH of 7.0, while RBCs boast a 7.2 pH.

-Acid = Proton donor (becomes its conjugate base).
-Base = Proton acceptor (becomes its conjugate acid).

*Monobasic phosphate (H2PO4-) in acidic medium act as a base (become H3PO4-), while in basic medium act as an acid (becomes HPO42-).

-Sources of acids include:

1. Anaerobic respiration (lactic acid).
2. Glycolysis (pyruvic acid).
3. Ketogenesis (ketone bodies).
4. Oxidation of sulfur-containing AA's (sulfuric acids)
5. Incomplete combustion of carbohydrates and fats (carbonic acid) 
6. Uric acid and inorganic phosphorus compounds (phosphoric acid).

-All acids dissociate into H+ ions. Some of which are used in metabolism and the rest is taken up by oxygen to form water. This keeps H ion concentration constant.

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-However, there is not always enough oxygen to bind H, and this is what buffer systems are for:

BICARBONATE/CARBONIC ACID (NaHCO3/H2CO3)

DIBASIC PHPSPHATE/MONOBASIC PHOSPHATE (Na2HPO4/NaH2PO4)

PROTEINATE/PROTEIN (Na protein/H protein)

HEMOGLOBINATE/HEMOGLOBIN

-The bicarbonate buffer system is the most important because it’s readily adjustable by altering the rate of CO2 removal by respiration as required.

-CO2 moves across the alveolar membrane and enters plasma as dissolved CO2. 5% remain free, while the rest diffuses from tissues into RBCs:

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

*H+ ions are taken up and buffered by deoxy Hb in RBCs (Hb è HHb)
*HCO3 goes out into the plasma in exchange for Cl- to maintain electrical neutrality.
*If an acid is added, H+ is taken up by HCO3, become H2CO3, and dissociate into H2O and CO2. Excess CO2 is exhaled. H2CO3 remains constant before and after addition, and hence pH does not change.

*If a base is added, H2CO3 increases and HCO3 decreases.

-Proteins are efficient buffers because of amino acid residues with different pKa values.

-Respiratory regulation:

-Short-term and don’t proceed to completion.

-Hyper and hypoventilation (expel or keep CO2). 

-Renal regulation:

-Slow, but long-term effect.

-Four main mechanisms:

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Excretion of H+ in PCT: This is coupled with HCO3 formation and reabsorption. H+ combines with base ions and excreted in urine in exchange for NaHCO3.

·      Excretion of NH4+ in DCT: This is coupled with HCO3 formation and reabsorption. Ammonium ion excretion buffers H+ secreted into tubular fluid.

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·    Excretion of acid phosphate (NaH2PO4) in PCT & DCT: NaH2PO4 in tubular fluid dissociate into NaHPO4 and Na (exchanged for H+ secreted into the tubular lumen and combine with NaHPO4 forming NAH2PO4). NaHCO3 (formed in tubular cells) reabsorbed into plasma.
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Reabsorption of HCO3 in PCT: Normal urine is free from HCO3. Filtered HCO3 combines with H+ in tubular fluid to form H2CO3 and finally HCO3 and H+. H+ secreted into fluid exchanged with Na. HCO3 reabsorbed into blood along with Na. There is no net excretion of H+ or generation of HCO3.

Pathology:

-Sample is arterial! The most convenient site is the radial artery. However, in cases of emergency or children, the femoral and brachial arteries could be used. Arterial catheter in one of these places may also be used.

-Heparin is the anticoagulant present in the syringe. Once the blood is drawn, air bubbles must be removed completely as they may dissolve in the sample and produce erroneous results. This is crucial!

-Send the syringe to the lab in a bag with 3-4 ice cubes; metabolic processes must be put on hold for a while. Exception: Plastic syringes can’t be iced. Analyze within 30 mins. If you ignored this, low O2 and high CO2 would result.

-You’ll be dealing with pulmonology clinicians here; these guys are always in a hurry! They want to know the status of gas exchange related to lung function, and it’s simply your job to tell them.

-What’s the concept of this partial pressure all about? We’re not physicists, but try to picture this: when a mixture of gases exist in a given place, they exert pressure. The partial pressure of a gas is the pressure that gas exerts alone in that place at the same temp. Now apply this to a dissolved gas in the blood.

(1) pH: This obviously diagnoses acidemia and alkalemia, and is the first result to look at when making a diagnosis.

(2) H+: Look up and tell me how it’s related! Hydrogen ion concentration is not used in diagnosis; PCO2 and HCO3- are more useful.

(3) PO2: A low O2 indicates that the patient is not respiring properly, and is hypoxemic. At a PO2 of less than 60 mmHg, supplemental oxygen should be administered. At a PO2 of less than 26 mmHg, the patient is at risk of death and must be oxygenated immediately. Again, not important for making a diagnosis.

(4) PCO2: Partial pressure of carbon dioxide. This is obviously controlled by the lungs, and is the respiratory component.

(5) HCO3-: Concentration of biarbonates (dissolved CO2) in the blood. It is controlled by the kidneys and represents the metabolic component.

-Blood gas analyzers run on multiple principles; the most common of which are ion-selective electrodes and potentiometry. These instruments are more friendly than what their names suggest (yes, names can be deceiving) and understanding of the situation; they will always provide you with more than you ask for. 

-RR:
pH = 7.35-7.45
PCO
2 = 35-45 mmHg
HCO
3 = 21-30 mmol/L.

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(6) Anion Gap: Measured cations minus measured anions. Na - [Cl + HCO3]. K+ is ignored due its very low concentration. Mg+2, PO4-3, and sulfates are unmeasured for a reason (discussed later). RR: 3-11 mEq/L.
 

(7) Osmolar Gap: Measured serum osmolality - calculated serum osmolality (discussed later). RR: <10 mOsm/kg.

(8) Base Excess: Increased bases in blood (discussed later). RR: -2 to +2 mEq/L.

 

METABOLIC ACIDOSIS

-Low pH; Low HCO3-; Low PCO2.

-Causes:

1.     Ketosis (DM or starvation)

2.     Tissue hypoxia (lactic acidosis)

3.     RTA or Renal failure  (no HCO3 reabsorption)

4.     Diarrhea (loss of HCO3 gastric secretions)

5.     Addison’s disease (decreased Na and HCO3 reabsorption)

-Always calculate the anion gap to aid in diagnosis: 

 

Anion Gap = Na+ – (Cl- + HCO3-) = 8-16

 

*The difference between anions and cations in blood.
*Always in balance, even in disease.

*HIGH = HIGH unmeasured anions as in ketoacidosis (untreated DM or starvation), lactic acidosis (intense exercise), renal failure (high phosphate and sulphate), and salicylate poisoning. Measurement of glucose, lactate, paracetamol, salicylate, ethanol (and sometimes hydroxybutyrate), in blood, with urine tested for ketones. In paediatric patients, metabolic screen (plasma lactate, ammonia, amino acids and urine amino acids and organic acids) is performed.
*HIGH = LOW unmeasured cations (K, Mg, Ca) or HIGH plasma proteins.
*NORMAL in hyperchloremic acidosis as in RTA and diarrhea.

*LOW = HIGH unmeasured cations or LOW unmeasured anions.

-Always calculate the osmotic gap to aid in diagnosis:

 

Osmotic Gap = Measured osmolality − Calculated osmolality

                       = Measured – (2 X Na) + glucose + urea = < 10

 

*HIGH with HIGH anion gap = Toxin such as ethanol, methanol or ethylene glycol. A fluoride oxalate sample with a urine sample should be sent for toxicology (with measurement of serum calcium and microscopy for crystals in suspected ethylene glycol poisoning). Very rarely measurement of D-lactate (produced in intestinal disease) may be useful.

*If calculated is higher than measured = analytical error.

-Hyperkalemia: H+ move into cells in exchange for K+.

-Compensation: Hyperventilation – Increased H+ excretion as NH4+ (acidic urine) with generation of HCO3 to increase in plasma.

METABOLIC ALKALOSIS
 

- High pH; High HCO3; High PCO2.

-Causes:

1.     Vomiting (loss of gastric HCl- decreases plasma H+ and Cl- is compensated by increasing HCO3).

2.     Cushing (high aldosterone increases Na+ and HCO3 reabsorption).

3.     Milk-alkali syndrome (excessive milk and alkali “sodium bicarb” given for peptic ulcer).

-Hypokalemia (vomiting ==> hypovolemia ==> renin-angiotensin system activation ==> water and Na reabsorption in exchange for K+ and H+ “acidic urine”).

-Always measure urinary Cl- to aid in diagnosis:

   *Saline responsive (hypovolaemic states): Low urinary Cl although not with current
     diuretic therapy.

*Saline resistant (due to Cushing leading to hypervolaemia): High urinary Cl

-Compensation: Hypoventilation – HCO3 excretion – Retention of acid and ammonia.

RESPIRATORY ACIDOSIS
 

-Low pH; High PCO2; High HCO3.

-Emphysema – Pneumonia (hypoventilation) – Morphine, barbiturates, and anaesthetics – CHF – COPD.

-Comp: H+ excretion as NaH2PO4+ and NH4+ with generation and reabsorption of HCO3.

RESPIRATORY ALKALOSIS
 

-High pH, Low PCO2, Low HCO3.

-Hysterical over breathing (hyperventilation decreases CO2) - High altitude - Stimulation of resp. center due to brain injury.

-Low plasma Ca2+ (tetany) and K+.

-Compensation: HCO3 excretion  – NaH2PO4 and NH3+retention.

*Case Studies:

-Make a diagnosis.
-Explain biochemical changes.
-Suggest further tests.

1) A hyperventilating patient is suffering from untreated diabetes. Over the past several days, he has experienced thirst, frequent urination, weight loss, and fatigue. Analysis of his blood reveals:    

pH = 7.31

[HCO3-] = 18 mmol/L

pCO2 = 31 mmHg

K = 6.1 mmol/L

2) A patient with chronic bronchitis. Blood gas results are:

pH = 7.28

PCO2 = 71 mmHg;

HCO3 = 39 mmol/L

3) A young man with a history of dyspepsia and excessive alcohol intake with a 24-hour history of vomiting. Blood gas results showed:

pH = 7.49

PCO2 = 54 mmHg

HCO3 = 48 mmol/L

4) pH = 7.48; PCO2 = 49 mmHg; HCO3 = 38 mmol/L

5) pH = 7.37;
 PCO2  = 75 mmHg;
HCO3 = 37 mmol/L