There are number of parameters which are measured: ph Oxygen (O 2 ) Carbon Dioxide (CO 2 ) Bicarbonate (HCO 3 -) AaDO 2 O 2 Content O 2 Saturation

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1 Arterial Blood Gases (ABG) A blood gas is exactly that...it measures the dissolved gases in your bloodstream. This provides one of the best measurements of what is known as the acid-base balance. The body is an active chemical reaction, requiring a precise balance of the acids and bases, in a measurement known as ph. The normal ph is 7.40 (it can also be expressed as H + concentration, normal being 40). An arterial blood gas (ABG) is done on a patient to determine the amounts or Oxygen and Carbon Dioxide dissolved in the blood. Also to determine the Acid/Base status of the blood. There are number of parameters which are measured: ph Oxygen (O 2 ) Carbon Dioxide (CO 2 ) Bicarbonate (HCO 3 -) AaDO 2 O 2 Content O 2 Saturation PH of the blood ph is the negative log of the Hydrogen Ion concentration. Simply put, its the measurement of the acidity or alkalinity of the blood. Most people know that the stomach produces acid, but many other processes do also. Muscles product lactic acid, CO 2 in the blood produces a mild acid, and other processes produce acid. The kidneys control the production and elimination of Bicarbonate (where we get HCO 3 ) which the body uses to buffer the acids produced. The body maintains the acid/base balance by the kidneys retaining HCO 3 and increasing the rate of breathing (lowering CO 2 ) when the ph is low (too acid). The kidneys eliminate HCO 3 and the rate of breathing is lowered (too some extent) when the ph is high (too alkaline). A normal ph value may be due to a compensated balance between both the respiratory side and the metabolic side. Compensation A primary metabolic derangement will be accompanied by some degree of respiratory compensation. The ability to detect the primary abnormality and the amount of compensation is hindered by other co-existing conditions causing respiratory acidosis and/or alkalosis. Also, coexisting medical problems can cause both metabolic acidosis and alkalosis.

2 PO 2 PO 2 is the amount of Oxygen dissolved in the blood plasma, not the amount held in the red blood cells bound to haemoglobin. The PO 2 is effected by the amount of oxygen in the air we breathe (20.9% at sea level), our depth and rate of breathing, the amount of air reaching the alveoli, and the amount able to move across the Alveolar/Capillary barrier (the tissue between the alveoli holding the air and the capillaries holding the blood). The body has receptor that react to the levels of oxygen in the blood, these receptors tell the brain to increase or decrease respirations. PCO 2 PCO 2 is the amount of Carbon Dioxide dissolved in the blood. The PCO 2, like PO 2, is affected by the depth and rate of breathing, and the amount of CO 2 that moves across the Alveolar/Capillary barrier. Note that CO 2 moves across this barrier easier than O 2. The amount of CO 2 increases with increased demands on the muscles, including those involved with respiration. There are also receptors for CO 2 that tell the brain to increase and decrease respiratory rate and depth. Note that these receptors are stronger than those for oxygen. The amount of carbon dioxide in the blood in the main drive to breathe. HCO 3 HCO 3, the bicarbonate ion and main buffering system of the body. The kidneys control the amounts of bicarbonate ions in the blood by eliminating or retaining the ion. CO 2 levels do affect HCO 3 to some extent, for every 10 to 15 mmhg increase of PCO 2 above 40 mmhb, the HCO 3 increases 1 meq/l. For every 5 mmhg decrease below the normal for PCO 2, the HCO 3 decreases 1 meq/l. B.E., or Base Excess, also relates to bicarbonate, plus the buffering effects of haemoglobin are taken into effect. Base Excess uses PCO 2, HCO 3, and the haematocrit (amount of red blood cells) to calculate the non-respiratory part of the acid/base balance. The O 2 Saturation is the total amount of oxygen bound to haemoglobin in the red blood cells in comparison to the total amount possible. For instance, if your O 2 Saturation is 50%, your haemoglobin is carrying only half of what it is capable of carrying. The O 2 Content is the sum of the oxygen carried by the red blood cells (O 2 Sat) plus the amount dissolve in the plasma (PO 2 ). 99% of the oxygen carrying capacity of blood is the haemoglobin and 1% is dissolved in blood plasma. Therefore, O 2 Content is affected most by the amount of haemoglobin or red blood cells present in the blood stream. An anaemic person has a much lower capacity to carry oxygen than a normal person. The AaDO 2, the Alveolar/Arterial Oxygen Difference is the difference of the amount of oxygen in the alveoli and arteries. Normally this difference is about 10 to 15 mmhg. If for some reason oxygen cannot make it across the alveolar/capillary barrier, this value and the difference between the oxygen in the lungs and the amount in the arteries increases.

3 Metabolic acidosis Metabolic acidosis can be due to a variety of conditions. Treatment of metabolic acidosis is treatment of the cause. Direct administration of alkali (sodium bicarbonate) is reserved for severe cases. A number of conditions can result in metabolic acidosis, the most important among them being the under perfusion of tissues resulting in accumulation of lactic acid. Differentiation of the causes of metabolic acidosis requires the estimate of an entity called the 'anion gap'. Anion gap Body fluids including blood may contain a variable number of ions, but the total number of anions (negative ions) and cations (positive ions) are roughly the same. The ions that are usually measured in blood are cations like sodium and potassium and anions including chloride and bicarbonate. The measured cations are usually greater than the measured anions by about 8-16mmol/L. This is because the unmeasured anions constitute a significant proportion of the total number of anions in blood. Proteins make this up predominantly, but also included are sulphates, phosphates, lactate and ketones. Causes of a decreased anion gap include hypoalbuminaemia and severe haemodilution. Rarer causes include increase in minor cation concentrations like calcium and magnesium. Causes of a raised anion gap include dehydration and any cause of raised unmeasurable anions, like lactate, ketones and renal acids, along with treatment with drugs given as organic acids such as penicillin, salicylates and poisoning with methanol, ethanol and paraldehyde. Rarely it may be due to decreased minor cation concentrations such as calcium or magnesium. Metabolic Alkalosis Metabolic alkalosis can result from the loss of acid, addition of alkali or both in the kidneys or elsewhere. Extra renal sites include stomach (loss of acid), redistribution of alkali from the intracellular stores to the ECF (as in potassium or chloride depletion), oral administration (antacids, ion-exchange resins, milk alkali syndrome, oral HCO 3 -) and parenteral administration of alkali (citrate in blood transfusions, bicarbonate in severe metabolic acidosis). Renal causes of alkali excess include mineralocorticoid excess, response to long-standing hypercapnia (persists even after correction of respiratory acidosis), hypokalemia (promotes H+ secretion in the distal nephron) and ECF volume depletion (impaired HCO 3 - excretion). Certain conditions can cause metabolic alkalosis by a number of mechanisms (eg diuretic use causes both ECF depletion and hypokalemia). Respiratory Alkalosis The principal cause of respiratory alkalosis (hypocapnia) is hypoxia and its causes (type I respiratory failure), further treatment of which has been detailed before. Other causes of acute respiratory alkalosis include anxiety, fever, pain, sepsis, hepatic failure, CNS disorders (stroke, infections), pulmonary disorders without hypoxia (infections and interstitial lung disease), delirium tremens and drugs (salicylate intoxication). Chronic causes include high altitude hypoxia, chronic hepatic failure, chronic pulmonary disease, CNS trauma, anaemia, hyperthyroidism, beriberi and pregnancy (2,4). Treatment should be directed towards the cause.

4 Problems with arterial blood gas analysis ABG analysis is associated with a number of problems including Pain Pre analytical errors: air contamination, heparin dilution, storage, excessive delay before analysis Analytical errors: accurate differences between models of blood gas analysers Post analytical errors: transcription errors, delays in reporting results Infection risk to patient (particularly with arterial catheter) Infection risk to clinician (particularly with arterial puncture) Thrombosis and distal embolisation (particularly with arterial catheter) and ischemia Blood loss (particularly with arterial catheter), arterial spasm, haematoma Intermittent information Spontaneous variability of blood gas levels without clinical change in the patient Cost Conclusion Arterial blood gases can provide invaluable clinical information in critically ill surgical patients. It must however be remembered that they are static measurements and do not necessarily reflect the changing physiologic status of a sick patient. Therefore, any decision-making should be directed keeping in mind the overall condition of the patient and not the blood gas report alone. Picking up a major acid base disorder might not be as difficult as identifying other coexisting acid base imbalances which might be masked by the main disorder, but might also require active treatment. A person can have a mixture of any of these acid/base disorders. Normal values in an ABG report. Arterial Blood Venous Blood ph (H + ) (45 35) (45 35) pao 2 in kpa (mm Hg) (80-100) (37-42) paco 2 in kpa (mm Hg) (35-45) (42-50) HCO 3 mmols/l BE (Base Excess) +/-2 +/-2 Sat O 2 (%) >95% AaDO mmhg Anion Gap 8-16 mmols/l Osmolar Gap 10 mmols/l PaO 2 (mmhg)/fio 2 (%) More than 3

5 Glossary PaO 2 FiO 2 PaCO 2 H + ph SaO 2 HCO 3 Base excess Base deficit Acid-base balance Compensated acidosis/alkalosis Partial pressure of oxygen in arterial blood Fraction of oxygen in inspired air (0.21 for atmospheric air) Partial pressure of carbon dioxide in arterial blood Hydrogen ion concentration expressed in nmol/l Negative logarithm of (H+) expressed in nmol/l Percentage of haemoglobin which oxygenated (oxyhaemoglobin), i.e. oxygen saturation serum concentration of bicarbonate in mmol/l Quantity of acid or base necessary to titrate 1 litre of blood to ph 7.4 at 37 0 C with a PaCO 2 of 5.3kPa Negative base excess The state in which the ph of the blood is maintained at approximately between 7.35 and 7.45 Underlying acidosis/alkalosis, but the ph of the blood has been returned to normal by compensatory mechanisms.