Arterial Blood Gases (ABG) PDF

RTT 125 – Arterial Blood Gases Metabolism and Arterial Blood Sampling Reading Resources ▪ Clinical Blood Gases: Chapter 1 & 3 ▪ Respiratory Care Anatomy and Physiology: Chapter 23 pg. 414-417 WHY THE ARTERIAL BLOOD GAS?  ▪ The ABG aids in diagnosis, assessment and trea...

RTT 125 – Arterial Blood Gases Metabolism and Arterial Blood Sampling Reading Resources ▪ Clinical Blood Gases: Chapter 1 & 3 ▪ Respiratory Care Anatomy and Physiology: Chapter 23 pg. 414-417 WHY THE ARTERIAL BLOOD GAS?  ▪ The ABG aids in diagnosis, assessment and treatment ▪ Provides information on pH, PaCO2 (mmHg), PaO2 (mmHg), HCO3 (mEq/L), and oxygen (or other gas) saturation in ARTERIAL blood. ▪ pH ▪ Indicates the body’s acid/base status. Can be altered by metabolic and respiratory components (CO2 or HCO3 or other acid). ▪ PaCO2 ▪ Indicative of ventilation adequacy. THE ABG ▪ PaO2 ▪ The amount of oxygen dissolved in the blood. Usually correlates to the SpO2. ▪ Allows the clinician to make a clinical judgment about oxygenation status at the tissues. ▪ HCO3 ▪ Bicarbonate, a byproduct of metabolism. This is the body’s largest acid buffer system and can significantly affect the pH. HCO3 levels are primarily managed by the kidney. ABG or VBG? Which would you choose, and why?  ▪ The arterial blood gas is the gold standard ABG or for assessment, diagnosis and management of oxygenation and acid- VBG: base disorders. ▪ However, the venous blood gas can Purpose reliably assess pH, PvCO2 and HCO3. The VBG is a reflection of local Dependent metabolism and is prone to more variability with unstable patients (i.e., hypotension, cardiac arrest). Metabolism ▪ The sum of all the chemical process in the body, resulting in growth, the generation of energy and other bodily functions. Metabolism has two steps: catabolism and anabolism. ▪ Catabolism: the destruction of complex molecules to create energy. ▪ Anabolism: the creation of more complex molecules from simpler molecules, requiring the addition of energy. Carbohydrates ▪ Also known as carbs, saccharides, sugars, etc. ▪ Primary energy source – they are easily absorbed into the bloodstream. ▪ Simple sugars are absorbed as glucose, more complex saccharides require glycogenolysis to be transformed to glucose in the liver. ▪ Other molecules like pyruvic acid, lactic acid, amino acids and glycerol can be transformed to glucose via gluconeogenesis (also primarily in the liver). ▪ Excess blood glucose ▪ Excreted in the urine when blood levels are abnormally high. ▪ Converted to fat for storage as adipose tissue. ▪ Stored in muscle as glycogen. ▪ When needed, glucose is utilized in the tissues in oxidation to produce energy. Protein ▪ Primarily for the growth, repair and maintenance of tissues (i.e., hemoglobin, muscle mass, enzyme buffers, etc.) ▪ RNA and DNA contain amino acid building blocks. ▪ Hormonal function relies on proteins to transfer messages and perform enzymatic reactions. ▪ Absorbed in the intestine as amino acids (digested protein). Amino acids are also utilized from the breakdown of tissue protein within the body. ▪ The liver synthesizes certain amino acids and plasma proteins. ▪ Through oxidation, protein can be broken down and will produce CO2, H2O and energy (citric acid cycle). This process produces urea. Lipids ▪ Function as energy stores, signal and transport molecules and provide structural support to cell membranes. ▪ Absorbed via the intestine, utilized from adipose tissue or manufactured by the liver from glucose, pyruvic acid, acetic acid and amino acids. ▪ The production glucose from lipids results in the formation of ketone bodies (keto acid). Although a normal process in the presence of low blood glucose levels, this process can dramatically alter the body’s pH level, inducing a condition called metabolic acidosis. Respiratory Quotient for Macromolecules ▪ Each metabolic process results in the production of at least CO2, H20 and energy. ▪ The respiratory quotient is the volume of CO2 produced each minute compared to the volume of O2 consumed each minute. ▪ CO2 produced each minute = VCO2 O2 consumed each minute VO2 ▪ Carbohydrate metabolism RQ is 1.0 ▪ Example: C6H12O6 + 6O2 = 6H20 + 6CO2 + energy ▪ Fat metabolism RQ is 0.7 ▪ Protein metabolism RQ is 0.8 ▪ The whole body has an RQ of 0.8 ▪ 200 ml CO2/min 250 ml O2/min ATP ▪ Adenosine triphosphate ▪ The primary and most useable form of energy within the body. ▪ Provides energy for enzymatic reactions, muscle contractions, metabolic functions, etc. ▪ ATP is made in the mitochondria of the cell. Citric Acid Cycle (Krebs Cycle) The process of oxidative phosphorylation ▪The complete oxidation of glucose, in the presence of oxygen, yields 38 ATP. ▪Only yields 2 ATP without the presence of oxygen. ▪Anaerobic metabolism produces an abundance of lactic acid which will reduce the body’s amount of natural buffer (HCO3). What are some other mechanisms of hypoxia? How might we end up with a low HCO3 in an ABG sample? Arterial Blood Gas Sampling ▪ We will discuss the technique, complications and procedure in lab. Preparation and Pre-analytical Considerations 1. Anticoagulants and Bleeding Disorders ▪ Some patients have medication to prevent blood clots, this can pose a serious risk to arterial puncture. There are lab tests to measure their risk of bleeding ▪ PT (Prothrombin Time) and INR (International Normalized Ratio) ▪ PT and INR are measurements of patient’s extrinsic clotting or the clotting tendency of blood. Medication like warfarin, heparin, Eliquis, conditions like liver damage and low vitamin K supply will increase the PT and INR ▪ PT = 9-14s ▪ INR = 0.9-1.2s ▪ aPTT (Activated partial thromboplastin time ) - 25 - 39 s ▪ PTT: intrinsic clotting pathway and is increased with heparin therapy ▪ ABG Sample - Simple Example Arterial Blood Gas Sampling Preparation and Pre-analytical Considerations 2. Status of the Patient ▪ The patient should be in a steady state. When you take an ABG, it only provides information about the patient at the time it was taken. ▪ Ideally, you would wait for 15-20 minutes for a patient to stabilize following a therapeutic intervention like ventilation changes, O2 changes, etc. 3. Temperature of the Patient ▪ A decrease in temperature will result in a decrease in PaCO2, increase in pH and decrease in PaO2. Often, ABG machines or a hospital lab will require a patient temperature for calibration. If they do not, consider the patient temperature during interpretation. Arterial Blood Gas Sampling ABG Sampling Errors (Chapter 3) ▪ Many things can cause an erroneous value to be obtained when testing the ABG. The responsibility of the RT is to minimize or account for any potential errors during the pre-analytical phase of ABG sampling. ▪ Possible sources of error: ▪ Air bubbles in the sample: PaCO2 will trend to 0, PaO2 will rise to atmospheric levels. ▪ Time to testing exceeded (30 min): metabolism will continue within the sample causing increased PaCO2, decreased pH and decreased PaO2. ▪ Heparin dilution: will cause a drop in PaCO2 and since heparin is slightly acidic, it will also drop the pH. ▪ Venous sampling: blood will not equate to arterial values. The blood in the VBG sample will not be red (deoxygenated hemoglobin) in a well oxygenated patient. Arterial Blood Gas Sampling Avoiding Errors Choose a bounding artery (strong, palpable pulse). Verify saturations with the oximeter during procedure (to correlate). Proper needle size. Ensure sample is adequately heparinized (plastic syringes will predominately come with heparin inside). Take your time to properly position the patient. Take a large enough sample for the machine to run (1.5-3mL for adults).  Oxygen Transport RTT125 Learning Objectives and Reading Resources ▪ CLO: 2.0, 3.5, 3.6 ▪ Reading Resources: ▪ Clinical Blood Gases: Chapter 7 ▪ Respiratory Care Anatomy and Physiology: Chapter 8 Oxygen Content Oxygen is carried in the blood in 2 distinct ways: 1. Dissolved in the blood ▪ 0.003 mL O2/100 mL of blood/mmHg 2. Combined with hemoglobin (Hb) ▪ 1.34 mL/O2/g of Hb (at 100% saturation) The total volume of dissolved oxygen + the total volume of combined oxygen is the TOTAL OXYGEN CONTENT Hb x SaO2 x 1.34 mL/O2/g Hb + (0.003 mL O2/100 mL of blood/mmHg) Total Oxygen Content Dissolved Oxygen Combined Oxygen Hemoglobin ▪ Each RBC (erythrocyte) contains roughly 280 million molecules of hemoglobin. ▪ The porphyrin molecule and ferrous ion combine with a covalent bond that composes the heme group on the hemoglobin molecule. There are four hemes per globin in hemoglobin, allowing the hemoglobin molecule to carry 4 oxygen molecules. ▪ Normal hemoglobin levels: ▪ Men: 15 g/100 mL ▪ Women: 13-14 g/100 mL Oxyhemoglobin Dissociation Curve Shifts of the Curve Shifts of the Curve ▪ Which directional shift is better? Why? ▪ A – Normal ▪ B – Left shift (increased affinity) ▪ C – Right shift (decreased affinity) 2,3 Diphosphoglycerate (DPG) Organic phosphate group in erythrocytes These will bind with hemoglobin and reduce its affinity for O2, a sustained effect. Rapid compensatory mechanism. Hemoglobin Variants and Abnormalities ▪ Small changes in amino acid sequence cause structural and functional changes. ▪ Fetal Hemoglobin (variant) ▪ 2 alpha and 2 gamma chains, increased affinity (p50 is 20mmHg). ▪ Term infant has 80% fetal hemoglobin, decreases to normal HbA in 12 weeks – 1 year. ▪ Newborns also have higher amounts of hemoglobin (18 g%), increasing O2 supply. ▪ Carboxyhemoglobin (abnormality) ▪ CO bines to ferrous ion, preventing binding with O2. ▪ Hemoglobin affinity for CO is nearly 245 times greater than for O2. ▪ Additionally shifts curve to the left (figure 7-19) reducing O2 availability at the tissues. ▪ Measured using CO-oximetry. ▪ Treatment? Hemoglobin Variants and Abnormalities ▪ Methemoglobin (Variant) ▪ Ferrous ion is oxidized to the ferric state. ▪ Unable to transport O2. ▪ Normally about 1% of total Hb, increased by: ▪ Ingestion of amyl nirate or nitroglycerin, well water high in nitrates, nitric oxide administration. ▪ Hemoglobin S (variant) ▪ Predominate variant present in patients with sickle cell anemia. ▪ A small change in amino acid causes the HbS to crystalize and create obstructions to blood flow. The presence of 3 g/dL of deoxygenated hemoglobin in a capillary bed. Seen as a blue discolouration in the skin, centrally and Cyanosis peripherally. Calculation: [(Hb) x arterial (Hb % desat) + (Hb) x venous (Hb % desat)] / 2 Levels of Oxygenation PaO2 SaO2 Normal 97 97 80-100 95-100 Normal Range Hypoxemia