Objectives Identify the indications/contraindications for blood gas sampling Discuss the process of ABG Highlight Acid base Regulation , ABG parameters and Acid base disorder To know the step wise approach of of acid base analysis of ABG
Milestones 1921 Barcroft and Nagahashi - aerotonometry for direct measurement of the partial pressure of oxygen in blood. Roughton and Scholander (1943) - idea of a one-piece syringe and gas analyser Clark's electrode(1956)- development of present commercial blood gas systems THE DEVELOPMENT OF BLOOD GAS ANALYSIS-C. S. BREATHNACH
Is Clinical Acid-base Interpretation Still a Problem A study in Australia from 2010- 29% of ABGs incorrectly interpreted by EM doctors. 31% incorrectly interpreted by critical care nurses ( 2011 Utah, USA) However, using graphical tools the result - approx. only 17% incorrectly interpreted. Austin K et al. Accuracy of interpretation of arterial blood gases by emergency medicine doctors. Emergency Medicine Australasia 2010;22:159-165 Doig AK et al. Graphical Arterial Bloood Gas Visualization Tool Supports Rapid and Accurate Data Interpretation. Computers Informatics Nursing 2011;29:204-211
Indication Of ABG
The results of ABG sampling only reflect the physiological state of the patient at the time of sampling I t is important they are correlated with the evolving clinical scenario and changes in a patient’s treatment
Contraindication
Hazards
Procedure for Radial Artery Puncture The radial artery is the one most often used in practice in the acute care setting because of easy access and the fact that the artery is superficial and easily palpated. Prior to any attempt at arterial puncture the practitioner must perform the Modified Allen’s Test
Modified Allen’s Test To determine that collateral circulation is present from the ulnar artery in the event of thrombosis of the radial artery. Position the patient’s arm on a firm flat surface with the wrist extended (Compress both the radial and ulnar arteries with the index and middle fingers of both hands Ask the patient to clench and unclench fist until blanching of distal skin occurs Release pressure over the ulnar artery and assess skin colour and refill – approximately 5 seconds after release of the artery, the extended hand should blush owing to capillary refilling . If blanching occurs, palmar arch circulation is inadequate and sampling could lead to ischaemia of the hand
pH stat management pH and pC02 of hypothermic blood to normal In Cardiopulm bypass- addition of Co2 via oxygenator Temperature correction of blood gas samples is required to interpret the values from a hypothermic patient but measured at 37 degree Celsius Used in congenital heart disease especially in cooling prior to hypothermic circulatory arrest
Alpha stat management Alpha- refers to charge portion of histidine in imidazole residue Objective- to maintain biologic neutrality by preserving the alpha imidazole and protein charge state OH/H ratio and enzyme function during hypothermia Most common strategy in adult cardiopulmonary bypass Doesn’t invove supplement co2 Doesn’t require temperature correction
NORMAL VALUES pH 7.35 - 7.45 PaCO 2 35 - 45 mm Hg PaO 2 70 - 100 mm Hg SaO 2 93 - 98% HCO 3 ¯ 22 - 26 mEq /L Base excess -2.0 to 2.0 mEq /L
After sampling ABG analysis Alveolar ventilation Oxygenation PaO2 Sa02 PaO2 / FiO2 ratio arterial-Alveolar O2 gradient a-A O2 ratio Acid base balance
Alveolar Ventillation PaCO2=K*(VCO 2 /V A )= k* [VCO 2 /V E (1-V D /V T )] PaCO2- 35 - 45 mm Hg Hypercapnea > 45 mm Hg (Hypoventilation) Respiratory Acidosis Hypocapnea < 35 mm Hg (Hyperventilation) Respiratory Alkalosis
Oxygenation Pao2 80-108 mm hg PaO 2 = 120 − Age/3 HYPOXEMIA Mild (60-80) mmHg Moderate(40-60) mmHg Severe <40 mmHg
The Alveolar arterial gradient PAO2=104 mmHg PaO2=100mmHg Venous admixture A-a = 4 -25 mm Hg Alveolar Air Arterial Blood
PaO2/FiO2 ratio Another common measure of oxygenation Most often employed in ventilated patients. PaO 2 /FiO 2 ratio – 300 to 500 mmHg Normal < 300 mmHg abnormal gas exchange <200 mmHg hypoxemia
Acid Base Balance
Brownsted - lowry concept An acid is a proton donor and a base is a proton acceptor
Hydrogen Ion Concentration and pH(in aqueous solution) pH = -log [H + ] [H +] nEq /L = 24 x (PCO2 / [ HCO3]) Henderson-Hasselbalch equation pH = 6.1 + log HCO 3 0.03 x PCO 2
Abnormal acid-base balance Acid-base imbalances can be defined as acidosis or alkalosis. Acidosis is a state of excess H+ Acidemia results when the blood pH is less than 7.35 Alkalosis is a state of excess HCO3- Alkalemia results when the blood pH is greater than 7.45
Acid base Regulation Three mechanisms to maintain pH Respiratory (CO2) Buffer (in the blood: carbonic acid/bicarbonate, phosphate buffers, Hgb ) Renal (HCO 3 - )
A buffer is a substance that can give or accept protons i.e. H+, in a manner that tends to minimise changes in the pH of the solution. Usually buffers are composed of a weak acid (proton donor) and a weak base (proton acceptor) as shown in the following equation. Acid base Regulation
Classification of Acid base disorder
Secondary Response Designed to limit the change in H + produced by primary change in acid base disorder Accomplished by changing the other component of paCO2/ HCO3 ratio in same direction Is not compensatory response
Metabolic Acidosis
Response to metabolic Acid Base Disorder Involves change in minute ventilation mediated by peripheral chemoreceptors located in carotid bifurcation and response to brain pH Metabolic acidosis: Increase in minute ventillaion ( Vt and RR)- Subsequent decrease in PaCO2 Appears in 30-120 minutes and take upto 24 hrs PaCO2= 1.2* HCO3 Expected PaCO2= 40-[1.2 * (24- current HCO3)]
Metabolic Alkalosis
Response to metabolic Acid Base Disorder Metabolic Alkalosis Decrease in Minute ventilation and increase in PaCO2 Not vigorous as response to metabolic acidosis – peripheral stimulator not active PaCO2= 0.7* HCO3 Expected PaC02=40+[0.7*(current HCO3-24)]
Response to Respiratory acid base disorder Secondary response to change in PaCO2 occurs in the kidneys – HCO3 absorption in proximal tubules adjusted to produce change in plasma HCO3 Relatively slow and can take 2-3 days to reach completion
Response to Respiratory acid base disorder Acute Respiratory disorder Acute change in PaCO2 have small effect on plasma HCO3 Acute Respiratory Acidosis HCO3=0.1* PaCO2 Acute Respiratory alkalosis HCO3=0.2* PaCO2
Response to Respiratory acid base disorder Chronic Respiratory disorders Increase in PaCO2- increase HC03 reabsorption in proximal tubules- raises HCO3 Decrease in PaC02- lowers HCO3 reabsorption – lowers plasma HCO3 HCO3=0.4* PaCO2 Chronic Respiratory acidosis Expected HCO3=24 + [ 0.4*(current PaCO2-40)]
Response to Respiratory acid base disorder Chronic respiratory alkalosis Expected HCO3=24-[0.4*(40-current PaCO2)]
Respiratory Acidosis
Respiratory alkalosis
STEPWISE APPROACH TO ACID-BASE ANALYSIS Stage I: Identify the Primary Acid-Base Disorder PaCO2 and pH are used to identify the primary acid base disorder . Rule 1 : If the PaCO2 and/or the pH outside the normal range - acid-base disorder.
STEPWISE APPROACH TO ACID-BASE ANALYSIS Rule 2(ROME) If the PaCO2 and pH are both abnormal- the directional change is compared 2a. If the PaCO2 and pH change in the same direction, there is a primary metabolic acid-base disorder. 2b. If the PaCO2 and pH change in opposite directions, there is a primary respiratory acid-base disorder.
pH- 7.12 PaCO2- 23.7 mm HG Primary metabolic acidosis
p H – 7.33 PaC02-56.4 mm hg Primary Resp disorder Primary respiratory acidosis
Response to Respiratory acid base disorder Rule 3 pH or PaCO2 is abnormal - mixed metabolic and respiratory disorder (i.e., equal and opposite disorders). 3a If the PaCO2 is abnormal, the directional change of PaCO2 identifies the type of respiratory disorder (e.g., high PaCO2 indicates a respiratory acidosis), and the opposing metabolic disorder 3b. If the pH is abnormal, the directional change in pH identifies the type of metabolic disorder (e.g., low pH indicates a metabolic acidosis) and the opposing respiratory disorder .
Ph-7.37 and PaCO2- 27.2 mmhg PaCO2- abnormal Mixed metabolic and resp disorder PaC02- low – resp alkalosis metabolic disorder- acidosis Primary metabolic acidosis with respiratory alkalosis
STEPWISE APPROACH TO ACID-BASE ANALYSIS Stage II: Evaluate the Secondary Responses The goal in Stage II - determine if there is an additional acid base disorder . Rule 4 : For a primary metabolic disorder, if the measured PaCO2 is higher than expected-secondary respiratory acidosis I f the measured PaCO2 is less than expected-secondary respiratory alkalosis.
STEPWISE APPROACH TO ACID-BASE ANALYSIS Rule 5 : For a primary respiratory disorder, a normal or near-normal HCO3 indicates that the disorder is acute .
STEPWISE APPROACH TO ACID-BASE ANALYSIS Rule 6: For a primary respiratory disorder HCO3 is abnormal , the expected HCO3 for a chronic respiratory disorder is determined 6a. Chronic respiratory acidosis , HCO3 < expected , - incomplete renal response HCO3>expected-secondary metabolic alkalosis 6b. chronic respiratory alkalosis, if the HCO3 > expected- an incomplete renal response , HCO3< expected - secondary metabolic acidosis.
If primary disorder is respiratory < 0.3–Chronic >0.8–acute 0.3–0.8–acute on chronic
STEPWISE APPROACH TO ACID-BASE ANALYSIS Stage III: Use The “Gaps” to Evaluate a Metabolic Acidosis The final stage of this approach is for patients with a metabolic acidosis, where the use of measurements called gaps can help
GAPS Anion gap The difference between unmeasured anion and cation Rough estimation of relative abundance of unmeasured anion Measured cation – measured anion AG(UA-UC)= Na- (Cl+ HCO3) 8-16 meq /L
GAPS Influence of albumin Albumin is principle unmeasured anion .. weak acid contribute 3meq/l to AG for each 1gm/dl albumin in plasma AGc (corrected AG) =AG+2.5*(4.5-Albumin)
Metabolic Acidosis
Gap Gap Ratio (delta ratio) In the presence of High anion Gap metabolic acidosis – presence of another metabolic acid base disorder Delta rato =AG excess/HCO3 Deficit =(AG-12)/ (24-HCO3)
Gap Gap Ratio (delta ratio)
Base excess and deficit Defined as the amount of acid (or base) required to be added to whole blood to achieve a pH of 7.4 at 37˚C and paCO2 of 40mmHg . -2 to + 2 If the base is in excess- may be due to decrease in metabolic acids may be due to increase in buffers (e.g. HCO3-) If the base is in deficit may be due to excess metabolic acids
Samples ABG -1 , 2 and 3 What is the primary acid base disorder?? What is the compensation What is the secondary response?? Final impression??
Can there be negative anion Gap??
Samples were obtained from 4 climbers who had just submitted Mount Everest at 8400 meter without 02 PB of 272 mm hg and PI02 of 47 mm Hg Alveolar o2 – 30 mmhg and had increased A-a gradient All had normal psychomotor function-result of aclimatization Pa02 – normal once they descended to 7000 meter Grocott MP et al . Arterial Blood Gases and Oxygen content in Climbers on Mount Everest. N Engl J Med. 2009 Jan 8; 360 (2) :140-9.
Summary ABG-quantifies response to therapeutic intervention, diagnostic evaluations , assess early goal-directed therapy and monitor severity and progression of documented disease processes Ventilation Status Oxgenation Status Normal , Acidemia Or Alkalemia ? Respiratory Or Metabolic Or Mixed? If Respiratory – Acute Or Chronic? If Metabolic – Anion Gap/Delta Gap? Is Compensation Adequate?
Summary ABG sampling- reflect the physiological state of the patient -correlation with the evolving clinical scenario and changes in a patient’s treatment
References The ICU Book 4th edition- Marino Clinical Anesthesiology- Morgan 5 th Edition The D evelopment of Blood G as A nalysis --C. S. Breathnach www.acutecaretesting.org www.derrangedphysiology.com Blood Gas and Critical Care Analyte Analysis