Arterial Blood Gas Analysis-Assesment of oxygenation Ventilation And A

Indications for Mechanical Ventilation & : 

Indications for Mechanical Ventilation & Dr. T.R.Chandrashekar Chief -Department of Critical Care K.R.Hospital , Bangalore Karnataka, India Arterial Blood Gas Analysis

Blood Gas Interpretation-means analyzing the data to determine patient’s state of:: 

Blood Gas Interpretation- means analyzing the data to determine patient’s state of: 2 Ventilation Oxygenation Acid-Base Discuss Indications for Mechanical Ventilation along with ABG interpretation and clinical examples

Slide 3: 

Approach to ABG Interpretation Assessment of Acid-Base Status Assessment of Oxygenation & ventilatory Status There is an interrelationship, but less confusing if considered separately….. Volume – Osmolality Electrolytes

Slide 4: 

Always mention and see… FiO 2 / ct Hb -----XXXX Diagnostics---- Blood Gas Report Measured 37.0 0 C pH 7.452 pCO2 45.1 mm Hg pO2 112.3 mm Hg Calculated Data HCO3 act 31.2 mmol / L O2 Sat 98.4 % O2 ct 15.8 pO2 (A -a) 30.2 mm Hg  pO2 (a/A) 0.78 Entered Data FiO2 % Ct Hb gm/dl -----XXXX Diagnostics----- Blood Gas Report 328 03:44 Feb 5 2006 Pt ID 3245 / 00 Measured 37.0 0 C pH 7.452 pCO2 45.1 mm Hg pO2 112.3 mm Hg Corrected 38.6 0 C pH 7.436 pCO2 47.6 mm Hg pO2 122.4 mm Hg Calculated Data HCO3 act 31.2 mmol / L HCO3 std 30.5 mmol / L B E 6.6 mmol / L O2 ct 15.8 mL / dl O2 Sat 98.4 % ct CO2 32.5 mmol / L pO2 (A -a) 30.2 mm Hg  pO2 (a/A) 0.78 Entered Data Temp 38.6 0C FiO2 30.0 % ct Hb 10.5 gm/dl The essentials of Blood gas… Calculated parameters Measured parameters

Why Order an ABG?: 

Why Order an ABG? Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management allows for optimal function of medications Acid/base status may alter electrolyte levels critical to patient status/care

Slide 6: 

Matching delivery = Requirement Assessment of Oxygenation O2 delivery is a Cardio-Respiratory function

Oxygen Cascade: 

Oxygen Cascade Atmospheric Air- 150 mmHg ( 21%) PAO2-Alveolar Oxygen-100 mmHg ( CO2 / Water Vapour) PaO2- 90mm Hg ( A-a difference) SaO2 ( can be measured if Co-oximeter / calculated ODC)- Limitations CaO2- Oxygen content ( 1.34 x Hb x Sao2) DaO2-Oxygen delivery- CaO2 x Cardiac output If A-a difference is more -does it tell us anything ?

Slide 8: 

O 2 CO 2 Alveoli PAO2 Atmospheric air /FIO2 Water vapour is added- Nose/ upper airway Alveolar Oxygen PaO 2 (2 % dissolved O2) Measured in ABG P(A-a)O 2 SaO2 O. D. C. Temp H+ 2,3-DPG 98% of O2 is Hb bound- 1.34 x Hb % x Sao2 CaO2-oxygen content +PaO2 x 0.003ml Oxygen Delivery=CaO2 x Cardiac output Cardiac output - SV x HR Preload / Afterload/ Contractility Oxygen delivery DO2 is a Cardio- Respiratory Function =

Slide 9: 

DO2-Oxygen delivery- CaO2 x Cardiac output Did oxygen delivery meet the demand? Patient with sepsis on ventilator has fever 103F ,BP 80/60 mmHg, HR 140/mt, PaO2 100 mmHg, PcO2 42 mmHg, PH 7.23, HCO3 20, SaO2 98% Hb 12 gm%, Not responding to Fluids/ inotropes Delivery (DO2 )looks OK How to assess the consumption? Lactate -Anaerobic meatabolism Lacti -time ScVo2 - oxygen saturation in Superior vena Cava ScVO2 DO2 Consumption O2

Slide 10: 

calculated PAO 2 CO2 O2 PaCO2=60 mmHg PAO2 = FIO2 (BP-47) – 1.2 ( PaCO2 ) =.21 (760-47) – 1.2 (60) = 150 – 72 = 78 An elevated PaCO 2 will lower the PAO 2 and as a result will lower the PaO2 FIO2 We always correlate PaO 2 with FiO 2 BUT…………………………. never forget to correlate with PaCO 2 PAO2=FIO2(Barometric Pressure-H2O)-1.2(PCO2) PAO2 = FIO2 (760– 47 mm Hg)- 1.2 (PaCO2) PAO2 = 0.21(713)-1.2(40)= 100 mmHg “1.2” is dropped when FIO2 is above 60%. 5 X FIO2=PaO2

A-aDo2: 

A-aDo 2 A-aDo 2 = PAO 2 -PaO 2 (from ABG)= 10-15 mmHg / Increases with age Increased P(A-a)O 2 -lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries. O 2 CO 2 PaO 2 Alveoli PAO2 P(A-a)O 2 Diffusion defect V/Q Mismatch-Dead Space Shunt P(A-a)O 2 signifies some sort of problem within the lungs

Oxygenation Physiology : 

Oxygenation Physiology PAO2 Diffusion defect Pao2 Shunt Does not respond to FIO2 Responds to FIO2 Diffusion defect is a rare cause 1µm Oxygenation over within 1/3 time If HR >240 it affects CO2 has over 20 times more Diffusion coefficient Severe ARDS/ILD CO2 Atmospheric air Nitrogen FIO2- O2 PaO2 V/Q Mismatch

Alveolar-arterial Difference: 

Alveolar-arterial Difference O 2 CO 2 Alveolar – arterial G. 100 - 45 = 55 ……………….Wide A-a Oxygenation Failure Wide Gap PCO 2 = 40 PaO 2 = 45 P A O 2 = 150 – 1.2 (40) = 150 - 50 = 100 Ventilation Failure Normal Gap PCO 2 = 80 PaO 2 = 45 PAO 2 = 150-1.2(80) = 150-100 = 50 Alveolar arterial G. 50 – 45 = 5 …………….Normal A-a

Interpretation of shunt fractions: 

Interpretation of shunt fractions <10% Normal 10-20% Mild shunt 20-30% Significant shunt >30% Critical shunt, even 100% O2 cannot restore Pao2

arterial-Alveolar O2 tension ratio : 

arterial-Alveolar O 2 tension ratio a/A ratio >0.75 normal 0.40-0.75 acceptable 0.29-0.39 poor <0.20 very poor

a/A ratio Nomogram: 

a/A ratio Nomogram

Oxygen Dissociation Curve: SaO2 vs. PaO2: 

Oxygen Dissociation Curve: SaO 2 vs. PaO 2 CaO2 A B

Which patient is more hypoxemic, and why?: 

Which patient is more hypoxemic, and why? Patient A : pH 7.48, PaCO 2 34 mm Hg, PaO2 85 mm Hg, SaO 2 95%, Hemoglobin 7 gm%- Patient B : pH 7.32, PaCO 2 74 mm Hg, PaO2 59 mm Hg, SaO 2 85%, Hemoglobin 15 gm%- Patient A: Arterial oxygen content = .95 x 7 x 1.34 = 8.9 ml O2/dl Patient B: Arterial oxygen content = .85 x 15 x 1.34 = 17.1 ml O2/dl Hypoxic/ Hypercarbic Anemic 98% of O2 is Hb bound- 1.34 x Hb % x Sao2 + ( 2% ) PaO2 x 0.003ml CaO2 =

The power of hemoglobin : 

The power of hemoglobin Normal Hypoxemia Anemia PaO2 90 mm Hg 45 mm Hg 90 mm Hg SaO2 98% 80% 98% Hb 15 g/dL 15 g/dL 7.5 g/ dL CaO2 200 ml/L 163 ml/L 101 ml/L % change - 18.6% - 49.5%

Slide 20: 

20 vol% 15 vol % O 2 Transport; Normal = C.O X arterial O 2 content 5 L blood x150 /L blood x 1.39 ml O2/g Hb (= 20 ml O 2 /dl blood, or 20 vol % = 1000 ml O 2 /min = 250 ml( oxygen consumption) 750 ml = Venous O 2 return( = 15 vol%) DO 2

ScVO2-60%-80% normal range: 

ScVO2-60%-80% normal range Is the central venous oxygen saturation measured from a CVP cannula Reflects the global balance between oxygen Delivery and consumption ScVO2 SVO2 ScVO2 Range 60-80% Normal 60-50% More extraction warning sign 50-30% Lactic acidosis Demand > Supply 30-20% Severe lactic acidosis Cell death > 5-7

Factors which alter ScVo2: 

Factors which alter ScVo2 Decreased Delivery DO2 Increased Consumption VO2 Fever, Shivering Trauma Pain / anxiety Dysarhythmia CCF/ MI Sepsis Hypoxia/hypoxemia Suctioning, ARDS/ COPD Hemorrhage Occult bleeding RBC disorders Anemia

Case ….: 

65 yr old male with DM IHD –in septic shock on ventilator ABG-PaO2-90 PH 7.42, PCO2 43 Hb-12 gm%, Spo2 98% CaCo2-17 Vol% BP 90/40 mmHg ,Temp 103F What is the problem ? ScVO2 48%, Lactate 8 mMoles/L Fluids Nor adrenaline / Dobutamine Fever control Case …. 65 yr old male with DM IHD –in septic shock on ventilator ABG-PaO2-90 PH 7.42, PCO2 43 Hb-12 gm%, Spo2 98% CaCo2-17 Vol% BP 90/40 mmHg ,Temp 103F What is the problem ? ScVO2 68%, Lactate 2 mMoles/L Microcirculatory Mitochondrial Dysfunction (MMDS) ScVo2

Lactate metabolism: 

Lactate metabolism Glucose Pyruvate Lactate Oxidative phosphorylation 2 ATP 36 ATP NAD+CO2+H2O O 2 + NADH Glycolysis ADP Cell Cytoplasm Mitochondria Oxygen

Energy Failure and Lacti-Time: 

c Energy Failure and Lacti-Time Aerobic metabolism 36 ATP Lack of O2 delivery Anaerobic metabolism 2 ATP + Lactic acid The time before lactate becomes less than 2 is important prognostic indicator-LACTI- TIME Septic patient admitted to ICU BP 90/50, HR 150/mt ScVO2-45%, Lactate 6 mmoles/L ,PH 7.16, PaO2/PCO2- 68/39 mmHg After 2hrs- fluid resuscitation/ Noradrenaline BP140/80 mmHg ScVo2-65% Lactate 3 mmoles /L After 2hrs- fluid resuscitation/ Noradrenaline BP 70/40 mmHg ScVo2-45% Lactate 7mmoles/L Microcirculatory mitochondrial dysfunction (MMDS)

Summary –Oxygenation assessment: 

Summary –Oxygenation assessment CaO2 x CO =Delivery ScVO2=consumption Lactate=Delivery not meeting demand Anaerobic metabolism- decreased ATP production -cell death Lacti-Time- prognostic indicator

Slide 28: 

Assessment of Ventilatory Status….

Slide 29: 

Oxygenation Acid-Base HCO3 PAO2 = FIO2 (BP-47) – 1.2 (PCO2) pH ~ ------------ PaCO2 PaO2 VCO2 x .863 PaCO2 = -------------------- VA VA=Minute ventilation-Dead space volume f(VT) – f(VD) PaCO2 is key to the blood gas universe; without understanding PaCO2 you can’t understand oxygenation or acid-base. The ONLY clinical parameter in PaCO2 equation is RR VCO2=CO2 production

Breathing pattern’s effect on PaCO2: 

Breathing pattern’s effect on PaCO2 Patient Vt f Ve Description A (400)(20) = 8.0L/min (slow/deep) B (200)(40) = 8.0L/min (fast/shallow) Patient Vt-Vd f Va A (400-150)(20) =5.0L/min (slow/deep) B (200-150)(40) =2.0L/min (fast/shallow) PaCO2 = alveolar ventilation Not on Minute ventilation which is measured Dead space quantification at bed side not possible

PaCO2 abnormalities…: 

Condition State of PaCO 2 in blood alveolar ventilation > 45 mm Hg Hypercapnia Hypoventilation 35 - 45 mm Hg Eucapnia Normal ventilation < 35 mm Hg Hypocapnia Hyperventilation PaCO2 abnormalities… PCO2-65 mmHg with rate 7/mt in Drug overdosage 65/7-true hypoventilation PCO2-65 mmHg with rate 37/mt in bilateral consolidation 65/37- Reduced alveolar ventilation/ dead space ventilation PCO2-22 mmHg with rate of 37/mt in post operative patient with pain and fever-Increased alveolar ventilation

Quantification of Dead space: 

Quantification of Dead space V D V T = 25-40% NORMAL (2ml/Kg) In MV pts till 55% is normal More than 60% is abnormal dead space

Quantification of Dead space : 

Quantification of Dead space VD/VT=(PaCO2-PETCO2)/PaCO2 Minute volume in liters Ҳ PaCO2(mmHg) Body weight in kg Normal index<5 More than 8 indicates an increase dead space Limitation-need to measure minute volume accurately Difficulties in sampling and accurate measurement limits the usefulness Of dead space in clinical practice

Case Scenarios ….: 

Case Scenarios …. 20 year old male with OP poisoning with fasciculation's, neck muscle weakness with RR 35/mt, increased WOB, SPO2 on 4l/mt on RBM 84%, pooling secretions, HR 150/mt on atropine drip, BP 140/60 ABG PH 7.37 Pao2-52 Pco2-32 Do we intubate this guy? YES Intubated minimal settings ABG stabilised Has Pulse oximeter/ ETCO2 Do we require to repeat ABG’s NO If pt develops hypotension On inotrope /not synchronising Yes

Treat the Patient not the ABG: 

Treat the Patient not the ABG ABG-PCO2-60mmHg, PO2-58mmHg with HR-80/min, BP- 130/80mmHg, RR-14/min, A 45 yr old patient with chronic neurological weakness conscious, comfortable ABG-PCO2-60mmHg, PO2-58mmHg and with HR-120/min,BP-100/70 mmHg,RR-40/min, A 24yr old asthmatic severe respiratory distress, drowsy Intubate

Case Scenario….: 

Case Scenario…. 40 yr old diabetic male pt with urinary sepsis Has BP 90/60 mmHg after fluid resuscitation, high dose noradrenaline,has tready pulse, is tachypenic 35/mt with increased WOB-is restless. On 6L of O2 RBM ABG PH-7.38 PaCO 2 -36 mmHg PCO 2- 100 mmHg Sao 2 -98%, ScVo2-50%, Lactate 6 mmoles/L Do we intubate this patient Normal respiratory effort-5% CO Nearly 20-30% CO Rest respiratory muscle and so CO is utilised by essential organs

Slide 37: 

55 year old chronic smoker, Diabetic male admitted with Lower limb cellulitis has Sepsis and Rt mid and lower zone pneumonia on 6L of O2 on RBM HR 140/mt BP 100/60 mmHg RR- 35 with increased WOB ABG PH-7.28 PaCO 2 -56 mmHg PCO 2 - 58 mmHg FIO2 70% Pao2-58 hypoxemic Pco2-56/35- decreased Alveolar ventilation Intubation

IF the same guy is already on 5L/O2 / on noradrenaline fluid resuscitation- we probably intubate: 

IF the same guy is already on 5L/O2 / on noradrenaline fluid resuscitation- we probably intubate 40 yr old male Diabetic in ketosis with pylonephritis Drowsy received in casualty- BP 70/50 mmHg, RR 28/mt, Fever-103F, HR 150/mt, WOB normal SC-1.6 WBC 20,000, LFT normal ABG done on room air PH-7.28 PCO 2 -36 mmHg PaO 2 - 58 mmHg HCO3 18 mmoles/L O2 4L RBM Fluids 2l Noradrenaline Imipenem +cilastin 1g IV, Paracetamol BP 140/80, HR 100/mt, UO 100ml/hr ABG PH-7.38 PaCO 2 -36 mmHg PCO 2 - 78 mmHg HCO3 20 mmoles/L Mentation better

Slide 39: 

A 29-year-old woman has excessive bleeding normal delivery has Hb of 5 g%, fluids-3L/mt given Bp 100/60mmHg HR 114/mt PH-7.38 PaCO 2 -33 mmHg PCO 2 - 78 mmHg HCO3 22 mmoles/L Cao2- 7 vol % ScVO2 55 % Lactate 5 mMoles/L What do we do? Packed cells FFP Platelet 1:1:1 (FFP to PRBC to platelets)

Slide 40: 

Causes of Respiratory failure Respiratory Center in Brain Neuromuscular Connections Thoracic Bellows Airways (upper & lower) Lung parenchyma (alveoli) Head injury Drug overdose Spinal cord injury Myopathies Myasthenia C COPD ARDS Brain Nerves Bellows Airways Alveoli It only requires one disrupted “link” to cause respiratory failure !

Some points which help us to decide when to ventilate patients?: 

Some points which help us to decide when to ventilate patients? Primary cause for Respiratory failure-time for the disease to resolve Hypoxemia on high FIO2 Increased PCO2 Increased WOB Airway protection ? +ABG values Do not treat the ABG, treat the patient If you’re not sure whether or not the patient needs a ventilator, the patient needs a ventilator

Acid Base analysis: 

Acid Base analysis

Slide 43: 

Basics [H+]= 40 nEq/L at pH-7.4 For every 0.3 pH change = [H+] double 160nEq/L 40 nEq/L 16nEq/L [ H + ] in nEq/L = 10 (9-pH)

Slide 44: 

Acid-Base Physiology

Slide 45: 

CO 2 + H 2 O H 2 CO 3 H + + HCO 3 - CO 2 H + HCO 3 - Acid-Base physiology Respiratory Metabolic Ventilation controls PCO2 Kidney losses H+ and reabsorbs bicarbonate (HCO3-) Bicarbonate is the transport from of CO2 hence should move in the same direction PCO2-Respiratory acidosis (Hypoventilation) PCO2-Respiratory alkalosis (Hyperventilation) HCO3- Metabolic acidosis HCO3- Metabolic Alkalosis

Slide 46: 

Very fast 80% in ECF Starts within minutes good response by 2hrs, complete by 12-24 hrs Starts after few hrs complete by 5-7 days

Slide 47: 

Acid-base Balance Henderson-Hasselbalch Equation [HCO 3 - ] pH = pK + log ------------- .03 [PaCO 2 ] For teaching purposes, the H-H equation can be shortened to its basic relationships: HCO 3 - ( KIDNEY) pH ~ -------------------- PaCO 2 (LUNG) Maximum compensation HCO3-= 40/10 CO2=60/10 24/40 36/60 24/40 18/30

Slide 48: 

Characteristics of  acid-base disorders DISORDER PRIMARY RESPONSES COMPENSATORY RESPONSE Metabolic acidosis  PH  HCO 3 -  pCO2 Metabolic alkalosis  PH  HCO 3 -  pCO2 Respiratory acidosis  PH  pCO2  HCO 3 - Respiratory alkalosis  PH  pCO2  HCO 3 -

How to identify the type of compensation…?: 

How to identify the type of compensation…? pH HCO 3 CO 2 7.20 15 40 7.25 15 30 7.37 15 20 Un Compensated Partially Compensated Fully Compensated ( pH abnormal ) ( pH in normal range )

Slide 50: 

Body’s physiologic response to Primary disorder in order to bring pH towards NORMAL limit Full compensation Partial compensation No compensation…. (uncompensated) BUT never overshoots, If a overshoot pH is there, Take it granted it is a MIXED disorder Compensation…. Normal functioning

Slide 51: 

Step 4 continued… RESPIRATORY disorders… Expected HCO 3 for a Change in CO 2 ......... 1 2 3 4 Acidosis…. (expected) HCO 3 = 0.1 x ∆ CO 2 Alkalosis…. (expected) HCO 3 = 0.2 x ∆ CO 2 Acidosis…. (expected) HCO 3 = 0.3 5 x ∆ CO 2 Alkaosis…. (expected) HCO 3 = 0.4 x ∆ CO 2 Acute respiratory Chronic respiratory HCO 3 - ( KIDNEY) pCO2 (LUNG) pH= what has changed ? CO2

Compensation : 

Compensation Metabolic Acidosis: Compensation Winters’ formula pCO2 = 1.5 x [HCO3-] + 8 ± 2 Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5

Slide 53: 

Na+ Unmeasured cations Unmeasured anions Cl- HCO3- ‘ Mind the gap’ cations = Anions Anion gap = metabolic acidosis

Slide 54: 

Anion Gap AG = [Na + ] - [Cl - +HCO3 - ] Elevated anion gap represents metabolic acidosis Normal value: 12 ± 4mmol/L Major unmeasured anions albumin phosphates sulfates organic anions

Mixed Acid-Base Disorders : Clues: 

Mixed Acid-Base Disorders : Clues -- Clinical history -- pH normal, abnormal PCO 2 and HCO 3 -- PCO 2 and HCO 3 moving opposite directions -- Degree of compensation for primary - disorder is inappropriate

Slide 56: 

Steps for Successful Blood Gas Analysis 7

Slide 57: 

2. Look at pH? 3. Look up HcO3-// PCo2 4. Match either pCO2ot the HCO3with pH 5. Fix the level of compensation. 6.If metabolic acidosis, calculate- Anion gap 7.Correlate clinically 1. Consider the clinical settings! Anticipate the disorder 7 steps to analyze ABG

First Step-Clinical History: 

First Step-Clinical History COPD- Chronic Respiratory Acidosis-Met alkalosis Asthma-Acute Respiratory Acidosis not well compensated Cardiac arrest-Acute Metabolic/Respiratory acidosis Septic shock-Acute Metabolic acidosis

The second step: 

The second step Look at the pH - Label it . pH of 7.30 , PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L. Na+ 143, CL-104 ACIDOSIS

Slide 60: 

Look at - pCO2. Label it. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L. Increased Normal pCO2 levels are 35-45mmHg. Below 35 is alkalotic, above 45 is acidic. The third step

Slide 61: 

look at the HCO3- Label it. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L INCREASED A normal HCO3 level is 22-26 mEq/L. If the HCO3 is below 22, the patient is acidotic. If the HCO3 is above 26, the patient is alkalotic

Slide 62: 

Next match either the pCO2 or the HCO3 with the pH to determine the acid-base disorder. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L pH is on acidotic side & PCO2 is increased. So it is respiratory acidosis The Fourth Step

Slide 63: 

Does either the CO2 or HCO3 go in the opposite direction of the pH? pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L To find the primary and what is compensatory HCO3 is going in opposite direction of pH. So it is metabolic compensation Fifth Step

Slide 64: 

Step 4 continued… RESPIRATORY disorders… Expected HCO 3 for a Change in CO 2 ......... 1 2 3 4 Acidosis…. (expected) HCO 3 = 0.1 x ∆ CO 2 Alkalosis…. (expected) HCO 3 = 0.2 x ∆ CO 2 Acidosis…. (expected) HCO 3 = 0.3 5 x ∆ CO 2 Alkaosis…. (expected) HCO 3 = 0.4 x ∆ CO 2 Acute respiratory Chronic respiratory HCO 3 - ( KIDNEY) pCO2 (LUNG) pH= what has changed ? CO2

Is the compensation full or partial??: 

Is the compensation full or partial?? Do the calculations…. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L PCO2 is increased by =40 HCO3-=should be increased by 4 i.e. 24+4=28( for full compensation)

Slide 66: 

Calculate the anion gap if it is more there is Metabolic acidosis AG = [Na+] - [Cl- +HCO3- ] Sixth Step pH of 7.30 , PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L. Na+ 143, CL-104 AG+143- (104+27)=140-131=12

Pathogenesis of Metabolic Acidosis with AG: 

Pathogenesis of Metabolic Acidosis with AG Fixed acid accumulation and low serum bicarbonate Renal failure Renal,GI Lactic Salicylate Ketones Methanol Phosphate Ethylene glycol HCl AG = [Na + ] - [Cl - +HCO3 - ]

Metabolic Acidosis……. + additional disorders: 

Metabolic Acidosis……. + additional disorders Equivalent rise of AG and Fall of HCO3…… …. Pure Anion Gap Metabolic Acidosis Discrepancy…….. in rise & fall + Non AG M acidosis, + M Alkalosis

PURE Anion Gap Acidosis +: 

PURE Anion Gap Acidosis + Delta gap = HCO 3 + ∆ AG Delta Gap = 24….Pure AG acidosis < 24 = non AG acidosis > 24 = metabolic alkalosis ∆ AG =Measured Anion gap-12 Delta Gap = 24 …… AG Met Acidosis < 24 ….. Non AG Met acidosis > 24 ….. Non AG Met acidosis + Meta. Alkalosis

Slide 70: 

Clinical correlation Finally

Slide 71: 

Step 4 continued… RESPIRATORY disorders… Expected HCO 3 for a Change in CO 2 ......... 1 2 3 4 Acidosis…. (expected) HCO 3 = 0.1 x ∆ CO 2 Alkalosis…. (expected) HCO 3 = 0.2 x ∆ CO 2 Acidosis…. (expected) HCO 3 = 0.3 5 x ∆ CO 2 Alkaosis…. (expected) HCO 3 = 0.4 x ∆ CO 2 Acute respiratory Chronic respiratory HCO 3 - ( KIDNEY) pCO2 (LUNG) pH= what has changed ? CO2

Compensation : 

Compensation Metabolic Acidosis: Compensation Winters’ formula pCO2 = 1.5 x [HCO3-] + 8 ± 2 Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5

Slide 73: 

pH............7.25 PaCO2.....58.5 HCO3.......25.1 Uncompensated Respiratory Acidosis pH = 7.4 PaCO2 = 40 HCO3 = 24 Post op pt –drowsy

Slide 74: 

pH............7.46 PaCO2.....34.0 HCO3.......26.0 Uncompensated Respiratory Alkalosis pH = 7.4 PaCO2 = 40 HCO3 = 24 Pt on vent pressure support has pain Acute asthmatic

Slide 75: 

pH............7.39 PaCO2.....39.0 HCO3.......23.4 Normal A.B.G. pH = 7.4 PaCO2 = 40 HCO3 = 24

Slide 76: 

pH............7.34 PaCO 2 .....33.9 HCO 3 .......18.2 Partially compensated Metabolic Acidosis pH = 7.4 PaCO2 = 40 HCO3 = 24 20 yr old male with Acute Gastroenteritis…..

Slide 77: 

Case A 46-year-old man has been in the hospital for two days with pneumonia. He was recovering but has just become diaphoretic, dyspneic, and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min. pH 7.41 PaCO 2 20 mm Hg HCO3- 12 mEq/L CaO2 17.2 ml O2/dl PaO 2 80 mm Hg SaO 2 95% Hb 13.3 gm% How would you characterize his state of oxygenation, ventilation, and acid-base balance? Normal pH Respiratory alkalosis and Metabolic acidosis. Winters formula pCo2=1.5 x 12 +8=26

Case: 

Case Mrs. H is found pulseless and not breathing this morning. After a couple minutes of CPR she responds with a pulse and starts breathing on her own. A blood gas is obtained: pH----------- 6.89 pCO 2 ------- 70 pO2 --------- 42 HCO3------- 13 SaO2-------- 50% What is your interpretation? What interventions would be appropriate for Mrs. H? Mrs. H has a severe metabolic and respiratory acidosis with hypoxemia

Case …..: 

Case ….. A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea. Electrolyte results: BP 90/60 mmHg Na+ 134, K+ 2.9, Cl- 108, BUN 31, Cr 1.5. ABG: pH 7.31 PCO2 33 mmHg HCO3 16 PaO2   93 mmHg What is the acid base disorder? History Acidosis from diarrhea or lactic acidosis as a result of hypovolemia and poor perfusion.

Normal anion gap acidosis with adequate compensation: 

Normal anion gap acidosis with adequate compensation Look at the pH- acidemic . What is the process? Look at the PCO2, HCO3- . PCO2 and HCO3- are abnormal in the same direction , therefore less likely a mixed acid base disorder. Calculate the anion gap The anion gap is Na - (Cl + HCO3-) = 134 -(108 + 16) = 10 Is compensation adequate ? Calculate the estimated PCO2. Winter's formula; PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.

Case....: 

Case.... A 50 year old insulin dependent diabetic woman was brought to the ED by ambulance. She was semi-comatose and had been ill for several days. Current medication was digoxin and a thiazide diuretic for CHF. Lab results Serum chemistry: Na 132,  K  2.7,  Cl  79,  Glu  815, Lactate 0.9   urine ketones 3+ ABG:  pH 7.41  PCO2 32 HCO3- 19     pO2 82 History : Elevated anion gap acidosis secondary to DKA Metabolic alkalosis in the setting of thiazide diuretics use.

Case......: 

Case...... 2 . Look at the pH . -     Note that the pH is normal which would suggest no acid base disorder. But remember, pH may be normal in the presence of a mixed acid base disorder. 3 . What is the process? Look at the PCO2, HCO3- . PCO2 is low indicating a possible respiratory alkalosis. The HCO3- is also low indicating a possible metabolic acidosis. Because the pH is normal, we are unable to distinguish the initial, primary change from the compensatory response. We suspect however that the patient has DKA, and therefore should have a metabolic acidosis with an anion gap that should be elevated. We can confirm this by calculating the anion gap. 4 . Calculate the anion gap The anion gap is Na - (Cl + HCO3-) = 132 -(79 + 19) = 34 Since gap is greater than 16, it is therefore abnormal and confirms the presence of metabolic acidosis. Why is the pH normal? If the patient has metabolic acidosis, we suspect a low ph unless there is another process acting to counteract the acidosis, i.e alkalosis.

Delta Gap 34-12=22 + 19=41 Met alk: 

Delta Gap 34-12=22 + 19=41 Met alk Since the delta ratio is greater than 2, we can deduce that there is a concurrent metabolic alkalosis . This is likely due to to the use of thiazide diuretic. Note that DKA is often associated with vomiting, but in this case;vomiting was not mentioned. Another possibility is a pre-existent high HCO3- level due to compensated chonic respiratory acidosis. But we have no reason to suspect chronic respiratory acidosis based on the history. Assessment : Mixed elevated anion gap metabolic acidosis and metabolic alkalosis likely due to DKA and thiazide diuretics.

THANKS: 

THANKS chandrakavi@gmail.com I shall practice gentle mechanical ventilation and not try to bring ABG to perfect normal. I shall treat the patient not the ABG report I shall always correlate ABG report clinically

Slide 85: 

PaO2 O2 CASCADE AIR ALVEOLAR POST PULMONARY ARTERIAL Hb MICRO- CIRCULATION MIXED VENOUS