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Arterial blood gas analysis assesment of oxygenation ventilation and acid base
 

Arterial blood gas analysis assesment of oxygenation ventilation and acid base

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ABG analysis of oxygenation/ ventilation /Acid base and indications of mechanical ventilation

ABG analysis of oxygenation/ ventilation /Acid base and indications of mechanical ventilation

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  • This simplistic picture shows the arterial blood being oxygenated and then returned to the right side of the heart after 5 volumes% oxygen has been extracted from it. The average arterial (20 vol%) and mixed venous (15vol%) oxygen content are also shown.
  • Figuratively speaking the metabolism of lactate is a cul-de-sac as it can only be converted from and into pyruvate. The key take home messages from this schematic flow diagram are that anything that causes pyruvate to accumulate will result in accumulation of lactate. Broadly speaking theses are A big push on glycolysis such that it overwhelmes the mitochondria A block on mitochondrial function either because there is no oxygen or reducing agent or there is other inflammatory mediated enzymatic dysfunction.

Arterial blood gas analysis assesment of oxygenation ventilation and acid base Arterial blood gas analysis assesment of oxygenation ventilation and acid base Presentation Transcript

  • 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: Discuss Indications for Mechanical Ventilation along with ABG interpretation and clinical examples Ventilation Oxygenation Acid-Base
  • 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
  • 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 Calculated parameters Measured parameters
  • 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
    • Matching delivery
    • =
    Requirement Assessment of Oxygenation O2 delivery is a Cardio-Respiratory function
  • 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 ?
  • 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 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 = O. D. C.
    • 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
  • 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
    • 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 We always correlate PaO 2 with FiO 2 BUT…………………………. never forget to correlate with PaCO 2
  • 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 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 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 <10% Normal 10-20% Mild shunt 20-30% Significant shunt >30% Critical shunt, even 100% O2 cannot restore Pao2
  • 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
  • Oxygen Dissociation Curve: SaO 2 vs. PaO 2 CaO2 A B
  • 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 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%
  • 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
    • Is the central venous oxygen saturation measured from a CVP cannula
    • Reflects the global balance between oxygen
      • Delivery and consumption
    ScVO2 SVO2 > 5-7 ScVO2 Range 60-80% Normal 60-50% More extraction warning sign 50-30% Lactic acidosis Demand > Supply 30-20% Severe lactic acidosis Cell death
  • 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 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 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 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
    • CaO2 x CO =Delivery
    • ScVO2=consumption
    • Lactate=Delivery not meeting demand Anaerobic metabolism- decreased ATP production -cell death
    • Lacti-Time- prognostic indicator
    • Assessment of Ventilatory Status….
    • 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
    • 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 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
    • 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
    • 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 ….
    • 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
    • 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….
    • 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
    • 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
    • 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
    • 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)
  • Causes of Respiratory failure Respiratory Center in Brain Neuromuscular Connections Thoracic Bellows Airways (upper & lower) Lung parenchyma (alveoli) It only requires one disrupted “link” to cause respiratory failure ! Head injury Drug overdose Spinal cord injury Myopathies Myasthenia C COPD ARDS Brain Nerves Bellows Airways Alveoli
  • 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
  • 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)
  • Acid-Base Physiology
  • 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
  • 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
  • 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
  • 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 -
  • Un Compensated Partially Compensated Fully Compensated ( pH abnormal ) ( pH in normal range ) pH HCO 3 CO 2 7.20 15 40 7.25 15 30 7.37 15 20
  • Normal functioning 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
  • 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
    • Metabolic Acidosis: Compensation
    • Winters’ formula
    • pCO2 = 1.5 x [HCO3-] + 8 ± 2
    • Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5
  • Na+ Unmeasured cations Unmeasured anions Cl- HCO3- ‘ Mind the gap’ cations = Anions Anion gap = metabolic acidosis
  • 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
    • -- 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
  •  
  • 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
    • 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
    • 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
    • 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
    • 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
    • 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
    • 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
  • 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??
    • 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)
    • 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 Fixed acid accumulation and low serum bicarbonate Renal failure Renal,GI Lactic Salicylate Ketones Methanol Phosphate Ethylene glycol HCl AG = [Na + ] - [Cl - +HCO3 - ]
  • Equivalent rise of AG and Fall of HCO3…… … . Pure Anion Gap Metabolic Acidosis Discrepancy…….. in rise & fall + Non AG M acidosis, + M Alkalosis
    • 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
  • Finally
  • 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
    • Metabolic Acidosis: Compensation
    • Winters’ formula
    • pCO2 = 1.5 x [HCO3-] + 8 ± 2
    • Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5
  • pH............7.25 PaCO2.....58.5 HCO3.......25.1 Uncompensated Respiratory Acidosis pH = 7.4 PaCO2 = 40 HCO3 = 24 Post op pt –drowsy
  • 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
  • pH............7.39 PaCO2.....39.0 HCO3.......23.4 Normal A.B.G. pH = 7.4 PaCO2 = 40 HCO3 = 24
  • Partially compensated Metabolic Acidosis pH = 7.4 PaCO2 = 40 HCO3 = 24 20 yr old male with Acute Gastroenteritis…..
  • 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
    • 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 …..
    • 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
    • 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....
    • 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......
    • 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
    • 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.
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    • 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
  • PaO2 O2 CASCADE AIR ALVEOLAR POST PULMONARY ARTERIAL Hb MICRO- CIRCULATION MIXED VENOUS