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  Indications for Mechanical Ventilation &   ,[object Object],[object Object],[object Object],[object Object],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? ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],Requirement Assessment of Oxygenation O2 delivery is a Cardio-Respiratory function
Oxygen Cascade ,[object Object],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.
[object Object],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 ,[object Object],[object Object],[object Object],[object Object],5 X FIO2=PaO2 We always correlate PaO 2  with FiO 2   BUT…………………………. never forget to correlate with PaCO 2
A-aDo 2 ,[object Object],[object Object],[object Object],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 ,[object Object],[object Object],[object Object],[object Object],[object Object]
a/A ratio Nomogram
Oxygen Dissociation Curve:  SaO 2  vs. PaO 2 CaO2 A  B
Which patient is more hypoxemic, and why? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],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 ,[object Object],[object Object],[object Object],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 ,[object Object],[object Object],[object Object],[object Object]
[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],PaCO2 is key to the blood gas universe; without understanding PaCO2 you can’t understand oxygenation or acid-base.  ,[object Object],VCO2=CO2 production
Breathing pattern’s effect on PaCO2 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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 ,[object Object],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 ,[object Object],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 …. ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],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 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Intubate
Case Scenario…. ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Normal respiratory effort-5% CO Nearly 20-30% CO Rest respiratory muscle and so CO is utilised by essential organs
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],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 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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? ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acid Base analysis
Basics  ,[object Object],[object Object],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 ,[object Object],[object Object],[object Object],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 ,[object Object],[object Object],[object Object],[object Object]
Na+ Unmeasured cations Unmeasured anions Cl- HCO3- ‘ Mind the gap’ cations = Anions  Anion gap = metabolic acidosis
Anion Gap ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]
 
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 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
The second step ,[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],Normal pCO2 levels are 35-45mmHg. Below 35 is alkalotic, above 45 is acidic. The third step
[object Object],[object Object],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
[object Object],[object Object],[object Object],[object Object],[object Object],The Fourth Step
[object Object],[object Object],[object Object],[object Object],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?? ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],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
[object Object],[object Object],[object Object],[object Object],∆  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 ,[object Object],[object Object],[object Object],[object Object]
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 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Normal pH  Respiratory alkalosis and Metabolic acidosis. Winters formula pCo2=1.5 x 12 +8=26
Case ,[object Object],[object Object],[object Object],Mrs. H has a severe metabolic and respiratory acidosis with hypoxemia
Case ….. ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],History Acidosis from diarrhea or  lactic acidosis as a result of hypovolemia and poor perfusion.
Normal anion gap acidosis with adequate compensation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Case.... ,[object Object],[object Object],[object Object],History : Elevated anion gap acidosis secondary to DKA  Metabolic alkalosis in the setting of thiazide diuretics use.
Case...... ,[object Object],[object Object],[object Object],[object Object],[object Object]
Delta Gap 34-12=22 + 19=41 Met alk ,[object Object],[object Object],[object Object]
[email_address] ,[object Object],[object Object],[object Object]
PaO2 O2 CASCADE AIR ALVEOLAR POST PULMONARY ARTERIAL Hb MICRO- CIRCULATION MIXED VENOUS

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Mechanical Ventilation Indications ABG Interpretation Clinical Examples

  • 1.
  • 2. 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
  • 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
  • 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 Calculated parameters Measured parameters
  • 5.
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  • 7.
  • 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 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.
  • 9.
  • 10.
  • 11.
  • 12. 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
  • 13. 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
  • 14. Interpretation of shunt fractions <10% Normal 10-20% Mild shunt 20-30% Significant shunt >30% Critical shunt, even 100% O2 cannot restore Pao2
  • 15.
  • 17. Oxygen Dissociation Curve: SaO 2 vs. PaO 2 CaO2 A B
  • 18.
  • 19. 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. 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
  • 21.  
  • 22.
  • 23. 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
  • 24. 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
  • 25. Lactate metabolism Glucose Pyruvate Lactate Oxidative phosphorylation 2 ATP 36 ATP NAD+CO2+H2O O 2 + NADH Glycolysis ADP Cell Cytoplasm Mitochondria Oxygen
  • 26. 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)
  • 27.
  • 28.
  • 29.
  • 30.
  • 31. 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
  • 32.
  • 33.
  • 34.
  • 35.
  • 36.
  • 37.
  • 38.
  • 39.
  • 40. 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
  • 41.
  • 43.
  • 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
  • 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
  • 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
  • 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 -
  • 49. 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
  • 50.
  • 51. 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
  • 52.
  • 53. Na+ Unmeasured cations Unmeasured anions Cl- HCO3- ‘ Mind the gap’ cations = Anions Anion gap = metabolic acidosis
  • 54.
  • 55.
  • 56.  
  • 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
  • 58.
  • 59.
  • 60.
  • 61.
  • 62.
  • 63.
  • 64. 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
  • 65.
  • 66.
  • 67. 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 - ]
  • 68. Equivalent rise of AG and Fall of HCO3…… … . Pure Anion Gap Metabolic Acidosis Discrepancy…….. in rise & fall + Non AG M acidosis, + M Alkalosis
  • 69.
  • 71. 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
  • 72.
  • 73. pH............7.25 PaCO2.....58.5 HCO3.......25.1 Uncompensated Respiratory Acidosis pH = 7.4 PaCO2 = 40 HCO3 = 24 Post op pt –drowsy
  • 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
  • 75. pH............7.39 PaCO2.....39.0 HCO3.......23.4 Normal A.B.G. pH = 7.4 PaCO2 = 40 HCO3 = 24
  • 76. Partially compensated Metabolic Acidosis pH = 7.4 PaCO2 = 40 HCO3 = 24 20 yr old male with Acute Gastroenteritis…..
  • 77.
  • 78.
  • 79.
  • 80.
  • 81.
  • 82.
  • 83.
  • 84.
  • 85. PaO2 O2 CASCADE AIR ALVEOLAR POST PULMONARY ARTERIAL Hb MICRO- CIRCULATION MIXED VENOUS

Editor's Notes

  1. 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.
  2. 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.