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Causes of Hypoxemia

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					Internal Respiration

      Module F
            Module F
• Chapter 9 – Assessment of
  Hypoxemia and Shunting
• Chapter 10 – Treatment of
  Hypoxemia and Shunting
• Chapter 11 – Hypoxia: Assessment
  and Intervention
                     Objectives
At the conclusion of this session the participant will:

• Still be awake! This covers 3 chapters!
   • Relax…most is a review and some will be covered in
      Winter 09.
• Define oxygen extraction.
• Describe the effects of anaerobic metabolism.
• State the formula for calculating RQ.
• List the 5 causes of hypoxemia.
• State the effect of an increase or decrease in cardiac
  output on the shunt fraction.
• List three methods, other than the shunt fraction, which
  can be used to assess the degree of physiologic
  shunting.
• State three ways to treat acute hypoxemia.
                   Objectives
• Define anemia.
• List three types of anemia and state the causes of
  the defect.
• Describe the effect of anemia on the presence of
  hypoxia.
• State the benefit, problems, and specific levels for
  each of the following as it relates to it being an
  indicator of cellular hypoxia:
   • Lactate
   • Mixed Venous Oxygenation
   • Oxygen Consumption & Utilization
   • Gastric Mucosal Acidosis
           Internal Respiration
• Exchange of oxygen and carbon dioxide at
  the cellular level.
  • Some control by local vasculature.
    • Increased distance from capillary to tissue will result
      in decreased delivery.
  • Some organs use more than others.
    • Table 7-1 (p. 188).
    • Note: % of blood flow is not equal to volume of
      oxygen consumed.
          Internal Respiration
• Normal metabolism exists when O2 is
  consumed and CO2 is produced.
  • Normal ratio of CO2 produced : O2 consumed
    is 0.8:1 (200/250)
  • Increased ratio with excess CHO utilization;
    decreased with fat & ETOH.
• When insufficient oxygen is present,
  anaerobic metabolism results.
  • Less ATP produced.
  • Lactic Acid is produced.
      Adequacy and Efficiency of
          Oxygen Delivery
• Adequacy: Is there sufficient oxygen present?
  (Hint: Is hypoxemia present?)
   • Causes of Hypoxemia
      • Low PIO2
      •   Hypoventilation
      •   Absolute Shunts
      •   Relative Shunts
      •   Diffusion Defects
      •   True or Absolute Deadspace (secondary mechanism)
• Efficiency: Is the PaO2 appropriate for the FIO2?
   • If not…assume a shunt is present!
 Effects of Cardiac Output on PaO2
• The normal decrease in PaO2 from alveolar
  oxygen levels is due to the small mixing of
  anatomically shunted blood (5%).
   • This blood is venous in nature and has a PO2 the
     same as the P O2.
• Four situations exist that can affect the PaO2:
   •   Decreased Cardiac Output with a Normal Shunt
   •   Increased Shunting with a Normal Cardiac Output
   •   Decreased Cardiac Output with an Increased Shunt
   •   Increased Cardiac Output with an Increased Shunt
 The Normal Ventilation/Perfusion
         Relationship
• Normal PAO2
  • Normal PćO2
• Normal P    O2
  • Normal CO
  • Normal Oxygen
    Consumption
• Normal PaO2
    Decreased Cardiac Output with a
            Normal Shunt
• P O2 decreases with a
  decrease in cardiac
  output because of an
  increased oxygen
  extraction (assuming
     O2 doesn’t change).
• Any shunted blood will
  have a reduced
  P O2 .
• Because the amount of
  shunted blood is so small,
  the decrease in PaO2 isn’t
  significant.
        Increased Shunting with a
          Normal Cardiac Output
• Example: ARDS
• Normal Cardiac
  Output = Normal
  P O2
• The problem here is
  a significant increase
  in intrapulmonary
  shunt, meaning more
  P O2 “contaminated”
  blood entering the
  pulmonary vein
  (arterial system).
     Decreased Cardiac Output with
          an Increased Shunt
• Similar to the first
  scenario, but here
  there is an increased
  intrapulmonary shunt.
   • Example: ARDS with
     an MI
• Reduced Cardiac
  Output yields a
  reduced P O2 (higher
  extraction).
• More of that low P O2
  blood is shunted in
  the lungs, resulting in
  a large reduction in
  PaO2.
   Increased Cardiac Output with an
           Increased Shunt
• Normal physiologic
  response to hypoxemia
  is to increase heart rate
  (peripheral
  chemoreceptors) and
  Cardiac Output.
   • P O2 is increased (better
     oxygen delivery).
• With an increased
  intrapulmonary shunt,
  however, there still is an
  increased amount of
  P O2 “contaminated”
  blood entering the
  system.
                    So What?
• Don’t always assume that an improvement or
  deterioration in PaO2 is occurring solely because
  of a change in pulmonary gas exchange.
• Suspect a change in cardiac output when an
  abrupt, unexplained hypoxemia is observed in
  critically ill patients.
• Also, consider other non-cardiac causes of
  reduced P O2.
  • Anemia
  • Increased metabolism (fever)
  • Maldistribution of systemic perfusion
        Assessment of Hypoxemia
  • Definition of “Hypoxemia”.
      • Severity?
  • Causes of Hypoxemia
  • Differential Diagnosis of Hypoxemia
  Abnormality       PaO2      PaCO2      RA P(A-a)O2     100% O2 P(A-a)O2
Hypoventilation                             N                 N
Absolute Shunt               N or                            
Relative Shunt               N, ,                           N
Diffusion Defect     N at     N or      N at rest,           N
                   Rest,               with exercise
                      w/
                   exercise
         Shunt Substitutes
• P(A-a)O2
• PaO2/PAO2
• PaO2/FIO2
                    PAO2
• PAO2 = [(PBARO - PH2O) x FIO2] –
  (PaCO2/0.8)
  • On FIO2 of less than 60%
• PAO2 = [(PBARO - PH2O) x FIO2] – PaCO2
  • On FIO2 greater than 60%
• Normal Values:
  • Room Air: 100 – 104 mm Hg
  • 100% Oxygen: 600
                   P(A-a)O2
• Normal values is around 10 mm Hg on
  room air.
  • Values increase with increasing age and the
    supine position.
• Normal values 25-65 mm Hg on 100%
• Difficult to use when FIO2 varies from 21
  or 100%
  • Normal values differ for each FIO2
     • Limited value when using supplemental oxygen.
        P(A-a)O2 on Room Air
• Normal A-a gradient on 21% is seen with:
  • Pure hypoventilation
  • High altitude
  • Diffusion defect (patient at rest)
• Abnormal A-a gradient on 21% is seen
  with
  • Relative shunt
  • Absolute shunt
          P(A-a)O2 on 100%
• Relative Shunt will improve
  • A-a gradient less than 300 mm Hg
• Absolute Shunt will not improve
  • A-a gradient is greater than 300 mm Hg
   Using P(A-a)O2 to Estimate
             Shunt
• On 100% FIO2, a 1% shunt is estimated
  for every 10 – 15 mm Hg P(A-a)O2
• Example: A-a gradient is 140 mm Hg
  • 140 = 9.3%      140 = 14.0%
     15             10
   Using P(A-a)O2 to Estimate
             Shunt
• Normal Shunt is 5%
• Add 5 % to the normal 5% shunt for every
  100 mm Hg gradient; Example:
  • 100 mm Hg – 10%
  • 200 mm Hg – 15%
  • 300 mm Hg – 20%
             Shunt Equation
• Classic Shunt Equation
  • “Gold Standard”
• Clinical Shunt Equation
• A shunt greater than or = 15% is significant
• Increased shunts will correlate with
  • “White out on x-ray unless its cardiac in origin.
  • Atelectasis, pneumonia, pulmonary edema, ARDS
      Classic Shunt Equation
 
 Qs        Cc O2  CaO 2
                         100
      Q t Cc O2  Cv O2
• Where:
  • CćO2= (1.34 x Hb x 1.0) + (PAO2 x .003)
    • Assumes 100% saturation in the ideal alveolus
• Requires a Pulmonary Arterial Catheter
  (BTFDC)
        Clinical Shunt Equation

Qs                 P A  a O2  .003
       P A  a O  .003  CaO  Cv O 
     Qt             2                2   2




• Requires a Pulmonary Arterial Catheter
  (BTFDC)
• Only accurate at lower FIO2
       PaO2 /PAO2 (a-A ratio)
• Normal value is greater than 75% on any
  FIO2
• Example: 100/104 = 96%
  • 96% of oxygen is diffusing across the A-C
    membrane
               PaO2/FIO2 ratio
•   Normal value is 400 – 500
•   Example: 100 mm Hg/.21 = 476
•   Value between 200 – 300 = ALI
•   Value less than 200 = ARDS
    • Values less than 200 correlate with a shunt
      of greater than 20%
    Treatment of Hypoxemia
• Increase FIO2
• Increase MAP
  • PEEP, Inspiratory Time, Vt
• Body Positioning
  • Prone Positioning
  • Lateral decubitus (good lung down)
• Good bronchial hygiene
  • Suction, bronchodilators, CPT/Flutter/PEP
      Oxygen Administration
• Treat hypoxemia/Hypoxia
• Decrease the work of breathing
• Decrease the work of the heart
    Hazards of Oxygen Therapy
•   Absorption atelectasis
•   Oxygen Toxicity
•   Retinopathy of prematurity
•   Oxygen induced hypoventilation in COPD
    • Look for oxygen levels above 60 mm Hg and
      a rising PaCO2
    • Evaluate FIO2 patient is receiving
    • Patient symptomatic: sleepy, lethargic
              Hyperoxemia
• PaO2 greater than 100 mm Hg
  • Usually undesirable
  • Very little oxygen content is gained
• A PaO2 above 130 mm Hg indicates the
  patient is breathing supplemental oxygen.
• Hyperoxemia is indicated in COHb%.
             Hyperoxemia
• SpO2% of 100% means the PaO2 could be
  between 100 mm Hg & 600 mm Hg
  • Very dangerous in infants
    Oxygen Administration in
     Chronic Hypercapnia
• PaO2 will increase 3 mm Hg for each 1%
  increase in FIO2
• Keep PaO2 around 60 mm Hg
• FIO2 = 60 - PaO2 on room air
                   3
               Example

• You are asked to draw an ABG on a
  CO2 retainer. The PaO2 is 39 mmHg on
  21%
  Where should the FIO2 be set?
  FiO2 = 60 - 39 = 7% Add to 21%
                3
• Set FIO2 at 28%
 Calculating the maximal PaO2
      for any given FIO2
• The PaO2 on room air during
  hyperventilation may go up to 130 mm Hg
• A PaO2 more than 5 times the % of
  oxygen is suspicious.
  •   30   x   5   =   150
  •   40   x   5   =   200
  •   50   x   5   =   250
  •   60   x   5   =   300
                 Problem
• pH 7.32, PaCO2 48, PaO2 200, FIO2 .30
• PAO2 = 760 – 47 x 0.30 – 48/.8
          = 154 mm Hg
• Can’t have a PaO2 greater than PAO2, so…
  • Either the FIO2 was not recorded accurately
  • Lab error (air bubble)
             Evaluating FIO2
• High flow devices may not be delivering
  the FIO2 that is set
  • If the patient’s total flowrate is exceeding the
    flow from the oxygen delivery device, the FIO2
    will decrease
  • Water in the aerosol tubing will increase FIO2
• High flow oxygen delivery systems should
  be analyzed
  Analyze High Flow Systems
• Polarographic (battery and electrolyte
  solution)
• Galvanic (fuel cell)
• Troubleshooting: If analyzer is not
  reading the FIO2 within + 2% then:
  • Calibrate analyzer first
  • Change fuel cell (galvanic) or
  • Change battery/electrolyte level
    (polarographic)
     Correlating ABG to the
      Patients Condition
• A patient who looks good but has bad
  ABG
  • Suspect a lab error
  • Venous blood gas sample
  • COPD (high PaCO2 and HCO3-)
      Correlating ABG to the
       Patients Condition
• A patient who looks and feels bad but
  ABG are good.
  • CO poisoning, MetHB%
  • Tissue hypoxia
     • Anemic hypoxia
     • Histotoxic hypoxia
     • Circulatory hypoxia
  • Pulmonary embolism – high Vd/Vt ratio and
    high E
         Analyzing an ABG
• On 21%, add PaCO2 and PaO2 to see if
  greater than 150.
• If one of the three acid base parameters
  is abnormal, there is an error.
  • pH 7.58, PaCO2 40, HCO3- 24
• PaO2 cannot be greater than PAO2 on any
  FIO2.
           Analyzing an ABG
• Know normal venous values and
  suspect when a venous sample may
  have been drawn
• Inaccurate FIO2
  • Improperly recorded
  • Patients total flow exceeds flow from
    delivery device
  • FIO2 recorded from low flow system
  • Water in the aerosol tubing
                 Objectives
• Define anemia.
• List three types of anemia and state the
  causes of the defect.
• Describe the effect of anemia on the
  presence of hypoxia.
• State the benefit, problems, and specific
  levels for each of the following as it relates
  to it being an indicator of cellular hypoxia:
  •   Lactate
  •   Mixed Venous Oxygenation
  •   Oxygen Consumption & Utilization
  •   Gastric Mucosal Acidosis
                      Hypoxia
• Definition: Reduced oxygen levels at the
  tissue.
• No “best” index for assessing tissue
  oxygenation.
• Begin assessment by assessing the
  components of oxygen delivery:
  •   Dissolved Oxygen
  •   Bound Oxygen
  •   Hemoglobin
  •   Cardiac Output (This will be covered in RSPT 2420)
• Then look at markers of the effects of possible
  tissue hypoxia.
            Types of Hypoxia
•   Hypoxemic Hypoxia
•   Circulatory (Stagnant) Hypoxia
•   Anemic Hypoxia
•   Histotoxic Hypoxia
          Oxygenation Indices
• Dissolved Oxygen as an index of hypoxia.
  • Not very useful
     • Pretty good bet hypoxia is present with severe hypoxemia
         • Be careful at extremes!
  • Keep PaO2 above 60 mm Hg.
• Combined Oxygen (SaO2) as an index of
  hypoxia.
  • Make sure how you know HOW it is reported
     • SaO2 with nomogram, 2-wavelength oximetry, CO-Oximetry,
       Pulse Oximetry
  • Better than PaO2, but has its faults.
     • Abnormal species of hemoglobin
     • Insensitive in telling deterioration or at high PaO2 levels.
                  Anemia
• RBC:
  • 5 million/mm3 in men; 4.5 million/mm3 in
    women.
• Hemoglobin
  • 15 g% in men, 13 to14 g% in women.
• Anemia defined as a reduction in the
  amount of circulating RBC or hemoglobin.
• Hematocrit (formed elements in blood)
  • 47% in men, 42% in women.
  • Too low is bad; too high is bad.
               Types of Anemia
• Presence of anemia means one of two things:
   • Decrease in production of RBC or Hb
      • Bone Marrow Failure (Aplastic Anemia)
          • Usually due to chemical or physical agent (normocytic)
      • Inadequate Hemoglobin synthesis
          • Iron deficiency 2° chronic blood loss or pregnancy (microcytic)
               • Pagophagia: Ice chip craving
          • Thalassemias – genetic disorder (microcytic)
      • Inadequate RBC formation
          • Folic Acid deficiency: Green vegetables & alcoholics (macrocytic)
          • B12 deficiency: Pernicious anemia 2° lack of intrinsic factor
            (macrocytic)
   • RBC & Hb are being lost or destroyed at an accelerated rate.
      • Blood loss
          • Acute bleeding (normocytic)
          • Excessive hemolysis
      • Sickle cell disease
           Analyzing FIO2
• Always correlate ABG to patients
  condition.
• When drawing from an A-line, always
  remove all heparin from the lines – this
  means withdrawing 3-5 cc and discarding.
• Understand the relationship of increased
  metabolism with leukocytosis (leukemia).
       Anemia and Hypoxia
• Mild anemia (10 g%) usually won’t cause
  hypoxia
  • 25% extraction
  • Cardiac output reserves (acute)
  • Changes in levels of 2,3 DPG (cardiac)
• Probably significant with Hb < 6 g%
• Transfuse when Hb levels fall below 7 g%
      Key Indicators of Hypoxia
•   Lactate
•   Mixed Venous Oxygen
•   Oxygen Consumption/Oxygen Extraction
•   Gastric Tonometry
•   Vital Organ Function
                           Lactate
• Immediate response to a reduced oxygen
  delivery is the onset of anaerobic metabolism.
  • Glycolysis: Pyruvate reduction to lactate.
  • Normal lactate is 0.9 to 1.9 mM/L or 8 to 17 mg/dL
  • Metabolic Acidosis + hypoxemia + CO = Hypoxia
  • Increase in mortality at levels above 2.5 mM/L; 90% at
    levels above 8 mM/L
  • Problem is lactate elevation is not linear (not a good
    early predictor)
      • Reduction is by liver. Poor perfusion/Liver failure worsens
        prognosis.
  • Cyanide poisoning (Histotoxic hypoxia) should be
    suspected with high lactates and no increase in HbCO
    with smoke inhalation.
      Mixed Venous Oxygenation
• Requires a pulmonary artery catheter.
• Assessment of oxygen supply vs. demand
• S O2: Continuous vs. Spot Check
   • Normal 75%
          • Decreased with increased O2, decreased SaO2, decreased Hb or
            decreased CO.

• P   O2: Average   end-capillary driving pressure.
   • Usefulness depends on distribution of cardiac output.
   • Decreases are associated with decreased supply or increased
     demands.
   • Increases are associated with reduced utilization (NOT
     ALWAYS A GOOD THING!)
 Oxygen Uptake and Utilization
• Normal oxygen uptake (consumption) by the
  tissue remains constant despite changes in
  cardiac output because of huge reserve (25%
  normal extraction).
  • Hypoxia is present when O2del falls below 8 to 10
    ml/kg/min.
• Covert Hypoxia: Normally, increasing oxygen
  delivery is not needed; in some situations (MOF
  secondary to ARDS, septic shock, ARF). The
  cause is suspected to be an altered oxygen
  utilization.
            Gastric Tonometry
• Blood shunting to key organs
  occurs with reduced oxygen
  supply at the expense of non-vital
  organ systems (GI tract).
• If hypoxic crisis is present, GI
  involvement will be a primary
  source.
• The mixing of gases to a point of
  equilibration is called tonometry.
• Use of a specialized catheter with
  a balloon can measure the
  gastric carbon dioxide and infer
  gastric blood flow.
     Sublingual Tissue PCO2
• Improvement on gastric
  tonometry.
• Uses CO2 sensor in
  “temperature” like probe.
• Results within 60 seconds.
          Vital Organ Function
• If compensatory mechanisms are intact,
  the presence of these compensatory
  mechanisms may be an indication that
  hypoxia is present.
  •   Urine output
  •   Mental status
  •   Skin coolness
  •   Great toe temperature