Morning Report

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					Oxygen Delivery
   Jenny Boyd, MD
Case #1
  12 mo male with a history of truncus
   arteriosus type I s/p repair with placement of a
   RV-PA who just a newborn who is now
12 mo maleconduit ashad heart surgery and is s/p
very sick. We have to take care of him until 7AM
   conduit replacement. Patient is being
when the morning crew arrives.
   admitted to the PCCU post-operatively.

   What are the goals of our care?

                              Images from American Heart Association
Care of the PCCU Patient

   2 main goals of critical care:

       Ensure adequate oxygen delivery!

       Buy time!
 Why Is Oxygen Important?
    Used in cellular respiration
         Needed for energy production by cells and tissues

Glucose              2 ATP

                                                    KREB’S CYCLE
     GLYCOLYSIS              Pyruvate                    +
                                                 ELECTRON TRANSPORT

                                                       34 ATP
Case #1 (cont.)
   Initial assessment: PERRL, clear BS
    bilaterally, RRR, soft belly, warm extremities,
    well-perfused, 2+ pulses, brisk cap refill.
   Initial CXR looks good, all tubes and lines in
    expected places.
   Initial ABG: pH 7.32, pCO2 52, pO2 142, BE -
    0.2, lactate 3.9 (nl <2)
       Initial elevation of lactate very common post-
        bypass, should resolve within 4 hours
Case #1 (cont.)
   Over the next few hours, patient is
    hemodynamically stable with good perfusion,
    decent UOP and minimal bleeding from
    surgical site.
   Repeat ABGs are normal except the lactate
    rises from 3.9  4.4  5.1
   Are you worried?
   Is an elevated lactate harmful?
 Where Does Lactate Come From?
Glucose           2 ATP

                                                  KREB’S CYCLE
     GLYCOLYSIS           Pyruvate              Lactate +
                                              ELECTRON TRANSPORT

    So, why is our patient’s lactate elevated?
                                            34 ATP
Oxygen Delivery
   O2 delivery dependent on cardiac output and
    O2 content of the blood
                   .         .
                     DO2 = CaO2 * Q

   O2 content is primarily due to hemoglobin
    saturation with little contribution of dissolved
    O2 in blood
             CaO2 = (SaO2* Hb * 1.34)+(0.003 * PaO2)
Oxygen Delivery (cont.)
   From previous equations, we can simplify to:
          O2 Delivery ≈ Hgb x SaO2 x Q

  So, there are 3 reasons for poor O2 delivery:
1) anemic anoxemia (low Hgb)
2) anoxic anoxemia (low SaO2)
3) stagnant anoxemia (low Q)

How much O2 delivery does our patient need?
Oxygen Consumption
   Goal: O2 delivery > O2 consumption

   Adequate O2 delivery may become
    insufficient if tissue O2 consumption
       Fever increases O2 consumption 10% per degree
       Agitation can increase O2 consumption by 40%
Back to the Patient!
   Due to the elevated lactate, we minimize O2
    consumption by ensuring our patient is afebrile and
    well sedated. However, our next lactate has risen to

   What’s wrong with our patient?
       Anemic?
       Low sats?
       Low cardiac output?
Our Patient (cont.)
   Since return from the OR, our patient’s Hgb
    has been > 10 and SaO2 has been >95%

   How do we know what our cardiac output is?
   What determines cardiac output?
Measuring Cardiac Output
   Thermodilution
       Need cardiac catheterization

   Echocardiography
       Need an echocardiographer
       Shortening fraction

   Surrogate markers
       Oxygen extraction
Oxygen Extraction
   Measure O2 consumption by looking at O2
    extraction: SaO2 – SvO2
       Should be ~20 - 30 mmHg
       Need arterial line and right atrial line
   Increased O2 extraction can be due to
    increased O2 consumption (hungry mouths) or
    decreased O2 delivery (not enough food)
Regional Oxygen Extraction
   NIRS (Near-Infrared
       Measures organ-
        specific oxygen
           Kidney – Surrogate for
            cardiac output
               ≈ SaO2 – 15
           Brain – Because the
            brain is important!
               ≈SaO2 – 30

                                     Image from Children’s Hospital of Wisconsin
Understanding Cardiac Output (Q)
   Q = Heart Rate x Stroke Volume

   What determines stroke volume?
       Preload
       Contractility
       Afterload
Frank-Starling Curve
   Increasing preload
    increases myosin-actin
    overlap, resulting in
    increased stroke volume

                                  Stroke Volume
   Increasing contractility
    increases stroke volume for
    a given preload
   Increasing afterload
    decreases stroke volume
    for a given preload                           Preload
Increasing cardiac output (Q)
   Remember: Q = Heart Rate x Stroke Volume
   Increase heart rate
       Pacing
       Inotropes
   Increase preload
       Preload ≈ CVP
   Increase contractility
       Inotropes
   Decrease afterload
       Vasodilators
Where were we?
   Our patient was having rising lactates despite minimizing O2
    consumption and having normal Hgb and SaO2. As we check
    on him, we note that he is normotensive, warm and well-
    perfused, with good peripheral pulses and brisk capillary
    refill. He has had adequate urine output since return from the
    OR. What other information do you want/need?
   Arterial SO2 = 100%
   Mixed venous SO2 = 75%
   Renal SO2 = 90%
   Cerebral SO2 = 80%
   CVP = 14
So why is our lactate so high?
   Increased production
       Dead tissue?

   Decreased clearance
       Liver failure?
   As the nurse is drawing a
    hepatic function panel,
    your patient begins to
    seize. After terminating
    his seizure, an emergent
    head CT is performed,
    revealing left-sided
    cerebral infarction,
    probably a bypass-related
   Patient discharged to home
    on POD #8 on Keppra with
    weakness of RUE

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