Oxygen Delivery

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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
12 mo
maleconduit
who just
heart surgery
RV-PA
ashad
a newborn
who isand
nowis s/p
veryconduit
sick. We
have to take
care of
until 7AM
replacement.
Patient
is him
being
when
the morning
admitted
to the crew
PCCUarrives.
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
GLYCOLYSIS
2 ATP
Oxygen
Pyruvate
KREB’S CYCLE
+
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 postbypass, 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
GLYCOLYSIS

2 ATP
Oxygen
Pyruvate
KREB’S CYCLE
Lactate +
ELECTRON TRANSPORT
34 ATP
So, why is our patient’s lactate elevated?
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
increases!


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
7.0.

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


Echocardiography



Need cardiac catheterization
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
Spectroscopy)
Monitoring

Measures organspecific oxygen
extraction

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



Increasing preload
increases myosin-actin
overlap, resulting in
increased stroke volume
Increasing contractility
increases stroke volume for
a given preload
Increasing afterload
decreases stroke volume
for a given preload
Stroke Volume
Frank-Starling Curve
Preload
.
Increasing cardiac output (Q)


.
Remember: Q = Heart Rate x Stroke Volume
Increase heart rate



Increase preload


Preload ≈ CVP
Increase contractility


Pacing
Inotropes
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 wellperfused, 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?
Conclusion


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
complication.
Patient discharged to home
on POD #8 on Keppra with
weakness of RUE
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