Jenny Boyd, MD
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!
Why Is Oxygen Important?
Used in cellular respiration
Needed for energy production by cells and tissues
Glucose 2 ATP
GLYCOLYSIS Pyruvate +
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
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
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
GLYCOLYSIS Pyruvate Lactate +
So, why is our patient’s lactate elevated?
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?
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?
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
Need cardiac catheterization
Need an echocardiographer
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
Kidney – Surrogate for
≈ 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?
overlap, resulting in
increased stroke volume
increases stroke volume for
a given preload
decreases stroke volume
for a given preload Preload
Increasing cardiac output (Q)
Remember: Q = Heart Rate x Stroke Volume
Increase heart rate
Preload ≈ CVP
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?
As the nurse is drawing a
hepatic function panel,
your patient begins to
seize. After terminating
his seizure, an emergent
head CT is performed,
probably a bypass-related
Patient discharged to home
on POD #8 on Keppra with
weakness of RUE