Oxygen DeliveryJenny Boyd, MD

Case #1 12 mo male with a history of truncus

arteriosus type I s/p repair with placement of a RV-PA conduit as a newborn who is now s/p conduit replacement. Patient is being admitted to the PCCU post-operatively.

What are the goals of our care?

Images from American Heart Association

12 mo male who just had heart surgery and is very sick. We have to take care of him until 7AM when the morning crew arrives.

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

GLYCOLYSISKREB’S CYCLE

+ELECTRON TRANSPORT

Pyruvate

Glucose Oxygen2 ATP

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?

GLYCOLYSISKREB’S CYCLE

+ELECTRON TRANSPORT

Pyruvate

Glucose Oxygen2 ATP

34 ATP

Lactate

So, why is our patient’s lactate elevated?

Oxygen Delivery O2 delivery dependent on cardiac output and

O2 content of the blood

O2 content is primarily due to hemoglobin saturation with little contribution of dissolved O2 in blood

CCaaOO22 = (S = (SaaOO22* Hb * 1.34)+(0.003 * P* Hb * 1.34)+(0.003 * PaaOO22))

DODO22 = = CCaaOO22 ** Q Q. .

Oxygen Delivery (cont.) From previous equations, we can simplify to:

So, there are 3 reasons for poor O2 delivery:

1) anemic anoxemia (low Hgb)

2) anoxic anoxemia (low SaO2)

3) stagnant anoxemia (low Q).

O2 Delivery ≈ Hgb x SaO2 x 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

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

Spectroscopy) Monitoring Measures organ-

specific 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

.

.

Frank-Starling Curve 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 Preload

Stro

ke V

olum

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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?

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