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 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 GLYCOLYSIS KREB’S CYCLE + ELECTRON TRANSPORT Pyruvate Glucose Oxygen 2 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, pCO 2 52, pO 2 142, 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? GLYCOLYSIS KREB’S CYCLE + ELECTRON TRANSPORT Pyruvate Glucose Oxygen 2 ATP 34 ATP Lactate  So, why is our patient’s lactate elevated?

Oxygen Delivery  O 2 delivery dependent on cardiac output and O 2 content of the blood  O 2 content is primarily due to hemoglobin saturation with little contribution of dissolved O 2 in blood C a O 2 = (S a O 2 * Hb * 1.34)+(0.003 * P a O 2 ) DO 2 = C a O 2 * Q..

Oxygen Delivery (cont.)  From previous equations, we can simplify to:  So, there are 3 reasons for poor O 2 delivery: 1) anemic anoxemia (low Hgb) 2) anoxic anoxemia (low S a O 2 ) 3) stagnant anoxemia (low Q). O 2 Delivery ≈ Hgb x S a O 2 x Q. How much O 2 delivery does our patient need?

Oxygen Consumption  Goal: O 2 delivery > O 2 consumption  Adequate O 2 delivery may become insufficient if tissue O 2 consumption increases! Fever increases O 2 consumption 10% per degree Agitation can increase O 2 consumption by 40%

Back to the Patient!  Due to the elevated lactate, we minimize O 2 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 S a O 2 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 O 2 consumption by looking at O 2 extraction: S a O 2 – S v O 2 Should be ~ mmHg Need arterial line and right atrial line  Increased O 2 extraction can be due to increased O 2 consumption (hungry mouths) or decreased O 2 delivery (not enough food)

Regional Oxygen Extraction  NIRS (Near-Infrared Spectroscopy) Monitoring Measures organ- specific oxygen extraction  Kidney – Surrogate for cardiac output ≈ SaO 2 – 15  Brain – Because the brain is important! ≈SaO 2 – 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 Stroke Volume

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 O 2 consumption and having normal Hgb and SaO 2. 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 SO 2 = 100%  Mixed venous SO 2 = 75%  Renal SO 2 = 90%  Cerebral SO 2 = 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