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Oxygen Delivery vs Oxygen Consumption

Oxygen Delivery vs Oxygen Consumption

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Oxygen Delivery vs Oxygen Consumption

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  1. Oxygen Delivery vsOxygen Consumption K. Allen Eddington, MD, MSc Assistant Professor Pediatric Critical Care Medicine Albert Einstein College of Medicine

  2. Objective: • Demonstrate a framework for the assessment, initial resuscitation, and ongoing reassessment and management of critically ill children, based on physiologic principles of tissue oxygen delivery and oxygen consumption.

  3. There are several physiologic principles and formulas which are introduced in the second year of medical school…and then often forgotten. • Reviewing these principles and formulas--without necessarily re-memorizing them--can help us prioritize and interpret the patient data we gather when a child is critically ill, and can help guide and prioritize our management. • In my experience, reviewing these principles after a few years of clinical experience, turns them into helpful tools.

  4. Let’s make this interactive! (I usually do this talk sitting at a table with a pen and paper.)

  5. Oxygen Delivery > Oxygen Consumption (DO2 > VO2) If this relationship is not maintained… • Tissue damage begins within minutes • If not corrected, organ damage and death ensue…rather rapidly

  6. Oxygen Delivery > Oxygen Consumption (DO2 > VO2) • There are a lot of disease entities out there with a lot of treatments we all have to know, but they tend to take time to work. • In critically ill patients, the focus is on maintaining DO2 > VO2, while we wait for other treatments to work.

  7. In simplistic terms, what are the steps a molecule of oxygen has to take to get from the outside environment to the mitochondria of a cell in your baby toe? If you need help reading my mind, I’m thinking of 4 major steps.

  8. Air (including oxygen) is drawn in from the environment to the alveoli • Oxygen diffuses across the alveolar and capillary membranes into the blood • Oxygen is carried in the blood to a capillary near a cell in your baby toe. • Oxygen diffuses across the capillary and cellular membranes into the mitochondria (where it is used in oxidative phosphorylation to generate ATP, which the cell uses to fill its energy requirements)

  9. Let’s look at the physiology of each of these steps more closely, to see • how patients (especially children) compensate when something doesn’t work well • what clinical data is most critical to gather • what interventions will most directly address maintaining DO2 > VO2 at each step

  10. Air (including oxygen) is drawn in from the environment to the alveoli • Oxygen diffuses across the alveolar and capillary membranes into the blood • Oxygen is carried in the blood to a capillary near a cell in your baby toe. • Oxygen diffuses across the capillary and cellular membranes into the mitochondria (where it is used in oxidative phosphorylation to generate ATP, which the cell uses to fill its energy requirements)

  11. Air is drawn in from the environment to the alveoli What parameters determine the content of oxygen transferred in this step? • Respiratory rate (RR) • Tidal Volume (Vt) • Fraction of inhaled oxygen (FiO2)

  12. Vt (ml) x RR (bpm) x FiO2 (%) = volume of inspired oxygen per minute (l/min) Examples; Healthy, 1 month-old, 4 kg 30 ml air x 35 bpm x 0.21 oxygen/volume air = 220 ml of oxygen/min Healthy, 16 year-old, 60 kg 450 ml air x 14 bpm x 0.21 oxygen/volume air = 1300 ml of oxygen/min

  13. In infants, the ability to accelerate RR > the ability to increase Vt (When RR increases greatly, Vt decreases) In teens and adults, the ability to increase Vt > the ability to accelerate RR

  14. Examples; Stressed, 1 month-old, 4 kg 25 ml x 90 bpm x 0.21 = 475 ml O2 /min (475-220)/220 x 100% = 115% increase Stressed 16 y/o, 60 kg 900 ml x 30 bpm x 0.21 = 5600 ml O2 /min (5600-1300)/1300 x 100% = 330% increase

  15. How is this clinically meaningful? Children of all ages have the capacity to significantly compensate for increased oxygen requirement by increasing RR and Vt.

  16. How is this clinically meaningful? Take home point: If a patient’s compensatory mechanism is intact, but not in use, respiratory failure is not imminent.

  17. How is this clinically meaningful? It is usually obvious when the compensatory mechanism is NOT intact. • Severe neurological impairment • Tiring after prolonged compensation Check if the baby accelerates when you approach or when you stick him, then calms back down. • Of note, most infants can breathe in the 70-90’s for several DAYS before “getting tired”.

  18. How is this clinically meaningful? When you communicate with the PICU about respiratory patients, we are AXIOUSLY awaiting a current and accurate respiratory rate! Right before you call, clock the kid yourself, and tell me EARLY in the presentation.

  19. How is this clinically meaningful? Other tidbits you might be tempted to tell me first • how impressive the stridor is • how deep the retractions are • or what poor air entry you hear on ausultation.… are all more meaningful in the context of a current RR.

  20. How is this clinically meaningful? I only barely care about the RR on initial presentation, so please tell me where we are now, then tell me about the journey to get there. (Telling the punchline and then the set-up makes for bad joke telling, but great critical care communication!)

  21. When you identify patients in respiratory distress, what fundemental treatments most directly address and maximize this step in oxygen transport? • 100% FiO2 • Mechanical assistance to optimize Vt and RR • (Various specific treatments for obstructive and restrictive airway and lung disease)

  22. Air (including oxygen) is drawn in from the environment to the alveoli • Oxygen diffuses across the alveolar and capillary membranes into the blood • Oxygen is carried in the blood to a capillary near a cell in your baby toe. • Oxygen diffuses across the capillary and cellular membranes into the mitochondria (where it is used in oxidative phosphorylation to generate ATP, which the cell uses to fill its energy requirements)

  23. Oxygen diffuses across the alveolar and capillary membranes into the blood What parameters determine the content of oxygen transferred in this step? • Permeability of the membranes to oxygen • Functional surface area of the membranes • Concentration gradient

  24. How do we assess the ability of oxygen to diffuse in a particular patient? A-a gradient….the classic answer PAO2 –PaO2 = FiO2 (Patm-PH2O) – PaCO2/0.8 Doable, but not handy.

  25. How do we assess the ability of oxygen to diffuse in a particular patient? Other estimates include : • PaO2/FiO2 ratio • SPO2/FiO2 ratio • Oxygenation Index, when mechanically ventilated • (Mean Airway Pressure x FiO2)/PaO2

  26. How do we assess the ability of oxygen to diffuse in a particular patient? Other estimates include : • PaO2/FiO2 ratio • SPO2/FiO2 ratio These are intuitive, simple to remember, and simple to calculate.

  27. How do we assess the ability of oxygen to diffuse in a particular patient? Examples calculations: Healthy lungs, on Room Air PaO2 = 100 mmHg SPO2 = 100% P/F = 100/0.21 = 476 Sp/F = 476

  28. How do we assess the ability of oxygen to diffuse in a particular patient? Examples calculations: Sick lungs, SPO2 = 95% on 30% FiO2 PaO2 = 80 mmHg P/F = 80/0.30 = 267 Sp/F = 95/0.30 = 317

  29. How do we assess the ability of oxygen to diffuse in a particular patient? P/F ratio is part of the criteria for Acute Lung Injury and Acute Respiratory Distress Syndrome (<300 ALI; <200 ARDS)

  30. How do we assess the ability of oxygen to diffuse in a particular patient? Of note, Healthy lungs, on 100% FiO2: PaO2 = 400-500 (P/F = 400-500) But SP/F ratio is meaningless… 100% sat/ 1 = 100

  31. How do we assess the ability of oxygen to diffuse in a particular patient? Take home point: To non-invasively assess oxygen requirement with SP/F ratio, patients on supplemental oxygen need to saturate 99% or less. You may still want to increase the FiO2 to 100% in the early stages of care, but be aware of the distinction between your assessment and your treatment.

  32. Oxygen moves slowly across the membrane in healthy patients, and even more slowly when lung disease is present, so the functional surface area of the alveolar/capillary membrane is paramount to oxygen movement.

  33. Carbon dioxide moves across the alveolar/capillary membrane rapidly. Functional alveolar surface area is rarely if ever a limiting factor to CO2 removal.

  34. Membrane diffusion is the rate limiting step in oxygen delivery to the blood, while movement from the alveoli to the outside environment is the rate limiting step for CO2 removal. In respiratory failure, it’s important to distinguish between oxygenation failure and failure of CO2 removal.

  35. How does this help me take better care of my patients? • Mechanical ventilator settings predominately address one or the other. • Settings that directly affect the minute ventilation will predominately affect CO2 removal. • RR • Vt or positive inspiratory pressure (PIP)

  36. How does this help me take better care of my patients? • Mean airway pressure (MAP) is the primary determinant of the lung’s volume. • With increased lung volume is increased functional alveolar surface volume

  37. How does this help me take better care of my patients? • MAP is determined by positive end-exipratory pressure (PEEP)>>Vt/PIP, RR, Inspiratory Time, slope of breath delivery. • And obviously, FiO2 influences O2 delivery without effecting CO2 removal

  38. Air (including oxygen) is drawn in from the environment to the alveoli • Oxygen diffuses across the alveolar and capillary membranes into the blood • Oxygen is carried in the blood to a capillary near a cell in your baby toe. • Oxygen diffuses across the capillary and cellular membranes into the mitochondria (where it is used in oxidative phosphorylation to generate ATP, which the cell uses to fill its energy requirements)

  39. Oxygen is carried in the blood to a capillary near a cell in your baby toe. What are the determinants of how much oxygen gets delivered to the tissues? Blood oxygen content Cardiac Output DO2=CO x O2 content

  40. What are the determinants of blood oxygen content? Hb bound O2 + Dissolved O2 1.34 x Hb x sat (as integer) + 0.003 x PaO2 To get familiar with the norms and implications of different derangements, we’ll do some example calculations.

  41. Normal kid, on room air Hb bound Dissolved (1.34 x 13 x 1) + (0.003 x 90) = 17.4 + 0.3 = 17.7 Normal kid, on 100% FiO2 17.4 + (0.003 x 500) = 17.4 + 1.5 = 18.9 (18.9-17.7)/17.7 = 6.7% increase

  42. Kid with lung disease, on RA (1.34 x 13 x 0.75)+ (0.003 x 40) = 13.1 + 0.1 = 13.2 Kid with lung disease, on 100% (1.34 x 13 x 0.9) + (0.003 x 60) = 15.7 + 0.2 = 15.7 (15.7-13.2)/13.2 = 18.9% increase

  43. Kid with anemia, on RA (1.34 x 2.5 x 1) + (0.003 x 90) = 3.4 + 0.3 = 3.7 Kid with anemia, on 100% 3.4 + (0.003 x 500) = 3.4 + 1.5 = 4.9 (4.9-3.7)/3.7 = 32.4% increase

  44. Kid with cyanotic heart disease, on RA (1.34 x 16 x 0.75) + (0.003 x 40) = 16.1 + 0.1 = 16.2 Kid with cyanotic heart disease, on 100% (Don’t try this at home!!) (1.34 x 16 x 0.9) + (0.003 x 60) = 19.3 + 0.2 = 19.5 (19.5-16.2)/16.2 = 20.4 % increase

  45. A few notes on cyanotic heart disease: High PAO2 can cause decreased pulmonary vascular resistance and lead to increased systemic-to-pulmonary shunting • Pulmonary edema • Systemic hypo-perfusion

  46. A few notes on cyanotic heart disease: • Children with cyanotic lesions generally have well balanced circulation with saturations of 75%-80%. • They can and do get pulmonary disease requiring oxygen. • To safely supplement them, you need an oxygen blender, and you need a close eye on the pulse ox, even if the kid isn’t that sick. • Titrate to the target, but if you can’t hit it, err on the low side.

  47. Take home points on blood oxygen content: • Children in distress should (almost) ALL get supplemental oxygen via non-rebreather in the initial phase of resuscitation. • The roll of dissolved oxygen is usually negligible, but not always. In cases of severe anemia, supplemental oxygen significantly increases DO2 until a transfusion can be given, even if the patient sats 100% on RA at presentation.

  48. Take home points on blood oxygen content: • Children with cyanotic lesions are polycythemic to compensate for their persistently desaturated state, so don’t let the low sats scare you. Don’t over-think them; unless peds cardio tells you differently for a particular child, a saturation as close to 75% as you can get should be the goal.

  49. Enough about blood oxygen content! On to Cardiac Output!

  50. What are the determinants cardiac output? CO = HR x Stroke Volume And the determinants of Stroke Volume? Preload, Contractility, Afterload CO = HR x SV / | \ Pre Con After