Oxygen Delivery vs Oxygen Consumption

Oxygen Delivery vs Oxygen Consumption

K. Allen Eddington, MD, MScAssistant ProfessorPediatric Critical Care MedicineAlbert Einstein College of Medicine

1Objective: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.

2There are several physiologic principles and formulas which are introduced in the second year of medical schooland 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.

3Lets make this interactive! (I usually do this talk sitting at a table with a pen and paper.)

4Oxygen Delivery > Oxygen Consumption (DO2 > VO2)If this relationship is not maintainedTissue damage begins within minutesIf not corrected, organ damage and death ensuerather rapidly

5Oxygen 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.

6In 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, Im thinking of 4 major steps.

7Air (including oxygen) is drawn in from the environment to the alveoliOxygen diffuses across the alveolar and capillary membranes into the bloodOxygen 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)

8Lets look at the physiology of each of these steps more closely, to seehow patients (especially children) compensate when something doesnt work wellwhat clinical data is most critical to gather

what interventions will most directly address maintaining DO2 > VO2 at each step

9Air (including oxygen) is drawn in from the environment to the alveoliOxygen diffuses across the alveolar and capillary membranes into the bloodOxygen 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)

10Air is drawn in from the environment to the alveoliWhat parameters determine the content of oxygen transferred in this step?

Respiratory rate (RR)Tidal Volume (Vt)Fraction of inhaled oxygen (FiO2)

11Vt (ml) x RR (bpm) x FiO2 (%) = volume of inspired oxygen per minute (l/min)Examples;Healthy, 1 month-old, 4 kg30 ml air x 35 bpm x 0.21 oxygen/volume air= 220 ml of oxygen/minHealthy, 16 year-old, 60 kg450 ml air x 14 bpm x 0.21 oxygen/volume air = 1300 ml of oxygen/min

12In 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

13Examples;Stressed, 1 month-old, 4 kg25 ml x 90 bpm x 0.21 = 475 ml O2 /min (475-220)/220 x 100% = 115% increase

Stressed 16 y/o, 60 kg900 ml x 30 bpm x 0.21 = 5600 ml O2 /min (5600-1300)/1300 x 100% = 330% increase

14How is this clinically meaningful?

Children of all ages have the capacity to significantly compensate for increased oxygen requirement by increasing RR and Vt.

15How is this clinically meaningful?

Take home point:

If a patients compensatory mechanism is intact, but not in use, respiratory failure is not imminent.

16How is this clinically meaningful?

It is usually obvious when the compensatory mechanism is NOT intact. Severe neurological impairmentTiring 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 70-90s for several DAYS before getting tired.

17How 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.

18How is this clinically meaningful?

Other tidbits you might be tempted to tell me firsthow impressive the stridor ishow deep the retractions areor what poor air entry you hear on ausultation.are all more meaningful in the context of a current RR.

19How 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!)

20When you identify patients in respiratory distress, what fundemental treatments most directly address and maximize this step in oxygen transport?

100% FiO2Mechanical assistance to optimize Vt and RR

(Various specific treatments for obstructive and restrictive airway and lung disease)

21Air (including oxygen) is drawn in from the environment to the alveoliOxygen diffuses across the alveolar and capillary membranes into the bloodOxygen 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)

22Oxygen diffuses across the alveolar and capillary membranes into the bloodWhat parameters determine the content of oxygen transferred in this step?

Permeability of the membranes to oxygenFunctional surface area of the membranesConcentration gradient

23How 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.

24How do we assess the ability of oxygen to diffuse in a particular patient?

Other estimates include :PaO2/FiO2 ratioSPO2/FiO2 ratioOxygenation Index, when mechanically ventilated(Mean Airway Pressure x FiO2)/PaO2

25How do we assess the ability of oxygen to diffuse in a particular patient?

Other estimates include :PaO2/FiO2 ratioSPO2/FiO2 ratio

These are intuitive, simple to remember, and simple to calculate.

26How do we assess the ability of oxygen to diffuse in a particular patient?

Examples calculations:Healthy lungs, on Room AirPaO2 = 100 mmHgSPO2 = 100%P/F = 100/0.21 = 476Sp/F = 476

27How do we assess the ability of oxygen to diffuse in a particular patient?

Examples calculations:Sick lungs, SPO2 = 95% on 30% FiO2PaO2 = 80 mmHg P/F = 80/0.30 = 267Sp/F = 95/0.30 = 317

28How 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(Vt/PIP, RR, Inspiratory Time, slope of breath delivery.And obviously, FiO2 influences O2 delivery without effecting CO2 removal

37Air (including oxygen) is drawn in from the environment to the alveoliOxygen diffuses across the alveolar and capillary membranes into the bloodOxygen 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)

38Oxygen 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 contentCardiac Output

DO2=CO x O2 content

39What are the determinants of blood oxygen content?Hb bound O2 +Dissolved O21.34 x Hb x sat (as integer) + 0.003 x PaO2

To get familiar with the norms and implications of different derangements, well do some example calculations.

40Normal kid, on room airHb boundDissolved(1.34 x 13 x 1) + (0.003 x 90) = 17.4 + 0.3= 17.7Normal kid, on 100% FiO217.4+(0.003 x 500)=17.4+ 1.5= 18.9 (18.9-17.7)/17.7 = 6.7% increase

41Kid with lung disease, on RA(1.34 x 13 x 0.75)+(0.003 x 40)= 13.1+0.1= 13.2Kid 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

42Kid with anemia, on RA(1.34 x 2.5 x 1) + (0.003 x 90)=3.4+ 0.3= 3.7Kid 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

43Kid with cyanotic heart disease, on RA(1.34 x 16 x 0.75) + (0.003 x 40) =16.1+ 0.1= 16.2Kid with cyanotic heart disease, on 100% (Dont 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

44A few notes on cyanotic heart disease:High PAO2 can cause decreased pulmonary vascular resistance and lead to increased systemic-to-pulmonary shuntingPulmonary edemaSystemic hypo-perfusion

45A 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 isnt that sick. Titrate to the target, but if you cant hit it, err on the low side.

46Take 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.

47Take home points on blood oxygen content:Children with cyanotic lesions are polycythemic to compensate for their persistently desaturated state, so dont let the low sats scare you. Dont 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.

48Enough about blood oxygen content!

On to Cardiac Output!

49What 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

50What is a childs primary compensatory mechanism when DO2 is insufficient for VO2?

Tachycardia, Tachycardia, Tachycardia

(Also brought on by fever, pain, anxiety, etc.)

51What is a childs primary compensatory mechanism when DO2 is insufficient for VO2?

In the first months of life, tachycardia to the 180s is common and not impressive. Breastfeeding may be enough to induce it.Intermittent tachycardia to 200s or 220s should raise a red flag, but isnt particularly rare, either.

52So how do I know what HR is worrisome?Watch for variability. A baby who works his way up to 220 for a few seconds and calms back down to 180 is not in SVT (which usually starts around 240), and is less worrisome than a baby stuck at 180 or stuck at 220.

53So how do I know what HR is worrisome?Watch the response to your interventions. Giving oxygen and giving fluid boluses should result in significant improvements in tachycardia.

54Take home point:A patient who has shown the capacity for tachycardia, who has a normal HR now, has adequate DO2 for his needs.

55As we look at the our initial interventions for critically ill patientseven without a diagnosisthey fall clearly within the paradigm of DO2 vs VO2.Deliver 100% FiO2Assess perfusion, assist if necessarySecure airway, assist breathing if necessary

56Continuous monitoring for HR, RR, Sat (and frequent BP)Maximize preload (bolus, bolus, bolus)Augment contractility (inotropes)Augment HR (chronotropes)

57When a baby is brought back to the resuscitation room grey and lifeless, the initial decisions are easy.Children not quite as sick, or those who respond well to initial interventions, but have persistant derangements in labs, vitals, or physical exam are more anxiety provoking for providers.

58What are the best objective measures to assess the relationship of DO2 and VO2 in your patient?

(IE, What can tell you that your patient is good enough for now versus that you need to continue active interventions?)

59HRBicRRBESatLactateBPSaO2-SVO2UOPpHPaCO2PaO2

60Vital SignsHRIn children, it is an early and powerful compensatory mechanism directly tied to DO2 and VO2Normal HR with frequent variability is extremely reassuringTachycardia is a red flag, but non-specificRRNormal RR with variability is also extremely reassuringIn an alert child, it trumps any scary noise

61Vital SignsSatImportant and telling, but doesnt directly address DO2 at the tissue levelBPThe VS which impresses me the least and tells me the least.If you dont have one, you die, but unless it is a very extreme value, its not very telling in children(Where is BP in the DO2 formula?)

62DO2=[O2 content in blood] x CO[(1.34 x Hb x Sat) + (0.003 xPaO2)] x HR x SV / | \ Pre Con After BP

63Tools to assess DO2 vs VO2UOPTells me about perfusion, a big chunk of the equation, but doesnt exactly answer the question.pHTells me if my pt acidemicInsufficient DO2 can cause acidemiaPaCO2Good infohelps me interpret my pH, but doesnt address my question.BICdoesnt directly address the question

64Tools to assess DO2 vs VO2LactateDirectly answers the question!Krebs cycle (CO2 and lots of ATP) O2Glucose (6 Cs) 2 Pyruvates (3 Cs) Lactate (3 Cs, 2 ATP)

65Tools to assess DO2 vs VO2LactateDirectly answers the question!Accumulates in minutesClears in minutes to hoursEasy to trend

Can be elevated in certain metabolic diseases

66Tools to assess DO2 vs VO2SaO2-SVO2 Directly answers the question!Measures oxygen extraction(Dont confuse SaO2 with PaO2)Normal 25ish, above 40 is worrisomeMaybe falsely reassuring in mitochondrial dysfunction (like in some cases of sepsis)

67Case #15 y/o, 20 kg boy presents with RR 40-50s and labored breathing, peri-oral cyanosis, and ill appearance, after 3 days of a bad cold. He has no significant PMH.

The pt remains cyanotic, though mildly improved, after non-rebreather, then a brief trial of BiPAP. Ultimately, he is intubated in the ED for saturations in the low 80s and persistent distress.

68Case #1(PICU attending is coming, but is stuck on a bridgeHe predicts he will another 2 hours, at least.)Post intubation CXR shows a tube in good position and diffuse bilateral infiltrates with areas of atelectasis.

69Case #1The patient has only stirred occasionally since intubation.Current vent settings are 150 ml/5 peep x 22, FiO2 100%Sats 85% RR 22 Peak Pressure 28ABG 7.25/60/50

70Case #1How do you assess this patients DO2 vs VO2?

If you determine it is necessary, how can you improve his oxygen balance?

71Case #21 m/o 4 kg girl is brought to the ED at 6am grey, with poor respiratory effort, and minimally responsive. HR 230 RR 20 BP not obt temp 35.9 sat 87%She is intubated, a pre-tibial IO is placed, and a 20 ml/kg bolus is initiated.An initial capillary blood gas shows 7.0/90/30 Lactate 15

72Case #290 minutes into her resuscitation, the patient has received 60 ml/kg crystalloid and Abx.Femoral venous and arterial lines have been placed.Dopamine and dobutamine drips have been initiated and progressively increased to 20 mcg/kg/min, in addition to a norepi drip at 1.5 mcg/kg/min

73Case #2HR is now 190-210, BPs 50/25, sat 100% temp 37.5Vent settings PIP 18 /5 PEEP x 25, FiO2 100%RR 32 measured Vt 20-35 mlCurrent ABG 7.15/40/350, lactate 13

74Case #2How do you assess this patients DO2 vs VO2?

If you determine it is necessary, how can you improve her oxygen balance?

75When you have maximized DO2, and your patient is still inadequately treated, we have many interventions to reduce VO2.

IntubateSedateParalyzeTreat Sz, even if subclinical(NPO)

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