Consumption K Allen Eddington MD MSc Assistant Professor Pediatric Critical Care Medicine Albert Einstein College of Medicine Objective Demonstrate a framework for the assessment initial resuscitation and ongoing reassessment and management of critically ill children based on p ID: 759549
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Oxygen Delivery vs Oxygen Consumption
K. Allen Eddington, MD, MScAssistant ProfessorPediatric Critical Care MedicineAlbert Einstein College of Medicine
Slide2Objective:
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.
Slide3There 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.
Slide4Let’s make this interactive! (I usually do this talk sitting at a table with a pen and paper.)
Slide5Oxygen Delivery > Oxygen Consumption (DO2 > VO2)
If this relationship is not maintained…Tissue damage begins within minutesIf not corrected, organ damage and death ensue…rather rapidly
Slide6Oxygen 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.
Slide7In 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.
Slide8Air (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)
Slide9Let’s look at the physiology of each of these steps more closely, to seehow patients (especially children) compensate when something doesn’t work well what clinical data is most critical to gatherwhat interventions will most directly address maintaining DO2 > VO2 at each step
Slide10Air (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)
Slide11Air 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)
Slide12Vt (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
Slide13In 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
Slide14Examples;Stressed, 1 month-old, 4 kg 25 ml x 90 bpm x 0.21 = 475 ml O2 /min (475-220)/220 x 100% = 115% increaseStressed 16 y/o, 60 kg 900 ml x 30 bpm x 0.21 = 5600 ml O2 /min (5600-1300)/1300 x 100% = 330% increase
Slide15How is this clinically meaningful?Children of all ages have the capacity to significantly compensate for increased oxygen requirement by increasing RR and Vt.
Slide16How is this clinically meaningful?Take home point:If a patient’s compensatory mechanism is intact, but not in use, respiratory failure is not imminent.
Slide17How is this clinically meaningful?It is usually obvious when the compensatory mechanism is NOT intact. Severe neurological impairmentTiring after prolonged compensationCheck 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”.
Slide18How 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.
Slide19How 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.
Slide20How 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!)
Slide21When 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)
Slide22Air (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)
Slide23Oxygen 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 oxygenFunctional surface area of the membranesConcentration gradient
Slide24How do we assess the ability of oxygen to diffuse in a particular patient?A-a gradient….the classic answerPAO2 –PaO2 = FiO2 (Patm-PH2O) – PaCO2/0.8Doable, but not handy.
Slide25How 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
Slide26How do we assess the ability of oxygen to diffuse in a particular patient?Other estimates include :PaO2/FiO2 ratioSPO2/FiO2 ratioThese are intuitive, simple to remember, and simple to calculate.
Slide27How do we assess the ability of oxygen to diffuse in a particular patient?Examples calculations:Healthy lungs, on Room AirPaO2 = 100 mmHg SPO2 = 100%P/F = 100/0.21 = 476 Sp/F = 476
Slide28How 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 = 267 Sp/F = 95/0.30 = 317
Slide29How 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)
Slide30How 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
Slide31How 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.
Slide32Oxygen 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.
Slide33Carbon dioxide moves across the alveolar/capillary membrane rapidly. Functional alveolar surface area is rarely if ever a limiting factor to CO2 removal.
Slide34Membrane 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.
Slide35How 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.RRVt or positive inspiratory pressure (PIP)
Slide36How 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
Slide37How 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
Slide38Air (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)
Slide39Oxygen 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 OutputDO2=CO x O2 content
Slide40What are the determinants of blood oxygen content?
Hb bound O2 + Dissolved O21.34 x Hb x sat (as integer) + 0.003 x PaO2To get familiar with the norms and implications of different derangements, we’ll do some example calculations.
Slide41Normal kid, on room airHb 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
Slide42Kid 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
Slide43Kid 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
Slide44Kid 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
Slide45A 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
Slide46A 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.
Slide47Take 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.
Slide48Take 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.
Slide49Enough about blood oxygen content!On to Cardiac Output!
Slide50What are the determinants cardiac output?
CO = HR x Stroke VolumeAnd the determinants of Stroke Volume? Preload, Contractility, AfterloadCO = HR x SV / | \ Pre Con After
Slide51What is a child’s primary compensatory mechanism when DO2 is insufficient for VO2?Tachycardia, Tachycardia, Tachycardia(Also brought on by fever, pain, anxiety, etc.)
Slide52What is a child’s 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 isn’t particularly rare, either.
Slide53So 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.
Slide54So 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.
Slide55Take home point:A patient who has shown the capacity for tachycardia, who has a normal HR now, has adequate DO2 for his needs.
Slide56As we look at the our initial interventions for critically ill patients—even without a diagnosis—they fall clearly within the paradigm of DO2 vs VO2.Deliver 100% FiO2Assess perfusion, assist if necessarySecure airway, assist breathing if necessary
Slide57Continuous monitoring for HR, RR, Sat (and frequent BP)Maximize preload (bolus, bolus, bolus)Augment contractility (inotropes)Augment HR (chronotropes)
Slide58When 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.
Slide59What 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?)
Slide60HR BicRR BESat LactateBP SaO2-SVO2UOPpHPaCO2PaO2
Slide61Vital Signs
HR In children, it is an early and powerful compensatory mechanism directly tied to DO2 and VO2 Normal HR with frequent variability is extremely reassuring Tachycardia is a red flag, but non-specificRR Normal RR with variability is also extremely reassuring In an alert child, it trumps any scary noise
Slide62Vital Signs
Sat Important and telling, but doesn’t directly address DO2 at the tissue levelBP The VS which impresses me the least and tells me the least. If you don’t have one, you die, but unless it is a very extreme value, it’s not very telling in children (Where is BP in the DO2 formula?)
Slide63DO2= [O2 content in blood] x CO[(1.34 x Hb x Sat) + (0.003 xPaO2)] x HR x SV / | \ Pre Con After ↑ BP
Slide64Tools to assess DO2 vs VO2
UOP Tells me about perfusion, a big chunk of the equation, but doesn’t exactly answer the question.pH Tells me if my pt acidemic…Insufficient DO2 can cause acidemiaPaCO2Good info…helps me interpret my pH, but doesn’t address my question.BIC doesn’t directly address the question
Slide65Tools to assess DO2 vs VO2
Lactate Directly answers the question! Krebs cycle (CO2 and lots of ATP) ↗O2 Glucose (6 C’s) → 2 Pyruvates (3 C’s) ↘ Lactate (3 C’s, 2 ATP)
Slide66Tools to assess DO2 vs VO2
Lactate Directly answers the question! Accumulates in minutes Clears in minutes to hours Easy to trend Can be elevated in certain metabolic diseases
Slide67Tools to assess DO2 vs VO2
SaO2-SVO2 Directly answers the question! Measures oxygen extraction (Don’t confuse SaO2 with PaO2) Normal 25ish, above 40 is worrisome Maybe falsely reassuring in mitochondrial dysfunction (like in some cases of sepsis)
Slide68Case #1
5 y/o, 20 kg boy presents with RR 40-50’s 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 80’s and persistent distress.
Slide69Case #1
(PICU attending is coming, but is stuck on a bridge…He 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.
Slide70Case #1
The 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
Slide71Case #1
How do you assess this patient’s DO2 vs VO2?If you determine it is necessary, how can you improve his oxygen balance?
Slide72Case #2
1 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
Slide73Case #2
90 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
Slide74Case #2
HR is now 190-210, BP’s 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
Slide75Case #2
How do you assess this patient’s DO2 vs VO2?If you determine it is necessary, how can you improve her oxygen balance?
Slide76When you have maximized DO2, and your patient is still inadequately treated, we have many interventions to reduce VO2.IntubateSedateParalyzeTreat Sz, even if subclinical(NPO)