Oxygen-Delivery-vs-Oxygen-Consumption

Report
Oxygen Delivery vs
Oxygen 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 physiologic principles of
tissue oxygen delivery and oxygen
consumption.
• 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.
• Let’s make this interactive!
(I usually do this talk sitting at a table with a
pen and paper.)
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
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.
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.
• 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)
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
• 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)
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)
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
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
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
How is this clinically meaningful?
Children of all ages have the capacity to
significantly compensate for increased oxygen
requirement by increasing RR and Vt.
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.
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”.
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.
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.
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!)
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)
• 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)
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
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.
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
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.
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
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
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)
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
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.
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.
Carbon dioxide moves across the
alveolar/capillary membrane rapidly.
Functional alveolar surface area is rarely if
ever a limiting factor to CO2 removal.
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.
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)
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
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
• 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)
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
What are the determinants of blood
oxygen content?
Hb bound O2
+
1.34 x Hb x sat (as integer) +
Dissolved O2
0.003 x PaO2
To get familiar with the norms and implications
of different derangements, we’ll do some
example calculations.
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
(18.9-17.7)/17.7 = 6.7% increase
=
= 18.9
Kid with lung disease, on RA
(1.34 x 13 x 0.75)+
13.1
+
(0.003 x 40)
0.1
Kid with lung disease, on 100%
(1.34 x 13 x 0.9) +
(0.003 x 60)
15.7
+
0.2
(15.7-13.2)/13.2 = 18.9% increase
=
= 13.2
=
= 15.7
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
(4.9-3.7)/3.7 = 32.4% increase
=
= 4.9
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
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
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.
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.
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.
Enough about blood oxygen content!
On to Cardiac Output!
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
What is a child’s primary
compensatory mechanism when DO2
is insufficient for VO2?
Tachycardia, Tachycardia, Tachycardia
(Also brought on by fever, pain,
anxiety, etc.)
What 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.
So 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.
So 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.
Take home point:
A patient who has shown the capacity
for tachycardia, who has a normal HR
now, has adequate DO2 for his needs.
As 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% FiO2
• Assess perfusion, assist if necessary
• Secure airway, assist breathing if
necessary
• Continuous monitoring for HR, RR, Sat
(and frequent BP)
• Maximize preload (bolus, bolus, bolus)
• Augment contractility (inotropes)
• Augment HR (chronotropes)
When 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.
What 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?)
HR
RR
Sat
BP
UOP
pH
PaCO2
PaO2
Bic
BE
Lactate
SaO2-SVO2
Vital Signs
HR
RR
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-specific
Normal RR with variability is also
extremely reassuring
In an alert child, it trumps any scary noise
Vital Signs
Sat Important and telling, but doesn’t directly
address DO2 at the tissue level
BP 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?)
DO2=
[O2 content in blood]
x CO
[(1.34 x Hb x Sat) + (0.003 xPaO2)] x HR x SV
/ | \
Pre Con After
↑
BP
Tools 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 acidemia
PaCO2Good info…helps me interpret my pH, but
doesn’t address my question.
BIC doesn’t directly address the question
Tools 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)
Tools 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
Tools 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)
Case #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.
Case #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.
Case #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 28
ABG 7.25/60/50
Case #1
How do you assess this patient’s DO2 vs VO2?
If you determine it is necessary, how can you
improve his oxygen balance?
Case #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
Case #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
Case #2
HR is now 190-210, BP’s 50/25, sat 100%
temp 37.5
Vent settings PIP 18 /5 PEEP x 25, FiO2 100%
RR 32 measured Vt 20-35 ml
Current ABG 7.15/40/350, lactate 13
Case #2
How do you assess this patient’s DO2 vs VO2?
If you determine it is necessary, how can you
improve her oxygen balance?
When you have maximized DO2, and your
patient is still inadequately treated, we have
many interventions to reduce VO2.
Intubate
Sedate
Paralyze
Treat Sz, even if subclinical
(NPO)

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