When Oxygen Goes Bad
or
How Not to Kill a Small
Child with O2
Karim Rafaat, MD
Nice Things Can Hurt You
First, a simple example
The PDA
Fetal Circulation
Fetal Circulation is Parallel
Oxygenated Blood from the
umbilical vein enters the RA
Some mixes with systemic
blood and is ejected by the
RV into the PA
Most gets preferentially
shunted across the Foramen
Ovale, joins with a touch of
blood from the pulmonary
veins in the LA, then is
ejected by the LV
The PA and Aortic flows are
connected by the Ductus
Arteriousus
Relative resistances of
systemic and pulmonary
vascular beds ensure a well
perfused body
Transitional Circulation
Once born, O2 ensures a decrease in the resistance of
the pulmonary vasculature, to below the level of SVR
The decrease in RVEDP, and thus RAP, leads to a
functional closure of the formaen ovale
Oxygen and a decrease of maternal prostaglandins
leads to the closure of the ductus arteriosus
But this closure does not always occur
Usually we see this secondary to extreme prematurity
PDA
Now, there exists a path of variable size (we will assume
big for this talk) through which blood from the aorta
may shunt through to the pulmonary circulation
Qp:Qs
So, what determines our ratio of pulmonary to systemic
blood flow?
Or, Qp:Qs
OHM’S LAW:
V=IxR
V is voltage, or, another way, driving force
V = Pressure difference
I is current or flow
I = CO
R is, in both cases, resistance
Qp:Qs and PDAs
Rearranged:
I=V/R
or
Q = ΔP / R
ΔP can be affected by way of inotropy, but this has little
effect on the ratio of pulmonary to systemic flow
The resistances of the two circuits are separate, and can thus
be manipulated in a way that can effect flow differentially
Resistance
Resistance to Pulmonary flow is determined by
Valvar or subvalvar pulmonary stenosis
Pulmonary arteriolar resistance
Pulmonary venous and left atrial pressure
In part determined by:
amount of pulmonary blood flow
restriction of outflow through left atrioventricular valve
Resistance
Resistance to systemic flow determined by:
Presence of anatomic obstructive lesions
Aortic valve stenosis
Arch hypoplasia or coarctation
Subaortic obstruction
Systemic arteriolar resistance
Qp:Qs
The most easily alterable aspects are thus the
resistances of the respective vascular beds
The problem of balancing the flows can be
somewhat simplified to balancing the ratio of
PVR:SVR
Useful, as the majority of therapies available to
us that affect flow differentially do so by way of
manipulation of the resistance of the respective
vascular beds
Why is this important?
Physiology with a high Qp:Qs brings with it a relatively
low systemic oxygen delivery
Low systemic DO2 leads to tissue hypoxia, anaerobic
metabolism, and eventual end organ damage
So…… Getting on with it
Not only will O2 hurt the retina of tiny babies with
ROP
It will decrease their PVR, increase their Qp:Qs, thus
decreasing their systemic oxygen delivery.
This can lead quickly to acidosis and end organ damage
It will also drastically decrease their DBP, to the point
that LV perfusion is impaired
This is why most NICU transporters have O2 blenders,
so a concentration of O2 other than 100% can be
delivered to the child.
So What, just PDAs?
Nope, this issue of balancing pulmonary and systemic
flows in the face of a parallel circulation to ensure
adequate peripheral DO2 occurs in quite a few other
lesions
Ill move through these quickly, as some of you may
never ever hear of them again
HLHS
The most common is
Hypoplastic Left Heart
Syndrome
1. PFO
2. hypoplastic aorta
3. Patent PDA
4. aortic atresia
5. Hypoplastic left ventricle
Mixing occurs via a patent
PDA
HLHS post Norwood Stage I
We see this lesion
usually after the stage 1
Norwood operation
BTS supplies
pulmonary flow
Atrial septectomy
Pulmonary trunk
disconnected from MPA
MPA and Aorta
anastomosed to form a
neo-aorta
DORV
Double Outlet Right
Ventricle
Both the aorta and
pulmonary artery arise
from the RV
Accompanied by a VSD
D-TGA with VSD
Aorta and Pulmonary
Artery arise from the
wrong ventricle
Mixing occurs through
the VSD
CAVC
Complete AV Canal
atrial septal defect
abnormal tricuspid
valve
abnormal mitral valve
ventricular septal defect
Truncus Arteriosus
single large arterial
trunk arises from both
ventricles,
large VSD just below
the trunk
Tetralogy of Fallot
ventricular septal defect
(VSD)
pulmonary (or right
ventricular outflow
tract) obstruction
overriding aorta.
Right ventricular
hypertrophy
Qp:Qs
In lesions with parallel circulation, the total CO of the
usually single ventricle is shared between pulmonary
and systemic circulations
The ratio of Qp:Qs describes the relative amount of
pulmonary and systemic blood flow
The absolute value, however, is a representation of
total cardiac output
Qp:Qs
With complete mixing lesions, the ventricular output is
the SUM of Qp and Qs
Cause there’s, effectively, one ventricle
The higher the ratio, the higher the demand on the
heart
So, a Qp:Qs of 2:1 means that the heart is pumping
about 3 “cardiac outputs”
It must maintain such a high output in an attempt to
allow for acceptable systemic oxygen delivery
What does this mean?
Ventricular wall tension and myocardial oxygen
demand are increased in the dilated, volume
overloaded ventricle
Leads to myocardial dysfunction and AV valve
regurgitation
Prolonged increased pulmonary volume will lead
to pulmonary vascular bed remodeling
can lead to increased pulmonary vascular resistance,
which makes single ventricle surgical repair impossible
So, even over the course of a 5 min transport from the
NICU to the OR
100% O2 will
Increase Qp:Qs
increasing total myocardial workload and oxygen demand
Decrease systemic oxygen delivery, leading to acidosis and
end organ damage
The combination of the above two can lead to myocardial
ischemia
How do we know when we
should exercise caution?
Our Clues for Caution
The Cath Report
If a pt has a complex cardiac lesion, they have probably either
had an echocardiogram or gone to the cath lab
The cath report will describe systemic and pulmonary resistences
in Woods units, and even give you the Qp:Qs
The Echo
The lesion will be described. Look it up…….
The Saturation that the ICU is allowing to be “acceptable”
If the patient has a cardiac lesion, and the ICU is allowing a
saturation of 70% as acceptable, this should (ideally and
hopefully) indicate that this is the point of optimal Qp:Qs and
thus optimal DO2.
Keep it there
Our Clues for Caution
The Bedside Nurse
If they insist theres a good reason for allowing this child
to have sats of 75% and be on 21% O2, there may be a
reason for it
Bottom Line
More isn’t always better
Except if its cowbell
Oxygen is a drug
It can dramatically alter
pulmonary vascular
resistance and thus systemic
perfusion in a way that may
cause acidosis and end organ
damage
We can delve into more detail
with Fick, graphs etc next
time.