When Oxygen Goes Bad

or

How Not to Kill a Small Child with O2Karim Rafaat, MD

Nice Things Can Hurt You

First, a simple example The PDA

Fetal CirculationFetal 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 occurUsually we see this secondary to extreme prematurity

PDANow, 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:QsSo, what determines our ratio of pulmonary to systemic blood flow?

Or, Qp:Qs

OHM’S LAW:

V = I x RV is voltage, or, another way, driving force

V = Pressure differenceI is current or flow

I = COR is, in both cases, resistance

Qp:Qs and PDAsRearranged:

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 pressureIn 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

HLHSThe 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 flowAtrial septectomyPulmonary trunk disconnected from MPAMPA and Aorta anastomosed to form a neo-aorta

DORVDouble Outlet Right Ventricle

Both the aorta and pulmonary artery arise from the RVAccompanied by a VSD

D-TGA with VSDAorta and Pulmonary Artery arise from the wrong ventricle

Mixing occurs through the VSD

CAVCComplete AV Canal

atrial septal defectabnormal tricuspid valveabnormal mitral valveventricular septal defect

Truncus Arteriosussingle large arterial trunk arises from both ventricles,

large VSD just below the trunk

Tetralogy of Fallotventricular 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 willIncrease 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 CautionThe 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 EchoThe 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 NurseIf 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 LineMore isn’t always better

Except if its cowbell

Oxygen is a drugIt 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.