When Oxygen Goes Bad or How Not to Kill a Small Child with O2

1. When Oxygen Goes BadorHow Not to Kill a Small Child with O2 Karim Rafaat, MD

2. Nice Things Can Hurt You

3. First, a simple example The PDA

4. 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 DuctusArteriousus • Relative resistances of systemic and pulmonary vascular beds ensure a well perfused body

5. 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 formaenovale • Oxygen and a decrease of maternal prostaglandins leads to the closure of the ductusarteriosus • But this closure does not always occur • Usually we see this secondary to extreme prematurity

6. 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

7. Qp:Qs • So, what determines our ratio of pulmonary to systemic blood flow? • Or, Qp:Qs • OHM’S LAW: V = I x R V is voltage, or, another way, driving force V = Pressure difference I is current or flow I = CO R is, in both cases, resistance

8. 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

9. 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

10. Resistance • Resistance to systemic flow determined by: • Presence of anatomic obstructive lesions • Aortic valve stenosis • Arch hypoplasia or coarctation • Subaortic obstruction • Systemic arteriolar resistance

11. 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

12. 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

14. 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

15. This is why most NICU transporters have O2 blenders, so a concentration of O2 other than 100% can be delivered to the child.

16. 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

17. 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

18. 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

19. DORV • Double Outlet Right Ventricle • Both the aorta and pulmonary artery arise from the RV • Accompanied by a VSD

20. D-TGA with VSD • Aorta and Pulmonary Artery arise from the wrong ventricle • Mixing occurs through the VSD

21. CAVC • Complete AV Canal • atrial septal defect • abnormal tricuspid valve • abnormal mitral valve • ventricular septal defect

22. Truncus Arteriosus • single large arterial trunk arises from both ventricles, • large VSD just below the trunk

23. Tetralogy of Fallot • ventricular septal defect (VSD) • pulmonary (or right ventricular outflow tract) obstruction • overriding aorta. • Right ventricular hypertrophy

24. 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

25. 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

26. 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

27. 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

28. How do we know when we should exercise caution?

29. 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

30. 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

31. 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.