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Anthony Rossi, MD Director, Cardiac Intensive Care Program Congenital Heart Institute Miami Childrens Hospital, Miami, FL USA
Warning!!!!!!
My comments are completely biased They are based on 21 years of clinical experience with SvO2 monitoring in the CICU They are based on some sound physiologic principles I believe in
Early detection of hemodynamic derangements Early correction of hemodynamic derangements a Goal oriented therapy in the critically ill
We must Identify shock states or impending shock states such as low cardiac output syndrome (LCOS) at the earliest possible moment.
a Last Exit before Eternity
Shock is a continuum
Warm shock
Cold shock
Irreversible shock
DEATH
Life isadependent on maintaining the most favorable relationship possible b/w VO2 and DO2
DO2/VO2
O2 O2 2 O O2 O 2 O2
In the relationship of DO2 and VO2, in fully saturated patients, 5 times as much oxygen is delivered to the tissues as utilized (in desaturated pts such as those with cyanotic heart disease, the a situation is much more precarious*).. * Rossi et al. Congenit Heart Dis. 2006 Nov;1(6):294-9.
2
VO2
5 omega
* Decreasing CV Reserve
Not the most important piece of information! Only relevant when taken in context of patients oxygen requirements of a demands (VO2).
Definition of MvO2
Mixture of ALL the blood that has traversed the capillary beds capable of extracting oxygen. The mixed venous oxygen content will reflect the total body balance b/w DO2 and VO2 of perfused tissues.
a
MvO2 Monitoring
MvO2 Monitoring must occur at the site where all the venous blood in the body has pooled, such as the PA in pts with structurally normal hearts SVC monitoring better reflects cerebral blood flow physiology than global systemic blood flow IVC blood flow may best reflect splanchnic a blood flow
MvO2 Monitoring
defines the relationship of DO2/VO2 estimate oxygen delivery (AVO2 difference, OER, OEF/omega) estimate cardiac output trends estimate Qp/Qs
SaO2 poor indicator of Qp/Qs (low SvO2 will decrease SaO2 in face of large Qp/Qs)
a
1. 2. 3. 4.
a
Rossi et al. Am J Cardiol; 1994
a
Rossi et al. Am J Cardiol; 1994
OER
survivors nonsurvivors
normal
6 hours tim e
24 hours
Liver
Intestine Brain
MUSCLE IS THE FIRST ORGAN SYSTEM TO BE AFFECTED BY LCOS. IT MAKES COMPLETE SENSE THAT WE SHOULD a BE TARGETING THAT ORGAN SYSTEM FOR MONITORING!!!
From: Pathologic Foundations of Critical Care. Pinsky and Dhainhaut
Redistribution of BF in Shock
Early shock (or LCOS) is marked by a maldistribution of blood flow to critical organs (such as the brain and heart) and away from organs like the mesenteric bed or the limbs. It is intuitive that the earliest signs of LCOS (such as low venous O2 sat) would be found in the less critical organ systems, prompting earlier recognition and response by clinicians SVC or MVO2 monitoring MIGHT be considerably less valuable than IVC (esp. low IVC, which really a measures venous saturation of lower extremities!)
Lactate Monitoring
Advantage: Lactate is measured and is not a derived variable Advantage: Association with outcomes in critical illness is clear Advantage: Goal oriented therapy targeted at lactate has been associated with improved outcomes Disadvantage: End product that is a result of very significant derangement in oxygen delivery/oxygen consumption equation Disadvantage: Intermittently monitored. Lots can happen b/w samples. a
NIRS Monitoring
Advantage: Continuous monitoring technique Advantage: Noninvasive Disadvantage: what the heck is it really monitoring and what is the physiologic significance of this monitored data? Requires the use of conformational bias in decision making.
All the data that is consistent with your assessment of the pts underlying status is accepted. Data that is in disagreement with your assessment is a rejected.
Can we be lead astray by the inaccuracies of NIRS monitoring? Two points circled here, one suggests SvO2 would be high when it is not, the second suggests SvO2 is pathologically low when it is not.
Assumed SvO2=65
Measured SvO2=30 Decrease inotropes Extubate? a
3 y.o. s/p subaortic membrane resection. SaO2 100%. a What physiologic state is associated with an a-vO2 difference of 5 after CHS?
7 mo s/p TOF repair. SaO2=100% a Is the a-vO2 difference 31 or 5? Which number do you treat? Are the numbers truly reflective of the underlying physiology?
NB with HLHS. Just off pump after S1P. LCOS or not? a Using NIRS technology introduces cognitive dissonance and the need for applying conformational bias to resolve the conflict.
The earliest warning sign that something is awry. Can monitoring splanchnic circulation or the venous oxygen sat from the major extremities in critical a illness achieve this?
Conclusions
Goal directed therapy is a valuable adjuvant to the management of critically ill patients, including those recovering after CHS SvO2 is an excellent hemodynamic parameter to target in GDT Monitoring individual, at risk tissue beds for hypoperfusion states may be of greater benefit than monitoring the admixture of all systemic venous blood a
Conclusions
Continuous monitoring of central venous oxygen saturation may be accomplished and of value in:
SVC RA Umbilical Vein Femoral Vein
a
Conclusions
Non-invasive SvO2 monitoring of the splanchnic bed may just be the Holy Grail! Maybe.
No hemodynamic monitoring technique should ever be considered a panacea or was intended to stand alone. Hemodynamic techniques should be accurate, objective, timely a (in real-time if possible) and most importantly complimentary.