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Anthony Rossi, MD Director, Cardiac Intensive Care Program Congenital Heart Institute Miami Children’s Hospital, Miami, FL USA
• 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
The Value and Clinical Utility of Continuous SvO2 Monitoring
• This slide show will address
– Relationship of DO2 to VO2 – Goal Oriented therapy in the critically ill – Definition of SvO2 – Use GDT and SvO2 monitoring in CHS – Pitfalls of other measures of cardiovascular well-being in the critically ill
Shock is a rest stop on the highway to death:
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
Last Exit before Eternity
The Constant Tug of War between DO2 and VO2
Life isadependent on maintaining the most favorable relationship possible b/w VO2 and DO2
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.
Relation of DO2 to VO2
critical point of DO2 Lactate increases DO2
* Decreasing CV Reserve
DO2 and Critical Illness
• Monitoring DO2 in the critically ill and developing treatment plans to optimize DO2, is a logical approach to pt management and has been shown to improve outcomes in a wide spectrum of critical illness • Pts achieving a normal or supernormal level of DO2 have lower mortality, less end organ damage, lower morbidity and shorter hospital stays a
Goal of Post-Op Care: Maintain Optimal Tissue Oxygenation • Global • Regional
• splanchnic - the correction of unrecognized perfusion defects seems to be a desirable addition to the standard clinical management of critically ill patients with regard to preservation of organ function* • coronary a * J.-L. Vincent. Intensive Care Med (1996) 22:3
Can You Measure DO2 Following CHS?
• CI usually impossible to measure because of intracardiac shunting • small patient size makes CI measurements impractical
Use indirect measures of DO2
Indirect Indicators of Systemic DO2
• • • • • • pH HCO3 BE SVO2 (Δ AVO2, OER) Δ CO2 (SvCO2-SaCO2) lactate
Why not Measure CO?
• Impractical in kids after CHS
– Small size – Intra-cardiac mixing
• Not the most important piece of information! • Only relevant when taken in context of patients oxygen requirements of a demands (VO2).
What does that CO measurement mean?
• I implant an artificial heart in you and set it at a “normal cardiac output” • Is that sufficient CO for the whole range of stresses in life or in the ICU? • Wouldn‟t it make sense to measure something that looks at the CVS ability to meet the metabolic needs of the body? • *Data suggests that in some pt populations after CHS, the most important derangement in PO hemodynamics is not the decrease in CO but actually the increase in VO2. We need to measure the end product of this balance, not the individual components. – *Li et al. JTCVS 2006
Common Cardiac Surgical Procedures
• • • • • • • • • • • • Arterial switch operation Repair of tetralogy of Fallot VSD closure ASD closure AVC repair Rastelli operation Norwood operation Bi-Glenn Fontan Repair IAA a BTS Central shunt • • • • • • • • • • • • Ross MV replacement AV replacement Aortic Valvotomy Konno Ross-Konno Repair TAPVC Repair coarctation Repair DORV Senning Mustard Double switch
Single Goal of PO Care
• Maintain optimal tissue oxygen delivery
Goal Directed Therapy
• Therapy directed at specific end points, usually related to indices of DO2 in intensive care patients. Indices have traditionally included CO or SvO2.
Psychological Benefits of GDT
• “Don‟t mess up!” • “Keep „em alive till 8:05” • Goal oriented tasks keeps team members focused • Little rewards (tangible results)
Definition of SvO2
• 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.
• SvO2 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
• 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)
Causes of Low SVO2 SVO2 = SaO2 – (VO2/Q x Hb x 13)
1 2 3 4
1. 2. 3. 4.
Hypoxemia Increased metabolic rate Low cardiac output anemia
SaO2 does not predict SvO2 after Norwood
Rossi et al. Am J Cardiol; 1994
SaO2 and Qp/Qs after Norwood
Rossi et al. Am J Cardiol; 1994
OER and OEF
• OER = O2 consumption/O2 delivery • OER = O2 Sat art - O2 Sat sys ven O2 Sat art • normal relationship of 5/1 DO2/VO2 • normal OER = 0.20 • normal OEF = 5 (Ω = 5)
AVO2 difference vs. OER
• AVO2 diff of 25 in pt with SaO2 100%
– OER = 25/100 = 0.25 – OEF = 4 – DO2/VO2 = 4/1 (normal)
• AVO2 diff of 25 in pt with SaO2 65%
– OER = 25/65 = 0.38 – OEF = 2.5
a –DO2/VO2 = 2.5/1 (2/1 = critical point of DO2!)
OER in Infants following Heart Surgery
0.55 0.5 0.45
0.4 0.35 0.3 0.25 0.2 admit
6 hours tim e
Rossi, Seiden, Gross, et al. Annals Thorac Surg. 1999
SvO2 Monitoring Decreases Morbidity and Mortality
Where to measure SvO2?
• • • • PA: only true “mixed venous sat” SVC: very dependant on cerebral BF RA: not for pts with L to R shunt (HLHS) IVC: lower body sat
– Could over estimate MvO2 because renal vein contribution – Measures splanchnic BF – Should never be low
• Umbilical Vein a • Femoral Vein
Hierarchies of Organ Hypoxia
V O2 Whole Body DO2
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
MEASURING REGIONAL OXYGEN DELIVERY MAY BE MORE IMPORTANT THAN GLOBAL!!!!
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!)
Alternatives to Continuous SvO2 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
How about Non-Invasive SvO2 Monitoring?
It sounds great but doesn’t exist!
• 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.
Measured SvO2=30 Decrease inotropes Extubate? a
Assumed SvO2=25 Measured SvO2=52
Augment DO2 Decrease VO2
NIRS incorrectly Predicts normal DO2
NIRS correctly predicts normal DO2
NIRS correctly a predicts low DO2
NIRS incorrectly predicts low DO2
Three site NIRS Monitoring
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?
Two Site NIRS Monitoring
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?
Two Site NIRS Monitoring
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.
We need the Canary in the Cave
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?
• 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
• Continuous monitoring of central venous oxygen saturation may be accomplished and of value in:
– SVC – RA – Umbilical Vein – Femoral Vein
• Non-invasive SvO2 monitoring of the splanchnic bed may just be the Holy Grail! Maybe.
Thanks for Listening!!!
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.
Special Thanks To: