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Why Cardiac Output?

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Case Study - “Flow-directed Goal-directed Therapy”


Summary
Traditional monitoring, using vital signs alone, has been shown to be inadequate in some clinical instances. While HR, SBP, CVP and MAP are useful indicators, relying solely on these can lead to unfavorable therapy, including over resuscitation or inappropriate resuscitation. Evidence suggests that early application of these indicators in conjunction with flow parameters in a goal-directed protocol can lead to significant clinical and economic benefits, including:
  • Reduced mortality
  • Fewer complications and reduced morbidity
  • Shorter length of hospital stay
  • Lower costs to hospitals
Minimally invasive cardiac output monitoring technologies, such as the FloTrac sensor and Vigileo monitor, benefit the clinician by providing key flow parameters to help guide the treatment of critically ill and high-risk patients. The FloTrac system sets up rapidly, is easy to use and requires no manual calibration. This ease of application may lead to earlier initiation of flow-directed goal-directed therapy, which has been shown to improve patient outcomes. When coupled with goal-directed therapy (such as a Rivers EGDT protocol), it enables clinicians and nurses to manage patients’ oxygen delivery more precisely than traditional vital sign monitoring alone.

Why flow-directed?
Clinical therapy has traditionally centered on monitoring various vital signs. A growing body of literature, however, suggests that goal-directed therapy focusing on maximizing effective blood flow, in conjunction with vital sign monitoring, bears the potential for considerable improvement to the outcome of both critically ill and high-risk surgical patients. Bennett has suggested that traditional vital sign monitoring that stresses blood pressure, heart rate (HR), respiratory rate and temperature may not be sufficient as a predictive indicator and should be monitored in combination with flow parameters.1

Traditional vital signs and monitoring parameters may include ECG, non-invasive and/or intra-arterial blood pressure, SpO2, and central venous pressure (CVP). However, in some instances, vital signs can be of limited use or lead to unfavorable therapy:
  • Baroreceptor-mediated vascular compensation by increasing vascular tone can sustain a constant blood pressure in a patient losing as much as 18% of blood volume before being associated with a drop in mean arterial pressure (MAP).1
  • MAP monitoring can be a poor predictive indicator because “…systemic hypoperfusion usually precedes hypotension, especially in patients with hemorrhage and sepsis.”2
  • Evidence suggests that no solid link exists between oxygen delivery and systolic blood pressure (SBP) in hemorrhaging trauma patients.3
  • HR, respiratory rate and SBP may be poor predictors of critically ill patients.4
  • Monitoring of HR and SBP alone may not adequately reveal hypovolemia or may “cloak” hypoperfusion.1,5
  • SBP, CVP and HR show considerable lack of sensitivity and specificity as predictors of fluid responsiveness in neurosurgery compared to stroke volume variation (SVV).6
Incorrect measurement and/or interpretation based on traditional vital signs alone can lead to imprecise interventions such as over or under resuscitation and inappropriate resuscitation. Instead, the clinician may consider the use of flow directed parameters to help guide and give confidence in the direction of therapy.

Evidence for flow-directed goal-directed therapy
Protocolized therapy based on flow-directed parameters can lead to considerable advantages in treatment of critically ill patients. Such flow parameters include cardiac output (CO) and cardiac index (CI), stroke volume (SV) and stroke volume index (SVI), and oxygen delivery (DO2). Mixed venous oximetry (SvO2) can be used as an indirect marker of oxygen delivery by determining the “adequacy of oxygen delivery” against oxygen consumption (VO2).4,7 Central venous oximetry (ScvO2) can also be used in determining the adequacy of oxygen delivery with the understanding that it usually differs ±7% higher than SvO2 and this difference can widen greatly in shock states. However, ScvO2 trends with SvO2 90% of the time.8 Flow-directed, goal-directed optimization using the above parameters in a rigorous and well designed treatment protocol has been effective in the treatment of a variety of patients, including those undergoing

Reduced Mortality
Investigator Flow
Parameter
Control Protocol Patient Type
Wilson CI, DO2 17% 3%
(P=0.007)
major elective surgery
Boyd DO2 22.2% 5.7%
(P=0.015)
high risk
surgery
Shoemaker CI, DO2 35% 12.5%
(P<0.02)
critical
post-op.
Shoemaker CI, DO2 35% 4%
(P<0.01)
high
risk surgery

Fewer Complications / Reduced Morbidity
Investigator Flow
Parameter
Control Protocol Patient Type
Morbidity % dIfference % dIfference
Pearce CO 68% 44%
(P=0.003)
high risk
surgery
Venn SV, CO 28% 7%
(P<0.05)
hip fracture
repair
Complications Complications
per patient
Complications
per patient
Boyd DO2 1.35 0.68
(P=0.008)
high risk
surgery
Shoemaker CI, DO2 1.34 0.76
(P<0.05)
critical
post-op.
Shoemaker CI, DO2 1.30 .39
(P<0.01)
high risk
surgery


Shorter Length of Stay - Hospital Days
Investigator Flow
Parameter
Control Protocol Patient Type
Pearse CO 14 11 high
risk surgery
Gan CO, SV 7±3 5±3 major
surgery
Wilson CI, DO2 22 13 major elective
surgery
Shoemaker CI, DO2 2.5.2±3.4 19.3±2.4 high
risk surgery
McKendry CI, DO2 14 11 high
risk surgery
Sinclair CO, Max SV 20 12 hip fracture
repair

Health-Economic Benefits
Investigator Flow
Parameter
Result
Fenwick CI, DO2 Mean cost of pre-optimized patients was
33% less than control group
Guest CI, DO2 Cost of obtaining a survivor in protocol group was
31% less than control group
Shoemaker CI, DO2 Hospital charge of protocol group was
26% less than control
major elective and high-risk surgery, cardiac surgery, in the emergency department and those suffering from hypovolemia or organ failure. Various studies suggest that significant benefits are realized from protocol-driven perioperative flow-directed therapy.9-17

Furthermore, optimization of flow-directed therapy using specific treatment protocols can lead to significant benefits in prevention of organ failure stemming from hypovolemia, particularly in cases of renal failure.1,19 While hypovolemia is poorly predicted by traditional vital sign monitoring, it can be predicted and prevented by monitoring and optimizing SV and CO.5,15,20 This can reduce the chances of a critically ill patient acquiring end-stage renal failure (ESRF), a condition which can cost a hospital more than $51,000/patient/year.19-21

Solution
A minimally invasive hemodynamic monitoring technology has been developed which can be used to monitor and optimize critically ill patients using various flow parameters. The FloTrac sensor and Vigileo monitor use an existing peripheral arterial line to monitor CO, SV and SVV in real time. ScvO2 is also available when the Vigileo monitor is used in conjunction with the PreSep central venous oximetry catheter. The FloTrac system can be set up in just a few minutes and is easy to use for both the nurse and the physician. The technology requires no manual calibration since the FloTrac algorithm automatically compensates for the continuously changing effects of vascular tone. The FloTrac sensor has been proven accurate and reliable in monitoring CO in clinical studies when compared against continuous cardiac output (CCO), intermittent cardiac output (ICO).22 The benefits seen in the previously mentioned studies using flowdirected goal-directed therapy should be equally realized with the FloTrac system. In addition, this ease of use and application can result in earlier initiation of flow directed goal-directed therapy, which in itself has been shown to provide better patient outcomes.

Oxygen Delivery




Any quotes used in this material are taken from independent third-party publications and are not intended to imply that such third party reviewed or endorsed any of the products of Edwards Lifesciences.


References
1. Bennett D. Arterial Pressure: A Personal View. Functional Hemodynamic Monitoring. Berlin: Springer-Verlag, 2005. ISBN: 3-540-22349-5.
2. Rackow EC: Pathophysiology and treatment of septic shock. JAMA 1991, 548-554. 3. Dutton RP: Hypotensive Resuscitation during Active Hemorrhage: Impact on In-Hospital Mortality. J Trauma 2002, 1141-1146.
4. Rady MY: Resuscitation of the Critically Ill in the ED: Responses of Blood Pressure, Heart Rate, Shock Index, Central Venous Oxygen Saturation, and Lactate. Am J Emerg Med 1996, 218-225.
5. Hamilton-Davies C: Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med 1997, 276-281.
6. Berkenstadt H: Stroke Volume Variation as a Predictor of Fluid Responsiveness in Patients Undergoing Brain Surgery. Anesth Analg 2001, 984-989.
7. Pinsky MR: Hemodynamic monitoring in the intensive care unit. Clin Chest Med 2003, 549-560.
8. Reinhart K: Continuous central venous and pulmonary artery oxygen saturation monitoring in the critically ill. Intensive Care Med. 2004,1572-8.
9. Wilson J: Reducing the risk of major elective surgery. BMJ 199,1099-1103.
10. Boyd O: A Randomized Clinical Trial of the Effect of Deliberate Perioperative Increase of Oxygen Delivery on Mortality in High-Risk Surgical Patients. JAMA 1993, 2699-2707.
11. Shoemaker WC: Use of Physiological Monitoring to Predict Outcome And to Assist in Clinical Decisions in Critically Ill Postoperative Patients. AM J Surg 1983, 43-50.
12. Shoemaker WC: Prospective Trial of Supranormal Values of Survivors as Therapeutic Goals in High-Risk Surgical Patients. Chest 1988, 1176-1186.
13. Pearse R: Early goal-directed therapy after major surgery reduces complications and duration of hospital stay. Critical Care 2005, R687-693.
14. Venn R: Randomized controlled trial to investigate influence of the fluid challenge on duration of hospital stay and perioperative morbidity in patients with hip fractures. Brit J Anaest 2002, 65-71.
15. Gan TJ: Goal-directed Intraoperative Fluid Administration Reduces Length of Hospital Stay after Major Surgery. Anesthesiology 2002, 820-826.
16. McKendry M: Randomised controlled trial assessing the impact of a nurse delivered, flow monitored protocol for optimization of circulatory status after cardiac surgery. BMJ, doi:10.1136/bmj.38156.767118.7C
17. Sinclair S: Intraoperative intravascular volume optimisation and length of hospital stay after repair of proximal femoral fracture. BMJ 1997, 909-912.
18. Fenwick E: Pre-operative optimisation employing dopexamine or adrenaline for patients undergoing major elective surgery Int Care Med 2002, 599-608.
19. Kellum JA: Primary prevention of acute renal failure in the critically ill. Curr Opin Crit Care 2005, 537-541.
20. O’Leary MJ: Preventing renal failure in the critically ill. BMJ 2001, 1437-1439.
21. Chikotas N: Uremic syndrome and end-stage renal disease. JAANP 2006 195-202.
22. Dr Gerry Manecke, Poster, SCCM 2005. Dr William McGee, Poster, ISICEM 2005.
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