Abstract

Hemodynamic monitoring is a central component of intensive care. Patterns of hemodynamic variables often suggest cardiogenic, hypovolemic, obstructive, or distributive (septic) etiologies to cardiovascular insufficiency, thus defining the specific treatments required. Monitoring increases in invasiveness, as required, as the risk for cardiovascular instability-induced morbidity increases because of the need to define more accurately the diagnosis and monitor the response to therapy. Monitoring is also context specific: requirements during cardiac surgery will be different from those in the intensive care unit or emergency department. Solitary hemodynamic values are useful as threshold monitors (e.g. hypotension is always pathological, central venous pressure is only elevated in disease). Some hemodynamic values can only be interpreted relative to metabolic demand, whereas others have multiple meanings. Functional hemodynamic monitoring implies a therapeutic application, independent of diagnosis such as a therapeutic trial of fluid challenge to assess preload responsiveness. Newer methods for assessing preload responsiveness include monitoring changes in central venous pressure during spontaneous inspiration, and variations in arterial pulse pressure, systolic pressure, and aortic flow variation in response to vena caval collapse during positive pressure ventilation or passive leg raising. Defining preload responsiveness using these functional measures, coupled to treatment protocols, can improve outcome from critical illness. Potentially, as these and newer, less invasive hemodynamic measures are validated, they could be incorporated into such protocolized care in a cost-effective manner.

Highlights

  • Hemodynamic monitoring is a cornerstone of care for the hemodynamically unstable patient, but it requires a manifold approach and its use is both context and disease specific

  • Hemodynamic monitoring must be considered within the context of proven medical therapies, success of which is dependent on the clinical condition, pathophysiological state and ability to reverse the identified disease process

  • One may ask just three questions regarding the cardiovascular system during resuscitation from shock [57]: will blood flow to the body increase with fluid resuscitation?; is arterial hypotension due to inadequate blood flow or loss of vasomotor tone, or both?; and is the heart capable of maintaining effective blood flow without going into failure? If the answer to the first question is ‘yes’, treatment must include volume expansion

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Summary

Introduction

Hemodynamic monitoring is a cornerstone of care for the hemodynamically unstable patient, but it requires a manifold approach and its use is both context and disease specific. Demonstration, using echocardiographic techniques, of more than 36% superior vena caval collapse during positive-pressure inspiration [14] or complete inferior vena caval collapse [15,16] identifies individuals whose CVP is below 10 mmHg. there is no threshold value of CVP that identifies patients whose cardiac output will increase in response to fluid resuscitation [17]. Volume challenge The time-honored method of assessing preload responsiveness is to administer a relatively small intravascular volume bolus rapidly and observe the subsequent hemodynamic response in terms of blood pressure, pulse, cardiac output, SvO2 and related measures. The extent to which these measures accurately track real stroke volume fluctuations is unclear Because these various devices calculate stoke volume differently, the threshold values for each parameter in predicting preload responsiveness may be different between devices, and may exhibit different degrees of robustness under varying clinical conditions. These studies underscore the importance of examining the utility of monitoring systems within the context of a specific disease process coupled to effective treatment protocols

Conclusion
Schmidt-Nielsen K
35. Pinsky MR
40. Pinsky MR
44. Perel A
Findings
50. Pinsky MR
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