Fundamental concepts in perioperative fluid management: Consensus statement by POQI
The Perioperative Quality Initiative (POQI-5) consensus conference has developed consensus statements applicable to the physiologically based management of intravenous fluid therapy in the perioperative setting. The consensus statement has been published in Perioperative Medicine.
Optimal fluid therapy in the perioperative and critical care settings depends on understanding the underlying cardiovascular physiology and individualizing assessment of the dynamic patient state.
In the consensus conference two key concepts emerged as follows: (1) The ultimate goal of fluid therapy and hemodynamic management is to support the conditions that enable the normal cellular metabolic function in order to produce optimal patient outcomes, and (2) optimal fluid and hemodynamic management is dependent on an understanding of the relationship between pressure, volume, and flow in a dynamic system which is distensible with variable elastance and capacitance properties.
Main consensus statements are hereunder-
Physiological principles of fluid resuscitation
1. The ultimate goal of fluid and hemodynamic management is to support normal cellular metabolic function.
2. Achieving normal cellular metabolic function requires maintenance or restoration of the effective coordinated function of the macrocirculation and the microcirculation, as well as intact cellular metabolism.
3. Practically speaking, most clinical management is currently targeted at macrocirculatory variables and surrogates of cellular metabolism (e.g., lactate, base excess).
4. The therapeutic rationale of intravenous fluid administration is to optimize macrocirculatory function in order to improve or optimize microcirculatory and cellular function.
5. There is a minimal intravascular volume required to maintain cardiac output and stroke volume and normal tissue perfusion. Below this volume, cardiac output and blood pressure may be maintained at the expense of microcirculatory blood flow and cellular function.
6. The majority of intravascular volume is in the venous circulation; therefore, the venous capacitance is a critical determinant of effective macrocirculatory function.
Physiology of fluid responsiveness
1.There is no readily available method of measuring intravascular volume and it is uncertain if knowing this static value would have clinical utility.
2. Optimal intravascular volume can only be characterized by dynamic evaluation.
3. Administration of a fluid bolus as part of a fluid challenge is a means of increasing intravascular volume to evaluate the effect on stroke volume.
4. Fluid responsiveness is defined as a state of recruitable stroke volume in response to intravascular fluid administration.
Venous capacitance
1.The venous circulation is comprised of stressed and unstressed volumes.
2. Stressed volume is the (theoretically measurable) volume of blood that exerts distending pressure against the venous wall. In contrast, the unstressed volume is the volume of blood up to the point of filling the veins but without exerting any pressure on the vessel walls.
3. Stressed volume determines the mean systemic filling pressure (MSFP, the pressure of venous return when cardiac activity is absent), related to the elastic recoil of the venous system. The difference between the MSFP and right atrial pressure is the major factor determining venous return to the heart. The MSFP provides driving pressure against right atrial pressure which creates a gradient promoting forward flow.
Practical implications
1. Full characterization of fluid responsiveness requires consideration of the type, amount, and timing of fluid as well as the expected change in stroke volume.
2. The best method of measuring fluid responsiveness is a continuous or rapidly repeatable measure of stroke volume.
3. A common approach to test fluid responsiveness is the administration of 250-500 mL bolus in < 15 min with a positive response defined by a 10-15% increase in stroke volume.
4. The passive leg-raise maneuver replicates a transient fluid bolus and predicts fluid responsiveness without administration of intravenous (IV) fluids (positive response defined as > 10% increase in stroke volume), thereby mitigating the risks of excess IV fluid administration. This maneuver has limited utility in the intraoperative setting.
5. Alternative methods for predicting fluid responsiveness include stroke volume variation (SVV), pulse pressure variation (PPV), systolic pressure variation (SPV), and (in certain mechanically ventilated patients) end-expiratory occlusion test and respiratory systolic variation test.
6. Sonographic evaluation of IVC size, distensibility, or collapsibility has limited and unproven utility at the present time.
7. The actions of vasoactive drugs are typically considered in relation to the arterial circulation but many have significant effects on the venous circulation.
8. Venoconstrictors (e.g., alpha agonists) increase venous tone and thereby reduce venous capacitance, thus increasing the stressed volume at the expense of the unstressed volume. In a hypovolemic patient, this reduction in unstressed volume may, in turn, reduce microcirculatory blood flow and thereby compromise cellular metabolism, due to reduced perfusion despite maintenance of normal blood pressure.
9. Vasodilators (e.g., nitroglycerin) reduce venous tone and thereby increase venous capacitance and decrease the stressed volume. This typically decreases venous return and left ventricular end-diastolic volume.
10. Intra-abdominal hypertension (e.g., pneumoperitoneum) may reduce venous return or venous capacitance.
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