Volume responsiveness is the evidence of a rise in cardiac output between 10-15% after administration of a fluid bolus or performance of a passive leg raise (Monnet, 2006). Volume responsiveness remains a hot topic with an exponential rise in publications over the past 10 years (Figure 1). Volume responsiveness may be important for resuscitation, but what about de-resuscitation? Empirical evidence for de-resuscitation remains sparse. Where evidence is limited we have to return to physiologic principles first, therefore this post should be seen in the realm of hypothesis generation. Today, I introduce volume de-responsiveness; but first, let us clarify some common terminology:
Volume Responsiveness- Evidence of a rise in cardiac output with increased preload.
Volume Intolerance– A physiologic state where further volume administration will lead to harm.
Volume De-Responsiveness– The converse of volume responsiveness in that removal of fluid will cause a significant reduction in cardiac output.
While I have changed some of the details surrounding this case for patient confidentiality reasons, this was a case that I remember well from fellowship.
68 F with a history of HFrEF (last known EF of 20%), COPD, obesity (250 kg), and DM presents with fevers, chills, and increased sputum production. Chest x-ray is difficult to interpret due to body habitus, but antibiotics were started due to concern for pneumonia. He requires High Flow Nasal Cannula at 40 L and 70% FiO2. He was found to be hypotensive and had a lactate of 4 mmol/L on admission. He received 7 liters of crystalloid in the setting of persistent hypotension, but became increasingly hypoxic after fluids and was eventually intubated. Lung ultrasound after fluid administration exhibits bilateral/fused B-lines with a LLL consolidation with dynamic air bronchograms. He is on 100% FiO2, lung protective strategy TV, and 17 of PEEP (best compliance at this PEEP). The patient was proned with minimal improvement; therefore, he was made supine again. He requires 15 mcg/min of norepinephrine (0.06 mcg/kg/min) to maintain a MAP of 65 mmHg. He is now oliguric, and his Cr has increased from 1.6 on admission to 2.3, 24 hours after admission. Portal vein pulsatility assessed and exhibits a biphasic pattern (consistent with venous congestion)1. TEE performed by the primary team demonstrating persistently reduced LVEF but with a new diagnosis of acute cor pulmonale (RV/LV ratio > 1 and septal flattening). Estimated Cardiac Index using doppler was 1.4 L/min/m2 leading to the determination that there is a cardiogenic component to the patient’s shock. The team would like to remove fluid. How can we methodically and systematically remove fluid safely?
Our patient is in shock. Diuresis/ fluid removal is often avoided due to an overly reductionist view that hypotension is always equivalent to hypovolemia. It is not. The patient has evidence of right-sided congestion. Figure 2 demonstrates the Guyton Diagram2. The figure illustrates the concept of volume responsiveness on two different cardiac function curves. Operating points 1 and 2 exist within a normal to hyperdynamic cardiac function state, whereas 3 and 4 are within a depressed cardiac function curve. The transition from 1 to 2 occurs with an increase in preload from maneuvers, such as a Passive Leg Raise (PLR). PLR delivers an auto bolus and is a well-validated method to assess volume responsiveness 3. The hyperdynamic curve demonstrates a significant increase in cardiac output with preload increase, whereas the depressed cardiac function curve does not. If we can use Guytonion physiology to infer a response to volume expansion, can the same be done for volume removal? Logically, if the patient’s physiologic milieu demonstrates volume responsiveness, then it can be surmised that there will be a significant cardiac output drop in the case of volume removal. Conversely, if the patient is not volume responsive, there is a lower likelihood of a hemodynamically significant drop in cardiac output with fluid removal. A study performed by Monnet et el; demonstrated that PLR induced an increase in CI > 9% predicted hypotension during dialysis (with ultrafiltration) with an AUC of 0.89 4. Physiologically this may be sound, but is there any empirical evidence to support this hypothesis? At the moment there are no major studies that completely fit the phenotype of our patient, but there is some demonstration of the physiologic principle for volume de-responsiveness. Furthermore, patients with minimal response to the PSL were less likely to have worsening hemodynamics with fluid removal.
The patient was deemed to be both volume intolerant and not responsive. We felt that a large amount of administered volume in the setting of sepsis-related capillary leak, a strong predisposition to cardiac insults, and positive pressure ventilation may have contributed to new cardiogenic shock. CRRT was initiated in the setting of AKI with oliguria and the need for ultrafiltration. Ultrafiltration titrated up 300 ccs/hr. Pressor requirements improved during this course and turned off on day 2. Daily volume responsiveness maneuvers were performed, and on day three, he was noted to be responsive. Ultrafiltration is reduced for even fluid balance. The patient’s ventilator settings improved, and he was extubated on day 4.
- Patients with sepsis require fluids but large volumes can be harmful. Fluid balance, weight, lung ultrasound, and IVC are some traditional methods to identify volume intolerant patients.
- A patient who is volume intolerant may warrant volume removal.
- Methods for volume responsiveness can be used to determine volume de-responsiveness (A physiologic hypothesis at this point that warrants further study).
- Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J. Apr 9 2020;12(1):16. doi:10.1186/s13089-020-00163-w
- Magder S. Bench-to-bedside review: An approach to hemodynamic monitoring–Guyton at the bedside. Crit Care. Oct 29 2012;16(5):236. doi:10.1186/cc11395
- Cherpanath TG, Hirsch A, Geerts BF, et al. Predicting Fluid Responsiveness by Passive Leg Raising: A Systematic Review and Meta-Analysis of 23 Clinical Trials. Crit Care Med. May 2016;44(5):981-91. doi:10.1097/ccm.0000000000001556
- Monnet X, Cipriani F, Camous L, et al. The passive leg raising test to guide fluid removal in critically ill patients. Ann Intensive Care. Dec 2016;6(1):46. doi:10.1186/s13613-016-0149-1