A 26-year-old male is admitted to the intensive care unit with general seizures, syncope, non-palpable blood pressure, and a suspicion of ventricular tachycardia whilst in the Emergency Room. The emergency room physician therefore (successfully) applied a DC shock to convert him to regular sinus rhythm. Afterwards the patient was alert and cooperative and he was transferred to the ICU for mere overnight “baby-sitting”. From his previous history, we know that he has been deprived of oxygen at birth, and consequently suffered a cerebrovascular accident (CVA) with left hemiparesis and seizures (managed with triple antiepileptic therapy, carbamazepine, topiramate and lamotrigine). Because of his cognitive deficit, he normally attends a special day care institution. For the last 9 years he had also been diagnosed with idiopathic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 52% (treated with an angiotensin converting enzyme inhibitor) and a mild mitral regurgitation.

Overnight in the ICU, he was initially hemodynamically stable with no further seizures. However, his need for supplemental oxygen increased from 2 liters via nasal cannula to 15 liters administered with a non-rebreathing mask. The patient was in respiratory distress with a respiratory rate of 34 breaths per minute. After failing a trial of non-invasive ventilation, he was intubated and mechanically ventilated within 24 hours of ICU admission, illustrating the dramatic chain of events. Respiratory rate was set at 24 breaths per minute and inspiratory pressures towards a tidal volume of 6ml/kg predicted body weight (PBW). Figure 1 shows the chest X-ray on admission and just after intubation. He then became hemodynamically unstable.  Therefore, a transthoracic cardiac ultrasound (US) was performed (Figure 2) and the results are listed in Table 1 together with the ventilator settings and blood gas results.

The FiO2 was increased to 100% and the PEEP was set according to the low flow pressure-volume (PV) loop (as can be automatically constructed with the Draeger Evita XL ventilator). Figure 4 shows the PV loop with detection of a lower inflection point at 16 cmH2O. During the PV loop, that also acted as a recruitment maneuver his systolic blood pressure decreased to 40 mmHg, so norepinephrine was started and swiftly increased to 0.4 ug/kg/min. Dobutamine was also started at 4 ug/kg/min. Saturation remained poor at 88% and he was switched to high frequency percussive ventilation (HFPV) with the VDR4 ventilator (Percussionaire Corporation, Sandpoint, Idaho, U.S.A). A transpulmonary thermodilution PiCCO catheter (Pulsion Medical Systems, Munich, Germany) was inserted in the femoral artery at this point. The evolution of the hemodynamic parameters obtained after insertion of the PiCCO catheter together with the respiratory variables are listed in Tables 2 and 3.

The initial hemodynamic picture showed a normal cardiac index (CI) of 3.5 L/min.m2 (normal range 3-5), a relatively low intravascular filling status with a GEDVI of 757 ml/m2 (normal range 680-800), a very low global ejection fraction GEF of 13%  (normal range 25-35) but a very severe capillary leak with high extravascular lung water index (EVLWI) of 38 ml/kg predicted body weight (normal range 3-7). The high EVLWI was suggestive of hyper permeability edema in view of the high pulmonary vascular permeability index (PVPI) of 7.4 (normal range 1-2.5).

At the same time however the patient seemed to be fluid responsive with a high pulse pressure variation (PPV) of 19% (normal range <10).  Heart rate was regular at 119 beats per minute with a MAP of 65 mmHg. The CVP was still 16 mmHg. His response to a passive leg raising (PLR) maneuver was positive (15% increase in CI and MAP) confirming that he was volume responsive despite the fact that he had such bad pulmonary edema (EVLWI 38) with a critical oxygenation status (P/F ratio of 57, at IPAP of 34 cmH2O and PEEP of 15 cmH2O).

In the case study (dating before the publication of the big fluid trials) the patient was given small volume resuscitation with hyperhaes (Fresenius Kabi) at a dose of 4ml/kg given as a bolus over 10-15 minutes combined with 1000 ml of balanced colloids (Volulyte, 6% hydroxyethyl starch 130/0.4), following the results obtained with the transpulmonary thermodilution.

Editorial Comment: “We have to note that after the EMEA PRAC recommendations, nowadays the use of starches cannot be advocated in patients with sepsis, burns or kidney injury. Instead of hyperhaes, a hypertonic salt solution 6% can be used.”

The patient remained on a dobutamine infusion (9 ug/kg/min) and norepinephrine (0.4 ug/kg/min). The following day (day 2) his CI increased to 5.7 L/min.m2, GEDVI increased to 900  ml/m2 and EVLWI had decreased to 14 ml/kg PBW (Table 2).  Despite the filling, his CVP decreased from 16 to 6 mmHg, illustrating the opposite changes between barometric and volumetric preload indices due to increased intrathoracic pressure.

This is an example of a therapeutic dilemma or conflict [25]. A therapeutic conflict is a situation where each of the possible therapeutic decisions carries some potential harm [26]. In high-risk patients, the decision about fluid administration should be done within the context of a therapeutic conflict. Therapeutic conflicts are the biggest challenge for protocolized cardiovascular management in anesthetized and critically ill patients. A therapeutic conflict is where our decisions can make the most difference. Although the patient had evidence of severe pulmonary edema (EVLWI 38 ml/kg PBW) the decision was made to give fluids because the PPV was high and the PLR test was positive. Also, the GEDVI was relatively low in relation to the GEF, despite the increased CVP and increased left ventricular end diastolic area (from the ultrasound) [6, 27]. Cardiac US further showed that his inferior vena cava collapsibility index (IVCCI) was almost 50% [28](Figure 6).

What was really important to know for this patient was the type of curve and where he was on his Frank Starling curve (Figure 7, panel A). Evidence shows that when the global end-diastolic volume and the right ventricular end-diastolic volume are corrected for the GEF they correlate more closely especially when compared to the change in CVP or PAOP (Figure 7, panel B) [6].  Observation of the transpulmonary thermodilution curve also allowed us to get further diagnostic clues (Figure 8 and Video 3).

By late afternoon of day 2, the patient had had a drop in urine output with production of only 350 mls over the last 12 hours despite a positive cumulative fluid balance of 4 litres. He was still on dobutamine 5 ug/kg/min, and norepinephrine 0.2 ug/kg/min.

Other parameters are listed in Tables 2 and 3, and can be summarized as follows: CI 5.4 L/min.m2, MAP 79 mmHg, CVP 8 mmHg, PPV 6 %, GEF 23 %, GEDVI 1080 ml/m2, EVLWI 18 ml/kg PBW, conclusive with overfilling and worsening pulmonary edema in the absence of fluid responsiveness.

Respiratory function deteriorated with a P/F ratio of 205, at an IPAP of 34 cmH2O, PEEP 11 cmH2O, while FiO2 was increased from 45 to 65%.

Lactate levels increased from 1.6 to 2.6 mmol/L

Finally, the physicians fully understand the clinical situation of this patient who after the initial ebb phase of shock did not enter the flow phase spontaneously. His PEEP was increased to 18 cmH2O, along with the administration of hypertonic albumin 20%, and he was given an infusion of Lasix® (frusemide, 60mg/hr for 2 hours then followed by 10 mg/hr according to urine output).

This treatment was recently referred to as PAL. PAL is one of the therapeutic options that can be used during deresuscitation. By day 3 his cardiorespiratory condition improved with a drop in EVLWI to 15 ml/kg PBW, a PVPI of 1.9 and P/F ratio of 266 (with IPAP 34 and PEEP at 18 cmH2O).

Vasopressors and inotropes were titrated to norepinephrine doses of 0.11 ug/kg/min and Dobutamine at 3 ug/kg/min respectively, and he required less albumin 20% and less frusemide.

Things continued to fluctuate for the patient over the next few days but with two more episodes of frusemide infusions eventually his EVLWI came down to 8 ml/kg PBW on day eight. The patient was extubated on day 10 and left the ICU after 2 weeks. Figure 11 shows the evolution of volumetric and barometric indicators during the first week (detail of first 2 days is shown in panel B showing opposite effects on volumetric and barometric preload indicators), while Figure 12 shows the daily and cumulative fluid balance.

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