The first line of treatment in patients with acute circulatory failure is fluid administration. The physiological rationale to administer fluids in patients with acute circulatory failure is to improve tissue oxygenation by increasing stroke volume and mean arterial pressure. . Only half the patients with circulatory failure respond positively to fluid administration.¹ Hence it is necessary to detect fluid responders. The decision to infuse fluids in very important since excessive fluid loading is associated with increased complications, length of intensive care unit stay and mortality ²especially in patients with acute respiratory distress syndrome (ARDS). The current SARS CoV2 pandemic has posted a real challenge with diverse presentation, with two lung phenotypes, (L-phenotype and H phenotyes) and most patients who required intensive care unit admission had ARDS.³â€¯The circulatory failure in such patients is more complex due to varied prevalence of myocardial injury, distributive shock, cytokine storm and right ventricular dysfunction (proportion of ARDS patients). Recent surviving sepsis campaign suggested restricted fluid strategy in patients with ARDS due to SARS CoV2 and to use appropriate dynamic parameters to decide fluid therapy.⁴ Thus, it is important to identify which patient will benefit from fluid therapy before administration.  However, predicting which patients will positively respond to fluid administration by increasing stroke volume and hence cardiac output (fluid responsiveness- FR) is challenging in critically ill patient with SARS CoV2.  

Various dynamic indices which depend on cardiopulmonary interactions like stroke volume variation (SVV) and pulse pressure variation (PPV) are superior to static indices and shown to accurately predict fluid responsiveness.⁵ The major limitation for using PPV and SVV are low tidal volume (Vt) ventilation i.e. Vt â‰¤6 mL/kg predicted body weight (PBW)^6,7 and poor lung compliance (Crs is <30 mL/cmH2O)⁸. Low tidal volume ventilation is commonly used nowadays in ICU, it is recommended not only in patients with adult respiratory distress syndrome (ARDS)⁹, but also in patients at risk of ARDS, with septic shock, potential organ donors, and patients undergoing high risk intra- abdominal and thoracic surgeries.⁹10. 

During low Vt ventilation the magnitude of change in airway driving pressure may not be enough to produce an adequate change in intra-cardiac pressure. Thus PPV  may be low even in fluid responders. To overcome this limitation with the use of PPV during low tidal volume we developed a new test called the “tidal volume challenge”.¹¹ This test involves transiently increasing the tidal volume from 6mL/kg predicted body weight (PBW) to 8mL /kg PBW for one minute and thereafter reducing the tidal volume back to 6mL/kg PBW. The change in PPV following the “tidal volume challenge” (i.e. Î”PPV_6-8 and Î”SVV_6-8) reliably predicts fluid responsiveness in patients ventilated at low Vt with cut off values of 3.5% and 2.5 % respectively. The tidal volume challenge has been subsequently tested in various settings and it has become  standard test of fluid responsiveness. ¹²1314But it is not tested well in patient having low lung compliance and in prone position.  

The PPV depends not only on the magnitude of driving pressure but also on how much of this driving pressure is transmitted to pleural and pericardial cavity, which in turn is proportional to  lung compliance. Thus PPV  do not reliably predict fluid responsiveness when the lung compliance is low. Monnet et al have shown that PPV was the unreliable when the respiratory system compliance was <30 mL/cmH2O and predictability varies with the lung compliance⁸. In our study on 19 out of the 30 occasion, patients had low respiratory compliance (<30 mL/cmH2O).¹¹ In all 19 situations PPV and SVV reliably predicted fluid responsiveness after the “tidal volume challenge”. Thus, our study suggested that the “tidal volume challenge” may also help improve the reliability of PPV and SVV in patients with low compliance who are ventilated using low Vt. Also, patients in prone ventilation for ARDS have low respiratory system compliance, varied or reduced chest wall elastance which may also affect the PPV probably by affecting pleural pressures, cardiac preload. The combination of altered lung compliance and chest wall elastance may affect the PPV in opposite direction leading to either increased or decreased value compared to supine position.¹⁵So, the behaviour of PPV is unpredictable and not tested as well.  

Prone position ventilation is frequently done in moderate to severe ARDS patients especially more during this COVID Pandemic. Prone ventilation is the standard of care and the rescue therapy for refractory hypoxia.  The prone position may also have influence on the hemodynamic status by increasing abdominal pressure, altered intrathoracic pressure affecting the venous return. The cardiac preload may be increased in prone position with increased intraabdominal pressure but when the IAP is high enough to compress the inferior vena cava, there will be a reduction in cardiac preload. The cardiac output may be increased with better right ventricular pressure with prone positioning.^16,17 On the other hand, there could be increased afterload with raised IAP. So, there may be unpredictable hemodynamic response to prone ventilation and previous studies have shown varying effect of prone position on hemodynamics.^16–19 

None of the commonly used tests are neither reliable nor feasible in prone ventilation. Passive leg raising test (PLRT) which is standard test commonly done to predict fluid responsiveness in ICU is not feasible in prone position.  Recently Trendelenburg position , moving the bed of patient in prone ventilation 13 degrees up to 13 degree down  has shown to predict FR. ^20 21But it requires cardiac output monitor, not feasible in resource limited setting, that too during COVID pandemic with constrained resource globally. In our previous study we have shown that the change in PPV following fluid bolus was more in fluid responders, PPV change could be  potential surrogate for cardiac output change. Recently the PPV change following passive leg raising test (PLRT) predicted FR with high accuracy.²² In that study authors showed that using PPV change with PLRT is easy, safe. Moreover, PPV is a number which is available in all mutipara monitor which is used to monitor heart rate, blood pressure, ECG in all ICU patients. This is very handy and can be used for all patients.   

Thus, we would like to test the reliability of the change in PPV following Trendelenburg manoeuvre in prone ventilation and to test whether “tidal volume challenge” can improve the reliability of PPV in patients with low compliance, prone ventilation.  

The test of fluid responsiveness that we are testing either require cardiac output monitor or not well tested in prone ventilation. PPV change is a good surrogate of change in cardiac out that has been proven in our previous study¹¹ as well as in recent study by Taccheri et al²². So, we hypothesise that the Trendelenburg manoeuvre using PPV change and “tidal volume challenge” in prone ventilation will be potential test for FR in both resource full and resource limited setting especially during COVID pandemic, as it is simple, safe, quickly doable at bedside and doesn’t require cardiac output monitor.