Capnogram and Fluid Responsiveness

Predicting fluid responsiveness in critically ill patients is of paramount importance. It can
help define an adequate fluid balance. Overzealous fluid administration is poorly tolerated
and has been associated with poor outcomes but so has insufficient administration. Currently
available predictors of fluid responsiveness rely on invasive monitors and require patients
to be on mechanical ventilation. It is thus important to develop non invasive novel methods
to assess fluid responsiveness to provide an accurate management for a favorable outcome. We
propose a readily available non-invasive method that relies on improvement of the ventilation
perfusion mismatch as recorded by end tidal CO2.

Ventilation of physiologic dead space is part of a spectrum of mismatch between ventilation
and perfusion of the lungs. The extent of pulmonary dead space varies depending on factors
affecting pulmonary perfusion (e.g. pulmonary capillary hydrostatic pressure) and alveolar
pressure (e.g. positive pressure ventilation). Compromised pulmonary capillary perfusion can
lead to ventilation-perfusion mismatch in a patient with clear conductive airway and adequate
alveolar oxygen pressure. Alveolar dead space results in decreased CO2 exchange that
translates into lower levels of expired CO2.

Stroke volume of the right ventricle is a major determinant of the pulmonary capillary
perfusion. Right ventricular cardiac output can be increased by passive lower limb elevation
maneuver, which ultimately results in improvement of the ventilation to perfusion ratio. This
effect leads to a higher participation of perfused (and ventilated) alveolar units in gas
exchange and narrowing of the gradient between arterial and expired CO2 concentration.
Performing a passive leg raising (PLR) maneuver leads to stroke volume enhancement in both
healthy patients and in those experiencing hemodynamic instability. Responsiveness to PLR can
be assessed by different methods including echocardiography and pulse pressure variation.
Left ventricular cardiac output (LVCO) can be easily measured by transthoracic echo and be
used as a surrogate of right ventricular preload changes. LVCO can thus be used to assess the
fluid responsiveness of PLR and the effects of on end tidal CO2 that ensue.

We propose this study to test the hypothesis that expired CO2 is a reliable predictor of
fluid responsiveness after performance of the PLR maneuver, based on the assumption that
increasing right ventricular output causes a reduction of the ventilation to perfusion ratio,
leading to increased levels of expired CO2. T