Respiratory Variation of Inferior Vena Cava Diameter in Mechanically Ventilated Patients with Spontaneous Breathing Effort: An Observational Study.
CCCF ePoster library. Shuster C. Oct 4, 2017; 198178; 86 Disclosure(s): No disclosures.
Constantin Shuster
Constantin Shuster
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Respiratory Variation of Inferior Vena Cava Diameter in Mechanically Ventilated Patients with Spontaneous Breathing Effort: An Observational Study.

Shuster, Constantin1; Hurlburt, Andrew1; Ong, Shaun1; Kaila, Ken1; Sirounis, Demetrios1,2; Boyd, John H.1,2

1 - Department of Critical Care Medicine, University of British Columbia, Vancouver, BC, Canada.

2 - Critical Care Research Laboratories, Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, BC, Canada.


The goal of fluid administration in patients with shock is to increase their cardiac output (CO) through the Frank-Starling mechanism1. However, increased fluid administration has been associated with hypoxemia, tissue edema and increased risk of mortality2. Only 30-50% of patients with shock remain able to increase their CO in response to volume expansion after initial fluid administration (30 mL/kg)3. Such patients are termed fluid responders and fluid responsiveness (FR) can be predicted by examining the respiratory variation of inferior vena cava diameter (IVCd) in mechanically ventilated, apneic patients4,5. However, this measure's utility is unknown in patients who are spontaneously breathing with assistance from a ventilator. Such patients form the majority in modern intensive care units and thus the ability to predict FR in this patient group must be revisited.
In critically ill patients who are mechanically ventilated in a pressure support mode, our aim was to examine how variation in positive end-expiratory pressure (PEEP) affected IVCd, and whether IVCd respiratory variation predicted FR while accounting for PEEP.
This was a prospective observational study of patients who were ≥18 years, admitted to the intensive care unit and mechanically ventilated in a pressure support mode. IVCd was measured throughout respiration using M-mode echocardiography from the subcostal view at PEEPs of 0, 5, 10, 15 and 20. To assess for FR, an 8 mL/kg intravenous bolus of crystalloid was administered. A peripheral pulse contour analysis device (FloTracTM/VigileoTM, Edwards Life Sciences, USA) was used to monitor cardiac output. Fluid responders were defined by an increase in cardiac index or mean arterial pressure ≥15%. Patients were excluded if it was unsafe to vary PEEP. Patients were excluded from the FR assessment only if they were not in sinus rhythm or if fluid administration was deemed unsafe.
Twenty-six patients were recruited, of which 21 underwent FR assessment. Elevations in PEEP increased inspiratory IVCd (slope=0.69±0.13, r2=0.18, p<0.0001), with little effect upon expiratory IVCd (slope=0.26±0.08, r2=0.07, p=0.0025). IVCd respiratory variation was a poor test for FR (AUROC 0.51±0.13, 95% CI 0.26-0.77), however, >55% respiratory collapse in IVCd was specific (100%) to predicting FR. We devised a new measure, IVC compliance (uL/cm H2O PEEP), which had good test characteristics (AUROC 0.70±0.12, 95% CI 0.46-0.93) and >25.5uL/cm H2O was specific (89%) to predicting FR.
In critically ill patients who are mechanically ventilated yet spontaneously breathing, IVCd respiratory variation and IVC compliance can be specific markers of FR.

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