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Fluid responsiveness. A 64-year-old man is admitted to the hospital with 2 days of worsening abdominal pain and intermittent fevers. He underwent a laparoscopic cholecystectomy. On postoperative day 1, the patient was hypotensive and oliguric. His blood pressure, heart rate, and urine output did not increase after administration of 3 L of lactated Ringer solution. His electrocardiogram showed a sinus rate of 120 bpm, his blood pressure was 89/45 mm Hg, and his central venous pressure was 12 mm Hg. Over the course of the morning, his mental status deteriorated, and his work of breathing increased. He was intubated and his lungs were mechanically ventilated. You are called by the resident physician in the postoperative anesthesia care unit and asked to guide further management.
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How can an ultrasound examination assess volume responsiveness?
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An intensivist assesses a patient's volume responsiveness to determine if a fluid bolus will increase a patient's stroke volume and cardiac output. Traditionally, static parameters of cardiac filling pressures, such as the central venous pressure (CVP) or the pulmonary artery occlusion pressure (PAOP), have been used as surrogates of a patient's volume status. Clinicians have also assessed volume status via echocardiographic parameters such as the left ventricular end-diastolic volume or estimated filling pressures. Most of these traditional parameters, however, poorly predict volume responsiveness because Frank-Starling forces, cardiopulmonary interactions, and changes in systolic, diastolic, intra-abdominal, and intrathoracic pressures influence the patient's response to volume loading.1, 2
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If a patient lies on the steep portion of the Frank-Starling curve, an increase in preload will increase the stroke volume (volume responsive). On the other hand, if the patient is on the flat portion of the Frank-Starling curve, an increase in preload will not increase stroke volume and indeed may reduce it (nonvolume responsive).
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Volume assessment aided by dynamic parameters, in contrast to static measurements, recognizes the characteristic respirophasic changes that occur as a patient's intrathoracic pressure changes with positive-pressure ventilation (Figures 30-1 and 30-2). These changes are more dramatic in the hypovolemic patient and can be recognized via the arterial pressure waveform. During a positive-pressure breath with mechanical ventilation, right ventricular (RV) stroke volume drops for two main reasons. First, the RV has less preload owing to decreased venous return from an increased intrathoracic pressure. Second, there is a concomitant increase in afterload to the RV secondary to the pneumatic compression of the pulmonary capillaries. Simultaneously, during mechanical insufflation, the venous return to the left ventricle (LV) is increased as the pulmonary capillaries are compressed and blood is pushed to the left side of the heart. Therefore, LV stroke volume increases during mechanical inspiration. After two to three cardiac cycles (pulmonary transit time), the LV stroke volume falls as a consequence of the aforementioned reduction in RV stroke volume and cardiac output. The converse is true for the expiratory phase of mechanical ventilation. As ...