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
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).
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 a patient becomes increasingly hypovolemic, this relationship becomes exaggerated and is manifested as arterial line waveform variation from inspiration to expiration.
Cardiorespiratory interactions in hypovolemic patient during mechanical ventilation. RV preload decreases because the increased pleural pressures (1) compress the SVC and (2) compress the RA, whereas (3) the RV afterload is increased in the upper lung regions (West zones I and II). (4) In the dependent lung regions (West III), the pulmonary veins are squeezed and the blood pushed into LA. (5) Higher pleural pressures finally decrease LV afterload. LA, left atrium; LV, left ventricle; Palv, alveolar pressure; Ppl, pleural pressure; RA, right atrium; RV, right ventricle; SVC, superior vena cava. (From Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology. 2005;103:419-428.)
Cardiorespiratory interactions in hypervolemic patients during mechanical ventilation. The vena cava and RA are well filled and thus poorly compliant and compressible; therefore, changes in pleural pressure will have no effect. The pulmonary capillary bed is mainly consistent with West zone III areas; thus, the left preload will increase with insufflation (4) and LV afterload is decreased with increasing pleural pressures. LA, left atrium; LV, left ventricle; Palv, alveolar pressure; Ppl, pleural pressure; RA, right atrium; RV, right ventricle. (From Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology. 2005;103:419-428.)
Dynamic parameters such as the arterial pulse pressure variation, systolic blood pressure variation, and stroke volume variation can be assessed via an arterial blood pressure tracing.
Measuring the inferior vena cava (IVC) variation is another dynamic measurement that is noninvasive and easy to perform.3, 4 The IVC returns 80% of the venous blood to the right atrium (RA). It briefly passes through the thoracic cavity before joining the inferior aspect of the right atrium. The vena cava is a collapsible vessel, and as such its diameter is dependent on the internal distending pressure and the external compressing pressure. The intrathoracic vena cava's diameter is determined by the right atrial pressure (RAP) minus the pleural pressure (Ppl). During mechanical ventilation, the greater the Ppl, the more likely the vena cava is to collapse. As the RAP rises, collapse becomes less likely. This relationship can be evaluated by assessing IVC respiratory diameter and respirophasic variation. The higher the change in IVC diameter, the more likely the patient will respond to fluid loading with an increase in stroke volume (SV) and carbon monoxide (CO). Typical cutoff values that differentiate between responders and nonresponders depend on the method used: 12% (using max IVC diameter − minimal IVC diameter/mean diameter) or 18% (using max IVC diameter − min IVC diameter/min IVC diameter) IVC respiratory variability during mechanical ventilation.3, 4
Respiratory variation of the superior vena cava (SVC) may also predict fluid responsiveness. In a study of 66 septic mechanically ventilated patients, SVC variability of greater than 36% predicted fluid-responsive hemodynamics with a 100% sensitivity and a 90% specificity.5 However, this imaging is only readily obtainable with a transesophageal echocardiography (TEE) and therefore may have limited utility. IVC imaging has the advantage of being easily performed even by physicians untrained in echocardiography.6