Implicit in any attempt to optimize the circulation are two key issues. First, it is important to identify those measures or parameters that constitute the most appropriate treatment options. Second, it is essential to define the actual goals that will drive resuscitation. Thus, we first define measures that identify volume responsiveness and circulatory failure. We then define the goals of resuscitation that these measures will be used to achieve.
Hemodynamic Monitoring-Defined Assessment of the Circulation
In acute circulatory failure, volume expansion is most often the first therapeutic choice. Fluid administration can be expected to increase cardiac output and oxygen delivery. Nevertheless, improvement can occur only if changes in cardiac preload result in significant changes in cardiac output (i.e., if both ventricles are preload dependent ; Fig. 16-1 ). If no test is used to predict preload dependence a priori, then volume expansion often will not result in the expected increase in cardiac output. Thus preload dependence should be tested before fluid is administered. This approach will help avoid fluid overload, which is an independent predictor of mortality in patients with septic shock or acute respiratory distress syndrome (ARDS). Several indices and tests have been developed to test volume responsiveness.
Ability of Static Indices of Cardiac Preload to Predict Volume Responsiveness
Static markers of cardiac preload, such as the central venous pressure (CVP), do not reliably predict fluid responsiveness. This failure can be explained by basic physiology. The slope of the cardiac function curve depends on the cardiac systolic function ( Fig. 16-1 ). Because this slope is unknown in a given patient at any given moment, an absolute ”static” value of any measure of preload could correspond to a point on any number of curves and thus to preload dependence and preload independence. Only extreme values can inform on the presence of fluid responsiveness. Furthermore, the measurement of any static marker is subject to error. For instance, the measurement of CVP requires a precise positioning of the pressure transducer with respect to the right atrium. The measurement must also be made at end expiration and should account for the transmission of intrathoracic pressure to the right atrium. Likewise, the pulmonary artery occlusion pressure suffers from many possible errors in its measurement and interpretation.
To address the shortcomings of static indices, dynamic alternatives have been developed to predict preload responsiveness within an overall concept of functional hemodynamic monitoring. Dynamic measures involve altering cardiac preload via mechanical ventilation, postural changes, or administration of small amounts of fluid and measuring the resultant change of cardiac output or stroke volume.
Dynamic Parameters to Predict Volume Responsiveness
Several tests have been developed to detect volume responsiveness before administering fluid. The appropriate approach is most often determined by the clinical setting and the patient’s condition. These tests allow the practitioner to avoid administering fluid if it is not hemodynamically effective.
Variations of Stroke Volume Induced by Mechanical Ventilation
During mechanical ventilation, insufflation increases the intrathoracic pressure and, as a result, decreases venous return. Furthermore, increased right ventricular afterload decreases right ventricular outflow and thus left ventricular preload. In conventional ventilation, these changes should occur at expiration. If the left ventricle is preload dependent, then the left ventricular stroke volume transiently decreases at expiration. Hence, a cyclic variation of stroke volume under mechanical ventilation indicates the preload dependence of either ventricle.
Several surrogates or estimations of stroke volume have been used to quantify its respiratory variations. These include the systemic arterial pulse pressure, which is proportional to stroke volume. Indeed, studies have demonstrated that pulse pressure variation (PPV) is a valuable indicator of fluid responsiveness, provided that the conditions of its validity are fulfilled. Overall, variation greater than 13% is significantly associated with fluid responsiveness. Of course, as for many tests, this is not a strict cutoff. The farther from 13% the PPV value, the higher its diagnostic value.
Other parameters used to estimate stroke volume responses to respiratory variation include pulse contour analysis, subaortic blood flow measured by descending echocardiography, aortic blood flow measured with esophageal Doppler monitoring, and amplitude of the plethysmography signal with pulse oximetry. These indices—in particular, those of PPV—are solidly evidence based. Indeed, several commonly used bedside monitors can measure PPV.
The respiratory variation of stroke volume as a marker of preload responsiveness is not valid under several conditions that are not uncommon. First, during spontaneous breathing, stroke volume variations relate more to the respiratory irregularity than to preload dependence. Second, arrhythmias directly affect stroke volume variability within the respiratory cycles, a response likely related to arrhythmia rather than heart-lung interactions. The third important limitation relates to ARDS. In such a case, the low tidal volume and/or the low lung compliance will reduce the transmission of changes in alveolar pressure to the intrathoracic structures; both diminish the amplitude of the ventilation-induced changes of intravascular pressure. The net result would be false-negative responses to PPV. Open chest surgery, a low ratio of heart rate over respiratory rate (corresponding in fact to respiratory rates at ≥40 breaths/min), or intra-abdominal hypertension also reduce the ability of PPV measurements to predict fluid responsiveness. Overall, the limitations to the use of PPV are much more frequently encountered in the intensive care unit than in the operating room.
Respiratory Variation of Vena Caval Diameter
Mechanical ventilation can alter the diameter of vena cava, an effect that is exaggerated in hypovolemia. The magnitude of this change in the inferior vena cava (IVC) at the diaphragmatic inlet, as well as collapse of the superior vena cava (SVC), reliably predicted fluid responsiveness.
The most important limitation of these methods is that they become unreliable during spontaneous breathing activity because respiratory efforts are variable and lack homogeneity. Mechanically ventilating poorly compliant lungs with a low tidal volume should minimize the effect of ventilation on the vena cava diameter and thus invalidate the method. Conversely, this approach is valuable in patients with cardiac arrhythmias.
Respiratory variation in the IVC can be measured with transthoracic echocardiography. This approach may be particularly valuable during the early phase of care, before arterial cannulation. The collapsibility of the SVC has been validated only in a single study and requires transesophageal echocardiography. In a patient equipped with an arterial catheter, it is easier to use PPV than SVC collapsibility.
End-Expiratory Occlusion Test
As stated previously, inspiration under mechanical ventilation cyclically reduces cardiac preload. Briefly holding mechanical ventilation at end expiration interrupts this cyclic decrease and induces a transient increase in cardiac preload. If the right ventricle is preload dependent, then the end-expiratory occlusion (EEO) test will increase right ventricular output and, if sufficient to increase flow into the pulmonary circulation, left ventricular preload. A preload-dependent patient will respond to EEO with an increase in cardiac output ( Fig. 16-1 ). Some studies have shown that cardiac output increases of more than 5% during a 15-second EEO test reliably predict volume responsiveness.
Beyond its simplicity, the EEO test is useful during cardiac arrhythmias because it exerts its effects over the course of several cardiac cycles ( Fig. 16-2 ). The EEO test can be used in patients who are not fully paralyzed or deeply sedated unless respiratory triggering interrupts the 15-second occlusion. The EEO test is also much easier to use with a real-time measurement of cardiac output, such as pulse contour analysis. The increase in arterial pulse pressure during EEO is also indicative of fluid responsiveness, but it requires a large-scale display of the arterial pressure curve. The EEO test also appears to be independent of the magnitude of positive end-expiratory pressure.
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