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Guiding Resuscitation in the Emergency Department

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References

Monitoring Devices

Background

As noted throughout this review, it is important not only to identify and rapidly treat shock, but to also correctly identify the type of shock, such that treatment can be appropriately directed at its underlying cause. However, prior work suggests that EPs are unable to grossly estimate CO or systemic vascular resistance when compared to objective measurements of these parameters.42 This is in agreement with the overall poor performance of physical examination and clinical evaluation as a means of predicting volume responsiveness or guiding resuscitation, as discussed previously. Fortunately, a wide variety of devices to objectively monitor hemodynamics are now available to the EP.

In 1970, Swan et al43 published their initial experience with pulmonary artery catheterization at the bedside, using a balloon-tipped, flow-guided PAC in lieu of fluoroscopy, which had been mandated by earlier techniques. The ability to measure CO, right heart pressures, pulmonary arterial pressures, and estimate LV end diastolic pressure ushered in an era of widespread PAC use, despite an absence of evidence for causation of improved patient outcomes. The utilization of PACs has fallen, as the literature suggests that the empiric placement of PACs in critically ill patients does not improve mortality, length of stay, or cost, and significant complication rates have been reported in large trials.44,45Subsequently, a number of non-invasive or less-invasive HDM devices have been developed. Amongst the more commonly encountered modern devices, the techniques utilized for providing hemodynamic assessments include thermodilution and pulse contour analysis (PiCCOTM), pulse contour analysis (FloTrac/VigileoTM), and lithium chemodilution with pulse power analysis (LiDCOplusTM).46 The primary utility of these devices for the EP lies in the ability to quantify CO, stroke volume, and stroke volume or pulse pressure variation (PPV) to predict or assess response to resuscitative interventions (volume administration, vasopressors, inotropes, etc).

Benefits

Many of these devices require placement of an arterial catheter. Some require the addition of a CVC. Both of these procedures are well within the clinical scope of the EP, and are performed with fair frequency on critically ill patients. This is a distinct advantage when compared to pulmonary artery catheterization, a higher risk procedure that is rarely performed outside of the intensive care unit or cardiac catheterization laboratory. In addition, all of the devices below present hemodynamic data in a graphical, easy-to-read format, in real time. All of the devices discussed report stroke volume variation (SVV) or PPV continuously.

Limitations

Though these measures have validated threshold values that predict volume responsiveness, they require the patient to be intubated with a set tidal volume of greater than or equal to 8 mL/kg without spontaneous respirations and cardiac arrhythmias, in order to accurately do so. All of the HDM devices that rely on pulse contour analysis as the primary means of CO measurement cannot be used in the presence of significant cardiac arrhythmias (ie, atrial fibrillation), or mechanical circulatory assistance devices (ie, intra-aortic balloon counterpulsation). None of these devices are capable of monitoring microcirculatory changes, felt to be of increasing clinical importance in the critically ill.

The use of HDM devices to monitor CO with a reasonable degree of accuracy, trend CO, and assess for volume responsiveness using a number of previously validated parameters such as SVV is now in little doubt. However, these devices are still invasive, if less so than a pulmonary artery. The crux of the discussion of HDM devices for use in ED resuscitation revolves around whether or not the use of such devices to drive previously validated, protocolized care results in better outcomes for patients. The EP can now have continuous knowledge of a large number of hemodynamic parameters at their fingertips with relatively minimal additional efforts. At the time of this writing, though, this is both untested and unproven, with respect to the ED population.

Point-of-Care Ultrasound

Background

Over the past two decades, ultrasound (US) has become an integral part of the practice of emergency medicine (EM), and is now included in all United States Accreditation Council for Graduate Medical Education Emergency Medicine Residency Programs.47,48 It has emerged as a very important bedside tool performed by the clinician to identify type of shock and guide resuscitation, and has been endorsed by both EM and critical care societies.49-51 This section reviews the utility of US as a modality in identifying shock and guiding resuscitation, in addition to the pitfalls and limitations of this important tool.

In 2010, Perera et al47 described in their landmark article the Rapid Ultrasound in SHock (RUSH) examination, which describes a stepwise (the pump, tank, pipes) approach to identify the type of shock (cardiogenic, hypovolemic, obstructive, or distributive) in the crashing, hypotensive ED patient. We do not describe the full RUSH examination in this review, but discuss key elements of it as examples of how POCUS can assist the EP to make a rapid diagnosis and aid in the management of patients in shock. The “pump” is the heart, which is assessed in four different views to identify a pericardial effusion and possible tamponade, assess contractility or ejection fraction of the LV (severely decreased, decreased, normal, or hyperdynamic), and right heart strain which is identified by an RV that is larger than the LV, indicative of a potential pulmonary embolus.

The “tank” is then assessed by visualizing the IVC in the subxiphoid plane, and is evaluated for respiratory collapsibility (CI) and maximum size. This has been quite the debated topic over the last two decades. In 1988, Simonson and Schiller52 were the first to describe a correlation in spontaneously breathing patients between IVC caliber (measured 2 cm from the cavoatrial junction) and variation and RAP, where a larger IVC diameter and less respiratory variation correlated with a high RAP. Kircher et al53 later went on to describe that a CI greater than 50% correlated with an RAP of less than 10 mm Hg and vice versa in spontaneously breathing patients. Since then there have been more studies attempting to verify these findings in both spontaneously breathing and mechanically ventilated patients.54-56 The purpose of performing these measurements is not to estimate CVP, but to assess fluid responsiveness (ie, a blood pressure response to a fluid challenge). It can be assumed in states of shock that a small IVC, or one with a high CI, in the presence of a hyperdynamic heart is indicative of an underfilled ventricle and fluid responsiveness, especially if the IVC size increases with fluid.55,57 However, there are several caveats to this. First, in mechanically ventilated patients, the IVC is already plethoric due to positive pressure ventilation, and increases in diameter with inspiration and decreases with expiration as compared to spontaneously breathing patients. Second, the CI value to predict volume responsiveness in ventilated patients is set at 15% instead of 50%.55 Third, it is important to always take the clinical scenario in context; a dilated IVC with small CI is not necessarily only due to volume overload and congestive heart failure, but can be due to elevated RAP from obstructive shock due to cardiac tamponade or massive pulmonary embolus, which is why it is important to assess the “pump” first.47,58 It is also crucial to not forget to assess the abdominal and thoracic cavities, as intraperitoneal or pleural fluid with a collapsed IVC can potentially make a diagnosis of hemorrhagic or hypovolemic shock depending on the clinical scenario.47 The final part of the RUSH protocol is to evaluate the “pipes,” inclusive of the lower extremity deep venous system for evaluation of potential thrombosis that could increase suspicion for a pulmonary embolism causing obstructive shock, and the aorta with the common iliac arteries if there is concern for aortic dissection or aneurysmal rupture.

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