Advanced Hemodynamic and Cardiopulmonary Ultrasound for Critically Ill Patients in the Emergency Department

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation ( Figure 11 ). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%. ^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients. ⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients. ^64,65

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation. ⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow.

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta. ^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT. ⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) ( Figures 7a and 7b ) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness. ⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output. ⁷¹

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output. ⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion. ^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid.

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% ( Figure 7c ).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver.