You have a patient in shock and after fluid boluses he remains hypotensive. How to know where your patient is on the Frank Starling curve is a very important relevant clinical question that cardiac ultrasound may aid you in answering. Persistent hypotension after an initial fluid resuscitation attempt is a common dilemma and your options include giving more fluid, start pressors or inotropic agents. Selecting the appropriate approach is paramount as there is an increased mortality associated with excessive fluid resuscitation so the key idea is to assess if a patient is fluid responsive before giving fluids. In this chapter we analyze physiologic responses dynamically with the use of cardiac ultrasound.
Although FoCUS does not require you to make any measurement, concepts explained in this chapter are of paramount importance to the practice of Anesthesiology and Critical Care.
1. Static Measures of Fluid Responsiveness.
Fluid responsive is defined as an increase of >15% in cardiac output in response to volume expansion, this being typically <1L of crystaloid. Static pressure parameters such as CVP or pulmonary artery occlusion pressure were previously used. The clinician measures baseline parameters, administers a bolus and then evaluates changes on these. This approach is unfavorable since there is poor to no correlation between these parameters and fluid responsiveness. Static echocardiographic parameters are available. These include estimating CVP from IVC measurements since there is a strong correlation between size of the IVC and CVP. However the size of the IVC does NOT predict fluid responsiveness. In fact static parameters are all poor predictors of fluid responsiveness unless there is obvious hypovolemia. To make matters more complicated even systolic left ventricular function is subject to change in the critically ill since in up to 60% of patients with septic shock there is LV dysfunction and thus difficult to predict where patients are on the Frank Starling curve based on static values alone.
2. Dynamic Measures of Fluid Responsiveness.
Dynamic parameters to estimate fluid responsiveness serve as a dichotomous decision making process. Is the patient on the steep portion of the Frank Starling curve? If they are, loading them with fluid is expected to increase their cardiac output (CO). We will be using breathing related variations in intrathoracic pressure that create changes in RV and LV preload in spontaneous or mechanically ventilated patients. Otherwise CO changes can be observed after passive leg raising (PLR) which cause a temporary increase in preload. Bear in mind that the following methods are not universally applicable specially in patients who are in vent dyssynchrony and high PEEP values, not in normal sinus rhythm or high intraabdominal pressure. If the patient is on mechanical ventilation there must be no spontaneous respiratory efforts which would alter preload and tidal volumes be around 8ml/kg
During spontaneous ventilation the negative intrathoracic pressure generated increases RV preload. The blood in the RV restricts full expansion of the LV limiting LV preload. The pulmonary veins also receive less blood as a consequence of the negative intrathoracic pressure. This also causes less LV preload. As a consequence stroke volume and CO drops to lower levels on inspiration when breathing spontaneously. This is the paradoxical pulse. The opposite occurs in a patient undergoing mechanical ventilation as the inspiration causes a drop of RV preload.
2.1 Pulsed Wave Doppler
So how do we measure CO as a response to changes in intrathoracic pressure? We interrogate the LV stroke volume so that it provides us with a dynamic evaluation of preload dependence. We do this by estimating it through Doppler analysis using Pulsed Wave Doppler (PWD). This US technique measures velocity flow across a sample box along an interval of time. We then trace the are of velocity across time in what is called the velocity time integral (VTI). You can also use the maximum and minimum velocity obtained from the VTI to determine fluid responsiveness.
Where to measure VTI with PWD and limits of normal.
Multiple sites can be used to interrogate the LV VTI. The ascending and descending aorta. The normal expected changes of ventilation and VTI is a cutoff value of 12%
1. Start by getting an Apical 4 chamber view and rotate the probe anticlockwise to get the LVOT. Alternatively you will have to flatten the probe more so you can see the LVOT.
2. Move the cursor line and place the sample box on the LVOT seen on the middle image. Proper alignment is paramount since measurements must be as parallel to the cursor line as possible.
3. Activate PWD. and change the baseline shown on the right image. Freeze the image to make measurements. You can either trace the envelope or measure the max and min velocities (shown in the image). The sweep speed on the machine needs to be changed to allow several resp cycles represented
4. The last image shows a VTI on the MV inflow with a clear difference between inspiration and expiration. This has been achieved by changing the sweep speed which allows more measurements to be made over a period of time.
Variation= VTImax-VTImin/(VTI average)
A variation of greater than 12 % on the LVOT is considered fluid responsive.
2.1a Apical 4 or 5 chamber interrogation
2.1b VTI using Arterial source.
We can also measure VTI when interrogating a major vessel so long as we can make the probe lie as parallel to the vessel as possible.
On the image to the left (1), the PW doppler placement is seen. This is not the ideal scan since the probe is perpendicular to the PW scan. On the right (2), the probe has been placed as parallel to the skin as possible and PWD has been activated. We use the same thresholds as above here.
2.2 IVC distensibility index
These are changes in IVC diameter that are measured over several respiratory cycles and the changes are compared with the following formula.
IVC DI= IVC max-IVC min/IVC min
A value >18% is suggestive of fluid responsive.