LV Systolic Function 3
This station covers LV systolic function evaluation. We will look at doppler evaluation of stroke volume and cardiac output. 2D evaluation of cardiac function is useful, but it can be sometimes difficult to determine hemodynamic effects from 2D data alone. This is where doppler evaluation of cardiac function and hemodynamics can help. We will illustrate this with a clinical case scenario.
A. Stroke Volume
1. LVOT Diameter
STEP 1:
- This measurement is made in 2D
- Obtain the PLAX view, zoom in on the LVOT & AV,
- Freeze the clip and scroll to the mid-systolic frame, when the aortic valve leaflets are open
- Measure the LVOT diameter in 2D just proximal to the aortic valve. Measure from inner edge to inner edge of the LVOT
- As the diameter (LVOTd) is squared to obtain the LVOT CSA, small errors can lead to significant overestimation of stroke volume.
2. LVOT VTI
STEP 2:
- Obtain the apical 5 chamber or apical 3 chamber view
- Use pulse wave doppler
- Place the sample volume in the LVOT where the diameter was measured
- Obtain the LVOT VTI by tracing the doppler envelope
3. Calculate Stroke Volume
STEP 3:
- Stroke volume (ml) is then obtained by multiplying LVOTcsa and LVOT VTI
- Cardiac output is given by SV x heart rate
Summary
B. Clinical Scenario
Scenario 1
Patient A
Patient A is a 69 year old man is admitted with acute pancreatitis. His past medical history includes ischaemic heart disease and he is known to have a LVEF < 30%. He is day 8 on the ICU and is hypotensive with a fever today. You suspect line sepsis but are unsure if his hypotension has a mixed etiology of hypovolaemic, cardiogenic or distributive.
- The LVOT VTI is 20.9cm
- LVOTd = 2.72cm
- Heart Rate = 70/min
This gives us a stroke volume of 119.6ml and a cardiac output of 8.4 l/min. Link to echo calculator
It is evident that the hemodynamics seen here do not fit with the 2D echo findings. It is likely that there is vasolidation/low svr state that is causing the hypotension. The patient should be started on vasopressors to increase SVR.
Patient B
A 48 year old man is found collpased at home. He received bystander CPR, followed by ALS by the EMT and regained cardiac output on arrival to hospital. His GCS is 3/15 on arrival. He is hypotensive with cool peripheries. First impressions suggest a cardiogenic cause
- The LVOT VTI is 9.7cm
- LVOTd = 2.2cm
- HR = 70/min
The stroke volume and cardiac output are 36.9ml and 2.6l/min respectively.
2D findings and doppler hemodynamic evaluation is consistent with a low cardiac output state secondary to cardiogenic shock.
Here are 2 patients on mechanical ventilation in the ICU. Both patients are hypotensive. Both of the above patients have very similar LV systolic function on 2D evaluation. The left ventricle is poorly contracting in both clips and visual estimate of EF is < 30%. Further interrogation of hemodynamics with doppler however reveals that the underlying cardiac hemodynamics are quite different. This has implications for clinical management.
Scenario 2
SV = LVOTcsa x LVOT vti
LVOT csa = 3.14 x LVOT radius x LVOT radius
The equation can also be written as
LVOT csa = 0.785 x LVOT diameter x LVOT diameter
LVOTcsa = 0.785 x 2.4 x 2.4 = 4.52cm2
Stroke volume = 4.52 x 25.32
= 114.5ml