36 Assessment of filling status

Question 1

What are the effects of filling status on the heart?

Answer 1

In acute volume overload, there is increased systolic and diastolic function but in chronic volume overload, there is decreased systolic and diastolic dysfunction.

IVC, SVC and hepatic vein dilatation and decreased inspiratory collapse.

Paradoxical septal motion.

In states of increased filling status (volume overload), there is increased preload, via the Frank-Starling mechanism (increase in stretch increases the SV), so there is improved LV/RV systolic function (e.g. normal or increased LVEF). However, chronic volume overload causes LV/RV dilatation and LV/RV systolic dysfunction (HFrEF). In states of increased filling status (volume overload), there is increased LVEDP so there is improved LV/RV diastolic function (e.g. increased E wave, E/E’ and E/A). However, chronic volume overload causes LV/RV diastolic dysfunction with increased filling pressures (HFpEF). In states of increased filling status, there are increased doppler velocities. The increased preload increases the SV which increases AV Vmax. However, chronic volume overload can cause AR.

In states of increased filling status (volume overload), there is increased venous return and increased central venous pressure. Therefore, the IVC and SVC are dilated with decreased inspiratory collapse and the hepatic veins are dilated and less pulsatile with less variation.

In states of increased filling status (volume overload), the RA pressure is increased so the IAS is forced to the left. This causes paradoxical septal motion.

Question 2

How is fluid status managed and assessed?

Answer 2

In shock patients, the assessment of LV function directs the management of inotropes and vasopressors, and the assessment of LV size and IVC size and collapsibility directs the management of fluids.

An increase in chamber size (indicates an increase in preload), chamber systolic function (LVEF), and SV, indicate a positive response to the fluids. An increase LA size, presence of pulmonary hypertension/congestion, and impaired diastolic function with increased filling pressures indicate fluid overload.

An increase in SV, CO and LV systolic function (e.g. LVEF, TDI, strain) indicate a positive response to inotropes. A significant increase in afterload, and therefore decrease in LV function, may indicate inotropic toxicity.