The Intensivist's Perspective of Shock, Volume Management, and Hemodynamic Monitoring

Abstract

One of the primary reasons for intensive care admission is shock. Identifying the underlying cause of shock (hypovolemic, distributive, cardiogenic, and obstructive) may lead to entirely different clinical pathways for management. Among patients with hypovolemic and distributive shock, fluid therapy is one of the leading management strategies. Although an appropriate amount of fluid administration might save a patient's life, inadequate (or excessive) fluid use could lead to more complications, including organ failure and mortality due to either hypovolemia or volume overload. Currently, intensivists have access to a wide variety of information sources and tools to monitor the underlying hemodynamic status, including medical history, physical examination, and specific hemodynamic monitoring devices. Although appropriate and timely assessment and interpretation of this information can promote adequate fluid resuscitation, misinterpretation of these data can also lead to additional mortality and morbidity. This article provides a narrative review of the most commonly used hemodynamic monitoring approaches to assessing fluid responsiveness and fluid tolerance. In addition, we describe the benefits and disadvantages of these tools.

Keywords: POCUS; critical care nephrology and acute kidney injury series; fluid responsiveness; fluid therapy; hemodynamic monitoring; shock.

Figure 1.

Fluid responsiveness on the basis of myocardial contractility. These Frank–Starling curves show two patients with normal and failing hearts. The normal heart can increase its stroke volume by preload expansion, whereas the failing heart cannot. Using a static measurement for fluid status by assessing ventricular preload (estimated by central venous pressure), two patients may have similar preload but completely different responses to fluid loading. However, dynamic measurements can assess the steepness of the curves (i.e., α- and β-angles) and identify if patients are fluid responsive or not (here, α is larger than β, indicating a higher increase in stroke volume for a given fluid bolus).

Figure 2.

Major components in and tools for shock evaluation. CV, cardiovascular; CVP, central venous pressure; EKG, electrocardiogram; ID, infectious diseases; JVD, jugular venous distention; POCUS, point-of-care ultrasound; SPO2, saturation of peripheral oxygen; VEXUS, venous excess ultrasound grading system.

Figure 3.

Venous flow patterns and organ congestion (76). Normal hepatic venous flow patterns should have a flow wave larger in systole than in diastole. During progressive liver congestion, the ratio of systolic to diastolic flow continues to decrease, and in severe congestion, the systolic flow becomes reversed. This is due to a progressive decline in right atrial compliance secondary to volume overload. Normally, there is no pulsation in portal venous flow. However, with progressive liver congestion, portal venous flow becomes increasingly pulsatile. Venous flow in the intrarenal parenchymal vessels is also nonpulsatile in normal conditions. This changes with a progressive increase in kidney intracapsular pressure and congestion. In mild to moderate congestion, pulsatile intrarenal venous flow is biphasic, becoming monophasic with progressive congestion (76).