PROFOUND HYPOTENSION AND end-organ hypoperfusion are most often the consequence of inadequate systemic blood flow from primary cardiac failure (cardiogenic shock) or hemorrhage (hemorrhagic shock). However, profound hypotension may also result from vasodilation and abnormally low systemic vascular resistance (SVR) called vasoplegic or vasodilatory shock.¹ While sepsis is the leading cause of vasodilatory shock, often patients who initially present with cardiogenic shock develop a component of vasodilatory shock due to end-organ hypoperfusion and subsequent release of vasodilatory mediators.² In the setting of persistently low SVR, these patients typically require very high doses of vasopressors to achieve adequate systemic blood pressure, placing an additional burden on already compromised cardiac function.³

SVR represents the ratio of systemic blood pressure and cardiac output (CO) and can be conceptualized as the increase in systemic blood pressure per unit of CO. Clinically, SVR is calculated by dividing the pressure gradient across the systemic circulation (mean arterial pressure [MAP] minus central venous pressure [CVP]) by the CO (L/min).⁴ The result represents the pressure increase (in mmHg) per liter of CO and is expressed in Wood units. When multiplied by a conversion factor of 80, SVR can also be expressed in units of dynes·s·cm⁻⁵.

Fluid administration and high-dose vasopressor therapy are the main pharmacologic approaches to normalization of hemodynamics in vasodilatory shock. However, increases in CVP and arteriolar vasoconstriction may actually worsen rather than improve oxygen delivery to end-organs.⁵ In fact, the use of multiple vasopressors at high doses is associated with a very high mortality⁶ and often these patients become resistant to pharmacologic therapies that normally increase vascular smooth muscle tone (termed vasoplegia).⁷ The recognition that improvement of oxygen delivery to tissues is a key goal of therapy has led to a dramatic rise in and earlier use of mechanical circulatory support devices. An increasingly common approach to treating a patient in acute cardiogenic shock is the initiation of venoarterial extracorporeal membrane oxygenation (VA-ECMO). VA-ECMO immediately restores blood pressure and oxygen delivery by increasing systemic flow. Its use, however, in patients with vasodilatory shock has not been as successful,⁸ likely due to inadequate flow rates achieved by ECMO in patients with profound vasodilation.^9,10

We present a simple method to estimate the systemic flow required to achieve a target MAP that uses Doppler echocardiography to estimate left ventricular (LV) stroke volume (SV). Adding to the measured ECMO flow rates provides an estimation of total systemic flow and hence SVR. Using this value of SVR allowed the calculation of the additional flow required to raise MAP to a target level and thus the need for two concurrent ECMO systems.