CHAPTER 32

#### KEY POINTS

• No hemodynamic monitoring device will improve patient outcome unless coupled to a treatment, which itself improves outcome.

• Low venous oxygen saturations need not mean circulatory shock but do imply circulatory stress, as they may occur in the setting of hypoxemia, anemia, exercise, as well as circulatory shock.

• There is no “normal” cardiac output, only one that is adequate or inadequate to meet the metabolic demands of the body. Thus, targeting a specific cardiac output value without reference to metabolic need, or oxygen-carrying capacity of the blood, is dangerous.

• Cardiac output is estimated, not measured, by all devices routinely used in bedside monitoring (though we shall call it measured in this text).

• Cardiac output estimates using arterial pulse pressure contour analysis cannot be interchanged among devices and all suffer to a greater or lesser extent by changes of peripheral vasomotor tone commonly seen in the critically ill.

• Since metabolic demands can vary rapidly, continuous or frequent measures of cardiac output are preferred to single or widely spaced individual measures.

• Integrating several physiologic variables in the assessment of the adequacy of the circulation usually gives a clearer picture than just looking at one variable.

• Integrating cardiac output with other measures, like venous oxygen saturation, can be very helpful in defining the adequacy of blood flow.

#### INTRODUCTION

The goal of the cardiorespiratory system is to sustain adequate delivery of oxygen to the tissues and removal of carbon dioxide to meet their metabolic demands. Under normal conditions, this system has significant flow and O2-carrying capacity reserve to handle all but the most demanding metabolic stresses or primary organ dysfunction. Indeed, once overt cardiorespiratory failure is present, the degree of cardiorespiratory impairment is often advanced with existing end-organ ischemic dysfunction. Hemodynamic monitoring plays an important role in the management of these critically ill patients with cardiovascular dysfunction. It is profoundly useful in the titration of therapies in patients with known cardiovascular disease processes, like hemorrhagic shock, acute mitral regurgitation, cor pulmonale, left-sided heart failure, and vasoplegic shock wherein knowing the underlying pathophysiologic process, physiologic state, and titrating-specific therapies represents the centerpiece of cardiovascular support. However, monitoring is also useful in identifying problems before they deteriorate to shock and/or in the management of high-risk patients with proven therapies. In this chapter, we will discuss monitoring the elements of oxygen delivery $(DO2)$, namely cardiac output and blood oxygen saturation. Hemoglobin is the other variable defining $DO2$, but usually does not change rapidly and can be estimated from venous oximetry. Although circulatory shock is due to inadequate $DO2$ to meet metabolic demands, targeting-specific cardiac output or $DO2$ values across all patients in an attempt to prevent occult or obvious tissue hypoperfusion and ischemia is not only unwarranted but potentially harmful, as the needs of different patients and the same patient over time can vary widely.

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