Preload refers to the tension or load on a muscle as it begins to contract. In the context of the cardiovascular system, preload is the length of the ventricular muscle fiber at end-diastole. The principal factor that determines muscle fiber length is the volume of blood in the ventricles at the point of maximal filling. Therefore, ventricular end-diastolic volume (EDV) is used as a reflection of preload for the intact heart. The pressure-volume curves in Figure 4-2 depict the influence of preload on the mechanical performance of the left ventricle during diastole (lower curves) and systole (upper curves). The solid lines on the curves represent the normal pressure-volume relationships during diastole and systole. Note that the uppermost curve in the figure has a rapid ascent, which indicates that small changes in EDV are associated with large changes in systolic pressure. For this reason, the most effective measure for preserving adequate cardiac output is to maintain an adequate EDV.

The intrinsic ability of the heart to adapt to alterations in the volume of blood returning to the heart is commonly known as the Frank-Starling phenomenon. The graph that is most often used to depict this relationship is known as a ventricular function curve (Fig. 4-3). Within certain physiologic limits, the more the ventricles are filled with blood during diastole, the greater the quantity of blood that will be ejected during systole.
Conversely, when the amount of blood returning to the ventricles is diminished, cardiac output may be impaired. For example, this may be evident in the patient with significant blood loss or hypotension who has decreased circulating blood volume or venous return to the heart.

The stretch imposed on cardiac muscle is determined not only by the volume of blood in the ventricular chambers but also by the tendency of the ventricular wall to distend or stretch at a given volume within the chamber. This property is described as the compliance of the ventricle. Compliance is determined by the relationship between changes in end-diastolic pressure (EDP) and end-diastolic volume. The lower curve in Figure 4-3 illustrates this concept. As the ventricle becomes less compliant (e.g., in ventricular hypertrophy), there is less change in diastolic volume relative to the change in diastolic pressure. Early in the process, the EDV remains normal, but the EDP increases above normal. As the compliance decreases further, the increase in EDP eventually reduces venous return to the heart, thereby causing a reduction in EDV.⁶

Afterload is the resistance or load that opposes ventricular ejection of blood during systole. The right ventricle pumps against pressure or resistance in the pulmonary vasculature, whereas the left ventricle pumps against the higher pressure or resistance in the systemic circulation. In contrast to preload, afterload and cardiac output have an inverse relationship. Within certain physiologic limits, the lower the afterload or resistance applied against the ventricles during systole, the greater the cardiac output. Conversely, patients with clinical conditions such as pulmonary or systemic hypertension, in which pressure in the pulmonary or systemic vessels respectively is increased, are at risk for decreased cardiac output. Forces that contribute to ventricular wall tension or afterload are listed in Box 4-1.

Because afterload is a transmural force, it is influenced by the pleural pressures at the outer surface of the heart. Negative pleural pressures increase transmural pressure and increase ventricular afterload, whereas positive pleural pressures have the opposite effect. Negative pressures surrounding the heart may impede ventricular emptying by opposing the inward displacement of the ventricular wall during systole.⁷ This action is responsible for the decrease in systolic blood pressure that occurs during the inspiratory phase of spontaneous breathing. Positive pleural pressures can promote ventricular emptying by facilitating the inward displacement of the ventricular wall during systole.

Contractility, also known as the inotropic state of the heart, is the intrinsic ability of the heart muscle to shorten or develop tension independent of variations in preload and afterload. Not easily measured in clinical situations, contractility may nonetheless be inferred by a change in cardiac output when afterload and preload remain constant. Under conditions of altered catecholamine production or following administration of medications that alter inotropic response, the Frank–Starling curve shifts upward with a higher cardiac output for a given filling pressure. Conversely, with decreased contractility, the heart pumps less well at a given filling pressure. Thus, patients with compromised heart function at higher pressures under normal conditions have less reserve and are more prone to heart failure when stressed.

Heart rate affects the strength of myocardial contraction and thus cardiac output. For example, at faster rates, the force of contraction is strong. At slower rates, the force is weaker. This intrinsic property of the heart muscle may be attributable to rate-driven variations in sarcoplasmic calcium concentration. It should be noted that an increased heart rate also results in decreased diastolic filling time and may thereby decrease preload. If continued over a period of time, this may lead to decreased cardiac output. In addition, a pause between heart contractions results in increased force of the next contraction, also known as rest potentiation, which may increase cardiac output. For these reasons, rate-related changes in the force of contraction, preload, and cardiac output interact in a complex manner.

Oxygen is transported to the tissues in two ways: dissolved under pressure in plasma and bound to hemoglobin in red blood cells. The oxygen dissolved in plasma makes up approximately 1 to 2 percent of the total oxygen content, whereas oxygen bound to hemoglobin makes up the remaining 98 to 99 percent.

The role of hemoglobin in the transport of oxygen is significant. Hemoglobin is composed of four subunits, each consisting of a protein chain with a heme group attached to a histidine residue. One molecule of oxygen is loosely bound with one of the six coordinate valencies of each of the heme iron atoms. Thus, each molecule of hemoglobin is associated with four molecules of oxygen. The kinetics of the association are such that all of the molecules of oxygen bind at the same rate. When a hemoglobin molecule is combined with oxygen, it is called oxyhemoglobin. The saturation of hemoglobin with oxygen is the ratio of oxyhemoglobin to the total amount of hemoglobin capable of transporting oxygen (Fig. 4-4).

Although it represents only a small fraction of total oxygen content, oxygen dissolved in plasma plays a crucial role. The ability of oxygen to combine with hemoglobin in the lungs, later to be released at the tissue level, is affected by oxygen in the plasma. This reversible binding of oxygen to hemoglobin is an important concept in oxygen transport and allows for the loading of oxygen in the lungs and unloading at the tissue level.

Affinity refers to the ability of oxygen to bind to hemoglobin. Both the uptake and the release of oxygen from hemoglobin molecules are represented visually by the oxyhemoglobin dissociation curve, depicted in Figure 4-5.

The curve portrays the relationship between the partial pressure of oxygen (PaO₂) in arterial blood and the saturation of hemoglobin (SaO₂). The sigmoid shape of the normal curve is the result of:

The position of the curve is defined more precisely by a reference point known as the P₅₀. This point represents the PaO₂ at which hemoglobin is 50 percent saturated. Under normal conditions in nonpregnant people, the P₅₀ is 26.3 mmHg (see Fig. 4-5).

The P₅₀ is not fixed in those who are critically ill. If the affinity and P₅₀ change, the oxyhemoglobin dissociation curve shifts to the right or left. Conditions known to change oxygen affinity are described in Table 4-1. Decreased oxygen affinity, resulting in a right shift of the
oxyhemoglobin dissociation curve, means that at any given PaO₂, there is decreased saturation. Thus, oxygen is released more readily to tissues. Conversely, increased oxygen affinity, resulting in a left shift of the curve, means that at any given PaO₂, there is increased saturation. This results in oxygen binding more tightly to hemoglobin.

It should be noted that pregnancy also affects the position of the oxyhemoglobin curve. The maternal curve normally shifts to the right, whereby oxygen is released more quickly from hemoglobin. The fetal curve normally shifts to the left, resulting in increased affinity of oxygen for hemoglobin. This concept is depicted in Figure 4-6.

Oxygen delivery (DO₂) is the amount of oxygen delivered to the tissues per unit of time. The delivery of oxygen from the lungs to the tissues depends on cardiac output as well as on the content of oxygen in arterial blood (CaO₂). It should be recalled that cardiac output is dependent on preload, afterload, contractility, and heart rate. Arterial oxygen content is determined by the arterial concentration of hemoglobin, the arterial saturation of hemoglobin (SaO₂), and the amount of oxygen dissolved under pressure in plasma within the arteries (PaO₂).

Factors that increase cardiac output (e.g., uterine contractions, increased metabolism, and certain medications) also increase DO₂. In addition, factors that increase total oxygen content (e.g., transfusion of packed red blood cells) increase DO₂. Such conditions may include hypovolemia, hypoxemia, anemia, and administration of certain medications. When oxygen supply is threatened, the body attempts to compensate in order to maintain delivery to the tissues by first increasing cardiac output. It should be noted that cardiac output may increase severalfold above normal in healthy people under stressful circumstances.

Oxygen consumption (VO₂) refers to the amount of oxygen consumed by the tissues each minute. At rest, VO₂ is approximately 25 percent of the total oxygen available. Oxygen consumption is increased by numerous conditions as well as by interventions, therapeutic procedures, and various other stressors. It should be noted that VO₂ also increases significantly during normal pregnancy.

The normal relationship between DO₂ and VO₂ is such that sufficient reserve exists to maintain VO₂ independent of DO₂ over a wide range of delivery values. However, situations may develop whereby prolonged decreased DO₂, below a critical threshold, eventually results in a linear fall in VO₂. This is known as delivery dependent VO₂ because the amount of oxygen consumed is limited by the amount of oxygen delivered. In such circumstances, VO₂ does not become independent of DO₂ except at very high levels of oxygen delivery, if at all. This pathologic response is related to the fixed oxygen-extraction ratio present in some critically ill patients.

The central venous pressure (CVP) catheter is a single- or multiple-lumen catheter advanced through a peripheral or central vein until the tip is in the proximal superior vena cava (Fig. 4-7). Central venous access is most commonly obtained via either the internal jugular or subclavian vein. The internal jugular vein is preferred during pregnancy because of the increased risk of pneumothorax with subclavian placement attempts during pregnancy.

Use of this catheter permits evaluation of right preload (expressed in mmHg as CVP), as well as access for administration of fluid or medications. The primary limitation with respect to central hemodynamic assessment is that right ventricular function may not accurately reflect left ventricular function. Thus, clinical use of the CVP may be misleading and possibly deleterious in certain clinical situations. In addition, a CVP catheter does not permit evaluation of data regarding other determinants of cardiac output or oxygen transport parameters. For these reasons, use of a CVP catheter for assessment of hemodynamic function in a critically ill obstetric patient is seldom, if ever, indicated. However, CVP catheters may be utilized for reasons other than assessment of hemodynamic function. Box 4-2 lists potential indications for use of a CVP catheter.⁸

Complications of central venous access that can occur during insertion and monitoring include pneumothorax, venous air embolism, inadvertent arterial puncture, and infection. Although pneumothorax has been reported in 1 to 5 percent of a general patient population undergoing central venous catheterization, Clark and associates observed no pneumothorax when the internal jugular approach was used in a compilation of obstetric and gynecologic patients.² Strategies to reduce the risk of central line–associated bloodstream infection (CLABSI) are presented later in this chapter.