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Recognition of obstetrical hemorrhage severity is crucial to its management. However, visual estimates, especially when blood losses are excessive, are notoriously inaccurate. In many cases, true volume losses are often two to three times the clinical estimate. Moreover, in obstetrics, part and sometimes even all of the lost blood may be concealed. Estimation is further complicated in that peripartum hemorrhage also includes the pregnancy-augmented blood volume. After pregnancy hypervolemia is lost at delivery, blood loss can be estimated by calculating 500 mL loss for each 3 volume percent drop in hematocrit. Its nadir depends on the speed of resuscitation with intravenous crystalloids and blood products. With ongoing blood loss, the real-time hematocrit is at its maximum whenever measured in the delivery, operating, or recovery room.

Prudently, if blood loss is considered more than average, the hematocrit is determined, and plans are made for close observation for potential physiological deterioration. Blood loss determination as recommended by the American College of Obstetricians and Gynecologists (2019b) is discussed in detail in Chapter 42. Urine output measured hourly is one of the most important “vital signs.” Unless diuretic agents are given—and these are seldom indicated with active bleeding—accurately measured urine flow reflects renal perfusion. This in turn reflects perfusion of other vital organs. The volume of urine output should be ≥30 mL/hr and preferably ≥50 mL/hr.

Another important factor to consider with management of hemorrhage is whether there are adequate procoagulants to achieve clot formation and stability. Many cases of severe obstetrical hemorrhage are further complicated by disseminated intravascular coagulation (DIC), in which blood has dysfunctional coagulation (p. 775).


Hypovolemic Shock

Shock from hemorrhage evolves through several stages (Cannon, 2018). Early, the mean arterial pressure, stroke volume, cardiac output, central venous pressure, and pulmonary capillary wedge pressure decline. Greater differences in arteriovenous oxygen content values reflect enhanced tissue oxygen extraction, although overall oxygen consumption falls.

Blood flow to capillary beds is controlled by arterioles, which are resistance vessels and partially controlled by the central nervous system (CNS). However, approximately 70 percent of total blood volume is contained in venules, which are passive resistance vessels controlled by humoral factors. Thus, the catecholamine release during hemorrhage prompts greater venular tone, and this provides an autotransfusion from this capacitance reservoir. This volume boost is accompanied by compensatory rises in heart rate, systemic and pulmonary vascular resistance, and myocardial contractility. At the same time, selective, CNS-mediated arteriolar constriction or relaxation, termed autoregulation, preferentially redistributes cardiac output and blood volume. Thus, more blood flow is diverted to the heart, brain, and adrenal glands, whereas perfusion to the kidneys, splanchnic beds, muscles, skin, and uterus is relatively diminished.

When the blood volume deficit exceeds approximately 25 percent, compensatory mechanisms usually are inadequate to maintain cardiac output and blood pressure. Importantly, additional small losses of blood ...

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