A prudent rule is that any time blood loss is considered more than average, then the hematocrit is determined and plans are made for close observation for potential physiological deterioration. 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-accuratey measured urine low relects renal pefusion, which in turn rlects pefusion of other vital organs. Urine low of at least 30 mL, and preferably :50 mL per hour, should be maintained.
Shock from hemorrhage evolves through several stages. Early in the course of massive bleeding, mean arterial pressure, stroke volume, cardiac output, central venous pressure, and pulmonary capillary wedge pressure decline. Increases in arteriovenous oxygen content diference relect a relative rise in tissue oxygen extraction, although overall oxygen consumption falls.
Blood low to capillary beds in various organs is controlled by arterioles. These are resistance vessels that are partially controlled by the central nervous system. However, approximately 70 percent of total blood volume is contained in venules which are passive resistance vessels controlled by humoral factors. Catecholamine release during hemorrhage prompts greater venular tone, which provides an auto transfusion from this capacitance reservoir (Barber, 1999). his is accompanied by compensatory rises in heart rate, systemic and pulmonary vascular resistance, and myocardial contractility. In addition, cardiac output and blood volume are redistributed from the efect of selective, centrally mediated arteriolar constriction or relaxation-autoregulation. hus, although perfusion to the kidneys, splanchnic beds, muscles, skin, and uterus is diminished, relatively more blood flow is diverted to the heart, brain, and adrenal glands.
When the blood volume deicit exceeds approximately 25 percent, compensatory mechanisms usually are inadequate to maintain cardiac output and blood pressure. Importantly, additional small losses of blood will now cause rapid clinical deterioration. Following an initial augmented total oxygen extraction by maternal tissue, maldistribution of blood flow results in local tissue hypoxia and metabolic acidosis. This creates a vicious cycle of vasoconstriction, organ ischemia, and cellular death.
Another important clinical efect of hemorrhage is activation of lymphocytes and monocytes, which in turn causes endothelial cell activation and platelet aggregation. These promote release of vasoactive mediators that occlude small vessels and further impair microcirculatory perfusion. Other common obstetrical syndromes-preeclampsia and sepsis-also lead to loss of capillary endothelial integrity, additional loss of intravascular volume into the extracellular space, and platelet aggregation. These then can incite DIC.
he pathophysiological events just described create important but often overlooked extracellular luid and electrolyte shifts involved in both the genesis and successful treatment of hypovolemic shock. hese include changes in the cellular transport of various ions such as sodium and water into skeletal muscle as well as potassium loss. Replacement of extracellular luid and intravascular volume are both necessary. Survival is enhanced in acute hemorrhagic shock if blood plus cystalloid solution is given compared with blood tranusions alone.
Whenever excessive blood loss is suspected in a pregnant woman, steps are simultaneously taken to identiy the bleeding source and to begin resuscitation. If she is undelivered, restoration of blood volume is beneficial to mother and fetus, and it also prepares for emergent delivery. If she is postpartum, it is essential to immediately identiy uterine atony, retained placental fragments, or genital tract lacerations. At least one and preferably more large-bore intravenous infusion systems are established promptly with rapid administration of crystalloid solutions, while blood is made available. An operating room is readied, and a surgical and anesthesia team are assembled immediately. Specific management of hemorrhage is further dependent on its etiology.