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While a serum potassium of 3.0 mEq/L is consistent with the hypokalemia seen in persistent vomiting, an arterial pH of 7.28 indicates a state of metabolic acidosis. Acidosis in hyperemesis would only occur late due to starvation ketosis, but it is not the primary result of losing gastric secretions. The question specifically asks for findings indicative of alkalosis, making this choice physiologically inconsistent with the primary gastric loss.

A serum sodium of 145 mEq/L is at the upper limit of normal, which can occur in dehydration, but a blood urea nitrogen of 10 mg/dL is within the normal range (7 to 20 mg/dL). In significant dehydration, the nurse expects to see an elevated BUN due to decreased renal perfusion and pre-renal azotemia. This combination fails to demonstrate the severity of the clinical dehydration typically associated with pathological hyperemesis gravidarum.

Normal electrolytes and a decreased hematocrit are findings that contradict the pathophysiology of severe emesis. Persistent vomiting leads to hemoconcentration, which causes the hematocrit to rise as plasma volume decreases. The presence of normal electrolytes suggests that the client has not yet experienced the significant ionic shifts that characterize the transition from simple nausea to hyperemesis gravidarum.

An elevated hemoglobin level is a common finding in hyperemesis gravidarum, but it is a marker of hemoconcentration rather than starvation. As the plasma volume decreases due to profound dehydration, the relative concentration of red blood cells increases. While this reflects the fluid volume status of the client, it does not provide information regarding the underlying metabolic pathways or the switch to ketosis.

Normal serum glucose levels are often maintained even in severe starvation states due to the body's highly efficient gluconeogenesis pathways. The liver can synthesize glucose from non-carbohydrate sources like amino acids and glycerol to protect fetal development and brain function. Therefore, a normal glucose reading does not rule out starvation, as the body may be maintaining that level by sacrificing maternal tissues.

A decreased white blood cell count, or leukopenia, is not a recognized feature of the pathophysiology of hyperemesis gravidarum. In fact, a client with severe dehydration and stress may actually exhibit a mild leukocytosis as a physiological response to systemic inflammation or hemoconcentration. A low count would be more suggestive of an immunological disorder or bone marrow suppression, which is unrelated to the emetic pathways.

A complete blood count is utilized to assess for hemoconcentration and infection, but it provides no information regarding the etiology of hormonal surges. While an elevated hematocrit can confirm the severity of dehydration, it cannot visualize the contents of the uterus to rule out abnormal placental growth. It is a supportive test for fluid management rather than a primary diagnostic tool for trophoblastic disease.

Liver function tests are often indicated in severe hyperemesis to monitor for transaminitis, which may occur due to starvation or hepatic stress. While these enzymes can be mildly elevated in approximately 50% of hospitalized cases, they are non-specific findings that do not identify the source of the emetic stimulus. Elevated AST or ALT levels do not help in ruling out a molar pregnancy or other gestational abnormalities.

An electrocardiogram is primarily used to monitor for cardiac arrhythmias secondary to electrolyte imbalances like hypokalemia. While essential for managing the systemic complications of persistent vomiting, it lacks the diagnostic capability to identify the hormonal or anatomical cause of the hyperemesis. It assesses the cardiovascular impact of the disease rather than the underlying pregnancy-related pathology.