A nurse is caring for a postoperative 70-kg patient who had major blood loss during surgery and now has acute kidney injury. The patient does not have signs of fluid overload. Which intervention would be most effective as a fluid challenge to promote kidney perfusion?

Choice A reason: Deep vein thrombosis is a condition where blood clots form in the deep veins, usually in the legs. While it is a serious condition, it is not directly associated with portal hypertension in patients with late-stage cirrhosis. Portal hypertension primarily affects the liver and its associated blood vessels, leading to complications within the portal circulation system rather than systemic venous thrombosis.

Choice B reason: Ascites is the accumulation of fluid in the abdominal cavity, and it is a common complication of portal hypertension in patients with cirrhosis. Increased pressure in the portal vein leads to leakage of fluid into the abdominal cavity, causing distension and discomfort. Ascites can significantly impact the patient's quality of life and requires careful management.

Choice C reason: Splenomegaly, or enlargement of the spleen, is another potential complication of portal hypertension. The increased pressure in the portal vein can cause blood to back up into the spleen, leading to its enlargement. Splenomegaly can result in hypersplenism, where the spleen becomes overactive and destroys blood cells, contributing to anemia, thrombocytopenia, and leukopenia.

Choice D reason: Esophageal varices are dilated blood vessels in the esophagus that develop as a result of portal hypertension. The increased pressure in the portal vein causes blood to divert through collateral vessels, including those in the esophagus. These varices can rupture and cause life-threatening bleeding, making them a critical complication to monitor in patients with cirrhosis.

Choice E reason: Increased platelet levels are not typically seen in patients with portal hypertension. In fact, portal hypertension and cirrhosis often lead to thrombocytopenia, or low platelet levels, due to splenic sequestration and reduced platelet production. Thrombocytopenia is a more common finding in this patient population.

Choice A reason: An increased heart rate is not an expected therapeutic response to adenosine. Adenosine is used to slow the heart rate by temporarily blocking the electrical conduction through the atrioventricular (AV) node. This action is crucial in managing supraventricular tachycardia (SVT), as it can help restore a normal heart rhythm. An increased heart rate would suggest that the medication is not working as intended, and the underlying tachycardia may persist or worsen.

Choice B reason: A short period of asystole is the correct and expected therapeutic response when administering adenosine. Adenosine works by briefly stopping the heart's electrical activity, leading to a brief asystole (lack of heartbeat). This allows the heart's natural pacemaker to reset and potentially restore a normal rhythm. Although this can be alarming, it is a known and anticipated effect of the drug, and it typically resolves quickly as the heart resumes normal activity.

Choice C reason: Hypertension is not an expected response to adenosine. Adenosine generally causes vasodilation, which can lower blood pressure. The primary focus of adenosine in the context of SVT is on its cardiac effects rather than influencing blood pressure significantly. If hypertension occurs, it may be unrelated to the administration of adenosine and could indicate another underlying issue that needs to be addressed.

Choice D reason: Decreased intraocular pressure is not a relevant or expected response to adenosine administration in the context of managing SVT. Adenosine's primary effect is on the heart's electrical conduction system, and it does not significantly impact intraocular pressure. The focus should remain on observing the cardiac responses to ensure the medication is effectively managing the SVT.