A 52-year-old man with dilated cardiomyopathy (left ventricular ejection fraction 25%), recently discharged from a heart failure (HF) admission, presented to the office with weakness and shortness of breath. On examination, his weight was stable, his blood pressure was 88/60 mm Hg, his jugular veins were difficult to assess owing to obesity, with a few bibasilar crackles, distant heart sounds with a 2/6 holosystolic murmur and a soft S3, a protruding abdomen, and 1 to 2+ pitting lower-extremity edema. Laboratory results showed a rise in creatinine from 1.5 to 2.6 mg/dL, a rise in serum urea nitrogen from 38 to 52 mg/dL, and a rise in brain natriuretic peptide from 106 to 280 pg/mL. This patient presented a clinical challenge, because it was not clear whether his symptoms were related to progressive HF with worsening cardiorenal syndrome, or conversely, to relative hypovolemia. Unfortunately, physical examination and laboratory studies can be misleading in the setting of HF exacerbation, 1 and changes in weight are known to lag behind important hemodynamic shifts.
2Traditionally, this patient would likely have been hospitalized, with consideration of right heart catheterization if hemodynamic assessment were needed to guide further treatment. However, in our efforts to improve the quality and safety of care, with potentially competing imperatives to reduce readmissions, length of stay, and costs, 3 we must revisit our approach. The use of pulmonary artery flotation catheter monitoring requires intensive care unit or specialty unit hospitalization, has significant procedure-related risks, may not be accurate in all A and B, The inferior vena cava is 2.6 cm in diameter, without respiratory collapse during inspiration (Ins), consistent with an elevated CVP. This is opposed to a patient with a small IVC (C and D) with inspiratory collapse, consistent with a normal CVP. IVC indicates inferior vena cava.