Does High BNP Always Mean High Filling Pressure

Because a major stimulus for the release of BNP is increased wall tension, BNP levels might be expected to correlate with elevated LV filling pressures. However, in the clinical setting there are circumstances in which a high level of BNP is not associated with high left heart filling pressures. These situations include right-sided failure secondary to advanced pulmonary disease, PE, or primary pulmonary hypertension; acute or chronic renal failure; and rapid lowering of the wedge pressure with diuretics and/or vasodilators before

Hours

Fig. 12. Concurrent measurement of PCWP and BNP in patients with acute heart failure admitted to intensive care unit. Data are limited to responders to therapy as assessed using PCWP. (From ref. 58, with permission.)

Hours

Fig. 12. Concurrent measurement of PCWP and BNP in patients with acute heart failure admitted to intensive care unit. Data are limited to responders to therapy as assessed using PCWP. (From ref. 58, with permission.)

a Swan-Ganz catheter is placed. In addition, under some circumstances, BNP levels might be normal when the wedge pressure is high. This situation is most likely to occur in acute mitral regurgitation in which the increase in capillary pressure is "upstream" from the left ventricle and in "flash" pulmonary edema in which BNP might not have had time to be synthesized.

In a given patient, the level of BNP does not always correlate tightly to wedge pressure. However, in a patient admitted with heart failure and high filling pressures secondary to volume overload, along with a high BNP ("wet BNP"), a treatment-induced decrease in wedge pressure will almost always be associated with a rapid drop in BNP concentration, as long as the patient is maintaining adequate urine output. Kazanegra et al. (58) obtained hemodynamic measurements (pulmonary capillary wedge pressure [PCWP], cardiac output, right atrial pressure, systemic vascular resistance), and BNP levels every 2-4 h for the first 24 h and every 4 h for the next 24-48 h in patients admitted for decompensated heart failure. PCWP dropped from 33 ± 2 to 25 ± 2 mmHg over the first 24 h, whereas BNP dropped from 1472 ± 156 to 670 ± 109 pg/mL (Fig. 12). The correlation between BNP levels and other indices of cardiac function-cardiac output (thermodilution), mixed venous oxygen saturation, and systemic vascular resistance was nonsignificant. It should be emphasized that patients with end-stage heart failure admitted for transplant workup who are not acutely volume overloaded may not show a drop in BNP levels as the wedge pressure is lowered ("dry BNP").

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