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(Chest. 2005;128:288-295.)
© 2005 American College of Chest Physicians

Utility of B-Type Natriuretic Peptide and N-terminal Pro B-Type Natriuretic Peptide in Evaluation of Respiratory Failure in Critically Ill Patients*

Dane Jefic, MD; John W. Lee, MD; Dijana Jefic, MD; Ruth T. Savoy-Moore, PhD and Howard S. Rosman, MD

* From the Departments of Medicine (Dr. Dane Jefic), Pulmonary and Critical Care (Dr. Lee), Nephrology (Dr. Dijana Jefic), Medical Education (Dr. Savoy-Moore), and Cardiology (Dr. Rosman), St. John Hospital, Wayne State University School of Medicine, Detroit, MI.

Correspondence to: Dane Jefic, MD, 22201 Moross Rd, PB II Ste 80, Detroit, MI 48236; e-mail: danejefic{at}yahoo.com


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: B-type natriuretic peptide (BNP) and N-terminal pro BNP (NTproBNP) have been shown to correlate with pulmonary arterial wedge pressure (PAWP) in patients with heart failure. We studied whether BNP and/or NTproBNP can differentiate high- vs low-PAWP respiratory failure in ICU patients. We also evaluated if BNP and NTproBNP will reflect accurately cardiac dysfunction and predict 30-day survival.

Design: Prospective observational study of ICU patients in an urban teaching hospital.

Patients: Forty-one consecutive patients with hypoxic respiratory failure undergoing pulmonary artery catheterization were enrolled between January and December, 2003.

Interventions: BNP and NTproBNP were assayed from a venous blood sample. Hemodynamic variables were obtained at the time blood was drawn. Survival was documented at day 30.

Measurements and results: BNP and NTproBNP correlated significantly with each other (r = 0.656, p < 0.001) and inversely with hemodynamic markers of contractility: BNP with cardiac index (CI) [r = – 0.481, p < 0.02], and left ventricular stroke work index (LVSWI) [r = – 0.384, p < 0.02]; NTproBNP with CI (r = – 0.441, p < 0.02) and LVSWI (r = – 0.623, p < 0.001). BNP and NTproBNP did not correlate with PAWP. We created receiver operating characteristic (ROC) curves for detection of contractile dysfunction using different LVSWI cutoffs. Area under the ROC (AUROC) values were larger and more consistent for NTproBNP than for BNP. For LVSWI < 35 g·m/m2: BNP AUROC = 0.643, NTproBNP AUROC = 0.885 (p < 0.02); for LVSWI < 30 g·m/m2: BNP AUROC = 0.754 (p < 0.02) and NTproBNP AUROC = 0.884 (p < 0.001). Mean (± SE) concentrations did not differ between the survi-vors and nonsurvivors: BNP, 909.3 ± 264.2 pg/mL vs 840.9 ± 171.2 pg/mL; NTproBNP, 11,630.6 ± 3,181.8 pg/mL vs 11,777.6 ± 2,989.9 pg/mL, respectively.

Conclusions: NTproBNP and BNP failed to differentiate high- vs low-PAWP respiratory failure but were inversely correlated with indexes of cardiac contractility. With higher accuracy, NTproBNP may be a more discerning marker than BNP in patients with milder cardiac dysfunction. Neither peptide predicted short-term mortality.

Key Words: accuracy • B-type natriuretic peptide • contractile dysfunction • critically ill • natriuretic peptide • N-terminal pro B-type natriuretic peptide • respiratory failure • Swan-Ganz catheter • wedge pressure


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Over the last several years, we have witnessed an increased interest in the diagnostic utility of natriuretic peptides (NPs).1234 Assays for B-type NP (BNP) and N-terminal pro B-type NP (NTproBNP) have shown comparable accuracy in diagnosing, monitoring and establishing prognosis in patients with heart failure.5678 The diagnostic use of NPs in the intensive care setting could be an attractive alternative as a noninvasive marker of heart failure that could obviate the need for some pulmonary artery catheterizations. It has been suggested that BNP could be used as a pulmonary artery wedge pressure (PAWP) surrogate, differentiating heart failure from ARDS in patients with bilateral lung infiltrates.91011 However, one report12 describes extreme elevations of NPs in patients with ARDS. Most recently, Tung et al13 found no correlation of BNP with PAWP in ICU patients with cardiogenic and noncardiogenic shock.

The range of normal values for BNP and NTproBNP was established in ambulatory and emergency department settings in dyspneic patients. Using these established cutoffs for BNP and NTproBNP for extremely ill ICU patients might therefore be an oversimplification for several reasons. Preexisting systolic or diastolic dysfunction is very prevalent in ICU patients; therefore, NPs are elevated at baseline, limiting the predictive value of these tests. In different lung diseases, increased pulmonary pressures elevate BNP via right ventricular strain.1014 Critical surgical illnesses and trauma alone can elevate NPs, although the mechanism is unclear (possibly through ventricular stretch or hypoxia).15 Hypoxia is a known stimulator of BNP release.1617 In sepsis and systemic inflammatory response syndrome, cardiomyopathy is prevalent and often reversible.1819 NPs have been shown to increase with the reduced glomerular filtration rate (GFR), and renal failure is very prevalent in the ICU.20

The diagnostic utility of BNP and NTproBNP has not been evaluated head-to-head in critically ill patients. Specifically, we performed the study to evaluate BNP and NTproBNP as possible surrogates of PAWP and correlated them with parameters of cardiac contractility to differentiate heart failure syndrome from other causes of respiratory failure. In addition, we determined if BNP and NTproBNP could predict mortality in critically ill patients with respiratory failure.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Design
This was a prospective observational study. Consecutive patients admitted to medical, cardiac, or surgical ICUs of a tertiary referral center and meeting inclusion criteria were enrolled. The study period was 12 months, from January to December 2003. Written informed consent was obtained from either the patient or next of kin. The St. John Hospital and Medical Center Institutional Review Board approved the study.

Patients were included who had respiratory failure (mechanical ventilation or documented hypoxemia on room air: oxygen saturation < 90%, PaO2 < 60 mm Hg), infiltrates on chest radiograph, pulmonary artery catheter (PAC) placed for clinically indicated purposes, and age > 18 years. Exclusion criteria were end-stage renal disease requiring hemodialysis and recent heart surgery.

Patient Characteristics
One hundred twenty consecutive patients were prescreened for enrollment if they had a PAC in place and were in a medical, surgical, or cardiac ICU. Most common reasons for exclusion were inability to obtain informed written consent from the patient or next of kin, absence of respiratory failure, and presence of end-stage renal disease. Forty-one subjects fulfilled our inclusion criteria (Table 1 ). All but two patients were intubated at the time of blood sampling. Fifteen patients had primarily intra-abdominal problems such as pancreatitis, cholecystitis, colitis, intra-abdominal abscess, hepatic or gastric malignancy, small-bowel obstruction, ischemia, or rupture. Five patients had pulmonary edema as their primary problem, and one patient was in cardiogenic shock. The remaining 20 patients had respiratory diseases including pneumonia, COPD, or cor pulmonale as the primary process. Sepsis or septic shock was a primary or secondary diagnosis for 20 patients among the above-described three groups. The majority of our patients had failure of two or more organ systems.


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  		Table 1.. Demographic Characteristics of the Study Population (n = 41)*

 
Measurements
Blood samples for BNP and NTproBNP were obtained from venous port of PAC or peripheral blood in two ethylenediamine tetra-acetic acid-containing tubes, and hemodynamic measurements and calculations were performed within 2 h of the first PAC profile. If blood sampling was delayed from PAC insertion for any reason, blood was drawn at one of the next PAC readings. Tubes were transported to the central laboratory at room temperature immediately and spun and frozen at – 70°C within 4 h. One of the specimens was sent to a reference lab for BNP testing (Triage fluorescence immunoassay; Biosite Diagnostics; San Diego, CA). The second tube was stored at – 70°C, and all specimens were run for NTproBNP at the end of the study (Elecsys 2010 electrochemiluminescent assay; Roche Diagnostics; Indianapolis, IN). Clinicians were blinded to BNP and NTproBNP results.

Hemodynamic, echocardiographic, radiographic, laboratory, and clinical values were obtained from the chart. Values nearest the blood sampling were chosen. Cardiac index (CI) and left ventricular stroke work index (LVSWI) were calculated using the standard formulas.21 The estimated creatinine clearance (CrCl) was calculated using the Cockroft-Gault formula.22 APACHE (acute physiology and chronic health evaluation) II scores23 were calculated retrospectively using data from the day of enrollment. Patients were followed up, and 30-day survival was documented.

Statistical Analysis
Of the 41 patients enrolled, 40 specimens were available for BNP and 37 for NTproBNP. To prevent extreme values from skewing the results, two NTproBNP values (66,382 pg/mL and 61,417 pg/mL) and one BNP value (3,810 pg/mL) were excluded after being identified by the outlier test.24 SPSS 12.0 software (SPSS; Chicago, IL) was used for all analyses. Pearson product moment correlation was used for calculating correlation coefficients. Results are presented as mean ± SEM; {chi}2 test was used for analysis of categorical variables, and analysis of variance was used for comparing continuous variables. Multiple linear regression analyses were performed using NTproBNP and BNP as the dependent variable and age, BNP, NTproBNP, CrCl, PAWP, LVSWI, and CI as potential predictor variables. Significant cardiac abnormality was arbitrarily defined as a LVSWI < 35 g·m/m2, and receiver operating characteristic (ROC) curves were constructed for BNP and NTproBNP separately. A probability of < 0.05 was taken as significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Demographic characteristics of our patient population are shown in Table 1.

BNP and NTproBNP
The mean BNP was 866 ± 729.1 pg/mL (range, 15 to 2,780 pg/mL). Four values were within the normal range. The mean NTproBNP was 11,421.1 ± 2,136 pg/mL (range, 542 to 46,309 pg/mL), and only one value was within normal range. BNP and NTproBNP correlated significantly (r = 0.656, p < 0.001). Mean NTproBNP/BNP ratio was 18 ± 3.8 (range, 0.6 to 135.8). Values for both peptides are plotted against PAWP in Figure 1 and against LVSWI in Figure 2 .



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  		Figure 1.. Neither the correlation between PAWP and NTproBNP (top left) nor that between PAWP and BNP (top right) were significant (r = < 0.2). Bottom: PAWP was divided at the value of 15 mm Hg, and patient values below and above this cutoff were compared. Again, there were no differences for either NTproBNP (bottom left) or for BNP (bottom right).

 


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  		Figure 2.. Both NTproBNP (left) and BNP (right) correlated with LVSWI (p < 0.02).

 
NPs and Hemodynamic Measures of Filling
Neither BNP nor NTproBNP correlated with PAWP, mean pulmonary artery pressure, or central venous pressure. Patients were classified into high- and low-PAWP groups using different PAWP cutoffs (15 mm Hg, 17 mm Hg, and 20 mm Hg), and no difference in mean or median concentrations was seen between groups (Fig 1 shows data using PAWP of 15 mm Hg as a cutoff).

Correlations of NPs and Measures of Contractility
Both NPs were inversely correlated with hemo-dynamic markers of contractility: BNP with CI (r = – 0.481, p = 0.008), BNP with LVSWI (r = – 0.384, p = 0.016); NTproBNP with CI (r = – 0.441, p = 0.008) and LVSWI (r = – 0.623, p < 0.001) [Fig 2].

Comparison of BNP and NTproBNP
Patients were classified into groups with significant cardiac abnormality (LVSWI < 35 g·m/m2) and those with near-normal cardiac function (LVSWI > 35 g·m/m2). There were differences in NTproBNP (abnormal, 13,528 ± 2,399 pg/mL; near-normal, 1,236 ± 83 pg/mL; p = 0.028) but not in BNP (916 ± 128 pg/mL vs 639 ± 286 pg/mL; not significant). Patients with ab-normal LVSWI also were older, more likely to have a history of chronic heart failure, have lower ejec-tion fraction (EF) and calculated CrCl (Table 2 ). NTproBNP has shown AUROC of 0.885 (p = 0.003) for the detection of significant contractile abnormality (defined as above). A NTproBNP value of 1,550 pg/mL had the best combination of sensitivity, specificity, and positive and negative predictive values at this LVSWI cutoff (86.2%, 83.3%, 83.8%, and 85.8%, respectively; Fig 3 ). BNP was not useful at the same LVSWI cutoff (area under ROC curve [AUROC], 0.643; p = 0.242). When LVSWI cutoff was decreased to 30 g·m/m2, accuracy for NTproBNP remained comparable (AUROC, 0.884; p < 0.001) but improved for BNP (AUROC, 0.754; p = 0.01).


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  		Table 2.. Characteristics of Groups Divided Into Near-Normal Contractility and Impaired Contractility*

 


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  		Figure 3.. ROC curves for NTproBNP (left) and BNP (right) using stroke work index cutoff of 35 g·m/m2. Area under the curve (AUC) was significant for NTproBNP but not for BNP. The discriminant value for NTproBNP was 1,550 pg/mL (arrow).

 
NPs and CrCl
NPs correlated inversely with calculated CrCl (BNP, r = – 0.495, p = 0.001; NTproBNP, r = – 0.600, p < 0.001). Cardiac contractility indexes correlated positively with CrCl (CI, r = 0.428, p = 0.005; LVSWI, r = 0.548, p < 0.001). Linear regression analysis with NTproBNP and BNP as outcome variables were separately performed using CrCl, LVSWI, PAWP, age, BNP, and NTproBNP as predictor variables. CrCl was not an independent predictor of either BNP or NTproBNP.

NPs and 30-Day Survival
Twenty-three patients were alive and 17 were dead at day 30. One patient was unavailable for follow-up. Mean NP concentrations did not differ between the survivors and nonsurvivors (BNP, 909.3 ± 264.2 pg/mL vs 840.9 ± 171.2 pg/mL; NTproBNP, 11,630.6 ± 3,181.8 pg/mL vs 11,777.6 ± 2,989.9, pg/mL, respectively), nor did median concentrations differ (Fig 4 ). Mean APACHE II score was higher in nonsurvivors than in survivors (22 ± 1.6 vs 16.1 ± 1.1, p < 0.05).



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  		Figure 4.. Box and whiskers plots for mortality showing NTproBNP (left) and BNP (right). Neither peptide was good at predicting mortality.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
NPs are frequently elevated in critically ill patients.1315 While cardiomyopathy is frequent in the critically ill, there are reasons to suspect that factors other than the left ventricular myocardial stretch or tension will stimulate the release of these hormones. Studies172526 have shown that critical illness in a setting of sepsis, systemic inflammatory response syndrome, trauma or surgery can elevate NPs by different mechanisms (through inflammatory cytokines, hypoxemia, or right ventricular overload). Decreased GFR is also postulated to affect NPs by unclear mechanisms, which most likely involve their renal extraction or clearance.20 Preexisting cardiac dysfunction is prevalent in the ICU population, and this by itself can make it difficult to interpret BNP and NTproBNP concentrations.25 Our study population had generally depressed left ventricular contractility (mean LVSWI, 25.6 ± 1.7 g·m/m2), even though only half had known or suspected heart failure. Only 17% of our patients had near-normal cardiac contractility, judged by LVSWI. Even though NPs have been shown to correlate with PAWP in patients with decompensated heart failure,9 we did not see this correlation. We have shown that neither BNP nor NTproBNP can be used as a surrogate for PAWP to differentiate high- vs low-wedge pressure respiratory failure in these critically ill patients. This is consistent with recent report by Tung et al,13 who also did not find a relationship between BNP and PAWP in patients with shock.

While cardiac output is a good objective measure of left ventricular function, it can frequently be elevated in the setting of lowered systemic vascular resistance that occurs in sepsis. LVSWI has been shown to be very good marker of cardiac function and is frequently used in both laboratory and clinical studies.2627 We have, therefore, arbitrarily defined significant left ventricular contractile abnormality as LVSWI < 35 g·m/m2, and NTproBNP was able to distinguish the abnormality. NTproBNP also showed a very strong discriminating ability at higher degrees of contractile abnormality (LVSWI < 30 g·m/m2 and LVSWI < 20 g·m/m2). In contrast, BNP only showed modest diagnostic accuracy when cardiac dysfunction was defined in this manner. The explanation for this discrepancy may be the fact that NTproBNP has much higher molar concentrations and steeper increments for any given level of cardiac dysfunction and that indeed it is the more sensitive measure of cardiac dysfunction particularly in its milder degrees. Interestingly, Seino et al28 observed similar findings in their comparison of the two peptides in patients with heart failure: NTproBNP was more predictive than BNP when an EF of 50% was used as a cutoff. When the EF cutoff was lowered to 40%, BNP showed comparable accuracy.

Using the cutoffs for NPs established for ambulatory populations, or using them as a rule-out/rule-in test, may be problematic in determining the etiology of pulmonary infiltrates (ARDS vs pulmonary edema) because of the high prevalence of preexisting cardiac impairment and unknown baseline NPs. McLean et al25 have shown that raising the upper limit of BNP might be needed in ICU patients. We agree that NP levels need to be interpreted not only in the context of age or gender but also of co-morbidities and renal function. We found the NTproBNP concentration of 1,550 pg/mL to have good accuracy for detecting impaired cardiac contractility. This value is at least two times the upper limit of normal for NTproBNP even after accounting for variations in age and gender. While NPs should not be used as surrogates of PAWP, they appear to be good surrogates of cardiac contractility and predictors of patients with respiratory failure who have additional cardiac dysfunction.

Impaired renal function is common in the ICU. To minimize the effect of renal failure on NP concentrations, we excluded patients on receiving hemodialysis2930; however, only 9 of our patients (22%) had CrCl > 90 mL/min. Interestingly, CIs strongly correlated with CrCl, reinforcing the relationship of renal function with cardiac function. We believe that this correlation most probably reflected diminished GFR in a decreased cardiac output state since in multivariate analysis CrCl was not an independent predictor of either BNP or NTproBNP. We observed that renal and cardiac abnormalities are tightly interrelated and that NPs could be viewed as markers of global cardiorenal axis as indicated elsewhere.2031

BNP and NTproBNP have been shown to be strong mortality predictors in a wide variety of cardiovascular syndromes including cardiogenic and other shock states.323334353637 Our study population had 41% mortality at 30 days. The mean BNP and NTproBNP concentrations did not significantly differ between survivors and nonsurvivors. This observation is in contrast to that of Tung et al,13 who found BNP to be a powerful mortality predictor in a population similar to ours. Our population was different in that only approximately half of our patients met their definition of shock. Another difference in our population is that our mean BNP concentration across all the patients was significantly lower and the range narrower. The smaller number of patients in our study also could account for the difference.

A limitation to our study is that we used only a single measurement of NPs. As NPs are known to fluctuate, serial measurement of NPs may be more useful than using a single measure with predefined cutoffs. A second limitation of our study was that we collected hemodynamic parameters from the chart after PAC measurements were performed with calculations done by the patient’s nurse and physician. Thus our measurements were not standardized, but are much more generalizable to a real-life setting in a community hospital ICU. Finally, APACHE II scores were calculated retrospectively based on information from the time of patient‘s enrollment, and not on the patient’s entry into the ICU.

BNPs are promising tools in the care of critically ill patients, but the experience in this population has been limited. Even though we did not find any correlation with PAWP, we observed an inverse correlation with measures of contractility for both BNP and NTproBNP. NTproBNP is a strong discriminator of cardiac dysfunction in patients with significant comorbidities, preexisting cardiac dysfunction, and impaired renal function. BNP may be a less strong discriminator. While we did not find either BNP or NTproBNP to predict survival, this will need to be confirmed in larger population.


   Footnotes
 
Abbreviations: APACHE = acute physiology and chronic health evaluation; AUROC = area under receiver operating characteristic; BNP = B-type natriuretic peptide; CI = cardiac index; CrCl = creatinine clearance; EF = ejection fraction; GFR = glomerular filtration rate; LVSWI = left ventricular stroke work index; NP = natriuretic peptide; NTproBNP = N-terminal pro B-type natriuretic peptide; PAC = pulmonary artery catheter; PAWP = pulmonary artery wedge pressure; ROC = receiver operating characteristic

Received for publication October 26, 2004. Accepted for publication December 15, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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E. B. Milbrandt, A. Ishizaka, and D. C. Angus
Update in critical care 2005.
Am. J. Respir. Crit. Care Med., April 15, 2006; 173(8): 833 - 841.
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 ChestHome page
M. Heringlake, L. Bahlmann, S. Klaus, D. Jefic, and H. S. Rosman
Plasma Levels of N-Terminal Pro-Brain Natriuretic Peptide in the Critically Ill: The Right Hormonal Marker in the Wrong Patients?
Chest, January 1, 2006; 129(1): 212 - 213.
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 NEJMHome page
L. B. Ware and M. A. Matthay
Acute Pulmonary Edema
N. Engl. J. Med., December 29, 2005; 353(26): 2788 - 2796.
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