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Croat Med J. 2009 April; 50(2): 133–142. doi: 10.3325/cmj.2009.50.133. | PMCID: PMC2681050 |
Copyright © 2009 by the Croatian Medical Journal. All rights reserved. Combination of Quantitative Capnometry, N-Terminal Pro-brain Natriuretic Peptide, and Clinical Assessment in Differentiating Acute Heart Failure from Pulmonary Disease as Cause of Acute Dyspnea in Pre-hospital Emergency Setting: Study of Diagnostic Accuracy Petra Klemen,1,3 Mirjam Golub,1 and Štefek Grmec1,4 1Center for Emergency Medicine Maribor, Maribor, Slovenia 2Department of First Aid and Emergency Medicine, University of Maribor School of Medicine, Maribor, Slovenia 3Faculty of Health Sciences, University of Maribor, Maribor, Slovenia 4Department of Family Medicine, University of Ljubljana School of Medicine, Ljubljana, Slovenia Received October 17, 2008; Accepted March 16, 2009. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Aim To determine the diagnostic accuracy of the combination of quantitative capnometry (QC), N-terminal pro-brain natriuretic peptide (NT-proBNP), and clinical assessment in differentiating heart failure (HF)-related acute dyspnea from pulmonary-related acute dyspnea in a pre-hospital setting. Methods This prospective study was performed in the Center for Emergency Medicine Maribor, Slovenia, January 2005 - June 2007. Two groups of patients with acute dyspnea apnea were compared: HF-related acute dyspnea group (n  = 238) vs pulmonary-related acute dyspnea (asthma/COPD) group (n = 203). The primary outcome was the comparison of combination of QC, NT-proBNP, and clinical assessment vs NT-proBNP alone or NT-proBNP in combination with clinical assessment, in differentiating HF-related acute dyspnea from pulmonary-related acute dyspnea (asthma/COPD) in pre-hospital emergency setting, using the area under the receiver operating characteristic curve (AUROC). The secondary outcomes were identification of independent predictors for final diagnosis of acute dyspnea (caused by acute HF or pulmonary diseases), and determination of NT-proBNP levels, as well as capnometry, in the subgroup of patients with a previous history of HF and in the subgroup of patients with a previous history of pulmonary disease. Results In differentiating between cardiac and respiratory causes of acute dyspnea in pre-hospital emergency setting, NT-proBNP in combination with PetCO2 and clinical assessment (AUROC, 0.97; 95% confidence interval [CI], 0.90-0.99) was superior to combination of NT-proBNP and clinical assessment (AUROC, 0.94; 95% CI, 0.88-0.96; P= 0.006) or NT-proBNP alone (AUROC, 0.90; 95% CI, 0.85-0.94; P= 0.005). The values of NT-proBNP≥2000 pg/mL and PetCO2 ≤ 4 kPa were strong independent predictors for acute HF. In the group of acute HF dyspneic patients, subgroup of patients with previous COPD/asthma had significantly higher PetCO2 (3.8 ± 1.2 vs 5.8 ± 1.3 kPa, P= 0.009). In the group of COPD/asthma dyspneic patients, NT-proBNP was significantly higher in the subgroup of patients with previous HF (1453.3 ± 552.3 vs 741.5 ± 435.5 pg/mL, P= 0.010). Conclusion In differentiating between cardiac and respiratory causes of acute dyspnea in pre-hospital emergency setting, NT-proBNP in combination with capnometry and clinical assessment was superior to NT-proBNP alone or NT-proBNP in combination with clinical assessment. ClinicalTrials.gov trial registration number NCT00878475 In patients presenting with acute dyspnea in pre-hospital setting, the early and correct diagnosis may present a significant clinical challenge ( 1, 2). Physical examination, chest radiography, electrocardiography, and standard biological tests often fail to accurately differentiate heart failure (HF) from pulmonary causes of dyspnea ( 3). Timely differentiation of HF from other causes of dyspnea may permit the early institution of appropriate medical therapy ( 4- 6). Brain natriuretic peptide (BNP) and amino-terminal pro-brain natriuretic peptide (NT-proBNP) have been proposed as early markers of HF and demonstrated to be useful for diagnosing and excluding HF in emergency department ( 7- 9). A combination of BNP or NT-proBNP testing and standard clinical assessment has been suggested to be superior to either tool used in isolation ( 7, 8, 10). Some previous studies have also suggested that quantitative capnometry (QC) may be useful in differentiating between cardiac and obstructive causes of respiratory distress ( 11, 12). Therefore, we hypothesized that a new combination of NT-proBNP testing, standard clinical assessment, and partial pressure of end-tidal CO2 (PetCO2) would optimize evaluation and differentiation of acute dyspnea in a pre-hospital setting. The aim of this study was to determine the accuracy of combination of QC, NT-proBNP, and clinical assessment in differentiating acute HF from obstructive pulmonary disease (COPD/asthma) as a cause of acute dyspnea in pre-hospital emergency setting. Study design and setting This prospective cohort study was performed in the pre-hospital emergency setting (Center for Emergency Medicine Maribor, Slovenia, Europe) between January 2005 and June 2007. The study was approved by the Ethical Review Board of the Ministry of Health of Slovenia. Patients During the period of the study, 546 consecutive patients with acute dyspnea were treated by emergency teams (emergency physician, register nurse, and medical technician/driver in an ambulance-car or at pre-hospital emergency medical center). After pre-hospital care, all patients were admitted to the University Clinical Center Maribor and followed until discharge. To be eligible for the study, a patient had to present with shortness of breath as the primary complaint (defined as either the sudden onset of dyspnea without history of chronic dyspnea or an increase in the severity of chronic dyspnea). Exclusion criteria were age <18 years, history of renal insufficiency, trauma, severe coronary ischemia (unless patient’s predominant presentation was dyspnea), and other causes of dyspnea: pneumonia, pulmonary embolism, carcinoma, pneumothorax, pleural effusion, intoxications (drugs), anaphylactic reactions, upper airway obstruction, bronchial stenosis, and gastroesophageal reflux disorder, according to the history, clinical status, and additional laboratory tests available in pre-hospital setting (D-dimer, troponin, C-reactive protein). There were 441 patients who met the criteria for inclusion in the survey. Hundred and five patients were excluded from the study. Recruitment, exclusion, and subsequent grouping of all patients are shown in the flowchart (). Data collection After enrollment, patient’s demographic characteristics, symptoms and signs, medical history, medication use, chest X-ray, and standard blood test results (after admission to the hospital) were recorded. Our protocol for clinical assessment of HF-related acute dyspnea (the pre-hospital clinical assessment for HF) was designed based on Boston ( 13) and Framingham criteria for HF ( 14) ( Table 1). We did not use certain criteria from the original protocols, which were not available in the prehospital setting (eg, chest radiography). | Table 1Study protocol for prehospital clinical assessment of HF (modified Boston criteria)* |
For additional evaluation of patients with suspect obstructive causes of dyspnea, we included criteria for clinical assessment of severe asthma (diffuse polyphonic bilateral and particular expiratory wheezes, chest tightness, shortness of breath, using accessory muscles of breathing, signs of hyperinflation, atopic condition, personal or family history of asthma, tachypnea, previous asthma and asthma medications, and the value of modified Boston criteria for HF≤5) ( 15, 16) and criteria for chronic obstructive pulmonary disease (COPD) exacerbation (history of COPD, COPD medications, cough, worsening dyspnea, increased sputum production and volume, increased sputum purulence, rhonchi and rales, modified Boston criteria for HF≤5) ( 17). The final hospital diagnosis of HF-related acute dyspnea and pulmonary-related acute dyspnea (the hospital reference standard for HF and pulmonary diseases: asthma/COPD) was confirmed by cardiologist and/or intensive care physician in the University Clinical Center Maribor, using the reference standard definition for HF and pulmonary diseases in accordance with previously cited instruments ( 13- 19), including chest X-ray, echocardiographic examination, cardiac functional assessment (exercise test), pulmonary function test, full blood count, biochemistry, and invasive investigation or angiography ( 17). According to these criteria, identification of independent predictors for final diagnosis of acute dyspnea (caused by acute HF or pulmonary diseases) was performed by examination of 26 variables ( Table 2): age, sex, nocturnal dyspnea, orthopnea, cough, sputum production, fever, murmur, lung rales, wheezes, pulse rate, jugular venous distension, lower extremity edema, ECG, history of COPD/asthma medications or HF medications, troponin T, PetCO 2, Sa o2, NT-proBNP, the need for endotracheal intubation, previous arrhythmia, history of previous, acute myocardial infarction (AMI), congestive heart failure (CHF), or COPD, and the value of modified Boston criteria for HF. Central venous pressure (CVP) in the field was assessed by the visualization of external jugular vein. This correlates well with catheter-measured CVP ( 18) and may give a reliable estimate of CVP, categorized as low (<5 cm H2O) or high (≥10 cm H2O) when the top of the external jugular veins is >3 cm of vertical distance above the sternal angle. | Table 2Univariate analysis for all demographic and clinical variables pertinent to diagnosis of acute HF or pulmonary disease (n=441)* |
Two groups of patients (HF-related acute dyspnea group and pulmonary-related acute dyspnea [asthma/COPD] group) were further divided according to previous history of HF or COPD/asthma (acute HF dyspneic patients with previous history of HF, acute HF dyspneic patients with previous history of COPD/asthma, acute COPD/asthma dyspneic patients with previous history of HF, acute COPD/asthma dyspneic patients with previous history of COPD/asthma) for determination of NT-proBNP levels, as well as for capnometry. Measurements NT-proBNP. During initial evaluation (before application of medicines), a 5-mL sample of blood was collected into a tube containing calcium disodium edetate for blinded measurement of NT-proBNP. The level of NT-proBNP was measured using a Cardiac Reader (Roche Diagnostics, Mannheim, Germany) and recorded in the special protocol. The test was finished within 15 minutes. PetCO2. PetCO2 was obtained by Lifepak 12 (Medtronic Physiocontrol, Corporate Headquarters, Redmond, WA, USA); an average PetCO2 value of the first three measurements in the first minute after endotracheal intubation or nasal measurement was registered. Blinding (masking) of physicians The raters who made the diagnosis (in pre-hospital setting – pre-hospital emergency physicians, at admission to hospital – internists at emergency department, and at discharge from the hospital with the final diagnosis – cardiologists or/and intensive care physicians) were blinded to the results of NT-pro-BNP. In addition, the investigators of NT-proBNP did not collaborate in making the final diagnosis. On the other hand, pre-hospital emergency physicians were not blinded to the value of PetCO2 because QC represents the routine method in Slovenian pre-hospital emergency medicine. To avoid bias, the value of PetCO2 was recorded by the emergency physician in the field but did not affect the diagnosis. The raters who made the diagnosis in the hospital were blinded to the values of prehospital PetCO2. Statistical analysis Univariate comparison was made with χ2 test for categorical variables and unpaired t test for continuous variables with normal distribution (age, pulse rate, PetCO2, NT-proBNP, Sao2, modified Boston criteria for HF). The normality of distribution was tested with Kolmogorov-Smirnov test. Odds ratio (OR) and 95% confidence interval (CI) were calculated to examine risk of acute HF (for adjusted using multiple logistic regression). The area under the receiver operating characteristic curve (AUROC) was used to determine the diagnostic accuracy of combination of QC, NT-proBNP, and clinical assessment vs NT-proBNP alone or NT-proBNP in combination with clinical assessment in differentiating acute HF from COPD/asthma in pre-hospital emergency setting. We compared the areas under different curves using the technique proposed by Hanley and McNeil ( 20) and Jannuzi ( 8). Single areas were calculated and compared with univariate Z score testing. Univariate analysis was performed for all variables pertinent to diagnose HF or pulmonary disease, and multivariate analysis was performed to simultaneously identify potential independent predictor variables of a final diagnosis of acute HF. Significant variables identified by univariate analysis with a P value <0.05 were entered into a logistic regression analysis. This enabled adjusted OR (for confounding) to be calculated and identified any factor that affected the primary outcome variable (HF). Variables considered in the analysis were age, nocturnal dyspnea, orthopnea, cough, sputum production, fever, murmur, rales, wheezes, jugular venous distension, lower extremity edema, ECG-normal sinus rhythm, asthma/COPD medications, HF medications, troponin t> 0.03 ng/mL, PetCO2, NT-proBNP, endotracheal intubation, previous AMI, HF, or COPD, and modified Boston criteria for HF. Sensitivity, specificity, and negative and positive predictive values were estimated for NT-proBNP and PetCO2 for different cut-off points. As established in PRIDE study ( 10), the suggested NT-proBNP concentrations for identifying acute HF were greater than 450 pg/mL for patients younger than 50 years and greater than 900 pg/mL for patients aged 50 years or more, whereas 300 pg/mL was suggested as an optimal cut-off point for excluding HF. The suggested PetCO 2 values for identifying acute HF were 4 kPa or less, and the cut-off point for excluding HF was PetCO 2≥8 kPa. NT-proBNP levels, as well as capnometry, were determined in the subgroup of patients with a previous history of pulmonary disease but finally diagnosed as acute HF, and in the subgroup of patients with a history of HF but finally diagnosed as acute pulmonary disease (COPD/asthma). AUROC analysis was performed using Analyze-It software (Leeds, UK) whereas other analyses were performed using SPSS software (SPSS, Inc., Chicago, IL, USA). The baseline clinical and demographic characteristics of the study population are presented in Table 2. Mean age in the group of patients with acute HF was 68.9 ± 10.5 years; 188 (58%) were men. HF group was significantly older. Diagnostic accuracy of combination of QC, NT-proBNP, and clinical assessment in differentiating HF-related acute dyspnea from pulmonary-related acute dyspnea By using of AUROC, the sensitivity and 1- specificity were compared for different cut-off points for NT-proBNP alone vs combination of NT-proBNP + clinical assessment vs combination of NT-proBNP + clinical assessment + PetCO2 (). The AUROC from NT-proBNP + PetCO2 + clinical assessment (AUROC, 0.97; 95% CI, 0.90-0.99) was superior to NT-proBNP + clinical assessment (AUROC, 0.94; 95% CI, 0.88-0.96; P= 0.006) and NT-proBNP testing alone (AUROC, 0.90; 95% CI, 0.85-0.94; P= 0.005). Diagnostic modality with the combination of the NT-proBNP + clinical assessment was superior to NT-proBNP testing alone ( P= 0.010). Identification of independent predictors for final diagnosis of acute dyspnea For the identification of a final diagnosis of acute HF, we examined 23 variables ( Table 2) in multivariable logistic regression analysis; 11 variables remained significant after analysis ( Table 3). These included an elevated NT-proBNP (as a strongest predictor of acute HF), rales, orthopnea, HF medications, troponin T, PetCO2, and previous HF. Asthma medications, cough, fever, and ECG with normal sinus rhythm independently predicted respiratory causes of dyspnea. | Table 3Multiple logistic regression analysis of factors used for differentiating between patients with HF-related acute dyspnea and pulmonary-related acute dyspnea in prehospital emergency setting |
Negative and positive predictive values for NT-proBNP and PetCO2 for different cut-off points In Table 4 and Table 5, sensitivity, specificity, positive and negative predictive value are presented for different cut-off points for NT-proBNP and PetCO2 for the diagnosis of acute HF. The value ≥2000 pg/mL for NT-proBNP and value ≤4 kPa for PetCO2 are strongly independent predictors for acute HF. | Table 4Test characteristics of NT-proBNP for the diagnosis of acute HF for different cut-off points* |
| Table 5Test characteristics of PetCO2 for the diagnosis of acute heart failure for different cut-off point* |
NT-proBNP levels, and capnometry, in subgroup of patients with a previous history of HF or of pulmonary disease In the group of acute HF dyspneic patients, we did not find any significant difference in the value of NT-proBNP between subgroup with previous acute HF and previous COPD/asthma, but we found significantly higher PetCO 2 in the subgroup with previous COPD/asthma. In the group of COPD/asthma dyspneic patients, we found significantly higher value of NT-proBNP in the subgroup with previous HF ( Table 6). We did not observe any adverse events from performing the index tests or the reference standard. To our knowledge, this is the first prospective study specifically designed to assess the utility of NT-proBNP testing in combination with PetCO2 and routine clinical assessment for the diagnosis of acute HF in pre-hospital setting. Our study showed that the combination of NT-proBNP, clinical assessment, and capnometry proved to be useful in differentiating HF from pulmonary causes of acute dyspnea and had a significantly better AUROC for the diagnostic accuracy than each method alone or a combination of two of them. Timely differentiation of HF from other causes of respiratory distress may permit the early institution of appropriate medical therapy. The symptoms and signs of COPD/asthma exacerbation may frequently be difficult to differentiate from those of acute HF and when the two diagnoses coexist, treatment decisions become incrementally more complex ( 21- 23). Routine BNP testing of dyspneic patients in emergency department has been demonstrated to be a useful method for diagnosing and excluding acute HF ( 7- 10). The introduction of BNP measurement in patients with uncertain diagnosis may reduce the error rate by over 50% ( 19). Measurement of the PetCO2 in the field has already become a standard procedure to ensure proper placement and function of the endotracheal tube and to monitor the adequacy of ventilation ( 24, 25). Some previous studies have also suggested that QC may be useful in differentiating between cardiac and obstructive causes of respiratory distress ( 11, 12). PetCO2 is reported to have a prognostic value in patients with HF at rest and during exercise testing ( 26, 27). Matsumato et al ( 28) found that PetCO2 could become a new ventilatory abnormality marker for impaired cardiac output response. Brown et al ( 11) found that PetCO2 levels for pulmonary edema/CHF patients differed significantly from those of asthma/COPD patients. We also found a significant difference in PetCO 2 values between HF and COPD/asthma, and concluded that capnometry could represent an objective additional method for differentiating acute dyspnea in pre-hospital setting. With adding the PetCO2 in our study, we improved the sensitivity and specificity in differentiating the cause of acute dyspnea (especially in COPD patients with severe exacerbation and coexisting HF). Combination of NT-proBNP and PetCO2 presents two different ways and mechanisms of verification of HF. It introduces an opportunity for integration of biochemical and pathophysiologic measurement in a new complementary method. Both devices are accessible in the field and present an effective way in differentiating respiratory distress in prehospital setting. Our study confirmed that the combination of these two parameters had a strong diagnostic value. We also found an association between the history of previous COPD/asthma or HF and the current values of NT-proBNP and PetCO2. Our results showed that higher values of NT-proBNP in acute dyspneic patients due to COPD/asthma correlated with a history of HF, and higher values of PetCO2 in acute dyspneic patients due to HF correlated with a history of COPD/asthma. Similarly, Morrison et al ( 23) reported significantly higher BNP levels in patients with HF than in patients with pulmonary disease. Patients with history of HF but with current COPD diagnosis had higher BNP levels than patients without history of HF. Tung et al ( 29) found that in patients without previous HF, median NT-proBNP levels were higher than in patients with new-onset HF than in those with COPD/asthma exacerbation. High clinical suspicion for acute HF detected only 23% of patients with new-onset HF, whereas 82% of these patients had elevated NT-proBNP levels. In patients who had both previous acute HF and COPD/asthma, median NT-proBNP levels were significantly higher in those with acute HF than in those with COPD/asthma exacerbation. McCullough et al ( 30) investigated whether BNP could distinguish new-onset HF in patients with a history of COPD/asthma presenting with dyspnea to the emergency department and concluded that the yield of adding routine BNP testing in these cases was approximately 20%. The prehospital emergency physicians offer the earliest treatment of acute dyspnea, performed as close as clinically possible to the event. Based on clinical judgment alone, it is sometimes very difficult to distinguish cardiac from respiratory causes of dyspnea. In fact, even in experienced centers, diagnostic accuracy is lower than 80% ( 19). If the prehospital physicians have the values of NT-proBNP and PetCO2 at their disposal, the diagnostic dilemmas in differentiating causes of respiratory distress are reduced and the treatment possibilities in clinical obscure cases are mainly improved. This is particularly important for more complex treatment (eg, diuretics, morphine, vasodilatators, or inotropes). This study has some limitations: 1) prehospital emergency physicians were not blinded to the values of PetCO2 because capnometry represents the routine prehospital test. In our opinion, this fact did not induce bias because the physicians were unaware of the differential diagnostic importance of PetCO2 for the purpose of the study (in the differentiation of cardiac and pulmonary causes of shortness of breath – blindness for the purpose of the study); 2) in the majority of patients, spirometry or simple forced expiratory volume in one second (FEV1) were not measured and evaluated, thus the severity of COPD/asthma is not differentiated in the study; and 3) severe additional factors may have an impact of the reliability of PetCO2 (some patients in the study hyperventilated, had periodic breathing, were intubated, or had ventilation/perfusion mismatch) ( 31). In conclusion, NT-proBNP in combination with capnometry and clinical assessment was superior to NT-proBNP alone or NT-proBNP in combination with clinical assessment in differentiating between cardiac and respiratory causes of acute dyspnea in prehospital emergency setting. QC and NT-proBNP measurement can improve the differentiation and treatment of acute dyspnea in the first hours of its appearance. Wider use of these routine procedures can be helpful for emergency physicians in everyday work, but further investigation (eg, a larger multicentric study) is needed to confirm the utility of these methods in the prehospital setting. 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