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Consecutive asthmatic children referred for pulmonary function testing were enrolled. The aim of this study was to assess whether FAno could be a marker of distal obstruction and/or mild symptoms. Thus, we first defined a detailed structured questionnaire (symptom and medications) that was prospectively recorded in our population. Recorded symptoms were part of those included in the Asthma Quality of Life Questionnaire (chest tightness, 6 questions; cough, 12 questions; chest heaviness, 14 questions; woken at night by asthma, 24 questions; lack of a good night’s sleep, 29 questions). Symptomatic children were defined as having at least one symptom within 72 h before testing. Since the evaluation was planed to enroll mildly symptomatic children, in order to assess whether exhaled NO measures could reflect the onset of exacerbation (before the occurrence of significant airflow Limitation as decrease in FEV₁), wheezing patients were not included. For the same reason daily peak expiratory flow (V) rate was not recorded in this young population. Consequently, only mild asthma symptoms were evaluated.

Only one investigator (B.M.) obtained all clinical histories. This study reports the results obtained in consecutive children or adolescents who were evaluated by functional respiratory tests in the follow-up of asthma. A group of healthy children without history of atopy (relatives of medical staff) was also evaluated.

NO Measurements

The breathing circuit consisted of a mouthpiece with a bacterial filter connected to a one-way valve, through which the children exhaled via an expiratory resistance while targeting a fixed mouth pressure of 16 cm H₂O displayed on a water column to prevent contamination from nose and sinuses. Each NO measurement was done as recommended by the American Thoracic Society (ATS).

Children exhaled via separate resistances in turn while maintaining the same expiratory pressure, thus producing multiple flows that were measured by a downstream pneumotachograph (Fleisch #1; Fleisch; Lausanne, Switzerland, connected to Vali-dyne ± 2 cm H₂O; Validyne Engineering; Northridge, CA). Each child was asked to perform at least one maneuver in five different ranges: very low flow (< 40 mL/s), low flow (40 to 60 mL/s), intermediate flow (60 to 100 mL/s), high flow (100 to 150 mL/s), and very high flow (> 150 mL/s). The criteria used for FEno interpretation were those in the ATS guidelines,¹⁷ the expiratory time being at least 6 s with a plateau of at least 3 s.

FEno was measured using a chemiluminescent NO analyzer (EVA4000; Seres; Aix en Provence, France), as previously described. NO concentration, V, and expired volume were displayed on a computer (Biopac Systems; Santa Barbara, CA).

Modeling the Qno/FIow Rate Relationship

We used two different approaches using multiple-flow analysis.

Asthma is characterized by an inflammation of both the proximal and the distal lung airways. Exhaled nitric oxide (NO) is considered a noninvasive marker of lung airway and alveolar inflamma-tion. Increased NO output ((Qno) in asthma has been extensively documented. Cellular inflammation located in the very small airways and alveoli could contribute to this increased QNO output. Along this line, increased numbers of total eosinophils, activated eosinophils, and lymphocytes have been found in the distal asthmatic lung. Furthermore, there is compelling evidence linking proinflammatory cytokine expression, eosinophil recruitment, and NO synthase expression or reactive nitrogen species in distal airspaces as evaluated by BAL. Consequently, we hypothesized that an increased QNO output could occur from distal airways and/or alveoli of asthmatic subjects.

The flow dependency of exhaled NO fraction

(FEno) has been extensively reported. Convincing mathematical models have related this experimental observation to a dual origin of NO, which is produced both by the proximal airway compartment and by the expansible compartment comprising the alveolar space and very small airways. More recently, Tornberg and colleagues demonstrated that oral cavity contributes significantly to exhaled NO; consequently, the nonexpansible compartment would better be named proximal or conducting airways (orotracheal plus bronchial parts). The ability of multiple-flow analysis to differentiate increase in FEno due to either distal (alveolitis or hepatopul-monary syndrome) or to bronchial (asthma) origin has been verified.

We previously demonstrated, as others, that the increased QNO observed in asthma is due to an increased maximal proximal airway (Qno (Qbr,maxNo), the alveolar NO concentration (FAno) being normal. However, these studies were not designed to assess whether FAno could be elevated owing to the presence of symptoms or bronchial obstruction. Consequently, our objectives were to evaluate the respective contributions of Qbr,maxNO and FAno to FEno in asthmatic children using multiple-flow analysis of (Qno, and to evaluate whether recent symptoms and/or airway obstruction in these children were related to significant increases in Qbr,maxNO or FAno. To ensure the validity of FAno calculation, two approaches of its determination were used using multiple-flow analysis, both of them based on the two-compartment model of the NO exchange dynamic.

Materials and Methods

Patients

Informed consent for the participation to the study was obtained from the parents in every case. Asthma was defined as a history of recurrent wheezing episodes,

Based on current knowledge, some modality of long-term and high degree of acid suppression or acid exclusion seems to be the most effective treatment strategy. Preselecting children with an abnormal extended pH monitoring finding and a favorable response to a therapeutic trial of aggressive anti-GER therapy seems to be the best way to implicate GER in inducing or exacerbating asthma.

The patients had daily Ws and ECGs recorded and printed routinely with the placement of the limb electrodes on the wrists and ankles, however, for the purposes of this study, the ECGs and Ws from hospital admission and at the point of half-PW gain (HF-W), and PW for the patients with AN, the hospital admission and discharge data for the control subjects, the prehemodialysis and posthemodialysis data for the patients undergoing this procedure, and the data from hospital admission and discharge for the patients with CHF were employed. An ECG unit was used that acquires data simultaneously and digitally from all ECG leads, instead of acquiring data from a few leads and calculating the rest of them online. Calibration of the unit was 1.0 mV = 1.0 cm. Measurements of the sum of the highest positive plus the lowest negative deflections of the QRS complex in all ECG leads of all study ECGs were made to the nearest 0.5 mm, employing hard copies and using manual calipers and a magnifying glass. For ECGs with atrial fibrillation, the average of measurements of three consecutive heart beats was used. Since the six limb leads can be calculated from leads 1 and 2, as per Einthoven law (leads 1 + 3 = 2), and the aV leads, as per formulas (lead aVR = 1/2[1 + 2], aVL = 1 — 1/2, [2], lead aVF = 2 — 1/2, [1], and lead aVR + aVL + aVF = 0), the 2QRS2 was employed as a variable, along with the £QRS12 and 2QRS6. It should be emphasized here that the use of SQRS2 as an ECG system is employed with the full realization that for the derivation of the remaining four limb leads, through the abovedescribed formulas, the values of leads 1 and 2 are treated algebraically in serial online measurements from the entire duration of the QRS complex in ECG machines, while in the present work the sum of the peak-to-peak (ie, positive-to-negative) amplitude values of the QRS complex of these two leads is implemented. Moreover, it should be understood that the same measurement approach was used for all three ECG systems. 2QRS12, SQRS6, and SQRS2 were calculated from the day of admission, the HF-W point, and the PW point for each of the 28 patients. Obviously, the HF-W point was determined after the PW was attained, and it represented a W value that was closest to one half of the PW gained. The mean (± SD) PW gain of the 28 patients with AN was 23.9 ± 14.8 lbs, and the mean HF-W gain was 16.9 ± 10.7 lbs. The corresponding ECG for the day when the HF-W was reached was used in the analysis.

In ECG syndrome has been reported that associated the development of peripheral edema of varying etiology with a decrease in the body surface QRS potentials involving all ECG leads. In that work, we employed the sum of QRS complexes of 12-lead ECGs from routine daily tracings, which were obtained by our technicians without the aid of marking of the thoracic wall to ensure intrasubject reproducible recordings from the precordial ECG sites. It is common knowledge that precordial ECGs display considerable intraindividual variation stemming from an alteration in the use of thoracic landmarks for V1-V6 recording, and that even a slight change of the recording sites can alter significantly the ECG waveforms. This problem remains without solution, despite the clear treatment of the topic on the appropriate recording of the precordial ECG provided by the ECG textbooks. In practice, this is of immense importance, since such inconsistencies frequently lead to erroneous diagnoses and a need for a cardiologic consultation.

Since the six standard (bipolar and unipolar) limb ECG leads are not subject to the vagaries of inconsistent recording that is inherent with the six precordial leads, it was hypothesized that the correlation of the weight (W) gain with a reduction in the sum of the QRS complexes from the six standard ECG leads (2QRS6) in our patients with anasarca (AN) would be better than the one we found with the employment of the 2QRS12 (r = 0.61; p = 0.0005) in our previous article.

Most modern ECG machines record only leads 1 and 2, and they calculate in real time the remaining limb leads. Accordingly, it was hypothesized that using merely the sum of QRS complexes of leads 1 and 2 (2QRS2) from a recorded 12-lead ECG will suffice to provide at a glance a quick index of body fluid retention. Such an index could be used at bedside for the evaluation of patients with an edematous state, thus obviating the inconvenience of calculating 2QRS6 or 2QRS12.

Consequently, the database of our previous study in conjunction with 2QRS6 and 2QRS2 in addition to the corresponding 2QRS12 used previously, was employed to investigate the two hypotheses cited above. In addition, similar ECG data from another recent study of three patients with idiopathic dilated cardiomyopathy who were admitted to the hospital with congestive heart failure (CHF) were included.

In this issue of CHEST, Japan’s leading investigator of pericardial disease, Tetsuro Sugiura, MD, and his colleagues contribute a unique report of patients free of heart disease with asymptomatic pericardial effusions, small to large, some of whom had PR segment and ST-T wave changes. The report raises as many questions as it answers, and these will require further investigation. By standard definition, 32 of 121 patients had low voltage QRS. In the entire group, widespread ST-segment elevation was found in only 8 patients, and widespread PR-segment depression in 32 patients. PR-segment depressions were significantly more frequent in those with low QRS voltage than in those free of low voltage (more cases may have escaped detection when low voltage applied to more than the QRS complexes). The authors appropriately lumped moderate and large pericardial effusions, as it has been shown that the physiologic effect—increased ventricular interaction of even asymptomatic effusions was similar in moderate-to-large effusions as opposed to small effusions.

Eight of 32 patients with PR-segment deviations had ST-segment deviations, while none with isoelectric PR segments had ST deviations, and significantly more patients with isoelectric PR segments had moderate-to-large effusions than small effusions. Small voltage and PR-segment deviations were rare in patients who had clinically silent pericardial effusions with an unsurprising trend to lower voltage in moderate-to-large effusions.

Certain findings are relatively remarkable: all patients with PR deviations had either a malignancy or a connective tissue disease. In contrast, it is not surprising that all patients with hypothyroidism and with renal disease had no ECG changes.

The authors conclude that there is subepicardial myocardial involvement by inflammation that they believe can cause low voltage despite small effusions and conclude “even a small but inflammatory effusion can cause low voltage in the presence of PR-segment depressions.” They thus assume the fluid to be inflammatory and, presumably because the patients were asymptomatic, they assumed that neither drainage nor biopsy was indicated. In this connection, no patients had tamponade, and Sugiura and colleagues did not describe any of the large effusions as massive. PR-segment deviations can be safely attributed to early appearance of the atrial T wave because they are always opposite to the direction of the P wave with an appropriate spatial vector. However, it is not certain that all PR-segment deviations must be inflammatory.

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