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EDITORIAL wheezing and respiratory insufficiency in pregnancy: was it bronchial or cardiac asthma? J.C. Yernault 1989 issue of Chest, 'I'ENHoLDER and the case of a 27 yr old pregnant gestation who presented with ng shortness of breath, cough sputum, and wheezing. When hospi3), 1987, she was receiving therapy inbalcd tcrbuLaiJne nnd oral lheophylwas begun two weeks earlier .(unction tests had shown "reactive , Unfortunately no figures are given to to fully appreciate the meaning of that to describe spirometric results. On was afebrile, had tachycardia (124 (22 breaths per min). Diffuse bilatheard with dullness to percussion on ·were no heart murmurs, nor jugular The chest X-ray showed bilateral lower lobes and pleural effusions. No e~l. Arterial blood gases showed 60.6 mmHg on 4 l oxygen by nypocaJpma (Paco1 29.5 mmHg). The the intensive care unit and treated aminophylline and methylpredniof terbutaline and atropine. On admission, a spirometry showed defect (FVC 59% predicted, FEV / a parallel 300 ml improvement in FVC .5. clearl y stated, I presume that the was concurrent bronchial asthma and patient without any past history of improved steadily during """>v•umzation and the chest film taken normal. The authors were puzzled . obstructive pattern of severe u to an out-of-proportion reduction .,,.,,,""'"''v and inability for the patient to their case history, I wonder whether might not have been considered, nuher than "bronchial" asthma. ActuCh~t issue, PtsoN et al. [2], describing s•vcncss to inhaled methacholine in left heart failure, remind us that the ng is as characteristic of exleft ventricular failure as it is of bronchial asthma, with dyspnoea present in their 12 patients (5 of them also complaining of chest tightness), cough in 7 and wheezing in 9. Hypoxaemia was also present in several of their patients during the acute phase with the lowest measured Pao1 at 6.9 kPa (52 mmHg). The chest X-ray, which was abnormal in all their patients during the exacerbation, returned to normal after increased diuretic therapy in several of them. Significant airway obstruction with reduced FEV 1 and FEV/FVC was initially presem in 6/12 patients. Several of the features of the patient described by TENHoLDER and SoUrH-PAUL [1) including the chest Xray findings with bilateral pleural effusions [3, 4], are thus compatible with a diagnosis of cardiac rather than bronchial asthma. Admittedly, this is an unusual problem in a young woman without a previously recognized heart problem, but the hypothesis should at least have been discussed because situations such as critical mitral regurgitation can present without audible murmur as recalled by SCHREIBER et al. [5] also in the same Chest issue. Moreover recent studies [6, 7] have emphasized the limited reliability of physical signs for estimating the pulmonary capillary wedge pressure in patients with impaired left ventricular function. A raised jugular venous pressure is a rather specific but poorly sensitive indicator of heart failure [7), and other signs such as a third heart sound or a displayed apex beat are difficult to appreciate [8, 9]. In the presented case, a significant heart problem cannot be excluded only on the basis of clinical data. Similarly the improvement under therapy cannot be taken as an argument pro bronchial rather than cardiac asthma, because bed rest, oxygen and theophylline administration might have contributed to an improvement of the haemodynamic status. Moreover, wheezing cannot be equated with bronchospasm nor wilh asthma [10]. It is produced when oscillations of the airway wall occur, induced by an acceleration of the gas flow through a narrowed lumen and/or by dynamic compression. In so-called cardiac asthma, narrowing of airway lumen most probably results from congestion and oedema of the bronchial wall [11). Following these lines, the bronchial hyperresponsiveness to inhaled methacholine observed in these circumstances has been attributed to its vasodilating effect on the bronchial arterioles [12]. To conclude, with the data that were summarized in the above case presentation, I believe that no definite diagnosis can be proposed, but that a simple diagnostic I.C. YERNAULT 248 manoeuvre would have been very useful. Should a thoracocentesis have been pcrfonned, the chemical analysis of the pleural Ouid demonsrraling a transudate might have pcnniucd very strong arguments in favour of a diagnosis of cardiac rather than bronchial asthma and pneumonia, in which case an exudate would have been expected. Rererences 1. Tenholder MF, South-Paul JE. - Dyspnea in pregnancy. Chest, 1989, 96, 381-382. 2. Pison C, Malo JL, Rouleau JL, Chal11oui J, Ohezzo H, Malo J. - Bronchial hyperresponsivencss lO inhaled methacholine in subjects with chronic left hean failure at a time of exacerbation and after increasing diuretic therapy. Chest, 1989, 96, 230-235. 3. Pist.olesi M. Miniali M, Milne ENC, Oiuntini C. - The chest roentgenogram in pulmonary edema. Clin CMst Med, 1985, 6, 3 15- 344. 4. Wiener-Kronish JP, Berthiaume Y. Albertine KH.- Pleural effusions and pulmonary edema. Clin Chest Med, 1985, 6, 509-519. S . Schteiber TL, Fisher I, Mangla A "silent" milral regurgitat.ion. A potential' refractory hean failure. Chest, 1989, 96 6. Editorial. - Clinical signs in heart fa'il 309- 3 10. ~. 7. Stevenson LW, Perloff JK. -The physical signs for estimating hemodynamics failure. JAMA, 1989. 261, 884-88. 8. lshmail AA, Wing S, Ferguson J, nut,e flb,_j S, Aegel KM. - Interobserver agreement by presence of a lhird heart sound in pauen11 heart failure. Chest, 1987, 91, 870-873, 9. O'Neill TW, Barry M. Smith IM. - Diagnostic value of the apex be.t 410-411. • 10. Yema.ult JC, Lenclud C. - Wheez.ing Progress In asthryta and COPD. P. V I.C. Yemault ed~. Amsterdam. Excerpta 61-69. 1t. Fi.~hman AP. - Cardiac asthma. A fresh wheeze. N Engl J Med, 1989, 320, l346-I l 2. Cabancs LR, Weber SN, Matran R, "ci!IWIIP MO, Oegeorges ME, Lockhart A. siveness to methacholine in patients with ventricular function. N Engl J Med, 1989, 320,