EDITORIAL

wheezing and respiratory insufficiency in pregnancy: was it bronchial or cardiac ?

J.C. Yernault

1989 issue of Chest, 'I'ENHoLDER and bronchial asthma, with dyspnoea present in their 12 the case of a 27 yr old pregnant patients (5 of them also complaining of chest tightness), gestation who presented with cough in 7 and wheezing in 9. Hypoxaemia was also ng , cough present in several of their patients during the acute phase

sputum, and wheezing. When hospi- with the lowest measured Pao1 at 6.9 kPa (52 mmHg). 3), 1987, she was receiving therapy The chest X-ray, which was abnormal in all their pa­ inbalcd tcrbuLaiJne nnd oral lheophyl­ tients during the exacerbation, returned to normal after was begun two weeks earlier increased diuretic therapy in several of them. Significant

.(unction tests had shown "reactive airway obstruction with reduced FEV1 and FEV/FVC , Unfortunately no figures are given to was initially presem in 6/12 patients. to fully appreciate the meaning of that Several of the features of the patient described by to describe spirometric results. On TENHoLDER and SoUrH-PAUL [1) including the chest X­ was afebrile, had (124 ray findings with bilateral pleural effusions [3, 4], are (22 breaths per min). Diffuse bilat­ thus compatible with a diagnosis of cardiac rather than heard with dullness to percussion on bronchial asthma. Admittedly, this is an unusual problem ·were no heart murmurs, nor jugular in a young woman without a previously recognized heart The chest X-ray showed bilateral problem, but the hypothesis should at least have been lower lobes and pleural effusions. No discussed because situations such as critical mitral regur­ e~l. Arterial blood gases showed gitation can present without audible murmur as recalled 60.6 mmHg on 4 l oxygen by by SCHREIBER et al. [5] also in the same Chest issue.

nypocaJpma (Paco1 29.5 mmHg). The Moreover recent studies [6, 7] have emphasized the the intensive care unit and treated limited reliability of physical signs for estimating the aminophylline and methylpredni­ pulmonary capillary wedge pressure in patients with of terbutaline and atropine. On impaired left ventricular function. A raised jugular venous admission, a spirometry showed pressure is a rather specific but poorly sensitive indicator defect (FVC 59% predicted, FEV / of [7), and other signs such as a third heart a parallel 300 ml improvement in FVC sound or a displayed apex beat are difficult to appreciate .5. [8, 9]. In the presented case, a significant heart problem clearly stated, I presume that the cannot be excluded only on the basis of clinical data. was concurrent bronchial asthma and Similarly the improvement under therapy cannot be taken patient without any past history of as an argument pro bronchial rather than cardiac asthma, improved steadily during because bed rest, oxygen and theophylline administra­ """>v•umzation and the chest film taken tion might have contributed to an improvement of the normal. The authors were puzzled haemodynamic status. . obstructive pattern of severe Moreover, wheezing cannot be equated with u to an out-of-proportion reduction bronchospasm nor wilh asthma [10]. It is produced when .,,.,,,""'"''v and inability for the patient to oscillations of the airway wall occur, induced by an acceleration of the gas flow through a narrowed lumen their case history, I wonder whether and/or by dynamic compression. In so-called cardiac might not have been considered, asthma, narrowing of airway lumen most probably nuher than "bronchial" asthma. Actu­ results from congestion and oedema of the bronchial wall Ch~ t issue, PtsoN et al. [2], describing [11). Following these lines, the bronchial hyperrespon­ s•vcncss to inhaled methacholine in siveness to inhaled methacholine observed in these left heart failure, remind us that the circumstances has been attributed to its vasodilating effect ng is as characteristic of ex­ on the bronchial arterioles [12]. left ventricular failure as it is of 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 248 I.C. YERNAULT manoeuvre would have been very useful. Should a S. Schteiber TL, Fisher I, Mangla A thoracocentesis have been pcrfonned, the chemical analy­ "silent" milral regurgitat.ion. A potential' sis of the pleural Ouid demonsrraling a transudate might refractory hean failure. Chest, 1989, 96 have pcnniucd very strong arguments in favour of a 6. Editorial. - Clinical signs in heart fa'il 309- 3 10. ~. diagnosis of cardiac rather than bronchial asthma and 7. Stevenson LW, Perloff JK. -The pneumonia, in which case an exudate would have been physical signs for estimating hemodynamics expected. failure. JAMA, 1989. 261, 884-88. 8. lshmail AA, Wing S, Ferguson J, nut,eflb,_j S, Aegel KM. - Interobserver agreement by Rererences presence of a lhird heart sound in pauen11 heart failure. Chest, 1987, 91, 870-873, 1. Tenholder MF, South-Paul JE. - Dyspnea in pregnancy. 9. O'Neill TW, Barry M. Smith Chest, 1989, 96, 381-382. IM. - Diagnostic value of the apex be.t 2. Pison C, Malo JL, Rouleau JL, Chal11oui J, Ohezzo H, 410-411. • Malo J. - Bronchial hyperresponsivencss lO inhaled methacho­ 10. Yema.ult JC, Lenclud C. - Wheez.ing line in subjects with chronic left hean failure at a time of Progress In asthryta and COPD. P. V exacerbation and after increasing diuretic therapy. Chest, 1989, I.C. Yemault ed~. Amsterdam. Excerpta 96, 230-235. 61-69. 3. Pist.olesi M. Miniali M, Milne ENC, Oiuntini C. - The 1t. Fi.~hman AP. - Cardiac asthma. A fresh chest roentgenogram in . Clin CMst Med, wheeze. N Engl J Med, 1989, 320, l346-I 1985, 6, 315- 344. l2. Cabancs LR, Weber SN, Matran R, "ci!IWIIP 4. Wiener-Kronish JP, Berthiaume Y. Albertine KH.- Pleu­ MO, Oegeorges ME, Lockhart A. - ral effusions and pulmonary edema. Clin Chest Med, 1985, 6, siveness to methacholine in patients with 509-519. ventricular function. N Engl J Med, 1989, 320,