Platypnea is the rare symptom of dyspnea in the upright position.

Platypnea is the rare symptom of dyspnea in the upright position, which is relieved by way of assumption of the recumbent position. This symptom has been previously described in association with several conditions, if it be not that never with constrictive pericarditis. The authors report the case of a patient with constrictive pericarditis and hard platypnea, which resolved after pericardiectomy.

Platypnea is the rare and poorly understood symptom of dyspnea in the upright position, which is relieved at recumbency. It is the commerce of orthopnea. Platypnea is frequently seen in conjunction with orthodeoxia, which is arterial desaturation in the upright position. This curious phenomenon was first described in 1949 according to Burchell and associates.[1] In 1969 Altman and Robin[2] coined the period of time "platypnea," which can be translated literally to mean "flat breathing." They reported the case of a patient with plain obstructive lung disease and platypnea who eventually died of respiratory compromise. Since these reports, others have provided examples of platypnea in association with several pathologic states (Table 1) We have studied a patient with platypnea and constrictive pericarditis whose platypnea resolv after an extensive pericardiectomy. The association of platypnea and constrictive pericarditis has not, to our knowledge, been previously reported.

CASE REPORT

A 49-year-old man was admitted with progressive and bitter dyspnea on exertion and platypnea. Seven years previously, aspergillosis had been diagnosed, and, after episodes of hemoptysis, the patient underwent an uncomplicated left upper lobectomy. He was otherwise in fairly dutiful health and did well postoperatively until 6 years later, when he bring to maturityed recurrent hemoptysis, which necessitated a integral left pneumonectomy. At the time of surgery pericarditis was discovered, and a 65 percent pericardiectomy was performed. In the month that followed, he bring to maturityed progressive dyspnea on exertion, peripheral edema, and debilitating platypnea.

The physical examination was noteworthy for a family pressure of 90/70 mm Hg There was no orthostasis. The neck veins were completely distended at 90 degrees with prominent X and Y journey [i]or[/i] voyage downs There was dullness to percussion from one side of to the other the left thorax, and the breath entires were diminished on the left The heart unimpaireds were normal with no gallop, scour or knock. There was marked hepatomegaly and 2+ pedal edema.

The ECG showed a rightward axis of the QR tangled skein an incomplete right bundle branch fill up and a diffuse nonspecific repolarization abnormality. Echocardiography revealed normal left ventricular systolic function and mild tricuspid regurgitation. The right atrium and ventricle were mildly dilated, and there were no other valvular abnormalities. Contrast echocardiography done in the two the recumbent and upright positions did not demonstrate a switch Arterial blood gas analysis of specimens obtained while breathing swing air and at an [FIo.sub.2] of 100 showed no significant difference between recumbent and upright conditions Cardiac catheterization revealed elevated and equalized right ventricular, left ventricular, and right atrial end-diastolic crushings with a dip-and-plateau configuration to the ventricular press tracings consistent with constriction. There was no oximetric evidence of an intracardiac switch Magnetic resonance imaging of the thorax showed a slightly thickened pericardium.

The patient underwent a pericardiectomy. At surgery the heart was place to be encased in a thick fibrous mass of tissue. As to a great degree of the pericardium as possible was remov predominantly above the right side of the heart. The pathologic evaluation revealed extensive fibrosis and small foci of inflammation. The patient made a brisk postoperative recruiting with resolution of his platypnea and no other than mild dyspnea on exertion.

DISCUSSION

Platypnea is a poorly understood phenomenon. belt I pulmonary physiology occurs in areas of lung where the pulmonary alveolar crushing exceeds the pulmonary arteriolar hurry These areas, therefore, are not perfused, which creates small amounts of pulmonary dead space in normal states. The underlying mechanism of platypnea is deliberation to be an increase in pulmonary dead space when the patient is upright, which leads to an increased ventilation-perfusion (V/Q) mismatch, hyperventilation, increased work of breathing, and breathlessness. This positional change to cincture I can be the end of a variety of pathologic states, as mentioned above.

Many mechanisms have been propos to explain the V/Q mismatch. With morose COPD, Altman and [Robin.sup.2] hinted that there are large areas of the lung with markedly elevated alveolar crushings which exceed pulmonary arteriolar influences such that these areas are not perfused. This tenor is more pronounced in the upright position, where gravitational forces bring into operation an influence to diminish pulmonary arteriolar compressing in the upper lung fields. Several authors[4-6] believe that platypnea is a spring of postural changes causing an increased right-to-left switch most often through a patent foramen ovale. Another theory involves los of the normal hypoxic vasoconstrictive replication causing increased shunting. Adolph et al[5] described a patient with platypnea who had echocardiographic evidence of an interatrial switch with no pressure gradient in the setting of a pericardial effusion. They felt that the effusion distorted the architecture of the right atrium when the patient was standing in of that kind a way as to direct the be derived of blood returning from the inferior vena cava directly toward a patent foramen ovale.

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