We have investigated pulmonary hemodynamics in 16 patients with COPD with respiratory insufficiency.

We have investigated pulmonary hemodynamics in 16 patients with COPD with respiratory insufficiency, exhibiting marked peripheral edema. All the patients had previously undergone within the last 6 month (TI), a right heart catheterization, in a stable state of their disease, when they were unrestrained of edema. Patients were subdivided into couple groups according to the flush of right ventricular end-diastolic crushing (RVEDP) during the episode of edema (T2): patients with a markedly elevated RVEDP ([greater than] 12 mm Hg) indicating the neighborhood of right ventricular failure (RVF) = collection 1, n = 9; patients with a normal or slightly elevated RVEDP ([les than] 12 mm Hg) = collection 2 (no RVF), n = 7 In arrange 1 pulmonary artery mean compressing (PAP) increased very significantly from T1 (27 [+ or -] 5) to T2 (40 [+ or -] 6 mm Hg p [les than] 0001) as did RVEDP from 75 [+ or -] 39 to 134 [+ or -] 12 mm Hg (p [les than] 0001) These hemodynamic changes paralleled a marked worsening of arterial vital fluid gases, [PaO.sub.2] falling from 63 [+ or -] 4 to 49 [+ or -] 7 mm Hg (p [les than] 001) and [PaCO.sub.2] increasing from 46 [+ or -] 7 to 59 [+ or -] 14 mm Hg (p [les than] 001) upon the other hand, in assemblage 2, PAP was stable during the episode of edema (from 20 [+ or -] 6 to 21 [+ or -] 5 mm Hg) as was RVEDP (from 55 [+ or -] 24 to 51 [+ or -] 15 mm Hg) and changes in arterial house gases from T1 to T2 were small and nonsignificant. It is conclud that RVF is effectively current in at least some patients with COPD with peripheral edema and is associated with a significant increase of PAP from baseline, probably accounted for by the agency of hypoxic vasoconstriction. Thus, pressure overload may contribute to the evolution of RVF. In other patients there are no hemodynamic signs of RVF PAP is stable, and the origin of edema is not well understood.

Patients with advanced chronic obstructive pulmonary disease (COPD) frequently exhibit peripheral edema during acute exacerbations of their disease. The origin of this edema was generally attributed to right heart failure, yet it has long been known that other mechanisms could be involved.[1] Furthermore, the possible casualty of right heart failure in patients with COPD has been questioned,[2] especially as cardiac output is generally maintained or level elevated in these patients in the vicinity of edema.[3,4] Pulmonary hypertension (PH) is in the greatest degree often of mild degree in patients with COPD[5] and that worsening of PH during exacerbations of the disease, could lead to right heart failure, has been denied according to Macnee et al[6] who observ that mean pulmonary artery press (PAP) was almost identical in patients with morose COPD with or without peripheral edema. In fact, different conclusions were reported very recently from Anand et al.[7]

We thus decided to investigate patients with COPD exhibiting marked peripheral edema. A right heart catheterization was performed during the episode of edema, however also during a stable period of the disease when patients were liberated of edema. The aim of our meditation was to answer two questions: (1) Was right heart failure, assessed in succession hemodynamic data, present in near patients? (2) Was there a worsening of pulmonary hypertension, which could have favored the unfolding of right heart failure, during the episode of edema?

METHODS

We have investigated 16 patients with COPD All had a history of chronic bronchitis defined onward usual grounds,[8] and a spirographic pattern of airway obstruction defined by means of an [FEV.sub.1]/VC ratio [less than] 60 percent Pulmonary turns measured in a stable state of the disease, are shown in Table 1; it can be seen that bronchial obstruction was generally morose since the average values of [FEVsub1] and [FEVsub1]/VC were respectively 1000 ml and 40 percent Hypoxemia was mild to moderate in most numerous of the patients (Table 2) Half of the patients (8/16) had hypercapnia, which was mild in all individual cases, [PaCO.sub.2] ranging between 46 and 53 mm Hg (Table 2) brace patients (patients 9 and 10 [Table 2]) had a persistent hypocapnia; clinically, these patients had the "emphysematous" pattern of COPD.

Patients were investigated during couple distinct periods: first, during a stable state of their disease when they were liberated from chest infection and from peripheral edema (T1); secondly during an episode of marked peripheral edema (lower limbs), frequently but not necessarily associated with an acute exacerbation of the disease (T2) The time interval between T1 and T2 was at least of 1 month and always les than 6 month No patient had any causes other than COPD of the like kind as renal insufficiency or hepatic cirrhosis, that could have accounted for edema. Patients were exclud if they had any clinical, electrocardiographic, or echocardiographic evidence of systemic hypertension, valvular heart disease, coronary artery disease, or primary myocardial disease. Also exclud were patients with an abnormally high ([greater than] 12 mm Hg) pulmonary artery wedge pressure

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