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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since hypoxemia is not known to be a sensitive indicator of acute pulmonary embolism, we performed a retrospective study to determine whether an increased P(A-a)O2 gradient or hypocapnia improved the sensitivity of blood gas analysis in acute embolism. The study group consisted of 78 patients with angiographically documented emboli who had blood gas samples obtained while breathing room air. None had a prior history of cardiopulmonary disease. Hypoxemia was present in 59 patients (76 percent), hypoxemia or hypocapnia in 73 patients (93 percent), an increased P(A-a)O2 gradient in 74 patients (95 percent), and an increased P(A-a)O2 gradient or hypocapnia in 77 patients (98 percent). Only one patient with acute embolism showed a normal P(A-a)O2 gradient and normal PaCO2 breathing room air. These results suggest that a normal P(A-a)O2 gradient and a normal PaCO2 obtained in a patient during room air breathing can be used as evidence against the presence of pulmonary emboli.
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PMID:Improved use of arterial blood gas analysis in suspected pulmonary embolism. 279 99

Recurrent pulmonary embolism sometimes (3% of hospital autopsies) determines a progressive obstruction of the pulmonary vascular bed, which in turn causes pulmonary arterial hypertension and in time right ventricular hypertrophy and failure. The first stages of this process are characterized by slight pulmonary arterial hypertension at rest and by few and deceiving symptoms which make the diagnosis very difficult. Regarding anatomy, in most cases recurrent thromboembolism obstructs one of the main branches of the pulmonary artery. At the beginning pulmonary embolism usually manifests itself in a spontaneous and atypical manner: paroxysmal dyspnea, tachycardia, lateral chest pain, mild hemoptysis and recurrent fever. The clinical signs of peripheral thrombophlebitis are not very frequent. The chest roentgenogram supplies diagnostic information in 20% of cases, the electrocardiogram in 10%. Very important is the contribution of the analysis of arterial blood gases: hyperventilation, moderate hypoxia associated with shunting, hypocapnia with a widened difference between alveolar and arterial CO2. Pulmonary perfusion scintiphotography shows vast unperfused areas, different to the "plexogenic" appearance in primitive pulmonary arterial hypertension, in about 50% of cases. Pulmonary angiography discloses the exact site and extension of the obstruction in 80-90% of cases. On catheterization pulmonary arterial hypertension results to be inconstant and may appear only during stress. Regarding the evolution of pulmonary embolism, the forms associated with pulmonary arterial hypertension may last several years, although recurrent embolism may shorten its course. When the stage of right ventricular hypertrophy is reached, the evolution is generally rapid (from 1 to 4 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pulmonary thromboembolism. 653 60

A cardiorespiratory monitoring system allows the measurement of FAECO2 and FECO2 in the expired air of the patient at the mouth (endtidal CO2) and in a mixing box. From these parameters, combined with the measured PACO2, the alveolo-expired (DuA = PECO2/PAECO2) and alveolar-arterial (Dua = PAECO2/PACO2) ductances which assimilate the respiratory system to a two-stage exchanger have brought about a lot of valuable information 1. DuA improves by 20% in 20 patients after removal of bronchial obstruction (p < 0.001) and by 9% in 7 intubated patients after tracheotomy (p < 0.02). DuA falls by 15% (p < 0.001) in 10 patients with hypocapnia (PaCO2 = 28 mmHg) after a dead space adjunction with the aim of normalizing PaCO2 (paCO2 = 35 mmHg). 2. Dua falls by 33% in six patients after pulmonary embolism, proved by angiography (p 0.001) by 9% in 34 patients after 30 min of pure oxygen breathing (p 0.001). On the other hand, inthe absence of clinical or radiological pulmonary edema, in increases by 19% in 38 patients with hypervolemia after diuresis (furosemide) (p < 0.001). Thus since DuACO2 varies with anatomical dead space and the air distribution disorder, DuaCO2 evolves according to the disorders of the blood distribution and arterial-alveolar diffusion. The determination of these coefficients, in the absence of significant changes in the arterial blood gases, helps the diagnosis, guides the early treatment and allows for the monitoring of its efficiency.
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PMID:The continuous monitoring of CO2 ductances in pulmonary intensive care. 677 20

Arterial blood gases (pH, pO2, p CO2) were studied in 100 patients with documented pulmonary embolism (Group A), confirmed by pulmonary angiography (n = 51) or scintigraphy ( n = 49). The pO2 ranged from 32 to 97 mm Hg (average 60,5 +/- 13 mm Hg). Hypoxaemia was found in 97 cases and would therefore seem to be a reliable sign of pulmonary embolism. In the three cases in which it was absent, the embolism was small. Hypoxaemia was associated with hypocapnia and alkalosis in 91 cases. However, hypoxaemia was not a specific finding; it was also present in 49 patients with suspected pulmonary embolism (Group B) in whom the diagnosis was excluded by pulmonary angiography or scintigraphy. A previous history of cardiovascular disease was found in 37 patients (76%) in this group: of the 12 remaining patients, 6 were heavy smokers and 4 were significantly obese. No correlation was found between the degree of hypoxaemia and the extent of amputation of the vascular bed on pulmonary angiography or scintigraphy. Nevertheless, a pO2 of under 50 mm Hg was always associated with a severe embolism with amputation of over 40% of the pulmonary vascular bed. A significant correlation was found between the severity of hypoxaemia and the degree of cyanosis (p less than 0,05) and ECG changes (p less than 0,01). The average pO2 was 59 +/- 12 mm Hg in patients with cardiovascular disease ( n = 21) and 55 +/- 11 mm Hg with known pulmonary disease ( n = 6). A higher average pO2 was found when these conditions were absent (61,5 +/- 13 mmHg). The difference was not statistically significant unless previous cardiac and pulmonary disease were associated (pO2 = 51 +/- 14 mm Hg, p less than 0,05).
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PMID:[Arterial blood gas analysis in acute pulmonary embolism]. 678 77

Mechanisms of hypoxemia and hypocapnia in pulmonary embolism (PE) are incompletely understood. We studied 10 patients at diagnosis (D) and five of these again after 10 to 14 d of heparin treatment (T). Patients had right heart catheterization, assessment of ventilation-perfusion ratio (VA/Q) distribution by inert gas, radioisotopic perfusion and ventilation scans, and angiography. At D, two-thirds of the pulmonary circulation was obstructed, patients were hypoxemic (PaO2 = 63.0 +/- 11.7 mm Hg) and hypocapnic (PaCO2 = 30.0 +/- 4.1 mm Hg), mixed venous oxygen pressure (PvO2) was reduced (30.9 +/- 3.9 mm Hg), minute ventilation (VE) markedly increased (14.1 +/- 5.1 L/min), and cardiac output measured by applying the Fick principle to arteriovenous oxygen content difference (QT) slightly low (4.7 +/- 1.7 L/min). Hypoxemia was mainly explained by VA/Q inequality, reduced PvO2 also contributed. Hypocapnia was the result of hyperventilation. VA/Q inequality was characterized by shift of VA and Q distribution mean to regions with higher VA/Q ratio through a fraction of blood flow (19.0 +/- 24.3% of cardiac output) went to lung units with low VA/Q ratio. Log SDQ and log SDvA were increased. Shunt, diffusion limitation, or true alveolar dead space occurred in occasional patients but were generally insignificant. Regional ventilation and perfusion maps indicated that in the unperfused lung segments, ventilation was reduced. Furthermore, they disclosed overperfused lung segments. At T, hypoxemia and hypocapnia improved considerably. However, temporal imbalances in recovery between regional ventilation and perfusion occurred with the former normalizing sooner. However, perfusion recovered sooner than ventilation in some regions.
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PMID:Mechanisms of hypoxemia and hypocapnia in pulmonary embolism. 759 43

The diagnosis of pulmonary embolism (PE) can be accurately made by perfusion lung scan and pulmonary angiography; however, when these diagnostic techniques are not promptly available, simple clinical procedures may be useful to identify patients with high probability PE. To this end, collection of clinical data through a standardized questionnaire and the use of findings from chest radiograph, ECG, and blood gas analysis may raise clinical suspicion and decide on therapeutic management. By reviewing published literature and our own experience, we found that unexplained dyspnea and chest pain are the most frequent symptoms, and sudden onset dyspnea and pleuritic chest pain are the most typical. Chest radiograph is abnormal in more than 80% of patients with PE, showing typical signs such as "sausage-like" descending pulmonary artery, Westermark sign, etc. The ECG may show findings characteristic of PE, such as tachycardia, T wave inversion in V1-V2, and PR displacement. Arterial blood gas data frequently demonstrate hypoxia and hypocapnia, being helpful in suspecting or excluding PE. Recent statistical techniques, such as discriminant or logistic analysis, may be applied to the above clinical assessment to refine and improve the noninvasive diagnosis of PE.
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PMID:Clinical features of pulmonary embolism. Doubts and certainties. 781 25

To contribute for making early diagnosis and treatment of acute pulmonary embolism (APE), we investigated on clinical pictures of 225 patients with APE. Common underlying factors were heart disease, prolonged bed rest, post-surgical state, thrombophlebitis, malignant tumor and post-catheterization state in this order. Dyspnea, chest pain, tachycardia and shock were frequently seen as initial symptoms and signs. Blood screening showed leukocytosis, hypoxemia, hypocapnia and elevated serum LDH. Electrocardiographic findings highly demonstrated were ST.T abnormalities, such as T inversion with ST elevation in V1-3, ST depression in V4-6 and sinus tachycardia. Chest X-rays showed diminished pulmonary vascular marking and pulmonary artery dilation. Right ventricular dilatation were frequently seen on 2-dimensional echocardiograms. Pulmonary artery pressure were elevated up to 49/20 (30) mmHg. Twenty-five percent of the patients died, and the recurrence was seen in 4%. Thus, as soon as APE is suspected by above clinical findings, definitive diagnosis should be obtained by the lung perfusion scan and pulmonary arteriography, then oxygen and thrombolytic agents should be given immediately to prevent the fatal outcome.
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PMID:[Early diagnosis and management of acute pulmonary embolism: clinical evaluation those of 225 cases]. 835 37

Twenty-five patients with acute pulmonary embolism without other pulmonary or heart diseases were analyzed for pulmonary hypertension. Doppler echocardiography was used to determine the systolic pressure of the pulmonary artery (PAPs) from the maximal velocity of the tricuspid regurgitation using corrected Bernoulli's formula (PAPs = 1.23 x 4 Vmax2 - 0.09). Pulmonary hypertension was found in 84% (21/25) of the patients with acute pulmonary embolism. PAPs values ranged between 34 and 90 mmHg (X = 54 +/- 7.5 mmHg) and hypocapnia with carbon dioxide partial pressure, PaCO2, ranged from 26 to 34 mmHg (X = 30 +/- 2 mmHg). PAPs showed a significant negative correlation with oxygen partial pressure (r = -0.87, P < 0.01). According to the findings of lung scintigraphy, all patients with pulmonary hypertension had submassive pulmonary embolism with perfusion abnormalities in two segments (X = 5 +/- 2 segments). It is concluded that pulmonary hypertension may be expected in more than 80% of the patients with submassive acute pulmonary embolism, and hypoxemia and hypocapnia. Doppler echocardiography is a noninvasive method useful in the diagnosis and follow-up of pulmonary hypertension in patients with acute pulmonary embolism.
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PMID:[Pulmonary hypertension in acute pulmonary embolism]. 864 78

The aims of this study were to compare the clinical features of patients with pulmonary embolism (PE) and patients in whom the initial suspected diagnosis was not confirmed by the complementary studies and to determine the possible clinical differences among patients with PE according to age. A retrospective review of the charts of a group of patients with PE (n, 96) and another without PE (n, 96) was carried out. The patients with PE over 65 years of age (n, 64) were compared with those under 66 years of age (n, 32). The variables related to PE were absence of known heart disease, duration of symptoms </=2 days, pleuritic chest pain, absence of cough, pCO(2) <4.8 kPa (36 mmHg), and normal chest X-ray. The variables associated with the existence of PE in patients over 65 years of age, when contrasted with younger patients, were female sex, absence of pleuritic chest pain, abnormal chest X-ray, hypoxemia (pO(2) < 8.7 kPa (65 mmHg) and absence of S1Q3T3 pattern in ECG.The duration of symptoms and the presence of hypocapnia, pleuritic chest pain, and normal chest X-ray may lead to the suspicion of PE. Pleuritic pain and S1Q3T3 pattern are less commonly found in old patients with PE.
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PMID:Influence of age on clinical presentation of acute pulmonary embolism. 1086 63

Pulmonary embolism alters the distribution of ventilation/perfusion relationships, and increases pulmonary vascular resistance. These changes lead to hypoxemia and hypocapnia, and eventually, to right heart failure. The thin-walled and compliant right ventricle adapts to any increase in afterload by dilatation and decreased stroke volume, but this is largely prevented or delayed by the pulmonary circulation being a low resistance, recruitable and distensible circuit. Pulmonary embolism cannot be associated with a mean pulmonary artery pressure higher than 40 mmHg. More severe pulmonary hypertension indicates the presence of a hypertrophied right ventricle in the context of preexistent cardiac or pulmonary disease. Gas exchange is initially affected because of increased ventilation/perfusion ratios in embolized lung areas, and decreased ventilation/perfusion ratios in remaining non embolized lung areas. Both physiologic shunt and physiologic dead space increase accordingly, resulting in hypoxemia and hypocapnia. However, these changes are rapidly affected by an increase in ventilation, and by a "pneumoconstriction" which decreases physiologic dead space in embolized areas. In addition, a series of secondary alterations contribute to increase perfusion to lung units with low ventilation/perfusion ratios, thereby aggravating hypoxemia, while hypocapnia persists.
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PMID:[Physiopathology of pulmonary arterial hypertension and gas exchange in acute pulmonary embolism]. 1090 37


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