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

Arterial pH, pO2 and pCO2 were analysed with Astup's micromethod on one hundred and three acute myocardial infarctions (A.M.I.) without metabolic, pulmonary and renal diseases. Following the clinical picute, the patients were divided into five groups and results were clinically and statistically evaluated (mean, standard deviation, Student's test "t", correlation coefficient "r" between pO2 and pulmonary arterial diastolic pressure): --Ist group (A.M.I. without complications): only mild hypoxemia; --IInd group (A.M.I. with slight left ventricular failure): more remarkable hypoxemia and hypocapnia, often with respiratory alkalosis; --IIIrd group (A.M.I. complicated by acute pulmonary oedema): mixed acidosis and severe hypoxemia; --IVth group (A.M.I. complicated by shock): prevailing metabolic acidosis and severe hypoxemia. Acidosis shows good correlations with the clinical picture; --Vth group (A.M.I. with serious arrhythmias): mixed and profound acidosis and important hypoxemia during ventricular fibrillation and cardiac arrest. In twenty patients hypoxemia and arterial pulmonary diastolic pressure showed a significant correlation.
G Ital Cardiol 1976
PMID:[Blood gas analysis and acid-base balance in acute myocardial infarction. Personal observations (author's transl)]. 1 Feb 18

We conducted a retrospective analysis on 311 patients with clinical diagnosis of pulmonary embolism (PE) in a period of 3 years. 163 patients were excluded based on clinical-laboratorial criteria. The remaining 146 patients had a median age of 69 years (range: 30-91 years). 54% of the patients were male. We found dyspnea (94%), abnormal cardiopulmonary observation (89%), risk factors for venous thromboembolism (74%), tachycardia (53%), cyanosis (49%), and neck vein distension (45%) to be the most frequent findings. 64% of the patients had heart failure, 32% had myocardial ischemia, 13% had cancer, and 11% had myocardial infarction. Lactic dehydrogenase (LDH) was higher than two-fold in 54% of the patients. There was severe hypoxemia in 55% of the cases and hypocapnia in 43% of the cases. Creatinine phosphokinase (CPK) was elevated in 16% of the cases. Electrocardiography was suggestive of PE in 37% of the cases. Echocardiography showed right heart dysfunction in 30% of the cases, 92% of the patients were treated with heparin, 37 patients (25%) died, 54% of which during the first 4 days after admittance. Trying to define an index of mortality in PE we evaluated all patients by discriminant analysis coming up with 14 items with good discriminative power. By approximation of their odds-ratios we determined how many points would correspond to each item in the total sum.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Port Cardiol 1992 Sep
PMID:[Pulmonary embolism--mortality risk]. 147 67

We report our experience with five children with pulmonary embolism and infarction. Two with congenital heart disease, one with rheumatic cardiopathy and two with a previously healthy cardiopulmonary system. The risk factors, clinical behavior and ECG were similar to those in adults. In chest roentgenogram we found pulmonary infarction with cavitations in three patients because of a delayed diagnosis. All patients had hypoxemia and hypocapnia, and diagnosis was made on the basis of segmentary or larger defects in perfusion gammagraphy. In just one case we obtained V/Q gammagraphy and pulmonary angiography. In one case we confirmed the clinical diagnosis by autopsy. We conclude that it is very important to keep this diagnosis in mind in all children with respiratory failure.
Arch Inst Cardiol Mex
PMID:[Pulmonary thromboembolism in children]. 177 17

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)
G Ital Cardiol 1984
PMID:Chronic pulmonary thromboembolism. 653 60

The syndrome of chronic heart failure is characterized by exercise intolerance. Exercise is limited by shortness of breath and fatigue, and either symptom occurs in the same patient depending on the type of exercise performed. Exercise capacity correlates poorly with indices of central hemodynamic function, but the increased ventilatory response in chronic heart failure correlates well with exercise capacity. Possible pulmonary causes have been explored, including increased dead space ventilation, abnormal airway function, and abnormal diffusion capacity. However, the finding of hypocapnia and hyperoxemia in arterial blood during exercise in patients with heart failure suggests that blood gas values reflect hyperventilation, and that any abnormality of pulmonary function is secondary to changes elsewhere. Skeletal muscle is abnormal in chronic heart failure, and shows changes in structure, bulk, exercise capacity, blood flow, and intrinsic metabolic activity. The relative importance of these abnormalities is not clearly determined, but the possible presence of an ergo- or metaboloreceptor connection between abnormal exercising muscle and the ventilatory response to exercise suggest a mechanism linking the two cardinal symptoms of chronic heart failure.
Curr Opin Cardiol 1994 May
PMID:Mechanisms of exercise intolerance in cardiac failure: abnormalities of skeletal muscle and pulmonary function. 804 88

The objective of this study was evaluate the relationships between abnormal pulmonary circulation, lung function, and respiratory response during exercise in Fontan patients. Pulmonary function and cardiopulmonary exercise tests were performed in 101 Fontan patients and 122 controls. A small vital capacity (VC) with a high residual volume-to-total lung capacity ratio and a slight but significant low arterial saturation with hypocapnia were observed in Fontan patients. The number of surgical procedures determined VC. Total cavopulmonary connection, fenestration, higher pulmonary arterial wedge pressure, and smaller VC were independent determinants of low arterial saturation, which was the only determinant of hypocapnia. Arterial saturation decreased during exercise and resting arterial saturation correlated with that at peak exercise. Improvement in dead space ventilation was less in Fontan patients and was independently determined by resting arterial saturation. A steeper minute ventilation-carbon dioxide production slope was determined by resting arterial saturation, arterial carbon dioxide tension, and peak oxygen uptake. In Fontan patients, in addition to dead space ventilation, surgery-related reduced VC, the type of repair, and high pulmonary arterial wedge pressure cause arterial desaturation with subsequent hypocapnia, resulting in accelerated inefficient ventilation at rest and during exercise.
Pediatr Cardiol
PMID:Restrictive ventilatory impairment and arterial oxygenation characterize rest and exercise ventilation in patients after fontan operation. 1513 7

Patients affected by pulmonary arterial hypertension (PAH) show a reduced exercise tolerance with early occurrence of dyspnoea and fatigue. The origin of functional capacity limitation is multifactorial and several mechanisms have been proposed, including right heart failure, which leads to a limited increase in cardiac output during exercise, and hyperventilation with a reduced perfusion of properly ventilated alveoli. In addition, abnormalities in arterial blood gases are observed, with the occurrence of hypoxemia and hypocapnia, related to an abnormal ventilation/perfusion match, gas diffusion abnormalities, low mixed venous oxygen saturation and to the development of intra- and extra-pulmonary right-to-left shunts. At present, the 6-minute walking test is the most used method to assess exercise tolerance in PAH; it is also useful to monitor the response to therapy and provides prognostic information. However, the assessment of functional capacity by cardiopulmonary exercise test (CPET) seems to be more complete, because CPET allows for discrimination between the metabolic, cardiovascular and pulmonary components of exercise limitation. Moreover, CPET estimates the severity of disease and assesses patients' prognosis and response to therapy. In PAH, a typical CPET-response is observed, characterized by a severe reduction in peak VO2, work rate, O2 pulse and anaerobic threshold and by a marked increase in VE/VCO2 slope and in the dead space to tidal volume ratio. However, the use of CPET should be limited to experienced centres. This review will focus on resting lung function and exercise tolerance tests, showing that CPET can provide the physiological explanation of functional limitation in PAH.
Eur J Prev Cardiol 2012 Oct
PMID:Exercise testing in the clinical management of patients affected by pulmonary arterial hypertension. 2312