Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute haemodynamic effects of intravenous infusion of adenosine, a dilator of most vascular beds, were studied in 16 patients (seven with coronary artery disease, nine with normal coronary arteries) undergoing cardiac catheterization for investigation of chest pain. At the lowest dose used (4.3 mg min-1) adenosine increased minute ventilation by 44% (P less than 0.01, n = 11) and reduced pulmonary vascular resistance by 20% (P less than 0.05) without causing other significant haemodynamic changes. Symptoms, including chest discomfort in 14 patients and dyspnoea in 11, limited the maximum dose to 8.5 +/- 2.3 mg min-1 (mean +/- SD, 108 +/- 24 micrograms kg-1 min-1). At this dose, adenosine reduced pulmonary and systemic vascular resistance (by 38% and 34%, respectively) and increased heart rate (by 34%), stroke index (by 12%) and cardiac index (by 52%). Systemic blood pressure and right atrial pressure did not change. Unexpectedly, adenosine increased left ventricular end-diastolic pressure (LVEDP) (from 5 +/- 6 to 14 +/- 10 mmHg, n = 8), pulmonary capillary wedge pressure (from 3 +/- 2 to 10 +/- 5 mmHg, n = 16) and consequently mean pulmonary artery pressure (from 10 +/- 2 to 16 +/- 5 mmHg). Minute ventilation increased by 84% (n = 11), resulting in hypocapnia (PCO2: 31 +/- 3 mmHg, n = 8) and alkalosis (pH: 7.46 +/- 0.02, n = 8). Oxygen consumption was unchanged during the infusion, but increased by 21% 5 min post infusion. All effects were similar in patients with and without coronary artery disease. Adenosine therefore causes pulmonary and systemic vasodilation and respiratory stimulation. Symptoms and an increase in LVEDP of uncertain cause, which occur with high doses, may limit the use of adenosine as a systemic vasodilator in conscious subjects. However at lower doses adenosine causes selective pulmonary vasodilation which merits further study.
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PMID:Acute haemodynamic effects of intravenous infusion of adenosine in conscious man. 228 21

Nitrofurantoin is a widely prescribed antibiotic used for the treatment of urinary tract infections. In some patients it can produce an acute pulmonary reaction ranging from mild dyspnea to noncardiogenic pulmonary edema. Symptoms include fever, dyspnea, chills, cough, and chest pain. Physical examination generally reveals an acutely ill, extremely apprehensive patient in varying degrees of respiratory distress. Fever is usually present and there is an increase in heart rate and respiratory rate. Cyanosis, rales, and a maculopapular rash are common findings. Laboratory studies typically demonstrate a leukocytosis with eosinophilia, varying degrees of hypoxia and hypocapnia, and a mild to moderate elevation of the erythrocyte sedimentation rate. The chest x-ray study may be normal but more often demonstrates bilateral lower lobe interstitial infiltrates frequently accompanied by pleural effusions. Treatment in the majority of cases requires only stopping the drug, but steroids, bronchodilators, or antihistamines may be used in selected cases. Once the diagnosis is made and the drug withdrawn, prognosis for full recovery is excellent.
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PMID:Acute pulmonary toxicity to nitrofurantoin. 270 84

The respiratory function of pregnant women is changed for more than one reason. There is a mechanical effect due to the increase in the uterine volume and the elevation of the diaphragm. However, there are only modest functional consequences, because the pulmonary volumes are only little changed, with the exception of a reduction in the functional residual capacity. Bronchial permeability is unaltered due to the balancing of constrictors (mechanical, hypocapnia) and dilators (hormonal influences). As regards pulmonary haemodynamics, the hypovolaemia of the pregnant woman has no repercussions on pulmonary vascular pressure. Gas exchange and alveolar-capillary diffusion are normal or even improved as a consequence of chronic hyperventilation. The latter is the most important functional change, sometimes expressed as a sensation of dyspnoea. The origin of this hyperventilation relates to the diminution of the threshold of sensibility in the respiratory centres to CO2 due to the effect of raised progesterone levels.
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PMID:[Pregnancy and the respiratory function]. 304 98

In prior studies at high altitude, we have found that pregnancy increases maternal hypoxic ventilatory response (HVR) but the factors responsible are unknown. Changes in metabolic rate and hormones that occur during pregnancy have previously been shown to influence HVR. We therefore sought to determine the contribution of metabolic rate and hormonal changes to the pregnancy-associated rise in HVR. Pregnancy increased HVR in each of 20 normal, low-altitude (1,600 m) residents. As measured by the shape parameter A, HVR at week 36 was 237 +/- 26 (SE) or twofold higher than the 124 +/- 13 value measured 3 mo postpartum (P less than 0.01) despite the presence of the potentially depressant effects of hypocapnia [change in alveolar partial pressure of CO2 (delta PACO2) = -4 +/- 1 mmHg] and alkalosis [change in arterial pH (delta pHa) = 0.02 +/- 0.01 U] during pregnancy. Sixty percent of the increase in HVR values had occurred by week 20 of gestation at which time O2 consumption (VO2) and CO2 production (VCO2) were unchanged relative to values measured postpartum. The remaining 40% rise in HVR paralleled increases in VO2 and VCO2, and further elevation in VO2 and VCO2 with moderate exercise produced an additional increase in HVR. Serum estradiol and progesterone levels increased with pregnancy, but levels did not correlate with HVR. The women reporting the greatest symptoms of dyspnea had higher HVR A values at week 36 than the least dyspneic women (285 +/- 28 vs. 178 +/- 34, respectively, P less than 0.05). We concluded that factors intrinsic to pregnancy in combination with increased metabolic rate raised HVR twofold with pregnancy and may have contributed to the often-reported symptoms of dyspnea in pregnant women.
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PMID:Increased HVR in pregnancy: relationship to hormonal and metabolic changes. 310 85

A patient with acute hyperleukocytotic myelogenous leukemia who presented with acute respiratory distress is reported. Clinical manifestations included dyspnea, tachypnea, hyperventilation, and cyanosis. Blood gas analysis revealed hypoxemia, hypocapnia, and metabolic acidosis. Chest X-ray and perfusion lung scanning were normal. Pulmonary leukostasis syndrome (PLS) was later confirmed at autopsy. In a patient with hyperleukocytosic from acute nonlymphocytic leukemia and respiratory distress, a normal perfusion lung scintigraph should make one consider the PLS.
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PMID:Acute respiratory failure in hyperleukocytotic acute myeloid leukemia: the role of perfusion lung scintigraphy. 316 47

We studied the relation between mood disorder and hyperventilation (hypocapnia) before and during exercise treadmill testing in 113 chest pain patients attending a cardiac clinic and 30 healthy controls. In most patients end-tidal PCO2 (PCO2) rose in the normal way on exercise but in a subset of 24 (21 per cent) there was no rise: these patients with initial hyperventilation had significantly higher anxiety scores than those with a normal exercise-induced rise in PCO2. Two of the 24 had ischaemic heart disease and 10 (42 per cent) complained of recent panic anxiety compared with 12 (13 per cent) of the 89 with normal rise in PCO2 (p less than 0.05). Rates of psychiatric morbidity were similar in patients with 'typical' and 'atypical' chest pain. Resting hypocapnia occurred more often in patients with panic anxiety than in either anxious or non-anxious patients without panic. Panic patients also reported more symptoms of breathlessness and hyperventilation-related complaints than those without panic. Our findings confirm the important association between panic and hyperventilation in patients with chest pain. Furthermore, patients with exercise-induced hyperventilation are more likely to have a psychiatric than a cardiac disorder. Early detection and treatment of these patients may reduce the potential morbidity associated with unnecessary invasive investigations.
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PMID:Panic anxiety and hyperventilation in patients with chest pain: a controlled study. 327 82

A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.
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PMID:Primary pulmonary hypertension. A national prospective study. 360

In the original description of the syndrome of hyperbradykininism, dyspnea on exertion was not described. However, in five women with the syndrome, ages 31 to 58, four of whom had at least one elevated value of blood kinin as determined by radioimmunoassay, dyspnea on exertion was a prominent complaint. During treadmill walking at a constant power requirement against gravity, expired air gas collections and equilibrium carbon dioxide rebreathing were performed. Seventeen apparently healthy women, ages 18 to 48, served as control subjects. Although oxygen uptake was the same in both groups by design (oxygen uptake 0.91 liters per minute, 0.11 standard deviation [SD], in the control subjects; oxygen uptake 0.97 liters per minute, 0.12 [SD] in the patients), cardiac output was significantly reduced in the patients (cardiac output 8.4 liters per minute, 1.3 [SD], in the control subjects; cardiac output 6.3 liters per minute, 0.9 [SD], in the patients, p less than 0.01). End-tidal carbon dioxide tension was significantly lower in the patients (end-tidal carbon dioxide tension 41 torr, 3 [SD], for the control subjects; end-tidal carbon dioxide tension 33 torr, 7 [SD], for the patients). In one patient, repeated studies over a 12-month period demonstrated a positive relationship between end-tidal carbon dioxide tension and the respiratory exchange ratio. (Respiratory exchange ratio = 0.01 + 0.027 X end-tidal carbon dioxide tension, 0.073 standard error of the estimate [SEE], 0.71 regular correlation coefficient, n = 20). This relationship was opposite to that expected with voluntary overbreathing; it was interpreted to mean that reduced cardiac output with exercise occurred to a variable degree and was the cause of hyperpnea and hypocapnia. In the same patient, studies at exercise with and without the Jobst (antigravity) garment and studies at exercise in the supine and erect position were consistent with the hypothesis that dyspnea and exercise intolerance were caused by venous pooling when standing. It is concluded that hyperbradykininism is characterized not only by orthostatic hypotension and tachycardia with light-headedness, as originally described, but also by severe dyspnea on exertion with exercise intolerance. The mechanism remains obscure, and the treatment is unsatisfactory, but temporary improvement in the abnormal physiology can be achieved in some patients with the use of an antigravity garment.
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PMID:Dyspnea in patients with hyperbradykininism and excessive venous pooling. 374 83

The clinical experience of 661 children with bronchiolitis is reported in four-years period to gain a better understanding of diagnosis and pathogenesis of bronchiolitis. Upper airways infections, expiratory dyspnea, clear sound by chest percussion, vesicular rales and whistling by chest auscultation, air trapping on the chest radiography were considered as essential data of diagnosis. It was found in 595 patients: expiratory dyspnea, air trapping, vesicular r. and whistling in 85% and whistling only in 15%; hypoxemia in 20% combined with hypercapnic acidosis in 10%; normoxemia in 80% combined with hypocapnia in 54%; hyperlactemia in 64% combined with an increment in the serum of CPK in 50% and of GPT in 30%; virus were cultured in 27%, adenovirus and RSV were identified in 90%. Instead it was found in 66 patients: air trapping but no difficult breath, with normal chest auscultation; crisis of cyanosis or paleness-cyanosis chilly sweat in 80% were motive of admission. The clinical and/or radiological features of "air trapping" were considered as essential symptoms and signs of bronchiolitis. The insufficient systemic perfusion was considered as a frequent occurrence and as cause for sudden respiratory and circulatory emergency.
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PMID:[Bronchiolitis. Our clinical experience in the 4 years from 1981 to 1984]. 383 40

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


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