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

The cardiorespiratory responses to exercise and forced hyperventilation were measured in 17 unselected patients with syndrome X (angina, positive exercise test, normal coronary arteriogram, no other cardiovascular disease) and compared with those in 15 healthy subjects. Forced hyperventilation produced hypocapnia and metabolic alkalosis but no chest pain or electrocardiographic change. Patients with syndrome X showed reduced maximum oxygen consumption with an increased respiratory exchange ratio at peak exercise, confirming that exercise was limited by skeletal muscle perfusion--and thus that the increase in cardiac output with exercise is limited in syndrome X as in heart failure. Arterial carbon dioxide tension (PCO2) homoeostasis during exercise was normal but the ventilatory cost of carbon dioxide excretion was increased in syndrome X (as in heart failure). End tidal PCO2 measurements correlated only poorly with arterial PCO2 in individual patients with syndrome X, providing a possible explanation for previous reports, based on end tidal PCO2 of inappropriate hyperventilation. Patients with syndrome X did not show inappropriate hyperventilation but they did show hyperventilation that was appropriate to maintain normal arterial PCO2 in the face of reduced cardiac reserve.
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PMID:Syndrome X and hyperventilation. 193 59

Seventeen (39%) of 44 patients with chest pain but without significant ST depression on treadmill exercise had their usual chest pain reproduced during or after 3 min of voluntary hyperventilation (VHV) at rest. These patients with hyperventilation positive tests had not only significantly more hyperventilation-related symptoms and respiratory complaints but also shorter breath-holding times, lower mean resting end-tidal pCO2 and higher mean respiratory rates than those with negative tests and normal controls. Of the psychological variables, only phobic avoidance scores for agoraphobia were higher in patients with positive tests. These findings suggest that in two fifths of patients with exercise tests negative for ischaemia, chest pain is associated with HV, but abnormalities of breath control and relative hypocapnia are present even in the absence of chest pain. It is possible that a chronic abnormality of respiratory control may interact with attitudinal factors in the experience of non-cardiac chest pain.
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PMID:Hyperventilation provocation in patients with chest pain and a negative treadmill exercise test. 202 44

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

A hyperventilation provocation test (HVPT) was performed on a group (n = 63) of consecutive patients, below the age of 40 years, attending an emergency care unit complaining of chest pain without obvious organic cause. The results were compared with those for a control group (n = 32). There was no tendency to hyperventilate in the patient group, either after discontinuing hyperventilation or during the ensuing relaxation period. PETCO2 measurements during this time thus showed no significant differences between the patient group and the control group. During the HVPT, 44% of patients reported three or more listed symptoms familiar to them from earlier occasions and regarded as typical of hyperventilation, compared to 23% of the controls (P less than 0.05). In a previously reported study, 38% of the patients were found to have similar symptoms during standardized mental stress, despite lack of hypocapnia. It is concluded that, on the basis of PETCO2 measurements, there were no signs of abnormal hyperventilation in the patient group. Moreover, the HVPT did not appear to be specific for diagnosis of hyperventilation syndrome, since mental stress itself was able to reproduce symptoms without concomitant hypocapnia, and since the provocation test was 'positive' in many control subjects.
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PMID:Acute chest pain without obvious organic cause before the age of 40 years: response to forced hyperventilation. 205 66

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 end tidal partial pressure of carbon dioxide (PCO2) was measured during treadmill exercise in 30 normal controls and 113 patients referred for assessment of chest pain. Among the 92 patients without significant ST depression hypocapnia occurred more often in those reporting "typical" than "atypical" chest pain (17 of 22 patients compared with 29 of 70; p less than 0.01). Hypocapnia was uncommon in patients with significant ST depression whether reporting typical or atypical chest pain (one of 10 patients and two of 11, respectively). Hypocapnia at rest (PCO2 less than 4 kPa) occurred in 16 (14%) patients but in only one control. Hypocapnia occurred during or after exercise in only one control and three of the 21 patients with significant ST depression on exercise (group 1). The remaining 92 patients were divided into those with a history suggestive of hyperventilation (group 2; n = 30) and those without (group 3; n = 62). Hypocapnia developed significantly more often in both these groups (21 and 25 patients respectively) than in controls or patients with significant ST depression. An abnormal response of the PCO2 to exercise provided objective data to support a clinical suspicion of chest pain induced by hyperventilation in 24 cases, suggested a cause for equivocal ST depression other than coronary stenosis in five patients, and led to the diagnosis of previously unsuspected respiratory disease in 14 patients. Measurement of end tidal PCO2 gives additional valuable diagnostic information during the conventional treadmill exercise test in patients with both typical and atypical chest pain.
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PMID:Value of measuring end tidal partial pressure of carbon dioxide as an adjunct to treadmill exercise testing. 313 51

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

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

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


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