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)

Thirty-five asthmatic patients (average age 28 years) who attended a pulmonary function laboratory when their mean ratio of forced expiratory volume in one second: forced vital capacity was 81 per cent (within the normal range for their age group) had arterial hypoxaemia and hypocapnia. These were probably secondary to lung hyperinflation and pulmonary ventilation/perfusion imbalance. The pulmonary abnormalities of bronchial asthma are not always detected by simple spirometric tests and the results of such tests should be interpreted cautiously.
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PMID:Pulmonary function in asthmatic patients in remission. 23 66

The Asthma Symptom Checklist (ASC), describing the subjective symptoms reported to occur during asthmatic attacks, has been developed previously. In the present study, the ASC key cluster solution was replicated and refined within a sample of 374 asthmatic inpatients. All of the original symptom categories were reporduced, including two mood categories, Panic-Fear and Irritability, a Fatigue category, and two somatic categories. Hyperventilation-Hypocapnia and Airway Obstruction. Two refinements were notable: (1) The Airway Obstruction category was empirically divided into two conceptually clear components, Dyspnea anc Congestion, and (2) three secondary mood categories, Worry, Loneliness, and Anger, were identified, which describe a continuum of mood between the polar extremes of panic and irritability. Of the symptom categories, only Panic-Fear was related to the intensity of the discharge drug regimens recommended 2 to 6 mouths after ASC administration. Panic-Fear scores were independent of pulmonary function measurements. A combined index based on pulmonary functions and panic-fear yielded the best prediction of discharge steroid regiments. Finally, those physicians rated highest in "sensitivity" to their patients by their supervisors prescribed less steroids overall, but most frequently prescribed discharge steriod regimens in relation to their patients' Panic-Fear scores. In contrast, physicians rated lower on sensitivity prescribed higher steroid regimens overall, but based these drug recommendations more cleary on objective pulmonary functioning, and not in relation to their patients' Panic-Fear scores. The results strongly suggest that the ASC Panic-Fear scale is associated with coping behaviors that importantly affect the patient's overall clinical picture by increasing the apparent severity of the asthma, thereby leading to intensified treatment. The findings stress the need to evaluate independently the objective medical condition and subjective symptomatology with its related coping behavior, in order to direct appropriate modes of therapy to each.
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PMID:Obervations on subjective symptomatology, coping behavior, and medical decisions is asthma. 40 66

The purpose of this investigation was to assess the relative contributions of hyperpnea and hypocapnia in the induction of postexercise asthma. To achieve these ends, eight young asthmatics were exercised on a treadmill while minute ventilations (VE) and end-tidal CO2 (PET CO2) tensions were continuously recorded. The subjects were then restudied using a partial rebreathing technique that allowed separation of minute and alveolar ventilations so that independent evaluations could be made of the relative effects of bulk airflow on pulmonary mechanics as well as a systematic study of hypocapnia in a dose-response fashion. Sustained hyperpnea with VEidentical to those recorded during exercise was totally without effect when the mean PET CO2 was isocapnic or lowered to approximately 30 Torr. Reduction in PETCO2 to 21.3 +/-0.9 Torr brought about significant changes in mechanics, but in every variable measured, exercise produced the greatest alterations and did so at PETCO2 values that had no effect when studied in a controlled fashion. Consequently, neither high VE per se, nor hypocapnia can be considered as the mechanisms underlying exercise induced asthma.
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PMID:Relative contributions of hypocarbia and hyperpnea as mechanisms in postexercise asthma. 83 72

Exercise-induced bronchospasm (EIB) in some cases of asthma is related to hypocapnia, hypoxemia, and acidosis, but studies have shown that children do not develop as abnormal PCO2, PO2, or pH levels with the induction of EIB. Gradient changes of alveolar-arterial oxygen differences reveal ventilation perfusion abnormalities existing at the onset of exercise in those patients who do develop EIB.
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PMID:Blood gas in exercise-induced bronchospasm: a review. 118 78

Forty adult patients with acute severe asthma were assessed for arterial blood gases and acid-base changes at presentation at the Casualty Unit, Kenyatta National Hospital, Nairobi, Kenya. Marked degrees of hypoxaemia (mean P(a)O2 of 8.02 kP(a)), hypocapnia (mean P(a)CO2 of 4.62kP(a)) with apparently normal pH (mean 7.384) were documented in the majority of these patients. Based on these findings, a significant number of the patients (68.5%) were either candidates (5.3%) or potential candidates (63.2%) for artificial ventilation. Records at this hospital suggest an increasing trend in asthma admissions and mortality. Additionally, Intensive Care Unit (ICU) admissions for asthma are associated with high mortality (54.4%). Pulsus paradoxicus emerged as the most significant (p = 0.002) clinical correlate to asthma severity. Central cyanosis was detected in none of the study patients suggesting that it is an unusual finding in the common presentation of acute severe asthma at this hospital. Its clinical detection would therefore imply an ominous clinical state. It is recommended that clinicians should take every opportunity to adequately assess their asthma patients before prescribing medications. They are also encouraged to more frequently request for blood gas studies in acute asthma. Those in charge of clinical teaching should direct appropriate efforts towards improved understanding of the pathophysiology and interpretation of acid-base disorders.
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PMID:Arterial blood gases and acid-base status of adult patients presenting with acute severe asthma at Kenyatta National Hospital, Nairobi. 150 18

The purpose of this study was to compare psychologic and physiologic variables during intense dyspnea to those at times of no or low dyspnea in people with asthma. Thirty-six adults ranging from 19 to 76 years old were tested when they first came to the emergency department in acute dyspnea and again when they had no or low dyspnea just prior to discharge. Clinical signs found to be higher during high dyspnea than low dyspnea were respiratory rate, pulse, wheezing, and accessory muscle use. Peak expiratory flow rates and oxygen saturation were significantly lower, while anxiety, depression, somatization, and hostility were higher during times of high dyspnea. The panic/fear, fatigue, dyspnea, hyperventilation/hypocapnia, congestion, and rapid breathing subscales of the Asthma Symptom Checklist were also higher during high dyspnea compared to low dyspnea.
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PMID:Psychologic and physiologic aspects of acute dyspnea in asthmatics. 185 43

Airflow-induced bronchoconstriction (AIB) may be initiated in asthmatic patients by inhaling dry air during eucapnic hyperventilation or exercise. Hypertonic aerosol-induced bronchoconstriction (HIB) also occurs in these patients, but it differs from AIB by exhibiting a faster time course. Although AIB and HIB probably increase airway fluid osmolality, only AIB is associated with airway cooling. In light of the similarities between our canine model and human AIB, we examined peripheral airway responses to dry air and hypertonic aerosol challenge. Specifically, we studied the magnitude and time course of these responses in an in situ, isolated, perfused lobe in which airway temperature was independently controlled. At body temperature, HIB peaked immediately after challenge, whereas transient airway cooling during aerosol challenge delayed HIB. In contrast, airway cooling attenuated AIB but did not alter its time course. Hypocapnia- and histamine-induced responses were not affected by airway cooling, suggesting that smooth muscle function was not impaired. To the extent that the mechanisms producing AIB in dogs and in humans are similar, our results suggest that (1) changes in airway fluid osmolality initiate AIB, (2) AIB = HIB + Cooling, and (3) exercise-induced asthma results from an imbalance between an excitatory pathway stimulated by airway drying and an inhibitory pathway initiated by airway cooling.
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PMID:Transient airway cooling modulates dry-air-induced and hypertonic aerosol-induced bronchoconstriction. 185 61

We report the case of an 82-year old male patient without history of chronic obstructive lung disease in whom a sudden respiratory distress syndrome with sibilant rales in both lungs revealed a moderately severe pulmonary embolism, later confirmed by angiography. Bronchospasm occurring in the acute phase of pulmonary embolism may be expressed as acute asthma refractory to bronchodilators. This bronchoconstriction, seldom detectable clinically, seems to be related to regional alveolar hypocapnia in the territories embolized and to platelet-produced mediators, through a vagus nerve-mediated reflex. It must not hide pulmonary embolism, particularly in a suggestive context and when bronchodilators are ineffective.
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PMID:[Bronchospasm disclosing pulmonary embolism]. 207 66

There has been considerable interest over the last years in gas exchange abnormalities that occur in patients with bronchial asthma, particularly during an acute attack. These are essentially characterized by moderate to severe hypoxemia and hypocapnia caused by considerable ventilation-perfusion (VA/Q) mismatch. Using the multiple inert gas elimination technique, the baseline pattern of VA/Q distribution reveals a bimodal bloodflow distribution of VA/Q ratios but no shunt. Inhaled salbutamol seems to be an efficient and safe therapeutic approach, owing to the lack of deleterious effect on VA/Q inequality. Following intravenous salbutamol there is development of further VA/Q mismatch for the same degree of bronchodilation, the resulting deleterious effect on PaO2 being offset by the improvement in mixed venous PO2 due to increased cardiac output.
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PMID:Gas exchange abnormalities in asthma. 211 69

Asthmatics seeking emergency care for severe acute asthma may show metabolic acidosis. We sought to determine the frequency of metabolic acidosis in such patients and to assess the relative contributions of renal bicarbonate loss and lactic acid accumulation to this acidosis. Twenty-two asthmatics (21-71 yr; four males, and 18 females) who came consecutively to the emergency department with severe acute asthma were studied. Most patients reported that their asthmatic symptoms had begun to worsen greater than or equal to 2 days before the emergency department visit. Within several hours, simultaneous measurements of arterial blood gases, whole blood lactate, and serum electrolytes were made. Ten of 22 patients were found to have metabolic acidosis (base deficit greater than 2 mEq/L). All ten patients had nonanion gap acidosis, while nine of ten had whole blood lactate values in the normal range (0.33 to 2.55 mmol/L). In the one patient with an elevated whole blood lactate level, the concentration of lactate in excess of normal (0.45 mmol/L) could not account for the magnitude of the base deficit (-4.9 mEq/L). We conclude that a) nonanion gap metabolic acidosis is very common in asthmatics with acute severe asthma (prevalence 45% in our series), and b) the mechanism of the base deficit in these patients is excessive renal bicarbonate excretion. We believe that the latter occurs as a renal compensatory response to a preceding period of hypocapnia due to hyperventilation related to worsening asthma.
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PMID:Metabolic acidosis not due to lactic acidosis in patients with severe acute asthma. 367 62


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