Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The respiratory effects of analgesia with nalbuphine were studied in 9 patients after thoracotomy. The pain score was measured by a visual analogue scale. Ventilatory pattern and occlusion pressure (P0.1) were studied during spontaneous breathing and during CO2 rebreathing, before and 0.5, 1, 2.5, 3.5 and 6 h after a 0.3-mg.kg-1 dose of intravenous nalbuphine. Compared to baseline values obtained before the injection, nalbuphine produced a decrease in the pain score (p < 0.001) during the 6-hour experiment period. In spontaneous breathing, P.01 was reduced by 15% in 1 h and remained decreased during 3.5 h (p < 0.05), whilst PaCO2 and ventilation (VE) remained unchanged. The P0.1 responsiveness to CO2 was decreased from 0.5 to 2.5 h after the nalbuphine injection (p < 0.05), but the VE responsiveness to CO2 was reduced only after 1 h (p < 0.01). This study shows that, while post-thoracotomy pain was reduced by analgesia, neuromuscular inspiratory drive and chemosensitivity to CO2 were weakened, without any change in spontaneous ventilation. A partial improvement in the thoracopulmonary mechanics induced by the reduction in chest pain could explain the maintenance of ventilatory level in spite of a decreased neuromuscular inspiratory drive.
 ...
PMID:Nalbuphine analgesia preserves ventilation after thoracotomy despite a reduction in inspiratory drive. 143 27

Hyperventilation is of little clinical relevance unless it causes symptoms. These are often non-specific. Their threshold for onset and relation to steady level of arterial (or its equivalent, end-tidal PCO2; PETCO2) are uncertain, and it has been suggested that they may relate better to the rate of fall of PCO2 than to the absolute level. We investigated this in nine normal subjects, who breathed to and fro through a pneumotachograph into an open circuit in which the concentration of CO2 could be varied. Tidal volume, respiratory frequency and ventilation was measured on-line by a Compaq computer, and PETCO2 at the mouth was measured by capnograph. Subjects overbreathed at a fixed rate and depth until symptoms consisting of dizziness, paraesthesiae and light headedness occurred. Then, without their knowledge and while they continued to overbreathe, inspired CO2 was increased to restore PETCO2 to normal and abolish symptoms, and was then withdrawn again over either approximately 0.1, 2.5 or 5 min until symptoms were again reported. The PETCO2 at this point was noted. The three protocols were performed in each subject in a random order and the same symptoms were reported each time. When averaged across all subjects, symptoms occurred at mean PETCO2 values of 20.3, 19.2 and 18.6 mmHg (2.71, 2.56 and 2.48 kPa), respectively. These were not significantly different, and it can be concluded that there was no influence of rate of fall of PCO2 on threshold for symptoms. Chest pain only occurred in one subject and may have a different mechanism.
 ...
PMID:Relation of hypocapnic symptoms to rate of fall of end-tidal PCO2 in normal subjects. 144 88

This article describes validating studies for diagnosing panic disorder in some patients with angiographically normal coronary arteries (NCA) and chest pain. Psychiatric interviews of 94 such patients showed that 34% met the diagnostic criteria for panic disorder. Further studies showed that NCA patients with panic disorder were more disabled at 3.5-year follow-up, had more relatives with panic disorder, were more likely to suffer from major depression, and were more likely to respond to 35% CO2 challenge with panic symptoms. Because panic disorder is highly disabling but responds well to psychological and pharmacologic treatments, screening NCA patients in the cardiology population for this disorder is recommended.
 ...
PMID:Validating studies for panic disorder in patients with angiographically normal coronary arteries. 189 11

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)
 ...
PMID:Chronic pulmonary thromboembolism. 653 60

The aim of this prospective study was to analyse the contribution of the measurement of alveolar arterial gradients of CO2 during forced expiration in the diagnosis of pulmonary emboli occurring in chronic airflow obstruction (COPD) as a result of smoking. The study was carried out on 178 patients: Group 1: 54 subjects without emboli (14 controls, 33 COPD and 7 patients with chest pain); Group 2: 72 patients with proved emboli (49 non COPD, 23 COPD); Group 3: 52 patients COPD presenting with varied non-embolic broncho-pulmonary pathology (pneumonia, bronchospasm, pulmonary oedema, bronchial neoplasm). The diagnosis of pulmonary emboli was confirmed by scintigraphy in patients with non COPD or angiography (in patients with COPD). The maximal fraction of CO2 was measured using a capnologue during a forced expiration which was long and prolonged until residual volume was achieved. The PaCO2 was measured simultaneously by an analysis of arterial blood gases. The D index was calculated according to the formula [(PaCO2-PEM CO2)/PaCO2] x 100. The D index was significantly lower in Group 1 (3.42 +/- 3.8% p < 0.0001) than in Group 2 (20.8 +/- 10%) and Group 3 (17.6 +/- 11.7%) (not significant between Groups 2 and 3). In patients with COPD the specificity and sensitivity and the predicted positive and negative value were 100% for a D limit of 7%. In COPD patients these values were respectively 82, 95, 75 and 96% for a D limit of 7%; on the other hand for a D below 5% the values were 60, 100, 64 and 100% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The significance of maximal expiratory concentrations of CO2 (MEC CO2) in the negative diagnosis of acute pulmonary embolism in chronic obstructive bronchopneumopathies]. 789 65

Using non-invasive monitors (such as blood pressure, O2 saturation, end-tidal CO2 pressure monitors and electrocardiograms), the application of total intravenous anesthesia with O2 mask in transthoracic endoscopic sympathectomy was evaluated. A total of 198 palmar hyperhidrosis patients were studied. In the study, the durations of surgery were 5-15 min (mean 8 min) with anesthesia duration of 8-20 min (mean 12 min), respectively. The cardiovascular system was quite stable during operation, with systolic blood pressures of 90-165 mmHg (mean 132 mmHg), diastolic blood pressures of 50-106 mmHg (mean 92 mmHg) and heart rates of 56-130 beats/min (mean 104 beats/min). The respiratory function was maintained within a safety range with O2 saturation of 95-100% (mean 99%) and end-tidal CO2 pressure of 32-40 mmHg (mean 36 mmHg). After surgery, the major discomfort was chest pain (132/198), but this could be improved with intravenous analgesics. Patients' consciousness returned within 1-3 min. After ensuring their general condition was stable, patients were discharged within 24 hr. Preliminary study showed that total intravenous anesthesia plus muscle relaxant, with O2 mask and assisted ventilation, could serve as a safe and simple anesthesia for palmar hyperhidrosis patients who received transthoracic endoscopic sympathectomy.
 ...
PMID:[Total intravenous anesthesia with O2 mask in transthoracic endoscopic sympathectomy for palmar hyperhidrosis]. 829 42

A 42-year-old man with one year history of cough and chest pain due to right upper lung cancer was scheduled for radical surgery. An echocardiogram and a lung scan showed a tumor mass in the left atrium, which was originating from carcinoma of the right upper lobe. Right pneumonectomy and atrial tumor extirpation were done successfully under the state of cardiac arrest using extracorporeal circulation with topical cooling by crushed ice in order not to spread the tumor cells into systemic circulation. He was extubated on the 1st postoperative day. But, thereafter he developed moderate dyspnea. On 7, 10 and 13th postoperative days he fell into the state of CO2 narcosis. Decreased capacity of the lung after the pneumonectomy and left phrenic nerve injury during the operation were considered factors causing the respiratory insufficiency. Patient was discharged 6 weeks later and continued to have consultations at the outpatient clinic.
 ...
PMID:[Extracorporeal circulation for removal of carcinoma of the lung invading the left atrium]. 858 64

Cardiopulmonary and radionuclear indices were used to evaluate and compare cardiac function during exercise testing in patients with symptomatic and silent ischemia. The study comprised 58 patients aged 35-74 years, divided into three groups: Group I-20 patients (controls) with neither ST depression nor chest pain; Group II-22 patients with ST depression > 1 mm and no chest pain; Group III-16 patients with both ST depression and chest pain. All patients in Groups II and III demonstrated significant coronary artery disease. No antianginal medication was taken at least 24 h before testing. All patients underwent a cardiopulmonary exercise test and a multigated acquisition radionuclear study. The following variables were measured: oxygen consumption (VO2), CO2 output (VCO2), minute ventilation (VE), O2-pulse, ventilatory anaerobic threshold (VAT), left ventricular ejection fraction (LVEF) at rest (r) and at maximal effort (ex). Probability values were significant for all variables (P < 0.01-0.0001) except left ventricular ejection fraction-rest (P not significant between the three groups). No significant differences in extent of coronary artery disease were noted between Groups II and III. These findings suggest that during exercise testing patients with silent ischemia have better overall cardiac function than patients with symptomatic ischemia. Their value for both cardiopulmonary and radionuclear indices are closer to those of the control group than to the symptomatic group, regardless of the severity of the coronary artery disease Summary of results: (mean +/- 1 S.D.) Group VO2-max O2-Pulse max VAT (%) VAT (ml/min) LVEF-rest delta LVEF (ex-r) I 25.2 +/- 6.3 15.7 +/- 3.4 51.2 +/- 6.6 1075 +/- 289 54.7 +/- 7 5.4 +/- 4.85 II 22.4 +/- 2.8 14.5 +/- 2 47.0 +/- 5.3 854 +/- 136 52 +/- 10 1.2 +/- 6.7 III 16.0 +/- 2.5 11.4 +/- 2 41.6 +/- 7.7 683 +/- 105 51 +/- 8.5 -5.87 +/- 6.3
 ...
PMID:Contribution of cardiopulmonary indices in the assessment of patients with silent and symptomatic ischemia during exercise testing. 879 79

1. Chest pain caused by myocardial ischaemia is mediated by cardiac sympathetic afferents. The mechanisms of activation of cardiac afferents during ischaemia remain poorly understood. Increased lactic acid production is associated closely with myocardial ischaemia. The present study examined the role of protons generated during ischaemia in activation of cardiac sympathetic C-fibre afferents. 2. Single-unit activity of cardiac afferents innervating both ventricles was recorded from the left sympathetic chain in anaesthetized cats. Epicardial tissue pH was measured within 1-1.5 mm of the surface by a pH-sensitive needle electrode. Responses of cardiac afferents to myocardial ischaemia, lactic acid, sodium lactate, acidic phosphate buffer and hypercapnia were determined. 3. Occlusion of the coronary artery for 5 min decreased epicardial tissue pH from 7.35 +/- 0.21 to 6.98 +/- 0.22 (P < 0.05). Epicardial placement of isotonic neutral phosphate buffer, but not saline, prevented the ischaemia-induced decrease in epicardial pH. This manoeuvre significantly attenuated the response of 16 afferents to 5 min of ischaemia (1.56 +/- 0.23 pre-treatment vs. 0.67 +/- 0.18 impulses s-1). Topical application of 10-100 microg ml-1 of lactic acid, but not sodium lactate, concentration-dependently stimulated 18 cardiac afferents. Inhalation with high-CO2 gas failed to activate 12 separate cardiac afferents. Furthermore, lactic acid stimulated cardiac afferents to a greater extent than acidic phosphate buffer solution, applied at a similar pH to the same afferents. 4. Collectively, this study provides important in vivo evidence that protons contribute to activation/sensitization of cardiac sympathetic C-fibre afferents during myocardial ischaemia.
 ...
PMID:Role of protons in activation of cardiac sympathetic C-fibre afferents during ischaemia in cats. 1042 20

The prevalence of panic disorder in patients who present with chest pain or palpitations to a First Heart Aid setting varies in the literature between 0%-59%. In a high percentage of cases, panic disorder is not recognized by the cardiologist in patients who present initially with chest pain or palpitations. Patients with panic disorder have a large and ongoing medical consumption. A selective serotonin reuptake inhibitor and/or cognitive therapy appear to be good treatment of panic disorder in patients who present initially with chest pain or palpitations. A CO2 challenge test elicits the symptoms in patients with panic disorder with high sensitivity and specificity but this test has not been validated in patients who present initially with chest pain or palpitations and in whom the diagnosis 'panic disorder' is not yet established.
 ...
PMID:[Panic disorder in patients with chest pain and palpitations: an often unrecognized relationship]. 1081 42


1 2 Next >>