Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute dyspnea represents a diagnostic challenge even for the experienced physician. There are no prospectively evaluated diagnostic algorithms dealing with this frequent clinical problem. First of all, the emergency has to be assessed and life supporting measures have to be considered. In addition to a thorough medical history and clinical examination, chest X-ray, spirometry, ECG, hemoglobin measurement, BNP and D-dimer testing represent valuable diagnostic tools and are available to GP's. Most commonly, acute dyspnoea is pulmonary or cardiac in origin. Up to one third of all cases will have several causes. Functional dyspnea is difficult to diagnose but should be taken into consideration after excluding any somatic cause. Hyperventilation is found in both, organic and non organic diseases, and is therefore an inappropriate criterion to differentiate between the two. The mainstay in the management of any symptom is to primarily treat the underlying disease. A significant hypoxemia (SO2 < 90%, pO2 < 60 mmHg) ought to be corrected by supplemental oxygen. It is inappropriate to withhold oxygen from patients with COPD and severe hypoxemia just to avoid hypercapnia. Besides oxygen, opiates efficiently relief dyspnoea but harbour the risk of respiratory depression, altered mental status or aspiration.
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PMID:[Acute dyspnea--what should I not forget?]. 1599 36

Increased chemosensitivity has been observed in HF (heart failure) and, in order to clarify its pathophysiological and clinical relevance, the aim of the present study was to investigate its impact on neurohormonal balance, breathing pattern, response to exercise and arrhythmic profile. A total of 60 patients with chronic HF [age, 66+/-1 years; LVEF (left ventricular ejection fraction), 31+/-1%; values are means+/-S.E.M.] underwent assessment of HVR (hypoxic ventilatory response) and HCVR (hypercapnic ventilatory response), neurohormonal evaluation, cardiopulmonary test, 24-h ECG monitoring, and assessment of CSR (Cheyne-Stokes respiration) by diurnal and nocturnal polygraphy. A total of 60% of patients had enhanced chemosensitivity. Those with enhanced chemosensitivity to both hypoxia and hypercapnia (i.e. HVR and HCVR), compared with those with normal chemosensitivity, had significantly (all P<0.01) higher noradrenaline (norepinephrine) and BNP (B-type natriuretic peptide) levels, higher prevalence of daytime and night-time CSR, worse NYHA (New York Heart Association) class and ventilatory efficiency [higher VE (minute ventilation)/VCO(2) (carbon dioxide output) slope], and a higher incidence of chronic atrial fibrillation and paroxysmal non-sustained ventricular tachycardia, but no difference in left ventricular volumes or LVEF. A direct correlation was found between HVR or HCVR and noradrenaline (R=0.40 and R=0.37 respectively; P<0.01), BNP (R=0.40, P<0.01), N-terminal pro-BNP (R=0.37 and R=0.41 respectively, P<0.01), apnoea/hypopnoea index (R=0.57 and R=0.59 respectively, P<0.001) and VE/VCO(2) slope (R=0.42 and R=0.50 respectively, P<0.001). Finally, by multivariate analysis, HCVR was shown to be an independent predictor of both daytime and night-time CSR. In conclusion, increased chemosensitivity to hypoxia and hypercapnia, particularly when combined, is associated with neurohormonal impairment, worse ventilatory efficiency, CSR and a higher incidence of arrhythmias, and probably plays a central pathophysiological role in patients with HF.
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PMID:Clinical significance of chemosensitivity in chronic heart failure: influence on neurohormonal derangement, Cheyne-Stokes respiration and arrhythmias. 1796 Nov 23

Central sleep apnea is highly prevalent in association with heart failure, some neurological diseases and chronic opioids use. There are two main categories of central sleep apnea respectively related with different underlying conditions. Some hypocapnic patients exhibit respiratory control system instability and central apnea occurs when PaCO(2) falls below the threshold for apnea during sleep. The other group are patients with chronic hypercapnia mainly in the context of neuromuscular disorders or obesity hypoventilation syndrome. All these patients should be assessed by recording blood gases, polysomnography and ventilatory responses to CO(2). Cardiologic assessment should include pro-brain natriuretic factor (pro-BNP) and cardiac echography whereas neurological examination requires brain imaging and/or electromyography. Ventilatory supports used for treating central sleep apnea are non-invasive ventilation and servo-assisted ventilation in hypercapnic and hypocapnic patients respectively.
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PMID:[Management of central sleep apnea]. 1978 53