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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.
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PMID:Effect of acute hypercapnia on alpha atrial natriuretic peptide, renin, angiotensin II, aldosterone, and vasopressin plasma levels in patients with COPD. 787 53

Obstructive sleep apnoea may be accompanied by various cardiovascular consequences resulting from alteration of the activity of the autonomous nervous system. These changes are mediated by: a--hypoxemia developing during the apnoea, b--severe hypoxemia, hypercapnia and acidosis in postapnoea, c--powerful but ineffective ventilatory efforts causing arousal and stimulation of the cardioexcitatory and vasomotor centres. There are four main pathogenetic mechanisms implementing the cardiovascular changes: 1--Functional alteration in the conduction system and the myocardium resulting in nocturnal cardiac dysrhythmias. 2--Vasoconstriction manifesting as angina pectoris, myocardial infarction, brain attacks and pulmonary or systemic hypertension. 3--Pulmonary congestion leading to cardiac or bronchial asthma or even lung oedema. 4--Neuroendocrine activation, including the sympathetic nervous system, renin-angiotensin-aldosterone system, atrial natriuretic peptide and erythropoietin, which may result in nycturia, nocturnal hypotension and diurnal hypertension.
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PMID:[Mechanisms in the development of cardiovascular complications in obstructive sleep apnea]. 1170 79

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

Water retention and hyponatraemia are typically observed in the final stages of Chronic Obstructive Pulmonary Disease (COPD) and the onset of edema is a poor prognostic factor. For several years the pathogenesis of edema in COPD patients was attributed to heart impairment because of pulmonary hypertension, but the evidence that cardiac output is often adequate for the metabolic demands has suggested, since 1960, that the pathogenesis of edema in these patients would be correlated with gas exchange impairment and in particular with carbon dioxide (CO2) retention. The gas exchange impairment induces, in these patients several hormonal abnormalities: renin (Rn), angiotensin II (AnII), aldosterone (Ald), atrial natriuretic peptide (ANP), vasopressin (ADH) and endothelial factors are some of the factors involved. The systemic response to hypercapnia has the effect of reducing the renal blood flow and, as a result, increasing water and sodium retention with the final effect of edema and hyponatraemia. The aim of this brief review is to highlight the current knowledge on renal/hormonal abnormalities in COPD and their therapeutic implications.
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PMID:Water and sodium imbalance in COPD patients. 1551 Jul 11

The combination of long-term hypercapnia and hypoxia decreases pulmonary vascular remodeling and attenuation of right ventricular (RV) hypertrophy. However, there is limited information in the literature regarding the first stages of acclimatization to hypercapnia/hypoxia. The purpose of this study was to investigate the effect of four-day hypoxia (10% O2) and hypoxia/hypercapnia (10% O2 + 4.4% CO2) on the protein composition of rat myocardium. Expression of the cardiac collagen types and activities of matrix metalloproteinases (MMPs) and of their tissue inhibitor TIMP-1 were followed. The four-day hypoxia changed protein composition of the right ventricle only in the hypercapnic condition; remodeling was observed in the extracellular matrix (ECM) compartments. While the concentrations of pepsin-soluble collagenous proteins in the RV were elevated, the concentrations of pepsin-insoluble proteins were decreased. Furthermore, the four-day hypoxia/hypercapnia increased the synthesis of cardiac collagen due to newly synthesized forms; the amount of cross-linked particles was not affected. This type of hypoxia increased cardiac collagen type III mRNA, while cardiac collagen type I mRNA was decreased. MMP-2 activity was detected on the zymographic gel through appearance of two bands; no differences were observed in either group. mRNA levels for MMP-2 in the RV were significantly lower in both the hypoxic and hypoxic/hypercapnic animals. mRNA levels for TIMP-1 were reduced in the RV of both the hypoxic and hypoxic/hypercapnic animals. Hypoxia with hypercapnia increased the level of mRNA (6.5 times) for the atrial natriuretic peptide (ANP) predominantly in the RV. The role of this peptide in remodeling of cardiac ECM is discussed.
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PMID:Protein remodeling of extracellular matrix in rat myocardium during four-day hypoxia: the effect of concurrent hypercapnia. 1766 May 88

The aim of this study is to evaluate the effect of fetal cardiac bypass on the production and secretion of fetal atrial natriuretic peptide (ANP) in the goat. Eighteen pregnant goats, at days 120 to 140 of gestation, were randomly divided into control (n = 8) and bypass (n = 10) groups. The control group underwent a sham procedure involving fetal sternotomy and cannulation. The bypass group underwent fetal cardiac bypass using a centrifugal pump for 30 min. Fetuses in the bypass group exhibited hypoxia, hypercapnia, and acidosis during and after cardiac bypass. The pulse index (PI) of the umbilical artery in the bypass group increased significantly after cardiac bypass compared with the control group. Tei indices of the left and right ventricles in the bypass group increased remarkably after cardiac bypass. Plasma troponin I levels in the bypass group increased significantly compared with that of the control group. Plasma ANP levels increased markedly in the bypass group after cardiac bypass, and the difference between two groups was significant. Transcriptional levels of ANP mRNA in the fetal heart elevated remarkably in the bypass group compared with the control group at 2 h after the bypass. A significant positive correlation between plasma ANP levels and Tei indices of the ventricles, plasma troponin I was observed (left ventricular Tei index, r = 0.606, P < 0.01; right ventricular Tei index, r = 0.581, P < 0.01; plasma troponin I, r = 0.275, P < 0.05). In conclusion, fetal cardiac bypass promoted the production and secretion of ANP and was associated with fetal cardiac dysfunction.
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PMID:Changes in atrial natriuretic peptide levels during cardiac bypass in the fetal goat. 1913 24

To avoid perioperative cardiac complications and deterioration of renal function in chronic kidney disease (CKD), anesthesiologists are required to manage respiration and circulation properly. Three mechanisms are considered to worsen renal function during inappropriate mechanical ventilation; first, hypercapnia or hypoxemia, second, unstable systemic hemodynamic, and third, systemic inflammatory mediators derived from pulmonary biotrauma. Many circulatory problems are present in CKD patients, for example, hypertension, cardiac hypertrophy, cardiomyopathy, ischemic heart disease, arterial sclerotic valve disease, salt and water retention etc. Blood pressure in CKD patients should be controlled properly before surgery. Renal blood flow and renal perfusion pressure should be maintained by aggressive fluid therapy to avoid perioperative acute kidney injury (AKI) on CKD, while cardiac congestion should also be avoided. Perioerative renal protective effects of human atrial natriuretic peptide (hANP) on CKD still needs further investigation. Appropriate hemodynamic monitoring, including direct arterial pressure, left ventricular preload, intravascular volume and cardiac output could be helpful for anesthesiologists to manage CKD patients safely. In the area of CKD and anesthesia, there is lack of evidence in respiratory and circulatory strategies. Prospective studies in these aspects are required in the future.
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PMID:[Perioperative respiratory and circulatory management for chronic kidney disease]. 2436 72