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

Friedreich's Ataxia (F.A.) is a degenerative disease which commonly leads to premature death of cardiorespiratory origin. To explain the early death of these patients, previous investigations have established the existence of 1) a cardiomyopathy in nearly 100% of cases, 2) a restrictive pulmonary syndrome of scoliotic origin and 3) a mild hypoxemia associated with slight respiratory alkalosis and a normal oxyhemoglobin dissociation curve. To further assess the cause of early death in patients with such neuromyopathy, we evaluated, in eleven F.A. patients, the sensitivity of the respiratory centers to hypercapnia, hypoxia, and hyperoxia. Ventilatory (VE, VT, F, VT/Ti) and occlusion pressure (P0.1) responses were taken as indices of the respiratory centers output during progressive hypercapnia (Read's method) and isocarbic hypoxia (Weil's method). We studied 11 Friedreich's Ataxia patients and 11 age, sex, and armspan matched controls. The responses of patients to hypercapnia were significantly greater than controls but their responses to hypoxia were similar to controls. Our study establishes that the respiratory centers are functioning adequately in early Friedreich's Ataxia and do not contribute to cardio-respiratory insufficiency in such neuromyopathy.
 ...
PMID:Regulation of respiration in Friedreich's ataxia. 48 4

The purpose of this investigation was to examine the effects of norepinephrine cardiomyopathy (NE-CM) on left ventricular (LV) performance in diabetic rabbits. Diabetes mellitus was produced in 11 rabbits by giving them alloxan monohydrate, 120 mg/kg. Cardiomyopathy was produced in five animals by a 90-min infusion of norepinephrine (2 micrograms/min/kg). Left ventricular contractility and pump function (VF) were examined 2 days later. The effects of hypercapnia and inotropic responsiveness to NE were also determined. VF was assessed by means of left ventricular function curves obtained with constant mean aortic pressure and heart rate and quantified by determining stroke volume (SV) at a left ventricular pressure of 10 cm H2O (SV10). Mean SV10 was 1.22 +/- 0.08 ml in control diabetics but averaged only 0.95 +/- 0.08 ml in diabetics with NE-CM (P less than 0.05). NE-CM markedly reduced LV dP/dt max responses to NE infusion but the increments in SV10 did not differ. Hypercapnia caused significantly greater ventricular depression in NE-CM than in control diabetic rabbits (P less than 0.001). The depressive effect of hypercapnia can be countered in part by the administration of NE in both groups, but differential depression in VF to hypercapnia was persistent between the two groups.
 ...
PMID:Ventricular performance in diabetic rabbits with norepinephrine cardiomyopathy. 394 45

Catecholamine cardiomyopathy (CM) was produced in rabbits by a 90-min infusion of norepinephrine (NE, 2 micrograms . kg-1 . min-1). Left ventricular (LV) contractility and pump function (VF) were examined 2 days later and compared with control animals. The effects of hypercapnia [CO2 tension (PCO2) greater than 70 mmHg] and inotropic responsiveness to NE were also determined. VF was assessed by means of left ventricular function curves obtained with constant aortic pressure and heart rate and quantified by determining stroke volume at left ventricular end-diastolic pressure of 10 cmH2O (SV10). Mean SV10 was 1.16 +/- 0.06 ml in controls but averaged only 0.93 +/- 0.05 in CM (P less than 0.02). Hypercapnia caused significantly greater depression of VF in CM than in controls. NE dose-response curves demonstrated increases in both LV dP/dtmax and SV10 in each group. The percent increase in LV dP/dtmax was markedly attenuated n CM, but the increments in SV10 did not differ. The mean histological score in the CM animals was 1.6 +/- 0.1, indicating extensive myofiber injury. No histological abnormalities were observed in the controls. Thus functional defects correlated with the presence of histopathological changes. In addition, a dissociation of velocity (dP/dtmax) and force (SV10) responsiveness to inotropic stimulation was identified in the CM group.
 ...
PMID:Ventricular function in norepinephrine-induced cardiomyopathic rabbits. 706 51

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
 ...
PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

Pulmonary hypertension (PH), defined as a mean pulmonary artery pressure greater than 25 mm Hg, is not a diagnosis, but rather the physiologic consequence of the interaction between pulmonary blood flow, pulmonary vascular impedance, and downstream pulmonary venous pressure. The diagnosis and appropriate treatment of PH in patients with or without heart failure (HF) requires an understanding of the underlying pathogenesis, whether it be due to increased pulmonary venous pressure, increased pulmonary vascular resistance (PVR), increased pulmonary blood flow, or a combination thereof. Furthermore, an explanation for the underlying cause must also be sought. For example, a rise in pulmonary venous pressure may relate primarily to an increase in left ventricular end-diastolic pressure in a patient with a known cardiomyopathy; however, it may be complicated by severe mitral regurgitation. Similarly, an increased PVR may reflect reactive changes in the pulmonary vasculature due to long-standing pulmonary venous hypertension, concomitant hypoxemia/hypercapnia, or it may be the harbinger of chronic thromboembolic disease. It is imperative that reversible causes of PH be considered. Although most often diagnosed by Doppler echocardiography, full hemodynamic characterization of PH requires right heart catheterization to measure biventricular filling pressures and PVR. Integration of invasive pulmonary hemodynamics with an assessment of right ventricular function is essential to appreciate the clinical and prognostic significance of PH of an individual patient. Right heart catheterization is not practically feasible in all patients with HF and PH; however, at a minimum it should be performed in patients with a Doppler-estimated pulmonary artery pressure greater than 60 mm Hg, those who present clinically with predominant right HF, significant mitral valve disease, and in particular, patients with impaired right ventricular function.
 ...
PMID:Approach to patients with heart failure and pulmonary hypertension. 1776 Nov 15

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.
 ...
PMID:[Perioperative respiratory and circulatory management for chronic kidney disease]. 2436 72

Sleep-disordered breathing in neuromuscular diseases is due to an exaggerated reduction in lung volumes during supine sleep, a compromised physiologic adaptation to sleep, and specific features of the diseases that may promote upper airway collapse or heart failure. The normal decrease in the rib cage contribution to the tidal volume during phasic REM sleep becomes a critical vulnerability, resulting in saw-tooth oxygen desaturation possibly representing the earliest manifestation of respiratory muscle weakness. Hypoventilation can occur in REM sleep and progress into non-REM sleep, with continuous desaturation and hypercarbia. Specific characteristics of neuromuscular disorders, such as pharyngeal neuropathy or weakness, macroglossia, bulbar manifestations, or low lung volumes, predispose patients to the development of obstructive events. Central sleep-disordered breathing can occur with associated cardiomyopathy (e.g., dystrophies) or from instability in the control of breathing due to diaphragm weakness. Mitigating factors such as recruitment of accessory respiratory muscles, reduction in REM sleep, and loss of normal REM atonia in some individuals may partially protect against sleep-disordered breathing. Noninvasive ventilation, a standard-of-care management option for sleep-disordered breathing, can itself trigger specific sleep-disordered breathing events including air leaks, patient-ventilator asynchrony, central sleep apnea, and glottic closure. These events increase arousals, reduce adherence, and impair sleep architecture. Polysomnography plays an important role in addressing pitfalls in the diagnosis of sleep-disordered breathing in neuromuscular diseases, identifying sleep-disordered breathing triggered by noninvasive ventilation, and optimizing noninvasive ventilation settings.
...
PMID:Sleep-disordered Breathing in Neuromuscular Disease. 2572 31

Respiratory failure affects up to 0.2% of pregnancies, more commonly in the postpartum period. Altered maternal respiratory physiology affects the assessment and management of these patients. Respiratory failure may result from pregnancy-specific conditions such as preeclampsia, amniotic fluid embolism or peripartum cardiomyopathy. Pregnancy may increase the risk or severity of other conditions, including thromboembolism, asthma, viral pneumonitis, and gastric acid aspiration. Management during pregnancy is similar to the nonpregnant patient. Endotracheal intubation in pregnancy carries an increased risk, due to airway edema and rapid oxygen desaturation following apnea. Few data are available to direct prolonged mechanical ventilation in pregnancy. Chest wall compliance is reduced, perhaps permitting slightly higher airway pressures. Optimizing oxygenation is important, but data on the use of permissive hypercapnia are limited. Delivery of the fetus does not always improve maternal respiratory function, but should be considered if benefit to the fetus is anticipated.
...
PMID:Acute respiratory failure in pregnancy. 2751 67

Pompe disease is an autosomal-recessive lysosomal storage disorder characterized by progressive myopathy with proximal muscle weakness, respiratory muscle dysfunction, and cardiomyopathy (in infants only). In patients with juvenile or adult disease onset, respiratory muscle weakness may decline more rapidly than overall neurological disability. Sleep-disordered breathing, daytime hypercapnia, and the need for nocturnal ventilation eventually evolve in most patients. Additionally, respiratory muscle weakness leads to decreased cough and impaired airway clearance, increasing the risk of acute respiratory illness. Progressive respiratory muscle weakness is a major cause of morbidity and mortality in late-onset Pompe disease even if enzyme replacement therapy has been established. Practical knowledge of how to detect, monitor and manage respiratory muscle involvement is crucial for optimal patient care. A multidisciplinary approach combining the expertise of neurologists, pulmonologists, and intensive care specialists is needed. Based on the authors' own experience in over 200 patients, this article conveys expert recommendations for the diagnosis and management of respiratory muscle weakness and its sequelae in late-onset Pompe disease.
 ...
PMID:Practical Recommendations for Diagnosis and Management of Respiratory Muscle Weakness in Late-Onset Pompe Disease. 2776 17

Respiratory failure affects up to 1 in 500 pregnancies, more commonly in the postpartum period. The causes of respiratory failure include several pregnancy-specific conditions such as preeclampsia, amniotic fluid embolism, and peripartum cardiomyopathy. Pregnancy may also increase the risk or severity of other conditions, such as asthma, thromboembolism, viral pneumonitis, and gastric acid aspiration. Changes to maternal respiratory physiology and the presence of a fetus may affect the assessment and management of these patients. In addition to identifying pregnancy-specific causes, some differences exist in the management of the pregnant woman with acute respiratory failure. Endotracheal intubation in pregnancy carries a significant risk, due to upper airway edema and rapid oxygen desaturation following apnea. Few studies have addressed prolonged mechanical ventilation management in pregnancy. Optimizing oxygenation is important, but whether permissive hypercapnia is tolerated during pregnancy remains unclear. Delivery of the fetus is often considered but does not always improve maternal respiratory function and should be reserved only for cases where benefit to the fetus is anticipated.
 ...
PMID:Management of Acute Respiratory Failure in Pregnancy. 2856 Dec 51


1