Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with heart failure are known to demonstrate periodic respiration during sleep. The mechanism behind periodic respiration is thought to be related to left heart enlargement causing an increased transit time between lung and chemoreceptors leading to an oscillation of the feed back loop controlling respiration. Additionally hyperventilation was shown to play an important role. We report of an 18 year old patient with idiopathic dilated cardiomyopathy (left atrial 52 mm, left ventricular end diastolic diameter 69 mm). Polysomnography revealed prolonged transit time and periodic respiration with impaired sleep. Hypocapnia and hyperventilation was demonstrated. Following successful cardiac transplantation periodic respiration was absent and transit time was normal. There was no hypocapnia or hyperventilation. Hypercapnic ventilatory response did no change. These findings support the model of an oscillation of the feed back loop controlling respiration as the main pathomechanism behind periodic respiration.
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PMID:[Elimination of periodic respiration in heart failure by heart transplantation]. 767 58

A 62 year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation of provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary ventilation. Progesterone (200 mg/d during 3 weeks) or naloxone did not improve either arterial blood gases (ABG) or the P 0.1/PCO2 curve. Hypoxemia and hypercapnia were not corrected during metabolic acidosis provoked by acetazolamide (250 mg/d). Nasal CPAP did not control hypoventilation periods. Mechanical ventilation was initiated with negative pressure (NPV) through a poncho. The patient presented severe discomfort with NPV and obstructive apneas were verified during it. She refused to continue NPV. Mechanical ventilation was initiated with positive intermittent pressure (IPPV) through a nasal mask. The patient had excellent tolerance to the procedure. SpO2 during IPPV was always higher than 95%. During sleep induction (under IPPV), respiration in phase with the ventilator 1: 1 was observed; instead, during consolidated sleep there was a complete dependence of the ventilator with apnea for over 2 min when IPPV was interrupted (Fig. 1). After 2 months of treatment, a relief of right ventricular failure occurred and hematocrit fell to 39%. There was an improvement of day-time ABG (Table I). The P. 0.1/PaCO2 curve 3 months after IPPV was the same as the previous one (Fig. 2). The patient has been for 18 months on home ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central alveolar hypoventilation with cor pulmonale: successful treatment by non-invasive intermittent positive pressure ventilation]. 771 33

Fenoldopam (FE), a dopamine DA1-receptor agonist, has been introduced for treatment of arterial hypertension and heart failure and for preservation of renal function. Vasodilators are generally assumed to affect all vascular beds including the cerebral circulation. We have evaluated effects of FE-induced (4 micrograms.kg-1.min-1) arterial hypotension on intracranial pressure (ICP) and intraocular pressure (IOP) under conditions of normal and increased intracranial elastance. ICP and IOP responses to hypertension were tested by infusion of angiotensin II (15 micrograms.kg-1.min-1), and the response to hypercapnia was tested by elimination and reintegration of soda lime canisters in the breathing circuit. Intracranial elastance was increased by infusing mock cerebrospinal fluid (CSF) into the lateral ventricle (20 +/- 3 ml.h-1). Arterial hypotension induced with FE did not increase ICP. With increased intracranial elastance, the infusion rate of mock CSF had to be reduced while administering FE to avoid a rise in ICP (p < 0.05 compared with preinfusion value); this indicates a shift on the volume-pressure curve to the right. There were no indicators that cerebral autoregulation or CO2 reactivity of the cerebral vasculature were affected by FE in this anesthetized porcine model, as speculated from analysis of the time course of delta ICP. There are, however, indicators of increased intracranial elastance, most likely caused by vasodilation. Caution should hence be exercised when FE is administered to patients with increased intracranial elastance.
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PMID:Effects of fenoldopam on intracranial pressure and hemodynamic variables at normal and elevated intracranial pressure in anesthetized pigs. 791 22

The abdominal pressure is a hydrostatic one, which can be measured in the bladder, the rectum and the stomach. In physiologic conditions, the abdominal pressure is variable, with peaks as high as 100 to 200 mmHg at the time of defecation, cough. The increase in abdominal pressure elicited by abdominal distension or compression acts directly on the abdominal compartment, indirectly on the thoracic compartment, and modifies the circulation and the ventilation. Venous return is decreased as the inferior vena cava is compressed. The systemic resistances are also increased as the abdominal vessels are compressed. Therefore the circulation is mainly distributed to the superior part of the body. Although the cardiac output is decreased, the usual haemodynamic parameters remain in the normal range: arterial pressure is increased, heart rate is unchanged, central venous pressure is increased, cardiac failure is unusual. The abdominal distension is also responsible for a restrictive respiratory syndrome, mainly due to the ascension of the diaphragm. The compression of the abdominal content explains renal effects and the decreased diuresis. A sustained increase in abdominal pressure occurs in several clinical conditions. During coelioscopy, abdominal pressure is a under control and the cardiovascular effects are minor. Insufflation with CO2 carries the risk of hypercapnia, gas embolism and pneumothorax. During abdominal tamponade, anuria is directly related to the level of pressures. At an abdominal pressure over 25 mmHg, anuria is common and decompression becomes essential. The G suit increases arterial pressure either by elevating vascular resistances or increasing blood content in the upper part of the body. Therefore cardiac tolerance can be decreased especially in cardiac patients. The adverse effects of abdominal pressure can also be observed in case of peritoneal dialysis and ascites. The risk of regurgitation associated with an increased abdominal pressure must also be kept in mind. The abdominal pressure plays an important role in anaesthesia as well as in surgery. Therefore its measurement, which is easy, should become a routine.
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PMID:[Intra-abdominal pressure]. 799 45

Pregnancy often poses a risk to patients with neuromuscular and skeletal disorders when these affect the respiratory muscles or the rib cage. The outlook is determined both by the severity of the underlying condition and the physiological changes during pregnancy. Patients with a vital capacity of less than 1 to 1.5 litres, hypercapnia, severe scoliosis, diaphragm weakness or pulmonary hypertension before pregnancy are particularly at risk. Pregnancy may adversely affect the conducting airways, respiratory pump and gas exchange in the lungs. Close monitoring of high risk patients during pregnancy is required and either a termination of pregnancy or mechanical respiratory support may be indicated if ventilatory or cardiac failure develops.
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PMID:Pregnancy in neuromuscular and skeletal disorders. 808 20

Theophylline is a bronchodilator used extensively in the management of obstructive pulmonary disease. Factors implicated in altered theophylline clearance include smoking, age, concomitant drug intake, liver disease and left ventricular heart failure. However, evidence now suggests that theophylline clearance may be altered by changes in severity of the pulmonary obstruction, hypoxia and variation in arterial pH. The in vitro disposition of theophylline has been evaluated in isolated rat livers and mouse hepatocytes. In vivo studies have assessed the metabolism of theophylline under hypoxia in rats, rabbits and dogs. In isolated mouse hepatocytes and rat livers, low oxygen concentrations resulted in higher theophylline concentrations, a longer elimination half-life and a decrease in the production of the metabolite 1,3-dimethyl uric acid, suggesting impaired metabolism of theophylline. In rabbits, hypoxia, hypercapnia and respiratory acidosis decreased total body clearance and increased plasma theophylline concentrations. On the other hand, experiments involving dogs showed no significant changes in theophylline concentrations or pharmacokinetic parameters with hypoxia. At present, animal studies remain inconclusive. This can be attributed to the use of different animal models and variations in study methodology, including the extent and duration of hypoxia and acidaemia, concurrent acid-base disorders such as hypercapnia, as well as the severity of pulmonary obstruction. Human studies assessing alterations in theophylline disposition secondary to the hypoxia present in pulmonary disease are few and include mostly case reports and observational studies. There is evidence suggesting decreased theophylline clearance and protein binding during acute illness and some consensus can be achieved using case reports and controlled studies. There is additional evidence that drug clearance decreases with age and that elderly patients may have a decreased theophylline clearance at baseline. However, the most obvious markers appear to be the severity of pulmonary disease and the rate of change in the patient's condition. Caution should be exercised when administering theophylline to elderly patients with chronic obstructive pulmonary disease presenting with acute exacerbations of a concomitant respiratory illness, as these patients appear to be most likely to exhibit altered theophylline metabolism. Therefore, they would be at increased risk for toxicity should conventional dosages be used during an acute respiratory event.
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PMID:Hypoxia, arterial pH and theophylline disposition. 826 13

A 62-year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation to provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary hyperventilation.
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PMID:Bilateral carotid body paraganglioma and central alveolar hypoventilation. 826 82

Patients with heart failure are known to demonstrate periodic respiration (PR) during sleep. The factors causing PR are not well known. We therefore studied 20 patients (aged 18-66 years) with idiopathic dilated cardiomyopathy. Full-night polysomnography and evaluation of respiration and transcutaneous oxygen saturation were performed. Hypercapnic ventilatory response (HCVR) was evaluated during daytime. The patients showed PR for 25 +/- 26% (mean +/- standard deviation) of total sleep time. During PR, oxygen desaturated 7.1 +/- 4.6%. Sleep was impaired. HCVR was normal. Oxygen desaturation during PR was predicted by HCVR (r = 0.47, P < 0.05) and left atrial diameter (r = 0.60, P < 0.05). The time period of PR expressed as a fraction of total sleep time was correlated with HCVR (r = 0.45, P < 0.05) and left atrial diameter (r = 0.51, P < 0.05). In conclusion, PR with oxygen desaturation, arousals, and impaired sleep was observed in stable heart failure. HCVR and left heart dimensions were related to PR. These findings confirm the concept of a feedback loop describing respiratory control in PR.
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PMID:Periodic respiration in patients with heart failure. 847 14

A 48-year-old man was referred to our hospital because of hypoxemia (PaO2 = 43 mmHg), hypercapnia (PaCO2 = 70 mmHg), complete atrio-ventricular block, and heart failure. He also had limitation of spine flexion, scoliosis, deformity of the rib cage, and constriction of the ankle joints, complicated by cor pulmonale. These findings were compatible with rigid spine syndrome. To avoid progressive pulmonary hypertension and hypoxemia, nasal BiPAP and home oxygen therapy (0.5 liters/minute) were begun. Rigid spine syndrome is clinically characterized by limitation of spine flexion, and the limitation of thoracic movement often causes severe constrictive respiratory dysfunction. This syndrome should be considered when evaluating patients who have both thoracic deformity, especially scoliosis, and respiratory failure.
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PMID:[Rigid spine syndrome associated with marked hypoxemia and hypercapnia]. 875 23

Patients with heart failure have, compared with normal subjects, an increased minute ventilation (VE) at matched workloads. This heightened ventilatory drive may contribute to their limitation of functional capacity through an increase in the work of breathing and further worsening in the lung ventilation-perfusion mismatch. To measure the ventilatory response to exercise, VE should not be assessed in absolute units but be related to one of its main determinants, e.g., carbon dioxide production (VCO2). Particularly, as VE is closely related to VCO2 during exercise, the ventilatory response to exercise has been assessed using the slope of the relation of VE versus VCO2. This slope is significantly increased in heart failure patients compared with normal subjects and is inversely related to other parameters of maximal exercise capacity, namely peak VO2. The mechanisms of exercise hyperpnea in heart failure patients are still unsettled. A first possibility is that it is a compensatory response to the abnormal exercise hemodynamics with secondary increase of the pulmonary dead space to tidal volume ratio. This mechanism should be aimed to maintain constancy of the arterial gas composition and acid-base balance. However, exercise-induced hypoxemia and/or hypercapnia do not generally develop in heart failure patients. This might imply that other mechanisms, such as an increased sensitivity of the arterial chemoreceptors and/or the activation of reflexes by the abnormal skeletal muscles, stimulate the ventilatory response in heart failure patients. Regardless of its mechanisms, exercise hyperpnea may be clinically relevant in the assessment of patients with chronic heart failure. In fact, it is inversely related with peak exercise capacity, and interventions known to improve peak functional capacity such as therapy with ACE inhibitors, physical training and heart transplantation, also tend to normalize exercise hyperpnea.
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PMID:Role of exercise ventilation in the limitation of functional capacity in patients with congestive heart failure. 889 41


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