UMLS:C0018801 - FACTA Search

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Query: UMLS:C0018801 (heart failure)
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Impaired pulmonary gas exchange can result from lung parenchymal failure inducing oxygenation deficiency and fatigue of the respiratory muscles, which is characterized by hypercapnia or a combination of both mechanisms. Contractility of and coordination between the diaphragm and the thoracoabdominal respiratory muscles predominantly determine the efficiency of spontaneous breathing. Sepsis, cardiac failure, malnutrition or acute changes of the load conditions may induce fatigue of the respiratory muscles. Augmentation of spontaneous breathing is not only achieved by the application of different technical principles or devices; it also has to improve perfusion, metabolism, load conditions and contractility of the respiratory muscles. Intermittent mandatory ventilation (IMV) allows spontaneous breathing of the patient and augments alveolar ventilation by periodically applying positive airway pressure tidal volumes, which are generated by the respirator. Potential advantages include lower mean airway pressure (PAW), as compared with controlled mechanical ventilation, and improved haemodynamics. Suboptimal IMV systems may impose increased work and oxygen cost of breathing, fatigue of the respiratory muscles and CO2 retention. During pressure support ventilation (PSV), inspiratory alterations of PAW or gas flow (trigger) are detected by the respirator, which delivers a gas flow to maintain PAW at a fixed value (usually 5-20 cm H2O) during inspiration. PSV may be combined with other modalities of respiratory therapy such as IMV or CPAP. Claimed advantages of PSV include decreased effort of breathing, reduced systemic and respiratory muscle consumption of oxygen, prophylaxis of diaphragmatic fatigue and an improved extubation rate after prolonged periods of mechanical ventilation. Minimum alveolar ventilation is not guaranteed during PSV; thus, close observation of the patient is mandatory to avoid serious respiratory complications. Continuous positive airway pressure breathing (CPAP) maintains PAW above atmospheric pressure throughout the respiratory cycle, which may increase functional residual capacity and decrease the effort of breathing. CPAP has been conceptually designed for the augmentation of spontaneous breathing and requires the intact central and peripheral regulation of the respiratory system. Airway pressure release ventilation (APRV) improves alveolar ventilation by intermittent release of PAW, which is kept above atmospheric pressure by means of a high-flow CPAP system. The opening of an expiratory valve for 1-2 s induces a decreased PAW and lung volume, which increases rapidly to pre-exhalation values after closure of the valve due to the high gas flow within the circuit (90-100 1/min). APRV may improve haemodynamics and VA/Q distribution as compared with conventional mechanical ventilation. Biphasic positive airway pressure (BIPAP) is characterized by the combination of spontaneous breathing and time-regulated, pressure-controlled mechanical ventilation. During the respiratory cycle the ventilator generates two alternating CPAP levels, which can be modified with regard to time and pressure. As with APRV, alveolar ventilation is maintained even if the spontaneous breathing efforts of the patient cease, which improves the safety of both modes of respiratory therapy. The contribution of spontaneous breathing to total minute ventilation may be important, since a decreased shunt and improved VA/Q relationship have been observed in experimental non-cardiogenic lung oedema. These data give support to the concept that spontaneous breathing should be maintained and augmented in the setting of acute respiratory failure.
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PMID:[Augmented spontaneous breathing]. 896 3

Sleep apnoea is common in patients with heart failure. While most patients have central sleep apnoea (CSA), a minority have obstructive sleep apnoea (OSA). The pathophysiology of CSA is not well understood. We hypothesized that central chemosensitivity would be an important pathophysiological factor in patients with CSA, and not in OSA. The aim of this study was to compare ventilatory responses between patients with CSA and those with OSA. Acute ventilatory responses to eucapnic hypoxia and hyperoxic hypercapnia were measured during wakefulness in 34 patients (33 males and one female, aged 59+/-8 yrs (mean+/-SD)), with stable medically-treated left ventricular dysfunction (LVD) and sleep apnoea (18 OSA and 16 CSA). Patients with CSA had a decreased awake end-tidal carbon dioxide tension (4.1+/-0.5 kPa), increased ventilatory response to carbon dioxide (0.65+/-0.43 L.min.(-1).kPa PCO2(-1)), and eucapnic hypoxic responses in the normal range (0.6+/-0.4 L.min(-1)/% fall in arterial oxygen saturation (Sa,O2)). In contrast, patients with OSA had normal end-tidal carbon dioxide tension (4.9+/-0.5 kPa), and normal ventilatory responses to hypercapnia (0.29+/-0.16 L.min(-1).kPa PCO2(-1)) and hypoxia (0.5+/-0.5 L-min(-1)/% fall in Sa,O2). These findings suggest that augmented chemosensitivity to hypercapnia may be an important factor in the pathophysiology of central sleep apnoea in patients with heart failure.
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PMID:Ventilatory control in patients with sleep apnoea and left ventricular dysfunction: comparison of obstructive and central sleep apnoea. 954 61

We sought to determine if predicted post-operative maximal oxygen uptake (VO2max/kg-PPO) was associated to the occurrence of respiratory or cardiac failure within the 60 days following lung surgery and to evaluate its validity as operability criterion. We studied 47 patients with chronic air-flow limitation (COPD) with FEV1 > 0.8 1 and without hypercapnia, that underwent lung surgery. Age was 56 (SD 11) years, FEV1 = 1.8 (SD 0.5) 1 (61% predicted (SD 13%) and FEV1/FVC = 55 (SD 7.5). Ten patients presented serious cardiac or respiratory complications (3 died). Significant correlation with complications was found for RV, TL-COsb-PPO, VO2max/kg, resection size and VO2max/kg-PPO. VO2max/kg-PPO correlation (-0.73) was significantly higher (p = 0.0016) than all the pulmonary function test (PFT) correlation and than VO2max/kg correlation (p = 0.049) as well. Cut-off points, positive and negative predictive values were respectively: 12.6 ml/min/kg, 0.75 y 0.90% for VO2max/kg-PPO; 17 ml/min/kg 0.83 and 0.87 for VO2max/kg and 148%, 0.67 and 0.82 for RV (the best of the pulmonary function tests). Multivariable models did not improve discriminant power. We conclude that, out of the studied variables, VO2max/kg-PPO showed higher correlation with the complications sought than PFT or VO2max/kg. As criterion to predict cardiac or respiratory failure, with the observed prevalence, its negative predictive values is good, but its positive predictive value is relatively low. None parameter was able to predict all the complications.
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PMID:[Role of postoperative estimate of maximum oxygen uptake in predicting cardiorespiratory insufficiency in the immediate postoperative period in thoracic surgery]. 961 37

Although midazolam has been proposed for the treatment of a variety of conditions such as anxiety, dyspnoea, hiccups and status epilepticus, terminal agitation is the only condition where its use is based on a reasonably large number of published clinical studies. A causal approach is generally recommended. Whenever possible, the aetiological condition (pain, fever, constipation, etc.) should be corrected. Such general measures as ensuring a peaceful, familiar environment, and the use of a night light, fluid therapy to counteract dehydration, and antipyretics for fever are beneficial. When symptomatic treatment is needed, drugs with little anticholinergic effect are to be recommended. The use of benzodiazepines as single drug treatment may exacerbate the condition. Haloperidol or risperidone (which has fewer side effects) are recommended. If the agitation is marked, a common strategy is to add lorazepam. Chlormethiazole is an alternative. Subcutaneous midazolam should be reserved for refractory cases. Attention should be paid to dosage, reduced doses being given to the elderly, patients on opioid medication, and patients with impaired liver or renal function. Overdosage may induce deep sedation, and result in carbon dioxide retention and subsequently heart failure and pulmonary oedema which may be fatal.
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PMID:[Midazolam (Dormicum) in terminal anxiety and agitation. The last choice alternative in palliative care]. 1035 70

Near-infrared (IR) light easily penetrates biological tissue, and the information offered by in vivo spectroscopy of cerebral oxygenation is detailed and comes with a high temporal resolution. Near-IR light spectroscopy (NIRS) reflects cerebral oxygenation during arterial hypotension, hypoxic hypoxaemia and hypo- and hypercapnia. As determined by dual-wavelength NIRS, the cerebral O2 saturation integrates the arterial O2 content and the cerebral perfusion, and as established for skeletal muscle, NIRS obtains information on tissue oxygenation and metabolism beyond that obtained by venous blood sampling. Caveats of cerebral NIRS include insufficient light shielding, optode displacement and a sample volume including muscle or the frontal sinus mucous membrane. The relative influence from the extracranial tissue is minimized by optode separation and correction for an extracranial sample volume, or both. The natural pigment melatonin and also water are of little influence to spectroscopic analysis of cerebral oxygenation, whereas bilirubin systematically lowers ScO2 and attenuates the detection of changes in cerebral oxygenation. By NIRS, reduction of cytochrome oxidase is demonstrated during hypoxic hypoxaemia and head-up tilt-induced arterial hypotension, but the changes are small. In the clinical setting, NIRS offers useful information in patients with both systemic and local cerebral circulatory impairment, for example, during cranial trauma, surgery on the cerebral arteries, orthostasis and acute heart failure. Whereas mapping of the brain circulation is needed for jugular venous sampling to reflect either global or local oxygenation, the determination of cerebral oxygenation by NIRS has the advantage of localized monitoring of the cerebral cortex.
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PMID:Near-infrared oximetry of the brain. 1040 56

The prehospital phase of head injury, also called the critical phase, consists of trauma-induced apnea and stress catecholamine release. This immediate period after head injury remains poorly summarized in the literature and essentially ignored with respect to treatment. A MEDLINE search of the literature on apneustic response and catecholamine surge after head injury and a review of literature from my acquired references revealed 116 references (from more than 600) that were pertinent. Apnea induced by head injury produces hypoxia, hypercarbia, and subsequent cardiac failure and hypotension, which, along with substantially elevated catecholamine values, promote secondary mechanisms of organ injury. Treatment for this immediate period after head injury requires a rapid response to the scene of trauma and development of treatment options that can be instituted at the scene of injury.
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PMID:The neglected prehospital phase of head injury: apnea and catecholamine surge. 1063 Jul 56

Physiological ageing of the lung is associated with dilatation of alveoli, enlargement of airspaces, decrease in exchange surface area and loss of supporting tissue for peripheral airways ("senile emphysema"), changes resulting in decreased static elastic recoil of the lung and increased residual volume and functional residual capacity. Compliance of the chest wall diminishes, thereby increasing work of breathing when compared with younger subjects. Respiratory muscle strength also decreases with ageing, and is strongly correlated with nutritional status and cardiac index. Expiratory flow rates decrease with a characteristic alteration in the flow-volume curve suggesting small airway disease. The ventilation-perfusion ratio (V'A/Q') heterogeneity increases, with low V'A/Q' zones appearing as a result of premature closing of dependent airways. Carbon monoxide transfer decreases with age, reflecting mainly a loss of surface area. In spite of these changes, the respiratory system remains capable of maintaining adequate gas exchange at rest and during exertion during the entire lifespan, with only a slight decrease in arterial oxygen tension, and no significant change in arterial carbon dioxide tension. Ageing tends to diminish the reserve of the respiratory system in cases of acute disease. Decreased sensitivity of respiratory centres to hypoxia or hypercapnia results in a diminished ventilatory response in cases of heart failure, infection or aggravated airway obstruction. Furthermore, decreased perception bronchoconstriction and diminished physical activity may result in lesser awareness of the disease and delayed diagnosis.
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PMID:Physiological changes in respiratory function associated with ageing. 1083 48

A 56-year-woman with type 2 respiratory failure due to diaphragmatic dysfunction in Charcot-Marie-Tooth disease (CMT) is reported. The patient, who had a 50-year history of CMT, was referred to our hospital because of nocturnal dyspnea. Arterial blood gas analysis on admission showed marked hypoxia with hypercapnia, and physical examination revealed thoracoabdominal paradoxus in the supine position. Chest radiography revealed elevation of both sides of the diaphragm. The vital capacity and arterial blood gas pressure in the sitting position were markedly higher than those in the supine position. Electrical phrenic nerve stimulation failed to produce any convincing muscle action potential in the diaphragm. These findings suggested that her respiratory failure was induced by both diaphragmatic dysfunction caused by bilateral phrenic nerve palsy due to CMT. Treatment of this patient was started at home with a pressure support ventilator, resulting in satisfactory clinical improvement. In general, respiratory muscle impairment is a rare phenomenon in a patient with CMT. However when a patient with CMT complains of dyspnea or if unexpected heart failure develops, it is important to keep in mind that CMT may be associated with phrenic nerve palsy.
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PMID:[Respiratory failure due to diaphragmatic dysfunction in Charcot-Marie-Tooth disease: a case report]. 1106 Oct 92

Cor pulmonale is defined as "hypertophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, as congenital heart disease". Pulmonary hypertension is a frequent hemodynamic complication associated with a wide variety of respiratory systems disorders whose only common physiologic abnormalities are alveolar hypoxia and consequent arterial hypoxemia of longterm duration. The sustained elevation in pulmonary arterial hypertension is thought to be mediated through two pathophysiologic vascular mechanism: 1) persistent vasoconstriction and 2) vascular structural remodeling. The combination of these processes causes vascular luminal narrowing and vessel obliteration that reduce pulmonary vascular surface area to the critical degree necessary for the development of the pulmonary hypertension. Cor pulmonale may be difficult to diagnose, particularly early in its course, when they symptoms manifested may be interpreted as representing progression of an underlying pathophysiological state, such as chronic obstructive airways disease. The treatment of cor pulmonale is directed toward reversing the pathogenetic process that can be directly treated, while at the same time relieving the hypoxemia, hypercapnia or acidosis. At present long-term oxygen therapy is the best treatment for pulmonary hypertension. Heart failure in cor pulmonale is usually transient once the initiating mechanism is controlled. The usual therapeutic measures for heart failure apply: a low-salt regimen, and diuretics.
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PMID:[Chronic cor pulmonale]. 1114 67

The chemoreflexes are important modulators of sympathetic activation. The peripheral chemoreceptors located in the carotid bodies respond primarily to hypoxaemia. Central chemoreceptors located in the region of the brainstem respond to hypercapnia. Activation of either the hypoxic or hypercapnic chemoreflex elicits both hyperventilation and sympathetic activation. During apnoea, when the inhibitory influence of stretch of the pulmonary afferents is eliminated, there is a potentiation of the sympathetic response to both hypoxia and hypercapnia. This inhibitory influence of the pulmonary afferents is more marked on the sympathetic response to peripheral compared with central chemoreceptor activation. The arterial baroreflexes also have a powerful inhibitory influence on the chemoreflexes. This inhibition is again more marked with respect to the peripheral compared with central chemoreflexes. In patients with hypertension, there is a marked increase in the sympathetic and ventilatory response to hypoxaemia. During apnoea, with elimination of the inhibitory influence of breathing, the sympathetic response in untreated mild hypertensive patients is strikingly greater than that seen in matched normotensive controls. This potentiated peripheral chemoreflex sensitivity in hypertension may be explained in part by impaired baroreflex function in these patients. Enhanced peripheral chemoreflex sensitivity is also evident in patients with obstructive sleep apnoea. This peripheral chemoreflex enhancement is not explained by obesity, as obese individuals have a selective potentiation of the central chemoreceptors with peripheral chemoreflex responses similar to those seen in lean controls. Increased sensitivity to hypoxaemia has important implications in patients with obstructive sleep apnoea who experience repetitive and severe hypoxaemic stress. Tonic activation of the chemoreflex may also contribute to the high levels of sympathetic activity evident even during normoxic daytime wakefulness in sleep apnoea patients. Administration of 100% oxygen in patients with sleep apnoea results in reductions in heart rate, blood pressure and central sympathetic outflow. In patients with heart failure, the central chemoreflex response to hypercapnia is markedly and selectively enhanced. This increased central chemoreflex sensitivity may contribute to the development of central sleep apnoea in heart failure patients. Administration of 100% oxygen does not lower sympathetic activity in patients with heart failure, providing further evidence against any peripheral chemoreflex potentiation. The peripheral and central chemoreflexes have powerful effects on sympathetic activity in both health and disease and may contribute importantly to disease pathophysiology, particularly in conditions such as hypertension, obstructive sleep apnoea and heart failure.
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PMID:Chemoreflexes--physiology and clinical implications. 1260 9

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