Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Decompressive craniectomy was purposed for the treatment of refractory intracranial hypertension after head injury. This review discusses results obtained by this surgery in severe head trauma. Several studies have confirmed a reduction in intracranial pressure secondary to decompressive craniectomy. Mortality decreased and the proportion of good outcome of the survivors increased. These results have not been confirmed prospectively, and indications have to be clarified. The positive effects of decompressive craniectomy compared to barbiturate or hypocapnia in the "second tier therapy" in refractory intracranial hypertension could be interesting to evaluate.
 ...
PMID:[Decompressive craniectomy and intracranial hypertension]. 1667 90

The ventilatory responses to immersion and changes in temperature are reviewed. A fall in skin temperature elicits a powerful cardiorespiratory response, termed "cold shock," comprising an initial gasp, hypertension, and hyperventilation despite a profound hypocapnia. The physiology and neural pathways of this are examined with data from original studies. The respiratory responses to skin cooling override both conscious and other autonomic respiratory controls and may act as a precursor to drowning. There is emerging evidence that the combination of the reestablishment of respiratory rhythm following apnea, hypoxemia, and coincident sympathetic nervous and cyclic vagal stimulation appears to be an arrhythmogenic trigger. The potential clinical implications of this during wakefulness and sleep are discussed in relation to sudden death during immersion, underwater birth, and sleep apnea. A drop in deep body temperature leads to a slowing of respiration, which is more profound than the reduced metabolic demand seen with hypothermia, leading to hypercapnia and hypoxia. The control of respiration is abnormal during hypothermia, and correction of the hypoxia by inhalation of oxygen may lead to a further depression of ventilation and even respiratory arrest. The immediate care of patients with hypothermia needs to take these factors into account to maximize the chances of a favorable outcome for the rescued casualty.
 ...
PMID:Respiratory responses to cold water immersion: neural pathways, interactions, and clinical consequences awake and asleep. 1671 16

Blood gas abnormalities in patients with idiopathic pulmonary arterial hypertension (IPAH) may be related to disease severity and prognosis. The present authors performed a 12-yr retrospective analysis assessing arterialised capillary blood gases, haemodynamics, exercise variables and survival in 101 patients with IPAH. At baseline, arterial oxygen tension (P(a,O(2))) and carbon dioxide arterial tension (P(a,CO(2))) were 9.17+/-1.86 and 4.25+/-0.532 kPa, respectively. While P(a,O(2) )was not associated with survival, a low P(a,CO(2 ))was a strong and independent prognostic marker. When patients were divided according to a baseline P(a,CO(2 ))value above or below 4.25 kPa, a cut-off value determined by receiver operating characteristics analysis, survival rates were 98 and 86% at 1 yr, 82 and 69% at 2 years, 80 and 51% at 3 yrs, 77 and 41% at 5 yrs, and 65 and 12% at 8 yrs, respectively. P(a,CO(2 ))after 3 months of medical therapy was strongly associated with survival. Hypocapnia at rest and during exercise correlated with low cardiac output, low peak oxygen uptake and reduced ventilatory efficacy. Multiple regression analysis revealed that 6-min walking distance, right atrial pressure and P(a,CO(2 ))were independently associated with survival. In patients with idiopathic pulmonary arterial hypertension, hypocapnia (carbon dioxide arterial tension <4.25 kPa) is an independent marker of mortality.
 ...
PMID:Prognostic value of blood gas analyses in patients with idiopathic pulmonary arterial hypertension. 1730 Nov

The objective of the treatment of intracranial hypertension is to decrease intracranial pressure (ICP) while maintaining cerebral blood flow (CBF). Despite numerous treatments, none of them associates total efficiency and security. Systemic secondary cerebral injuries, which are responsible for cerebral ischemia, lead us to administer non specific treatments in order to optimize CBF and cerebral oxygenation. Thus, the goals are: 1) to maintain cerebral perfusion pressure> or =70 mmHg; 2) to control metabolic status by preventing hyperglycaemia, anaemia and hyperthermia; 3) to maintain normoxia and normocapnia (hypercapnia increases ICP and hypocapnia decreases CBF). Beside the neurosurgical evacuation of extra- and intraparenchymatous haematomas, osmotherapy and cerebrospinal fluid (CSF) evacuation are the two specific treatments of intracranial hypertension. Osmotherapy consists in an administration of a hypertonic solution which induces a decrease in cerebral water and finally in ICP. Mannitol (20%), which is the reference, associates osmotic and rheologic effects, and decreases CSF production too. Recent data conduct us to administer larger doses, between 0.7 and 1 g/kg in 15 minutes. Hypertonic saline solution associates osmotic effects and plasma volume loading. Thus, this solution is particularly appropriate in severe head injury with arterial hypotension. CBF evacuation decreases rapidly ICP without any major side-effect. Until now, there is no proof of a superior efficiency of a treatment for intracranial hypertension compared to another. Considering their mechanism of action, all of them are efficient but potentially dangerous too. Indeed, the choice between treatments depends on data which are issued from the multimodal monitoring. General non specific treatments are always necessary. Specific treatments are indicated if ICP is above 20-25 mmHg. Maintaining cerebral perfusion pressure represents the first therapeutic goal. If intracranial hypertension persists, evacuation of CBF or osmotherapy may be advocated. In case of refractory intracranial hypertension, it may be useful to deepen neurosedation. Controlled hypocapnia and barbiturates remain a third line therapy providing to monitor and maintain an appropriate CBF and cerebral oxygenation. Controlled hypothermia and decompressive craniectomy must be individually discussed.
 ...
PMID:[Hierarchical strategy for treating elevated intracranial pressure in severe traumatic brain injury]. 1785 Oct 25

Patients with FHF have a high risk of cerebral edema and intracranial hypertension. The pathophysiological background for this phenomenon is not completely settled, but alteration in CBF as well as cerebral metabolism seems to be of importance. Mechanical hyperventilation has a prompt effect on intracranial pressure. This effect is assumed to be caused by the hypocapnia induced alkalosis which produces vasoconstriction and thereby a decrease in CBF and cerebral blood volume. It has been stated that hyperventilation may be harmful to patients with FHF, but only few studies have addressed the effect of hyperventilation upon cerebral metabolism. In the present clinical studies we evaluated the effect of short-term mechanical hyperventilation upon cerebral circulation and metabolism in patients with FHF. Although global CBF was reduced in patients with FHF it tightly matched the cerebral oxidative requirements. Already in the early phase of FHF there was a prominent cerebral efflux of glutamine that could not be accounted for by cerebral ammonia uptake. Moderate hyperventilation reduced global CBF without compromising cerebral oxidative metabolism. In addition, moderate hyperventilation restored cerebral autoregulation in most patients with FHF, and normalised the cerebral nitrogen balance during short-term interventions. Studies of global and regional cerebral carbon dioxide reactivity showed normal global as well as regional cerebral carbon dioxide reactivity in almost all patients with FHF. However, cerebral perfusion in frontal brain regions as well as basal ganglia is low in FHF as compared to healthy subjects, which may make these regions at risk of hypoperfusion during pronounced hyperventilation. It is concluded that moderate short-term hyperventilation does not compromise cerebral oxidative metabolism. Recommendation of its prolonged use in FHF awaits further studies. Furthermore, the data of this thesis demonstrates that alterations in cerebral glutamine and ammonia metabolism precedes increases of CBF, which seems to be a phenomenon that takes place later during the disease course, i.e., immediately before intracranial pressure is rising.
 ...
PMID:The effect of hyperventilation upon cerebral blood flow and metabolism in patients with fulminant hepatic failure. 1752 26

The report presents a definition and causes of syncope in children. Syncope differs from other states with loss of consciousness by causes leading to decreased perfusion and resultant transient cerebral dysfunction with decreased muscle tone. The most common causes of syncope noted in almost 15% of children are neurocardiogenic. This group includes vasovagal, carotid sinus reflexive, situational (coughing, dysphagia, micturation and defecation disturbances) and post-exercise syncope. Another group is represented by orthostatic syncope that may be triggered by primary and secondary dis-autonomy, decreased blood volume (hemorrhage, diarrhea, Addison's disease), some medications and substances of abuse (alcohol). An important group, accounting for 2%-6% of all cases, are cardiogenic syncope, caused mainly by congenital/acquired obstructive cardiac sub- and valvar heart defects, various cardiomyopathies, some heart tumors (e.g. myxoma), exudative pericarditis, pulmonary embolus and hypertension, congenital and acquired coronary anomalies, various significant brady-tachyarrhythmias (sick sinus syndrome, supra- and ventricular tachycardias, congenital and acquired atrio-ventricular blocks). Subclavian steal syndrome as the cause of syncope is exceptional in children. Syncope does not include loss of consciousness due to neurological and metabolic (hypoglycemia) causes, hypoxia, hyperventilation with hypocapnia or CO intoxication. Differential diagnosis should also include pseudo-syncope (hysteria). Preliminary diagnostic management should include a detailed medical history, including family history, on the frequency and circumstances of syncope, sudden deaths, a physical exam with orthostatic assessment of peripheral blood pressure and standard ECG (heart rate, intraventricular and atrioventricular conduction defects, cardiac hypertrophy, arrhythmias, L-QT, changes in ST-T). Further specialist tests depend on preliminary findings.
 ...
PMID:[Syncope in children and adolescents]. 1843 21

The usefulness of therapeutic hypothermia is highly debated after traumatic brain injury. A neuroprotective effect has been demonstrated only in experimental studies: decrease in cerebral metabolism, restoration of ATP level, better control of cerebral edema and cellular effects. Despite negative multicenter clinical studies, therapeutic hypothermia is still used to a better control of intracranial pressure. However, important issues need to be clarified, particularly the level and duration of hypothermia, the depth and modalities of sedation. A clear understanding of blood gases variations induced by hypothermia is needed to understand the cerebral perfusion and oxygenation changes. It is essential to recognize and to use hypothermia-induced physiological hypocapnia and alkalosis under strict control of cerebral oxygen balance (jugular venous saturation or tissue PO(2)) and also to take into account the increased affinity of hemoglobin for oxygen. Management of post-traumatic intracranial hypertension using hypothermia, directed by intracranial pressure level, and consequently for long duration, is potentially beneficial but needs further clarification.
 ...
PMID:[Hypothermia and cerebral protection after head trauma. Influence of blood gases modifications]. 1933 51

Obstructive sleep apnea is characterized by repeated upper airway obstruction during sleep and affects between 5% and 20% of the population. Epidemiological studies reveal that sleep apnea and associated intermittent hypoxemia increase the risk for hypertension and vascular disease but the mechanisms underlying these effects are incompletely understood. This review reports the results of rodent models of intermittent hypoxia (IH) and relates them to the observed hemodynamic and vascular consequences of sleep apnea. These animal studies have demonstrated that IH exposure in the absence of any other comorbidity causes hypertension, endothelial dysfunction, and augmented constrictor sensitivity, all due at least in part to increased vascular oxidative stress. Animal studies have used a variety of exposure paradigms to study intermittent hypoxia and these different exposure protocols can cause hypocapnia or hypercapnia-or maintain eucapnia-with accompanying alterations in plasma pH. It appears that these different profiles of arterial blood gases can lead to divergent results but the impact of these differences is still being investigated. Overall, the studies in rodents have clearly demonstrated that the vascular and hemodynamic impact of intermittent hypoxia provides a strong rationale for treating clinical sleep apnea to prevent the resulting cardiovascular morbidity and mortality.
 ...
PMID:Vascular effects of intermittent hypoxia. 1950 14

The central goal in the management of a patient with acute encephalopathy and encephalitis is the prevention of hypoxemic of hypoxic secondary insults. It is recommended that partial pressure of arterial oxygen should be more than 80 mmHg with mechanical ventilation and supplemental oxygen. About carbon dioxide tension, it is standard practice to ventilate to normocapnia instead of routine setting of hypocapnia. Hyperventilation therapy is limited to specialized conditions with intracranial hypertension which is refractory to other therapy and induces neurological deteriorations. And it is presumed that increasing positive end-expiratory pressure could be related to increase intracranial pressure and decrease cerebral perfusion pressure in these patients especially with low blood pressure. To avoid unfavorable sequelae in brain, lung, and all other organs, we consider that under multimodal brain monitoring, ventilator setting should be decided on a case-by-case basis.
 ...
PMID:[Mechanical ventilation]. 2140 Aug 49

In about 20% of patients admitted to an Intensive Care Unit (ICU) the indication of mechanical ventilation (MV) is a neurological disease. These patients have a prolonged MV stay and high mortality. The appropriate use of MV in patients with acute brain injury (ABI) is critical considering that MV by itself is able to induce or worsen an underlying lung injury. Patients with ABI have a higher risk to develop pulmonary complications. During endotracheal intubation the activation of airway reflexes should be prevented, because they may increase intracranial pressure. Tracheostomy is indicated to improve airway management and it is performed in about 33% of these patients. Indications for MV are loss of spontaneous respiratory effort, changes in lung compliance, gas exchange impairment and ventilatory failure due to muscle fatigue or neuromuscular junction dysfunction. During MV, hypoxemia should be avoided. The pC0(2) level has a critical role in cerebral blood flow regulation; therefore a normal pCO must be maintained in order to guarantee an optimal cerebral blood flow. Despite that, hypocapnia has been used in patients with increased intracranial pressure, at the present it is not recommended. Its use should be limited to the emergency management of intracranial hypertension, while the underlying cause is being treated. Non-conventional ventilatory modes as prone position ventilation, high-frequency oscillatory ventilation and extracorporeal C02 removal can be used in patients with ABI. All of them have specific risks and should be employed cautiously This paper reviews upper airway management and MV in patients with acute brain injury.
 ...
PMID:[Mechanical ventilation in patients with acute brain injury]. 2187 73


<< Previous 1 2 3 4 5 6 7 8 9 Next >>