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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiopulmonary effects resulting from the combination of xylazine and ketamine hydrochloride were evaluated in the adult horse. Xylazine (1.1 mg mg/kg) administered intravenously prior to or simultaneously with ketamine hydrochloride (2.2 mg/kg; intravenous) provided excellent analgesia and light anesthesia in all horses. Cardiac output, arterial blood pressure, pulmonary arterial pressure, central venous pressure, and pulmonary arterial wedge pressure remained within normal limits for the adult horse. Evidence of respiratory acidosis developed with time during the anesthetic period. Induction and recovery from anesthesia appeared smooth and excitement-free. In the horse, larger dosages of ketamine hydrochloride (6.6 mg/kg) following sedation with xylazine (1.1 mg/kg; intravenous) were accompanied by muscular tremor and rigidity, mydriasis, oculogyric movements, sweating, hypertension, tachycardia, and increased rectal temperature during recovery from anesthesia. Providing there is good sedation from xylazine, the combination of xylazine and ketamine hydrochloride as a short-term intravenous anesthetic technique in the horse appears safe and acceptable providing reasonably stable cardiopulmonary function. If the sedative properties of xylazine are not apparent or if excessive dosages of ketamine hydrochloride are used, the drug combination results in serious side effects precluding its use for anesthesia in the horse.
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PMID:Evaluation of xylazine and ketamine hydrochloride for anesthesia in horses. 84 17

Twelve patients with predominantly obstructive type sleep apnea underwent cardiac catheterization, hemodynamic monitoring, and arterial blood gas analysis during wakefulness and sleep. Abnormalities during wakefulness included systemic hypertension in four of 12, exercise-induced mild pulmonary hypertension in five of 12, and alveolar hypoventilation in one. During sleep nine patients had cyclic elevations of arterial pressure with each apneic episode, exceeding 200 mm Hg systolic in three of 12. Pulmonary artery pressures increased in 10 of 12, exceeding 60 mm Hg systolic in five. Marked degrees of hypoxemia (arterial P02, less than 50 mm Hg in eight of 12) and moderate hypercapnia with respiratory acidosis were associated with these hemodynamic changes. Cyclic upper airway obstruction during sleep may result in hypercapnia, acidosis, and pronounced hypoxemia, which can lead to hemodynamic abnormalities during sleep. Sustained pulmonary hypertension and possibly systemic hypertension may follow. Tracheostomy is an effective therapy and is recommended to symptomatic patients who have predominantly obstructive apnea but no relievable anatomic cause of upper airway obstruction.
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PMID:Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. 99 7

Circumstances under which the use of oxygen-therapy in lung disease can be effective and harmless, depend upon a careful evaluation of its indications: they are suggested by the clinical need of correction of hypoxaemia as well as by the awareness of factors determining respiratory failure and of problems concerning O(2) transport and supply to tissues in health and disease. Blood gases monitoring enables to control the effects of treatment on arterial O2 and CO2 tensions thus giving all the useful data for oxygen administering particularly as far as components of hyperoxygenated mixtures, flow rate, duration, use of very effective low-risk devices (Venturi masks) are concerned. Correction of hypoxaemia involves the reduction of hypertension of the pulmonary circulation and hyperglobulia, improvement of tolerance of exertion, and attention to the metabolic compensation of respiratory acidosis. These results are influenced by the nature of the pathogenetic factors behind broncho-obstructive disease, which may lead to either a primarily "bronchitis" or a primarily "emphysematous" syndrome. An interesting feature relates to prognosis in the case of patients making home use of hyperoxygenated mixtures as part of a rehabilitation program, or to improve their quality of life. The cost and benifits of such treatment should be carefully weighed. Lastly, in the event of protracted treatment, attention must be paid to the possibility of toxicity and the means to be adopted for its prevention.
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PMID:[Oxygen therapy in pneumology]. 101 8

When a patient with chronic obstructive pulmonary disease (COPD) requires medical therapy for systemic hypertension, a number of special considerations may affect the choice of antihypertensive drug and subsequent management. Thiazide diuretics have no adverse effect on airway function and are the agents of choice for initial therapy. beta-Antagonists are usually considered first-line agents in antihypertensive therapy, but even relatively cardioselective ones may increase airway resistance in patients with obstructive lung diseases, and they should be used with caution, if at all, in such patients. Although potassium-wasting diuretics are the preferred agents for treating hypertension in patients with COPD, they may worsen carbon dioxide retention in hypoventilating patients and potentiate hypokalemia in those receiving corticosteroids. In addition, beta-agonists may substantially lower serum potassium levels in patients already rendered hypokalemic by diuretics. Patients with COPD receiving potassium-wasting diuretics who have chronic respiratory acidosis or are receiving corticosteroids or beta-agonists should undergo close monitoring of electrolyte levels and be considered for therapy with potassium supplements or, preferably, potassium-sparing agents.
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PMID:Fluid and electrolyte considerations in diuretic therapy for hypertensive patients with chronic obstructive pulmonary disease. 286 47

Experiments were performed to assess the effect of left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either: (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to an acute respiratory acidosis (by varying the concentration of inspired PCO2). In association with left ventricular hypertrophy (secondary to hypertension), left ventricular pHi became significantly alkaline in all experimental hypertensive groups compared with control values; pHi control (in response to an acidosis) was also significantly improved. There was no change in resting levels of pHi or pHi control in right ventricular or skeletal muscle tissue in any hypertensive group. There was no change in resting levels of pHi or pHi control in left ventricular, right ventricular or skeletal muscle tissue from sham-operated animals. This suggests that these changes are the result of hypertrophy per se, rather than due to a generalised mechanism secondary to hypertension and operating on all tissues. There was no change in intracellular electrolyte concentration or content in association with hypertension in any tissue or group studied.
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PMID:The effects of short-term hypertensive left ventricular hypertrophy on intracellular pH and intracellular electrolytes in rats. 296 94

Experiments were performed to assess the effect of long-standing (4-8 weeks) left ventricular hypertrophy (induced by experimental hypertension) on intracellular pH (pHi) and intracellular electrolytes in left ventricular tissue. They were undertaken on: (1) hypertensive rats (hypertension being induced by either (a) subdiaphragmatic aortic constriction, (b) unilateral renal artery clipping, or (c) unilateral renal artery clipping with contralateral nephrectomy); (2) sham-operated rats for the above 3 subgroups; and (3) control (unoperated) rats. In this study the hypertension (and therefore the hypertrophy) was of long (4-8 weeks) duration. Intracellular pH and intracellular electrolytes were measured in left ventricular, right ventricular and skeletal muscle tissue from these animals. Intracellular pH control was assessed by exposing a number of animals in each group to a respiratory acidosis (by varying the concentration of inspired PCO2). As described previously [Oldershaw PJ, Cameron IR, Int J Cardiol 1988;18:131-141], in the earlier stages of left ventricular hypertrophy (1-4 weeks duration) left ventricular pHi was significantly alkaline at normal levels of extracellular pH. At this late stage, with the exception of animals with aortic constriction, pHi had returned to control values. There was no change in resting levels of pHi in right ventricular or skeletal muscle tissue in any hypertensive group. The improved control of pHi in left ventricular tissue observed with hypertrophy of short duration (1-4 weeks [Oldershaw PJ, Cameron IR. Int J Cardiol 1988;18:131-141]) persisted in all experimental groups at this stage (4-8 weeks) after the onset of development of left ventricular hypertrophy. There was no change in pHi control in right ventricular or skeletal muscle tissue. Neither was there any change in intracellular electrolyte concentrations or content in association with hypertension in any tissue or group studied.
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PMID:The effects of long-standing hypertensive left ventricular hypertrophy on intracellular pH and intracellular electrolytes in rats. 296 95

A 52-year-old apparently healthy, normotensive woman who presented for elective cholecystectomy experienced intra-operative hypertension and tachycardia, which were controlled by propranolol. Oesophageal temperature increased, there was a metabolic and respiratory acidosis with hypoxaemia, and malignant hyperthermia was diagnosed. Severe cardiogenic pulmonary oedema ensued, and was treated with intravenous glyceryl trinitrate. Ventricular fibrillation caused cardiac arrest, and this was treated successfully. Postoperatively a phaeochromocytoma was discovered, and removed at a subsequent operation. The case illustrates the similarities in presentation of malignant hyperthermia and phaeochromocytoma, and the possibility that misdiagnosis may exacerbate the crisis.
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PMID:Phaeochromocytoma--a presentation mimicking malignant hyperthermia. 323 80

An 87-year-old female, with a history of hypertension controlled with hydrochlorothiazide, was scheduled for excision of a cystic mass of the left lobe of the thyroid. In the course of the anaesthetic, she developed partial airway obstruction that resulted in respiratory acidosis (PaCO2 108 mmHg, pH 7.06), developed premature ventricular contractions and experienced a reduction in plasma potassium concentration from 3.9 to 2.9 mmole X L-1. We interpret this hypokalaemia as a consequence of the epinephrine discharge due to hypercapnia. The case is reported to emphasize the importance of minimizing the sympathetic response to induction of anaesthesia, intubation and surgery in patients with marginal potassium stores.
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PMID:Hypokalaemia and respiratory acidosis following partial obstruction of the airway. 360 55

This study examined the cardiovascular, respiratory, and sympathetic effects of selective mu and delta opioid agonists microinjected into the hypothalamic nucleus preopticus medialis (POM) of conscious SHR and WKY rats. The mu receptor agonist D-Ala2-MePhe4-Gly5-ol-enkephalin (DAGO) at a dose of 0.6 or 6.0 nanomoles (Nmol) increased the blood pressure and heart rate in WKY rats. In SHR rats, the lower dose of DAGO similarly had a pressor effect whereas the higher dose was depressor; heart rat was increased only by the 6.0 nmol dose in these animals. In both SHR and WKY rats, this opioid caused respiratory acidosis and elevation of plasma norepinephrine (NE) and epinephrine (E); plasma vasopressin was reduced by the higher dose of DAGO. All of these effects of the mu agonist were reversed by the opiate receptor antagonist naloxone (0.5 mg/kg, i.a.). The delta opiate-receptor agonist D-Ala2-D-leu5-eukephalin at a dose of 6.0 or 20.0 nmol increased blood pressure and heart rate in both SHR and WKY rats without affecting respiratory variables. Plasma NE and EPI were elevated at the peak of the pressor period. These studies suggest that the anteroventral hypothalamic region may be an important site in central autonomic regulation by opioid peptides. The mu-receptor agonist was more potent than the delta agonist in eliciting cardiovascular and respiratory effects and associated sympatho-adrenomedullary activation.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Opiate receptors and cardiovascular control in conscious SHR and WKY rats. 631 37

During a retrospective multicentric study of the encountered congenital pathology of the diaphragmatic domes, we focused our special attention on the prevalence of the congenital Bochdalek hernia. 140 charts were statistically analysed. The seriousness of the medical and surgical emergency situation enticed the authors to examine the most important prognostic clinical features. The interval between diagnosis and surgical therapy should be as short as possible. Respiratory acidosis and resuscitation were a common denomination in all infants who succumbed in the post-operative period. The early occurrence (less than 6 hrs) of respiratory distress disclosed the seriousness of the associated pulmonary hypoplasia. Surgical technical problems were rare. This in contrast to the struggle against pulmonary arterial and capillary hypertension. Pulmonary vasodilator drugs have not convinced those who initiated their use.
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PMID:[Bochdalek's congenital diaphragmatic hernia: a clinical review of 114 cases]. 671 Dec 39


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