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

Time-compressed Fourier analysis of the electroencephalogram has proven to be a useful analytical procedure during anesthesia and surgery which simplifies data interpretation by presenting the EEG in a time-compressed frequency domain rather than the conventional time domain. This method of data analysis graphically accentuates the electroencephalographic correlates of ischemia-induced cerebral dysfunction and other cerebral oxygen consumption abnormalities. The ability to accentuate trends in frequency and power is derived from sequential plotting of spectra to produce a graph with three dimensional axes of frequency, time, and power. In carotid endarterectomies the system has proven more useful than the conventional EEG in assessing the need for a vascular shunt to maintain internal carotid flow during endarterectomy. In open-heart surgery time-compressed EEG spectral analysis has allowed early recognition of cerebral ischemia resulting from arterial hypotension and venous hypertension. Five cases are presented which demonstrate the ability of our system to reflect developing cerebral ischemia.
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PMID:Monitoring of cerebral perfusion during anesthesia by time-compressed Fourier analysis of the electroencephalogram. 32 37

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

We reviewed retrospectively 75 renal transplant arteriograms done during a 7-year period. Acute rejection and vasomotor nephropathy were not differentiated. Generalized cortical ischemia was diagnosed correctly in 23 of 30 cases but there were 7 falsely negative results. Renal artery stenosis was found in 7 of 17 cases in which the main indication for arteriography was hypertension. We conclude that the major role of transplant arteriography is in the diagnosis of larger vessel disease.
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PMID:Angiography in the diagnosis of renal allograft dysfunction. 34 73

We measured indices of the renin-aldosterone system and body-fluid spaces in 11 adolescents who had received a renal transplant after removal of their own diseased kidneys. None had hypervolemia but 6 had hypertension. Renal angiography revealed greater than 50% luminal occlusion by allograft renal-artery stenosis (RAS) in only the 3 patients who had severe hypertension refractory to conventional medical therapy. Excessive peripheral plasma renin activity (PRA) distinguished these patients from those who had less severe stenosis or normal angiogram, and diuretic stimulation heightened the PRA differences. We conclude that significant allograft RAS does not necessarily act like a typical single-kidney Goldblatt model until after volume depletion. Our findings indicate that peripheral PRA values can be used to assess the degree of graft ischemia clinically. This permits early identification of patients who have severe RAS that probably will be difficult to control medically, and, therefore, should be followed closely with a view of reconstructive vascular surgery before further deterioration of renal function.
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PMID:Allograft renal-artery stenosis: increased peripheral plasma renin activity as an early indicator of uncontrollable hypertension. 36 8

The pattern and pathogenesis of nonlocalizing visual disturbances, associated with optic disc edema (ODE). raised cerebrospinal fluid pressure, and intracranial space-taking lesions were investigated experimentally in rhesus monkeys with simulated progressive brain tumor and clinically in patients with benign intracranial hypertension. The visual disturbances occurring in one of both eyes were of three types: recurrent attacks of transient obscuration, permanent blindness, and various types of visual field defects. The studies indicate that the visual disturbances are usually due to two mechanisms. The most common is ischemia of the optic disc secondary to ODE. The other, rarer mechanism probably consists of the space-taking lesion causing downward herniation of the parahippocampal gyrus into the tentorial notch, producing compression of the lateral geniculate body and optic tract.
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PMID:Optic disc edema in raised intracranial pressure. VI. Associated visual disturbances and their pathogenesis. 40 82

Two cases of atypical localization of an aortic coarctation are described. One patient was a hypertensive girl with a hypoplastic type of coarctation in the descending aorta. After insertion of a bypass graft the hypertension disappeared. The other patient was a hypertensive girl with a total aplasia of the distal abdominal aorta and a hypoplasia of a right renal artery. After right nephrectomy the blood pressure became normal. There were no symptoms or signs of ischemia of the legs. This is the second case, known in literature, with a total aplasia of the abdominal aorta. Some general considerations about atypical coarctations are made.
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PMID:Uncommon congenital anomalies of the aorta. 42 52

A total of 25 cases (12 men, 13 women) of complete left bundle branch block (LBBB) were found among 1,400 consecutive autopsy in the aged. Their ages ranged from 70 to 86 years (average 78.9). ECG was analyzed as for the occurrence of LBBB and myocardial infarction (MI). Pathological examinations included observations of the conduction system by serial sections. They were divided into group A with MI and group B without MI. Duration of LBBB was 1 to 3 days in 4 cases, more than 1 month in 7, and more than 1 year in 14. From the temporal sequence of LBBB and MI in group A, cases were classified into (1) MI preceding LBBB in 5, (2) both coexistent in 5, and (3) LBBB preceding MI in 1. There were 8 cases of normal electrical axis, 17 left axis deviation, 7 first degree A-V block, and 2 atrial fibrillation. Various heart diseases were underlying in 21 cases, including hypertension, MI, mitral and aortic regurgitation, and primary myocardial disease, and there were 4 cases with no cardiac diseases. Cause of death was cardiac in 12; MI, congestive heart failure, and sudden death. Heart weight was 410 Gm on the average (240 to 550 Gm). MI was found in 11, with stenotic index of 12/15, while it was 9/15 in group B. Lesions of the conduction system were slight to moderate (1.5 to 2.4) except left bundle branch, which showed marked changes in posterior (4.9) and anterior (4.8) fascicles. Site of interruption of the left bundle branch was the junction between the branching portion of the A-V bundle and the left bundle branch (Junctional type) in 17, and peripheral portion of the left bundle branch about 10 mm or more below the junction in 8 (Peripheral type). In conclusion, 2/3 of cases of LBBB belonged to the junctional type and most of them were not related to MI, but to the lesions caused by mechanical injuries at the septal summit. One third of the cases were as peripheral type, which was mainly related to the various types of lesions including septal ischemia (necrosis and fibrosis).
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PMID:A clinicopathological study on 25 cases of complete left bundle branch block. 44 51

Eleven patients with vascular sequelae of thoracic outlet syndrome were operated on at the University of California, SanFrancisco, during the past 17 years. Five patients presented with episodes of ischemia of the arm and hand secondary to microemboli released from subclavian arterial lesions produced by chronic compression at the thoracic outlet. Treatment consisted of arterial reconstruction, removal of the compressive structure, and cervical sympathectomy to relieve or lessen distal ischemia. Four of the five patients had good or excellent results; one patient required amputation of the forearm. The results were inversely proportional to the extent of distal arterial embolic occlusions present at the time of surgical treatment. Six patients presented with symptoms of chronic venous hypertension. Four of the six had subclavian venous thrombosis and were treated by transaxillary resection of the first rib to decompress the collateral veins within the costoclavicular space. All four were symptomatically improved. Two patients had venous hypertension due to extrinsic compression of the subclavian vein. One patient became asymptomatic and the other was markedly improved after resection for external compression. In this small series transaxillary resection of the first rib has resulted in symptomatic improvement in chronic venous hypertension of the arm.
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PMID:Thoracic outlet syndrome. 46 6

The handling of patients with cerebral ischemia is reviewed, taking into consideration recent concepts regarding etiopathogenesis along with new diagnostic and therapeutic methods. A particularly important new diagnostic method is computerized axial tomography. The subject is divided into four sections in order to present a practical outline. The first section deals with the arterial circulatory system. Evaluation of patients with arteriosclerosis of the vessels in the neck and/or intracranial are reviewed in some detail, according to whether the clinical manifestation was transitory ischemia, progressive cerebral infarction, or complete cerebral infarction. Emphasis is placed on the proper selection of diagnostic tests and application of therapy in each case. The second part is a discussion of the changes in arterial blood pressure in the etipathogenesis of stroke. Arterial hypertension is an important factor in production of small infarctions. In the third section a review is made of the role of the heart in transitory ischemia and as a cause of cerebral infarctions. Lastly, the hematologic factors which might contribute to the development of cerebral ischemia, along with the other causes, are mentioned.
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PMID:[Practical considerations in dealing with cerebral ischemia (author's transl)]. 47 Apr 90

Hemodynamic monitoring and care of the patient at high risk for anesthesia require a careful and systematic approach. During preoperative evaluation the patient at increased risk must be identified and correctable problems must be solved. The patient's current medications must be reviewed because they may influence the choice of anesthetic approach and may alter the physiologic response to the stresses commonly associated with anesthesia. In addition to conventional clinical and electrocardiographic monitoring, perioperative hemodynamic monitoring may be desirable for patients at special risk, who are likely to have significant associated medical problems or to undergo complicated surgical procedures. No ideal induction agent exists, and hypotension secondary to peripheral vasodilation or myocardial depression, or both, is a potential problem. Patients with an inordinately high risk may benefit from mechanical circulatory assistance prior to induction of anesthesia. Attention to oxygenation, blood volume replacement and the prevention of hypertensive episodes are particularly important during anesthesia so that optimal cardiac performance is ensured and ischemia avoided. The stresses during emergence from anesthesia contribute to lability of the cardiovascular status and hypoxemia. The period of risk does not conclude with immediate recovery from anesthesia but extends through the postoperative phase. Careful monitoring and attention to the control of pain, prevention of hypotension and hypertension, adequate oxygenation, early mobilization and resumption of the administration of cardiac medications are important factors in a successful outcome.
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PMID:Hemodynamic monitoring and care of the patient of high risk for anesthesia. 49 83


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