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

A prospective study was performed in our center on 60% (n = 36) of patients with systemic lupus erythematosus (SLE) to determine the prevalence and severity of pulmonary hypertension. Twenty-six healthy subjects of similar age and sex served as controls. Pulmonary artery systolic pressure was calculated from the sum of the peak tricuspid insufficiency Doppler pressure gradient and an estimate of right atrial pressure based on inferior vena cava size and its degree of inspiratory collapse. Five patients with SLE (14%) had pulmonary hypertension, defined as pulmonary artery systolic pressure greater than 30 mm Hg. Cardiac indices determined by planimetry of biplane apical 2-dimensional echocardiographic images were low or normal in the patients with pulmonary hypertension implying increased pulmonary vascular resistance as the etiology for elevated pulmonary artery pressure. The mean pulmonary artery systolic pressure in patients with SLE was 25 +/- 10 mm Hg vs 20 +/- 2 in controls (p = 0.002). No control had a pulmonary artery systolic pressure greater than 23 mm Hg. Patients with pulmonary hypertension had a shorter duration of SLE and steroid therapy and a higher prevalence of cytotoxic treatment and Raynaud's phenomenon in comparison to those with normal pulmonary artery pressures. The prevalence of systemic hypertension, interstitial lung disease, pleurisy, pericarditis, cutaneous manifestations, arthritis, renal disease, central nervous system involvement, and hematologic abnormalities was similar in patients with SLE with normal and elevated pulmonary artery pressure. Our study suggests that pulmonary hypertension in SLE is common but usually mild.
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PMID:Pulmonary hypertension in systemic lupus erythematosus. 233 68

In hypertension, coronary flow is augmented and oxygen balance is adequate despite an increase in coronary resistance. For the maintenance of flow in the presence of and after regression of ventricular hypertrophy, the ratio of pressure and ventricular mass must remain normal. Coronary reserve would be altered if treatment normalized pressure but not ventricular mass or if pressure were lowered too fast. We investigated 42 patients with primary hypertension. In 28 (Group I) left ventricular mass index (by ultrasound) was within the mean value +2 SD (96 + 38 g/m2) of 145 controls and exceeded these values in the remaining 14 patients (Group 2). The diastolic pressure was lowered rapidly to between 85 and 90 mm Hg with two potent vasodilators, nifedipine (sublingually) and nitroprusside, while a 12-lead electrocardiogram was recorded continuously. During both tests, seven patients in Group 2 (responders) showed inversion of normal T waves, in lead I, aVL, and V3-6. These changes waxed and waned in parallel with the pressure fall and recovery and were not attributable to alterations in adrenergic tone, conduction disturbances, variations, or group differences in the QRS axis, QTc interval, heart rate, left ventricular fractional shortening, wall stress, rate of dimension increase in early diastole, or isovolumic relaxation. A ""steal phenomenon'' or passive collapse in compliant coronary lesions during vasodilatation seems unlikely; in fact, patients were free from coronary symptoms, and the electrocardiographic alterations occurred only in seven patients in Group 2, who had a greater left ventricular mass index and required a larger pressure drop to return the diastolic pressure to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Jan
PMID:Cardiac hypertrophy in hypertension. Repolarization abnormalities elicited by rapid lowering of pressure. 296 41

Calcium blockers (CB) are routinely used. This could lead to possible interference with anaesthetic drugs. CB prevent calcium from entering the cell by inhibiting the slow voltage-dependent calcium channels. They act mostly on heart and smooth muscle. Of all the possible indications, the three that are confirmed are coronary heart disease, arterial hypertension and supraventricular rhythm disturbances. Most of the work published and the cases reported concerns interactions between CB and halogenated anaesthetic agents; the latter's actions on the heart depend on cellular calcium exchange. Also, the cardiovascular effects of these anaesthetics are similar to that of CB. Experimentally, halothane and enflurane have direct cardiac inhibitory effects similar to verapamil and diltiazem, whereas isoflurane's properties seem closer to the dihydropyridines (nifedipine and nicardipine). Giving verapamil or diltiazem increases the number of sino-atrial and atrio-ventricular blocks when using a halogenated agent. Clinically, interpreting the effects of CB during anaesthetic induction is difficult because of the pathology (coronary heart disease, cardiac failure), the other drugs (beta-blockers and nitrates) and the type of anaesthesia (emergency or elective). Interactions can give rise to anything from a severe cardiovascular collapse, requiring catecholamines, to a mild fall in blood pressure which responds well to plasma expansion, or even no effect on blood pressure. Rebound is seen on stopping CB in patients with coronary heart disease or arterial hypertension; stopping them before surgery does not therefore seem justified. However, extreme care must be taken when using halogenated agents for patients under treatment with CB and/or beta-blockers. A wary anaesthetist will be able to adapt the technique to the patient. It has been suggested that CB could be used to treat preoperatively myocardial ischaemia (diltiazem), hypertensive crises (nifedipine, nicardipine) and ventricular rhythm disturbances (verapamil); this must be done with caution, the patient being closely monitored (haemodynamic and electrocardiographic monitoring). Postoperatively, intranasal nifedipine, continuous intravenous nicardipine or diltiazem have been used to treat increases in arterial blood pressure during recovery and to adapt the cardiovascular system to the increased metabolic needs. Here again, close patient monitoring is essential. In any case, treatment with CB which has been stopped should be started up again as soon as possible.
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PMID:[Calcium inhibitors and anesthesia]. 297 26

Effects of brevetoxin were evaluated in cats anesthetized with pentobarbital under conditions of controlled end-expiratory pCO2 and constant body temperature. Recordings were made of arterial blood pressure, heart rate, respiratory pattern, diaphragm EMG, evoked tibialis muscle twitch and evoked contraction of the nictitating membrane. Electrical stimulation was employed for periodic excitation of the medullary respiratory center, the phrenic nerve, the peroneal nerve and the cervical sympathetic nerve. Brevetoxin was prepared at a concentration of 1.0 mg/ml in an aqueous medium of 2.5% ethanol plus 2.5% Emulphor 620 (General Aniline and Film Corp., New York). Small i.v. bolus injections of the toxin (40 micrograms/kg) evoked, without tachyphylaxis, the Bezold-Jarisch reflex triad of bradycardia, hypotension and bradypnea. This effect was essentially abolished by vagotomy. Continued injections then resulted in pressor reactions and tachycardia, along with the development of respiratory dysrhythmia. Large doses of brevetoxin (160 micrograms/kg i.v.) caused somatomotor seizures accompanied by severe hypertension, that occurred even after decerebration and cervical spinal cord transection. Cranial intra-arterial and intra-cerebroventricular injections of brevetoxin produced hypertension and respiratory depression more effectively than did i.v. injections. Systemic cumulation of the toxin, with the respiration supported artificially, caused death from cardiovascular collapse, without significant blockade of neuromuscular and ganglionic transmission. It is concluded that brevetoxin exerts its major toxic effects on the circulation and respiration through reflex and central actions, largely sparing peripheral motor mechanisms.
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PMID:Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats. 299 23

This paper summarizes the role of the renal pressure natriuresis and diuresis mechanisms in maintaining sodium and water balance in hypertension. In all forms of chronic hypertension studied to date, the renal pressure natriuresis and diuresis mechanisms are abnormal, since increased arterial pressure is required to maintain normal excretion of sodium and water, and therefore fluid balance. When renal perfusion pressure is prevented from increasing in various forms of experimental hypertension, caused by infusion of mineralocorticoids, angiotensin II, vasopressin, or norepinephrine and adrenocorticotrophic hormone (ACTH), sodium and water retention continues until ascites, pulmonary oedema and circulatory collapse occur within a few days. Thus, chronic hypertension appears to be an essential homeostatic response that permits sodium and water balance to be maintained despite various abnormalities which tend to decrease renal excretory capability. The intrarenal mechanisms by which increased renal perfusion pressure maintains sodium and water balance in hypertension have not been fully elucidated, but appear to involve small changes in glomerular filtration rate (GFR) and reductions in fractional sodium reabsorption, due either to the direct hydraulic effects of pressure or to various indirect effects, such as changes in angiotensin II formation.
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PMID:Mechanisms of sodium balance in hypertension: role of pressure natriuresis. 302 42

Physiologic and morphologic techniques were used to study kidneys of cardiac transplant recipients treated with either low-dose (low-CsA) or high-dose (high-CsA) cyclosporine. After 12 months both low-CsA (4.6 +/- 0.4) and high-CsA (6.3 +/- 0.3 mg/Kg/24 hr, p less than 0.01) were associated with azotemia and hypertension; GFR with each regimen was depressed below values in a third group treated without CsA (no-CsA) by 40-47%, while corresponding renal vascular resistance was elevated greater than 2-fold (P less than 0.01). Morphologic changes in both CsA groups included an obliterative arteriolopathy with downstream collapse or sclerosis of glomeruli. Determination of renal arcuate vein occlusion pressure revealed an increasing renal artery-to-peritubular capillary pressure gradient between 1 and 12 months of CsA therapy. Fractional clearances of dextrans of graded size were elevated at each time compared with the no-CsA group. Analysis of dextran transport with an isoporous membrane model indicates that transglomerular hydraulic pressure difference (delta P) approximated 39 with no-CsA, but was reduced with low-CsA therapy to about 30 at 1 month, and about 34 mmHg after 12 months. We conclude that chronic CsA therapy induces constriction and eventual occlusion of afferent arterioles, causing downstream glomerular damage that is irreversible. Low versus high dosage of CsA confers only marginal protection against this serious microvascular injury.
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PMID:Chronic injury of human renal microvessels with low-dose cyclosporine therapy. 305 92

Pulmonary arterial rupture due to the use of a Swan-Ganz catheter is a rare accident, with an estimated 2% incidence rate. It is fatal in almost 50% of cases. Predisposing factors are age greater than 60 years, pulmonary arterial hypertension and anticoagulant treatment. In patients older than 60 years, changes in the arterial wall increase the risk of rupture; pulmonary hypertension leads to too distal a movement of the catheter, and a concomitant treatment with anticoagulant drugs increases the amount of blood lost. Handling errors when setting up the catheter are often the cause of these accidents, especially a balloon too blown up and a catheter pushed too far. A subsequent movement of the catheter can be a cause of rupture during cardiac surgery. Haemoptysis is the major symptom of this accident, being found in 90% of cases. It can however be of minor importance; if it is ignored, this can lead to a secondary overwhelming haemorrhage. The haemorrhage can be life-threatening because of the cardiovascular collapse and acute respiratory failure by asphyxia. The treatment can only be carried out in intensive care. It will depend on the severity of the accident. It can go from an expectant wait after partial or total removal of the catheter, to an emergency thoracotomy for vascular suture, segmentectomy or even lobectomy. Intermediate measures include turning the patient onto the healthy side, injecting adrenaline or a clot of the patient's blood by the distal end of the catheter, placing a Fogarty catheter in the affected bronchus, or tracheal intubation with a double-lumen catheter and using mechanical ventilation with PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Perforation of the pulmonary artery following Swan-Ganz catheterization]. 306 41

A case of inadvertent intravascular injection of PGF2alpha during induction of labor by intraamniotic injection for fetal demise, involving alternating extreme hypotension and hypertension, is described. The woman was a 29-year old in late 2nd trimester with oligohydramnios, but no other related history. She was given epidural anesthesia, 7.5 mg midazolam and 5 mg morphine S04 for anxiety. Because of oligohydramnios, 300 ml Ringers lactate was instilled to dilute the PG. A test dose of 1 mg PGF2alpha was tolerated well. 80 g urea and 20 mg PGF2alpha were injected over 10 minutes. A few minutes later contractions began, followed by complaints of burning on face and chest and dyspnea. Oxygen was given by mask. Systolic pressure fell to 70 mm by cuff; peripheral pulses could not be palpated, but the patient remained alert and oriented. She was given 35 mg ephedrine and increased iv fluids. She remained dyspneic, her extremities became mottled, and she complained of chest pressure, severe headache and severe breast tenderness. Blood pressure rose to 220/135 mm Hg; pulse to 95, and respiratory rate to 44. Pulse oximetry, detectable at the earlobe only, was 94% saturation. After 50 mg labetalol, blood pressure fell to 134/77, but symptoms remained. For 2 hours blood pressure swung between 76/50 and 225/125, until delivery of the fetus. An arterial line could not be started because of extreme vasoconstriction. Central venous pressure was 13 cm H20. After artificial rupture of the membranes and removal of remaining PG, blood pressure stabilized. Delivery was accomplished without incident. The symptoms and labile blood pressure were considered to be due to intravascular injection of PGF2alpha, caused by repeated bolus injection at each uterine contraction. In case of PG induction for fetal demise, it is recommended that anesthesiologists be prepared to treat intravascular collapse, hypertension and bronchoconstriction.
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PMID:Life-threatening effects of intravascular absorption of PGF2 alpha during therapeutic termination of pregnancy. 318 4

Myocardial infarction and cerebrovascular accidents kill more people than all other causes of death combined, and hypertension is the single most important risk factor involved. From studies it is known that about 7% to 10% of adult dental patients will suffer previously unsuspected hypertension and which can be detected as a result of blood pressure screening programmes. Dentists can provide this valuable service in regard to total health care of their patients. Also by having base-line records of blood pressure for their patients and by maintaining competence in blood pressure measurement, a dentist is much better prepared to accurately assess and manage cases of collapse which may occur at any time.
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PMID:Dental office screening for hypertension. 327 May 64

We evaluated a chronic renal injury in 37 cardiac transplant recipients treated for 12 to 24 months with cyclosporine (CsA). Twenty-four cardiac transplant recipients treated with azathioprine for more than 24 months served as controls. Despite equivalent cardiac performance, GFR in those treated with CsA was depressed, 47 +/- 3 versus 94 +/- 4 ml/min/1.73 m2 (P less than 0.001). CsA therapy was also associated with significant elevation of renal vascular resistance (RVR), proteinuria, arterial hypertension, and impaired intrarenal conversion of inactive prorenin to active renin. Histopathological changes associated with CsA included an obliterative arteriolopathy with deposition of proteinaceous material in necrotic arteriolar walls, and associated tubulointerstitial damage. A minority of glomeruli exhibited either ischemic collapse or sclerosis. Area perimeter analysis revealed enlargement of the remaining glomeruli with significant expansion of the mesangium. Longitudinal examination over a 48 month period (N = 15) during which CsA was reduced in dosage or withdrawn revealed persistent hypofiltration, increasingly elevated RVR and heavier proteinuria. Further histopathological deterioration was observed when renal tissue was sampled a second time in six patients, and three members of the experimental group developed end-stage renal disease. We conclude that continuous CsA therapy for more than 12 months causes a chronic injury to renal microvessels that is rarely reversible and potentially progressive.
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PMID:The long-term course of cyclosporine-associated chronic nephropathy. 328 2


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