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

The renin-angiotensin system has been implicated in the genesis of pre-eclampsia. To avoid fetal toxicity, five women were studied who developed hypertension, proteinuria, and edema in the last trimester of pregnancy and whose BP elevation persisted immediately postpartum. At about 6 hours after delivery the CE enzyme inhibitor (SQ 20,881) was given in incremental doses ranging from 0.25 to 3.0 mg. per kilogram intravenously, before and after diuresis with furosemide, 40 mg. intravenously. BP was measure every 2 minutes and PRA and angiotensin II concentration before treatment, 30 minutes after 0.25 to 0.30 mg. per kilogram, and 30 minutes after 2.0 to 3.0 mg. per kilogram. Echocardiographic assessment of CI and PVR was performed before treatment and after a maximum dose in three patients. Before diuresis, CE blockade had no effect on heart rate, BP, CI, PVR, or PRA, regardless of whether the patient was in positive or negative fluid balance or was sodium loaded or restricted over the preceding 24 hours. Angiotensin II fell by 77 and 10 per cent, respectively, after 0.25 mg. per kilogram was given to two patients, but rose slightly in the other three patients, then fell an average of 46 per cent after 1.0 to 3.0 mg. per kilogram were given. After diuresis, 1.0 mg. per kilogram resulted in a 24 per cent fall in BP which persisted for 3 hours in two patients and a 14 per cent fall which lasted for 30 minutes after 1.0 or 3.0 mg. per kilogram in a third patient. It is concluded that the BP elevation which persists after delivery in certain patients with pre-eclampsia is not angiotensin II dependent.
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PMID:SQ 20,881: effect on eclamptic--pre-eclamptic women with postpartum hypertension. 68 62

The modified Fontan operation has gained wide acceptance as a functional corrective procedure for patients with CHD with single ventricle physiology. Long-term survival and palliation of symptoms are excellent with most patients able to lead normal lives. The absence of a pulmonary contractile ventricle means that the single ventricle is responsible for perfusion of both the pulmonary and systemic circulations. Elevated systemic venous pressure is required to overcome PVR and this state of systemic venous hypertension has a significant impact on the anesthetic and postoperative care of these patients.
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PMID:The modified Fontan procedure: physiology and anesthetic implications. 149 5

In order to evaluate the hemodynamic effects of INPV, eight patients with COPD (FEV1/FVC, 54 +/- 6 percent; mean +/- SD), respiratory failure (PaO2, 52 +/- 6 mm Hg; PaCO2, 56 +/- 4 mm Hg), and clinical signs of inspiratory muscle fatigue underwent right cardiac catheterization while performing 20 minutes of INPV by a cuirass ventilator at a pressure (-20 to -40 cm H2O) able to reduce the diaphragmatic electromyographic activity. Patients showed a mild basal pulmonary artery hypertension. During INPV, no changes in the mean values of HR (from 79 +/- 20 to 80 +/- 18 beats per minute), systolic BP (141 +/- 19 to 139 +/- 16 mm Hg), CO (5.2 +/- 0.8 to 5.1 +/- 1.3 L/min), mean PAP (23.8 +/- 3.8 to 23.9 +/- 4.4 mm Hg), RAP (4.3 +/- 2.6 to 5.5 +/- 2.5 mm Hg), PWP (10.3 +/- 4.5 to 9.4 +/- 2.9 mm Hg), TPR (369 +/- 76 to 392 +/- 124 dynes.s.cm-5), and PVR (199 +/- 51 to 233 +/- 94 dynes.s.cm-5) were observed. Direct systemic BP monitoring could be performed in six patients. During INPV, three patients showed "pulsus paradoxus," as assessed by an inspiratory fall in systolic BP of 11, 13, and 20 mm Hg, respectively. We conclude that INPV by cuirass ventilator does not induce adverse hemodynamic effects in patients with COPD who have pulmonary artery hypertension.
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PMID:Hemodynamic effects of negative-pressure ventilation in patients with COPD. 218 97

Pulmonary blood volume (PBV) measurements have been reported in chronic lung disease that do not include diffuse interstitial lung disease (ILD) and cor pulmonale (CP). In this study, PBV was measured using the double injection single sampling method, at rest and at exercise in ten patients with ILD due to extrinsic allergic alveolitis (n = 6) or usual interstitial pneumonia (n = 4). Lung biopsies were obtained in 8 patients, and in none of them the stage of fibrosis was predominant over inflammation. The degree of vascular lesions was in four patients grade I and in four grade II (Heath-Edwards classification). At rest, most of the patients had elevated mean pulmonary artery pressure (PAP) and vascular resistance (PVR), (mean PAP 30 +/- 4 mmHg and 336 +/- 171 d.s. cm.-5, respectively), hypoxemia (paO2 = 48 +/- 2 mmHg) and a severely reduced PBV (53.6 +/- 11 ml.s.qm.). At exercise, pulmonary arterial hypertension worsened and, although PBV value increased significantly (rest = 53.6 +/- 11.6 ml.m2, s.qm. exercise 132 +/- 28 ml.s.qm.p less than 0.01) it remained abnormally low with respect to normal value. Comparison of the mean intravascular pressure-PBV measurements relationship in different lung diseases showed that ILD patients with CP have the greatest abnormality. Possible explanations for the severe reduction in PBV include restriction of extra-alveolar vessels as a consequence of lung volume loss, restriction of intra-alveolar vessels due to structural and functional changes imposed by the inflammation-fibrosis process and vascular restriction due to vasoactive factors (alveolar hipoxia).
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PMID:[Pulmonary blood volume in patients with interstitial pneumopathy and pulmonary heart disease. Its study at rest and during exercise]. 319 Mar 62

A combined haemodynamic and radionuclide approach was used to evaluate right ventricular performance in 16 adolescent and adult patients with cystic fibrosis (CF). There were nine patients with mild arterial hypoxaemia (PaO2 greater than 80% of predicted) and normal resting pulmonary artery pressure and seven patients with severe arterial hypoxaemia (PaO2 less than 70% of predicted) and resting pulmonary arterial hypertension (PH). The right ventricular ejection fraction (RVEF) by equilibrium angiocardiography using krypton 81m as a tracer and stroke volume index (SVI) by thermodilution techniques were measured simultaneously and right ventricular end-diastolic and end-systolic volumes were derived. RVEF was normal in CF patients without PH (58.9 +/- 7.2%) but was reduced in those with PH (45.4 +/- 2.6%). There was a statistically significant inverse linear correlation between RVEF and afterload as assessed by mean pulmonary artery pressure (Pap: r = -0.76) and pulmonary vascular resistance (PVR: r = -0.78), indicating that RVEF ist afterload-dependent. Right ventricular function, however, as assessed by right ventricular end-systolic pressure-volume relations was even higher in CF patients with PH, indicating preserved or even increased right ventricular function in the face of an increased afterload stress.
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PMID:Right ventricular performance and pulmonary haemodynamics in adolescent and adult patients with cystic fibrosis. 321 93

Mild pulmonary artery hypertension (PAP, 29.6 +/- 10.6 mm Hg, mean +/- SD) due to a 3-fold elevation of pulmonary vascular resistance (PVR, 2.2 +/- 1.1 mm Hg X L/min) is a common finding in severe ARDS. A vasodilator such as nitroprusside (151 micrograms/kg X min) can be administered in early ARDS and will lower PAP and PAOP (capillary wedge pressure) while increasing cardiac output (CO) from 6.9 to 8.75 L/min X M2 and venous admixture from 23% to 31.6%. This suggests diffuse vasoconstriction is present in early ARDS. In 19 patients with severe ARDS, 13 had vascular occlusions on balloon occlusion angiography, and these occlusions correlated with increased post mortem counts of PA thrombi. At autopsy, there was a considerable increase of PA medial thickness and a reduction of lumen diameter. This hemodynamic and morphologic evidence suggests both vasoconstrictor and anatomic changes play major roles elevating the PVR in ARDS.
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PMID:Vascular components of ARDS. Clinical pulmonary hemodynamics and morphology. 361 11

In this study we measured high fidelity pulsatile pressure and flow waveforms at the inlet to the pulmonary vascular bed to assess the differences in adaptation to acute and chronic pulmonary venous hypertension in awake dogs. Acute elevations in left atrial pressure (P1a) were effected by inflation of left atrial balloons, while chronic elevations were accomplished by placement of aorta to left atrial shunts. Pulmonary artery hydraulic impedance was calculated and analysis of these data revealed marked differences between the responses to acute and chronic elevations of left atrial pressure. The acutely stressed dogs (n = 12) had significantly decreased pulmonary vascular resistance (when P1a = 16.9 +/- 1.0 mm Hg, PVR = 212 +/- 57 dynes sec/cm5; when P1a = 28.6 +/- 1.4 mm Hg PVR = 18 +/- 115 dynes sec/cm5; control P1a = 6.1 +/- 1.5 mm Hg, and PVR = 355 +/- 69 dynes sec/cm5) and normal characteristic impedances (ZO) (210 +/- 36, 227 +/- 39, 178 +/- 14 dynes sec/cm5, respectively), indicating recruitment of arteriolar-capillary perfusion density and no change in proximal pulmonary arterial physical properties. The chronic pulmonary venous hypertension group (n = 11) retained normal PVR (496 +/- 30 dynes sec/cm5) but demonstrated a markedly higher characteristic impedance, ZO = 361 +/- 11 dynes sec/cm5 (P < 0.001). This indicated a measurably different and extremely potent effect of chronic venous hypertension on the physical properties of the pulmonary vessels with an apparently increased arterial stiffness correlating with a 4-fold increase in Young's elastic modulus. These changes were not reversed by alpha-adrenergic blockade or acute lowering of left atrial pressures.
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PMID:An analysis of the pulsatile hemodynamic responses of the pulmonary circulation to acute and chronic pulmonary venous hypertension in the awake dog. 610 64

A woman with moderate PA hypertension and elevated PVR due to congenital heart disease experienced no serious complications from pregnancy. Although the outcome of this pregnancy in this patient was successful, this case suggests that the presence of even moderate maternal pulmonary hypertension with pregnancy should be viewed with caution.
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PMID:A pregnant woman with moderate pulmonary hypertension. 775 99

Fibromuscular dysplasia (FMD) is a nonatherosclerotic segmental disease of unknown etiology primarily affecting muscular arteries of intermediate size. The pathology affects the renal arteries in the majority of cases, followed by the carotid, vertebral, and ilio-femoral arteries. There have been only six reported cases of FMD involving the brachial artery. This case report describes the seventh case and illustrates an endovascular approach to this clinical entity. A 63-year-old female with a history of hypertension presented to vascular surgery clinic with a 4-day history of numbness, pain, and coolness of her left hand. On physical exam, the patient had a normal axillary and brachial pulse, but had only a Doppler signal of the left ulnar artery. There was no Doppler signal of the radial artery. Segmental pressures and PVR waveforms were normal in the upper arm, but there was a significant blunting of the waveform and decrease in pressure at the level of the wrist. An arteriogram revealed significant narrowing and irregularity of the brachial artery with a characteristic "string-of-beads" appearance. There was complete thrombosis of the radial artery and evidence of fresh thrombus in the distal brachial artery. The patient was treated with intra-arterial infusion of urokinase with restoration of the radial pulse and resolution of her symptoms. Subsequently, the patient had a percutaneous transluminal balloon angioplasty of the involved segment of brachial artery, with normal PVR's and segmental pressures upon completion. FMD of the brachial artery and its sequelae are extremely rare, and therefore, there is no consensus on proper management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibromuscular dysplasia of the brachial artery: an endovascular approach. 785 78

Nitric oxide (NO) has been reported to be an endothelium-derived relaxing factor, and hypoxic pulmonary vasoconstriction seems to be enhanced by inhibitors of endothelially dependent vascular relaxation. We examined the circulatory effects of inhalation of 15 ppm NO in air in 14 hypoxic patients suffering from chronic obstructive pulmonary disease (COPD). Of these patients 4 breathed 100% O2 before NO. The effects of NO inhalation on pulmonary gas exchange were also studied in 12 of these patients using the multiple inert gas elimination technique, 3 of whom breathed air, 100% O2, and 15 ppm NO in air in succession. Under baseline conditions, both mean +/- SD pulmonary artery pressure and pulmonary vascular resistance were increased (Ppa = 24.3 +/- 10.4 mm Hg and PVR = 3.3 +/- 1.1 mm Hg/L/min, respectively). Although the pulmonary circulatory effects were not immediate, with no detectable changes after 1 min NO inhalation, Ppa and PVR fell significantly (-19.1 +/- 10.5%, p < 0.02 and -29.3 +/- 15.1%, p < 0.02, respectively) after 10 min NO inhalation. Moreover, the extent of the NO-induced reduction in Ppa was found to depend on the level of baseline pulmonary arterial hypertension. No systemic circulatory effects were observed. The mean VA/Q ratio and the dispersion of ventilation and blood flow distributions were not altered by NO inhalation, although there was a significantly higher percentage of ventilation (7.3 +/- 7.3%, p < 0.05) in poorly and unperfused areas (VA/Q > 10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of inhaled nitric oxide on hemodynamics and VA/Q inequalities in patients with chronic obstructive pulmonary disease. 800 2


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