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

This report describes the case of a 59-year-old man who was scheduled for general anesthesia with propofol, sufentanil and sevoflurane for removal of a metal implant. The patient was classified as American Society of Anesthesiologists (ASA) II status because of an asymptomatic mitral valve prolapse and medically treated arterial hypertension. During induction of narcosis a pulsoxymetrically measured inadequate increase in oxygen saturation after preoxygenation was noticed and a moderate respiratory obstruction occurred intraoperatively, but anesthesia was uneventfully completed and the patient was extubated. However, 3 h later the patient developed severe dyspnea, hypoxia, tachycardia and arterial hypotension. Physical examination revealed a new grade 4/6 systolic murmur radiating to the axilla and X-ray showed bilateral pulmonary edema. Neither electrocardiographic nor biochemical manifestations of acute myocardial infarction were identified but transthoracic echocardiography revealed fluttering of the posterior leaflet of the mitral valve with grade III regurgitation and dilation of the left atrium. Coronary angiography was normal and left ventriculography confirmed severe mitral regurgitation. Mitral valve repair was successfully performed 22 h after presentation of symptoms. Mitral regurgitation is a common finding on echocardiography, seen to some degree in over 75% of the population. The etiology of mitral valve insufficiency which can be caused by pathologic changes of one or more of the components of the mitral valve, including the leaflets, annulus, chordae tendineae, papillary muscles, or by abnormalities of the surrounding left ventricle and/or atrium are discussed. Rupture of mitral chordae tendineae is infrequent and causes acute hemodynamic deterioration and needs corrective surgery. Valve replacement should be performed only if mitral valve repair is not possible. Echocardiography is an invaluable tool in determining the severity of regurgitation, the integrity of the mitral valve apparatus, the extent of left ventricular enlargement, and the ejection fraction. Acute mitral valve regurgitation caused by a rupture of chordae tendineae should be considered in the differential diagnosis of perioperative acute pulmonary edema.
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PMID:[Postoperative acute mitral regurgitation. Unexpected finding after minor non-cardiac surgery]. 1860 54

Many kinds of side effects are likely to occur while managing difficult airway. This article describes a case of a man who fell into pulmonary edema and heart failure during the difficult airway management. He was to undergo arthroscopic surgery on his knee. At first, we planed spinal anesthesia but he took an antiplatelet drug (aspirin). Since we wanted to avoid the epidural hematoma, we chose general anesthesia. After induction of general anesthesia, positive pressure ventilation via face mask was possible, but laryngeal mask ventilation was impossible. Although tracheal intubation was attempted, we recognized that he had difficult airway. After some intubation trials, we decided to quit the operation and awoke the patients. Spontaneous breathing appeared soon, but the oxygenation was getting worse. We performed fiberoptic nasal intubation under spontaneous breathing. Although his blood pressure was quite high during intubation, after intubation the vasopressor was needed to maintain blood pressure. Ventilation with 100% O2 could not maintain the oxygenation well. Chest X-ray revealed the pulmonary edema. We presumed that hypertension associated with airway stimulation had caused acute pulmonary edema and heart failure resulting from diastolic dysfunction induced by increased catecholamine.
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PMID:[Case of pulmonary edema and transient heart failure during difficult airway management]. 1917 26

A patient was presented with four days of vomiting, abdominal pain and sweating. At presentation the Capillary Blood Glucose (CBG) was 1.7 mmol/L, the Blood Pressure (BP) was 182/102 mmHg, and the pulse 100 bpm. On examination, he was sweaty, pale and cold. The initial differential diagnosis was hypoglycaemia secondary to insulin abuse, hypoadrenalism or insulinoma, the transient hypertension being considered a consequence of sympathetic stimulation. He remained clinically well overnight with a CBG of 10-14 mmol/L following intravenous glucose. The next morning he complained of nausea and abdominal pain. The BP had risen to 203/127 mmHg when he was later reviewed, having been given 10mg intramuscular metoclopramide. Shortly afterwards, he developed acute pulmonary oedema and had become hypoglycaemic again; a phaeochromocytoma crisis was suspected. Treatment with alpha-adrenoceptor blockade with intravenous phenoxybenzamine was advised. However, the patient deteriorated and died in the Intensive Care Unit within two hours. Autopsy examination confirmed a phaeochromocytoma in the left adrenal, with haemorrhage within the head of pancreas, but no evidence of a pancreatic tumour.
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PMID:Phaeochromocytoma crisis presenting with profound hypoglycaemia and subsequent hypertension. 1926 23

A 55-years-old woman, with a history of hypertension and ischemic stroke with residual left hemiparesis, was admitted to our hospital because of dyspnoea with clinical evidence of acute pulmonary edema. She was found to have a sinus tachycardia with ST-elevation in leads D1, aVL and V1-V4 in the electrocardiogram, and akinesis of the left ventricular apex with overall left ventricular systolic function being severely impaired and an ejection fraction of 28% on echocardiography. Orotracheal intubation was performed and mechanical ventilation was immediately started. Emergency cardiac catheterization was performed 2 h after the symptom onset. Coronary angiography showed no significant coronary artery disease. Blood analysis revealed an increase in the creatine kinase MB fraction, a significant positive detection in troponin T, a white blood cell count of 35000 per microliter, C-reactive protein of 59,9 mg/dl, and transient elevation in the concentration of free triiodothyronine, free thyroxine, thyroid globulin antibody, and thyroid peroxidase antibody. The symptoms improved during the next days, and follow-up echocardiography 18 days later showed complete resolution of the left ventricular dysfunction. These data suggest that tako-tsubo cardiomyopathy may be induced in patients with sepsis and transient hyperthyroidism.
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PMID:Tako-tsubo cardiomyopathy observed in a patient with sepsis and transient hyperthyroidism. 1964 11

In this study, we describe the development of acute pulmonary oedema and cardiac arrest after therapeutic ascitic paracentesis, in a gentleman with decompensated liver cirrhosis. There was no previous history of cardiorespiratory symptoms or disease. Postmortem examination revealed oedematous and congested lungs with bilateral pleural effusions; in addition, the right heart was dilated and congested. Micronodular cirrhosis was present with histological features of alpha1 antitrypsin deficiency. This is the first study of acute cardiac decompensation after large volume paracentesis. Owing to the postmortem findings, underlying asymptomatic cardiorespiratory disease may have been present. Cirrhosis is associated with cardiovascular complications including cirrhotic cardiomyopathy, portopulmonary hypertension and hepatopulmonary syndrome which may manifest or worsen under situations of haemodynamic stress. This report thus raises the question whether routine screening for cardiovascular abnormalities is warranted in patients with decompensated cirrhosis, particularly before the procedures such as paracentesis that impose significant haemodynamic strain.
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PMID:Pulmonary oedema after therapeutic ascitic paracentesis: a case report and literature review of the cardiac complications of cirrhosis. 2063 44

1. The presence of proteinuria is not essential to the diagnosis of pre-eclampsia under many diagnostic consensus statements. The aim of the present study was to assess maternal and perinatal outcomes after proteinuric pre-eclampsia compared with other non-proteinuric disease presentations. 2. An individual patient data review (n = 670) was undertaken for 2003-2006 at a tertiary referral centre in Sydney (NSW, Australia). Women were diagnosed in accordance with the Australasian Society for the Study of Hypertension in Pregnancy Consensus Statement. Data were analysed with the Chi-squared test, t-tests and non-parametric tests. Statistical significance was set at P < 0.05. 3. The proteinuric cohort had higher systolic and diastolic blood pressure recordings than the non-proteinuric cohort (160/102 and 149/94 mmHg, respectively; P < 0.001), and were also administered magnesium sulphate more frequently (44 vs 22%, respectively; P < 0.001), delivered at earlier gestation (37 vs 38 weeks, respectively; P < 0.001), required operative delivery more frequently (63 vs 48%, respectively; P < 0.001) and received more antihypertensive medications during the antenatal period (72 vs 57%, respectively; P < 0.001). Acute renal failure and acute pulmonary oedema were rare. Four cases of eclampsia all occurred in non-proteinuric women. The perinatal mortality rate was lower for the offspring of women with proteinuric pre-eclampsia compared with offspring of non-proteinuric women (13/1000 and 31/1000, respectively; P = 0.006). 4. The results of the present study indicate that the presence of proteinuria denotes a group of women who have higher antenatal blood pressure, who deliver at earlier gestation and require operative delivery more commonly, although it is not an indicator of other markers of maternal morbidity or perinatal mortality.
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PMID:Role of proteinuria in defining pre-eclampsia: clinical outcomes for women and babies. 1993 Apr 27

Transfusion-related acute lung injury is a clinical syndrome that occurs within 6 hours of transfusion. It is the leading cause of transfusion-related mortality. It presents with shortness of breath, acute pulmonary edema, fever, hypotension, or hypertension followed by hypotension. Treatment consists of respiratory support and fluid administration to support blood pressure. A majority of cases are associated with antibodies to white blood cells in the blood donor. Blood centers in the United States are currently taking measures to reduce the risk of transfusion-related acute lung injury from blood components.
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PMID:Transfusion-related acute lung injury. 2007 82

Most chronic dialysis patients are volume overloaded. This has two consequences. The first is hypertension. Even though the pathophysiologic mechanism causing this blood pressure (BP) elevation is well known, many patients are treated with antihypertensive drugs. These are often ineffective and, even if they lower BP, they do not eliminate its cause and the associated cardiac damage. But at least as harmful to the heart as the pressure load is the volume load. In the early phase of dialysis, this may lead to acute pulmonary edema, which is often erroneously referred to as "heart failure." Later, it causes dilatation of the heart compartments, stretching of their walls, and regurgitation through the valves. This dilated cardiomyopathy eventually leads to liver congestion, decreased ejection fraction, and low blood pressure. It is considered to be irreversible and incorrectly called "uremic" by many authors, but can be markedly improved and even cured by judicious ultrafiltration. This may take many months, since the heart muscle needs time to become "remodeled." All these unwanted effects could be prevented by strong dietary salt restriction. We tried to analyze why this and other "old truths" are being forgotten. While the reasons are clearly multifactorial, the unfortunate introduction of the Kt/V concept seems the most important one. The claim that adequacy of dialysis can be solely defined by urea removal, disregarding all other factors, above all salt retention, has diverted the nephrologist's attention from the most important issue, giving them the false conviction that the prescribed treatment is "adequate."
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PMID:Unpleasant truths about salt restriction. 2033 8

The hemodynamic and cardiovascular changes seen during PE vary according to the natural history of the disease, its severity and eventual therapeutic measures taken. In the early stages of pregnancy, patients who will eventually develop PE, present with a blood pressure which even though within normal limits, is higher than in other women. Similarly, their cardiac output is higher with a normal or decreased peripheral vascular resistance. As soon as the clinical signs of the disease appear, the hemodynamic picture usually shifts toward that of a high peripheral resistance with low cardiac output. Sometimes however, a clinically hyperkinetic circulation may be demonstrated. In PE patients, cardiac preload pressures are usually normal even though the circulatory volumes are lower by 600 to 800 ml when compared to those found in normal pregnancy. The cardiac function is however usually preserved during PE. PE induces an exaggerated capillary permeability. This results in the worsening of the airway edema which may render the intubation very difficult. The increased capillary permeability contributes, among other factors, to the heightened risk of acute pulmonary edema. It is not justified to administer an anti-hypertensive treatment to PE women presenting with only moderate hypertension. An anti-hypertensive treatment must only be initiated whenever the hypertension is severe (i.e. SBP> or =160 mmHg and/or DBP> or =110 mmHg) in order to reduce the risk of maternal complications. In the absence of objective comparative data assessing anti-hypertensive agents for the PE patient, the choice of therapy relies predominantly on the practitioners' own experience. Systematic circulatory volume expansion has not been proven to improve the maternal nor the neonatal prognosis. Such treatment is to be reserved solely for situations in which correcting a hypo-volemia is absolutely necessary. The treatment of acute pulmonary edema in a PE patient is symptomatic and includes the administration of vasodilating agents and of diuretics. A benefit in setting-up an invasive monitoring of the pulmonary artery occlusive pressure has not been demonstrated. The sonographic surveillance of the hemodynamic state can however be useful in these circumstances.
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PMID:[Circulatory and respiratory problems in preeclampsia]. 2034 59

Here we report an unusual development of peripartum cardiomyopathy (PPCM) in a parturient woman with preeclampsia. A 36-year-old nulliparous parturient woman underwent elective cesarean section for delivery of twins under spinal anesthesia. Both preoperative workup and past history were unremarkable except for proteinuria and hypertension for 1 week. Approximately 4 hours after cesarean section, progressive orthopnea developed. Chest plain film showed acute pulmonary edema, bilateral pulmonary infiltration with interstitial patches, and cardiomegaly. Postpartum cardiomyopathy was diagnosed afterward by echocardiography. This showed general hypokinesia and severe dysfunction of the left ventricle with ejection fraction of 15-20%. She was admitted to the intensive care unit for further management. Fortunately, the patient recovered after treatment and was discharged 15 days later. This case illustrates that we should bear in mind the possibility of PPCM if orthopnea develops while delivery is approaching in a parturient with preeclampsia. Echocardiography is helpful for early diagnosis of PPCM.
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PMID:An unusual case of peripartum cardiomyopathy in a parturient with preeclampsia. 2043 11


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