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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study on pulmonary hemodynamics, radionuclide right ventricular ejection fraction and blood gas analysis in 62 cases of COPD induced cor pulmonale at different stages showed the following results: 1. In early stage of cor pulmonale, stroke volume could not increase after exercise, it proved that cardiac reserve has been reduced; 2. With the progression of the disease, cardiac stroke volume reduced but cardiac output increased gradually, it could be considered as the evolutionary characteristic of cardiac function in chronic cor pulmonale; 3. The right ventricular stroke work was normal and could increase with the rise of after-load, reflecting the relatively effective functional compensation; 4. In acute exacerbation of cor pulmonale, the cardiac failure should be attributed to hyperdynamic type with hypervolemia; 5. Correlation analyses suggested that cardiac output decreased along with the increase of right ventricular afterload only in acute exacerbation of late cor pulmonale; PaO2 and PaCO2 have only slight influence on right ventricular function.
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PMID:[The changes of right ventricular function in the course of COPD induced cor pulmonale]. 840 24

To develop criteria for determining predisposition to pulmonary edema in patients with glomerulonephritis, clinical, laboratory and X-ray examinations were made in 697 patients with glomerulonephritis at different stages of its development. X-ray examination included chest tele X-ray and its densitometric analysis. Twenty two patients underwent computerized tomography with histographic analysis. In 106 patients, X-ray findings were compared with the volume of circulating blood, cardiac and stroke indices. Changes in the lungs and pleural cavities were found in 22.7%, pulmonary edema was revealed in 15.7% of the patients. The prognostically unfavourable criteria for the development of pulmonary edema were found to be Stage II pulmonary venous hypertension with hypervolemia and peripheral edemas. The densitometrically detected increase in the density of the lower lungs in patients with Stage II venous hypertension suggests early manifestations of interstitial edema of the lung and the narrowing of the histogram angle limited by its ascending and descending lines is indicative of the fact that interstitial edema progresses to alveolar one.
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PMID:[The x-ray diagnosis of a predisposition to nephrogenic pulmonary edema in glomerulonephritis patients]. 875 10

Exercise induced hypervolemia is well documented following the initial onset of chronic exercise. In trained man, however, it might be difficult to induce further PV expansion with exercise induced hypervolemia already present. Therefore the primary goal of this study was determine the effect of acute high intensity exercise on plasma volume (PV), cardiac output (CO), stroke volume (SV), heart rate (HR), and oxygen consumption (VO2), in fourteen male competitive runners (VO2max 60.7 +/- 6.4 ml.kg-1.min-1) in the middle of their season. In this well trained state, subjects twice performed three steady state runs at different speeds, and one maximal graded exercise test (baseline). After this baseline evaluation, subjects exercised at a high intensity (approximately 90-95% of VO2max) on 2 consecutive days (short-term high intensity STHI exercise). Subjects then repeated the submaximal runs and maximal exercise test (post high intensity exercise, PHIE). Following the intense exercise period, the subjects experienced an increase in PV of 4.4% (p < 0.05), HR was significantly reduced for any given running speed (p < 0.05) as was blood lactate concentration (p < 0.05), and SV was significantly increased by 4% (p < 0.05). Both CO and VO2 at submaximal running speeds were unaffected by the acute increase in exercise intensity. Maximal HR was also significantly reduced following the intense exercise (p < 0.05), but VO2max was unchanged. These data illustrate that STHI exercise can induce a secondary hypervolemia at a given work rate in trained man. These findings support scientific and anecdotal reports of a reduced HR response at a given work rate PHIE.
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PMID:Evidence of a secondary hypervolemia in trained man following acute high intensity exercise. 881 3

It seems that hypervolemia and vasodilatation coincide in compensated cirrhosis, but neither rank nor importance of these factors has been fully clarified in adaptive response to postural change. We studied, with gated equilibrium radionuclide angiography and thoracic electrical bioimpedance the hemodynamic status of 19 patients with compensated cirrhosis and 18 healthy subjects in upright and supine positions. In the upright position, the cirrhotic patients were hypotensive and had decreased peripheral vascular resistance despite increased cardiac output. The transition to the supine position was accompanied by a significant fall in the heart rate and an increase in the stroke volume in both controls (92 +/- 22 to 63 +/- 10 beats/min, and 38 +/- 9 to 62 +/- 19 ml/m2, respectively) and cirrhotic patients (101 +/- 20 to 79 +/- 13 beats/min, and 44 +/- 15 to 63 +/- 19 ml/m2, respectively). Besides, the diastolic arterial pressure fell in controls from 89 +/- 9 mmHg to 81 +/- 11 mmHg; p < 0.01, while it remained unchanged in cirrhotic patients (77 +/- 17 vs 82 +/- 13 mmHg). In the supine position, the cirrhotic patients presented tachycardia and left ventricular hyperkinesy (increased velocity of left ventricular filling and emptying). In conclusion, these results show that in compensated cirrhosis the decreased arterial tone and peripheral blood pooling are important factors of adaptive hemodynamic reaction to postural change.
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PMID:Cardiovascular status after postural change in compensated cirrhosis: an argument for vasodilatory concept. 906 72

Continuous positive airway pressure (CPAP) is used to treat congestive heart failure (CHF). Mechanisms for improved cardiac output (CO) include increased left ventricular (LV) surface pressure, changes in sympathoadrenal tone, nonadrenergic vasodilation, or shifting blood volume from intra- to extrathoracic compartments. At CPAP = 0 and CPAP = 5 cm H2O we measured CO, LV surface pressure, plasma norepinephrine (PNE), and systemic vascular resistance (SVR) in normal and hypervolemic pigs and pigs with CHF (rapid ventricular pacing). In normovolemia CPAP led to no change in CO. With both hypervolemia and CHF. CPAP led to increased CO (10-20%). With CPAP, LV surface pressure increased slightly in normovolemia, but did not increase, or even decreased, in hypervolemia. With CPAP, PNE did not change in normovolemia, increased in hypervolemia, and decreased in CHF, SVR always decreased when cardiac output increased with CPAP. We conclude that changes in cardiac surface pressure and overall sympathoadrenal tone cannot explain changes in CO with CPAP. Non-adrenergic mediated vasodilation could lead to unloading the LV. Alternatively, volume shift from intra- to extrathoracic compartments could lead to greater decreases in systolic than diastolic volume, thus increasing stroke volume. CPAP increases CO in the presence of cardiac distension whether or not myocardial function is impaired.
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PMID:Effects of continuous positive airway pressure on cardiac output in experimental heart failure. 908 21

Left ventricular functions were evaluated in 25 adult patients of chronic renal failure by 2-D echocardiography before and after four hours of standard hemodialysis session. Eighteen patients showed clinical evidence of fluid overload. Predialysis left ventricular end-diastolic diameter, left ventricular end-diastolic volume, left ventricular end-systolic diameter and left ventricular end-systolic volume were comparable in patients with or without fluid overload. Similarly, predialysis stroke volume and left ventricular ejection fraction were not significantly different in the two subsets. However, following hemodialysis there was a significant decrease in the left ventricular systolic and diastolic volumes and diameters in patients with fluid overload. The improvement in the left ventricular ejection fraction was of the same magnitude in the two subsets. The significant improvement in the left ventricular functions both in patients with and without fluid overload indicates that fluid overload may not be the only determinant of left ventricular functions in patients of chronic renal failure, but other factors, such as various uraemia toxins and metabolic changes might also be inhibiting the myocardial functions.
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PMID:Evaluation of left ventricular functions in chronic renal failure before and after acute hemodialysis. 935 65

Stroke is a leading cause of death and disability, particularly in the elderly population. The evolution of stroke prevention and treatment has reached a new stage whereby rapid evaluation and intervention can prevent stroke occurrence and its consequences. A stroke system much like a trauma system can be useful in getting patients to recognize signs and symptoms of stroke, mobilizing the emergency medical system (EMS), conducting diagnostic studies promptly, treating patients in a timely manner consistent with their disease process, stopping progression through monitoring and treatment, and beginning rehabilitation as early as feasible. The neurointensive care unit (neuro-ICU) is a key component of the system. It provides the monitoring and treatment for progressing stroke and its complications. Patients who might be suitable for neurointensive care are those with severe strokes, those receiving thrombolytic therapy, those receiving hypervolemia-hypertensive-hemodilution therapy, those at risk for intracranial and medical complications, and inhospital strokes following medical and surgical procedures. In order for patients to reach the neuro-ICU, education of patients, EMS providers, physicians, and hospital administrators with regard to the need for rapid response and intensive care is needed. The saga of myocardial infarction reaction is an example of the way a system of response can be developed. The concept of brain attack should alert the community and the healthcare providers of the urgency of stroke care and the need for a stroke system with neurointensive care as the therapeutic key.
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PMID:Epidemiology of stroke in requiring intensive care. 943 94

Key questions remain unresolved regarding the advantages and limitations of colloids for fluid resuscitation despite extensive investigation. Elucidation of these questions has been slowed, in part, by uncertainty as to the optimal endpoints that should be monitored in assessing patient response to administered fluid. Colloids and crystalloids do not appear to differ notably in their effects on preload recruitable stroke volume or oxygen delivery. Limited evidence nevertheless suggests that colloids might promote greater oxygen consumption than crystalloids. It remains unclear, in any case, to what extent such physiological parameters might be related to clinically relevant outcomes such as morbidity and mortality. Recent randomized controlled trial results indicate that, at least in certain forms of fluid imbalance, albumin is effective in significantly reducing morbidity and mortality. Much further investigation is needed, however, to determine the effects of colloid administration on clinically relevant outcomes in a broad range of critically ill patients. The ability of administered colloids to increase colloid osmotic pressure (COP) constitutes one mechanism by which colloids might reduce interstitial oedema and promote favourable patient outcomes. However, the applicability of this mechanism may be limited, due to the operation of compensatory mechanisms such as increased lymphatic drainage. Attempts to increase COP might also be less useful in states of increased vascular permeability such as acute respiratory distress syndrome, although this issue has by no means been settled by empirical data. Colloids are clearly more efficient than crystalloids in attaining resuscitation endpoints as judged by the need for administration of far smaller fluid volumes. Among the colloids, albumin offers several advantages compared with artificial colloids, including less restrictive dose limitations, lower risk of impaired haemostasis, absence of tissue deposition leading to severe prolonged pruritus, reduced incidence of anaphylactoid reactions, and ease of monitoring to prevent fluid overload. The cost of albumin, nevertheless, limits its usage. Crystalloids currently serve as the first-line fluids in hypovolaemic patients. Colloids can be considered in patients with severe or acute shock or hypovolaemia resulting from sudden plasma loss. Colloids may be combined with crystalloids to obviate administration of large crystalloid volumes. Further clinical trials are needed to define the optimal role for colloids in critically ill patients.
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PMID:Albumin and artificial colloids in fluid management: where does the clinical evidence of their utility stand? 1125 94

Cerebral vasospasm and related ischemic stroke continue to be significant complicating factors in the course of many patients with subarachnoid hemorrhage from berry aneurysm rupture. The risk of this well-recognized but poorly understood complication can be estimated on the basis of patient medical history, neurologic examination, and head CT findings. Every patient with possible risk needs specialized neurologic intensive care unit care after aneurysm obliteration. Surgical and pharmacologic wash-out of subarachnoid blood around the basal arteries, proper management of intracranial pressure and fluid status, hyponatremia, hypomagnesemia, and fever, as well as use of calcium channel blockers, have been considered helpful in patient management prior to and with the symptomatic vasospasm development. Transcranial Doppler (TCD) ultrasound is important in detecting vasospasm before the patient suffers ischemic neurologic deficit or infarct. Elevated TCD velocities often initiate the use of triple-H (HHH: hypertension, hemodilution, and hypervolemia) therapy and subsequently guide it. Up to the end of the first 3 weeks after subarachnoid hemorrhage and aneurysm obliteration, development of any focal neurologic deficit or mental deterioration, unless convincingly proven otherwise, is assumed to be from cerebral vasospasm. When a hemodynamically significant vasospasm in the arterial segments of clinical concern is suggested, emergency cerebral angiography with balloon dilatation angioplasty or intra-arterial infusion of vasodilating agents may be helpful in relieving ischemic symptoms.
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PMID:Cerebral Vasospasm Following Subarachnoid Hemorrhage. 1219 10

Cerebral vasospasm is a recognised but poorly understood complication for many patients who have aneurysmal subarachnoid haemorrhage and can lead to delayed ischaemic neurological deficit (stroke). Morbidity and mortality rates for vasospasm are high despite improvements in management. Since the middle of the 1970s, much has been written about the treatment of cerebral vasospasm. Hypervolaemia, hypertension, and haemodilution (triple-H) therapy in an intensive-care setting has been shown in some studies to improve outcome and is an accepted means of treatment, although a randomised controlled trial has never been undertaken. In this review, the rationale for this approach will be discussed, alongside new thoughts and future prospects for the management of this complex disorder.
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PMID:Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage. 1450 83


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