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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Starting from general assumptions on the clinical aspects of homeostasis and on the functional correlations lung-heart in physiological and pathological states, the difficulty to diagnose an individual pulmonary heart disease is stressed, as well as the necessity to differentiate it from the cases of coronary heart disease, when respiratory failure aggravates the latent cardiac ischemia and induces a global cardiac failure. The diagnosis criteria of the two distinct pathological pictures are established, emphasizing the importance of this differentiation for clinical practice and epidemiological research.
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PMID:Clinical aspects of cardio-respiratory homeostasis. 66 38

The purpose of this study was to find out whether acute massive pulmonary embolism can produce myocardial changes visible by light and electron microscopy. Ww therefore produced pulmonary embolism in rats using plastic microspheres (diameter, 15 +/- 5 mu). Two experimental protocols were used: lethal embolism, with a dose of microspheres known to kill in 3 to 15 hours (these rats were killed after 1 hour), and sublethal embolism, with a dose compatible with 100% survival (these rats were killed after 24 hours). In both groups, the left ventricle was normal. The right ventricle showed two tyes of changes: a) A distinctive lesion of the myocytes, more diffuse after lethal enbolism and different from the "zonal lesion" of shock. It consisted primarily in a localized shredding of the myofibrillar system; hence, the name shredding is proposed. Earlier stages of this lesion were represented by focal dissolution of the Z line (Z lysis). The pathogenesis of these lesions appeared to be primarily mechanical. b) Necrosis was already apparent at 1 hour and was more extensive after 24 hours. The pathogensis of the necrotic lesions is best explained by a temporary ischemia followed by delayed reflow; a possible potentiating role of endogenous catecholamines cannot be excluded. Most capilaries in the necrotic foci remained functional; this explains the rapid rate of the healing process of such lesions. A comparison is drawn between the observed foci of necrosis and the human myocardial lesions knowns as "miliary infarcts" and "myocytolysis." It is proposed that a factor common to all three is the preservation of the microcirculatory vessels and that our experimental model helps illuminate the pathogenesis of the human lesions. It is concluded that the right ventricle of acute cor pulmonale may develop cellular changes with a complex pathologenesis (mechanical, ischemic, and possibly hormonal). The nature of the changes found in our model could represent the morphologic substrate of right-sided failure; it can be correlated with the electrocardiographic abnormalities found in the comparable human condition.
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PMID:Ultrastructure of the myocardium after pulmonary embolism. A study in the rat. 67 69

The approach to fluid resuscitation in burn shock continues to be refined in step with improved knowledge of the complex fluid, electrolyte, and protein shifts that characterize this form of shock. Local burn tissue and generalized nonburn tissue edema occur initially after injury because of the release of histamine, which causes increased microvascular permeability. Subsequent edema formation in burned and nonburned tissue occurs according to distinctly different mechanisms. Burn tissue edema forms because of direct thermal injury to endothelial cells and increased burn tissue osmolarity. Nonburn tissue edema is attributed to severe hypoproteinemia caused by protein flux into burn-injured tissue. Interstitial protein depletion in nonburn tissue also increases the ease of water transport into the interstitial space. Cell damage occurs with ischemia caused by decreased perfusion. More cell damage can occur with reperfusion and the subsequent formation of oxygen radicals. Fluid therapy is designed to support the patient's cardiovascular system so as to restore and maintain tissue perfusion. General formulas serve as guidelines for the amount of fluid to infuse; however, fluid therapy should be tailored to the individual patient's needs based on factors such as extensiveness of burns, extremes of age, inhalation injury, pre-existing cardiopulmonary disease, and delayed fluid resuscitation. Ringer's lactate solution is the most common fluid used in the early postburn period. The addition of colloid to resuscitation efforts should begin as microvascular permeability is restored or immediately if the patient presents in frank shock. Continuous monitoring is necessary to judge the adequacy of fluid replacement.
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PMID:Burn shock. 235 24

Cardiac and circulatory failure are the main causes of hypoxic hepatitis. In a prospective study of 142 cases of hypoxic hepatitis collected during a 10-year period, we encountered two cases resulting from extreme arterial hypoxemia without congestive heart failure, cor pulmonale, or circulatory failure. Both patients were morbidly obese women admitted to the intensive care unit for carbonarcosis. Oxygen arterial saturation was very low, less than 35% in both patients, but there was no history of cardiac or respiratory failure and no clinical evidence of circulatory failure. Cardiac function, evaluated by isotopic scintigraphy, was normal. After the episode of hypoxic hepatitis, a diagnosis of obstructive sleep apnea was made clinically and confirmed by performing nocturnal oximetry, which showed multiple episodes of oxygen desaturation in both patients. Polysonography could be performed in one case and was typical of obstructive sleep apnea. Liver ischemia is the main mechanism leading to hypoxic hepatitis. More recently, the role of passive congestion of the liver has been emphasized. Arterial hypoxemia, however, is generally considered to be a minor factor. Our two cases support the hypothesis that severe arterial hypoxemia may lead to hypoxic hepatitis even in the absence of cardiac and circulatory failure.
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PMID:Hypoxic hepatitis caused by severe hypoxemia from obstructive sleep apnea. 925 50

The benefits of a Hct range of 30 to 35 percent include improved oxygen delivery and enhanced hemostasis, which help minimize complications in patients at high risk for ischemia and perioperative nonsurgical bleeding. In these settings, the conservative transfusion practice of using a lower Hct range should be replaced with a more aggressive approach. The known risks of blood transfusion would appear to be sufficiently low and the benefits sufficiently high to justify maintaining a Hct of at least 30 percent. An even higher Hct, of 35 percent, may be desirable in patients who have overt cardiopulmonary disease or who are at high risk for myocardial ischemia. Many retrospective studies have been conducted to persuade us that a conservative transfusion trigger is a safe and prudent practice, but retrospective studies are not what we need. What we need is a series of well-designed, prospective, randomized trials to evaluate the impact of a more aggressive transfusion policy on perioperative mortality, morbidity, and nonsurgical bleeding in patients with known cardiopulmonary disease or who are at high risk for myocardial and cerebrovascular ischemia.
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PMID:The red cell transfusion trigger: has a sin of commission now become a sin of omission? 966 95

In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.
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PMID:Two cases of right ventricular ischemic injury due to massive pulmonary embolism. 1118 71

The present review is focused on chronic RV pressure overload or Cor Pulmonale as it may occur in the setting of two distinct disorders: those associated with abnormal pulmonary gas exchange (hypoxemia and/or hypercapnia) where chronic obstructive pulmonary disease (COPD) is the leading cause, and those associated with pulmonary vascular obstruction where primary pulmonary hypertension (PDDH) is the representative example. The clinical curse, prognostic, implications, and therapeutic strategies differ considerably in these two clinical entities. Right ventricular failure (RVF) may adversely influence the natural history and prognosis of patients with diverse cardiopulmonary disorders. It has been long established that right ventricular (RV) ischemia, RV overload, and RV pressure overload, alone or in combination, are the main factors involved in the pathogenesis of RVF. From the pathophysiologic point of view, RVF of COPD is more a congestive type of failure, in which activation of renin-angiotensin system is involved. In PPH, a low cardiac output state is predominant and the precise mechanism of RVF remains unknown. Current evidence in favor of the pathogenetic role of ischemia, adrenergic overdrive, and genetic determination are all reviewed during the course.
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PMID:[Right ventricle insufficiency in pulmonary arterial hypertension. Physiopathologic considerations]. 1156 26

Pulmonary hypertension (PH) is a threatening condition that can be associated with a great variety of both pulmonary and extrapulmonary diseases. In all forms of severe PH the pulmonary vascular bed looses its physiological features of a "high flow-low pressure system", putting an increased afterload on the right ventricle (RV). Acute pulmonary hypertension in the intensive care unit often represents a clinical problem secondary to acute respiratory failure, left heart failure, pulmonary embolism, or decompensation of prior PH by concurrent pulmonary or cardiovascular disease. Right ventricular failure (acute cor pulmonale) occurs when relevant increases in pulmonary vascular resistance overwhelm its compensatory mechanisms, both abruptly on a previously normal RV, or gradually on a chronic cor pulmonale. This review addresses the main pathophysiological aspects of severe PH, focusing on the hemodynamic derangements occurring in the setting of acute cor pulmonale, and emphasizing the role of ventricular interdependence (the way right ventricular failure greatly affects diastolic and systolic function of the left ventricle), the risk of RV ischemia (the end stage of RV failure) and systemic organ hypoperfusion (caused by antegrade and retrograde heart failure). The understanding of the peculiar features of this type of cardiovascular insufficiency is necessary to both provide effective monitoring and adequate supportive therapy.
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PMID:Pathophysiology of severe pulmonary hypertension in the critically ill patient. 1517 2

Chronic dyspnea is defined as dyspnea lasting more than one month. In approximately two thirds of patients presenting with dyspnea, the underlying cause is cardiopulmonary disease. Establishing an accurate diagnosis is essential because treatment differs depending on the underlying condition. Asthma, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, cardiac ischemia, interstitial lung disease, and psychogenic causes account for 85 percent of patients with this principal symptom. The history and physical examination should guide selection of initial diagnostic tests such as electrocardiogram, chest radiograph, pulse oximetry, spirometry, complete blood count, and metabolic panel. If these are inconclusive, additional testing is indicated. Formal pulmonary function testing may be needed to establish a diagnosis of asthma, chronic obstructive pulmonary disease, or interstitial lung disease. High-resolution computed tomography is particularly useful for diagnosing interstitial lung disease, idiopathic pulmonary fibrosis, bronchiectasis, or pulmonary embolism. Echocardiography and brain natriuretic peptide levels help establish a diagnosis of congestive heart failure. If the diagnosis remains unclear, additional tests may be required. These include ventilation perfusion scans, Holter monitoring, cardiac catheterization, esophageal pH monitoring, lung biopsy, and cardiopulmonary exercise testing.
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PMID:Evaluation of chronic dyspnea. 1586 93

48 year old man with chronic obstructive pulmonary disease (COPD) secondary to pulmonary hypertension with domiciliary non-invasive ventilation was seen. He came to the emergency department with acute exacerbation of COPD. The patient was admitted to the Cardiology Service with the diagnosis of congestive heart failure. Diagnostic imaging (chest X-ray, transthoracic Doppler-echocardiography, multidetector row spiral CT and myocardial perfusion imaging) revealed an enlarged right ventricle. ECG was consistent with right ventricular failure. The heart perfusion imaging (pharmacologic stress testing with dobutamine) showed cor pulmonale and right ventricle ischemia induced by drug stress with dobutamine. Although right ventricle myocardial chronic dysfunction rarely causes right ventricular failure, it can occur when cor pulmonale and ischemia heart disease are present.
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PMID:[Ischemia of right ventricle and cor pulmonale]. 1612 9


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