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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied 12 surgical patients in the intensive care unit post coronary artery bypass graft surgery and ten nonsurgical patients in the coronary care unit with chronic heart failure to determine the usefulness of the pulmonary arterial wedge pressure as an indicator of left ventricular preload. Left ventricular end diastolic volume was derived from concomitant determination of ejection fraction (gated blood pool scintigraphy) and stroke volume (determined from thermodilution cardiac output). In the nonsurgical patients, there was a significant correlation between changes in pulmonary arterial wedge pressure and left ventricular end-diastolic volume (P less than 0.05, r = 0.57). In the 12 patients studied during the first few hours after surgery, there was a poor correlation between changes in pulmonary wedge pressure (range = 4-32 mmHg) and left ventricular end-diastolic volume (range = 25-119 ml/m2), and a poor correlation between pulmonary arterial wedge pressures and stroke work index. In contrast, there was a good correlation between left ventricular end-diastolic volume and stroke work index. The poor correlation between the pulmonary arterial wedge pressure and left ventricular end-diastolic volume was not explained by changes in systemic or pulmonary vascular resistance. The altered ventricular pressure-volume relationship may reflect acute changes in ventricular compliance in the first few hours following coronary artery bypass graft surgery. While measurement of pulmonary arterial wedge pressure remains valuable in clinical management to avoid pulmonary edema, it cannot reliably be used as an index of left ventricular preload while attempting to optimize stroke volume in patients immediately following coronary artery bypass graft surgery.
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PMID:Poor correlation between pulmonary arterial wedge pressure and left ventricular end-diastolic volume after coronary artery bypass graft surgery. 348 61

In order to define the mechanisms whereby cardiac output and arterial oxygen transport are reduced by acute permeability pulmonary edema and by positive end-expiratory pressure (PEEP), hemodynamic, respiratory, and lung water changes were measured in 12 mechanically ventilated dogs prior to the injection of oleic acid and at 1, 2.5, and 4 hr after the injection. Measurements were performed at each interval before and after the addition of 20 cm H2O PEEP. Positive end-expiratory pressure was not continued between measurements. One hour after the oleic acid injection, the lung water content and the pulmonary vascular resistance had increased more than 100% while the right ventricular (RV) volume, RV stroke volume, and PaO2 had decreased more than 35%. Each application of PEEP increased the PaO2 to control levels. However, PEEP also significantly increased the lung water content and pulmonary vascular resistance, and decreased the RV volume and stroke volume by 33%. The extravasation of fluid from the intravascular to the interstitial and alveolar spaces of the lung with oleic acid pulmonary edema is associated with substantial decreases in right ventricular volume and stroke volume and significant increases in the pulmonary vascular resistance. Treatment with 20 cm H2O PEEP further increases the lung water content and pulmonary vascular resistance and substantially reduces the right ventricular volume and stroke volume.
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PMID:Cardiopulmonary effects of oleic acid-induced pulmonary edema and mechanical ventilation. 352 83

Transmural cardiac pressures, stroke volume, right ventricular volume, and lung water content were measured in normal dogs and in dogs with oleic acid-induced pulmonary edema (PE) maintained on positive-pressure ventilation. Measurements were performed prior to and following application of 20 cmH2O positive end-expiratory pressure (PEEP). Colloid fluid was given during PEEP for ventricular volume expansion before and after the oleic acid administration. PEEP significantly increased pleural pressure and pulmonary vascular resistance but decreased right ventricular volume, stroke volume, and mean arterial pressure in both normal and PE dogs. Although the fluid infusion during PEEP raised right ventricular diastolic volumes to the pre-PEEP level, the stroke volumes did not significantly increase in either normal dogs or the PE dogs. The fluid infusion, however, significantly increased the lung water content in the PE dogs. Following discontinuation of PEEP, mean arterial pressure, cardiac output, and stroke volume significantly increased, and heart rate did not change. The failure of the stroke volume to increase despite significant right ventricular volume augmentation during PEEP indicates that positive-pressure ventilation with 20 cmH2O PEEP decreases right ventricular function.
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PMID:Effects of positive end-expiratory pressure on the right ventricle. 353 Nov 46

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

During 1977 to 1985 2008 patients suffering from acute ischemic cerebral infarcts were admitted to the Department of Neurology, Giessen University. 213 (10.6%) died during their stay at hospital of 28 days in average. Time of survival, cause of death, localization and etiology of the infarcts were evaluated retrospectively on base of the medical reports, the angiographic, doppler-sonographic, computerized tomographic, and autopsy findings. The same number of patients died because of direct sequelae of stroke and secondary complications respectively. Those with supratentorial infarcts, who died in consequence of a vegetative dysregulation generally did not survive the first week after ictus, often had infarcts exceeding the supply area of one large cerebral artery and frequently had evidence of cardiac embolism. Pathogenetic factors for extension of the ischemic cerebral damage subsequently causing transtentorial herniation were spreading thrombosis, reinfarction, and fatal secondary hemorrhage. Patients dying in consequence of an infratentorial infarct often had a thrombosis of the basilar artery or a large cerebellar infarction. Secondary fatal complications mostly occurred after the first week after stroke. Pulmonary edema, pulmonary embolism and myocardial infarction predominated with different time pattern.
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PMID:[Fatal outcome of ischemic cerebral infarct]. 369 19

By definition, the pulmonary "venous" system consists of the pulmonary veins and the left atrium. The stiffness of the pulmonary "venous" (P'V') system and the left ventricle (LV) at the end of the slow filling period (at the point of pre-a) were estimated sequentially in a total of 26 patients, divided into a control group and mitral stenosis (MS), angina pectoris (AP), hypertrophic cardiomyopathy (HCM) groups. The stiffness (delta P/delta V) of the P'V' system was estimated from the pulmonary artery wedge (PAW) pressure tracings and the stroke volume. The stiffness (dP/dV) of LV was obtained from the pressure-volume (P-V) relationship of LV with a model of P = beaV. The present study is aimed primarily at obtaining factual information. The stiffness of the P'V' system was 0.063 +/- 0.022 mmHg/ml (mean +/- SD) in the control group and 0.052 +/- 0.006 mmHg/ml in the HCM group (p greater than 0.1). The stiffness of LV in diastole was 0.091 +/- 0.016 mmHg/ml in the control group and 0.199 +/- 0.056 mmHg/ml in the HCM group (p less than 0.01). The ratio of the stiffness of LV in diastole to that of the P'V' system was 1.6 +/- 0.6 in the control group and 3.8 +/- 0.7 in the HCM group. The volume elastic constant (a) of the P'V' system was 0.008 +/- 0.005 ml-1 in the control group and the values of (a) occupied a range of 0.007 to 0.008 ml-1 in the remaining 3 groups of patients. The values of (a) of LV were 0.011 +/- 0.004 ml-1 in the control group and 0.022 +/- 0.007 ml-1 in the HCM group (p less than 0.01). The present study suggests that the P'V' system is usually 2 to 3 times more complaint than LV in diastole. On the other hand, the P'V' system remained compliant in spite of the decreased compliance of LV in diastole in the HCM group, maintaining the reservoir function with which pulmonary edema is prevented.
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PMID:A quantitative analysis of reservoir function of the human pulmonary "venous" system for the left ventricle. 373 56

The purpose of this study was to evaluate changes in pulmonary function after running five miles. Of particular interest was the reaffirmation of the previously reported 'uncoupling' or dissociation of pulmonary diffusing capacity (DLCO) and cardiac output (Q) after moderate or strenuous exercise. Cardiopulmonary assessments were made on eight runners before and after completing three separate five mile runs. There were significant reductions in vital capacity (5.7%) and volume at closing with increases in residual volume (22.5%) and closing capacity post-run. Although DLCO did not change, significant change in cardiac output occurred during the DLCO 10 sec breathhold maneuver. The pre-run DLCO maneuver produced a fall in stroke volume (SV) with an increase in HR while maintaining Q. The post-run Q fell during the DLCO maneuver due to a fall in SV with HR remaining constant. The primary basis for previous speculation of the development of a transient pulmonary edema during exercise has been the failure of DLCO to increase immediately after exercise when HR and presumably Q is elevated. To avoid any misinterpretation of changes in DLCO produced by exercise, Q should be measured at the time of the DLCO determination. Our findings suggest that values for DLCO post-exercise are entirely appropriate for the pulmonary blood flow at the time of the DLCO maneuver.
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PMID:Interpretation of changes in DLCO and pulmonary function after running five miles. 380 53

Breathing against positive expiratory pressure has been used to improve gas exchange in many forms of pulmonary edema, and forced expiration against resistance during exercise has been advocated for climbing at high altitude as a method to optimize performance. To evaluate the effect of expiratory positive airway pressure (EPAP) on climbers with high altitude pulmonary edema (HAPE) and on exercise at high altitude, we studied four climbers with HAPE at rest and 13 healthy climbers during exercise on a bicycle ergometer at 4400 m. We measured minute ventilation (VI, L/min), arterial oxygen saturation (SaO2 percent), end-tidal carbon dioxide (PACO2, mm Hg), respiratory rate (RR), and heart rate (HR) during the last minute of a five minute interval at rest in the climbers with HAPE, and at rest, 300, and 600 kpm/minute workloads on a bicycle ergometer in the healthy subjects. The HAPE subjects demonstrated an increased SaO2 percent, no change in HR or VI, and a decrease in RR on EPAP as compared to control. In normal subjects, SaO2 percent, VI, and heart rate were significantly higher on EPAP 10 cm H2O than 0 cm H2O control (p less than 0.01, 0.01, and 0.05, respectively). The RR and PaCO2 were not significantly different. In summary, EPAP improves gas exchange in HAPE subjects at rest. The EPAP in normal subjects at high altitude resulted in a higher SaO2 percent at the expense of a higher VI and higher HR. These results suggest that the work of breathing is higher and the stroke volume lower on EPAP. The positive pressure mask may be an effective temporizing measure for victims of HAPE who cannot immediately go to a lower altitude.
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PMID:High altitude pulmonary edema and exercise at 4,400 meters on Mount McKinley. Effect of expiratory positive airway pressure. 388 50

Electrolytic lesions of the ventrolateral medulla, coinciding with the A1 catecholamine cells of the conscious rabbit (A1 lesions) cause acute hypertension and bradycardia and in some animals, pulmonary oedema. We have assessed the change in cardiac performance after an A1 lesion, the role of cardiac autonomic effectors in this change; and the mechanism of the pulmonary oedema. Following A1 lesions there was a profound (over 100%) rise in total peripheral resistance and a fall in cardiac output which was mainly due to a fall in stroke volume since it occurred even in animals in which the heart rate was held constant by atrial pacing. This reduced stroke volume occurred despite a 40% increase in myocardial contractility (peak LV dP/dt) and elevation of left ventricular end diastolic pressure. beta-Adrenoceptor blockade with propranolol abolished the rise in peak LV dP/dt, while vagal blockade with methylscopolamine abolished the bradycardia and combined blockade with propranolol and methylscopolamine abolished the rise in peak LV dP/dt and reduced the bradycardia. In rabbits which developed pulmonary oedema, left ventricular end diastolic pressure rose to 35 +/- 3.5 compared to 16 +/- 2.7 mmHg in those which did not, suggesting that the pulmonary oedema was due to raised left ventricular filling pressure.
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PMID:Cardiac performance in the conscious rabbit with acute hypertension following brainstem lesions coinciding with the A1 group of catecholamine neurons. 615 79

We undertook a randomised between-group comparison of the haemodynamic effects of arteriolar dilatation and venodilatation in 20 males, following acute myocardial infarction, with persisting left ventricular failure after pretreatment with intravenous frusemide. All had radiographic pulmonary oedema and a pulmonary artery occluded pressure (PAOP) exceeding 15 mm Hg. The average cardiothoracic ratio was 52% (range 48-65%). Following control haemodynamic measurements, 10 patients received intravenous hydralazine (0.15 mg/kg) and 10 received intravenous isosorbide dinitrate infusion (50-200 micrograms/kg/h). Subsequent measurements were made at 30, 60, and 90 min. Isosorbide dinitrate reduced the PAOP by 3 mm Hg (p less than 0.01) and the mean systemic arterial pressure by 9 mm Hg (p less than 0.05) without significant change in the heart rate, cardiac output, or systemic vascular resistance. In contrast, hydralazine reduced the PAOP and systemic arterial pressure by a similar amount, but this was accompanied by a reduction in the systemic vascular resistance (p less than 0.01) and an increase in the cardiac output (p less than 0.01), heart rate (p less than 0.01), and stroke volume (p less than 0.01). This randomised study defines the contrasting haemodynamic results of arteriolar dilatation and venodilation in patients with resistant left ventricular failure following acute myocardial infarction. The different pharmacodynamic effects of these two methods of circulatory manipulation suggest that they are not mutually exclusive and together may offer therapeutic advantages.
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PMID:Arteriolar or venous dilatation in left ventricular failure following acute myocardial infarction: a haemodynamic trial of hydralazine and isosorbide dinitrate. 619 53


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