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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report two cases of heroin induced pulmonary edema. In both cases the severity of respiratory failure, attested by a deep hypoxemia (paO2 28 and 32 mmHg) and a metabolic and respiratory acidosis (pH 7.07 and 7.14) imposed an artificial ventilation with positive end expiratory pressure (PEEP). Hemodynamic study revealed a noncardiogenic edema. In both cases, a cardiac insufficiency was also present : in the first case it's etiology remained unclear, in the second it was a complication of hyperkalemia.
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PMID:[Pulmonary edema caused by heroin. Hemodynamic study of 2 cases]. 634 28

The effects of oral captopril on pulmonary haemodynamics were studied in two groups of 6 patients, one of subjects with chronic respiratory failure (PaO2 52 +/- 5.1 mmHg, PaCO2 54 +/- 2.1 mmHg), and the others with chronic heart failure and high plasma renin activity. Two potential mechanisms of its actions were assessed, namely inhibition of hypoxic vasoconstriction and inhibition of the possible effects of angiotensin II on the pulmonary circulation. There were significant (p less than 0.05) decreases in mean arterial pressure, pulmonary wedge pressure and in systemic arterial resistance associated with improvement in cardiac index in both groups. In the chronic respiratory failure group there was no change in blood gases, mean pulmonary arterial pressure or pulmonary vascular resistance. An increase in driving pressure (p less than 0.05) indicated that captopril had had no effect on pulmonary haemodynamics. In chronic heart failure, mean pulmonary arterial pressure and pulmonary capillary wedge pressure were decreased by a similar extent, so that driving pressure and pulmonary vascular resistance were not changed. It is concluded that oral captopril did not inhibit hypoxic vasoconstriction, and that it modified pulmonary haemodynamics in chronic heart failure patients with high renin activity only as a consequence of reduction in systemic afterload.
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PMID:Effects of captopril on pulmonary haemodynamics. 638 89

We have sequentially measured the daily extravascular lung water (EVLW) changes in 16 severely traumatized patients to better define the principal etiologic factors causing post-traumatic interstitial fluid accumulation and subsequent respiratory failure. We found that severe hemorrhagic shock (mean initial BP = 40 mm Hg), massive transfusion (12.7 liters of blood), and crystalloid resuscitation with resulting hemodilution of plasma colloid osmotic pressure (PCOP) (PCOP less than or equal to 15 mmHg) do not cause EVLW accumulation. Post-traumatic elevations in EVLW were seen after lung contusion (average EVLW = 15.3 +/- 2.5 ml/kg), sepsis (average EVLW = 17.1 +/- 2.9 ml/kg) and cardiac failure (EVLW = 15.3 +/- 0.3 ml/kg). Severe hemorrhagic shock, massive transfusion, and crystalloid resuscitation with resulting hemodilution of plasma colloid oncotic pressure do not cause EVLW accumulation. Post-traumatic elevations in EVLW are seen after lung contusion, sepsis, and cardiac failure. We conclude that after trauma elevations in capillary hydrostatic pressure and capillary permeability alterations resulting from lung contusion or sepsis are the primary determinants of interstitial fluid accumulation.
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PMID:Determinants of pulmonary interstitial fluid accumulation after trauma. 675 34

A program of respiratory muscle sparing in 9 patients with late stage Duchenne muscular dystrophy is presented. Results indicate that regular efficient night-time support by body respirator provides a constant significant improvement in daytime gas exchange for periods averaging up to 2 years following the occurrence of moderately severe respiratory failure. Until now, the longest survival is more than 4 years at the age of 28. the average PaCO2 and PaO2 before night ventilation were 60.8mmHg and 59.3mmHg, respectively. The levels after the program was begun were 45.5 (PaCO2) and 74.6 (PaO2). These arterial blood gas levels are acceptable for good cardiopulmonary homeostasis. There have been no deaths or episodes of cardiac failure since the program began. The ease of integrating the program into the patient's lifestyle and home are important advantages. Cost of equipment is discussed. The view that these patients are terminal must be qualified. A case is also made for early aggressive conservative measures including body respirators, postural drainage, chest physiotherapy with abdominal assisted coughing, intratracheal suctioning and bronchoscopy to combat respiratory infection, and decreasing the need of tracheostomy and volume ventilators which can be so disabling to the chronic restrictive lung disease (CRLD) patient. Research and development into better design of body respirators is vitally needed. Acute care hospitals must prepare themselves for such patients who now attain more independent living and longer lifespan. For this reason there is a growing need for these facilities to acquire tank ventilators for handling such patients who may need hospitalization for acute medical complications.
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PMID:Night ventilation by body respirators for patients in chronic respiratory failure due to late stage Duchenne muscular dystrophy. 678 53

Patients with progressive muscular dystrophy rarely survive beyond the second or third decades: the commonest causes of death are respiratory failure and cardiac failure. An easily repeatable method for early recognition of cardiac dysfunction and its follow-up would therefore be valuable. We performed a polycardiographic study of systolic time intervals in 11 patients with dystrophy (each subject representing an age from 7 to 17 years) in a group comprising 10 of their mothers and in control groups matched for age and sex. The mean values of QS2, PEP and QS1 were significantly higher in patients compared to controls (QS2 : 543 +/- 26 msec compared to 519 +/- 19 msec; PEP : 142 +/- 21 msec compared to 123 +/- 18 msec, and QS1 : 105 +/- 22 msec compared to 75 +/- 12 msec) whilst mean ICT was shorter (36 +/- 11 msec, compared to 49 +/- 5 msec). Mean LVET was comparable in patients and control. These results indicate a reduction in compliance and an increase in end diastolic left ventricular tension. When the systolic time intervals were analysed in each child, an increase in PEP and reduction in LVET were characteristic of the more serious phases of the disease with cardiac failure. It is emphasized that early stages of the disease are characterised by restrictive changes resulting in a reduction in ICT whilst terminal stages with reduced cardiac output cause a reduction in LVET and an increase in PEP. No significant changes were found in the mothers of patients compared to the control group. These results indicate that systolic time intervals may be useful in following up patients with Duchenne's cardiomyopathy.
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PMID:[Evaluation of systolic intervals in Duchenne cardiomyopathy]. 681 20

Incidence and extent of pulmonary complications were evaluated retrospectively in 101 patients with hepatic coma (34 patients with acute liver failure, 57 patients with hepatic encephalopathy and 10 patients with mixed forms). 76 patients (73.3%) had pulmonary complications (pulmonary edema 57 cases, pneumonia 20 cases, tracheobronchitis 30 cases). Lethality of the group with pulmonary complications was 97% as compared to 16% in the group without pulmonary complications. Pathogenesis of pulmonary complications is not completely clear; different mechanisms are being discussed like central mechanisms, vascular lesions caused by metabolic or toxic factors, cardiac failure, and increased susceptibility to infection. In 9 out of 59 cases (15.3%) with respiratory failure no morphological changes could be observed in the lungs; in these cases intrapulmonary shunts might have been the cause for the pulmonary complications. The incidence of pulmonary complications increased by a factor of 2.4 during intensive care unit treatment of the patients; this increase shows, that intensive care unit treatment still has to be improved.
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PMID:[Pulmonary complications in hepatic coma]. 682 Jun 75

Fluoroacetate was dosed per stomach tube to 17 Merino sheep at the rate of 0,05-1,0 mg/kg/day. The clinical signs, haemodynamic changes, chemical pathology and pathology of acute, subacute and chronically intoxicated cases are described. Tetanic convulsions were seen in acutely intoxicated animals and in them respiratory failure, occurring concomitantly with cardiac failure, may have been the cause of death. Subacute intoxication resulted in less conspicuous clinical signs when the sheep were at rest, but they developed apparent nervous signs on being handled, and later tended to lie down. Chronically intoxicated animals were only mildly affected. At all levels of intoxication changes in the chemical pathological parameters were either absent or were mild and transient. The microscopic lesions in the hearts of acutely intoxicated sheep included degeneration as well as necrosis of individual or small groups of myocardial fibres. In the subacutely and chronically intoxicated animals the multifocal myocardial lesions were more widespread and in various stages of development or resolution.
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PMID:Observations on the clinical, cardiac and histopathological effects of fluoroacetate in sheep. 718 40

In the operating room, 66 preterm infants weighing between 710 and 2,700 gm (23 less than 1,000 gm) underwent ligation of a patent ductus arteriosus (PDA). Respiratory distress syndrome was present in 53 patients; the rest had apnea-bradycardia syndrome. PDA ligation was indicated for intractable congestive heart failure in 52 patients or progressive respiratory failure in 14. There were no intraoperative deaths. Fifteen infants died 1 to 120 days postoperatively. Seven deaths resulted from intracranial bleeding, 3 from diffuse coagulopathy, and 1 from respiratory failure. The condition of patients with heart failure improved postoperatively, with the mean left atrium to aorta ratio reduced from 1.56 to 1.02 (p = 0.05). Respiratory function improved in 25 patients extubated by the third postoperative day. Late follow-up (one to five years) of the 51 survivors showed 1 late death. Seventeen survivors had roentgenographic evidence of bronchopulmonary dysplasia. Infants with bronchopulmonary dysplasia required longer postoperative ventilation (mean, 21.5 days compared with 4.75 days). Twenty-four infants were normal. Ligation of PDA in preterm infants has low intraoperative risk and improves the condition of those with heart and respiratory failure. Late follow-up showed good recovery of nearly two-thirds of the patients.
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PMID:Ligation of patent ductus arteriosus in premature infants. 725 56

Four thousand seven hundred twenty-eight autopsies performed at the Roswell Park Memorial Institute were reviewed to determine causes of death from cancer. The duration of the disease from the date of diagnosis to death, the primary site of the tumor, a detailed description of the presence or absence of metastatic tumor at a series of sites, and an estimate of the total tumor mass were included in the evaluation. Twenty-three common primary sites were selected for investigation. These sites represented 99% of the total series. Nine causes of death were described. These were respiratory failure, infection, toxic drug reaction, hepatic failure, renal failure, shock or heart failure, adrenal gland failure, electrolyte imbalance, and central nervous system failure. Some of these associations were obviuosly due to the direct destruction of the organ in question. There are some differences, however, comparing lung lesions to hepatic lesions. These and other factors are recited in the text.
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PMID:An investigation of the cause of death from cancer. 735 17

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60


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