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

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure]. 221 87

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6-10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.
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PMID:Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits. 311 22

The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.
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PMID:Effects of He-O2 breathing during experimental decompression sickness following air dives. 357 43

A prospective study on 150 infants with a birthweight of 1250 g or less was carried out to investigate the effects of patent ductus arteriosus (PDA), haemorrhagic pulmonary oedema (HPO), Indomethacin therapy and surgical ligation on the development of periventricular haemorrhage (PVH) or the extension of pre-existing PVH. The incidence of PVH, diagnosed by serial cerebral ultrasonography was 44% and the incidence of PDA, diagnosed by serial M-mode and contrast echocardiography, was 45%. During the first 8 days after birth when the infants were vulnerable to PVH, the development of PDA did not lead to the development or extension of PVH in 85% of infants. Haemorrhagic pulmonary oedema also had no effect on PVH in 71% of infants. Compared with infants whose PDA or HPO had no effect on PVH, those who had development or extension of haemorrhage had significantly more severe hypercapnia, blood gas instability and hypotension associated with the occurrence of PDA or HPO. Early Indomethacin therapy was not associated with the development or extension of PVH in 93% of infants. Although an elevation of arterial blood pressure was demonstrated after ductal ligation, surgery was performed after 1 week of age in all infants and in no instance was there an effect on PVH. This study suggests that PDA leads to PVH only if it causes significant blood gas and blood pressure disturbances which are known to affect cerebral blood flow adversely.
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PMID:Periventricular haemorrhage: association with patent ductus arteriosus and its treatment with indomethacin or surgery. 361 70

Severe head trauma patients frequently develop pulmonary failure. The aetiology of this respiratory distress may be central (neurogenic pulmonary oedema, delayed neurogenic pulmonary dysfunction, abnormal respiratory patterns) or peripheral, due to chest trauma, multiple trauma or lung infection. Hypoxia and hypercarbia alter cerebral haemodynamics, increase intracranial pressure and cause secondary deterioration of neurological function. Ventilatory support is of utmost importance in supportive care of head trauma patients. Continuous mechanical ventilation and intermittent mandatory ventilation are most frequently employed. Hyperventilation is used to lower intracranial pressure and positive end-expiratory pressure (PEEP) is applied in lung disorders characterized by interstitial oedema and alveolar collapse. The effects of PEEP on cerebral perfusion pressure and on intracranial pressure depend on the interaction of pulmonary compliance, cerebral pressure/volume relationship and cerebral vascular autoregulation. High levels of PEEP may be deleterious in patients with altered cerebral autoregulation. High frequency ventilation theoretically has less influence on intrathoracic pressures and on cerebral haemodynamics but has not been shown superior in the respiratory support of severe head trauma patients.
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PMID:Ventilatory support for pulmonary failure of the head trauma patient. 389 Sep 90

We describe continuous positive airway pressure (CPAP) by mask to reduce hypercarbia in two patients who had pulmonary edema due to congestive heart failure. In such patients, beside reducing venous return and filling pressures, CPAP improves compliance and decreases the work of breathing, thereby improving effective ventilation. Hence, CPAP may be useful to combat not only hypoxemia but also hypercarbia that is associated with pulmonary edema.
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PMID:Effectiveness of CPAP by mask for pulmonary edema associated with hypercarbia. 633 82

Disease secondary to heroin abuse constitutes a rarity in Spain. While there had been no previous cases in earlier years four young heroin addicts were admitted to the Hospital "1st de Octubre" for severe medical complications of their addiction within the last twelve months. Two patients were admitted in deep coma due to drug overdose, being cardiac arrhythmias and pulmonary edema the main associated complications. Cardiac rhythm disturbances are due to a heightened vagal tone, either secondary to inhibition of acetylcholine hydrolysis or to hypoxia, hypercapnia, and acidosis, factors that diminish cholinesterase activity and act synergistically to increase vagal tone. Pulmonary edema secondary to heroin overdose is non-cardiogenic and probably due to hypoxia added to the local action of heroin on the alveolocapillary membrane. The goal of therapy in such cases is to obtain an appropriate alveolar ventilation, the use of continuous positive pressure ventilation being required when there is pulmonary edema. The third patient had staphylococcal pneumonia with multiple abscess formation secondary to venous septic embolization originated peripherally where the drug was injected. Finally, the fourth patient was admitted because of a clinical and biochemical picture of HBsAg negative acute viral hepatitis, having suffered a similar clinical picture three years previously.
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PMID:[Severe medical sequelae in heroin addicts]. 720 89

Heroin lung is the most frequent complication of heroin intoxication. In September 1991 and January 1993, two young men aged 19 and 22 years presented with a sudden loss of consciousness and cyanosis after injecting heroin. They were both brought to our emergency department in the night and were immediately intubated and given 100% oxygen. Following intravenous naloxone, they both regained consciousness. The first patient's chest X ray revealed increased bilateral perihilar lung markings and mild patchy alveolar edema while the second patient showed a bat's wing shaped confluent alveolar edema. The blood gases in both cases revealed hypoxemia and hypercapnia. Follow-up chest roentgenograms on the second hospital day in case 1 and the third hospital day in case 2 revealed partial clearing of the lung fields. Fever developed on the second hospital day and they both received two weeks of antibiotics prior to discharge. Case 1 had normal pulmonary function testing, but case 2 developed mild restrictive lung changes. Review of the literature shows that heroin can cause a fulminant but rapidly reversible form of pulmonary edema. The treatment for this noncardiogenic pulmonary edema is adequate ventilation, good pulmonary toilet, and naloxone to reverse the respiratory and central nervous system depression. Diuretics, digitalis and morphine are not recommended in the treatment of heroin lung.
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PMID:Heroin lung: report of two cases. 791 90

A total of 52 patients with myocardial infarction have been examined. The patients have been subjected to HBO procedures. 40-62 min sessions with a working pressure of 0.3-1.1 atm were performed. The optimal pressure during the first days is 0.3 atm with a gradual increase to 0.7 atm. It is important to prepare the patient before the session with the end in view to achieve hemodynamic normalization and pain relief and to ensure a possibility of coronarolytic intake during the session. By session 4-5 hypercapnia and hypoxia, hyperventilation syndrome were eliminated, hemodynamic and respiratory parameters normalized, and immunity recovered. Only in one case a session had to be interrupted because of pulmonary edema recurrence. In 7 patients usual complications which were easily relieved have been observed. HBO shortened the patients' stay in an intensive care unit by 1.6 days and decreased lethality by 9.5%.
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PMID:[Hyperbaric oxygenation in myocardial infarct]. 808 Jan 31

In Norway the number of deaths per year from drowning is approximately nine persons per 100,000, most of them men between 25 and 40 years of age. About 60% of these persons can swim, and 50% of the deaths are related to intake of alcohol. About 6% of the drowned are children, most of them boys. In disaster medicine, drowning is associated with accidents at sea, involving large vessels or small boats, or connected to offshore activities. The important pathological events are directly related to asphyxia, hypoxemia, hypercarbia, pulmonary oedema, and circulatory arrest. This paper describes various aspects of drowning and the pathophysiological processes involved, and discusses differences between drowning and near drowning in fresh water and salt water. Although treatment is basically centred on effective cardiopulmonary resuscitation, there are certain differences with regard to further treatment and fluid/electrolyte management. Hypothermia is often a prominent feature, and if cardiopulmonary resuscitation is successful, hypoxic brain damage may be ameliorated by the fall in body temperature.
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PMID:[Drowning--near drowning]. 826 93


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