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

Of 22 patients with the classical clinical signs of pulmonary oedema (orthopnoe, cyanosis, sweating and rales heard at a distance) 15 (Group A) were observed clinically, while seven (Group B) underwent haemodynamic studies. Those in Group A were given 0.8-2.4 mg nitroglycerin sublingually one to six times at 5--10 minute intervals. Within five minutes of nitroglycerin administration 7 of the 15 had their first signs of clinical improvement. In 11 patients the rales had disappeared after 15--20 minutes or had regressed. In the remainder the dyspnoea had decreased so that at this point in 14 of the 15 patients various degrees of improvement had occurred. Four patients were completely without clinical signs after 30 minutes. The increased arterial blood pressure and heart rate had fallen markedly. In the seven patients of Group B mean left ventricular filling pressure fell within ten minutes of nitroglycerin administration (1.6 mg) from 33 +/- 10 to 24 +/- 8 mmHg, cardiac output rising sifnificantly from 3.3 +/- 0.8 to 3.7 +/- 0.8 1/min. Such favourable results with nitroglycerin are to be expected only if the pulmonary oedema is of cardiac origin.
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PMID:[Effect of nitroglycerin sublingually in the emergency management of "classical" pulmonary oedema (author's transl)]. 40 57

A patient experienced episodic pulmonary edema accompanying nocturnal angina pectoris. The symptoms were provoked at cardiac catheterization by atrial pacing. Simultaneous onset of chest pain, shortness of breath, and sudden appearance of a large V wave in the pulmonary artery wedge pressure contour confirmed acute mitral valve regurgitation. Rapid reversal of these changes after nitroglycerin administration supported "papillary muscle dysfunction" as the explanation for these hemodynamic changes.
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PMID:Severe papillary muscle dysfunction substantiated by atrial pacing during cardiac catheterization. 40 54

The haemodynamic effects of intravenous injections of furosemide and ethacrynic acid as well as those of peroral administration of nitroglycerin were studied in 32 patients (4-12 weeks after acute myocardial infarction) during rest and exercise. Cardiac output, heart rate and arterial blood pressure showed no significant changes after administration of nitroglycerin, furosemide and ethacrynic acid (fig 3). A few minutes after application of nitroglycerin or furosemide there were significant falls of pulmonary arteria diastolic pressure and right atrial pressure (fig. 1 and 2), whereas no changes were seen after injection of ehtacrynic acid. This initial effect of furosemide as well as the effect of nitroglycerin is primarily of vascular origin, causing an increased peripheral venous capacitance. Ethacrinic acid failed to exhibit any direct vascular effect. Therefore during pulmonary oedema nitroglycerin together with furosemide should be given.
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PMID:[Nitroglycerin, furosemide and ethacrynic acid effect on hemodynamics in rest and during ergometric load in coronary disease patients]. 81 11

In 15 patients with left heart failure due to coronary heart disease (10 acute and 5 old infarcts) the enddiastolic pressures in the pulmonary artery (left ventricular filling pressure) were elevated to 25 +/- 8 mm Hg and signs of pulmonary congestion were present. After nitroglycerin sublingually (0.8-1.6 mg) the left ventricular filling pressure fell to 17 +/- 8 mm Hg and caridac output tended to increase. Mean arterial pressure did not change significantly. In 6 patients with pulmonary edema, clinically an impressive improvement was observed within 5-15 min after administration of the drug. In 1 case the left ventricular filling pressure decreased from 50 to 27 mm Hg within 5 min. In left heart failure, especially in the presence of pulmonary edema, sublingual nitroglycerin is a potent drug with a favorable influence on hemodynamic and clinical parameters.
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PMID:Sublingual nitroglycerin in the treatment of left ventricular failure and pulmonary edema. 82 29

To determine whether nitroglycerin is as effective as nifedipine in lowering the blood pressure in severe hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg nitroglycerin sublingually or a 10-mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mmHg to 171/95 mmHg and after nifedipine from 210/118 to 185/102 mmHg. The greater effect of nitroglycerin may result from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15-20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mmHg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant differences in side effects were determined. Since a hypertensive crisis is usually accompanied by left ventricular failure, pulmonary edema, angina pectoris, or infarction, nitroglycerin has been definitively shown positively to influence these conditions, and preference should be given to nitroglycerin in the treatment of hypertensive crises.
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PMID:Comparison of nitroglycerin with nifedipine in patients with hypertensive crisis or severe hypertension. 146 34

A 32-year-old man (weight 132 kg, height 190 cm) suddenly became unconscious and cyanosed with an unrecordable pulse and ventricular flutter on ECG. After resuscitation, the blood pressure was 200/100 mm Hg; the patient moved his arms and legs at times, but he did not regain consciousness. Focal neurological signs and meningism were not demonstrable. Subsequent ECGs showed a raised ST segment, followed later by terminal T wave inversion; marked pulmonary oedema was present clinically and radiologically. The creatine kinase activity was 344 U/l. As lateral myocardial infarction was suspected, the patient received heparin (1000-1700 IU/h) and nitroglycerin intravenously. Because the CK-MB isoenzyme failed to rise significantly and there was no reduction of R wave on the ECG, a CT scan of the brain was performed: this showed brain oedema as well as severe subarachnoid haemorrhage in the basal subarachnoid space, the posterior horn of the lateral ventricles and over the cerebral hemispheres. Despite implantation of an epidural pressure gauge, hyperventilation and administration of dexamethasone, osmotic diuretics and thiopental, the patient died 14 days after collapsing. At autopsy the heart showed no signs of myocardial infarction. The cause of the subarachnoid haemorrhage was a ruptured aneurysm of the anterior communicating artery.
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PMID:[Subarachnoid hemorrhage with pulmonary edema and electrocardiographic changes. The differential diagnosis of myocardial infarct]. 157 49

For the emergency care of respiratory disorders, in addition to clearing of the airways and keeping them open, drug treatment has an important role to play. The bronchodilatory effect of beta-sympathicomimetics brings about a marked decrease in the resistance to flow, but potential cardiovascular side effects must be considered. In the case of theophylline, the solvent, ethylene diamine has its own pharmacodynamic effects that can make it necessary to select different theophylline preparations. The drugs with a primarily cardiac effect, nitroglycerin, dobutamine and dopamine can produce pulmonary relief. Furosemide is specifically indicated for pulmonary edema. In addition to experience in the use of emergency drugs, an appropriate basic knowledge of the pharmacodynamics and pharmacokinetics is indispensable.
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PMID:[Emergency drugs in respiratory disorders. A choice of commonly used substances]. 168 8

An understanding of the physiological principles involved in lung fluid balance is useful in the initial treatment of pulmonary edema. Normally, a very small volume of fluid is filtered from the pulmonary vasculature into the interstitial space. This interstitial fluid enters the pulmonary lymphatics and is transferred to mediastinal lymphatics at an estimated rate of 20 ml/hr. Under abnormal circumstances, fluid filtration may occur at such a rapid rate that it overwhelms the lymphatics and interstitial space and results in alveolar flooding. This may occur as a result of increased pulmonary vascular pressure or increased vascular permeability. The two general goals of initial therapy are (1) to relieve hypoxemia and (2) to reduce pulmonary capillary pressure. Relieving hypoxemia may require the use of supplemental oxygen by nasal prongs or mask, continuous positive airway pressure (CPAP) mask, or even endotracheal intubation and mechanical ventilation. Measures to decrease preload and thereby reduce pulmonary capillary pressure include sitting the patient up, administering a loop diuretic or morphine intravenously, and in some circumstances using sublingual nitroglycerin. After initial treatment is underway, a search for and specific management of the underlying cause of pulmonary edema can proceed.
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PMID:Initial treatment of pulmonary edema: a physiological approach. 177 26

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 +/- 4 to 14 +/- 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from -10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p less than 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 +/- 4 to 33 +/- 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur.
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PMID:Role of intravenous nitroglycerin in the treatment of severe pregnancy-induced hypertension complicated by pulmonary edema. 308 Aug 87

Eight patients with pulmonary oedema and 6 patients with cardiac asthma (primary disease: in 7 patients acute myocardial infarction, in 6--hypertension, in 1--mitral defect) were given sublingually a combination of 0.5 mg nitroglycerin, 10 mg Isodinit (isosorbid dinitrate) and 4 mg Sidnofarm (molsidomine) in powder form. This resulted in a rapid, pronounced and protracted reduction of dyspnoea, pulmonary congestion, respiration rate, and heart rate in the course of a four-hour observation rate, in more than 80% of cases. In patients with high blood pressure it dropped by 27% vs. the initial level; in patients with hypotension the change was only minimal. Pulmonary diastolic pressure began to drop from the 3rd minute after administration of the agents and the maximal decrease was attained after 30 min (34% of the initial value); even 4 hours after administration the values were below the initial level. The mentioned drug combination appears to be valuable especially in the first stage of treatment of cardiac asthma and pulmonary oedema.
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PMID:Application of a combination of sublingually administered vasodilating drugs for rapid action on pulmonary hypertension in patients with cardiac asthma and with pulmonary oedema. 311 25


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