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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of phentolamine was studied in 5 patients with pulmonary hypertension, of whom 3 had primary pulmonary hypertension and 2 had secondary pulmonary hypertension after pulmonary embolism. They received intravenous phentolamine in doses of 0.5 mg/min to 2 mg/min (i.e. up to a total dose of 27.5 mg in 25 minutes) during diagnostic cardiac catheterization. Under phentolamine infusion only 2 of the 3 patients with primary pulmonary hypertension showed a significant rise in cardiac index, from 1.4 to 2.0 and from 1.8 to 2.2 l/min/m2 respectively, a fall in pulmonary artery mean pressure from 100 to 93 and from 42 to 33 mm Hg respectively, and a decrease in pulmonary vascular resistance from 2950 to 1900 and from 1160 to 725 dyn X sec X cm-5 respectively. In 1 patient with primary, and 2 patients with secondary pulmonary hypertension, infusion of phentolamine had no effect. Interestingly, in the two patients with primary pulmonary hypertension who responded well to phentolamine the condition was very severe. It appears that even in cases with very advanced primary pulmonary hypertension there is a vasospastic component which can be influenced by vasodilators.
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PMID:[Therapy of primary pulmonary hypertension with phentolamine]. 682 47

Nifedipine is a calcium antagonistic drug which reduces elevated vascular resistances. The hemodynamic effects of 20 mg of sublingual nifedipine were studied in 10 patients with chronic pulmonary hypertension. The etiology of pulmonary hypertension was chronic lung disease in 4, congenital heart disease in 2, mitral stenosis in 1, recurrent pulmonary embolism in 2 and primary pulmonary hypertension in one case. 30' after the drug administration there was a fall both of total pulmonary vascular resistance (from 992 +/- 586 to 648 +/- 428 d s cm-5, p less than 0.02) and of systemic vascular resistance (from 1416 +/- 868 to 896 +/- 440 d s cm-5 p less than 0.02) with an increase of systemic cardiac index from 3.2 +/- 1 to 4.5 +/- 2 l/min/m'2 (p less than 0.02). No significant change in systemic arterial oxygen saturation was noted, while pulmonary arterial oxygen saturation increased from 56 +/- 16 to 62 +/- 13% (p less than 0.01). These hemodynamic changes persisted for 120' when a significant fall of mean pulmonary arterial pressure was also noted (from 59 +/- 11 to 52 +/- 9 mm Hg, p less than 0.02). These data indicate that nifedipine may be useful to reduce pulmonary resistance in pulmonary hypertension. However this effect was less pronounced in patients with chronic lung disease compared to the other cases. It is suggested that the type of pulmonary arterial changes may determine the hemodynamic response. Nifedipine may be particularly indicated when vasoconstriction (as in primary pulmonary hypertension) is the main determinant of pulmonary hypertension.
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PMID:Hemodynamic effects of nifedipine in pulmonary hypertension. 716 46

The echocardiographic and clinical study was performed in six patients (three acute pulmonary embolism, one for each hypertensive cardiomyopathy, ischemic heart disease and primary pulmonary hypertension) who had a diastolic monophasic triangular pattern of the tricuspid valve echogram. Left-sided and right-sided IRT / square root R-R, ICT / square root R-R, PEP, Q-Mc and Q-Tc, and PEP / ET (IRT; isovolumic relaxation time, ICT; isovolumic contraction time, PEP; preejection time, Q-Mc or Q-Tc; interval of the Q wave of the ECG to the closing point of the mitral or tricuspid valve, and ET; ejection time) were measured from echocardiograms, and the comparisons of these parameters were made between two kinds of echogram with or without triangular pattern of the tricuspid valve. There were no significant differences in the left-sided parameters between the two kinds of echocardiograms. The mitral valve echogram showed a persistent M-shaped pattern irrespective of the pattern of the tricuspid valve. Right-sided IRT / square root R-R and ICT / square root R-R were significantly prolonged and Q-Tc was significantly shortened in the echogram with a triangular pattern of the tricuspid valve. Right ventricular (RV) catheterization was performed using a Swan-Ganz catheter in four patients with the triangular pattern of the tricuspid valve echogram. The mean pulmonary artery pressure ranged from 24 to 96 mmHg (40 mmHg on an average) and RV end-diastolic pressure from 8 to 17 mmHg (12 mmHg on An average). The possible explanation for the production of the triangular tricuspid valve echogram was an impaired early diastolic relaxation and increased stiffness of the RV due to the acute pressure overloading, resulting in a delayed opening and an early closing of the tricuspid valve. We conclude that a diastolic monophasic triangular pattern of the tricuspid valve echogram is a reflection of an impaired early diastolic relaxation and an increased end-diastolic stiffness of the RV.
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PMID:[Echocardiograms of a monophasic triangular wave of the tricuspid valve]. 718 4

The collateral pulmonary blood flow was measured by the dye dilution method in four patients with chronic obstructive pulmonary disease, in 16 patients with diffuse pulmonary fibrosis, in 15 patients with pulmonary embolism, and in three patients with primary pulmonary hypertension. The authors found that collateral pulmonary circulation was small in the first two groups (0.3 % and 1.7% of the pulmonary blood flow, respectively), absent in primary pulmonary hypertension, and high (14.0% of pulmonary flow) in pulmonary embolism. The magnitude of the bronchopulmonary collateral circulation did not correlate with degree of precapillary pulmonary hypertension, left atrial pressure and left ventricular enddiastolic pressure. It seems that the bronchopulmonary collateral flow does not produce diastolic left ventricular overload in chronic pneumopathies.
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PMID:Left ventricular overload caused by collateral pulmonary circulation in chronic pneumopathies-myth or reality? 724 59

Definite diagnosis of pulmonary embolism (PE) by conventional methods such as angiography is frequently difficult. If residual thromboemboli incorporated into the pulmonary arterial wall or in the distal small segments are visible, differential diagnosis of PE versus primary pulmonary hypertension (PPH) can be made without open-chest pulmonary biopsy. Six patients suspected of having acute PE, 6 suspected of having chronic PE, and 4 with PPH diagnosed by pulmonary biopsy underwent percutaneous pulmonary angioscopy. In patients suspected of having PE, globular and mural thromboemboli were detected by both angioscopy and angiography in 4 and 1 patients, respectively. By angioscopy, emboli incorporated into the arterial wall were detected in 7 and microemboli obstructing the distal small segments were detected in 6. However, these emboli were detected by angiography in none. In patients with PPH, no embolus was detected by angioscopy and angiography. Angioscopically, however, stenoses were observed in the distal small segments in all patients. The results indicate that residual pulmonary thromboemboli in PE and stenoses of distal pulmonary arteries in PPH are detectable by percutaneous angioscopy, and therefore this method is feasible for differential diagnosis of PE.
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PMID:Angioscopic detection of residual pulmonary thrombi in the differential diagnosis of pulmonary embolism. 757 97

12 patients with pulmonary hypertension, primary pulmonary hypertension 3, secondary to recurrent pulmonary embolism 4, chronic obstructive pulmonary disease 2, and complicated with congenital heart disease 3, inhaled nitric oxide (NO). The NO concentration was adjusted in the range between 20-160 ppm to get a maximum hemodynamic effects. On inhaling NO, pulmonary artery pressure decreased in all patients. The maximum hemodynamic effects showed that pulmonary systolic, diastolic and mean artery pressure dropped by 22.9%, 21.0% and 20.3% (P < 0.001) respectively. Total pulmonary resistance decreased by 32.7% (P < 0.01). Cardiac index and oxygen delivery increased by 33.2% and 24.8% (P < 0.01) respectively. The ratio of pulmonary systolic artery pressure and systemic systolic artery pressure changed from the baseline 0.73 to 0.54. It is indicated that NO dilated pulmonary artery selectively in patients with hyperkinetic, obliterative and hypoxic pulmonary hypertension.
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PMID:[Hemodynamic effects of inhaled nitric oxide in patients with pulmonary hypertension]. 765 63

Medical therapy for pulmonary hypertension is very limited and surgical interventions can only be performed in cases with acute or chronic pulmonary embolism. Secondary pulmonary hypertension of other origin (Eisenmengers' Syndrome) as well as primary pulmonary hypertension can only be treated with lung transplantation. In selected cases, three different techniques are available, heart-lung transplantation (HLTx), single, and double lung transplantation (SLTx; DLTx). The indication for any of these operations has to be made on an individual basis, and the degree of pulmonary hypertension and right ventricular failure have to be encountered. Also, correctability of the underlying congenital disorder in Eisenmenger Syndromes has to be taken into account. In principle, combined heart-lung transplantation will allow for the best results. Due to the restricted number of donor organs, SLTx and DLTx are performed in increasing numbers. SLTx for pulmonary hypertension, however, is characterized by a high number of early (reperfusion injury) and late complications (ventilation-perfusion-mismatch). Following lung transplantation in pulmonary hypertension, 1- and 5-year survival rates of 70 and 60% can be expected, respectively. Which type of transplantation will ultimately prove to be the best therapy for pulmonary hypertension has not yet been defined.
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PMID:[Lung transplantation in pulmonary hypertension]. 786 95

The diagnosis of chronic primary and secondary pulmonary hypertension is difficult. Important indications result from physical examination and the patient's history. Non-invasive diagnostic tools are chest X-ray, ECG, blood gas analysis and 2-D-Doppler-echocardiography. If, despite these investigations, no reason for the pulmonary hypertension is found, perfusion scintigraphy of the lungs and a right-heart catheter investigation should be performed. If there is no intracardiac shunting and perfusion scintigraphy of the lungs is normal, repeated pulmonary embolism must be excluded by pulmonary angiography. Only after elimination of this possibility can primary pulmonary hypertension be regarded as the reason for the patient's condition. Pulmonary hypertension is usually more acute in the critically ill patient. Under these circumstances, only direct pressure measurements are of clinical relevance. In the critical care setting, many of the non-invasive methods are either difficult to perform or hard to interpret. Furthermore, many of the typical signs of pulmonary hypertension derived from non-invasive investigations do not appear in acute pulmonary hypertension.
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PMID:[Invasive and non-invasive diagnosis of pulmonary hypertension in the intensive care unit]. 813 5

Despite the development of several lung transplantation procedures, the most advantageous for pulmonary hypertension remains controversial. Between 1986 and February 1992, 30 patients with end-stage primary pulmonary hypertension (n = 24), chronic pulmonary embolism (n = 4), and hystiocytosis X (n = 2) underwent heart-lung (n = 21), double lung (n = 8), or single lung (n = 1) transplantation. Indications for double lung transplantation were similar to those for heart-lung transplantation, and the preoperative clinical and hemodynamic parameters were not significantly different between the two groups. There were no intraoperative deaths, but two reoperations were needed for pleural hematoma. Five early deaths were related to graft failure (two heart-lung transplantations), mediastinitis (one heart-lung transplantation), multiorgan failure (one double lung transplantation), and aspergillosis (one double lung transplantation). There was a similar improvement in early (days 0 and 2) and late (6 months postoperatively) right-sided hemodynamic function in patients undergoing heart-lung and double lung transplantation. Three double lung transplant recipients had early and reversible left ventricular-failure. The early postoperative course of the one patient who had single lung transplantation was characterized by severe pulmonary edema, left ventricular failure, and persistent desaturation and later on by moderate pulmonary hypertension and an important ventilation/perfusion mismatch. The pulmonary function results were also similar in the heart-lung and double lung transplantation groups. The overall projected 2- and 4-year survivals were 49% and 41%, respectively, and were not significantly different between the heart-lung and double lung recipients. Results demonstrate that heart-lung and double lung transplantation are equally effective in obtaining early and durable right-sided hemodynamic and respiratory improvement and similar respiratory function. In patients with pulmonary hypertension, double lung transplantation should be preferred to single lung transplantation because of the critical postoperative course and the uncertain long-term results of single lung transplantation.
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PMID:Comparative outcome of heart-lung and lung transplantation for pulmonary hypertension. 834 Oct 71

This study analyzed the regional pattern of right ventricular (RV) dysfunction on transthoracic echocardiograms in patients with and without acute pulmonary embolism. Quantitative (centerline) and qualitative (wall motion score) analyses of segmental RV free wall motion were performed on a "training" cohort of 41 patients (group 1), including 14 patients with acute pulmonary embolism, 9 patients with primary pulmonary hypertension, and 18 normal subjects. Patients with acute pulmonary embolism had a distinct regional pattern of RV dysfunction, with akinesia of the mid-free wall (centerline excursion: -0.2 +/- 0.8 mm, p = 0.0001 vs normal) but normal motion at the apex (centerline excursion: 5.7 +/- 0.8 mm, p = NS vs normal). In contrast, patients with primary pulmonary hypertension had abnormal wall motion in all regions (p <0.03 vs normal). This echocardiographic finding of normal wall motion at the apex and abnormal wall motion in the mid-free wall in acute pulmonary embolism was then tested in a "validation" cohort of 85 patients (group 2), consisting of hospitalized patients with RV dysfunction from any cause, including 13 patients with acute pulmonary embolism. The finding had a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism, with a positive predictive value of 71% and a negative predictive value of 96%. Thus, a distinct echocardiographic pattern of regional RV dysfunction, in which the apex is spared occurs in acute pulmonary embolism. This finding should raise the level of clinical suspicion for the diagnosis of acute pulmonary embolism.
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PMID:Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. 875 95


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