Pulmonary artery

About: Pulmonary artery is a research topic. Over the lifetime, 27278 publications have been published within this topic receiving 595835 citations. The topic is also known as: pulmonary arterial tree & pulmonary arteries.

Definitions and diagnosis of pulmonary hypertension

Abstract: Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure 25 mm Hg at rest, measured during right heart catheterization. There is still insufficient .evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) 15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone. (J Am Coll Cardiol 2013;62: D42-50) ©2013 by the American College of Cardiology Foundation.

Pulmonary Hypertension in Severe Acute Respiratory Failure

Abstract: We repeatedly assessed pulmonary and systemic hemodynamics in 30 patients undergoing therapy for severe acute respiratory failure of diverse causes. Pulmonary-artery hypertension and elevated pulmonar vascular resistance were observed in all patients after correction of systemic hypoxemia. Increasing pulmonary blood flow by isoproterenol infusion or decreasing pulmonary blood flow by partial bypass of the right side of the heart minimally altered pulmonary-artery pressure. Although neither elevated pulmonary vascular resistance nor low cardiac index reliably predicted death, survivors had preogressive decreases of pulmonary vascular resistance with time, whereas nonsurvivors tended to maintain or increase pulmonary vascular resistance. Right ventricular stroke-work index was markedly elevated in all patients. The work load imposed upon the right ventricle by elevation of pulmonary vascular resistance may be a factor limiting survival in severe acute respiratory failure.

Right ventricular infarction. Clinical and hemodynamic features.

Abstract: Six patients with acute myocardial infarction presented with hemodynamic evidence of predominant right ventricular failure, characterized by a mean right atrial pressure averaging 20.2 mm Hg and left ventricular filling pressure averaging 16.3 mm Hg. Autopsy in two cases revealed extensive involvement of the right as well as the left ventricle. Clinically the patients usually had evidence of diaphragmatic wall infarction, distended neck veins, hypotension and heart block. Pressure contours and mean pressure often showed no significant change as the catheter was advanced from the right atrium to the pulmonary artery. Shock in three patients was effectively treated with plasma volume expansion, to increase further right-sided pressure, or the administration of sodium nitroprusside, to reduce left-sided filling pressure. It is suggested that when right ventricular infarction accompanies left ventricular infarction, a unique clinical and hemodynamic syndrome occurs because the ability of the right ventricle to maintain adequate left ventricular filling is impaired. Recognition of this syndrome is vital if appropriate therapy is to be instituted.

Lung sequestration: report of seven cases and review of 540 published cases

Abstract: We present an analysis of 400 intralobar and 133 extralobar sequestrations, six cases presenting intra- and extralobar sequestration simultaneously, five sequestrations of one whole lung, and two bilateral intralobar sequestrations. This anomaly comprises 0·15-6·4% of all congenital pulmonary malformations. Usually the posterior basal segment is affected. The aberrant artery in intralobar sequestration originated in 74% of all cases from the thoracic aorta, and in 14·8% there was more than one anomalous artery. The mean diameter of the aberrant arteries was 6·3-6·6 mm. Usually arteries with predominantly elastic fibres were found. Arteriosclerotic changes were common, even in children. The venous return of the intralobar sequestration is, in 95·7% of all cases, via the pulmonary veins. In 13·7% of all cases other congenital malformations were observed. Symptoms arose within the first decade of life in 37·2% Bronchography and retrograde arteriography are the mainstay of diagnosis. Sequestrations are not supplied by a bronchial artery. Treatment of choice is operation as early as possible. Altogether seven operative deaths were reported, five of which were due to haemorrhage during operation. Of the 133 extralobar sequestrations, 77·4% were located between diaphragm and lower lobe. The arterial supply was provided by branches of the aorta. Some cases were supplied with venous blood by branches of the pulmonary artery. In six cases secondary changes, such as tuberculosis or carcinoma were found. In 60% of all the patients symptoms occurred within the first decade of life. Preoperative diagnosis was correct in only six cases. There were four postoperative deaths.