Pulmonary Artery Hemodynamics Research Articles

Pulmonary artery hemodynamics in primary pulmonary hypertension

Objectives. The present investigation compared and contrasted steady and pulsatile pulmonary hemodynamics at rest and during exercise in patients with primary pulmonary hypertension and normal control subjects.Background. A complete description of the relation between pressure and flow in the pulmonary circulation includes both steady and pulsatile hemodynamic behavior. Patients with primary pulmonary hypertension provide a unique opportunity to study the effects of primary alterations in pulmonary vasculature on pulmonary artery vascular hydraulic load.Methods. Catheter tip pressure and velocity recordings from the main pulmonary artery in 8 patients with primary pulmonary hypertension and 10 control subjects were used to derive the pulmonary artery input impedance spectrum and the extent of pulse wave reflection at rest and during exercise.Results. As expected, in patients with primary pulmonary hypertension, mean pulmonary artery pressure (50 ± 10 mm Hg) and pulmonary vascular resistance (880 ± 446 dynes·s·cm−5) were markedly elevated at rest and remained so during exercise (mean pressure 71 ± 15 mm Hg, mean resistance 750 ± 530 dynes·s·cm−5). Pulmonary artery characteristic impedance was elevated at rest and did not change with exercise (rest 55 ± 25 dynes·s·cm−5; exercise 66 ± 33 dynes·s·cm−5). Measures of arterial wave reflection indicated that the extent of wave reflection in the pulmonary bed in those with primary pulmonary hypertension is large at rest (reflection coefficient 0.89 ± 0.09) and that the composite reflected wave arrived during the midportion of right ventricular ejection. Although the extent of wave reflection decreased with exercise (reflection coefficient 0.81 ± 0.10, p < 0.05), the magnitude and timing of these reflections remained adverse. Furthermore, in patients with primary pulmonary hypertension, the stroke volume response to exercise was strongly related to rest levels of pulmonary artery diastolic pressure, pulmonary vascular resistance and the reflection factor, whereas no such relation was found in the control subjects.Conclusions. In addition to the expected abnormalities in steady measures of pulmonary artery hemodynamics at rest in patients with primary pulmonary hypertension, rest and exercise measures of oscillatory behavior (characteristic impedance and pulse wave reflection) are perturbed. Measures of steady and pulsatile behavior, particularly wave reflection, appear to have an important role in the exercise response of these patients.

Morphometry of parenchymal and vascular alterations in ARDS after extracorporal carbon dioxide removal therapy (ECCO 2-R-therapy)

The lungs of 12 patients suffering from ARDS treated by ECCO2-R-therapy were examined. The thickness of the interlobular septa, area portions of honeycombing, bleeding and lung parenchyma with diffuse alveolar damage were assessed by semi-automatic image analysis. Medial thickness of the pulmonary arteries with an external radius ranging between 40 microns and 150 microns was assessed planimetrically. The area portion of honeycombing ranged from 0% to 66% (average: 28.8%, standard deviation: 17.0%). The thickness of interlobular septa was increased with values between 74.0 microns and 195.5 microns (average: 140.4 microns, standard deviation: 41.7 microns; normal controls: 72.0 microns +/- 19.5 microns). Parenchymal and vascular changes were closely related: Average medial thickness rose from nearly normal values (4.9%) in cases with low area portions of honeycombing and bleeding to the double (11.1%) of normal values in cases with area portions of honeycombing and bleeding greater than 40%. We conclude that parenchymal changes due to shock and high inspiratory O2 concentration lead to changes of the pulmonary arterial hemodynamics which result in a quickly developing medial hypertrophy.

Leukocyte CD11b/18 antigen-directed monoclonal antibody improves early survival and decreases hypoxemia in dogs challenged with tumor necrosis factor.

This study examined the effect of monoclonal antibody (MAb) directed against leukocyte CD11b/18 glycoprotein complex (904MAb) on cardiopulmonary injury induced by tumor necrosis factor (TNF), and death. Eighteen 2-yr-old, purpose-bred beagles with chronic tracheostomies were challenged with TNF (60 micrograms/kg of body weight) intravenously. Nine of 18 animals were treated with 0.5 to 1.0 mg/kg of body weight 904MAb intravenously 45 min before and 12, 36, and 48 h after TNF infusion. Serial femoral and pulmonary arterial catheter hemodynamics, blood gas analysis, and radionuclide cineangiographic left ventricular ejection fractions (EF) were done before and after a fluid challenge. Serial bronchoalveolar lavages (BAL) with cell and protein analysis also were performed using the chronic tracheostomies. Compared with animals given TNF alone, animals treated with 904MAb did not differ in overall survival (TNF alone, 2/9; 904MAb, 3/9); however, the group of animals treated with 904MAb had significantly (p less than 0.01) fewer deaths within the first 30 h of TNF challenge. At 4 h after TNF challenge, all animals had significantly (p less than 0.05) reduced PaO2 after fluid challenge; however, animals given 904MAb (compared with animals given TNF alone) had significantly (p less than 0.05) smaller reductions in PaO2. Throughout the study, animals given 904MAb before TNF or TNF alone had similar changes in cardiac index, mean arterial pressure, EF, and BAL protein and neutrophil concentration. Thus, MAb directed against the leukocyte CD11b/18 glycoprotein complex prolonged survival and reduced the hypoxemia occurring after TNF challenge, but this antibody did not improve overall survival or cardiopulmonary function.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of a twenty-four-hour milrinone infusion in patients with severe heart failure and cardiogenic shock as a function of the hemodynamic initial condition

The systemic and pulmonary arterial hemodynamics of 40 patients with severe congestive heart failure were determined during a 24-hour infusion of milrinone (0.5 micrograms/kg/min) after a loading dose of 50 micrograms/kg. A subgroup (n = 18) with severe cardiac pump dysfunction and three patients in cardiogenic shock were analyzed separately; their hemodynamic response was compared with that of the total group (n = 40). After 15 minutes of intravenous therapy with milrinone, the total group (n = 40) showed an increase of 65% in cardiac index; in the subgroup (n = 18) cardiac index increased by 94% after 15 minutes and by 106% after 30 minutes. Likewise, pulmonary capillary wedge pressure decreased after 30 minutes in both the total group (n = 40) and the subgroup (n = 18). The heart rate showed an overall tendency to decrease. The systolic blood pressure tended upward and remained statistically unchanged in the total group, whereas in the subgroup in which pressure was initially low, there was an increase in the systolic pressure after 1 hour and a further increase after 24 hours. Mean arterial pressure also rose in this subgroup. The early improvement in all measured hemodynamic parameters was sustained throughout the 24-hour infusion period. Development of tolerance was not observed, nor were any clinically symptomatic side effects or symptomatic arrhythmias. Thus intravenous milrinone is a safe medication for the rapid and prolonged improvement in hemodynamics, specifically in patients with severely restricted cardiac pumping function.

Pulmonary artery morphology and hemodynamics in pulmonic valve atresia with ventricular septal defect before and after repair

Cardiac catheterization and angiography were performed in 22 patients with pulmonic valve atresia and ventricular septal defect to evaluate pulmonary morphology and hemodynamics before and after repair. In 12 of the 22, pulmonic valve atresia and ventricular septal defect were associated with major aortopulmonary collateral arteries, which were ligated in most. Mean postoperative pulmonary artery pressure (PAP) ranged from 9 to 92 mm Hg (mean 28 ± 19) and pulmonary vascular resistance ranged from 1.1 to 35.2 U · m 2 (mean 6.4 ± 8.0). These data correlated (r = 0.89, p < 0.001). The number of pulmonary artery subsegments connected to the central pulmonary arteries was 22 to 42 (mean 38 ± 6). Univariate analysis revealed that the mean postoperative PAP correlated with the number of pulmonary artery subsegments connected to the central pulmonary arteries (r = −0.81, p < 0.001), with mean preoperative PAP (r = 0.79, p < 0.001), with the postoperative pulmonary artery area index of the right and left pulmonary arteries at prebranching (r = −0.76, p < 0.001), and with the sum of the pulmonary artery areas after branching (r = −0.69, p < 0.005). Pulmonary vascular resistance correlated with the number of pulmonary artery subsegments connected to the central pulmonary arteries (r = −0.85, p < 0.001), with the mean preoperative PAP (r = 0.79, p < 0.001), with the sum of the pulmonary artery areas after branching (r = −0.73, p < 0.001), and with the postoperative pulmonary artery area index (r = −0.70, p < 0.001). The incidence of pulmonary vascular resistance being <3 U · m 2 was significantly higher in patients with >36 pulmonary artery subsegments connected to the central pulmonary arteries and with a preoperative pulmonary artery area index >0.5 (88%) (p < 0.01). These results indicate that postoperative PAP and pulmonary vascular resistance in patients with pulmonic valve atresia and ventricular septal defect may be predictable when the pulmonary artery area at prebranching and the number of pulmonary artery subsegments connected to the central pulmonary arteries are measured before repair. Early palliation to increase pulmonary artery size and the number of pulmonary artery subsegments connected to the central pulmonary arteries is recommended for obtaining normal pulmonary hemodynamics after repair.

Influence of aging on pulmonary hemodynamics in a population free of coronary artery disease

Previous studies showing an increase in pulmonary artery (PA) pressures and vascular resistance with aging have not systematically excluded subjects with coronary artery disease or left ventricular systolic dysfunction. To better determine the influence of aging on PA hemodynamics in the absence of disease, we identified 47 normal subjects anglographically free of coronary artery disease (18 men, 29 women) with normal left ventricular systolic function (ejection fraction ≥50% and left ventricular end-diastolic pressure <14 mm Hg) from 5,508 consecutive patients undergoing cardiac catheterlzation and coronary angiography between September 10, 1982 and March 9, 1987. AN subjects met a set of clinical and laboratory criteria identifying them as normal. In group I (age ≥60 years) mean PA pressure was 16 ± 3 mm Hg, pulmonary vascular resistance was 124 ± 32 dynes s cm −5 and the pulmonary/systemic vascular resistance ratio was 0.099 ± 0.046. In contrast, in group II (age <60 years), these values were lower at 12 ± 2 mm Hg, 70 ± 25 dynes s cm −5 and 0.057 ± 0.019, respectively (all p values <0.01 to 0.001). AN these parameters increased linearly with age (r = 0.69, p <0.001 for pulmonary vascular resistance). The differences were not attributable to body surface area or gender. There was no difference in cardiac output, PA wedge pressure, aortic pressure or systemic vascular resistance between the 2 groups. Thus, PA pressure and vascular resistance increase with aging, a change not attributable to coronary disease or left ventricular systolic dysfunction.

Abnormal pulmonary artery hemodynamics as a cause of pulmonary edema during resuscitation : Joseph P. Ornato, Jan L. Bredthauer. University of Nebraska, Omaha, NE 68105

Abnormal pulmonary artery hemodynamics as a cause of pulmonary edema during resuscitation : Joseph P. Ornato, Jan L. Bredthauer. University of Nebraska, Omaha, NE 68105

The pulmonic valve echogram in the assessment of pulmonary hypertension in children.

Echocardiographic patterns of pulmonary valve motion and right-sided systolic time intervals were correlated with pulmonary arterial hemodynamics in 56 children with congenital heart defects. The sensitivity of an abnormal a-dip, reduced e-f slope or mid-systolic valve closure in detecting elevated pulmonary artery diastolic or mean pressures or pulmonary to systemic resistance ratio varied from 36 to 62%. Specificities ranged from 50% (e-f slope for increased Rp:Rs) to 93% (mid-systolic closure for PA diastolic pressure greater than 10 mm Hg). Systolic-time-intervals (RPEP/RVET) did not significantly correlate with pulmonary hemodynamics. We therefore conclude that these echocardiographic features are insufficiently sensitive to be clinically applied to detect pulmonary hypertension in pediatric patients, and that only 2 (a-dip and mid-systolic closure) were of sufficient specificity to be useful.

Hypoxemia, pulmonary hypertension, and low cardiac output in newcomers at low altitude.

ARTICLESHypoxemia, pulmonary hypertension, and low cardiac output in newcomers at low altitudeF. Sime, D. Penaloza, L. Ruiz, N. Gonzales, E. Covarrubias, and R. PostigoF. Sime, D. Penaloza, L. Ruiz, N. Gonzales, E. Covarrubias, and R. PostigoPublished Online:01 May 1974https://doi.org/10.1152/jappl.1974.36.5.561MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByPhysiological Changes to the Cardiovascular System at High Altitude and Its Effects on Cardiovascular DiseaseHigh Altitude Medicine & Biology, Vol. 18, No. 2Effect of Increased Blood Flow on Pulmonary Circulation Before and During High Altitude AcclimatizationHigh Altitude Medicine & Biology, Vol. 17, No. 4The Impact of Moderate-Altitude Staging on Pulmonary Arterial Hemodynamics after Ascent to High AltitudeHigh Altitude Medicine & Biology, Vol. 11, No. 2Effect of Altitude on the Heart and the LungsCirculation, Vol. 116, No. 19Insights by Peruvian scientists into the pathogenesis of human chronic hypoxic pulmonary hypertensionJohn T. Reeves†, and Robert F. Grover1 January 2005 | Journal of Applied Physiology, Vol. 98, No. 1Role of Vascular Smooth Muscle in the Development of High Altitude Pulmonary Hypertension: An Interspecies EvaluationHigh Altitude Medicine & Biology, Vol. 2, No. 2Echocardiographic assessment of left ventricular function and wall motion at high altitude in normal subjectsThe American Journal of Cardiology, Vol. 68, No. 17Environmental Considerations for ExerciseCardiology Clinics, Vol. 5, No. 2 More from this issue > Volume 36Issue 5May 1974Pages 561-565 Copyright & PermissionsCopyright © 1974 the American Physiological Societyhttps://doi.org/10.1152/jappl.1974.36.5.561PubMed4826319History Published online 1 May 1974 Published in print 1 May 1974 Metrics

Oxygen toxicity; respiratory responses of normal men to inhalation of 6 and 100 per cent oxygen under 3.5 atmospheres pressure.

ARTICLESOxygen Toxicity. Respiratory Responses of Normal Men to Inhalation of 6 and 100 Per Cent Oxygen Under 3.5 Atmospheres PressureC. J. Lambertsen, M. W. Stroud 3RD, R. A. Gould, R. H. Kough, J. H. Ewing, and C. F. SchmidtC. J. Lambertsen, M. W. Stroud 3RD, R. A. Gould, R. H. Kough, J. H. Ewing, and C. F. SchmidtPublished Online:01 Mar 1953https://doi.org/10.1152/jappl.1953.5.9.487MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByArterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygenLindell K. Weaver, Steve Howe, Gregory L. Snow, and Kayla Deru1 July 2009 | Journal of Applied Physiology, Vol. 107, No. 1Hyperoxia-Induced HypocapniaChest, Vol. 128, No. 1Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neuronsJay B. Dean, Daniel K. Mulkey, Richard A. Henderson, Stephanie J. Potter, and Robert W. Putnam1 February 2004 | Journal of Applied Physiology, Vol. 96, No. 2Normocapnia improves cerebral oxygen delivery during conventional oxygen therapy in carbon monoxide–exposed research subjectsAnnals of Emergency Medicine, Vol. 40, No. 6Changes in respiratory control in humans induced by 8 h of hyperoxiaXiaohui Ren, Marzieh Fatemian, and Peter A. Robbins1 August 2000 | Journal of Applied Physiology, Vol. 89, No. 2The effect of oxygen administration on gas exchange and cardiopulmonary function in normal subjectsRespiration Physiology, Vol. 12, No. 3 More from this issue > Volume 5Issue 9March 1953Pages 487-494 https://doi.org/10.1152/jappl.1953.5.9.487PubMed13034676History Published online 1 March 1953 Published in print 1 March 1953 Metrics