Showing papers on "Pulmonary artery published in 1997"
TL;DR: Early failure has declined over the study period and is related in part to procedural modifications, and a continuing late hazard phase is associated with few patient-related variables and does not appear related to procedural variables.
553 citations
TL;DR: Increased atrial pressure in the isolated rabbit heart resulted in a significant increase in vulnerability to AF that was closely correlated to shortening of the AERP and no correlation was found with the spatial dispersion between right and left AERPs.
Abstract: Background Atrial fibrillation (AF) is frequently observed under conditions that are associated with atrial dilatation. The aim of this study was to investigate the effects of atrial dilatation on the substrate of AF. Methods and Results In 15 Langendorff-perfused rabbit hearts, the interatrial septum was perforated, and after occlusion of the caval and pulmonary veins, biatrial pressure was increased by raising the level of an outflow cannula in the pulmonary artery. Right and left atrial effective refractory periods (AERPs), monophasic action potentials (MAPs), and inducibility of AF by single premature stimuli were measured as a function of atrial pressure. Increasing the atrial pressure from 0.5±0.7 to 16.2±2.2 cm H2O resulted in a progressive shortening of the right AERP from 82.2±9.8 to 48.0±5.1 ms. In the left atrium, an increase in pressure up to 7.4±0.3 cm H2O had no effect on the AERP. At higher pressures, however, the left AERP also shortened, from 67.5±7.5 to 49.3±2.0 ms. The duration of MAPs ...
458 citations
TL;DR: G gadolinium-enhanced magnetic resonance angiography of the pulmonary arteries had high sensitivity and specificity for the diagnosis of pulmonary embolism and shows promise as a noninvasive method of diagnosing pulmonary emblism without the need for ionizing radiation or iodinated contrast material.
Abstract: Background Diagnosing pulmonary embolism may be difficult, because there is no reliable noninvasive imaging method. We compared a new noninvasive method, gadolinium-enhanced pulmonary magnetic resonance angiography, with standard pulmonary angiography for diagnosing pulmonary embolism. Methods A total of 30 consecutive patients with suspected pulmonary embolism underwent both standard pulmonary angiography and magnetic resonance angiography during the pulmonary arterial phase at the time of an intravenous bolus of gadolinium. All magnetic resonance images were reviewed for the presence or absence of pulmonary emboli by three independent reviewers who were unaware of the findings on standard angiograms. Results Pulmonary embolism was detected by standard pulmonary angiography in 8 of the 30 patients in whom pulmonary embolism was suspected. All 5 lobar emboli and 16 of 17 segmental emboli identified on standard angiograms were also identified on magnetic resonance images. Two of the three reviewers reporte...
434 citations
TL;DR: The presence of right ventricular afterload stress detected by echocardiography is a major determinant of short term prognosis in patients with clinically suspected acute pulmonary embolism.
Abstract: OBJECTIVE: To investigate the prognostic value of echocardiographic findings in patients who present with symptoms suggestive of acute pulmonary embolism. DESIGN: 317 patients with clinically suspected pulmonary embolism were prospectively evaluated by echocardiography for the presence of right ventricular afterload stress and right heart or pulmonary artery thrombi. Objective confirmation of pulmonary embolism by lung scan or pulmonary angiography was obtained in 164 (52%). The presence of deep venous thrombosis was established in 90 of 158 patients (57%) who underwent phlebographic or Doppler sonographic studies. RESULTS: Right ventricular afterload stress was diagnosed in 87 patients (27%). Objective confirmation of pulmonary embolism and diagnosis of deep venous thrombosis was more common in patients with right ventricular afterload stress than in those without (83% v 40% and 46% v 22%, respectively; P < 0.001). This was also true for the detection of thrombi in the right heart and major pulmonary arteries (12 patients v 1 patient; P < 0.001) as well as for the in-hospital mortality from venous thromboembolism (13% v 0.9%; P < 0.001). One year mortality from pulmonary embolism was 13% in patients with right ventricular afterload stress at presentation compared with 1.3% in those without (P < 0.001). CONCLUSIONS: The presence of right ventricular afterload stress detected by echocardiography is a major determinant of short term prognosis in patients with clinically suspected acute pulmonary embolism.
404 citations
TL;DR: The hypothesis that central obesity raises intra-abdominal pressure, which increases pleural pressure and cardiac filling pressure,Which impede venous return from the brain, leading to increased intracranial venous pressure and increased intrACranial pressure associated with pseudotumor cerebri is supported.
Abstract: Objectives.: To determine whether intra-abdominal pressure (as estimated from urinary bladder pressure) is elevated in patients with central obesity (as measured by sagittal abdominal diameter) and pseudotumor cerebri and whether this increased intra-abdominal pressure is associated with increased pleural pressure and cardiac filling pressure, implying a resistance to venous return from the brain. Design.: Nonrandomized, prospective. Setting.: University hospital, operating room. Main outcome measurements.: Intracranial pressure, urinary bladder pressure, sagittal abdominal diameter, transesophageal pleural pressure, central venous pressure, pulmonary artery pressure, and pulmonary artery occlusion pressure. Subjects.: Six women with pseudotumor cerebri (one with CSF leak, one with lumboperitoneal shunt). Results.: Urinary bladder pressure (22 ± 3 cm H 2 O) and sagittal abdominal diameter (29 ± 3 cm) were significantly elevated in these patients with elevated intracranial pressure (293 ± 80 mm H 2 O) compared with a previously reported group of nonobese control patients. The transesophageal pleural pressure (15 ± 10 mm Hg), central venous pressure (20 ± 6 mm Hg), mean pulmonary artery pressure (31 ± 6 mm Hg), and pulmonary artery occlusion pressure (21 ± 7 mm Hg) were all markedly elevated compared with published normal values and with previous data from obese patients without pseudotumor cerebri. Conclusions.: These data support the hypothesis that central obesity raises intra-abdominal pressure, which increases pleural pressure and cardiac filling pressure, which impede venous return from the brain, leading to increased intracranial venous pressure and increased intracranial pressure associated with pseudotumor cerebri.
337 citations
TL;DR: Early surgical management of CAF is a safe and effective treatment resulting in 100% survival and 100% closure rate and transcatheter embolization is a reasonable alternative to standard surgical closure in only a very small, select group of patients.
310 citations
TL;DR: Long-term follow-up of this single-center patient group demonstrated improved long-term survival during epo therapy compared with that in historical control subjects and confirms predicted improved outcomes based on shorter follow- up periods.
303 citations
TL;DR: Pulmonary hypertension is frequent and highly variable in patients with left ventricular dysfunction but is strongly associated with diastolic dysfunction (shorter mitral deceleration time) and the degree of functional mitral regurgitation (larger effective regurgitant orifice).
266 citations
TL;DR: It is concluded that NOS 3 is a key enzyme responsible for providing basal pulmonary NO release, and Congenital Nos 3 deficiency produces mild pulmonary hypertension in mice.
Abstract: NO, synthesized in endothelial cells by endothelial NO synthase (NOS 3), is believed to be an important endogenous pulmonary vasodilator substance that contributes to the normal low pulmonary vascular resistance. To selectively investigate the role of NOS 3 in the pulmonary circulation, mice with targeted disruption of the NOS 3 gene were studied. Pulmonary hemodynamics were studied by measuring pulmonary artery pressure, left ventricular end-diastolic pressure, and lower thoracic aortic flow by using a novel open-chest technique. Transient partial occlusion of the inferior vena cava was used to assess the pulmonary artery pressure-flow relationship. Tension developed by isolated pulmonary artery segments after acetylcholine stimulation was measured in vitro. The histological appearance of NOS 3–deficient and wild-type murine lungs was compared. NOS 3–deficient mice (n=27), when compared with wild-type mice (n=32), had pulmonary hypertension (pulmonary artery pressure, 19.0±0.8 versus 16.4±0.6 mm...
254 citations
TL;DR: The view that in most patients who have severe pulmonary hypertension associated with advanced liver disease, it is caused by fixed pathological changes in the pulmonary vasculature, is not reversible with liver transplantation, and is associated with a very high perioperative mortality rate is supported.
245 citations
TL;DR: It is concluded that L-arginine ameliorated the changes associated with PH in rats, perhaps by modifying the endogenous nitric oxide production.
Abstract: Background Endothelium-dependent nitric oxide–mediated vasodilation is impaired in rats with pulmonary hypertension (PH) induced by chronic hypoxia or by monocrotaline injection. We therefore investigated whether the prolonged administration of the nitric oxide precursor l-arginine would alleviate PH in both rat models. Methods and Results Fifty-nine rats were exposed to hypobaric hypoxia (380 mm Hg, 10 days) or room air and injected intraperitoneally with l-arginine (500 mg/kg), d-arginine (500 mg/kg), or saline once daily from day −3 to day 10. An additional 38 rats injected subcutaneously with monocrotaline (60 mg/kg) or saline were treated similarly with l-arginine or saline from day −3 to day 17. At the end of the experiment, awake mean pulmonary arterial pressure was determined. The heart was dissected to weigh the right ventricle, and the lungs were obtained for vascular morphometric analysis. Hypoxic rats developed PH (30.8±0.7 versus 19.2±0.4 mm Hg in controls; P<.05) and right ventricular hypert...
TL;DR: Increased endothelial NOS levels correlated with alterations in gas exchange and were accompanied by enhanced NO activity and a blunted response to phenylephrine, reversible by NOS inhibition, in pulmonary artery rings.
TL;DR: Many of the findings in the various syndromes of PE can be understood in terms of the severity of PE as it increases from mild with the pulmonary infarction syndrome to moderate with the isolated dyspnea syndrome to severe with circulatory collapse.
TL;DR: Because of high prevalence of bilateral central pulmonary thromboemboli in patients with hemodynamically significant PE, both sCT and TEE allow its definitive confirmation in most cases.
TL;DR: It is concluded that in patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration ofNocturnal hypox aemia.
Abstract: It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.
Journal Article•
TL;DR: In APE without prior cardiopulmonary disease, increases in PAP and TPR are correlated in a nonlinear fashion with the degree of pulmonary vascular obstruction as assessed by lung scanning, consistent with previous reports that pulmonary hypertension in CTEPH is due not only to the obstruction of proximal pulmonary arteries but also to remodeling of small distal arteries in nonoccluded areas.
Abstract: UNLABELLED To assess the relationship between pulmonary vascular obstruction and hemodynamic status in acute pulmonary embolism (APE) and in chronic thromboembolic pulmonary hypertension (CTEPH), perfusion lung scan and hemodynamic measurements were obtained in 31 consecutive patients with APE and in 45 with CTEPH. METHODS Lung scans were scored independently by two experience observers who determined the percentage of vascular obstruction (PVOs). Mean pulmonary artery pressure (PAP) and total pulmonary resistance (TPR) were obtained during right heart catheterization. In patients with APE, measurements were recorded within a 1-hr interval before and 12 hours after thrombolysis. This yielded 62 paired PVOs values with concomitant PAP and TPR measurements. In patients with CTEPH, data were recorded within a 3-day interval. RESULTS Mean PVOs (%) values were similar in APE and CTEPH patients (59 +/- 13 vs. 58 +/- 15), whereas PAP and TPR were significantly higher in CTEPH patients (51 +/- 17 mmHg and 23 +/- 11 U/m2, respectively) than in APE patients (23 +/- 8 mmHg and 9 +/- 5 U/m2, respectively, p < 0.001). In APE patients, significant hyperbolic correlations were found linking PVOs with PAP and TPR (r = 0.75, p < 0.01 for PAP; r = 0.71, p < 0.01 for TPR). In CTEPH, there were no significant correlations between PVOs and PAP or TPR. For the same level of PVOs, patients with CTEPH had higher PAP and TPR value than patients with APE. CONCLUSION In APE without prior cardiopulmonary disease, increases in PAP and TPR are correlated in a nonlinear fashion with the degree of pulmonary vascular obstruction as assessed by lung scanning. In CTEPH patients, the higher PAP and TPR values as compared to APE patients with comparable degrees of PVOs are consistent with previous reports that pulmonary hypertension in CTEPH is due not only to the obstruction of proximal pulmonary arteries but also to remodeling of small distal arteries in nonoccluded areas.
TL;DR: The degree of preoper MR was predictive of outcome, whereas the severity of preoperative cardiac dysfunction and ventricular dilation were not, and complete recovery from myocardial dysfunction is expected after dual coronary repair of ALCAPA.
Journal Article•
TL;DR: An important role for hemodynamics is demonstrated in determining the pattern of pulmonary vascular remodeling after injury and severe RVH developed in Sprague-Dawley rats but were not seen in animals receiving either MCT or anastomosis only.
Abstract: Hemodynamic factors have profound influences on blood vessels. To test the hypothesis that hemodynamic conditions modify the pattern of remodeling in response to injury, monocrotaline (MCT) injury in Sprague-Dawley rats was followed 1 week later by left pneumonectomy to increase blood flow to the right lung. Right pulmonary artery remodeling in these MCT plus pneumonectomy animals was compared with animals receiving MCT or pneumonectomy alone. Neointimal changes developed in more than 90% of all right lung intra-acinar vessels 5 weeks after MCT injury (4 weeks after pneumonectomy). Neointimal lesions did not develop in untreated animals or in animals receiving MCT or pneumonectomy only. Animals with a neointimal pattern of remodeling developed severe right ventricular hypertrophy (RVH) whereas animals with a medial hypertrophy pattern of remodeling (MCT only) developed moderate RVH compared with control animals. Neointimal lesions and RVH were similar whether injury preceded pneumonectomy or vice versa. To exclude the possibility that neointimal lesions resulted from injury plus post-pneumonectomy compensatory lung growth, rather than injury plus increased flow, a left subclavian-pulmonary artery anastomosis was substituted for pneumonectomy. Neointimal lesions and severe RVH developed in these animals but were not seen in animals receiving either MCT or anastomosis only. These studies demonstrate an important role for hemodynamics in determining the pattern of pulmonary vascular remodeling after injury.
TL;DR: It is concluded that pulmonary hypertension, as another cardiovascular complication of multiple factors of cause, seems to occur more frequently and at an early stage of the cardiac involvement in patients with thalassemia major.
TL;DR: Using transesophageal pulsed wave Doppler technique, four PVFV components are identifiable and determined by PV-LA hemodynamic pressure gradients, and these gradients appear to be influenced by a combination of physiologic events that include RV stroke volume, the compliance of the pulmonary vasculature and left atrium and phasic changes in LA pressure.
TL;DR: A mosaic pattern of lung attenuation can be seen on CT scans in patients with PAH due to vascular disease, cardiac disease, or lung disease, however, the mosaic pattern is seen significantly more often in Patients with PAh due toascular disease than in patientsWith PAHDue to cardiac or lung Disease.
Abstract: The purpose of this study was to determine the frequency with which a mosaic pattern of lung attenuation is seen on chest CT scans in patients with various causes of pulmonary artery hypertension (PAH).Chest CT scans of 64 patients with known PAH were reviewed to assess the patterns of lung attenuation. Patterns of lung attenuation were divided into three categories: class I, homogeneous lung parenchymal attenuation; class II, slightly heterogeneous lung attenuation that does not conform to the anatomic boundaries of the secondary pulmonary lobule; and class III (mosaic pattern), heterogeneous lung attenuation in geographic regions with well-defined borders corresponding to the anatomic units of single or multiple secondary pulmonary lobules. The patients medical histories were reviewed to determine the primary cause of PAH for each patient.Peak pulmonary artery pressure of the patients in our study averaged 74 mm Hg (range, 36-194 mm Hg). Twenty-one patients had PAH due to lung disease: 17 patients, due ...
TL;DR: In one patient coronary artery fistula closed spontaneously, and in one patient, the right coronary was arising from left coronary artery.
TL;DR: The total neopulmonary artery index correlates with postrepair right ventricular/left ventricular pressure ratio and is useful in deciding when to close the ventricular septal defect if it is larger than 200 mm2/m2.
TL;DR: It is concluded that ET(A) receptor stimulation contributes to the pathogenesis and pathophysiology of experimental perinatal pulmonary hypertension.
Abstract: Based on past studies of an experimental model of severe intrauterine pulmonary hypertension, we hypothesized that endothelin-1 (ET-1) contributes to high pulmonary vascular resistance (PVR), hypertensive lung structural changes, and right ventricular hypertrophy (RVH) caused by prolonged closure of the ductus arteriosus. To test this hypothesis, we studied the effects of BQ 123, a selective ET(A) receptor antagonist, after ligation of the ductus arteriosus in utero. In 19 late gestation fetal lambs (126+/-3 d; 147 d, term) we ligated the ductus arteriosus at surgery, and treated animals with either BQ 123 (1 mg/d) or vehicle (0.1% DMSO, HTN) in the pulmonary artery for 8 d. Chronic BQ 123 treatment attenuated the rise in mean pulmonary artery pressure (PAP) 8 d after ductus arteriosus ligation (78+/-2, HTN vs. 70+/-4 mmHg, BQ 123, P < 0.05). To study the effects of ET(A) blockade at birth, 15 animals were delivered by cesarean section and ventilated with 10% oxygen (O2), 100% O2 and inhaled nitric oxide (NO). Lambs treated with BQ 123 had lower PVR after delivery during ventilation with 10% O2, 100% O2, and inhaled NO (HTN vs. BQ 123, P < 0.05 for each intervention). Acute BQ 123 treatment (2 mg/30 min) lowered PVR in three HTN animals ventilated with 100% O2 and inhaled NO (P < 0.05). Chronic BQ 123 treatment prevented the development of RVH as determined by the ratio of the right ventricle/left ventricle + septum (0.79+/-0.03, HTN vs. 0.57+/-0.06, BQ 123, P < 0.05) and attenuated the increase in wall thickness of small pulmonary arteries (61+/-2, HTN vs. 50+/-2%, BQ 123, P < 0.05). In summary, chronic intrauterine ET(A) receptor blockade decreased PAP in utero, decreased RVH and distal muscularization of small pulmonary arteries, and increased the fall in PVR at delivery. We conclude that ET(A) receptor stimulation contributes to the pathogenesis and pathophysiology of experimental perinatal pulmonary hypertension.
TL;DR: The prevalence of PE limited to subsegmental pulmonary arteries is low, 6%, and was most prevalent among patients with low-probability ventilation/perfusion scans, particularly if they had no prior cardiopulmonary disease.
TL;DR: These results proved that, when the full dose of streptokinase has been given over 12 h, its efficacy is as good as that of 2 h of recombinant tissue plasminogen.
Abstract: Objective The aim of the study was to test the efficacy of recombinant tissue plasminogen activator and streptokinase in massive pulmonary embolism, the primary endpoints being haemodynamic improvement and thrombus lysis, and the secondary endpoints efficacy and safety.
Design Fifty patients with massive pulmonary embolism were randomly allocated either to a 100 mg 2 h infusion of recombinant tissue plasminogen activator followed by a 20 IU.kg−1.h−1 infusion of heparin, or to a 100 000 IU.h−1 12 h infusion of streptokinase after a initial bolus of 250 000 IU over 15 min, followed by heparin infusion of 10 IU.kg−1.h−1. Total pulmonary resistance and right ventricular ejection fraction were monitored over a 12 h period. Pulmonary vascular obstruction was assessed at 24 to 48 h and 10 days after thrombolytic therapy.
Results Thrombolysis occurred more rapidly with recombinant tissue plasminogen activator than with streptokinase, but without any significant difference in terms of right heart haemodynamics at 12 h or in improvement of pulmonary vascular obstruction at 24–48 h or at 10 days. There was no significant difference in bleeding complication rates and no patients suffered intracranial haemorrhage.
Conclusion These results proved that, when the full dose of streptokinase has been given over 12 h, its efficacy is as good as that of 2 h of recombinant tissue plasminogen. A further trial aimed at comparing recombinant tissue plasminogen activator and streptokinase infused over a 2 h period is needed to determine whether a similar efficacy can be obtained.
TL;DR: Pulmonary arterial hypertension, or altered vascular mechanical forces associated with hypertension, may be responsible for the augmented EDNO-dependent arterial dilation and upregulation of arterial eNOS in lungs from CH and MC-treated rats.
Abstract: We have previously demonstrated that arterial, but not venous, vasodilatory responses to endothelium-derived nitric oxide (EDNO)-dependent agonists are enhanced in lungs isolated from rats with chronic hypoxia (CH)-induced pulmonary arterial hypertension. These data suggest that CH is associated with increased endothelial nitric oxide synthase (eNOS) activity within the pulmonary arterial vasculature. In addition, the correlation of increased pulmonary arterial pressure with selectively enhanced arterial responsiveness to EDNO-mediated agonists suggests that arterial hypertension, rather than hypoxia per se, is a contributing factor in this response. Therefore, we hypothesized that 1) CH selectively upregulates eNOS within the pulmonary arterial vasculature and 2) monocrotaline (MC)-induced pulmonary arterial hypertension selectively enhances pulmonary arterial dilation to EDNO-dependent dilators and upregulates arterial eNOS. We examined the responses to the EDNO-dependent dilators arginine vasopressin and ionomycin in U-46619-constricted isolated perfused lungs from control and MC-treated rats. Microvascular pressure was assessed by the double-occlusion technique, allowing calculation of segmental resistances. Lungs from MC-treated rats exhibited augmented arterial dilation to arginine vasopressin compared with control lungs. However, the responses to ionomycin were not different between the two groups. Quantitative immunocytochemistry was used to compare pulmonary eNOS immunoreactivity in vessels from control, CH, and MC-treated rats. eNOS staining was more intense in the arteries of CH and MC-treated rats compared with those of control animals, whereas CH and MC treatment had no effect on eNOS staining in veins. We conclude that pulmonary arterial hypertension, or altered vascular mechanical forces associated with hypertension, may be responsible for the augmented EDNO-dependent arterial dilation and upregulation of arterial eNOS in lungs from CH and MC-treated rats.
TL;DR: Exacerbation of PR by increased airway pressure and branch pulmonary stenosis may be relevant to the acute postoperative and long-term management, respectively, of patients after repair of tetralogy of Fallot.
Abstract: Background Pulmonary regurgitation (PR) is an important determinant of outcome after repair of tetralogy of Fallot. Baseline PR was measured by magnetic resonance (MR) phase velocity mapping and from real-time right ventricular pressure-volume loops with a conductance catheter. Subsequently, the impact of two loading maneuvers (increased airway pressure, simulated branch pulmonary artery stenosis) on PR was assessed by the conductance catheter method. Methods and Results Thirteen patients, 3 to 35 years after tetralogy of Fallot repair or pulmonary valvotomy, had PR measured by MR phase velocity mapping while breathing spontaneously. During catheterization under general anesthesia, PR was estimated from right ventricular pressure-volume loops generated by conductance and microtip pressure catheters. The effect of increased airway pressure (continuous positive airway pressure, 20 cm H2O; n=12) and simulated branch pulmonary artery stenosis (transient balloon occlusion of a branch pulmonary artery, n=7) was...
TL;DR: Prior hemorrhage and resuscitation caused an earlier decline in cardiopulmonary function in the setting of increased intra-abdominal pressure, suggesting that, when interpreting intra-ABdominal pressures, the clinical scenario must be considered.
Abstract: Background: Intra-abdominal hypertension has been associated with pulmonary and cardiac dysfunctions. We have noted in the clinical scenario of hemorrhagic shock and resuscitation that avoidance of even moderate levels of increased intra-abdominal pressure, using prophylactic decompression, improves outcomes when compared with patients who were decompressed when intra-abdominal pressures went over 20 cm H 2 O. We hypothesized that prior hemorrhage and resuscitation exacerbates the cardiopulmonary dysfunction associated with intra-abdominal hypertension. Methods: Ten anesthetized pigs underwent placement of arterial and pulmonary artery catheters and a Silastic intra-abdominal catheter for measuring and manipulating intra-abdominal pressure. Group 1 animals (n = 5) were subjected to increasing intra-abdominal pressures at 10 mm Hg increments up to a level of 40 mm Hg. Group 2 animals (n = 5) were exposed to a severe hemorrhage and resuscitation before the increasing intra-abdominal pressure protocol. Results: Compared with baseline, hemorrhage and resuscitation caused a significant deterioration in cardiac output at intraabdominal pressures of 10 mm Hg and above. Oxygenation was reduced at 30 and 40 mm Hg. These changes were not seen in group 1 animals. A significant difference was found between groups 1 and 2 in VT, Paco 2 , and Paco 2 /Fio 2 ratio at an intra-abdominal pressure of 20 mm Hg. This difference was not seen at lower or higher pressures. Conclusions: Prior hemorrhage and resuscitation caused an earlier decline in cardiopulmonary function in the setting of increased intra-abdominal pressure. These data suggest that, when interpreting intra-abdominal pressures, the clinical scenario must be considered. Prior hemorrhage and resuscitation produce the adverse consequences of intra-abdominal hypertension at lower pressures than when intra-abdominal hypertension is the only insult.
TL;DR: In this article, the relationship between pulmonary artery size at computed tomography (CT) and PA pressures was determined, and a noninvasive CT method of PA pressure measurement was developed to determine a PA diameter that can enable differentiation of normal subjects from those with ptfimonary hypertension.