Increased Pulmonary Artery Pressure Research Articles

Early echocardiographic predictors of unfavorable yearly prognosis in patients with acute myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. Objective to determine the most informative in the prognostic plan echocardiographic indices in patients with acute myocardial infarction and diabetes mellitus. Methods A retrospective analysis of outcomes of 97 diabetic patients with acute myocardial infarction (AMI), with lesions of two or more coronary arteries was performed. All patients received conventional basic therapy comprising, acetylsalicylic acid, clopidogrel, beta-blocker, an ACE inhibitor, statins, and insulin therapy on a stationary phase for a minimum of 2 weeks, followed by a transition to oral antidiabetics. According to the 12 month follow depending on the outcomes two groups were established: favorable prognosis n = 46 and unfavorable prognosis n = 51, having one or more of the following complications: death, reinfarction (nonfatal), development or progression of heart failure. Results Differences in echocardiographic parameters, characterizing myocardial hypertrophy of left ventricular (LV) were revealed between patients with different outcomes of AMI. Thus, patients with adverse outcome were characterized by a significant increase of LV mass (from 191.2 ± 35.7g to 255.7 ± 46.2 g, p = 0.004) and LV posterior wall thickness (from 8.7 ± 1.04mm to 10.6 ± 1.37mm, p = 0.004) in dynamics. Moreover, a smaller LV ejection fraction (LVEF) was observed in the group with an unfavorable outcome (both initially and in dynamics), as well as large LV end-diastolic volume and end-systolic volume. Single-factor analysis has shown, that EF <40%, LV aneurysm, the involvement of the apical LV myocardial segments at any location were echocardiography predictors of poor outcome. In the group of patients with unfavorable course of AMI, the index of left atrium (LA) increased from 35.8 ± 3.8mm to 37.3 ± 1.8mm (p = 0.04), which is significantly higher than in the second group, where the LA index was 33.8 ± 3.2mm and 34.2 ± 2.9mm (p = 0.7). In the first group, the right ventricle (RV) remained practically unchanged (22.3 ± 2.7mm and 22 ± 3.5 mm, respectively, p = 0.89), while in the second group the size of the RV decreased from 23.2 ± 3.9mm to 20.7 ± 2.9mm (p = 0.38). Initially, when comparing between groups, p = 0.38) and after 1 month p = 0.5). The negative role of pressure in the pulmonary artery (PA) in patients with AMI was also demonstrated. The systolic pressure in the PA index in the group with a favorable outcome in the dynamics significantly decreased, in contrast to the group with an unfavorable outcome (from 19.9 ± 4.5 mmHg to 16.2 ± 2.6 mmHg, p = 0.03 and from 22.1 ± 5.7mmHg to 18.0 ±3.6 mmHg, p = 0.15, respectively). Conclusion AMI with a high risk of adverse 12-month outcomes, characterized by the following echocardiographic signs: engagement apical segments of the LV regardless of the localization of myocardial infarction, reduced LVEF, as well as increased PA pressure, combined with the increase in the size of RV.

Abstract 17233: Primary Intimal Sarcoma Of The Pulmonary Artery In A Patient With Laboratory Confirmed Heterozygous Factor V Leiden Mutation: A Case Report

Pulmonary artery intimal sarcoma (PAIS) is a rare tumor associated with progressively increasing dyspnea, atypical chest pain, and pulmonary hypertension. Owing to overlap in presentation, PAIS can be misdiagnosed as pulmonary thromboembolism (PTE). Here we present the case of a 59-year-old male with heterozygous Factor V Leiden mutation, history of deep vein thrombosis (DVT), and recent PTE presenting to urgent care with cough, mild orthopnea, and exertional dyspnea. Transthoracic echocardiogram (TTE) revealed severely dilated right ventricle with moderately decreased function and severe pulmonary hypertension with pulmonary arterial (PA) pressure of 93mmHg. Computed tomography angiography of the chest revealed massive central PTE. Given hemodynamic stability, saturating well on room air and simplified PESI score of 0, Pulmonology recommended discharge with anticoagulation. The patient returned a month later with three weeks of increased dyspnea on exertion, worsened right ventricular function as well as possible new mobile thrombus extending into the right ventricular outflow tract (RVOT). Due to presumed failure of medical therapy, Cardiology placed the patient on venoarterial extracorporeal membrane oxygenation (VA-ECMO) followed by attempted mechanical thrombectomy using both the Angiovac and Penumbra CAT12 systems. Both systems failed to remove substantial material from the PA. The next day, TTE revealed increased PA pressure of 132mmHg.The patient underwent emergent bilateral thromboendarterectomy with a mass discovered involving the pulmonary valve (PV), RVOT, both left and right PAs, along with invasion into the PA wall. The mass was resected, the PV valve replaced, the main PA and left PA reconstructed, and pericardial patch reconstruction of the RVOT was performed. The mass was determined to be a PAIS of French Federation of Comprehensive Cancer Centres (FNCLCC) Grade 3. Two months after uncomplicated recovery, chemotherapy was initiated. Securing the diagnosis of PAIS is challenging. However, collaboration between clinicians, radiologists, and pathologists increases the likelihood of recognizing subtle markers that can differentiate PAIS from illnesses with a similar presentation.

Cardiovascular magnetic resonance 4D flow analysis has a higher diagnostic yield than Doppler echocardiography for detecting increased pulmonary artery pressure

BackgroundPulmonary hypertension is definitively diagnosed by the measurement of mean pulmonary artery (PA) pressure (mPAP) using right heart catheterization. Cardiovascular magnetic resonance (CMR) four-dimensional (4D) flow analysis can estimate mPAP from blood flow vortex duration in the PA, with excellent results. Moreover, the peak systolic tricuspid regurgitation (TR) pressure gradient (TRPG) measured by Doppler echocardiography is commonly used in clinical routine to estimate systolic PA pressure. This study aimed to compare CMR and echocardiography with regards to quantitative and categorical agreement, and diagnostic yield for detecting increased PA pressure.MethodsConsecutive clinically referred patients (n = 60, median [interquartile range] age 60 [48–68] years, 33% female) underwent echocardiography and CMR at 1.5 T (n = 43) or 3 T (n = 17). PA vortex duration was used to estimate mPAP using a commercially available time-resolved multiple 2D slice phase contrast three-directional velocity encoded sequence covering the main PA. Transthoracic Doppler echocardiography was performed to measure TR and derive TRPG. Diagnostic yield was defined as the fraction of cases in which CMR or echocardiography detected an increased PA pressure, defined as vortex duration ≥15% of the cardiac cycle (mPAP ≥25 mmHg) or TR velocity > 2.8 m/s (TRPG > 31 mmHg).ResultsBoth CMR and echocardiography showed normal PA pressure in 39/60 (65%) patients and increased PA pressure in 9/60 (15%) patients, overall agreement in 48/60 (80%) patients, kappa 0.49 (95% confidence interval 0.27–0.71). CMR had a higher diagnostic yield for detecting increased PA pressure compared to echocardiography (21/60 (35%) vs 9/60 (15%), p < 0.001). In cases with both an observable PA vortex and measurable TR velocity (34/60, 56%), TRPG was correlated with mPAP (R2 = 0.65, p < 0.001).ConclusionsThere is good quantitative and fair categorical agreement between estimated mPAP from CMR and TRPG from echocardiography. CMR has higher diagnostic yield for detecting increased PA pressure compared to echocardiography, potentially due to a lower sensitivity of echocardiography in detecting increased PA pressure compared to CMR, related to limitations in the ability to adequately visualize and measure the TR jet by echocardiography. Future comparison between echocardiography, CMR and invasive measurements are justified to definitively confirm these findings.

P2766Increased right ventricular burden in patients with chronic thromboembolic disease

Abstract Introduction Patients with chronic thromboembolic disease (CTED) have residual perfusion defects after pulmonary embolism (PE) but not increased pulmonary artery (PA) pressure. These patients suffer from functional limitation and have a higher risk of venous thromboembolism recurrence. Purpose In this study we wanted to explore if CTED patients had signs of increased PA pressure and right heart burden by echocardiography Methods Inclusion criteria were history of PE, age 18–75 years and PE diagnosed 6–72 months prior to inclusion. Patients with left ventricular systolic or diastolic heart failure, valvular disease, chronic pulmonary disease and chronic thromboembolic pulmonary hypertension were excluded. All patients underwent echocardiography with standard and novel methods and ventilation/perfusion (VQ)-scan. The echocardiographic examinations were blinded to the result of the VQ-scan. VQ-scan were analyzed according to the European Association of Nuclear Medicine-criteria, and deemed either positive or negative. Data are presented as mean ± SD or median ± IQR as appropriate. Independent sample t-test or Mann-Whitney U test was used for the primary statistical analysis. Multiple linear regression was used to adjust for age, BMI and systolic blood pressure. Results Table 1 VQ negative (n=58) VQ positive (n=20) p-value Adjusted Age (years) 59±8 67±6.5 0.71 Time since PE event (months) 37±19 33±17 0.42 Pulmonary artery acceleration time (ms) 145±22 119.5±26 &lt;0.001 &lt;0.001 Pulmonary artery diameter (mm) 21±3.3 25±3.6 &lt;0.01 &lt;0.01 TAPSE (mm) 25.7±3.6 24.9±4.0 0.45 RV (right ventricle) S' (cm/s) 12.7±2.3 12.8±2.7 0.78 RV isovolumic relaxation time (ms) 33±23.9 50±22 &lt;0.01 &lt;0.01 RV myocardial performance index 0.36±0.10 0.44±0.15 0.04 0.02 Tricuspid regurgitation maximum velocity (m/s) 2.3±0.3 2.7±0.4 &lt;0.001 &lt;0.001 LV (left ventricle) ejection fraction (%) 62.5±4.2 61.3±6.0 0.41 E/A 1.02±0.26 0.90±0.23 0.09 E/e' 6.8±2.0 6.5±2.2 0.75 E/A: ratio between transmitral pulsed doppler peak early (E) diastolic and atrial (A) velocity; E/e': ratio between E and peak early velocity (e') by tissue velocity. Figure 1 (error bars - mean and 95% CI) Conclusion Patients with CTED after PE have increased PA pressure and impaired RV systolic and diastolic function compared to those without residual perfusion defects. These findings indicate that CTED patients should be more thoroughly followed up.

Effect of Ketamine in Pulmonary Hypertensive Children

Pulmonary hypertension is not an uncommon condition in clinical setting. Pulmonary artery (PA) pressure may increase during anesthesia because of the hypoxia, hypoventilation and acidosis. Keeping these factors constant there are also other possibilities which can increase the PA pressure, for example drugs. Among them ketamine is known to increase PA pressure in adults especially when they have baseline increased PA pressure. In few literatures it is claimed that in children ketamine may be safe even in those with pulmonary hypertension. We are using ketamine as a component of intravenous anesthesia in catheterization lab during right heart catheterization, pressure measurement and saturation evaluation. We thought it was necessary to evaluate the effect to ketamine on pulmonary artery pressure in pediatric patients in our setting. Altogether fifteen children diagnosed with pulmonary hypertension wer anesthetized with ketamine based anesthesia and the pulmonary artery pressure was evaluated in cardiac catheterization laboratory before and after 5, 10 and 15 min of injection of the ketamine (2mg/kg body weight) intravenously. We found in our study only about 6.2% increment in pulmonary artery pressure after 5 minutes of the injection of the ketamine and the pressure came to the pre-injection level at 10 to 15 minutes of the injection In conclusion of this preliminary study with limited number of the cases, ketamine can be used safely without much problems in pulmonary hypertensive children secondary to the increased blood flow to the lungs.

Eukaryotic elongation factor 2 kinase mediates monocrotaline-induced pulmonary arterial hypertension via reactive oxygen species-dependent vascular remodeling.

Pulmonary arterial (PA) hypertension (PAH) is a progressive and lethal disease that is caused by increased vascular contractile reactivity and structural remodeling. These changes contribute to increasing pulmonary peripheral vascular resistance, finally leading to right heart failure and death. Eukaryotic elongation factor 2 kinase (eEF2K) is a Ca(2+)/calmodulin-dependent protein kinase. We previously revealed that eEF2K protein increases in the mesenteric artery from spontaneously hypertensive rats and partly mediates the development of hypertension via a promotion of ROS-dependent vascular inflammatory responses and proliferation and migration of vascular smooth muscle cells. However, a role of eEF2K in the pathogenesis of PAH is unknown. In the present study, we tested the hypothesis that eEF2K may be involved in the pathogenesis of PAH. PAH was induced by a single intraperitoneal injection of monocrotaline (MCT; 60 mg/kg) to rats. A specific eEF2K inhibitor, A-484954 (2.5 mg·kg(-1)·day(-1)), was intraperitoneally injected for 14 days. Long-term A-484954 treatment inhibited MCT-induced increased PA pressure. It was revealed that A-484954 inhibited MCT-induced PA hypertrophy and fibrosis but not impairment of endothelium-dependent and -independent relaxation. Furthermore, A-484954 inhibited MCT-induced NADPH oxidase-1 expression and ROS generation as well as matrix metalloproteinase-2 activation. In conclusion, the present results suggest that eEF2K at least partly mediates MCT-induced PAH via stimulation of vascular structural remodeling perhaps through NADPH oxidase-1/ROS/matrix metalloproteinase-2 pathway.

Increase in pulmonary arterial pressure after atrial fibrillation ablation: incidence and associated findings

The stiff left atrial (LA) syndrome is defined as pulmonary hypertension (PH) secondary to reduced LA compliance and has recently been shown to be one cause of PH after atrial fibrillation (AF) ablation. We aimed to determine the incidence of an increase in pulmonary arterial (PA) pressure post-ablation and examine the clinical and echocardiographic associations. Patients who underwent AF ablation between 1999 and 2011 were included if they had both an echocardiogram pre-ablation and 3 months post-ablation. Patients were then separated into two groups with the increased PA pressure group defined as patients with >10 mmHg increase in right ventricular systolic pressure (RVSP) post-ablation and a post-ablation RVSP >35 mmHg. Of the 499 patients meeting the study criteria, 41 (8.2%) had an increase in RVSP >10 mmHg and RVSP >35 mmHg post-ablation. On echocardiogram, the two groups had similar E/A and E/e' ratios pre-ablation. However, post-ablation, the increased PA pressure group had higher E/A (2.12 vs. 1.49, p < 0.01) and E/e' (14.7 vs. 11.2, p < 0.01) ratios. LA expansion index values were lower in the increased PA pressure group pre-ablation (51 vs. 92%, p < 0.01), but not significantly different post-ablation (82 vs. 88%, p = 0.44). Around 8% of patients develop an increase in estimated PA pressure after AF ablation. Echocardiographic parameters suggest that patients who develop increased PA pressure are developing (or unmasking) left ventricular diastolic dysfunction.

Decreased Kv1.5 expression in intrauterine growth retardation rats with exaggerated pulmonary hypertension

Chronic hypoxia pulmonary hypertension (CH-PHT) in adulthood is likely to be of fetal origin following intrauterine growth retardation (IUGR). Oxygen (O₂)-sensitive voltage-gated potassium channels (Kv channels) in resistance pulmonary artery smooth muscle cells (PASMCs) play an important role in scaling pulmonary artery (PA) pressure. Expression and functional changes of Kv channels are determined, in part, by embryonic development. We hypothesized that O₂-sensitive Kv channels play an important role in exaggerated CH-PHT following IUGR. We established a rat model of IUGR by restricting maternal food during the entire pregnancy and exposed IUGR rats and their age-matched controls aged 12 wk to hypoxia for 2 wk. We found that hypoxia exposure significantly induced increased PA pressure and thicker smooth muscle layer in the IUGR group relative to controls. We compared the constriction of the resistance PA to inhibitors of K⁺ channels, 4-aminopyridine (4-AP), tetraethylammonium, and BaCl₂. Despite the thickness of the smooth muscle layer, the constriction to 4-AP was significantly reduced in the IUGR group exposed to hypoxia. Consistent with these changes in pulmonary vascular reactivity, 2 wk of hypoxia induced weaker 4-AP-sensitive Kv currents in a single IUGR PASMC. Moreover, after 2 wk of hypoxia, Kv1.5 expression in resistance PAs decreased significantly in the IUGR group. Overexpression of Kv1.5 in cultured PASMCs could offset hypoxia-induced cell proliferation and hypoxia-inhibited Kv currents in the IUGR group. These results suggest that the inhibited expression of Kv1.5 in PASMCs contribute to the development of exaggerated CH-PHT in IUGR rats during adulthood.

Changes in pulmonary arterial pressure after atrial fibrillation ablation: incidence, causes, and implications on the stiff left atrial syndrome

Purpose: The left atrial (LA) syndrome is defined as pulmonary hypertension (PH) secondary to reduced LA compliance. While decreased LA compliance is one possible cause of PH after atrial fibrillation (AF) ablation, our study examines the incidence of an increase in pulmonary arterial (PA) pressure post-ablation and the potential underlying mechanisms. Methods: Patients who underwent AF ablation between 1999 and 2011 were included if they had both an echocardiogram within 6 months prior to the procedure and between 1 week and 6 months after the procedure. Patients were then separated into two groups with the increased PA pressure group defined as patients with > 10 mmHg increase in right ventricular systolic pressure (RVSP) post-ablation and a post-ablation RVSP > 35 mmHg. Categorical parameters were compared using a Chi-square test for independence. Continuous parameters were compared with a Wilcoxon rank-sum test. Results: Of the 499 patients meeting study criteria, 41 (8.2%) had an increase in RVSP > 10 mmHg and RVSP > 35 mmHg post-ablation. The group which developed an increase in PA pressure had an older age, higher BMI, larger LA volume, and greater prevalence of coronary artery disease and valvular disease. On echo, the two groups had similar E/A and E/e' ratios pre-ablation. However, post-ablation the increased PA pressure group had higher E/A (2.12 versus 1.49, P=0.002) and E/e' ratios (14.7 vs. 11.2, P=0.006). LA expansion index values were lower in the increased PA pressure group pre-ablation (51% vs. 92%, P<0.0001), but not significantly different post-ablation (82% vs. 88%, P=0.44). Conclusions: Around 8% of patients develop an increase in estimated PA pressure after AF ablation. However, a stiff left atrium does not appear to be the most common mechanism, as evidenced by LA expansion index values. Echocardiographic parameters suggest that patients who develop increased PA pressure are developing (or unmasking) left ventricular diastolic dysfunction. These data do not rule out the LA syndrome as a cause of an increase in PA pressure in some patients, but suggest that LV diastolic dysfunction is a prominent cause of an increase in PA pressure after AF ablation.

Frequency and Clinical Implications of Increased Pulmonary Artery Pressures in Liver Transplant Patients

To characterize the pulmonary hemodynamics and identify predictors of pulmonary hypertension in a group of patients before liver transplantation and to determine whether pulmonary hypertension in these patients is related to survival. In 362 patients before their first liver transplantation (between 1985 and 1993), the clinical history, laboratory data, and results of pulmonary function tests were recorded. Pulmonary artery (PA) catheterization was performed after induction of anesthesia at the time of transplantation. Monthly follow-up was maintained. A hyperdynamic circulation was often present -- an increased mean cardiac output (7.6 L/min), increased mean PA pressure (20.9 mm Hg), correlation of mean PA pressure with cardiac output (r = 0.25; P<0.001), and decreased mean pulmonary vascular resistance (60 dynes times s/cm5). Mean PA pressures were more than 25 mm Hg in 72 patients (20%). Pulmonary hypertension (defined as mean PA pressure of more than 25 mm Hg and pulmonary vascular resistance in excess of 120 dynes times s/cm5) occurred in 15 patients (4%). Pulmonary function tests revealed obstruction in 7%, restriction in 18%, and low diffusing capacity in 46%. By univariate analysis, lower forced expiratory volume in 1 second, forced vital capacity, and total lung capacity were the only preoperative factors associated with pulmonary hypertension (P<0.05). Survival was significantly lower in patients with acute fulminant hepatitis (P<0.001), the group with the highest mean PA pressure, than in those with other diagnoses. Increased PA pressures or mild to moderate pulmonary hypertension was not found to be associated with a worse survival by univariate or multivariate analysis. Increased PA pressure is common in liver transplant patients (20%). "True" pulmonary hypertension occurred in only 4% of our patients and was not associated with an adverse outcome.

A new noninvasive method for estimation of pulmonary arterial pressure in mitral stenosis

The appearance of an increased pulmonary artery (PA) pressure is an important moment in the clinical history of mitral stenosis. A direct measurement of PA pressure levels is possible only with rightsided cardiac catheterization. This technique, being invasive is not risk-free and, consequently, many noninvasive methods for the evaluation of PA pressure have been proposed. 1 These procedures usually lack sensitivity and are limited in their ability to detect and quantify mild to moderate modifications of PA pressure. The introduction of Doppler echocardiography allowed the development of new procedures. 2–6 Unfortunately this method is not applicable in the absence of Doppler-detectable tricuspid regurgitation. 7 Furthermore, the computed systolic PA pressure value is approximate because a clinical estimation of the right atrial pressure is necessary. Moreover, a good acoustic window and satisfactory flow tracings are indispensable. To avoid the aforementioned drawbacks we attempted a different approach to the noninvasive estimation of PA pressure, devising a method based on the modifications induced by an increased PA pressure on the power spectrum of the pulmonary component of the second heart sound. We used fast-Fourier analysis to examine the acoustic characteristics of this heart sound and to define its frequency distribution in patients with normal and increased PA pressure to search for a relation between the PA pressure level and the spectral characteristics of the pulmonary component of the second heart sound.

Alterations in elastin and collagen related to the mechanism of progressive pulmonary venous obstruction in a piglet model. A hemodynamic, ultrastructural, and biochemical study.

We created an animal model to understand better the pathogenesis and underlying mechanism of progressive central pulmonary venous (PV) obstruction, a condition not amenable to current therapy. Twenty piglets underwent banding of their PVs, 18 had a sham operation, and 12 were nonoperated controls. After 1, 3, and 6 weeks hemodynamic data were obtained and correlated with ventricular weights, PV and pulmonary artery (PA) distensibilities (at 1 week), morphometric structural and ultrastructural analyses, and biochemical assessment of elastin determined gravimetrically (and by desmosine level at 1 week), collagen, and elastase activity. At 1 week, PV banding was associated with increased PV compliance (p less than 0.05). At 3 weeks, an increased PA pressure (Ppa) (p less than 0.05) was observed, unaccompanied by a rise in PV pressure (Pcw). In the PV, however, there was breakdown of the internal elastic lamina with apparent migration of smooth muscle cells from media to subendothelium. At 6 weeks, a rise in Pcw (p less than 0.01), a further rise in Ppa (p less than 0.01), and right ventricular hypertrophy (p less than 0.005) were observed. We also observed mild PV intimal thickening (p less than 0.01), complete degradation of elastic laminae (p less than 0.05), and an increase in collagen assessed morphometrically (p less than 0.01). The banding procedure resulted in an overall increase in PV elastin synthesis and in the proportion of elastin determined gravimetrically (p less than 0.05 for both) but not by desmosine level, suggesting the possibility of poor cross-linking of elastin, which might account for the early increased distensibility of the PV. However, our assay could not detect an increase in elastase activity associated with either the increased distensibility or the ultrastructural changes of elastin degradation. The increased Ppa was not associated with significant PA biochemical or structural changes. We speculate that in response to distal venous obstruction, early remodeling of the PVs increases distensibility, protecting the lung from venous congestion and blunting a rise in Pcw. PA hypertension precedes the rise in Pcw, likely because of reflex vasoconstriction. The subsequent modest rise in Pcw is already associated with extensive fibrosis of the PV, suggesting a reason for unsuccessful current therapy and a need for consideration of earlier assessment and intervention.

Do changes in fraction of inspired oxygen affect pulmonary artery acceleration time?

Pulmonary artery (PA) pressure is difficult, but important, to estimate by noninvasive methods. Accordingly, numerous noninvasive methods have been used. Perhaps the most accurate noninvasive method is determination of tricuspid regurgitation velocity gradient, which estimates instantaneous difference between right atrial and ventricular systolic pressure. In the absence of pulmonary stenosis and with addition of right atrial pressure, the result can be used to approximate PA pressure. 1 Reliable recording of tricuspid regurgitation in some individuals, however, has proven difficult. Accordingly, many centers have used the inverse relations between PA pressure and PA acceleration time to predict PA pressure. 2 PA acceleration time is derived from Doppler PA velocities. Although PA acceleration time has been used to estimate PA pressure, full characterization of the measurement has yet to be determined. PA acceleration time has been reported to vary over a small range in adults (75 to 170 ms) 2 and a smaller range in children (51 to 140 ms). 3 Ranges are not truly continuous because the Doppler waveform is obtained by intermittent Fourier analysis, a method that depends on a time history of the waveform, especially for low velocities such as those inscribed at the very beginning of systole. Finally, information is unavailable to suggest whether PA acceleration time is variable for a given individual as the result of small changes in PA pressure. Alveolar oxygen partial pressure alteration inversely affects PA pressure and vascular resistance. 4 Accordingly, increased fraction of inspired oxygen should decrease PA pressure and resistance and lengthen the PA acceleration time. Conversely, lowering inspiratory oxygen percentage below room air should increase PA pressure and resistance and shorten PA acceleration time. The hypothesis for this study is that PA acceleration time is variable for a given individual and that changes in fraction of inspired oxygen cause inverse changes in PA acceleration time.

The mechanism of nitrous oxide-induced changes in pulmonary vascular resistance in a dog model of left atrial outflow obstruction

Nitrous oxide has been reported to increase pulmonary vascular resistance (PVR) in patients with pulmonary hypertension secondary to mitral stenosis. Additional data suggest this response involves sympathetic stimulation because the increase in PVR can be prevented by a-adrenergic and ganglionic blockade. Whether or not active pulmonary vasoconstriction occurs remains unclear. This study was designed to more fully characterize the influence of N 2O on pulmonary hemodynamics during left atrial outflow obstruction (LAO). Responses in an in situ blood-perfused lung lobe were compared with those in the remaining intact lung of six dogs anesthetized with pentobarbital, 30 mg/kg, and morphine, 1.5 mg/kg, and prepared for measurement of peak left ventricular (LV) pressure, LV end-diastolic pressure (LVEDP), LV dP/dt, systemic arterial and pulmonary arterial (PA) pressures, and cardiac output (CO). The pulmonary artery branch supplying the left middle lung lobe was cannulated and perfused at a constant rate with warmed blood. LAO was produced by filling the balloon of a Foley catheter positioned in the left atrium (LA) with enough saline to increase PA pressure by 50%; the balloon was subsequently left filled for the entire protocol. Measurements were first obtained during ventilation with 67% N 2, and 33% O 2. The inspired gas was then changed to 67% N 2O and 33% O 2 for 10 minutes, and then returned to the N 2/O 2 mixture. Once baselines had been reestablished (about 10 minutes), phentolamine, 0.75 mg/kg, was administered, and the response to 10 minutes of N 2O again observed. N 2O did not change vascular resistance in the isolated lobe, but increased intact-lung PVR. The pressure differential across the lung (mean PA pressure — LA pressure) was not altered by N 2O in either the isolated or intact lung. CO (pulmonary blood flow) was slightly but significantly reduced by N 2O while the perfusion flow rate remained constant. Concomitantly, systemic vascular resistance (SVR) and LVEDP both rose; the increase in LVEDP was not accompanied by an increase in LV dP/dt max Following phentolamine treatment, N 2O did not change hemodynamics in either the intact lung or isolated lobe, nor did it alter CO, SVR, or LVEDP; however, it did produce a fall in LV dP/dt max This study suggests that under conditions of experimental LAO, nitrous oxide increases PVR primarily by reducing pulmonary blood flow. The findings do not support an active pulmonary arteriolar vasoconstriction by N 2O.

Factors affecting use of the Doppler-determined time from flow onset to maximal pulmonary artery velocity for measurement of pulmonary artery pressure in children

Measurement of the time from onset to maximal or peak velocity (TPV) of pulmonary artery (PA) flow has been proposed as a noninvasive means of determining PA pressure. The effects of age, heart rate, increased PA pressure and flow, pulmonary valve obstruction and altered PA vascular resistance on this measurement were evaluated. In 84 children, aged 1 day to 18 years, TPV was measured using continuous-wave Doppler echocardiography. The children were separated into 3 groups. Group I (n = 33) consisted of children with no cardiovascular abnormalities. Group II (n = 33) consisted of children with a variety of cardiovascular diseases producing varying PA pressures and flows. Group III (n = 18) consisted of children who had valvular pulmonic stenosis with PA to right ventricular gradients greater than 40 mm Hg. Doppler studies of group II and III patients were performed in conjunction with measurement of PA pressures and flows at the time of cardiac catheterization. In group I TPV showed a significant negative linear correlation with heart rate (r = −0.86, p < 0.001). The ratio of observed TPV to predicted TPV (TPVN) determined using the regression equation for TPV vs heart rate or TPV/TPVN was heart rate- and age-independent (p > 0.1) and ranged from 0.81 to 1.31 (mean 1.005). In group II TPV/TPVN was inversely related to the natural log of the PA pressures (systolic, r = −0.91; mean, r = −0.87; diastolic, r = −0.82; all p < 0.01), whether pressure elevation was due to increased flow, resistance or left atrial hypertension. It was not affected by increased flow in the absence of pressure elevation. In group III TPV/TPVN was prolonged beyond that expected for the PA pressures and beyond the group I range, but did not correlate with transvalvular pressure gradient. Changes in TPV/TPVN reflect changing PA input characteristics due to either decreasing vascular capacitance from pressure elevation or increased resistance from valvular obstruction.

Cardiac catheters for diagnosis and treatment of venous air embolism: a prospective study in man.

One hundred consecutive patients undergoing neurosurgical procedures in the seated position were monitored for venous air embolism with a Swan-Ganz pulmonary artery (PA) catheter, precordial Doppler ultrasound device, and continuous end-tidal CO2 (FETCO2) analysis. Simultaneous determinations of right atrial and pulmonary capillary wedge pressures were also performed during each operation. Although 80 episodes of air embolism were detected by changes in Doppler sounds, only 36 were associated with increased PA pressure, and only 30 developed a decrease in FETCO2. Changes in PA pressure and FETCO2 agreed closely (r = 0.86), and only marked changes were associated with systemic hypotension. Air was recovered from the right atrium and PA only in small amounts (2 to 20 ml) during air embolism, although it was possible to aspirate large quantities of blood. Twenty-nine patients were found to have right atrial pressures that were higher than pulmonary capillary wedge pressures. Paradoxical air embolism from a probe-patent foramen ovale was possible in these patients, and one developed signs and symptoms of systemic air embolism postoperatively. We conclude that noninvasive monitoring with the combination of a precordial Doppler device and end-tidal CO2 analysis is satisfactory for rapid detection of clinically significant venous air embolism. The unique advantage of Swan-Ganz monitoring, however, is that it permits identification of patients who may sustain paradoxical air embolism, and that it differentiates the hemodynamic effects of brain-stem manipulation from those caused by air embolism.

Atrial septal defect of secundum type in the middle-aged: Clinical results of surgery and correlations between symptoms and hemodynamics

Summary This study comprised 98 of 100 patients above 40 years of age who underwent surgery in Norway for atrial septal defect of secundum type (ASD II) up to 1972. A follow-up study was performed on average 74 months (range 22 to 174) after surgery. Pulmonary hypertension was found in 30 per cent. The pulmonary arteriolar resistance (PAR) was increased in only one patient. Increasing degrees of arrhythmias, Dyspnea, edema, and functional class (NYHA) before surgery were significantly correlated to increasing pressures in the right atrium, right ventricle, pulmonary artery (PA), left atrium (pulmonary capillary venous pressure), and to increasing PAR. No significant correlations between the shunt ratio and different degrees of the symptoms were found. The hospital mortality rate was 3 per cent, and was not related to high age or increased PA pressure. There were no deaths among the last 65 patients. Before surgery, 13 per cent of the patients were in functional Class I, and 22.6 per cent in Class II or IV. The corresponding figures after surgery were 58.1 per cent and 0 per cent. The frequency of arrhythmias was high, and this was the symptom which showed the least improvement. Cerebral embolism occurred in six patients who also had arrhythmias, and five of the embolisms occurred after surgery. All patients with ASD II complicated with arrhythmias should be given anticoagulant therapy, whether they are operated on or not. In middle-aged patients disabled by ASD II, a marked improvement after surgery can be expected.

Influence of vessel distension and myogenic tone on pulmonary arterial input impedance. A study using a computer model of rabbit lung.

A computer model of the pulmonary arterial (PA) bed of rabbit lungs was designed in order to test experimental observations of changes in PA input impedance and pulsatile hydraulic power (cap.) during increased PA pressure. The computer model was based on a simple 3-component analog representation of single vessels (i.e. resistance, inertance and compliance). 16 generations of arterial vessels, from PA to 60 mum diameter, were combined to calculate PA input impedance. Input impedance was found to mimic closely that observed experimentally. Both venous pressure elevation and arteriolar constriction was found to reduce input impedance and Wp. By combining arteriolar constriction with increased myogenic tone of the larger arteries, Wp was found to show a minimum level at a certain PA pressure, dependent on the degree of arterial stiffening. Wp was found to follow changes in arterial volume and resistance during stimulated vasoconstriction. Wp dissipation in arterial vessels was calculated to approx. 50% of total imput Wp at physiological pressure conditions, and could be reduced by one half after PA pressure increase from 20 to 50 cm H2O, despite a concurrent halving of arterial compliance. Arterial vessels smaller than 200 mum diameter were found to have negligible direct influence on PA input impedance.

Prostaglandin F and E levels during endotoxin-induced pulmonary hypertension in calves.

Prostaglandin F and E (PGF and PGE) concentrations in sequential blood samples obtained simultaneously from the pulmonary artery (PA) and pulmonary vein (PV) during endotoxin-induced pulmonary hypertension in calves were determined by radioimmunoassay. Three groups of calves were studied. In nine control calves in which no endotoxin was given PA pressure and PGF and PGE concentrations in four pairs of samples taken at 0, 5, 15, and 45 min did not change. In 17 calves given 1 mg E. coli endotoxin, PGF concentrations were increased significantly in the PV and to a lesser degree in the PA in the 15-and 45-min samples. The increased PGF concentration in the 15-min sample corresponded to an increased PA pressure of 74 plus or minus 4 mmHg (mean plus or minus SE). In three of the endotoxin-treated calves studied a second time and three separate calves indomethacin pretreatment completely blocked the hemodynamic effect of endotoxin as well as PGF release. PGE concentrations did not change in either group. These data suggest that endotoxin-induced pulmonary hypertension may be mediated by PGF, a known pulmonary pressor agent in the bovine, and that blockade of this effect by indomethacin may be due to inhibition of prostaglandin synthesis and/or release.