scholarly journals Enhanced Pulmonary Vasodilator Reserve and Abnormal Right Ventricular

2015 ◽  
Vol 8 (3) ◽  
pp. 542-550 ◽  
Author(s):  
Mads J. Andersen ◽  
Seok-Jae Hwang ◽  
Garvan C. Kane ◽  
Vojtech Melenovsky ◽  
Thomas P. Olson ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pulmonary Vasodilator ◽  
Vasodilator Reserve

Prostaglandins and fetal cardiac output distribution in the lamb

1985 ◽  
Vol 248 (6) ◽  
pp. H853-H858
Author(s):  
E. B. Sideris ◽  
K. Yokochi ◽  
F. Coceani ◽  
P. M. Olley
Keyword(s):  
Cardiac Output ◽  
Right Ventricular ◽  
Main Pulmonary Artery ◽  
Left Ventricular ◽  
Base Line ◽  
Pulmonary Flow ◽  
Pulmonary Vasodilator ◽  
Distribution Right ◽  
Output Ratio ◽  
Left Ventricular Output

With the use of a triple thermodilution technique in 17 fetal lambs, combined with microsphere estimations in 7, the effects of indomethacin prostaglandin (PG) I2 and PGE2 on cardiac output and its distribution were measured. Indomethacin (0.2 mg/kg) induced a main pulmonary artery-to-aorta pressure gradient, which peaked within 45–60 min and persisted for 2–3 h. PGE2 abolished this gradient (threshold 50 ng X kg-1 X min-1), while PGI2 in doses up to 100 ng X kg-1 X min-1 increased it. Indomethacin did not change total cardiac output but altered its distribution (right ventricular output, left ventricular output) and increased the percentage of right ventricular output flowing to the lungs. Ductal flow decreased concomitantly. After indomethacin, PGI2 further decreased ductal flow, increased pulmonary flow, and decreased pulmonary vascular resistance. PGE2 restored the original right ventricular-to-total cardiac output ratio, although ductus flow did not return to base-line levels. Pulmonary resistance increased slightly, reflecting decreased pulmonary flow, associated with decreased right ventricular output. Thus PGE2 was more effective on the ductus than on the pulmonary circulation. PGI2 did not relax the ductus but was a potent pulmonary vasodilator. Neither PGI2 nor PGE2 nor indomethacin changed total cardiac output but all altered its distribution.

Abstract 15452: Low Dp/dt Max , When Indexed to Central Venous Pressure, is Associated With Severe Right Ventricular Failure Following Left Ventricular Assist Device Implantation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Leila Y Beach ◽  
William Hiesinger ◽  
Matthew T Wheeler
Keyword(s):  
Right Ventricular ◽  
Continuous Flow ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Right Ventricular Failure ◽  
Heart Catheterization ◽  
Ventricular Contractility ◽  
Ventricular Failure ◽  
Mean Values ◽  
Pulmonary Vasodilator

Introduction: Right ventricular failure (RVF) is a common complication following LVAD implantation and a significant driver of post-LVAD mortality. dP/dt max , the maximum rate of rise in ventricular pressure, is a validated hemodynamic parameter of ventricular contractility that, when indexed to CVP, accounts for loading conditions. This parameter has not, however, been studied in the context of post-LVAD RVF. We therefore evaluated the relationship between dP/dt max /CVP and post-LVAD RVF in a cohort of LVAD recipients at Stanford. Methods: We conducted a retrospective, single-center analysis of patients who underwent continuous-flow LVAD implant at Stanford between January 2010 and June 2019. Preoperative RV dP/dt max /CVP values were extracted from right heart catheterization (RHC) reports. For cases in which dP/dt max /CVP was not reported, preoperative RA and RV pressure tracings were utilized to manually calculate the index. We then performed unpaired t-tests to evaluate for the presence of associations between dP/dt max /CVP and early post-LVAD RVF, defined as the prolonged (>7 days) requirement for inotropic or pulmonary vasodilator therapy or the need for RVAD support, and between dP/dt max /CVP and severe post-LVAD RVF, defined only by the requirement for RVAD support. Results: This cohort included 202 LVAD recipients who had available preoperative RHC data. Of these, 14.4% (n = 29) required an RVAD and 50.5% (n = 102) experienced early post-LVAD RVF. Mean values of dP/dt max /CVP amongst patients with and without early post-LVAD RV failure were 94.9 ± 128.5 s -1 and 105.6 ± 125.5 s -1 (p = 0.56), respectively, while mean values of dP/dt max /CVP amongst those who did and did not require an RVAD were 53.2± 42.0 s -1 and 108.2 ± 129.5 s -1 (p = 4.2 х 10 -5 ), respectively. Conclusion: In continuous-flow LVAD recipients, low preoperative RV dP/dt max /CVP is strongly associated with severe post-LVAD RVF requiring RVAD support but not early post-LVAD RVF more generally.

scholarly journals Increased incidence of Persistent Pulmonary Hypertension of the Newborn following third trimester maternal COVID-19 infection

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Ishqeir ◽  
A Nir ◽  
I Aptowitzer ◽  
M Godfrey ◽  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Persistent Pulmonary Hypertension ◽  
Third Trimester ◽  
Term Neonates ◽  
Live Births ◽  
Pulmonary Vasodilator ◽  
Near Term

Abstract Background Novel coronavirus (COVID-19) has been a world concern since December 2019. The knowledge about vertical transmission and fetal morbidity and mortality from maternal COVID-19 infection is limited. We detected an increase in the number of cases of term and near-term neonates with persistent pulmonary hypertension (PPHN) during the COVID-19 pandemic in 2020. Methods and results We collected data on all newborns with PPHN born between 2018 and 2020. We excluded premature infants (<34+0 weeks) and infants with other significant pathology or genetic syndromes. Compared to 5 cases of PPHN of 22930 live births in 2018, and 6 cases of PPHN of 22270 live births in 2019 (2-year average 0.02%, 95% CI 0.013%-0.043%), there were 16 PPHN cases from 22323 live births in 2020 (0.07%, 95% CI 0.044%-0.12%), a 3 fold increase (p<0.01). We report 5 cases of term and near-term neonates born to mothers who had highly suspected (2) and PCR proven (3) COVID-19 infection during the third trimester of pregnancy, who presented with PPHN during COVID-19 pandemic in 2020. All had otherwise unexplained pulmonary hypertension, right ventricular hypertrophy (RVH) and dilatation. Two patients needed endotracheal intubation, one was supported by nasal continuous positive airway pressure (CPAP) without intubation, two needed O2 support by nasal cannula only ant two newborns (one of them was intubated) needed Nitric oxide (NO) as pulmonary vasodilator therapy. No patient required Extracorporeal membrane oxygenation (ECMO) or died, and no prolonged residual cardiovascular or pulmonary morbidity was recorded during a median follow up of 4.8 months (range 4–6 months). Conclusions The increase in the incidence of PPHN during the COVID-19 pandemic, and the cases presented, suggest an intrauterine effect of maternal COVID-19 infection on the fetal pulmonary circulation. It is possible that the maternal infection affected the fetal pulmonary vascular resistance, or altered the normal decline in the resistance after birth. The right ventricular hypertrophy and dilatation with reduced function may be secondary to this hypothetical increased afterload or a direct effect of the infection. Further studies are warranted to elucidate the pathogenesis and clinical implications of this phenomenon. FUNDunding Acknowledgement Type of funding sources: None.

Inhaled nitric oxide has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute pulmonary embolism

2020 ◽  
pp. 204887262091871 ◽  
Author(s):  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jacob Gammelgaard Schultz ◽  
Mads Dam Lyhne ◽  
Asger Andersen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Embolism ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Porcine Model ◽  
Inhaled Nitric Oxide ◽  
Intermediate Risk ◽  
Ventricular Afterload ◽  
Pulmonary Vasodilator ◽  
Acute Pe

Background Inhaled nitric oxide (iNO) effectively reduces right ventricular afterload when administered in the immediate phase of acute pulmonary embolism (PE) in preclinical animal models. In a porcine model of intermediate-risk PE, we aimed to investigate whether iNO has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute PE. Methods Anesthetized pigs ( n = 18) were randomized into three subgroups. An acute PE iNO-group ( n = 6) received iNO at 40 ppm at one, three, six, nine and 12 hours after onset of PE. Vehicle animals ( n = 6) received PE, but no active treatment. A third group of sham animals ( n = 6) received neither PE nor treatment. Animals were evaluated using intravascular pressures, respiratory parameters, biochemistry and intracardiac pressure-volume measurements. Results The administration of PE increased mean pulmonary artery pressure (mPAP) (vehicle vs sham; 33.3 vs 17.7 mmHg, p < 0.0001), pulmonary vascular resistance (vehicle vs sham; 847.5 vs 82.0 dynes, p < 0.0001) and right ventricular arterial elastance (vehicle vs sham; 1.2 vs 0.2 mmHg/ml, p < 0.0001). Significant mPAP reduction by iNO was preserved at 12 hours after the onset of acute PE (vehicle vs iNO; 0.5 vs –3.5 mmHg, p < 0.0001). However, this response was attenuated over time ( p = 0.0313). iNO did not affect the systemic circulation. Conclusions iNO is a safe and effective pulmonary vasodilator both in the immediate and prolonged phase of acute PE in an in-vivo porcine model of intermediate-risk PE.

scholarly journals Practice patterns of pulmonary hypertension secondary to left heart disease among pediatric pulmonary hypertension providers

2021 ◽  
Vol 11 (1) ◽  
pp. 204589402199144
Author(s):  
Hythem Nawaytou ◽  
Jeffrey R. Fineman ◽  
Shahin Moledina ◽  
Dunbar Ivy ◽  
Steven H. Abman ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
North America ◽  
Right Ventricular ◽  
Ventricular Dysfunction ◽  
Practice Patterns ◽  
Right Ventricular Dysfunction ◽  
Pulmonary Vasodilators ◽  
Pulmonary Vasodilator ◽  
International Pediatric

Development of pulmonary hypertension (PH) in patients with left side heart disease (LHD) is a predictor of poor prognosis. The use of pulmonary vasodilators in PH associated with LHD (PH-LHD) is controversial. In this study, we describe the practice patterns regarding the use of pulmonary vasodilators in PH-LHD among a group of international pediatric PH specialists. A survey was distributed to the members of three pediatric PH networks: PPHNet, PVRI, and REHIPED. The survey queried participants on the rationale, indications, and contraindications of the use of pulmonary vasodilators in children with PH-LHD. Forty-seven PH specialists from 39 PH centers completed the survey. Participants included PH specialists from North America (57%), South America (15%), and Europe (19%). The majority of participants (74%) recommended the use of pulmonary vasodilators only in patients with combined pre-capillary and post-capillary pulmonary hypertension. Participants required the presence of clinical symptoms or signs of heart failure (68%) or right ventricular dysfunction by echocardiography (51%) in order to recommend pulmonary vasodilator therapy. There was no agreement regarding hemodynamic criteria used to recommend pulmonary vasodilators or the etiologies of LHD considered contraindications for using pulmonary vasodilators to manage PH-LHD. Of the available PH-targeted drugs, most participants preferred the use of phosphodiesterase-5-inhibitors for this indication. In conclusion, the practice of recommending pulmonary vasodilators in PH-LHD is highly variable among international pediatric PH specialists. Most specialists of those surveyed (57% in North America) would consider the use of pulmonary vasodilators in PH-LHD only if pre-capillary pulmonary hypertension and right ventricular dysfunction are present.

Coronary Vasodilator Reserve in Young Dogs with Moderate Right Ventricular Hypertrophy

1984 ◽  
Vol 38 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Mark J. Botham ◽  
John H. Lemmer ◽  
Richard A. Gerren ◽  
Richard W. Long ◽  
Douglas M. Behrendt ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Coronary Vasodilator ◽  
Vasodilator Reserve ◽  
Coronary Vasodilator Reserve

Combination of PGE1 and Pulmonary Vasodilator Therapy in Managing a Challenging Case of Severe PAH Secondary to CDH

2020 ◽  
Vol 11 (4) ◽  
pp. 525-527
Author(s):  
Othman A. Aljohani ◽  
Rohit Rao ◽  
Duncan Mackie ◽  
Shylah Haldeman ◽  
Tara Karamlou
Keyword(s):  
Right Ventricular ◽  
Congenital Diaphragmatic Hernia ◽  
Diaphragmatic Hernia ◽  
Right Ventricular Dysfunction ◽  
Vasodilator Therapy ◽  
Venoarterial Extracorporeal Membrane Oxygenation ◽  
Pulmonary Vasodilator ◽  
Pulmonary Parenchyma ◽  
Pulmonary Arterial ◽  
Severe Pulmonary Arterial Hypertension

Congenital diaphragmatic hernia (CDH) is a rare disease, which affects 1 in 2,500 newborns. Congenital diaphragmatic hernia can interfere with the normal development of the pulmonary parenchyma and vascular bed, and in severe cases, it can lead to the development of severe pulmonary arterial hypertension (PAH) and right ventricular failure. We present a neonate with CDH who developed severe PAH and right ventricular dysfunction and was managed with a unique strategy combining venoarterial extracorporeal membrane oxygenation, prostaglandin E1, and a variety of PAH therapies.

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