Impact of pericardial restraint on right atrial mechanics during acute right ventricular pressure load

2003 ◽  
Vol 284 (1) ◽  
pp. H350-H357 ◽  
Author(s):  
Hersh S. Maniar ◽  
Sunil M. Prasad ◽  
Sydney L. Gaynor ◽  
Celeste M. Chu ◽  
Paul Steendijk ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Right Atrium ◽  
Right Atrial ◽  
Compensatory Response ◽  
Before And After ◽  
The Right ◽  
The Impact

Optimization of right atrial (RA) mechanics is important for maintaining right ventricular (RV) filling and global cardiac output. However, the impact of pericardial restraint on RA function and the compensatory role of the right atrium to changes in RV afterload remain poorly characterized. In eight open-chest sheep, RA elastance (contractility) and chamber stiffness were measured (RA pressure-volume relations) at baseline and during partial pulmonary artery (PA) occlusion. Data were collected before and after pericardiotomy. With the pericardium intact and partial PA occlusion, RA elastance increased by 28% ( P < 0.04), whereas RA stiffness tended to rise ( P = 0.08). However, after pericardiotomy, there was a significant fall in both RA elastance (54%, P < 0.04) and stiffness (39%, P < 0.04), and subsequent PA occlusion failed to induce a change in elastance ( P > 0.19) or stiffness ( P > 0.84). After pericardiotomy, RA elastance and stiffness fell dramatically, and the compensatory response of the right atrium to elevated RV afterload was lost. The ability of the right atrium to respond to changes in RV hemodynamics is highly dependent on pericardial integrity.

Reservoir and conduit function of right atrium: impact on right ventricular filling and cardiac output

2005 ◽  
Vol 288 (5) ◽  
pp. H2140-H2145 ◽  
Author(s):  
Sydney L. Gaynor ◽  
Hersh S. Maniar ◽  
Sunil M. Prasad ◽  
Paul Steendijk ◽  
Marc R. Moon
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Right Atrium ◽  
Artery Occlusion ◽  
Right Atrial ◽  
Reservoir Function ◽  
The Right ◽  
Conduit Function ◽  
Inotropic Stimulation

The purpose of this study was to investigate the relationship between right atrial (RA) reservoir and conduit function and to determine how hemodynamic changes influence this relationship and its impact on cardiac output. In 11 open-chest sheep, RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. Conduit function was separated into early (before A wave) and late (after A wave) components. The effects of inotropic stimulation, partial pulmonary artery occlusion, and pericardiotomy were tested. At baseline with the pericardium intact, reservoir function accounted for 0.56 (SD 0.13) of RA inflow, early conduit for 0.29 (SD 0.07), and late conduit (during RA contraction) for 0.16 (SD 0.11). Inotropic stimulation decreased conduit function and increased reservoir function, but these effects did not reach statistical significance. With partial pulmonary artery occlusion, early conduit function fell to 0.20 (SD 0.11) ( P < 0.04), and the conduit-to-reservoir ratio decreased by 41% ( P < 0.03). Similarly, after pericardiotomy, early conduit function fell to 0.14 (SD 0.09) ( P < 0.004), reservoir function increased to 0.72 (SD 0.08) ( P < 0.04), and, consequently, the early conduit-to-reservoir ratio decreased by 63% ( P < 0.006). Cardiac output was inversely related to the conduit-to-reservoir ratio ( r = 0.39, P < 0.001). This study demonstrated that the right atrium adjusts its ability to act more as a reservoir than a conduit in a dynamic manner. The RA conduit-to-reservoir ratio was directly related to the right ventricular pressure-RA pressure gradient at the time of maximum RA volume, with increased ventricular pressures favoring conduit function, but it was inversely related to cardiac output, with an increase in the reservoir contribution favoring improved cardiac output.

scholarly journals Right Atrial and Ventricular Adaptation to Chronic Right Ventricular Pressure Overload

Circulation ◽  
2005 ◽  
Vol 112 (9_supplement) ◽  
Author(s):  
Sydney L. Gaynor ◽  
Hersh S. Maniar ◽  
Jeffrey B. Bloch ◽  
Paul Steendijk ◽  
Marc R. Moon
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Right Atrium ◽  
Systolic Function ◽  
Pressure Overload ◽  
Right Atrial ◽  
Chronic Pulmonary Hypertension ◽  
The Right ◽  
Conduit Function

Background— Increased mortality in patients with chronic pulmonary hypertension has been associated with elevated right atrial (RA) pressure. However, little is known about the effects of chronic right ventricular (RV) pressure overload on RA and RV dynamics or the adaptive response of the right atrium to maintain RV filling. Methods and Results— In 7 dogs, RA and RV pressure and volume (conductance catheter) were recorded at baseline and after 3 months of progressive pulmonary artery banding. RA and RV elastance (contractility) and diastolic stiffness were calculated, and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. With chronic pulmonary artery banding, systolic RV pressure increased from 34±7 to 70±17 mm Hg ( P <0.001), but cardiac output did not change ( P >0.78). RV elastance and stiffness both increased ( P <0.05), suggesting preserved systolic function but impaired diastolic function. In response, RA contractility improved (elastance increased from 0.28±0.12 to 0.44±0.13 mm Hg/mL; P <0.04), and the atrium became more distensible, as evidenced by increased reservoir function (49±14% versus 72±8%) and decreased conduit function (51±14% versus 28±8%; P <0.002). Conclusions— With chronic RV pressure overload, RV systolic function was preserved, but diastolic function was impaired. To compensate, RA contractility increased, and the atrium became more distensible to maintain filling of the stiffened ventricle. This compensatory response of the right atrium likely plays an important role in preventing clinical failure in chronic pulmonary hypertension.

scholarly journals P686 Right atrial, right ventricular and pulmonary cement embolism: a rare complication of percutaneous vertebroplasty

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Akhunova ◽  
R Khayrullin ◽  
N Stekolshchikova ◽  
M Samigullin ◽  
V Padiryakov
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Atrium ◽  
Percutaneous Vertebroplasty ◽  
Rare Complication ◽  
Clinical Manifestations ◽  
Stable Condition ◽  
Right Atrial ◽  
Cement Embolism ◽  
The Right

Abstract A 68-year-old man was admitted to the hospital with complaints of pain in the lumbar spine. He had L5 disc herniation, Spinal stenosis of the L5 root canal - S1 on the right in the past medical history. Percutaneous vertebroplasty at the level of L3 and Th8 vertebral bodies was performed six months ago due to painful vertebral hemangioma. The man is suffering from arterial hypertension, receives antihypertensive therapy. During routine transthoracic echocardiography, a hyperechoic structure with a size of 9.5 x 0.9 cm was found in the right atrium and right ventricle. Chest computed tomography with contrast enhancement revealed signs of bone cement in the right atrium and right ventricle, in the right upper lobe artery, in the branches of the upper lobe artery, in the paravertebral venous plexuses. Considering the duration of the disease, the stable condition, the absence of clinical manifestations and disorders of intracardiac hemodynamics, it was decided to refrain from surgical treatment. Antiplatelet therapy and dynamic observation were recommended. Conclusion Percutaneous vertebroplasty is a modern minimally invasive surgical procedure for the treatment of degenerative-dystrophic diseases of the spine. However, the cement can penetrate into the paravertebral veins and migrate to the right chambers of the heart and the pulmonary artery. This clinical case demonstrates asymptomatic cement embolism of the right chambers of the heart and pulmonary artery after percutaneous vertebroplasty, detected incidentally during routine echocardiography. Abstract P686 Figure.

Abstract 15388: Persistent Pulmonary Hypertension After Transcatheter Aortic Valve Implantation: Impact on Mortality

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Maria Drakopoulou ◽  
Konstantinos Stathogiannis ◽  
Konstantinos Toutouzas ◽  
George Latsios ◽  
Andreas Synetos ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Aortic Stenosis ◽  
Pulmonary Artery ◽  
Severe Aortic Stenosis ◽  
Systolic Pressure ◽  
Right Atrial ◽  
Pulmonary Artery Systolic Pressure ◽  
End Point ◽  
The Right ◽  
The Impact

Objective: Severe aortic stenosis leads to increased pulmonary arterial systolic pressure. A controversy still remains regarding the impact of persistent pulmonary hypertension (PHT) on prognosis of patients undergoing transcatheter aortic valve implantation (TAVI). We sought to investigate the impact of persistent PHT on 2-year all-cause mortality of patients with severe aortic stenosis following TAVI. Methods: Patients with severe and symptomatic aortic stenosis (effective orifice area [EOA]≤1 cm 2 ) who were scheduled for TAVI with a self-expanding valve at our institution were prospectively enrolled. Prospectively collected echocardiographic data before and after TAVI were retrospectively analyzed in all patients. Pulmonary artery systolic pressure was estimated as the sum of the right ventricular to the right atrial gradient during systole and the right atrial pressure. PHT following TAVI was classified as absent if <35 mmHg and persistent if ≥35 mmHg. Primary clinical end-point was 2-year all-cause mortality defined according to the criteria proposed by the Valve Academic Research Consortium-2. Results: Hundred and forty patients (mean age: 82±9 years) were included in the study. The primary clinical end point occurred in 17 patients (12%) during a median follow-up period of 2 years. Mean pulmonary artery systolic pressure was reduced in all patients following TAVI (45±9 versus 41±6 mmHg, p<0.01). Mortality rate was higher in patients with persistent PHT compared to patients with normal pulmonary artery systolic pressure following TAVI (26% versus 14 %, p<0.01). Patients that reached the primary clinical end point had a higher post procedural mean systolic pulmonary pressure (43±9 versus 39±6 mmHg, p=0.02). In multivariate regression analysis, persistence of PHT (OR: 2.51, 95% CI: 1.109-7.224, p=0.01) was an independent predictor of long-term mortality. Conclusions: The persistence of pulmonary hypertension after TAVI is associated with long term mortality. Identifying the population that will clearly benefit from TAVI is still need to be validated by larger trials.

Right atrium mediates a vasomotor reflex

1981 ◽  
Vol 241 (3) ◽  
pp. R163-R166
Author(s):  
R. F. Munzner ◽  
D. G. Ward ◽  
D. S. Gann
Keyword(s):  
Right Atrium ◽  
Carotid Arteries ◽  
Right Atrial ◽  
Vagus Nerves ◽  
Vascular Responses ◽  
The Right ◽  
Vasomotor Reflex ◽  
Atrial Receptors ◽  
Volume Pulsation

To examine the role of right atrial receptors in mediating reflex vascular responses we measured, in cats anesthetized with chloralose/urethan, changes in mean arterial pressure (MAP) in response to volume pulsation of the right atrium (+/- 1 ml, 1 Hz). Changes in MAP were measured 1) with pressure in the carotid arteries normal and vagus nerves intact: right atrial pulsation led to a very small and transient fall in MAP; 2) with pressure in the carotid arteries at 75 mmHg and the vagus nerves intact: right atrial pulsation led to a larger and sustained fall in MAP; 3) with pressure in the carotid arteries at 75 mmHg and the vagus nerves cooled or sectioned bilaterally: right atrial pulsation of the right atrium led only to a very small and transient fall in MAP. These data suggest strongly that signals from right atrial receptors traveling in the vagus nerves mediate a reflex change in MAP that is normally masked by signals from carotid receptors.

Prognostic Factors for Late Ventricular Arrhythmias after Repair of Tetralogy of Fallot

1997 ◽  
Vol 5 (1) ◽  
pp. 20-24
Author(s):  
Fumikazu Nomura ◽  
Seiichiro Ikawa ◽  
Keishi Kadoba ◽  
Masataka Mitsuno ◽  
Yoshiki Sawa ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Tetralogy Of Fallot ◽  
Ventricular Arrhythmias ◽  
Right Atrial ◽  
Age At Surgery ◽  
Group A ◽  
Group B ◽  
The Right

During a median follow-up period of 9 years (ranging from 9 months to 25 years), 24-hour ambulatory electrocardiographic studies were undertaken in 155 patients after repair of tetralogy of Fallot. The patients were divided into two groups. Group A consisted of 76 patients in whom the right ventricular approach was used and group B comprised 79 patients whose repair was through the right atrium. A transannular patch was employed in all patients in group A and in none of the patients in group B. Age at surgery was between 1 and 37 years (median age 4.8 years). During follow-up, 37 patients (48.6%) in group A had significant ventricular arrhythmias (Lown grade 2 or higher) and 13 patients (15.4%) in group B had significant ventricular arrhythmias. A close relationship was observed between age at surgery and Lown grade (R2 = 0.374, p < 0.001) and between follow-up duration and Lown grade (R2 = 0.514, p < 0.001), especially when the two groups were analyzed separately (R2 = 0.502, 0.476, p < 0.001). In contrast, no significant relationship was observed between the ratio of right ventricular to left ventricular pressure and Lown grade or between right ventricular systolic pressure and Lown grade. Discriminant analysis revealed risk factors associated with postoperative ventricular arrhythmias are follow-up duration (partial F = 3.22, p < 0.01), right ventricular to pulmonary artery pressure gradient (partial F = 3.35, p < 0.01), and operative method (partial F = 2.4, p < 0.05). Despite antiarrhythmic therapy, 11 of 22 late postoperative deaths occurred suddenly, presumably from ventricular arrhythmias. In this series of patients, the right atrial and pulmonary artery approach significantly reduced the risk of life-threatening ventricular arrhythmias after repair of tetralogy of Fallot.

scholarly journals P1488 Anomalous origin of left coronary artery from right pulmonary artery in association with scimitar syndrome

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Aly ◽  
R Lizano Santamaria ◽  
S J Yoo
Keyword(s):  
Pulmonary Hypertension ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Scimitar Syndrome ◽  
Right Atrial ◽  
Anomalous Origin ◽  
Coronary Perfusion ◽  
Antegrade Flow ◽  
The Right

Abstract Clinical Presentation A full-term neonate was referred to our institution because of respiratory distress. CXR was significant for right lung hypoplasia and mild cardiomegaly. ECG showed normal sinus rhythm, right atrial enlargement, and right ventricular hypertrophy with no signs of ischemia. Imaging Findings The initial echocardiogram demonstrated PAPVD with the right upper pulmonary vein draining into IVC/RA junction with flow acceleration (mean gradient= 7 mmHg), moderate ASD, small muscular VSD with left-right shunting, moderate PDA with bidirectional shunting. Forward flow was seen in the proximal part of left main coronary artery (LMCA). RV systolic pressure was supra-systemic with a qualitatively moderately reduced RV systolic function. The patient was taken to the catheterization lab where MPA angiography revealed an antegrade flow from the RPA into LMCA supplying both the anterior descending and the circumflex arteries. A selective injection within the scimitar vein showed drainage of the right lung into a vertical vein connecting with stenosis to IVC. A follow up echocardiogram to re-examine the coronary origin revealed an anomalous origin of LMCA from proximal RPA; 3 mm distal to branch pulmonary artery bifurcation with mainly antegrade low velocity flow into LMCA and LAD. (Image 1) Role of Imaging in Patient Care - Imaging of the coronary origin in patients with ALCAPA can be challenging especially if the LMCA originates from RPA. Also, the presence of pulmonary hypertension might contribute to maintain coronary perfusion and lead to misinterpretation of the antegrade flow in LMCA and its branches. - In certain situations, cardiac catheterization is essential to make the diagnosis of ALCAPA which prevented a potentially catastrophic outcome. Catheter intervention with a series of balloon dilations of the stenotic scimitar vein was successful in relieving the stenosis. Summary/Discussion Points: - Extensive review of the available literature revealed only three cases of Scimitar syndrome associated with ALCAPA. In all of these cases, the LMCA originated from the posterior sinus of MPA. Our case is the first to report ALCAPA from RPA in association with Scimitar syndrome. This presentation might have led to the initial misinterpretation of the echocardiography images. - The presence of pulmonary hypertension in our patient maintained an adequate antegrade flow across the LMCA preventing significant coronary steal and signs of myocardial ischemia. - The report highlights the challenges in making the diagnosis of ALCAPA with echocardiograms. Moreover, we discuss the role of cross-sectional and invasive imaging to rule out potential coronary arteries anomalies in patients with Scimitar syndrome, as this a rare although a very significant association that may have important implications in their outcomes. Abstract P1488 Figure. ALCAPA origin from RPA

Afferent sympathetic nerve fibers with mechanoreceptors in the right heart

1975 ◽  
Vol 228 (1) ◽  
pp. 223-230 ◽  
Author(s):  
Y Uchida
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Sympathetic Nerve ◽  
Nerve Fibers ◽  
Right Atrial ◽  
Right Heart ◽  
Unmyelinated Fibers ◽  
Myelinated Fibers ◽  
Sympathetic Nerve Fibers ◽  
The Right

Mechanosensitivity of afferent sympathetic nerve fibers from the right heart and the pulmonary artery has been examined. Action potentials of the afferent fibers that responded to tapping the right heart and the pulmonary artery were derived from upper thoracic communicating rami of both sides of anesthetized dogs. The fibers were composed of myelinated Adelta fibers and unmyelinated fibers. The receptive fields of both groups of fibers were located widely in the right heart and the pulmonary artery. Myelinated fibers ceased to fire quickly whereas unmyelinated fibers continued to fire after withdrawl of a brief mechanical stimulus. In the myelinated group, the pressure threshold was 3-50, 6-58, and 3-10 mmHg for right ventricular, pulmonary and right atrial threshold was 15-58, 22-34, and 4-8 mmHg for right ventricular, pulmonary, and right atrial fibers, respectively. Spontaneous discharge of myelinated fibers was synchronous with each rise and/or fall in intracardiac or pulmonary pressure whereas that of unmyelinated fibers was irregular and independent. A rise in pressure produced by pulmonary embolization or occlusion caused an augumented discharge whereas a fall caused by caval vein occulsion eliminated the discharge. The results indicate the existence of both myelinated and unmyelinated fibers with mechanoreceptors in the right heart and the pulmonary artery.

Limitations of thermodilution cardiac output measurements in the rat

1984 ◽  
Vol 246 (6) ◽  
pp. H754-H760 ◽  
Author(s):  
B. E. Hayes ◽  
J. A. Will ◽  
W. C. Zarnstorff ◽  
G. E. Bisgard
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Heat Loss ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Vena Cava ◽  
Right Atrial ◽  
Thermodilution Cardiac Output ◽  
The Right

Heat loss from the vascular system could introduce an error in thermodilution cardiac output determinations. Cardiac output measured in the rat via the thermodilution technique following right atrial injection yielded different values (P less than 0.001), depending whether sampling was from the pulmonary artery (460 +/- 31 ml X min-1 X kg-1), right ventricle (311 +/- 19), or thoracic aorta (245 +/- 15). Recirculation errors could not account for the differences. Heat loss from the vascular system was measured from extravascular thermistors within both the thorax and the abdomen. These dilutions were 22-57% in peak height of aortic curves recorded at approximately the same location. Differences in calculated cardiac output between sampling sites could be attributed to rapid heat conduction directly from the right atrium and inferior vena cava to the thoracic aorta with progressive loss of indicator from both the right ventricle and pulmonary artery.

scholarly journals Mechanical support of the pressure overloaded right ventricle: an acute feasibility study comparing low and high flow support

2015 ◽  
Vol 309 (4) ◽  
pp. H615-H624 ◽  
Author(s):  
Tom Verbelen ◽  
Jelle Verhoeven ◽  
Motohiko Goda ◽  
Daniel Burkhoff ◽  
Marion Delcroix ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
High Flow ◽  
Low Flow ◽  
Mechanical Support ◽  
Arterial Blood ◽  
The Right

The objectives of this study were to assess the feasibility of low flow right ventricular support and to describe the hemodynamic effects of low versus high flow support in an animal model of acute right ventricular pressure overload. A Synergy Pocket Micro-pump (HeartWare International, Framingham, MA) was implanted in seven sheep. Blood was withdrawn from the right atrium to the pulmonary artery. Hemodynamics and pressure-volume loops were recorded in baseline conditions, after banding the pulmonary artery, and after ligating the right coronary artery in these banded sheep. End-organ perfusion (reflected by total cardiac output and arterial blood pressure) improved in all conditions. Intrinsic right ventricular contractility was not significantly impacted by support. Diastolic unloading of the pressure overloaded right ventricle (reflected by decreases in central venous pressure, end-diastolic pressure and volume, and ventricular capacitance) was successful, but with a concomitant and flow-dependent increase of the systolic afterload. This unloading diminished with right ventricular ischemia. Right ventricular mechanical support improves arterial blood pressure and cardiac output. It provides diastolic unloading of the right ventricle, but with a concomitant and right ventricular assist device flow-dependent increase of systolic afterload. These effects are most distinct in the pressure overloaded right ventricle without profound ischemic damage. We advocate the low flow strategy, which is potentially beneficial for the afterload sensitive right ventricle and has the advantage of avoiding excessive increases in pulmonary artery pressure when pulmonary hypertension exists. This might protect against the development of pulmonary edema and hemorrhage.

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