Sympathetic afferent nerve activity of right heart origin

1975 ◽  
Vol 229 (4) ◽  
pp. 911-915 ◽  
Author(s):  
DR Kostreva ◽  
EJ Zuperku ◽  
RV Purtock ◽  
RL Coon ◽  
JP Kampine

Six mongrel dogs anesthetized with sodium pentobarbital and paralyzed with gallamine triethiodide were studied on total cardiopulmonary bypass. This study verified the existence of right heart mechanoreceptors whose afferent nerves traverse the upper thoracic white rami communicantes. these mechanoreceptors were studied by observing changes in average maximum, and total nerve spike frequency when right atrial and right ventricular systolic and diastolic pressures were altered by means of intracardiac balloons. Receptors that responded to volume and pressure changes were found in both the right atrium and right ventricle. Nerve activity in these afferents increased with increasing right atrial and right ventricular pressures. These mechanoreceptors were more responsive in the upper physiological ranges of right heart pressures. In most nerve fibers studied, maximum activity occurred during both right atrial and right ventricular diastole.

1975 ◽  
Vol 228 (1) ◽  
pp. 223-230 ◽  
Author(s):  
Y Uchida

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.


2016 ◽  
Vol 17 (suppl 2) ◽  
pp. ii161-ii163
Author(s):  
R. Enache ◽  
N. Sawada ◽  
L. Molina Ferragut ◽  
P. Monney ◽  
A. Jobbe Duval ◽  
...  

2014 ◽  
Vol 45 (3) ◽  
pp. 680-690 ◽  
Author(s):  
Stefan Buchner ◽  
Michael Eglseer ◽  
Kurt Debl ◽  
Andrea Hetzenecker ◽  
Andreas Luchner ◽  
...  

Structural and functional integrity of the right heart is important in the prognosis after acute myocardial infarction (AMI). The objective of this study was to assess the impact of sleep disordered breathing (SDB) on structure and function of the right heart early after AMI.54 patients underwent cardiovascular magnetic resonance 3–5 days and 12 weeks after AMI, and were stratified according to the presence of SDB, defined as an apnoea–hypopnoea index of ≥15 events·h−1.12 weeks after AMI, end-diastolic volume of the right ventricle had increased significantly in patients with SDB (n=27)versusthose without (n=25) (mean±sd14±23%versus0±17%, p=0.020). Multivariable linear regression analysis accounting for age, sex, body mass index, smoking, left ventricular mass and left ventricular end-systolic volume showed that the apnoea–hypopnoea index was significantly associated with right ventricular end-diastolic volume (B-coefficient 0.315 (95% CI 0.013–0.617); p=0.041). From baseline to 12 weeks, right atrial diastolic area increased more in patients with SDB (2.9±3.7 cm2versus1.0±2.4 cm2, p=0.038; when adjusted for left ventricular end systolic volume, p=0.166).SDB diagnosed shortly after AMI predicts an increase of right ventricular end-diastolic volume and possibly right atrial area within the following 12 weeks. Thus, SDB may contribute to enlargement of the right heart after AMI.


Author(s):  
Alexander C. Egbe ◽  
William R. Miranda ◽  
C. Charles Jain ◽  
Heidi M. Connolly

Background: Chronic elevation of left heart filling pressure causes pulmonary vascular remodeling, pulmonary hypertension, and right heart dysfunction. Although diastolic dysfunction is relatively common in patients with coarctation of aorta, there are limited data about the prevalence and prognostic implications of pulmonary hypertension and right heart dysfunction in this population. The purpose of the study was to assess right heart function and hemodynamics in patients with coarctation of aorta and to determine the relationship between right heart indices and cardiovascular events defined as heart failure hospitalization, heart transplant, or cardiovascular death. Methods: Right heart structure, function, and hemodynamics were assessed with these indices: right atrial volume, right atrial pressure, right atrial reservoir strain, right ventricular global longitudinal strain, right ventricular end-diastolic area, right ventricular systolic pressure, and tricuspid regurgitation severity. Right heart hemodynamic score, range 0 to 5, was generated based on the correlation between the right heart indices and cardiovascular events, using half of the cohort (derivation cohort, n=411), and then tested on the validation cohort (n=410). The goodness of fit and discrimination power was compared using C statistics and risk score. Results: The median follow-up in the derivation cohort was 8.2 (4.0–11.1) years, and 59 (14%) patients had cardiovascular events during this period. Right heart hemodynamic score was independently associated with cardiovascular events (hazard ratio, 1.64 [95% CI, 1.38–2.17]) for every unit increase in right heart hemodynamic score after adjustment for clinical and echocardiographic indices (C statistic, 0.718 [95% CI, 0.682–0.746]). The right heart hemodynamic score was also independently associated with cardiovascular events in the validation cohort (C statistic, 0.711 [95% CI, 0.679–0.741]). The C statistic difference (0.007 [95% CI, 0.014–0.022]) and risk score (0.86 [95% CI, 0.54–1.17]) suggest a good model fit. Conclusions: The current study underscores the prognostic importance of right heart dysfunction in patients with coarctation of aorta and suggests that right heart indices should be used for risks stratification in this population.


2021 ◽  
Vol 5 (7) ◽  
pp. 456-461
Author(s):  
O.N. Titova ◽  
◽  
N.A. Kuzubova ◽  
A.L. Aleksandrov ◽  
V.E. Perley ◽  
...  

Aim: to assess the functionality of the right heart in patients with chronic obstructive pulmonary disease (COPD), mixed cystic fibrosis (CF), and cystic fibrosis lung disease by Doppler echocardiography. Patients and Methods: 30 adults with CF and 82 adults with COPD underwent ultrasonography to evaluate pulmonary and cardiac hemodynamics. All patients were divided into four groups based on the presence/absence of clinical signs of right ventricular failure and pulmonary hypertension. Results: in COPD, diastolic dysfunction of the right heart can be subclinical preceding systolic impairment. Right ventricular hypertrophy and failure in CF occur in relatively low pulmonary artery pressure. Thus, in systolic pulmonary pressure less than 40–50 mm Hg, hypertrophy and dilation were concomitant. As the diastolic function of the right ventricle worsens, right atrial contractility increases while the ratio of left ventricular filling velocities during the early atrial diastole and systole reduces in patients with CF. Conclusion: in severe COPD, significant structural and functional impairments of the right ventricle occur. Compensatory potentialities of the right and left ventricles exhaust, thereby providing the conditions for the progression of heart failure and the development of the chronic pulmonary heart. In CF, diastolic dysfunction of the right heart often precedes systolic dysfunction, as illustrated by changes in the proportion of various filling phases of the right ventricle. In right ventricular diastolic dysfunction, an increase in right atrial contractility occurs that reduces only in severe decompensation of the chronic pulmonary heart. KEYWORDS: chronic obstructive pulmonary disease, cystic fibrosis, echocardiography, Doppler cardiography, pulmonary hypertension, right ventricular failure, diastolic function. FOR CITATION: Titova O.N., Kuzubova N.A., Aleksandrov A.L. et al. Pulmonary and cardiac hemodynamics in COPD and cystic fibrosis by Doppler echocardiography. Russian Medical Inquiry. 2021;5(7):456–461 (in Russ.). DOI: 10.32364/2587-6821-2021-5-7-456-461.


2021 ◽  
pp. 204589402110136
Author(s):  
Tailong Zhang ◽  
Weitao Liang ◽  
Longrong Bian ◽  
Zhong Wu

Right heart thrombus (RHT) accompanied by chronic thromboembolic pulmonary hypertension (CTEPH) is a rare entity. RHT may develop in the peripheral veins or in situ within the right heart chambers. The diagnosis of RHT is challenging, since its symptoms are typically non-specific and its imaging features resemble those of cardiac masses. Here, we report two cases of RHT with CTEPH that presented as right ventricular masses initially. Both patients underwent simultaneous pulmonary endarterectomy (PEA) and resection of the ventricular thrombi. Thus, when mass-like features are confirmed by imaging, RHT should be suspected in patients with CTEPH, and simultaneous RHT resection is required along with PEA.


1975 ◽  
Vol 229 (3) ◽  
pp. 761-769 ◽  
Author(s):  
JF Green

Mean systemic pressure-flow (Ps-Q) and volume-flow (V-Q) relationships of the systemic vascular bed were determined in two groups of dogs anesthetized with sodium pentobarbital (group I) and with methoxyflurane (group II). All blood returning to the heart (Q) was removed from the right atrial appendage and passed through a Starling resistor, a pump, a flowmeter , and then returned directly into the pulmonary artery. Ps was estimated from plateau values of right atrial pressure obtained during stop-flow procedures. Both the Ps-Q and V-Q relationships were nonlinear. This nonlinearity may be attributed to a redistribution of blood flow between systemic vascular compartments of unequal time constants. With group II, the Ps-Q and V-Q curves were shifted markedly to the right along the Ps and V axes, respectively. Evidence is presented which suggests that this shift was due to an effective back pressure other than right atrial pressure produced by a hepatic waterfall. The beta-adrenergic antagonist practolol increased the effective back pressure and augmented the shift in the Ps-Q and V-Q curves.


1992 ◽  
Vol 263 (5) ◽  
pp. R1071-R1077 ◽  
Author(s):  
D. H. Carr ◽  
D. B. Jennings ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay

We have reported that increased left heart pressure inhibits increases in plasma renin activity (PRA), arginine vasopressin (AVP), and cortisol during arterial hypotension. The goal of this study was to determine whether increases in right heart pressure also inhibited hormonal responses to hypotension. Seven dogs were chronically instrumented with inflatable cuffs around the ascending aorta (AA), the pulmonary artery (PA), and the thoracic inferior vena cava (IVC), as well as with catheters in both atria, the abdominal aorta, and vena cava. The IVC, the PA, and the AA cuffs were inflated on different days to cause step reductions in mean arterial pressure (MAP) of 5, 10, 20, and 30% below control MAP. Graded constriction of the AA caused large increases in left atrial pressure and plasma atrial natriuretic peptide (ANP), but had no effect on plasma AVP or cortisol and caused only a small increase in PRA at the maximal reduction of MAP. Constriction of the IVC reduced both atrial pressures and plasma ANP, but stimulated increases in PRA, AVP, and cortisol. Constriction of the PA increased right atrial pressure and plasma ANP and caused increases in plasma AVP and cortisol that were similar to responses during IVC constriction, but the PRA response was only half (P < 0.05). These results indicate that increasing pressure on the right side of the heart can attenuate the PRA response to hypotension, and suggest that the inhibition is mediated by the rise in plasma ANP.


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