Effect of increased left atrial pressure on breathing frequency in anesthetized dog

1990 ◽  
Vol 69 (6) ◽  
pp. 1973-1980 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Left Heart ◽  
Breathing Frequency ◽  
Anesthetized Dogs ◽  
The Right

Distension or loading of the isolated canine left heart caused reflex tachypnea in prior studies. The object of the present effort was to explore the possibility that this depended primarily on atrial distension. Cardiopulmonary bypass perfusion and ligation of pulmonary veins were used to isolate the left-heart chambers of anesthetized dogs. Simultaneous distension of the beating left atrium and fibrillating ventricle stimulated breathing frequency (f), whereas isolated ventricular distension did not. At other times, intervals of atrial fibrillation were imposed under two different conditions: 1) while the right heart and lungs were bypassed and systemic perfusion was provided by the left ventricle using blood returned to the left atrium by pump and 2) while the ventricles fibrillated and systemic perfusion was supplied directly by the pump. Atrial fibrillation increased left atrial pressure and stimulated f in condition 1. In condition 2, f increased only if fibrillation was associated with a rise in left atrial pressure. Vagal cooling blocked the effect of fibrillation. I conclude that left atrial distension may initiate reflex tachypnea.

Control of breathing in anesthetized dogs by a left-heart baroreflex

1986 ◽  
Vol 61 (6) ◽  
pp. 2095-2101 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Vagal Afferents ◽  
Low Flow ◽  
Base Line ◽  
Left Heart ◽  
Breathing Frequency ◽  
Autonomic Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Vagal Cooling

Anesthetized open-chest dogs on cardiopulmonary bypass were used to test the hypothesis that breathing reflexly responds to distension of the left-heart chambers. Bypass perfusion withdrew systemic flow from the right atrium and returned it to the aorta after gas exchange. Ventricles were fibrillated. The left heart was isolated by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle. Left-heart pressure was intermittently raised abruptly from a nominal base line of 0 by partial occlusion of outflow. Pressures from approximately 10 to 50 cmH2O caused proportional increases in breathing frequency and decreases in expiratory and inspiratory times. Changes occurred immediately, reached a plateau within approximately 20 s, and were sustained for periods of observation as long as 3 min. Recovery to base line followed stimulus removal. Vagal cooling to 8 degrees C prevented responses, but autonomic ganglion blockade with hexamethonium had no effect. I conclude that breathing may be stimulated by left-heart distension and that this is mediated by large myelinated vagal afferents.

Pulmonary venous waterfall and perivenous pressure in the living dog

1975 ◽  
Vol 38 (2) ◽  
pp. 304-308 ◽  
Author(s):  
H. C. Smith ◽  
J. Butler
Keyword(s):  
Left Atrium ◽  
Lung Tissue ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Transpulmonary Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Living Animal ◽  
Alveolar Pressure ◽  
Flow Through

Evidence has been obtained that a waterfall effect occurs in the pulmonary veins of the living dog. Anesthetized open-chest dogs were used. Small catheters were passed from the left atrium retrogradely up the pulmonary veins and venous tributaries until they finally pierced the venous walls. They were then pulled out through the surface of the lung until their bellshaped inner ends wedged in small side branches of the vein. They were used to measure upstream venous pressures via the occluded tributary without occlusion of the vein. The pulmonary lymphatics and bronchial circulation were untouched. Alveolar pressure (transpulmonary pressure, Ptp) was held constant during the periods of measurement. We found that intrapulmonary (upstream) venous pressures did not rise with elevation of left atrial (downstream) pressures at any Ptp until a pressure of at least 7 cmH2O above the base of the lung was exceeded. This left atrial pressure (below which a venous waterfall or flow-limiting segment effect was present) increased with Ptp when Ptp exceeded about 15 cmH2O. The waterfall occurs in the larger veins at the lung surface. Its presence and location suggest that intrapulmonary veins in the living animal are held open by the surrounding lung tissue and that neither the flow through them nor their contained volume is influenced by left atrial pressure when this is low.

scholarly journals Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model

2021 ◽  
Author(s):  
Liuyang Feng ◽  
Hao Gao ◽  
Nan Qi ◽  
Mark Danton ◽  
Nicholas A. Hill ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Left Atrium ◽  
Left Atrial ◽  
Left Atrial Appendage ◽  
Pulmonary Veins ◽  
Three Dimensional ◽  
Left Heart ◽  
Structure Interaction ◽  
Acute Mitral Regurgitation ◽  
Reversal Flow

AbstractThis paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

scholarly journals GW26-e4379 Left Atrial Pressure Predicts Atrial Fibrillation Recurrence after Catheter Ablation

2015 ◽  
Vol 66 (16) ◽  
pp. C177
Author(s):  
Xiaobo Liao ◽  
Yanzong Yang ◽  
Lianjun Gao ◽  
Yunlong Xia ◽  
Dong Chang ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Atrial Fibrillation Recurrence

Pulmonary congestion enhances responses of lung rapidly adapting receptors to cigarette smoke in rabbit

1994 ◽  
Vol 77 (6) ◽  
pp. 2633-2640 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda ◽  
A. C. Bonham
Keyword(s):  
Left Atrium ◽  
Cigarette Smoke ◽  
Left Atrial ◽  
Venous Congestion ◽  
Transient Increase ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pulmonary Congestion ◽  
Stimulation Of

We examined the effects of low-nicotine cigarette smoke, pulmonary venous congestion, and their combination on the activity of rapidly (RAR) and slowly adapting receptors (SAR) in anesthetized rabbits. Pulmonary venous congestion was achieved by inflating a balloon in the left atrium to increase left atrial pressure. We examined smoke effects on RARs (averaged over 15 breaths) at baseline left atrial pressure and at subthreshold and suprathreshold increases in left atrial pressure. At baseline, smoke significantly increased RAR activity from 12.1 +/- 4.2 to 16.2 +/- 4.2 impulses/breath (P < 0.05). At subthreshold increases in left atrial pressure (2.9 +/- 0.6 mmHg), smoke produced larger increases in RAR activity (12.3 +/- 3.3 to 22.5 +/- 4.1 impulses/breath; P < 0.05). Suprathreshold increases in left atrial pressure (9.2 +/- 1.1 mmHg) alone increased RAR activity from 10.9 +/- 3.2 to 19.8 +/- 5.9 impulses/breath (P < 0.05). Smoke had no additional effect (22.3 +/- 4.8 impulses/breath; P > 0.05). There was, however, a transient increase in RAR activity (1st 3 breaths of smoke) under all three conditions. Of nine SARs examined, only two were stimulated by smoke. We conclude that in the rabbit smoke-induced stimulation of RARs is augmented by mild pulmonary venous congestion. of RARs is augmented by mild pulmonary venous congestion.

Reflex effects of left atrial pressure elevation on total intravascular volume

1981 ◽  
Vol 241 (5) ◽  
pp. H760-H765 ◽  
Author(s):  
D. L. Rutlen
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Intravascular Volume ◽  
Pressure Elevation ◽  
Reservoir Volume ◽  
Baroreceptor Stimulation ◽  
Mitral Orifice ◽  
Autonomic Reflex ◽  
The Right

The reflex autonomic influence of left atrial baroreceptor stimulation on the total capacitance vasculature has not been examined. To this end, left atrial pressure was increased in 25 anesthetized dogs, in which blood from the vena cavae was drained into an extracorporeal reservoir and returned to the right atrium at a constant rate, so that changes in intravascular volume could be recorded as reciprocal changes in reservoir volume. Left atrial pressure was elevated from 5 +/- 1 (mean +/- SE) to 11 +/- 1 mmHg by inflating a balloon at the mitral orifice for 12-20 min. With left atrial pressure elevation, total intravascular volume decreased 25 +/- 10 ml (P less than 0.025). In six of the dogs, intravascular volume decreased 37 +/- 12 ml with left atrial pressure elevation before bilateral cervical vagectomies and increased 66 +/- 8 ml with atrial pressure elevation after vagectomies (P less than 0.001). In eight of the dogs, volume decreased 42 +/- 19 ml with atrial pressure elevation before propranolol administration and increased 44 +/- 29 ml after propranolol (P less than 0.03). Phenoxybenzamine in five of the animals and atropine in three did not attenuate the change in intravascular volume with left atrial pressure elevation. Thus left atrial baroreceptor stimulation is associated with an autonomic reflex, which acts to decrease intravascular volume. The afferent limb is mediated by the vagi, and the efferent limb, by beta-adrenergic receptor stimulation.

Reference sites not influenced by hydrostatic pressure for right and left atrial pressures

1964 ◽  
Vol 207 (2) ◽  
pp. 357-360 ◽  
Author(s):  
George G. Armstrong ◽  
John C. Hancock
Keyword(s):  
Hydrostatic Pressure ◽  
Reference Point ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Lateral Border ◽  
Zero Reference ◽  
The Right ◽  
Made In

Simultaneous recordings of left and right atrial pressures made in dogs being rotated into all positions in space allowed the location of rotational axes where right or left atrial pressure became independent of hydrostatic pressure. Utilization of these axes as zero reference levels made possible the measurement of right or left atrial pressure without the influence of hydrostatic factors. The right zero reference point lay 62.8% of the distance from the manubrium to the xiphoid, 61.2% of the posterior to anterior thoracic diameter, and 47.7% of the greatest transverse thoracic diameter as measured from the right lateral border. The left atrial zero reference point lay 62.1% of the manubrium to xiphoid distance, 57.2% of the posterior to anterior diameter of thorax, and 53.0% of the greatest transverse thoracic diameter as measured from the right lateral border. When referred to the anatomy of the dog, these points lay in the immediate vicinity of the right and left atrioventricular valves, respectively.

P1415Wide antral circumferential pulmonary vein isolation ablation using a novel balloon cryoablation catheter

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
A P Martin ◽  
M Fowler ◽  
N Lever
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Pulmonary Vein ◽  
Pulmonary Vein Isolation ◽  
Paroxysmal Atrial Fibrillation ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Posterior Wall ◽  
The Novel ◽  
Median Treatment

Abstract Background Pulmonary vein isolation using cryotherapy is an established treatment for the management of patients with paroxysmal atrial fibrillation. Ablation using the commercially available balloon cryocatheter has been shown to create wide antral pulmonary vein isolation. A novel balloon cryocatheter (BCC) has been designed to maintain uniform pressure and size during ablation, potentially improving contact with the antral anatomy. The extent of ablation created using the novel BCC has not previously been established. Purpose To determine the anatomical extent of pulmonary vein isolation using electroanatomical mapping when performing catheter ablation for paroxysmal atrial fibrillation using the novel BCC. Methods Nine consecutive patients underwent pre-procedure computed tomography angiography of the left atrium to quantify the chamber dimensions. An electroanatomical map was created using the cryoablation system mapping catheter and a high definition mapping system. A bipolar voltage map was obtained following ablation to determine the extent of pulmonary vein isolation ablation. A volumetric technique was used to quantify the extent of vein and posterior wall electrical isolation in addition to traditional techniques for proving entrance and exit block. Results All patients had paroxysmal atrial fibrillation, mean age 56 years, 7 (78%) male. Electrical isolation was achieved for 100% of the pulmonary veins; mean total procedure time was 109 min (+/- 26 SD), and fluoroscopy time 14.9 min (+/- 2.4 SD). The median treatment applications per vein was one (range one - four), and median treatment duration 180 sec (range 180 -240). Left atrial volume 32 mL/m2 (+/- 7 SD), and mean left atrial posterior wall area 22 cm2 (+/- 4 SD). Data was available for quantitative assessment of the extent of ablation for eight patients. No lesions (0 of 32) were ostial in nature. The antral surface area of ablation was not statistically different between the left and right sided pulmonary veins (p 0.63), which were 5.9 (1.6 SD) and 5.4 (2.1 SD) cm2 respectively. In total 50% of the posterior left atrial wall was ablated.  Conclusion Pulmonary vein isolation using a novel BCC provides a wide and antral lesion set. There is significant debulking of the posterior wall of the left atrium. Abstract Figure.

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