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

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

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Effects of arteriovenous fistula on systemic and pulmonary circulations

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1964.207.6.1319 ◽

1964 ◽

Vol 207 (6) ◽

pp. 1319-1324 ◽

Cited By ~ 31

Author(s):

Jiro Nakano ◽

Christian De Schryver

Keyword(s):

Cardiac Output ◽

Blood Transfusion ◽

Arterial Pressure ◽

Left Atrial ◽

Pulmonary Arterial Pressure ◽

Peripheral Resistance ◽

Systemic Arterial Pressure ◽

Left Ventricular ◽

Stroke Work ◽

Pulmonary Arterial

The effects of arteriovenous fistulas of different magnitudes on cardiovascular dynamics were studied in anesthetized dogs. It was found that A-V fistula decreases mean systemic arterial pressure, effective systemic blood flow, total and pulmonary peripheral resistances, whereas it increases heart rate, total cardiac output, stroke volume, left atrial pressure, pulmonary arterial pressure, and systemic peripheral resistance. The magnitude of the above hemodynamic changes was essentially proportional to the size of the fistula. At equivalent increments in total cardiac output produced by A-V fistula and blood transfusion, the former condition causes a greater increase in pulmonary arterial pressure than the latter, although both conditions decrease the pulmonary peripheral resistance by the same degree. It was also found that, at equivalent left atrial pressures, left ventricular stroke work with A-V fistula was greater than that with blood transfusion.

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Developmental differences in vascular responses to hypoxia in lungs of rabbits

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.2.507 ◽

1994 ◽

Vol 77 (2) ◽

pp. 507-516 ◽

Cited By ~ 5

Author(s):

C. D. Fike ◽

M. R. Kaplowitz

Keyword(s):

Arterial Pressure ◽

Left Atrial ◽

Pulmonary Arterial Pressure ◽

Developmental Differences ◽

Age Group ◽

Co2 Gas ◽

Micropuncture Technique ◽

Age Related ◽

Hypoxic Vasoconstriction ◽

Pulmonary Arterial

Our purpose was to determine whether postnatal age and prostaglandins influence the sites of hypoxic vasoconstriction in lungs of rabbits. To do this, we used the micropuncture technique to measure pressures in 20- to 80-microns-diam subpleural arterioles and venules during sequential inflation of lungs of newborn and adult rabbits with normoxic (21% O2–7–10% CO2–69–72% N2) and hypoxic (90–93% N2–7–10% CO2) gas mixtures. Indomethacin (40 micrograms/ml) was added to the perfusate of some lungs of each age group. During hypoxia in untreated lungs of newborn rabbits, both pulmonary arterial and 20- to 80-microns-diam arteriolar pressure increased by 5%, whereas 20- to 80-microns-diam venular pressure remained the same. In contrast, during hypoxia in untreated lungs of adult rabbits, pulmonary arterial pressure increased by 48%, whereas 20- to 80-microns-diam arteriolar pressure decreased slightly and 20- to 80-microns-diam venular pressure did not change. Regardless of the presence of indomethacin, location of vessels used for micropuncture, or level of left atrial pressure, pulmonary arterial pressure was the only measured vascular pressure that increased with hypoxia in adult lungs. Thus, in adult lungs, the site of hypoxia-induced vasoconstriction was limited to arteries > 80 microns diam, whereas in newborn lungs the site of hypoxia-induced vasoconstriction included vessels both larger and smaller than 20- to 80-microns-diam arteries. This age-related difference in the sites of hypoxia-induced vasoconstriction was not found in indomethacin-treated lungs.

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Effect of Renal and Left Ventricular Function on Serial Pulmonary Arterial Pressure Changes after Device Closure of Atrial Septal Defect

Journal of Interventional Cardiology ◽

10.1155/2021/8846656 ◽

2021 ◽

Vol 2021 ◽

pp. 1-8

Author(s):

Chul Shin ◽

Young Won Yoon ◽

In-Soo Kim ◽

Jong-Youn Kim ◽

Pil-Ki Min ◽

...

Keyword(s):

Atrial Fibrillation ◽

Arterial Pressure ◽

Septal Defect ◽

Pulmonary Arterial Pressure ◽

Left Ventricular ◽

Volume Index ◽

Device Closure ◽

Pulmonary Arterial ◽

One Year ◽

Pressure Changes

Background. The age of candidates for device closure of atrial septal defect (ASD) has been increasing. Thus, concerns exist about dyspnea aggravation or atrial fibrillation development after device closure due to augmentation of left ventricular (LV) and left atrial (LA) preload. This study aimed to examine patterns and determinants of serial pulmonary arterial pressure and left ventricular filling pressure changes after device closure of ASD. Methods. Among the 86 consecutive patients who underwent percutaneous device closure of ASD, those with end-stage renal disease or those without pre- or postprocedural Doppler data were excluded. The clinical, transesophageal, and transthoracic echocardiographic findings of 78 patients were collected at baseline, one-day postprocedure, and one-year follow-up. Results. The mean age of study patients was 49.8 ± 15.0 years, and the average maximal defect diameter and device size were 20.2 ± 6.0 mm and 23.8 ± 6.4 mm. Four patients (5.6%) underwent new-onset atrial fibrillation, and five patients (6.4%) took diuretics within one-year after closure. Some patients (n = 21; 27%) exhibited paradoxically increased tricuspid regurgitant velocity (TRV) one-day postprocedure; they also were older with lower e’, glomerular filtration rate, and LV ejection fraction and a higher LA volume index. However, even in these patients, TRV deceased below baseline levels one-year later. Both E/e’ and LA volume index significantly increased immediately after device closure, but all decreased one-year later. Larger defect size and higher TRV were significantly correlated with immediate E/e’ elevation. Conclusion. In older, renal, diastolic, and systolic dysfunctional patients with larger LA and scheduled for larger device implantation, peri-interventional preload reduction therapy would be beneficial.

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Microvascular pressures during hypoxia in isolated lungs of newborn rabbits

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.1.283 ◽

1988 ◽

Vol 65 (1) ◽

pp. 283-287 ◽

Cited By ~ 7

Author(s):

C. D. Fike ◽

S. J. Lai-Fook ◽

R. D. Bland

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Airway Pressure ◽

Left Atrial ◽

Pulmonary Arterial Pressure ◽

Hypoxic Conditions ◽

Hypoxic Vasoconstriction ◽

Pulmonary Arterial ◽

Isolated Lungs ◽

Ventilation Of The Lungs

The purpose of this study was to determine the sites of hypoxic vasoconstriction in lungs of newborn rabbits. We isolated and perfused with blood the lungs from 19 rabbit pups, 7-23 days old. We maintained blood flow constant, continuously monitored pulmonary arterial and left atrial pressures, and alternated ventilation of the lungs with 95% O2-5% CO2 (control), and 95% N2-5% CO2 (hypoxia). Using micropipettes and a servonulling device, we measured pressures in 20-60-micron-diam subpleural arterioles and venules during control and hypoxic conditions. We inflated the lungs to a constant airway pressure of 5-7 cmH2O and kept left atrial pressure greater than airway pressure (zone 3) during micropuncture. In eight lungs we measured microvascular pressures first during control and then during hypoxia. We reversed this order in four lungs. In seven lungs we measured microvascular pressures only during hypoxia. We found a significant increase in pulmonary arterial pressure with no change in microvascular pressures. These results indicate that the site of hypoxic vasoconstriction in lungs of newborn rabbits is arteries greater than 60 micron in diameter.

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Lymph flow and lung weight in isolated sheep lungs

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.5.1830 ◽

1986 ◽

Vol 61 (5) ◽

pp. 1830-1835 ◽

Cited By ~ 13

Author(s):

W. Mitzner ◽

J. T. Sylvester

Keyword(s):

Weight Gain ◽

Arterial Pressure ◽

Left Atrial ◽

Pulmonary Arterial Pressure ◽

Lymph Flow ◽

Atrial Pressure ◽

Left Atrial Pressure ◽

Lung Water ◽

Lung Weight ◽

Pulmonary Arterial

To study the relationship between lung weight and lymph flow, we used an in situ, isolated sheep lung preparation that allowed these two variables to be measured simultaneously. All lungs were perfused for 4.5 h at a constant rate of 100 ml X min-1 X kg-1. In control lungs, the left atrial pressure (Pla) was kept at atmospheric pressure. In experimental lungs, Pla was kept atmospheric except for a 50-min elevation to 18 mmHg midway through the perfusion. During this period of left atrial hypertension, pulmonary arterial pressure rose from 18 to 31 mmHg, lymph flow rose from 3 to 12 ml/h, and the lymph-to-plasma oncotic pressure ratio (pi L/pi P) fell from 0.7 to 0.48. After left atrial pressure was returned to control, pulmonary arterial pressure, lymph flow, and pi L/pi P all returned to control levels. The rate of weight gain after the return of left atrial pressure to control was also the same as that in the control group. However, during the period of left atrial hypertension 135 ml of fluid were filtered into the lung, and this large increase in lung weight remained after the pressure was lowered. The presence of this substantial excess lung water despite control values for vascular pressures, lymph flow, rate of weight gain, and pi L/pi P suggests that the absolute amount of lung water has little influence on the dynamic aspects of lung fluid balance. These results are consistent with a two-compartment model of the interstitial space, where only one of the compartments is readily drained by the lymphatics.

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Minimally Invasive Left Atrial Appendage Excision and Atrial Fibrillation Ablation as Secondary Prevention of Thromboembolic Stroke—Weighing the Risk Versus the Benefit

Seminars in Thoracic and Cardiovascular Surgery ◽

10.1053/j.semtcvs.2020.09.014 ◽

2020 ◽

Author(s):

Stephen J. Huddleston ◽

Sara J. Shumway

Keyword(s):

Atrial Fibrillation ◽

Minimally Invasive ◽

Secondary Prevention ◽

Left Atrial ◽

Left Atrial Appendage ◽

Atrial Fibrillation Ablation ◽

Atrial Appendage ◽

Thromboembolic Stroke

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PAF increases vascular permeability without increasing pulmonary arterial pressure in the rat

Journal of Applied Physiology ◽

10.1152/jappl.2001.90.1.261 ◽

2001 ◽

Vol 90 (1) ◽

pp. 261-268 ◽

Cited By ~ 18

Author(s):

Leonardo C. Clavijo ◽

Mary B. Carter ◽

Paul J. Matheson ◽

Mark A. Wilson ◽

William B. Wead ◽

...

Keyword(s):

Arterial Pressure ◽

Pulmonary Edema ◽

Pulmonary Arterial Pressure ◽

Ex Vivo ◽

Platelet Activating Factor ◽

Microvascular Permeability ◽

Blue Dye ◽

E Coli ◽

Pulmonary Arterial

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.

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