Should the mean left atrial pressure be the ultimate goal after TMVR?

2021 ◽  
Vol 97 (6) ◽  
pp. 1250-1251
Author(s):  
Mehmet Cilingiroglu ◽  
Konstantinos Marmagkiolis

1991 ◽  
Vol 70 (5) ◽  
pp. 1991-1995 ◽  
Author(s):  
S. A. Gu ◽  
J. Ducas ◽  
U. Schick ◽  
R. M. Prewitt

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.



1990 ◽  
Vol 259 (1) ◽  
pp. H93-H100 ◽  
Author(s):  
P. Lejeune ◽  
J. M. De Smet ◽  
P. de Francquen ◽  
M. Leeman ◽  
S. Brimioulle ◽  
...  

To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital sodium-anesthetized dogs ventilated alternately in hyperoxia [fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In hyperoxia, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.



2011 ◽  
Vol 27 (Supplement) ◽  
pp. OP12_1
Author(s):  
Yuji Konishi ◽  
Shingo Maeda ◽  
Hiroyuki Okada ◽  
Susumu Tao ◽  
Nobuyuki Kagiyama ◽  
...  


1992 ◽  
Vol 70 (1) ◽  
pp. 68-76 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda

The effects of cardiogenic and noncardiogenic pulmonary edema on the activities of rapidly adapting receptors (RARs) and pulmonary C-fibre receptors were investigated in dogs anaesthetized with chloralose. Cardiogenic pulmonary edema was produced by elevating the mean left atrial pressure by 25 mmHg (1 mmHg = 133.32 Pa) above the control value for a period of 45 min, by partial obstruction of the mitral valve. Noncardiogenic pulmonary edema was produced by injecting alloxan (100 mg/kg) intravenously. The effect of the latter was examined on RARs alone. Cardiogenic edema activated RARs (n = 8) and the activity was greatest during the first few minutes after elevation of mean left atrial pressure. The pulmonary C-fibre receptors (n = 6) were also activated by cardiogenic edema, but these responses were variable. Noncardiogenic pulmonary edema also activated RAR (n = 6), and this response was maintained during the entire recording period (20 min). The extravascular lung water (%), measured 15 min (n = 5) and 45 min (n = 5) after the elevation of the mean left atrial pressure, was significantly elevated above control values. However, these two values were not significantly different from each other. The extravascular lung water increased significantly after the injection of alloxan also (n = 5). These results show that during pulmonary edema, there is significant stimulation of the RARs and the pulmonary C-fibre receptors. It is suggested that the reflex respiratory responses observed in pulmonary edema may be due to the activation of both the RARs and the pulmonary C-fibre receptors.Key words: alloxan, cardiogenic edema, vagus.



2021 ◽  
Vol 77 (18) ◽  
pp. 1200
Author(s):  
Prince Sethi ◽  
Nikhil Parimi ◽  
Prakash Acharya ◽  
Amandeep Goyal ◽  
Emmanuel Daon ◽  
...  


2011 ◽  
Vol 25 (2) ◽  
pp. 244-250 ◽  
Author(s):  
S. Suzuki ◽  
T. Ishikawa ◽  
L. Hamabe ◽  
D. Aytemiz ◽  
H. Huai-Che ◽  
...  


Cardiology ◽  
1996 ◽  
Vol 87 (3) ◽  
pp. 224-229 ◽  
Author(s):  
Jer-Min Lin ◽  
Yi-Heng Li ◽  
Kwan-Lih Hsu ◽  
Juey-Jen Hwang ◽  
Yung-Zu Tseng


2015 ◽  
Vol 8 (7) ◽  
pp. e117-e119 ◽  
Author(s):  
Mackram F. Eleid ◽  
Saurabh Sanon ◽  
Guy S. Reeder ◽  
Rakesh M. Suri ◽  
Charanjit S. Rihal


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