Effects of acute changes in load and inotropic state on the exponential rate of fiber shortening and other indices of myocardial contractility in the anesthetized intact dog

1987 ◽  
Vol 65 (1) ◽  
pp. 46-53 ◽  
Author(s):  
José Suarez de Lezo ◽  
Pierre Casey ◽  
Anita Casey ◽  
José Luis Carrasco ◽  
José M. Arizon ◽  
...  

The effects of an acute increase in preload, afterload, and inotropic state on several indices of left ventricular contractility were studied in 20 anesthetized intact dogs. The behaviour of the exponential rate of fiber shortening (ERFS), a newly described index, which is based on the instantaneous fiber length – time relationship through ejection, was compared with other classical ejection and isovolumic indices of left ventricular contractility. Acute volume overload by dextran 40 infusion produced a significant increase in preload as reflected by a 103% (p < 0.01) increase in left ventricular end-diastolic pressure and a 121% (p < 0.001) increase in end-diastolic circumferential wall stress. There was also a smaller but significant increase (p < 0.05) of heart rate (30%) and of peak systolic circumferential wall stress (24%). None of the left ventricular contractility indices showed any significant change. Acute pressure overload, produced mechanically by an aortic balloon, increased the afterload significantly as reflected by a 33% (p < 0.05) rise of end-systolic circumferential wall stress and a 43% (p < 0.001) increase in systemic resistance. Stroke volume decreased significantly by 23% (p < 0.05). All ejection indices, including ERFS, were significantly diminished by 30 – 37%; all isovolumic indices showed no significant changes. Positive inotropic intervention was induced by dopamine infusion, which caused a significant 28% (p < 0.05) increase in cardiac output. End-diastolic and end-systolic circumferential wall stress were significantly diminished. All indices of left ventricular contractility increased significantly and ERFS showed the quantitatively greatest change. This study suggests that ERFS is an ejection index of myocardial contractility, which is quite sensitive to inotropic intervention, independent of preload but sensitive to afterload.

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
SKT Ma ◽  
WC Sin ◽  
CW Ngai ◽  
ASK Wong ◽  
WM Chan ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is an advanced technique in extracorporeal life support (ECLS) used to support extreme circulatory failure including patients with cardiac arrest and cardiogenic shock refractory to conventional support. It is a long-standing belief that peripheral V-A ECMO poses increased afterload to the inured heart, but conventional echocardiographic measurements are often insensitive in detecting subtle changes in loading conditions. Purpose This study aimed to evaluate the effects of varying blood flow during peripheral V-A ECMO on intrinsic myocardial contractility, using detailed echocardiographic assessment including speckle tracking echocardiography (STE). Methods Adult patients with acute cardiogenic shock who were supported by peripheral V-A ECMO from April 2019 to September 2020 were recruited. Serial hemodynamic and cardiac performance parameters were measured by transthoracic echocardiogram (TTE) within 48 hours after implementation of V-A ECMO, at different levels of extracorporeal blood flow – 100%, 120% and 50% of target blood flow (TBF). Results A total of 30 patients were included. 22 (71%) were male, and the mean (SD) age was 54 (13) years. The major indications for V-A ECMO were myocardial infarction (19, 63% patients), and myocarditis (5, 17%). With a decrease in extracorporeal blood flow from 100% to 50% of TBF, mean arterial pressure (MAP) dropped from 76+/-3 to 64+/-3mmHg (p &lt;0.001), and cardiac index (CI) increased from 0.89+/-0.13 to 1.27+/-0.18L/min/m2 (p &lt; 0.001). All indices of left ventricular contractility improved at a lower extracorporeal blood flow: the myocardial contractility measured by global longitudinal peak systolic strain (GLPSS) improved from -3+/-0.7% to -5+/-0.8% (p &lt; 0.001); left ventricular ejection fraction (LVEF) increased from 21.5+/-2.6% to 30.9+/-2.7% (p &lt; 0.001) and 19.7+/-3.1% to 28.4+/-3.2% (p &lt; 0.001) by biplane and linear methods, respectively; left ventricular index of myocardial performance (LIMP) improved from 1.51+/-0.12 to 1.03+/-0.09 (p &lt; 0.001). Similar findings were reproduced when comparing left ventricular contractility at extracorporeal blood flows of 120% and 50% of TBF. Conclusions The ECMO blood flow rate in peripheral V-A ECMO is inversely related to myocardial contractility, and is quantifiable by myocardial strain measured by STE.


1992 ◽  
Vol 73 (6) ◽  
pp. 2530-2537 ◽  
Author(s):  
D. J. Cooper ◽  
C. R. Thompson ◽  
K. R. Walley ◽  
R. P. Gillis ◽  
P. E. Wolinski-Walley ◽  
...  

To determine whether histamine alters human left ventricular contractility we measured heart rate, calibrated carotid arterial pressure, and left ventricular dimensions (echocardiogram) in nine healthy volunteers. We assessed baseline contractility using the end-systolic pressure-dimension relationship and the end-systolic meridional wall stress-rate-corrected velocity of circumferential fiber shortening relationship determined over a wide range of afterloads using phenylephrine and nitroprusside infusions. We then infused histamine for 3–5 min at a dose predetermined to decrease mean arterial pressure by 20%, both before and after H1 receptor antagonist pretreatment (diphenhydramine 50 mg i.v.). Histamine decreased end-systolic pressure but, unlike an equally hypotensive infusion of nitroprusside, did not decrease end-systolic dimension or increase fractional shortening. Histamine also decreased velocity of circumferential fiber shortening at the same end-systolic meridional wall stress as controls (P < 0.05). These effects of histamine were inhibited by H1 antagonist pretreatment. We conclude that the dominant effect of histamine on the human heart is to decrease left ventricular contractility and that this decrease in contractility is dependent, at least partially, on H1-receptor activation.


1995 ◽  
Vol 82 (6) ◽  
pp. 1389-1395. ◽  
Author(s):  
Axel W. Goertz ◽  
Tobias Mehl ◽  
Karl H. Lindner ◽  
Michael G. Rockemann ◽  
Uwe Schirmer ◽  
...  

Background Although a positive inotropic effect of hypertonic saline has been demonstrated in isolated cardiac tissue as well as in animal preparations, no information exists about a possible positive inotropic action of hypertonic saline in humans. The aim of this investigation was to determine whether a clinically relevant positive inotropic effect can be demonstrated in humans. Methods Twenty-six patients without cardiovascular disease were randomized to receive 4 ml/kg of either 7.2% hypertonic saline/6% hetastarch or 6% hetastarch (control) at a rate of 1 ml.kg-1.min-1 while under general endotracheal anesthesia. Transesophageal echocardiography was used to evaluate left ventricular function. Arterial pressure, heart rate, and left ventricular end-systolic and end-diastolic diameter, area, and wall thickness were measured immediately before and after administration of either solution. Fractional area change, end-systolic wall stress, and the area under the end-systolic pressure-length relationship curve (ESPLRarea) were calculated. ESPLRarea was used to assess left ventricular contractility. Results Administration of hypertonic saline/hetastarch resulted in a significant decrease of mean arterial pressure and end-systolic wall stress from 77 +/- 14 (mean +/- SD) to 64 +/- 17 mmHg (P &lt; 0.01) and from 52 +/- 14 to 32 +/- 11 10(3) dyne/cm2 (P &gt; 0.01), respectively. End-diastolic area and fractional area change increased from 16.5 +/- 2.9 to 21.7 +/- 3.3 cm2 (P &lt; 0.01) and from 0.53 +/- 0.07 to 0.70 +/- 0.06 (P &lt; 0.01), respectively, whereas there was only a minor change of ESPLRarea from 38 +/- 13 to 44 +/- 13 mmHg.cm (P &lt; 0.05). Conclusions The apparent improvement of left ventricular systolic function in response to hypertonic saline/hetastarch is caused mainly by the combined effect of increased left ventricular preload and reduced left ventricular afterload. A possible positive inotropic action of hypertonic saline/hetastarch is not likely to be clinically relevant.


2020 ◽  
Vol 13 (2) ◽  
pp. 357-369 ◽  
Author(s):  
Saki Ito ◽  
Cristina Pislaru ◽  
William R. Miranda ◽  
Vuyisile T. Nkomo ◽  
Heidi M. Connolly ◽  
...  

2019 ◽  
Vol 46 (5) ◽  
pp. 2137-2144
Author(s):  
Sahmin Lee ◽  
Seunghyun Choi ◽  
Sehwan Kim ◽  
Yeongjin Jeong ◽  
Kyusup Lee ◽  
...  

2021 ◽  
Author(s):  
Bálint Károly Lakatos ◽  
Mihály Ruppert ◽  
Márton Tokodi ◽  
Attila Oláh ◽  
Szilveszter Braun ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jorge Enrique Tovar Perez ◽  
Jesus Ortiz-Urbina ◽  
Celia Pena Heredia ◽  
Thuy T. Pham ◽  
Sridhar Madala ◽  
...  

An amendment to this paper has been published and can be accessed via a link at the top of the paper.


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