Mechanical heart-lung interaction with positive end-expiratory pressure

1983 ◽  
Vol 54 (4) ◽  
pp. 1039-1047 ◽  
Author(s):  
T. W. Wallis ◽  
J. L. Robotham ◽  
R. Compean ◽  
M. K. Kindred
Keyword(s):  
Cardiac Output ◽  
Compressive Force ◽  
Left Ventricular ◽  
Lv Function ◽  
Respiratory System Compliance ◽  
Positive End Expiratory Pressure ◽  
Heart Volume ◽  
Chest Wall Compliance ◽  
Diastolic Compliance ◽  
Wall Compliance

Recent reports have suggested that positive end-expiratory pressure (PEEP) depresses left ventricular (LV) function or shifts LV pressure-volume (PV) relationships due to neural, humoral, or mechanical events. These studies have usually utilized pressures measured during expiration. To study the mechanical effects of PEEP in expiration and inspiration, the circulation was arrested in 12 open-chest dogs, and the coronaries were perfused with a cold cardioplegic agent. Balloons were placed in the ventricles to measure ventricular pressures. Shifts in cardiopulmonary blood volume were prevented by venting the atria to atmosphere. Having ablated neural reflexes and humoral changes, we varied ventricular volumes, chest wall compliance, tidal volume, and PEEP. We found that isovolumic ventricular pressures (relative to atmosphere) increase with PEEP (P less than 0.001), and heart-lung interaction with PEEP is significantly greater in inspiration (P less than 0.001). The effect of PEEP is modified by heart volume (P less than 0.01) and respiratory system compliance (P less than 0.01). We conclude that a mechanical compressive force can be applied to the heart by the lungs as they expand, and this may explain the previous reports of diminished LV function or LV diastolic compliance with PEEP and, in part, explain the decreased cardiac output associated with PEEP. The marked increase in mechanical compressive forces applied to the heart during inspiration with PEEP may have far greater hemodynamic consequences than events during expiration.

Effects of decreasing lung compliance with oleic acid on the cardiovascular response to PEEP

1977 ◽  
Vol 233 (6) ◽  
pp. H635-H641 ◽  
Author(s):  
S. M. Scharf ◽  
R. H. Ingram
Keyword(s):  
Oleic Acid ◽  
Venous Return ◽  
Cardiovascular Response ◽  
Lung Compliance ◽  
Back Pressure ◽  
Right Atrial ◽  
Positive End Expiratory Pressure ◽  
Chest Wall Compliance ◽  
Before And After ◽  
Wall Compliance

In 12 anesthetized mongrel dogs on a constant volume ventilator, the response of the cardiovascular system to increasing positive end-expiratory pressure (PEEP) was examined before and after inducing acute lung injury with oleic acid. As PEEP was raised to approximately 16 mmHg, lung volume increased by approximately 900 ml before oleic acid and only 350 ml after. Pleural pressure increased by the same amount, indicating that both lung and chest wall compliance decreased with oleic acid. Right atrial pressure, the back pressure to venous return, also increased by the same amount. Although cardiac output at PEEP = 0 was lower after oleic acid, the relative decrements produced by increasing PEEP were the same as before oleic acid.

Positive end-expiratory pressure shifts left ventricular diastolic pressure-area curves

1980 ◽  
Vol 48 (4) ◽  
pp. 670-676 ◽  
Author(s):  
J. B. Haynes ◽  
S. D. Carson ◽  
W. P. Whitney ◽  
G. O. Zerbe ◽  
T. M. Hyers ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Pressure Area ◽  
Radiopaque Markers ◽  
Peep Ventilation ◽  
Volume Characteristics ◽  
Area Data

Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.

Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Acute Heart Failure ◽  
Coronary Blood Flow ◽  
Drug Effects ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Energetic Cost ◽  
Lv Function

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.

Effect of positive end-expiratory pressure on ventricular function in dogs

1979 ◽  
Vol 236 (4) ◽  
pp. H534-H544 ◽  
Author(s):  
R. M. Prewitt ◽  
L. D. Wood
Keyword(s):  
Cardiac Output ◽  
Left Ventricular Function ◽  
Pulmonary Edema ◽  
Ventricular Function ◽  
Diastolic Pressure ◽  
Intrathoracic Pressure ◽  
Esophageal Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Positive End Expiratory Pressure

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.

scholarly journals Relationship between Abdominal Pressure, Pulmonary Compliance, and Cardiac Preload in a Porcine Model

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Joost Wauters ◽  
Piet Claus ◽  
Nathalie Brosens ◽  
Myles McLaughlin ◽  
Greet Hermans ◽  
...  
Keyword(s):  
Chest Wall ◽  
Respiratory System ◽  
Cardiac Preload ◽  
Volume Index ◽  
Abdominal Pressure ◽  
Stroke Index ◽  
Respiratory System Compliance ◽  
Chest Wall Compliance ◽  
End Diastolic Volume ◽  
Wall Compliance

Rationale. Elevated intra-abdominal pressure (IAP) may compromise respiratory and cardiovascular function by abdomino-thoracic pressure transmission. We aimed (1) to study the effects of elevated IAP on pleural pressure, (2) to understand the implications for lung and chest wall compliances and (3) to determine whether volumetric filling parameters may be more accurate than classical pressure-based filling pressures for preload assessment in the setting of elevated IAP.Methods. In eleven pigs, IAP was increased stepwise from 6 to 30 mmHg. Hemodynamic, esophageal, and pulmonary pressures were recorded.Results. 17% (end-expiratory) to 62% (end-inspiratory) of elevated IAP was transmitted to the thoracic compartment. Respiratory system compliance decreased significantly with elevated IAP and chest wall compliance decreased. Central venous and pulmonary wedge pressure increased with increasing IAP and correlated inversely (r=-0.31) with stroke index (SI). Global end-diastolic volume index was unaffected by IAP and correlated best with SI (r=0.52).Conclusions. Increased IAP is transferred to the thoracic compartment and results in a decreased respiratory system compliance due to decreased chest wall compliance. Volumetric filling parameters and transmural filling pressures are clearly superior to classical cardiac filling pressures in the assessment of cardiac preload during elevated IAP.

End-systolic pressure-volume relationships in dogs during ventilation with PEEP

1988 ◽  
Vol 254 (4) ◽  
pp. H664-H670 ◽  
Author(s):  
A. J. Crottogini ◽  
P. Willshaw ◽  
J. G. Barra ◽  
G. J. Breitbart ◽  
R. H. Pichel
Keyword(s):  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Closed Chest ◽  
Inotropic State ◽  
Anesthetized Dogs ◽  
Lv Volume

Whether left ventricular (LV) contractility changes during ventilation with positive end-expiratory pressure (PEEP) remains controversial. To assess LV inotropic state during PEEP using a load-independent index, we generated end-systolic pressure-volume relationships (ESPVRs) in eight closed-chest, chronically instrumented, anesthetized dogs undergoing 0 [zero end-expiratory pressure for the 1st time (ZEEP1)], 5 (PEEP-5), 10 (PEEP-10), and again 0 (ZEEP2) cmH2O PEEP. LV volume was calculated from three orthogonal internal diameters (sonomicrometry), and LV pressure was measured using an implanted transducer. ESPVRs at each level of PEEP were generated by transient inflation of a vena caval occluder. Despite significant decreases in cardiac output with PEEP-5 (1.81 +/- 0.38 l/min, means +/- SE; P less than 0.05) and PEEP-10 (1.70 +/- 0.46; P less than 0.01) with respect to ZEEP1 (2.12 +/- 0.41), no change was found in the slope (ZEEP1: 6.99 +/- 1.03 mmHg/ml; PEEP-5: 7.48 +/- 1.20; PEEP-10: 7.17 +/- 1.02; ZEEP2: 7.38 +/- 1.02), the volume intercept (ZEEP1: 7.4 +/- 3.4 ml; PEEP-5: 6.6 +/- 3.0; PEEP-10: 7.2 +/- 4.0; ZEEP2: 6.6 +/- 3.6), or the new index area beneath the ESPVR (ZEEP1: 304 +/- 98; PEEP-5: 329 +/- 104; PEEP-10: 310 +/- 98; ZEEP2: 343 +/- 114). We conclude that these levels of PEEP do not affect LV contractility as assessed by the ESPVR.

β-Adrenergic-mediated improvement in left ventricular function by exercise training in older men

1998 ◽  
Vol 274 (2) ◽  
pp. H397-H404 ◽  
Author(s):  
Robert J. Spina ◽  
Michael J. Turner ◽  
Ali A. Ehsani
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Exercise Training ◽  
Velocity Ratio ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Lv Function ◽  
Adrenergic Blockade ◽  
Age Related ◽  
Inotropic Responses

To test the hypothesis that the training-induced improvement in the age-related decline in left ventricular (LV) function is mediated by enhanced inotropic responses to β-adrenergic stimulation, 10 sedentary healthy men, 65 ± 1 yr (mean ± SE) of age, exercised for 9 mo, which resulted in a 28% increase in aerobic exercise capacity. Training induced a greater increase in LV systolic shortening, assessed with two-dimensional echocardiography, in response to isoproterenol with a steeper slope of the fractional shortening-end-systolic wall stress (ςes) relationship and an upward shift of the ςes-systolic diameter relationship without an acute increase in heart rate or preload. The increase in the early-to-late diastolic flow velocity ratio, normalized for heart rate and preload, in response to isoproterenol was larger after training. LV systolic reserve and cardiac output during peak exercise were higher after training. β-Adrenergic blockade with esmolol HCl abolished the adaptive increases in LV systolic reserve capacity and cardiac output during peak exercise in the trained state. The results suggest that one of the underlying mechanisms responsible for the adaptive increase in LV systolic function in response to exercise training is an enhanced inotropic sensitivity to catecholamines. Furthermore, the enhanced inotropic responses are associated with increased diastolic filling.

scholarly journals The Cardiovascular Implications of Thoracic Endovascular Aortic Repair: how aortic stenting impacts LV function and coronary artery flow

2021 ◽  
Author(s):  
David P Stonko ◽  
Hossam Abdou ◽  
Joseph Edwards ◽  
Noha N Elansary ◽  
Eric Lang ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiovascular System ◽  
Coronary Flow ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Aortic Compliance ◽  
Flow Measurements ◽  
Aortic Stenting

Abstract Aortic stents are known to have harmful effects on the cardiovascular system. They augment left ventricular function by decreasing aortic compliance. How these cardiovascular parameters change during and immediately after deployment of aortic stents has not been rigorously quantified, despite the development of heart failure in as many as 40% of post-TEVAR survivors within one-year. Without a comprehensive understanding of how the cardiovascular system changes in response to aortic stenting, surgical or medical strategies to augment prevent these changes cannot be developed. The goal of this study is to evaluate alterations in cardiovascular physiology that develop during and after total aortic endografting in a swine model. We will employ left ventricular (LV) pressure-volume (PV) loop analysis, which provides comprehensive pump mechanical information about LV function including stroke work and cardiac output, coupled with direct coronary flow measurements to understand how these parameters change when an aortic stent is placed. Our hypotheses are that aortic stenting: 1) is associated with decreased aortic compliance and increased LV afterload, 2) augments the LV end systolic pressure relationship (i.e., stroke work and end systolic pressure increase) and 3) increases coronary blood flow but decreases the coronary flow/cardiac output ratio.

Systolic and diastolic dysfunction of the left ventricle induced by dietary taurine deficiency in cats

1991 ◽  
Vol 261 (1) ◽  
pp. H121-H127 ◽  
Author(s):  
M. J. Novotny ◽  
P. M. Hogan ◽  
D. M. Paley ◽  
H. R. Adams
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Lv Function ◽  
Once Daily ◽  
Taurine Deficiency ◽  
Diastolic Compliance ◽  
Myocardial Contractile ◽  
The Right

Isovolumic left ventricular (LV) preparations were used to assess myocardial failure associated with dietary taurine deficiency in cats. Adult female cats (n = 12) were fed a purified diet devoid of taurine for 6-8 mo. Six of the cats received 1,000 mg of crystalline taurine orally once daily. The remaining six cats were not provided taurine replacement. Compared with control preparations, hearts isolated from taurine-deficient cats generated significantly lower values for developed LV systolic pressure (107 +/- 6 vs. 66 +/- 15 mmHg; P less than 0.05), maximal rate of LV pressure rise (+dP/dtmax; 1,103 +/- 38 vs. 718 +/- 172 mmHg/s; P less than 0.05), and fall (-dP/dtmax; 930 +/- 46 vs. 587 +/- 129 mmHg/s; P less than 0.05). LV function curves generated by hearts from taurine-deficient cats were shifted downward and to the right of control curves, demonstrating inotropic depression. In addition, end-diastolic pressure-volume (compliance) relationships in hearts from taurine-deficient cats were shifted downward and to the right of controls in the direction of increased chamber compliance or distensibility. Ten millimolar taurine significantly improved inotropic indexes only in hearts from taurine-deficient cats but failed to affect diastolic compliance. Myocardial contractile dysfunction and LV chamber dilatation in hearts from taurine-deficient cats verify a causal association between dietary deficiency of this amino acid and dilated cardiomyopathy in this species.

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