PV Loops and REBOA During Hemorrhage and Resuscitation

2021 ◽  
Author(s):  
David P Stonko ◽  
Joseph Edwards ◽  
Hossam Abdou ◽  
Noha N Elansary ◽  
Eric Lang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Aortic Occlusion ◽  
Loop Analysis ◽  
Time Period ◽  
Great Vessels ◽  
The Brain

Abstract Retrograde Endovascular Balloon Occlusion of the Aorta (REBOA) is frequently used in hemorrhagic shock to facilitate resuscitation. In theory, aortic occlusion increases afterload and focuses perfusion to the coronary arteries and great vessels; also to focus perfusion to the brain. It is, however, unknown exactly how and to what extent REBOA impacts cardiovascular parameters such as preload, afterload and contractility, or coronary artery blood flow. It is also not known how these parameters evolve over time during REBOA as it is shifted from fully to partially occlusive, or weaned down entirely. We aim to use left ventricular Pressure-Volume (PV) loop analysis and directly measure coronary flow in swine as they descend into hemorrhagic shock, are resuscitated with full aortic occlusion with REBOA, transitioned to partial aortic occlusion with REBOA, and then weaned completely off of the REBOA and are resuscitated. We will examine, specifically, measures of preload, afterload, contractility and coronary blood flow during each study time period (baseline, hemorrhagic shock, full aortic occlusion, partial aortic occlusion, and post-occlusion during resuscitation).

Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stig Müller ◽  
Ole-Jakob How ◽  
Stig E Hermansen ◽  
Truls Myrmel
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Arterial Blood ◽  
Time Flow ◽  
The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

Continuous Airway Pressure Breathing With the Head-Box in the Newborn Lamb: Effects on Regional Blood Flows

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Airway Pressure ◽  
Left Ventricular Pressure ◽  
Blood Gases ◽  
Ocular Blood Flow ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Blood Flows ◽  
Arterial Blood

Continuous airway pressure delivered by a head-box is an accepted means of treating clinical hyaline membrane disease. To investigate hemodynamic alterations resulting from its use, eight newborn lambs, 1 to 6 days of age, were studied at 6 and 11 mm Hg of positive pressure, while spontaneously breathing room air. Organ blood flows and cardiac output were measured with 25 µ-diameter radioactive microspheres. Heart rate, left ventricular pressure, and arterial blood gases did not change during the study. Jugular venous pressures increased from 6.4 mm Hg to 18.6 and 24.2 mm Hg at 6 and 11 mm Hg, respectively (P < .005). Cardiac output decreased approximately 20% at either intrachamber pressure setting. Renal blood flow fell 21% at 11 mm Hg. No significant changes in blood flow were found in the brain, gastrointestinal tract, spleen, heart, or liver when compared to control flows. Of particular interest was the finding of a 28% reduction in ocular blood flow at 6 mm Hg and 52% at 11 mm Hg. From these results, we conclude that substantial cardiovascular alterations may occur during the application of head-box continuous airway pressure breathing, including a significant reduction in ocular blood flow.

Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta

1980 ◽  
Vol 238 (4) ◽  
pp. H423-H429 ◽  
Author(s):  
O. Stokland ◽  
M. M. Miller ◽  
A. Ilebekk ◽  
F. Kiil
Keyword(s):  
Inferior Vena Cava ◽  
Superior Vena Cava ◽  
Inferior Vena ◽  
Superior Vena ◽  
Vena Cava ◽  
Spinal Column ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Aortic Occlusion ◽  
Systolic Volume

To examine left ventricular responses to aortic occlusion, changes in end-diastolic volume (EDV) and end-systolic volume (ESV) were estimated by ultrasonic recordings of myocardial distances in atropinized open-chest dogs. During aortic occlusion EDV and ESV increased equally, systolic left ventricular pressure (LVP) rose by 86 +/- 8 mmHg, and blood flow more than doubled in the superior vena cava and fell by 90% in the inferior vena cava. During combined occlusion of aorta and inferior vena cava, systolic LVP and superior vena cava flow did not rise above control and EDV declined. By infusing 25 +/- 2 ml/kg body wt of blood during combined occlusion, the effects of aortic occlusion could be reproduced; control values before blood infusion were reestablished by withdrawal of only one-third of the infused volume, indicating a shunt line along the spinal column. Thus during aortic occlusion, transfer of blood accounts for the rise in EDV and increased activation of the Frank-Starling mechanism; increased afterload raises ESV as much as EDV in anesthetized dogs not subjected to sympathetic stimulation. Consequently, stroke volume is maintained and systolic LVP increased.

Fluid-Structure Interaction Simulation of Blood Flow Inside a Diseased Left Ventricle With Obstructive Hypertrophic Cardiomyopathy in Early Systole

2009 ◽  
Author(s):  
Ahmad Moghaddaszade-Kermani ◽  
Peter Oshkai ◽  
Afzal Suleman
Keyword(s):  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Left Ventricle ◽  
Fluid Structure Interaction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Systolic Phase

Mitral-Septal contact has been proven to be the cause of obstruction in the left ventricle with hypertrophic cardiomyopathy (HC). This paper presents a study on the fluid mechanics of obstruction using two-way loosely coupled fluid-structure interaction (FSI) methodology. A parametric model for the geometry of the diseased left ventricular cavity, myocardium and mitral valve has been developed, using the dimensions extracted from magnetic resonance images. The three-element Windkessel model [1] was modified for HC and solved to introduce pressure boundary condition to the aortic aperture in the systolic phase. The FSI algorithm starts at the beginning of systolic phase by applying the left ventricular pressure to the internal surface of the myocardium to contract the muscle. The displacements of the myocardium and mitral leaflets were calculated using the nonlinear finite element hyperelastic model [2] and subsequently transferred to the fluid domain. The fluid mesh was moved accordingly and the Navier-Stokes equations were solved in the laminar regime with the new mesh using the finite volume method. In the next time step, the left ventricular pressure was increased to contract the muscle further and the same procedure was repeated for the fluid solution. The results show that blood flow jet applies a drag force to the mitral leaflets which in turn causes the leaflet to deform toward the septum thus creating a narrow passage and possible obstruction.

Volume expansion potentiates cardiac sympathetic afferent reflex in dogs

2001 ◽  
Vol 280 (2) ◽  
pp. H576-H581 ◽  
Author(s):  
Wei Wang ◽  
Harold D. Schultz ◽  
Rong Ma
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Volume Expansion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Volume Expansion ◽  
Cardiac Sympathetic Afferent Reflex

Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 μg) and capsaicin (10 and 100 μg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 μg) of epicardial bradykinin (17. 3 ± 1.9 vs. 10.6 ± 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 ± 4.1 vs. 5.0 ± 1.3% for 5 μg, P < 0.05, and 28.9 ± 3.7 vs. 10.6 ± 4.8% for 50 μg, P < 0.05) and capsaicin (29.8 ± 6.0 vs. 9.3 ± 3.1% for 10 μg, P < 0.05, and 34.2 ± 2.7 vs. 15.1 ± 2.7% for 100 μg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.

Hemodynamics during transcatheter aortic valve implantation in patients with severe aortic stenosis measured by invasive pressure volume loop analysis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P.C Seppelt ◽  
R De Rosa ◽  
S Mas-Peiro ◽  
I Murray ◽  
A.M Zeiher ◽  
...  
Keyword(s):  
Energy Efficiency ◽  
Aortic Valve ◽  
Aortic Stenosis ◽  
Severe Aortic Stenosis ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Loop Analysis ◽  
Transcatheter Aortic Valve ◽  
Aortic Valve Implantation ◽  
Valve Implantation

Abstract Introduction Transcatheter aortic valve implantation (TAVI) for a stenotic aortic valve reduces the ventricular to aortic gradient and is expected to improve diastolic and systolic left ventricular function over the long-term. However, information about the early hemodynamic changes are lacking. To address this open question, we performed invasive pressure volume loop analysis prior and immediately after TAVI. Methods Invasive left ventricular pressure volume loop analysis was performed in 8 patients with aortic stenosis (mean 81.3 years) prior and immediately after transfemoral TAVI (conductance catheter). Parameters for global hemodynamics, afterload, contractility and the interaction of the cardiovascular system were analyzed. Results After TAVI, left ventricular ejection fraction (53.9% vs. 44.8%, p=0.018) as well as parameters for myocardial contractility such as preload recruitable stroke work (68.5 vs. 44.8mmHg, p=0.012) and endsystolic elastance (3.55 vs. 2.17, p=0.036) declined significantly compared to baseline. As sign of impaired diastolic function, TAU, a preload-independent measure of isovolumic relaxation (37.3 vs. 41.8ms, p=0.018) and enddiastolic pressure (13.1 vs. 16.4mmHg, p=0.015) increased after valve implantation. Contrarily, decreased ventricular-arterial coupling indicated early improvements in global cardiovascular energy efficiency (1.40 vs. 0.97 p=0.036). Arterial elastance had a strong correlation with the number of conducted rapid ventricular pacings (Pearson correlation coefficient, 0.772, p=0.025). Conclusion Invasive left ventricular pressure volume loop analysis revealed impaired systolic and diastolic function in the early phase after TAVI in patients with severe aortic stenosis. Contrarily, decreased ventricular-arterial indicated early improvement of global cardiovascular energy efficiency. PV Loop pre and post TAVI Funding Acknowledgement Type of funding source: None

Reflex cardiovascular changes with veratridine in the conscious dog

1982 ◽  
Vol 242 (5) ◽  
pp. H810-H817 ◽  
Author(s):  
K. W. Barron ◽  
V. S. Bishop
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Left Ventricular Pressure ◽  
Peripheral Circulation ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Inotropic Response ◽  
Inotropic Effects ◽  
Conscious Dog ◽  
Renal Vascular

The present study was undertaken to examine the reflex responses of activation of cardiac sensory receptors in the conscious dog. Intracoronary (left circumflex coronary artery) injection of veratridine (0.10 micrograms/kg) reduced mean arterial pressure (-40 mmHg, P less than 0.05), heart rate (-34 beats/min, P less than 0.05), and maximum rate of rise of left ventricular pressure (LV dP/dtmax) (-419 mmHg/s, P less than 0.05). Bilateral cervical vagal cold block (BVB) eliminated the depressor and bradycardic responses of veratridine. BVB not only eliminated the negative inotropic response to veratridine but reversed it to a positive inotropic response (LV dP/dtmax increased 313 +/- 76 mmHg/s). Ganglionic blockade abolished all effects of veratridine. The bradycardia and negative inotropic effects caused by veratridine were attenuated by either atropine or metoprolol and completely eliminated by the combination of the two antagonists. Veratridine also produced a decrease in renal artery blood flow but had no effect on renal vascular resistance. In contrast, iliac blood flow was increased with veratridine, and this, combined with the depressor effect, resulted in a decrease in iliac vascular resistance (-37%), P less than 0.05). BVB abolished the changes in renal and iliac blood flow or resistance caused by veratridine. The results indicate that activation of cardiac receptors in the conscious dog elicits inhibitory reflexes to the heart and peripheral circulation that are mediated by vagal afferents. After vagotomy, veratridine elicited a reflex positive inotropic response, which may have resulted from activation of cardiac sympathetic afferent fibers.

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