Abstract 30: Incomplete Chest Recoil During Piglet CPR Worsens Hemodynamics

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mathias Zuercher ◽  
Ronald W Hilwig ◽  
Jon Nysaether ◽  
Vinay M Nadkarni ◽  
Marc D Berg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Parametric Data ◽  
Wilcoxon Rank Sum Test ◽  
The Right

Background : Incomplete chest recoil during cardiopulmonary resuscitation (CPR) (ie, leaning on the chest during the decompression phase) is purported to decrease venous return, and thereby decrease forward blood flow. Aim To determine the effect of 10% and 20% lean on hemodynamics during piglet CPR. Methods : 10 piglets (10.7±1.2 kg) were anesthetized with isoflurane and instrumented with micromanometer-tipped catheters in the right atrium (RA) and aorta (Ao). After induction of ventricular fibrillation, CPR was provided in three-minute epochs with no lean, 10% lean, or 20% lean while aortic systolic pressure (AoS) was targeted at 80–90 mmHg. Because the mean force to attain 80 –90 mm Hg AoS was 18 kg in preliminary studies, 10% and 20% lean were provided as 1.8 and 3.6 kg weights on the chest, respectively. Left ventricular myocardial blood flow (MBF) and cardiac index (CI) were determined by fluorescent, color-microsphere technique. Statistics: paired t -test and repeated measurement ANOVA for parametric, Wilcoxon Rank Sum Test and Friedman’s ANOVA for non-parametric data. Results : 10% and 20% lean resulted in higher right atrial diastolic pressure (RAD) and lower coronary perfusion pressure (CPP) than no lean. Hemodynamics were not different with 10% lean vs. 20% lean. Mean 10%–20% lean resulted in substantially lower MBF and CI than no lean (Table ). Conclusions : 10–20% leaning during CPR increases RAD, decreases CPP, and substantially decreases MBF and CI. Table

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.

Abstract 17334: The Detrimental Effect of Chest Compression Interruptions on Coronary Perfusion Pressure Dynamics

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Norman A Paradis ◽  
Karen L Moodie ◽  
Christopher L Kaufman ◽  
Joshua W Lampe
Keyword(s):  
Blood Flow ◽  
Chest Compression ◽  
Detrimental Effect ◽  
Perfusion Pressure ◽  
Vena Cava ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Over Time

Introduction: Guidelines for treatment of cardiac arrest recommend minimizing interruptions in chest compressions based on research indicating that interruptions compromise coronary perfusion pressure (CPP) and blood flow and reducing the likelihood of successful defibrillation. We investigated the dynamics of CPP before, during, and after compression interruptions and how they change over time. Methods: CPR was performed on domestic swine (~30 Kg) using standard physiological monitoring. Blood flow was measured in the abdominal aorta (AAo), the inferior vena cava, the right common carotid and external jugular. Ventricular fibrillation (VF) was electrically induced. Mechanical chest compressions (CC) were started after four minutes of VF. CC were delivered at a rate of 100 compressions per minute (cpm) and at a depth of 2” for a total of 12 min. CPP was calculated as the difference between aortic and right atrial pressure at end-diastole per Utstein guidelines. CPP was determined for 5 compressions prior to the interruption, every 2 seconds during the CC interruption, and for 7 compressions after the interruption. Per protocol, 12 interruptions occurred at randomized time points. Results: Across 12 minutes of CPR, averaged CPP prior to interruption was significantly greater than the averaged CPP after the interruption (22.4±1.0 vs. 15.5±0.73 mmHg). As CPR continued throughout the 12 minutes, CPP during compressions decreased (First 6 min = 24.1±1.4 vs. Last 6 min = 20.1±1.3 mmHg, p=0.05), but the effect of interruptions remained constant resulting in a 20% drop in CPP for every 2 seconds irrespective of the prior CPP. The increase (slope) of CPP after resumption of compressions was significantly reduced over time (First 6 min = 1.47±0.18 vs. Last 6 min = 0.82±0.13 mmHg/compression). Conclusions: Chest compression interruptions have a detrimental effect on coronary perfusion and blood flow. The magnitude of this effect increases over time as a resuscitation effort continues. These data confirm the importance of providing uninterrupted CPR particularly in long duration resuscitations.

Abstract 289: Effect of Elevated Legs on Hemodynamic Performance During Cardiopulmonary Resuscitation in a Porcine Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eric Qvigstad ◽  
Andres Neset ◽  
Theresa M Olasveengen ◽  
øystein Tømte ◽  
Morten Eriksen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Supine Position ◽  
Life Support ◽  
Advanced Life Support ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Positive Pressure ◽  
Coronary Perfusion ◽  
End Tidal

Purpose of the study: During advanced life support (ALS) end-tidal carbon dioxide (EtCO 2 ) reflects cardiac output (CO). A recent clinical study found an association between passive leg raising (PLR) and increased EtCO 2 during ALS. This may reflect a transient increase in pulmonary blood flow and CO, but might cause a detrimental decrease in coronary perfusion pressure (CPP). We evaluated the effect of PLR during experimental ALS in a randomized, factorial design. Materials and methods: In nine anesthetized domestic pigs (30±1.8 kg) ventricular fibrillation was induced electrically. After 3 minutes of no-flow, mechanical chest compressions (5cm @ 100 min -1 ) were started. During four 5-minute segments of CPR we measured CO, EtCO 2 , perfusion pressures, carotid and cerebral cortical microcirculatory blood flow (MBF) and CPP (the average of the positive pressure difference between decompression aortic pressure (AP) and right atrial pressure (RAP)) at minute 2 and 4. Interventions were provided in a randomized sequence with PLR vs supine position, with or without epinephrine (0.5mg iv). Values are given as mean±standard deviation. Results: PLR did not increase EtCO2 compared to supine position (3.1±0.7 vs 3.0±0.8 kPa), but CO was minimally increased from 1.1±0.3 to 1.2±0.3 Lmin -1 ,(p=0.003). PLR did not significantly increase AP (57±15 vs. 48±18 mmHg, p=0.3), but RAP was higher (43±10 vs. 31±7, p=0.003). However, no difference was found in CPP due to marked variation in both groups (median(range): PLR 20 (9,43) and supine 17(9,58)). The effect of epinephrine during this experimental setup was minimal. Conclusion: We did not find a positive effect of PLR during experimental ALS, but there were no obviously detrimental effects either.

Activation of PKC decreases myocardial O2consumption and increases contractile efficiency in rats

2001 ◽  
Vol 281 (5) ◽  
pp. H2191-H2197 ◽  
Author(s):  
Teruo Noguchi ◽  
Zengyi Chen ◽  
Stephen P. Bell ◽  
Lori Nyland ◽  
Martin M. LeWinter
Keyword(s):  
Perfusion Pressure ◽  
Diastolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Regulatory Proteins ◽  
Basal Metabolism ◽  
Coronary Perfusion ◽  
Kinase C ◽  
Rat Hearts ◽  
Pkc Activation

The effect of protein kinase C (PKC) activation on cardiac mechanoenergetics is not fully understood. To address this issue, we determined the effects of the PKC activator phorbol 12-myristate 13-acetate (PMA) on isolated rat hearts. Hearts were exposed to PMA with or without pretreatment with the PKC inhibitor chelerythrine. Contractile efficiency was assessed as the reciprocal of the slope of the linear myocardial O2consumption (V˙o 2) pressure-volume area (PVA) relation. PMA decreased contractility ( E max; −30 ± 8%; P < 0.05) and increased coronary perfusion pressure (+58 ± 11%; P < 0.01) without altering left ventricular end-diastolic pressure. Concomitantly, PMA decreased PVA-independentV˙o 2 [nonmechanical energy expenditure for excitation-contraction (E-C) coupling and basal metabolism] by 28 ± 8% ( P < 0.05) and markedly increased contractile efficiency (+41 ± 8%; P < 0.05) in a manner independent of the coronary vascular resistance. Basal metabolism was not affected by PMA. Chelerythrine abolished the PMA-induced vasoconstriction, negative inotropy, decreased PVA-independent V˙o 2, and increased contractile efficiency. We conclude that PKC-mediated phosphorylation of regulatory proteins reduces V˙o 2 via effects on both the contractile machinery and the E-C coupling.

Effects of intensive exercise training on myocardial performance and coronary blood flow

1980 ◽  
Vol 49 (3) ◽  
pp. 444-449 ◽  
Author(s):  
R. J. Barnard ◽  
H. W. Duncan ◽  
K. M. Baldwin ◽  
G. Grimditch ◽  
G. D. Buckberg
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Work Capacity ◽  
Left Ventricular ◽  
Maximum Exercise ◽  
Time Index ◽  
Significant Difference ◽  
Tension Time

Five instrumented and eight noninstrumented dogs were progressively trained for 12-18 wk on a motor-driven treadmill. Data were compared with 14 instrumented and 8 noninstrumented control dogs. Gastrocnemius malate dehydrogenase activity was significantly increased in the trained dogs (887 +/- 75 vs. 667 +/- 68 mumol . g-1 . min-1). The trained dogs also showed significant increases in maximum work capacity, cardiac output (7.1 +/- 0.5 vs. 9.1 +/- 0.7 1/min), stroke volume (25.9 +/- 2.0 vs. 32.0 +/- 2.0 ml/beat), and left ventricular (LV) positive dP/dtmax (9,242 +/- 405 vs. 11,125 +/- 550 Torr/s). Negative dP/dtmax was not significantly different. Peak LV systolic pressure increased with exercise, but there was no significant difference between the trained and control dogs. LV end-diastolic pressure did not change with exercise and was the same in both groups. Tension-time index was lower in the trained dogs at rest and submaximum exercise (9.7 km/h, 10%) but was not different at maximum exercise. Diastolic pressure-time index was significantly higher in the trained dogs at rest and during submaximum exercise but was not different at maximum exercise. LV coronary blood flow was significantly reduced at rest (84 +/- 4 vs. 67 +/- 6 mo . min-1 . 100 g-1) and during submaximum exercise (288 +/- 24 vs. 252 +/- 8 ml . min-1 . 100 g-1). During maximum exercise flow was not significantly different (401 +/- 22 vs. 432 +/- 11 ml . min-1 . 100 g-1) between the control and trained groups. The maximum potential for subendocardial flow was unchanged with training despite the development of mild hypertrophy.

Arterial pressure-flow relations in the awake standing dog

1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rate Increase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Heart Rate Increase ◽  
Underlying Mechanisms ◽  
The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

Influence of coronary perfusion and myocardial edema on pressure-volume diagram of left ventricle

1961 ◽  
Vol 201 (1) ◽  
pp. 102-108 ◽  
Author(s):  
Cecil E. Cross ◽  
P. Andre Rieben ◽  
Peter F. Salisbury
Keyword(s):  
Diastolic Pressure ◽  
Myocardial Edema ◽  
Ventricular Volume ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Similar Degree ◽  
Coronary Perfusion ◽  
Fluid Accumulation ◽  
Tension Development ◽  
Isolated Hearts

Pressure-volume diagrams of paced, isolated hearts were derived from isovolumic contractions and auxotonic contractions (simultaneous changes of pressure and volume). Coronary perfusion, fluid accumulation in heart muscle, and left ventricular volume and pressure were measured and controlled. Pressure-volume diagrams from isovolumic and auxotonic contractions were virtually identical in the same heart and were influenced by the same factors to a similar degree. At equal diastolic volumes the magnitude of systolic, as well as of diastolic pressures, and the occurrence of a systolic descending limb were directly related to coronary perfusion pressure. At equal diastolic volumes, other factors being constant, myocardial edema did not influence the contractile strength (i.e., maximum contractile tension development) of a ventricle, but did decrease its distensibility (i.e., increase diastolic pressure) in proportion to fluid accumulation. Myocardial water content and coronary factors (coronary arterial and venous pressures, coronary blood volume and flow) therefore constitute intrinsic mechanisms which can regulate the performance of a ventricle by changing its contractile strength, its distensibility, or both. The effects of coronary factors and of myocardial edema on the distensibility of a ventricle are sufficient in magnitude to explain hemodynamic abnormalities which characterize certain types of congestive heart failure.

scholarly journals Novel Neuromodulation Approach to Improve Left Ventricular Contractility in Heart Failure

2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Vivek Y. Reddy ◽  
Jan Petrů ◽  
Filip Málek ◽  
Lee Stylos ◽  
Steve Goedeke ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Diastolic Pressure ◽  
Acute Decompensated Heart Failure ◽  
Systolic Pressure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Right Pulmonary Artery ◽  
The Right

Background: Morbidity and mortality outcomes for patients admitted for acute decompensated heart failure are poor and have not significantly changed in decades. Current therapies are focused on symptom relief by addressing signs and symptoms of congestion. The objective of this study was to test a novel neuromodulation therapy of stimulation of epicardial cardiac nerves passing along the posterior surface of the right pulmonary artery. Methods: Fifteen subjects admitted for defibrillator implantation and ejection fraction ≤35% on standard heart failure medications were enrolled. Through femoral arterial access, high fidelity pressure catheters were placed in the left ventricle and aortic root. After electro anatomic rendering of the pulmonary artery and branches, either a circular or basket electrophysiology catheter was placed in the right pulmonary artery to allow electrical intravascular stimulation at 20 Hz, 4 ms pulse width, and ≤20 mA. Changes in maximum positive dP/dt (dP/dt Max ) indicated changes in ventricular contractility. Results: Of 15 enrolled subjects, 5 were not studied due to equipment failure or abnormal pulmonary arterial anatomy. In the remaining subjects, dP/dt Max increased significantly by 22.6%. There was also a significant increase in maximum negative dP/dt (dP/dt Min ), mean arterial pressure, systolic pressure, diastolic pressure, and left ventricular systolic pressure. There was no significant change in heart rate or left ventricular diastolic pressure. Conclusions: In this first-in-human study, we demonstrated that in humans with stable heart failure, left ventricular contractility could be accentuated without an increase in heart rate or left ventricular filling pressures. This benign increase in contractility may benefit patients admitted for acute decompensated heart failure.

Transmural distribution of blood flow during activation of coronary muscarinic receptors

1981 ◽  
Vol 240 (6) ◽  
pp. H941-H946 ◽  
Author(s):  
G. J. Gross ◽  
J. D. Buck ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Muscarinic Receptors ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Tissue Blood Flow ◽  
Coronary Perfusion ◽  
Coronary Vasodilator ◽  
Blood Flow Ratio

The role of coronary muscarinic receptors in the distribution of transmural blood flow across the left ventricular wall of the working heart was studied in anesthetized open-chest dogs. Tissue blood flow in subepicardium, midmyocardium, and subendocardium was determined with radioactive microspheres before and during activation of muscarinic vasodilator receptors by intracoronary infusions of acetylcholine. Myocardial and coronary vascular beta-receptors were blocked by sotalol (2.0 mg/kg iv). Equivalent submaximal coronary vasodilator doses of acetylcholine and adenosine were compared for effects on transmural blood flow. Intracoronary infusions of acetylcholine (5.0 and 10.7 micrograms/min) produced a dose-related increase in the subendocardial-subepicardial blood flow ratio (endo/epi) from 1.07 to 1.32 and 1.57, respectively. A progressively larger decrease in coronary vascular resistance occurred in the subendocardium than midmyocardium or subepicardium following acetylcholine administration. In contrast, intracoronary administration of adenosine (54.4 micrograms/min) produced no change in endo/epi. Atropine effectively blocked acetylcholine-induced coronary vasodilation but not vasodilation produced by adenosine. Neither agent affected heart rate, left ventricular pressure, coronary perfusion pressure, or myocardial contractility. These results suggest that activation of muscarinic coronary vasodilator receptors redistributes blood flow preferentially to the subendocardium independent of cardiac mechanical influences.

Effect of ischemic zone size on nonischemic zone function

1990 ◽  
Vol 258 (6) ◽  
pp. H1786-H1795 ◽  
Author(s):  
T. Aversano ◽  
P. N. Marino
Keyword(s):  
Systolic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Acute Ischemia ◽  
Coronary Perfusion ◽  
Zone Size ◽  
Reduced Pressure ◽  
Systolic Performance ◽  
Shortening Deactivation

To study the influence of ischemic zone size on function in nonischemic regions, wall thickening and the end-systolic pressure-thickness (ESPTR) relationship were measured before and during a 90-s coronary occlusion, which produced either a small or large (24 or 35% of left ventricular mass) area of ischemia. With both size ischemic areas, nonischemic zone isovolumic and ejection phase wall thickening increased during occlusion, primarily because of increased preload and, to a lesser extent, a reduced pressure component of afterload. The nonischemic region ESPTR was unchanged from preocclusion control with small ischemic mass. With larger ischemic mass, the nonischemic region ESPTR was shifted downward and to the left, indicating reduced end-systolic performance. The decline in the nonischemic zone ESPTR with large ischemic zone size was not due to reduced blood flow, shortening deactivation, reflex effects, or "tethering" but rather to the associated decline in coronary perfusion pressure. Thus the increase of nonischemic region wall thickening during acute ischemia is due to a change in ventricular loading conditions and not augmentation of contractile performance. Larger ischemic zone size can impair function in nonischemic myocardium by reducing the erectile component of end-systolic performance.

Sign in / Sign up

Export Citation Format

Share Document