ECG-synchronized thoracic vest inflation during autonomic blockade, myocardial ischemia, or cardiac arrest

1992 ◽  
Vol 73 (6) ◽  
pp. 2263-2273 ◽  
Author(s):  
J. Peters ◽  
P. Ihle
Keyword(s):  
Cardiac Arrest ◽  
Myocardial Ischemia ◽  
Stroke Volume ◽  
Coronary Occlusion ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Pleural Pressure ◽  
Beta Blockade ◽  
Autonomic Blockade ◽  
Late Systole

To evaluate, in the absence of lung inflation, the cardiovascular effects of single and repetitive pleural pressure increments induced by thoracic vest inflations and timed to occur during specific portions of the cardiac cycle, seven chronically instrumented dogs were studied. Reflexes and left ventricular (LV) performance were varied by autonomic blockade, circumflex coronary occlusion (with and without beta-blockade), or cardiac arrest. Single late systolic, but not early systolic, vest inflations significantly increased LV stroke volume both before (+12.4%) and after myocardial depression by coronary occlusion+beta-blockade (+18.5%) when performed after a period of apnea to control preload and rate. During vest inflations, LV and aortic pressures increased to a greater degree than esophageal pressure (by 51 vs. 39 mmHg, P = 0.0001). Lung inflations (26 trials in 3 dogs) during early or late systole failed to increase stroke volume, despite peak esophageal pressures of 11–26 mmHg. With autonomic reflexes intact, repetitive vest inflations coupled to early systole, late systole, or diastole induced a large (40%) but unspecific systemic flow increase. In contrast, during autonomic blockade, flow increased slightly (7.5%, P < 0.05) with late systolic compared with diastolic inflations but not relative to baseline. During coronary occlusion (with or without beta-blockade), no cycle-specific differences were seen, whereas matched vest inflations during cardiac arrest generated 20–30% of normal systemic flow. Thus only single late systolic thoracic vest inflations associated with large increments in pleural pressure increased LV emptying, presumably by decreasing LV afterload and/or focal cardiac compression. However, during myocardial ischemia and depression, coupling of vest inflation to specific parts of the cardiac cycle revealed no hemodynamic improvement, suggesting that benefits of this circulatory assist method, if any, are minor and may be restricted to conditions of cardiac arrest.

scholarly journals Early detection of acute transmural myocardial ischemia by the phasic systolic-diastolic changes of local tissue electrical impedance

2016 ◽  
Vol 310 (3) ◽  
pp. H436-H443 ◽  
Author(s):  
Esther Jorge ◽  
Gerard Amorós-Figueras ◽  
Tomás García-Sánchez ◽  
Ramón Bragós ◽  
Javier Rosell-Ferrer ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Electrical Impedance ◽  
Coronary Occlusion ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Mechanical Activity ◽  
Aortic Blood Flow ◽  
Resistivity Curve ◽  
Acute Coronary Occlusion ◽  
The Mean

Myocardial electrical impedance is influenced by the mechanical activity of the heart. Therefore, the ischemia-induced mechanical dysfunction may cause specific changes in the systolic-diastolic pattern of myocardial impedance, but this is not known. This study aimed to analyze the phasic changes of myocardial resistivity in normal and ischemic conditions. Myocardial resistivity was measured continuously during the cardiac cycle using 26 different simultaneous excitation frequencies (1 kHz–1 MHz) in 7 anesthetized open-chest pigs. Animals were submitted to 30 min regional ischemia by acute left anterior descending coronary artery occlusion. The electrocardiogram, left ventricular (LV) pressure, LV dP/d t, and aortic blood flow were recorded simultaneously. Baseline myocardial resistivity depicted a phasic pattern during the cardiac cycle with higher values at the preejection period (4.19 ± 1.09% increase above the mean, P < 0.001) and lower values during relaxation phase (5.01 ± 0.85% below the mean, P < 0.001). Acute coronary occlusion induced two effects on the phasic resistivity curve: 1) a prompt (5 min ischemia) holosystolic resistivity rise leading to a bell-shaped waveform and to a reduction of the area under the LV pressure-impedance curve (1,427 ± 335 vs. 757 ± 266 Ω·cm·mmHg, P < 0.01, 41 kHz) and 2) a subsequent (5–10 min ischemia) progressive mean resistivity rise (325 ± 23 vs. 438 ± 37 Ω·cm at 30 min, P < 0.01, 1 kHz). The structural and mechanical myocardial dysfunction induced by acute coronary occlusion can be recognized by specific changes in the systolic-diastolic myocardial resistivity curve. Therefore these changes may become a new indicator (surrogate) of evolving acute myocardial ischemia.

scholarly journals Pulseless Electrical Activity as the Initial Cardiac Arrest Rhythm: Importance of Preexisting Left Ventricular Function

2021 ◽  
Author(s):  
Daniel I. Ambinder ◽  
Kaustubha D. Patil ◽  
Hikmet Kadioglu ◽  
Pace S. Wetstein ◽  
Richard S. Tunin ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Left Ventricular Dysfunction ◽  
Coronary Occlusion ◽  
Ventricular Dysfunction ◽  
Pulseless Electrical Activity ◽  
Left Ventricular ◽  
Severe Left Ventricular Dysfunction ◽  
Acute Coronary Occlusion ◽  
Coronary Ischemia

Background Pulseless electrical activity (PEA) is a common initial rhythm in cardiac arrest. A substantial number of PEA arrests are caused by coronary ischemia in the setting of acute coronary occlusion, but the underlying mechanism is not well understood. We hypothesized that the initial rhythm in patients with acute coronary occlusion is more likely to be PEA than ventricular fibrillation in those with prearrest severe left ventricular dysfunction. Methods and Results We studied the initial cardiac arrest rhythm induced by acute left anterior descending coronary occlusion in swine without and with preexisting severe left ventricular dysfunction induced by prior infarcts in non–left anterior descending coronary territories. Balloon occlusion resulted in ventricular fibrillation in 18 of 34 naïve animals, occurring 23.5±9.0 minutes following occlusion, and PEA in 1 animal. However, all 18 animals with severe prearrest left ventricular dysfunction (ejection fraction 15±5%) developed PEA 1.7±1.1 minutes after occlusion. Conclusions Acute coronary ischemia in the setting of severe left ventricular dysfunction produces PEA because of acute pump failure, which occurs almost immediately after coronary occlusion. After the onset of coronary ischemia, PEA occurred significantly earlier than ventricular fibrillation (<2 minutes versus 20 minutes). These findings support the notion that patients with baseline left ventricular dysfunction and suspected coronary disease who develop PEA should be evaluated for acute coronary occlusion.

Hemodynamic effects of cardiac cycle-specific increases in intrathoracic pressure

1986 ◽  
Vol 60 (2) ◽  
pp. 604-612 ◽  
Author(s):  
M. R. Pinsky ◽  
G. M. Matuschak ◽  
L. Bernardi ◽  
M. Klain
Keyword(s):  
Stroke Volume ◽  
Cardiac Cycle ◽  
Intrathoracic Pressure ◽  
Canine Model ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Cardiac Performance ◽  
Hemodynamic Effects ◽  
Volume Measurements ◽  
Systemic Venous Return

Changes in intrathoracic pressure (ITP) can influence cardiac performance by affecting ventricular loading conditions. Because both systemic venous return and factors determining left ventricular (LV) ejection may vary over the cardiac cycle, phasic increases in ITP may differentially affect preload or afterload if delivered at specific points within the cardiac cycle. We studied the hemodynamic effects of cardiac cycle-specific increases in ITP (pulses) delivered by a high-frequency jet ventilator in an acute closed-chested canine model (n = 11), using electromagnetic flow probes to measure biventricular stroke volume. Measurements were taken during a control condition after the induction of acute ventricular failure (AVF) by propranolol hydrochloride and volume infusion. ITP was independently varied without changing lung volume by the inflation of thoracoabdominal binders. Although synchronous pulses had minimal hemodynamic effects in unbound controls, binding pulses timed to occur in early diastole resulted in decreases in LV filling pressure and left ventricular stroke volume (SVlv) (P less than 0.05). In the AVF condition, pulses increased LV performance, evidenced by increases in SVlv (P less than 0.01), despite decreases in LV filling pressure (P less than 0.05). This effect is maximized by binding and by timing the pulses to occur in systole. We conclude that cardiac cycle-specific increases in ITP can significantly affect cardiac performance. These effects appear to be related to the ability of such timed pulses to selectively affect LV preload and afterload.

Reduced stroke volume related to pleural pressure in obstructive sleep apnea

1983 ◽  
Vol 55 (6) ◽  
pp. 1718-1724 ◽  
Author(s):  
F. A. Tolle ◽  
W. V. Judy ◽  
P. L. Yu ◽  
O. N. Markand
Keyword(s):  
Obstructive Sleep Apnea ◽  
Cardiac Output ◽  
Sleep Apnea ◽  
Stroke Volume ◽  
Human Subjects ◽  
Left Ventricular ◽  
Pleural Pressure ◽  
Impedance Method ◽  
Similar Reduction ◽  
Obstructive Sleep

Left ventricular stroke volume (LVSV) falls during obstructed inspiration in animals and normal human subjects through mechanisms that may be closely related to pleural pressure. In this study we postulated that a similar reduction in LVSV should occur in patients with obstructive sleep apnea (OSA). Daytime polysomnograms were performed in 10 patients with OSA. A noninvasive electrical impedance method was used to determine LVSV. Pleural pressure was measured by esophageal balloon. In comparison with awake values, during OSA we found reductions in LVSV, cardiac output, and heart rate of 18, 27, and 11%, respectively (P less than 0.01). We observed that systolic pleural pressure did not have a significant effect on LVSV (P greater than 0.05). However, at pleural pressures lower than 10 cmH2O below resting expiratory level, there was a linear relationship between falls in LVSV and falls in middiastolic pleural pressure (P less than 0.0001). We concluded that reduced LVSV shown in patients with OSA was significantly related to diastolic pleural pressure level. Our findings suggested reduced preload as the most likely mechanism for decreased cardiac output in OSA.

Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia

2006 ◽  
Vol 101 (4) ◽  
pp. 1091-1096 ◽  
Author(s):  
Xiangshao Fang ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Lei Huang ◽  
Yun-Te Chang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Cardiopulmonary Resuscitation ◽  
Myocardial Ischemia ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Chronic Myocardial Ischemia

Our group has developed a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. Left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 wk postsurgery. Coronary constriction provoked significant decreases in ejection fraction, increases in left ventricular end-diastolic volume, and increases left ventricular end-systolic volume at 4 wk postintervention, just before induction of ventricular fibrillation (VF). After 6 min of untreated VF, CPR was initiated on three groups: 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by rate of left ventricular pressure increase at 40 mmHg and the rate of left ventricular pressure decline was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. There were no differences in the total shock energy required for successful resuscitation and duration of survival among the groups. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 wk postintervention and subsequently with severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.

Conductance catheter measurement of left ventricular volume: evidence for nonlinearity within cardiac cycle

1995 ◽  
Vol 268 (4) ◽  
pp. H1490-H1498 ◽  
Author(s):  
R. S. Szwarc ◽  
D. Laurent ◽  
P. R. Allegrini ◽  
H. A. Ball
Keyword(s):  
Stroke Volume ◽  
Cardiac Cycle ◽  
Time Derivative ◽  
Reference Method ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Conductance Catheter ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

The conductance catheter gain factor, alpha, is usually determined by an independent measure of stroke volume and, as such, is assumed to be constant. However, nonlinearity of the conductance-volume relation has been proposed on theoretical grounds. The present study was designed to establish the extent of nonlinearity, or variability of alpha, within the cardiac cycle using magnetic resonance imaging (MRI) as the reference method. Pentobarbital-anesthetized minipigs (n = 10, 10–13 kg) were instrumented with left ventricular (LV) conductance and Millar catheters. Conductance catheter signals were recorded, and volumes were corrected for parallel conductance using a saline-dilution technique. Animals were then placed in a 4.7-T magnet, and first time derivative of LV pressure-gated transverse MRI images (5-mm slices) acquired during isovolumic contraction (end diastole) and relaxation (end systole). LV cavity volumes were then determined using a third-order polynomial model. The gain alpha was computed three ways: by dividing conductance stroke volume by MRI stroke volume (alpha SV), by dividing conductance end-diastolic volume by MRI end-diastolic volume (alpha ED), and by dividing conductance end-systolic volume by MRI end-systolic volume (alpha ES). alpha SV was 0.62 +/- 0.15, with alpha ED (0.71 +/- 0.17) significantly lower than alpha ES (0.81 +/- 0.21; P < 0.001). Using alpha SV to adjust conductance gain (i.e., assuming constant gain) resulted in a significantly larger end-diastolic volume (25.8 +/- 4.6 ml) and smaller ejection fraction (46.8 +/- 7.2%) than those obtained with MRI (23.0 +/- 4.1 ml and 53.1 +/- 7.3%, respectively; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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