Abstract 149: Role of Pre and Intra-Arrest Hemodynamics in Evolution of the Ventricular Fibrillation Electrocardiogram Waveform

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Caelie E Kern ◽  
David D Salcido
Keyword(s):  
Ventricular Fibrillation ◽  
Trajectory Analysis ◽  
Venous Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Pressure Transducers ◽  
Surface Ecg ◽  
Electrical Induction

Purpose: Quantitative waveform measures (QWM) of the ventricular fibrillation (VF) waveform have been shown in laboratory and clinical studies to be predictive of return of spontaneous circulation (ROSC) and survival to hospital discharge. During resuscitation, QWM are responsive to hemodynamic changes resulting from CPR. It is not known whether the trajectory of QWM are affected by pre-arrest hemodynamics or intra-arrest arterio-venous pressure equilibration. We sought to investigate the role of hemodynamics on the evolution of VF before and during prolonged VF. Methods: We pooled data from six previous porcine experiments. Each modeled prolonged VF and included electrical induction of VF which was left untreated for up to 10 minutes, followed by attempted resuscitation. All animals were instrumented with pressure transducers (Millar, MikroTip) placed via femoral cutdown in the aorta and right atrium, as well as Lead II surface ECG. Signals were recorded continuously at 1000Hz with a data acquisition unit (PowerLab, ADInstruments). Mean baseline central arterial (CAP) and central venous pressure (CVP) were calculated from 1- minute of immediate pre-VF pressure traces. Coronary perfusion pressure (CPP) during untreated VF was calculated as the continuous difference between the CAP and CVP channels. Median slope (MS), a QWM, was calculated in 1-second windows and interpolated to the full length of the intra-arrest ECG. For trajectory analysis, CPP and MS traces were normalized on a 0-1 scale and grouped by morphological similarity. Pearson’s Correlation coefficient was calculated between corresponding CPP and MS traces. Results: A total of 141 experiments were included in the analysis. Overall mean (SD) correlation between CPP and MS was 0.56 (0.29). CPP-MS correlation strength did not correlate with baseline pressures. However, trajectory analysis revealed multiple patterns of hemodynamic and QWM evolution through untreated VF, with the most well-defined (mean coeff. = 0.58) indicating a shared bimodality temporally offset between CPP and MS. Conclusions: Hemodynamics during untreated VF show some correlation with the trajectory of QWM of the VF signal. More work is needed to understand the mechanism of this relationship.

Abstract 2225: A Blinded, Randomized Controlled Evaluation Of An Impedance Threshold Device During Cardiopulmonary Resuscitation In Swine

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Timothy J Mader ◽  
Adam Kellogg ◽  
Jeremy Smith ◽  
Brett Murphy ◽  
Rachael Hynds-Decoteau ◽  
...  
Keyword(s):  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Continuous Variables ◽  
Active Device ◽  
Exact Test ◽  
Threshold Device ◽  
Baseline Characteristics ◽  
Controlled Evaluation ◽  
Impedance Threshold Device

Background: An impedance threshold device (ITD) has been designed to enhance circulation during CPR. A recent study suggests that the ITD does not improve hemodynamics and that it may worsen outcomes. We sought to determine, in a blinded fashion, the effect of the ITD on coronary perfusion pressure (CPP), passive ventilation (paO2 & paCO2), and return of spontaneous circulation (ROSC), in a porcine model of prolonged ventricular fibrillation (VF). We hypothesized that, when compared to sham, the active device would have no significant impact on these variables. Methods: Thirty devices (15 active/15 sham) were purchased from the Resuscitation Outcomes Consortium. Thirty male Yorkshire swine were instrumented under anesthesia. VF was electrically induced. After 8” of untreated VF, baseline characteristics were documented and CPR was begun (chest compressions rate 100/minute and ventilations at a ratio of 30:2). The device used on a given animal (active or sham) was randomly assigned. After 3 cycles of basic CPR, a second ABG was drawn and a drug cocktail was given followed by 6 CPR cycles. We recorded CPP continuously. The first 150J rescue shock (RS) was delivered after 9 complete cycles (3 minutes) of CPR. A third ABG was drawn just prior to the first RS. ROSC was defined as systolic blood pressure >80 mmHg for >60s continuously. The randomization code was revealed once preliminary data analysis was completed. Group comparisons were assessed using descriptive statistics, Student’s t -test for continuous variables and Fisher’s Exact Test for dichotomous variables. Proportions with 95% confidence intervals were calculated for the rate of ROSC. Results: Baseline characteristics between the two groups were the same. ROSC occurred in 14/15 animals in both active and sham. The table summarizes the results (mean) by group after each event/intervention (CPP in mmHg, paO2 & paCO2 in torr). Conclusions: Use of the active device had no impact on CPP, paO2 & paCO2 or ROSC compared to sham.

Abstract P22: An Impedance Threshold Device Combined with an Automated Active Compression Decompression CPR Device (LUCAS) Improves the Chances For Survival in Pigs in Cardiac Arrest

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Timothy R Matsuura ◽  
Scott H McKnite ◽  
Anja K Metzger ◽  
Demetris Yannopoulos ◽  
Tom P Aufderheide ◽  
...  
Keyword(s):  
Venous Blood ◽  
Blood Gases ◽  
Intrathoracic Pressure ◽  
Organ Damage ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Adverse Outcomes ◽  
Coronary Perfusion ◽  
Threshold Device ◽  
Impedance Threshold Device

Background: By lowering intrathoracic pressure during the chest recoil phase of CPR, the impedance threshold device (ITD) increases circulation and the rate of return of spontaneous circulation (ROSC). This study evaluated the ITD combined with a new automated CPR device, the US version of the LUCAS, that compresses the chest and then pulls upwards with a 3 lb force. Methods and Results: After 6 min of untreated ventricular fibrillation, anesthetized female pigs (40.0±0.7 kg) were randomized to 6 min of CPR (100 compressions/min with LUCAS and ventilation: 1.0 FiO2, tidal volume of 10ml/kg, rate 12/min) with an active (−10 cm H2O resistance) (n=12) or sham ITD (n=12), and then shocked once with 120 joules of direct current. Epinephrine (0.04 mg/kg) and more CPR and shocks were used if ROSC was not achieved. Results (in mmHg) after 6 min of CPR with an active vs. sham ITD were: coronary perfusion pressure (PP) 20.8±1.2 vs. 21.0±0.9 (p=0.94); cerebral PP 8.8±1.0 vs. 10.0±0.9 (p=0.62); and end tidal CO2 38.1±1.5 and 37.1±1.3 (p=0.61). Peak and mean carotid artery blood flow (ml/min) was 323.9±15.2 vs. 256.6±21.1 (p=0.17) and 95.3±5.4 vs. 77.0±6.0 (p=0.22) with an active vs. sham ITD, respectively. Mean endotracheal pressures (mmHg) during chest recoil with an active vs. sham ITD were −2.0±0.5 vs. −0.2±0.2 (p<0.01). Arterial and venous blood gases were similar after 6 min of CPR between groups. ROSC, the primary survival endpoint for comparing the active vs. sham ITD, was 7/12 vs. 2/12 after 1 shock (p= 0.09), 12/12 vs. 5/12 after 2 shocks (p<0.01), and 12/12 vs. 7/12 after 3 shocks (p=0.04). With up to 14 shocks, 10/12 sham animals had a ROSC. All animals with ROSC lived for 30 min. There was no evidence of pulmonary edema or organ damage on autopsy with either ITD. Conclusions: After 6 min of CPR, LUCAS and active ITD resulted in lower mean airway pressures during chest recoil versus controls but hemodynamic findings were similar. However, ROSC was significantly easier to achieve with an active ITD; with up to 3 shocks twice as many animals were resuscitated with an active ITD. This benefit is most likely explained by carotid blood flows that trended higher with the active ITD. These positive findings and lack of any adverse outcomes support the safety and efficacy of this device combination.

Abstract 167: Epinephrine Plus Chest Compressions May Be Superior to Epinephrine Alone in a Hypoxia-Induced Porcine Model of Lifeless Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Felipe Teran ◽  
Claire Centeno ◽  
Alex L Lindqwister ◽  
William J Hunckler ◽  
William Landis ◽  
...  
Keyword(s):  
Chest Compression ◽  
Porcine Model ◽  
Contractile Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Swine Model ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Fraction Of Inspired Oxygen ◽  
External Chest Compressions

Background: Lifeless shock (LS) (previously called EMD and pseudo-PEA) is a global hypotensive ischemic state with retained coordinated myocardial contractile activity and an organized ECG. We have previously described our hypoxic LS model. The role of standard external chest compressions remains unclear in the setting of LS and its associated intrinsic hemodynamics. Although it is known the patients with LS have better prognosis compared to PEA, it is unclear what is the best treatment strategy. Prior work has shown that chest compressions (CC) when synchronized with native systole results in significant hemodynamic improvement, most notably coronary perfusion pressure (CPP), and hence it is plausible that standard dyssynchronous CC may be detrimental to hemodynamics. Furthermore, retrospective clinical data has shown that LS patients treated with vasopressors and no CC, may have better outcomes. We compared epinephrine only versus epinephrine and chest compression, in a porcine model of LS. Methods: Our porcine model of hypoxic LS has previously been described. We randomized pigs to episodes of LS treated with epinephrine only (control) (0.0015 mg/kg) versus epinephrine plus standard external chest compressions (intervention). Animals were endotracheally intubated and mechanically ventilated, and the fraction of inspired oxygen (FiO 2 ) was gradually lowered from room air (20-30% O 2 ) to a target FiO 2 of 3-7% O 2 . This target FiO 2 was maintained until the systolic blood pressure (SBP) dropped to 30 mmHg for 30 seconds, or the animal became bradycardic (HR less than 40), which was defined as the start of LS. FiO 2 was then raised to 100%, and then animal would receive control or intervention. Return of spontaneous circulation (ROSC) was defined as SBP 60 mmHg, stable after 2 minutes. Results: Twenty-six episodes of LS in 11 animals received epinephrine only control and 21 episodes the epinephrine plus chest compression intervention. The rates of ROSC in two minutes or less were 5/26 (19%) in the control arm vs 14/21 (67%) in the intervention arm (P=0.001;95% CI 19.7 %-67.2%). Conclusions: In a swine model of hypoxia induced LS, epinephrine plus CPR may be superior to epinephrine alone.

Cardiac Arrest and Resuscitation

2015 ◽  
Author(s):  
Charles N. Pozner ◽  
Jennifer L Martindale
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Arrhythmias ◽  
Perfusion Pressure ◽  
Pulseless Electrical Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Cardiac Resuscitation ◽  
Neurologic Function

The most effective treatment for cardiac arrest is the administration of high-quality chest compressions and early defibrillation; once spontaneous circulation is restored, post–cardiac arrest care is essential to support full return of neurologic function. This review summarizes the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of cardiac arrest and resuscitation. Figures show the foundations of cardiac resuscitation, ventricular arrhythmias, coronary perfusion pressure as a function of time, an algorithm for initial treatment of cardiac arrest, sample capnographs, and the electrocardiographic appearance of varying degrees of hyperkalemia. Tables include components of suboptimal cardiac resuscitation and corrective actions, recommended doses of medications commonly used in cardiac resuscitation, causes of pulseless electrical activity/asystolic arrest to consider, immediate post–return of spontaneous circulation checklist, and resuscitation goals during post–cardiac arrest care. This review contains 6 highly rendered figures, 5 tables, and 142 references.

Downregulation of ventricular contractile function during early ischemia is flow but not pressure dependent

1998 ◽  
Vol 275 (5) ◽  
pp. H1520-H1523 ◽  
Author(s):  
Miao-Xiang He ◽  
H. Fred Downey
Keyword(s):  
Coronary Artery ◽  
Perfusion Pressure ◽  
Contractile Function ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Rat Hearts ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
Artery Obstruction

The mechanism responsible for the abrupt fall in myocardial contractile function following coronary artery obstruction is unknown. The “vascular collapse theory” hypothesizes that the fall in coronary perfusion pressure after coronary artery obstruction is responsible for contractile failure during early ischemia. To test the role of vascular collapse in downregulating myocardial contractile force at the onset of ischemia, coronary flow of isolated rat hearts was abruptly decreased by 50, 70, 85, and 100% of baseline, and subsequent changes in coronary perfusion pressure and ventricular function were recorded at 0.5-s intervals. At 1.5 s after flow reductions ranging from 50 to 100%, decreases in contractile function did not differ, although perfusion pressure varied significantly from 45 ± 1 to 20 ± 2 mmHg. When function fell to 50% of baseline, perfusion pressures ranged from 35 ± 0.5 to 2.5 ± 1 mmHg for flow reductions ranging from 50 to 100%. Identical contractile function at widely differing coronary perfusion pressures is incompatible with the vascular collapse theory.

Role of myocardial oxygen and carbon dioxide in coronary autoregulation

1992 ◽  
Vol 262 (4) ◽  
pp. H1231-H1237 ◽  
Author(s):  
T. P. Broten ◽  
E. O. Feigl
Keyword(s):  
Carbon Dioxide ◽  
Left Main Coronary Artery ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Vascular Conductance ◽  
Anesthetized Dogs ◽  
Coronary Conductance ◽  
A Prospective Study

Myocardial oxygen (PO2) and carbon dioxide tensions (PCO2) are likely mediators of the local control of coronary blood flow. A previous study demonstrated that myocardial PO2 and PCO2, estimated by coronary venous values, interact synergistically to determine coronary flow. This synergistic relation was used in a prospective study to test the hypothesis that myocardial PO2 and PCO2 mediate changes in coronary vascular conductance during autoregulation. The left main coronary artery was pump perfused at controlled pressures in closed-chest anesthetized dogs. Autoregulation curves were obtained by increasing coronary perfusion pressure from 80 to 160 mmHg in 20-mm increments. Steady-state measurements of coronary venous PO2 and PCO2 and coronary conductance were obtained at each perfusion pressure. The coronary venous PO2 and PCO2 were used in the previously determined synergistic relation to predict the coronary vascular conductance during autoregulation. The predicted changes in coronary vascular conductance were compared with the actual changes in coronary vascular conductance for the pressure range of 80-160 mmHg. The data indicate that the synergistic interaction of oxygen and carbon dioxide accounts for approximately 23% of the change in coronary vascular conductance during autoregulation. These results suggest that other factors are also involved in autoregulation.

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.

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