Showing papers by "Wanchun Tang published in 2006"

Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation.

Abstract: (7.7 0.9 to 15.7 2.4; p < .0001); and mixed venous oxygen saturation (26 5to365, p<.05). Hemodynamics improved further with the ITD. Oxygenation and arterial pH were similar. Only one of nine pigs had return of spontaneous circulation with 15:2, vs. six of nine with 30:2 (p < 0.03). Humans: Fatigue and quality of CPR performance were evaluated in 20 BLS-certified rescuers randomized to perform CPR for 5 mins at 15:2 or 30:2 on a recording CPR manikin. There were no significant differences in the quality of CPR performance or measurement of fatigue. Significantly more compressions per minute were delivered with 30:2 in both the animal and human studies. Conclusions: These data strongly support the contention that a ratio of 30:2 is superior to 15:2 during manual CPR and that the ITD further enhances circulation with both C:V ratios. (Crit Care Med 2006; 34:1444‐1449)

Microcirculation during cardiac arrest and resuscitation.

Abstract: Objective: Direct observations of the microcirculation using orthogonal polarization spectral imaging have attracted attention and revealed that, especially in cardiogenic and distributive shock, there is discordance between the macrocirculation and the microcirculation. We evaluated serial changes and the effects of epinephrine on microcirculatory blood flow in the most severe form of circulatory failure, namely, cardiac arrest. Design and Setting: Controlled laboratory animal study. Subjects and Interventions: A total of 15 pigs were subjected to 5 mins of ventricular fibrillation and 5 mins of precordial compression before electrical defibrillation was attempted. In a subset, six animals received 1 mg of epinephrine after 1 min of precordial compression. Measurements and Main Results: Microcirculatory blood flow was visualized in the sublingual mucosa at baseline and 0.5, 1, and 5 mins of ventricular fibrillation, at 1 and 5 mins of precordial compression, and at 1 and 5 mins after return of spontaneous circulation. In addition, coronary perfusion pressure was re corded. Microcirculatory blood flow decreased dramatically in the 0.5 min after the onset of ventricular fibrillation. Precordial compression partially restored microcirculatory blood flow in each animal but to a significantly greater extent in animals that achieved return of spontaneous circulation. These changes were paralleled by similar changes in coronary perfusion pressure. Both variables were highly correlated. Administration of epinephrine resulted in a massive reduction of microcirculatory blood flow that lasted for ≥5 mins. Conclusions: In this model, microcirculatory blood flow was highly corretated with macrocirculatory hemodynamics, including coronary perfusion pressure in distinction with septic shock. Administration of epinephrine dramatically decreased microcirculatory blood flow. (Crit Care Med 2006; 34[Suppl.]:S454-S457)

Increases in tissue Pco2 during circulatory shock reflect selective decreases in capillary blood flow.

Abstract: Objectives: Tissue Pco 2 reflects metabolic alterations due to circulatory failure during circulatory shock. This study addresses simultaneous changes in gastric and buccal tissue Pco 2 with changes in microcirculatory blood flow in a rat model of circulatory shock induced by cecal ligation and puncture. Design: Prospective controlled laboratory study. Setting: University-affiliated research laboratory. Subjects: Male breeder Sprague-Dawley rats. Interventions: Induction of polymicrobial, abdominal sepsis by cecal ligation and puncture. Measurements and Main Results: Tissue Pco 2 was continuously measured with the aid of a miniature carbon dioxide electrode. Using orthogonal polarization spectral imaging, recordings of the microcirculation were taken at baseline and hourly intervals until death and compared with sham-operated animals. Gastric and buccal tissue Pco 2 values progressively increased in animals after cecal ligation and puncture and terminated in death. Microcirculatory blood flow in vessels >20 μm was well preserved during progression of shock, whereas there was an early and progressive decrease in microcirculatory blood flow in vessels <20 μm, mostly representing capillaries. Tissue Pco 2 , the tissue Pco 2 -Paco 2 gradient, and blood flow in vessels <20 μm were highly correlated. This contrasted with sham control animals in which no significant hemodynamic, blood gas, lactate, microcirculatory, and tissue Pco 2 abnormalities were observed. Conclusions: These observations suggest that microcirculatory failure in capillaries appears as an early defect in close association with anaerobic metabolism during progression of circulatory shock in an animal model of septic peritonitis.

Comparison of buccal microcirculation between septic and hemorrhagic shock.

Abstract: Objective: Microcirculatory perfusion is disturbed in sepsis, and global hemodynamics does not necessarily reflect microcirculatory blood flow. In this study, we investigated the effect of the same level of mean arterial pressure (MAP) or cardiac index on the changes in buccal microcirculation between septic and hemorrhagic shock. Design: Prospective, controlled laboratory study. Setting: University-affiliated research laboratory. Interventions: A total of 20 Sprague-Dawley rats were divided into four groups : 1) septic shock induced by cecal ligation and perforation: when MAP decreased to 80 mm Hg, saline was infused at a rate of 25 mL.kg -1 .hr -1 for 2 hrs; 2) both time- and MAP-matched hemorrhagic shock : ?30% of total blood volume was withdrawn during the corresponding interval, followed by infusion aiming to restore MAP as required when MAP decreased to 80 mm Hg; 3) both time- and cardiac index-matched hemorrhagic shock : ?40% of total blood volume was withdrawn during the corresponding interval until MAP decreased to 50 mm Hg, which generally generated a cardiac index similar to those in septic animals, followed by infusion at the same rate for 2 hrsand 4) sham control : animals underwent the same procedure except no cecal ligation and perforation, bleeding, and infusion. Measurements and Main Results : Buccal microcirculation was visualized with the aid of an orthogonal polarization spectral image device. A semiquantitative score was calculated for vessels of <20 μm, primarily representing the capillaries. Impaired buccal capillary blood flows in septic animals were more severe than those in MAP-matched hemorrhagic animals and were similar to those in cardiac index-matched hemorrhagic animals during the hypoperfusion period before infusion. Significantly improved global hemodynamics after resuscitation cannot effectively improve the buccal capillary blood flows in septic animals, in contrast to those in MAP-matched and cardiac index-matched hemorrhagic animals. Conclusions: Impaired microcirculatory alteration in septic shock is more severe than hemorrhagic shock; microcirculation is relatively independent of improved systemic hemodynamics, in contrast to those in hemorrhagic shock. (Crit Care Med 2006; 34[Suppl.]:S447-S453)

One-Shock Versus Three-Shock Defibrillation Protocol Significantly Improves Outcome in a Porcine Model of Prolonged Ventricular Fibrillation Cardiac Arrest

Abstract: Background— The success of resuscitation with a 1-shock versus the conventional 3-shock defibrillation protocol was investigated subject to the range of treatment variation imposed by automated ext...

Mechanism by which activation of δ-opioid receptor reduces the severity of postresuscitation myocardial dysfunction

Abstract: Objective Postresuscitation myocardial dysfunction has been recognized as a leading cause of early death after initially successful cardiopulmonary resuscitation. We have previously demonstrated that opening adenosine triphosphate (ATP)-sensitive K (KATP) channels or activation of delta-opioid receptors minimized the severity of postresuscitation myocardial dysfunction and increased the duration of postresuscitation survival. In the present study, we investigated the potential mechanism of myocardial protection following delta-opioid receptor activation in a rat model of cardiac arrest and cardiopulmonary resuscitation. Design Randomized prospective animal study. Setting Animal research laboratory. Subjects Male Sprague-Dawley rats. Interventions Ventricular fibrillation was induced in 24 Sprague-Dawley rats. Mechanical ventilation and precordial compression were initiated after 8 mins of untreated ventricular fibrillation. Defibrillation was attempted after 6 mins of cardiopulmonary resuscitation. The animals were randomized to four groups: a) pentazocine (0.3 mg/kg), a delta-opioid receptor agonist; b) pentazocine pretreated with KATP channel blocker, glibenclamide (0.3 mg/kg), administered 45 mins before induction of ventricular fibrillation; c) glibenclamide pretreated alone 45 mins before induction of ventricular fibrillation; and d) placebo. Pentazocine or saline placebo was injected into the right atrium after 5 mins of untreated ventricular fibrillation. Measurements and main results Postresuscitation myocardial function, as measured by the rate of left ventricular pressure increase at 40 mm Hg, left ventricular end-diastolic pressure, and cardiac index, was significantly improved in pentazocine-treated animals. This was associated with significantly prolonged duration of survival. Except for ease of defibrillation, the beneficial effects of pentazocine were abolished by pretreatment with the KATP channel blocker glibenclamide. Conclusions The postresuscitation myocardial protective effects provided by activation of delta-opioid receptor may be mediated via opening KATP channels.

Cardiopulmonary resuscitation in a rat model of chronic myocardial ischemia

Abstract: 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.

Role of buccal PCO2 in the management of fluid resuscitation during hemorrhagic shock.

Abstract: Arterial pressure is a widely used measurement for estimating the severity of hemorrhagic shock and to guide its management. However, this capability is reduced when very low arterial pressure values cannot be reliably measured by noninvasive methods. Moreover, hypoperfusion may be masked by compensatory hemodynamic changes, and therefore, in the presence of near normal blood pressure, tissue hypoperfusion may progress undetected. Accordingly, hypercarbia is a general phenomenon of perfusion failure, which occurs in coincidence of the onset of hypotension and is promptly reversed with restoration of normal blood flows. Increases in buccal mucosa Pco 2 sublingual mucosa Pco 2 hemorrhagic shock. In both clinical and experimental settings, tissue Pco 2 measured in the oral mucosa proved to be a practical and reliable measurement for the diagnosis of circulatory failure states and an indicator of its severity. In contrast to intraarterial pressure, buccal Pco 2 after large-volume blood loss. Buccal Pco 2 emerges as a useful predictor for survival and outcome and a useful guide to manage fluid resuscitation during hemorrhagic shock. (Crit Care Med 2006; 34[Suppl.]:S442-S446)

Buccal capnometry to guide management of massive blood loss

Abstract: In both clinical and experimental settings, tissue Pco2 measured in the oral mucosa is a practical and reliable measurement of the severity of hypoperfusion. We hypothesized that a threshold level ...

δ-Opioid–induced pharmacologic myocardial hibernation during cardiopulmonary resuscitation

Abstract: Objectives: Cardiac arrest and cardiopulmonary resuscitation is an event of global myocardial ischemia and reperfusion, which is associated with severe postresuscitation myocardial dysfunction and fatal outcome. Evidence has demonstrated that mammalian hibernation is triggered by cyclic variation of a δ-opiate-like compound in endogenous serum, during which the myocardial metabolism is dramatically reduced and the myocardium tolerates the stress of ischemia and reperfusion without overt ischemic and reperfusion injury. Previous investigations also proved that the δ-opioid agonist elicited the cardioprotection in a model of regional ischemic intact heart or myocyte. Accordingly, we were prompted to search for an alternative intervention of pharmacologically induced myocardial hibernation that would result in rapid reductions of myocardial metabolism and therefore minimize the myocardial ischemic and reperfusion injury during cardiac arrest and cardiopulmonary resuscitation. Design: Prospective, controlled laboratory study. Setting: University-affiliated research laboratory. Interventions: In the series of studies performed in the established rat and pig model of cardiac arrest and cardiopulmonary resuscitation, the δ-opioid receptor agonist, pentazocine, was administered during ventricular fibrillation. Measurements and Main Results: The myocardial metabolism reflected by the concentration of lactate, or myocardial tissue Pco 2 and Po 2 cardiopulmonary resuscitation. These are associated with less severe postresuscitation myocardial dysfunction and longer duration of postresuscitation survival. Conclusions: δ-Opioid-induced pharmacologic myocardial hibernation is an option to minimize the myocardial ischemia and reperfusion injury during cardiac arrest and cardiopulmonary resuscitation. (Crit Care Med 2006; 34[Suppl.]:S486-S489)

Simultaneous blockade of α1- and β-actions of epinephrine during cardiopulmonary resuscitation

Abstract: Objective: Experimental and clinical studies have implicated that α 1 and β-adrenergic effects of epinephrine significantly increased the severity of postresuscitation myocardial dysfunction by increasing myocardial oxygen consumption during ventricular fibrillation. This prompted experimental studies to investigate the effect of simultaneous blockade of α 1 - and β-actions of epinephrine during cardiopulmonary resuscitation. Design: Literature review. Results: Improved postresuscitation myocardial dysfunction was observed in epinephrine-treated animals after its α 1 - and β-actions were blocked, which were associated with less pos tresuscitation arrhythmia, lower blood lactate level, better neurologic recovery, and longer duration of survival. Conclusions: After simultaneous α 1 - and β-adrenergic blockade, epinephrine administered during cardiopulmonary resuscitation yielded improved postresuscitation myocardial functions and significantly better postresuscitation outcomes. (Crit Care Med 2006; 34[Suppl.]:S483-S485)

Effects of biphasic waveforms on outcomes of cardiopulmonary resuscitation in a porcine model of prolonged cardiac arrest.

Abstract: OBJECTIVES The effects of two clinically available biphasic waveforms on the success of defibrillation and postresuscitation myocardial dysfunction after prolonged ventricular fibrillation were compared with two newly designed dual-path sequential and simultaneous rectilinear biphasic waveforms. Defibrillation via sequential pulses and encircling, overlapping multiple pathway may depolarize a larger myocardial mass and facilitate transthoracic defibrillation. DESIGN Animal study. SETTING Experimental laboratory. SUBJECTS Thirty-two 40 +/- 3 kg pigs. INTERVENTIONS Ventricular fibrillation was ischemically induced in 32 pigs. After 7 mins of untreated ventricular fibrillation, cardiopulmonary resuscitation was initiated and continued for 5 mins. Animals were then randomized to receive up to three shocks with a) single-path rectilinear biphasic waveform; b) single-path biphasic truncated exponential waveform; c) dual-path rectilinear biphasic sequential defibrillation; or d) dual-path rectilinear biphasic simultaneous defibrillation. MEASUREMENTS AND MAIN RESULTS Rectilinear biphasic, dual-path sequential defibrillation, and simultaneous defibrillation had significantly fewer shocks (1.1 +/- 0.4, 1.4 +/- 0.5, 1.3 +/- 0.7, respectively) before restoration of spontaneous circulation than biphasic truncated exponential waveform (2.6 +/- 1.4, p < .005) and less postresuscitation myocardial dysfunction (p < .05). Also, dual-path sequential defibrillation had higher postresuscitation ejection fraction than rectilinear biphasic and dual-path simultaneous defibrillation (p < .005). CONCLUSIONS The energy requirements for terminating ischemically induced ventricular fibrillation were significantly lower and minimized early postresuscitation myocardial dysfunction in the rectilinear biphasic, dual-path sequential defibrillation, and simultaneous defibrillation than the biphasic truncated exponential waveform. Dual-path sequential defibrillation had less postresuscitation myocardial dysfunction than rectilinear biphasic and dual-path simultaneous defibrillation, but at 72 hrs these differences were no longer significant.

The Ninth Wolf Creek Conference on Cardiopulmonary Resuscitation: Addressing the scientific basis of reanimation.

Abstract: More than 45 yrs have elapsed since the combined techniques of mechanical ventilation, external precordial compression, and electrical defibrillation were introduced. These ushered in the modern era of cardiopulmonary resuscitation (CPR). The outcomes, however, have been very disappointing. In the United States alone, more than 350,000 previously healthy adults die suddenly of cardiac causes each year. Typically, fewer than 5% of the victims are likely to be successfully resuscitated to the extent that they are returned to productive lives. The so-called Wolf Creek Conferences of CPR researchers were initiated by Drs. James Elam, James Jude, and Peter Safar. The objective was to improve the clinical practices of CPR by stimulating laboratory and clinical research. There was great need of objective data such that guidelines on CPR might be more secure. The first meeting of some 20 investigators was hosted in 1975 by Dr. James Jude at his “Wolf Creek Lodge” in Georgia. The proceedings were published by Drs. Safar and Elam as part of a monograph entitled Advances in Cardiopulmonary Resuscitation by Springer-Verlag in 1977 (1). The second meeting occurred approximately 5 yrs later in Key West, FL. It was chaired by the late Dr. Joseph Redding. The proceedings appeared in Critical Care Medicine in 1981 (2). The third meeting was held approximately 5 yrs later in Lake Geneva, WI. It was organized by Drs. Nicholas Bircher, Mickey Eisenberg, and Charles Otto, and the proceedings of the meeting were published in Critical Care Medicine in 1985 (3). The initial objective of these conferences was at least partially accomplished, and the field of resuscitation science has grown impressively. New capabilities for cardiac resuscitation using automated external defibrillators, greatly expanded emergency medical systems, and a number of promising new mechanical resuscitation methodologies have emerged. The Fourth Wolf Creek Conference featured exciting exchanges of information and view points among spirited experts in the field of CPR research. Hosted by the Institute of Critical Care Medicine and University of Southern California School of Medicine and chaired by Max Harry Weil, it was held between April 14 and 16, 1996, in Palm Springs, CA. This conference included 38 discussants and a much larger number of active researchers. Also in attendance were representatives of voluntary health organizations, industry, and government. The proceedings of the meeting were published in New Horizons in 1997 (4). The Fifth and the Sixth Wolf Creek Conferences were hosted by the Institute of Critical Care Medicine on September 8 and 9, 1999, and between June 4 and 7, 2001, at the Ritz-Carlton Hotel in Rancho Mirage, CA. The Seventh Wolf Creek Conference was also hosted by the Institute of Critical Care Medicine between June 13 and 16, 2003, at The Lodge in Rancho Mirage, CA, and these three conferences were chaired by Max Harry Weil and Wanchun Tang. More than 50 international experts on CPR and representatives of voluntary health organizations, industry, and government participated. The proceedings of the conferences were published in Critical Care Medicine in 2000 (5), 2002 (6), and 2004 (7). The Eighth Wolf Creek Conference was also hosted by the Institute of Critical Care Medicine between June 10 and 13, 2005, at The Lodge in Rancho Mirage, CA, and this conference was again chaired by the undersigned. The proceedings of this meeting are included in this issue. The Eighth Wolf Creek Conference was again remarkable in that the large hiatus between current concepts and practices of CPR and the scientific bases that supported these concepts and practices were exposed. The presentations by Drs. Aufderheide and Yannopoulos documented the effectiveness of the impedance threshold device for augmenting systemic blood flow during both CPR and hypovolemic shock. Dr. Hickey and his colleagues further supported the concept that the so-called “agonal gasping” actually improves both cardiac output and pulmonary gas exchange during cardiac arrest and CPR. The presentations by Dr. Rudolph Koster challenged the current definition of defibrillation success and proposed to use return of organized rhythm as the primary outcome measure of defibrillation success. Drs. Russell and White presented evidence that electrocardiographic waveform analyses offer promise for realtime guidance of CPR interventions, especially the priority of chest compression or defibrillation. Direct observation of the microcirculation during the low-flow states has recently attracted attention. Dr. Michael Fries reported that microcirculatory hemodynamics is highly correlated with macrocirculatory hemodynamics in the absence of epinephrine during CPR. In contrast to CPR, however, Dr. Fang reported that during septic shock, changes in microcirculation are relatively independent of changes in systemic hemodynamics. Recent clinical studies on hypothermia induced immediately after resuscitation provide additional evidence of improved cerebral outcomes after successful CPR. Dr. Merchant, however, demonstrated that unintentional overcooling below target temperature is common. Better mechanisms for temperature control are required to prevent potential complications of profound hypothermia. The search for an optimal vasopressor agent for administration during CPR continues. The detrimental effects of the 1and -actions of epiThe Eighth Wolf Creek Symposium was supported, in part, by unrestricted grants from the American Heart Association, Advanced Circulatory Systems, Cardiac Science, Asmund S. Laerdal Foundation for Acute Medicine, Medtronic Physio-Control, Philips Medical Systems, and Zoll Medical. Copyright © 2006 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins

The Effects of Gasping During Cardiac Arrest and Cardiopulmonary Resuscitation

Abstract: Gasping, observed commonly at the beginning and at the end of life [1]–[5], is a striking phenomenon characterised by fast and forceful inspirations. Gasping is especially prominent in the human newborn. In 1812, Legallois [6] described gasping in a variety of animal species and also in human patients. The Glossary Committee of the International Union of Physiologic Sciences defined a gasp as ‘an abrupt, sudden transient inspiratory effort’ [7].

Abstract 92: Outcomes of CPR in a Rat Model of Chronic Myocardial Ischemia

Abstract: Introduction: A majority of sudden cardiac deaths occur in victims who have ischemic heart disease. In such patients, lesser success of CPR and lower likely ultimate survival are assumed. In the pr...

Microcirculation During Low Flow States

Abstract: Microcirculation represents the ultimate determinant of the outcomes of circulatory shock states. Microcirculatory function is the prerequisite for adequate tissue oxygenation and therefore organ function. It transports oxygen and nutrients to tissue cells, ensures adequate immunological function, and, during disease, delivers therapeutic drugs to target cells. It consists of the smallest blood vessels: arterioles, capillaries and venules [1] (Fig. 1). Previous techniques for studying microcirculation (microscopes, laser Doppler and plethysmography) were able to provide only global measurements of microvascular blood flow, expressed as average values of the diameter or direction of a single vessel. Recent technological developments using orthogonal polarisation spectral (OPS) imaging techniques allow the direct visualisation and monitoring of microcirculation at the bedside [2], [3] (Fig. 2). The OPS imaging technology is a non-invasive method for directly visualising multiple conditions of the microcirculation that have clinical applications for humans. It allows the quantitative measurement of the diameter of vessels, the velocity of red blood cells and functional capillary density [4]. The technique uses a linearly polarised light to illuminate the area of interest. The light is reflected from the tissue source and forms an image of the illuminated region within the target of the video camera. The image is then captured through a polariser, which is oriented orthogonally to the plane of the illuminating light [5].