Showing papers by "Wanchun Tang published in 1997"

High-Energy Defibrillation Increases the Severity of Postresuscitation Myocardial Dysfunction

Abstract: Background The fatal outcome of victims after initially successful resuscitation from cardiac arrest has been attributed both to global myocardial ischemia during the interval of cardiac arrest and to the adverse effects of reperfusion. The present study was prompted by earlier experimental observation that the magnitude of myocardial dysfunction was in part related to the energy delivered during electrical defibrillation. Methods and Results Ventricular fibrillation (VF) was induced in 15 Sprague-Dawley rats. Precordial compression was begun together with mechanical ventilation after 4 minutes of untreated VF and continued for 6 minutes. Spontaneous circulation was restored in each animal after external defibrillation with a single stored 2-, 10-, or 20-J countershock. Cardiac index and the rate of left ventricular pressure rise at left ventricular pressure of 40 mm Hg (dP/dt40) and fall (negative dP/dt) during the 240-minute interval after successful resuscitation were decreased, and left ventricular di...

Adverse effects of interrupting precordial compression during cardiopulmonary resuscitation.

Abstract: ObjectivesIn the current operation of automated external defibrillators, substantial time may be consumed for a "hands off" interval during which precordial compression is discontinued to allow for automated rhythm analyses before delivery of the electric countershock. The effects of such a pause on

Phased chest and abdominal compression-decompression: A new option for cardiopulmonary resuscitation

Abstract: Background We describe a new manual method of phased chest and abdominal compression-decompression with a Lifestick resuscitator for cardiopulmonary resuscitation (CPR). Methods and Results Ventricular fibrillation (VF) was induced in 20 domestic pigs. After either 5 or 7 minutes of untreated VF, either phased chest and abdominal compression-decompression (Lifestick resuscitator) or precordial compression was initiated. Defibrillation was attempted at 2 minutes after the start of CPR. For the animals in which VF was untreated for 7 minutes, epinephrine was administered in doses of 20 μg/kg at 2 minutes after start of CPR. The coronary perfusion pressure generated by the Lifestick resuscitator was more than twofold greater ( P P P P Conclusions Phased chest and abdominal compression-decompression substantially increased hemodynamic efficacy of CPR and outcome in terms of successful resuscitation, 48-hour survival, and cerebral recovery.

Esophageal PCO2 as a monitor of perfusion failure during hemorrhagic shock.

Abstract: Sato, Yoji, Max Harry Weil, Wanchun Tang, Shijie Sun, Jianlin Xie, Joe Bisera, and Hidehiro Hosaka. Esophageal P CO 2 as a monitor of perfusion failure during hemorrhagic shock. J. Appl. Physiol. 82(2): 558–562, 1997.—Measurement of gastric wall P CO 2 ( Pg CO 2 ) by tonometric method has emerged as an attractive option for estimating visceral perfusion during circulatory shock. However, gastric acid secretion obfuscates the tonometric measurement. We, therefore, investigated the option of measuring P CO 2 in the esophagus to minimize these restraints. Hemorrhagic shock was induced in five Sprague-Dawley rats, and five rats served as sham controls. Pg CO 2 was measured with an ion-sensitive field effect transistor that was surgically implanted into the gastric wall. Esophageal luminal P CO 2 ( Pe CO 2 ) was measured by a second ion-sensitive field effect transistor sensor. During hemorrhagic shock, mean aortic pressure declined from 150 to 50 mmHg. Gastric blood flow decreased from 58 to 12 ml ⋅ min−1 ⋅ 1...

Management of acidosis: the role of buffer agents.

Abstract: 52cc-1-2-051 Full text For more than 50 years, continuing up to about 1980, sodium bicarbonate was used for the treatment of metabolic acidosis. The rationale was that administration of an alkaline fluid would correct an acidotic state. However, the potential value of sodium bicarbonate was called into question when more recent studies demonstrated that it induced venous hypercarbia, and decreases in tissue and cerebrospinal fluid pH, as well as provoking tissue hypoxia, circulatory congestion, hypernatremia, and hyperosmolality, with consequent brain damage [1-6]. Bicarbonate buffers may intensify rather than ameliorate cellular acidosis because sodium bicarbonate generates CO2 and thereby increases intracellular (hypercarbic) acidosis [7]. Sodium bicarbonate administered to patients with diabetic ketoacidosis failed to favorably alter the clinical course or outcome. More specifically, the survival rate was similar in patients who did not receive bicarbonate [8]. During hypoxic lactic acidosis, sodium bicarbonate produced a decline in both systemic arterial pressure and cardiac output without improvement in outcome [9]. The declines in arterial pressure and cardiac output were associated with the hypertonicity of buffer agents which produced arterial vasodilation [10]. Several other agents have been investigated for the treatment of lactic acidosis. The intent was to increase blood pH during hypoxic states, without reducing oxygen delivery or increasing blood and tissue CO2. Among the most promising are the organic buffers, including TRIS (THAM), and a mixture of equimolar concentrations of sodium carbonate and bicarbonate named Carbicarb. Both of these agents are CO2-consuming, rather than CO2-generating, bicarbonate buffers. In animal studies, both THAM and Carbicarb appeared to have advantages over sodium bicarbonate in the treatment of lactic acidosis and diabetic ketoacidosis [5,11]. However, no well-controlled human trials are available at this time and neither agent is as yet regarded as appropriate for routine management. Only in exceptional circumstances, particularly in cases of poisoning, drug intoxication, life threatening hyperkalemia or acute epinephrine-fast broncho-constriction, is there likely to be an indication for the reversal of acidosis by the administration of buffer agents. In settings of cardiac arrest, there is currently no secure evidence of improved outcome after buffer administration. Moreover, measurements indicate that buffer agents including sodium bicarbonate, THAM and Carbicarb do not alter myocardial pH during cardiac resuscitation [12]. Nevertheless, a minority of data, based on experimental cardiopulmonary resuscitation (CPR) studies in dogs, are cited to encourage continued use of sodium bicarbonate during CPR [13,14]. A very recent study in our laboratory may be of interest as it indicates that buffer agents, when administered during CPR, may reduce the severity of post-resuscitation myocardial dysfunction and prolong survival in animals [15] We must await confirmation from studies on patients before we see whether this will prove to be clinically applicable. In conclusion, we cannot, at the time of writing, recommend routine bicarbonate or other buffer administration for the reversal of acidosis associated with low flow states.