Wanchun Tang

Augmented efficacy of external CPR by intermittent occlusion of the ascending aorta.

BackgroundAfter prolonged cardiac arrest, conventional methods of closed-chest cardiac compression are ineffective. This is primarily because of failure to generate minimal threshold levels of coronary perfusion pressure for cardiac resuscitation. This report introduces a new option for cardiac resuscitation by use of a combination of intermittent ascending aortic balloon occlusion, aortic infusion, and precordial compression to increase the pressure gradient for coronary perfusion. Methods and ResultsTwenty anesthetized, mechanically ventilated, normovolemic domestic pigs were investigated. A lOF balloon catheter was advanced from the left femoral artery into the ascending aorta. Ventricular fibrillation was induced with an AC current delivered through an electrode catheter advanced into the right ventricle. Precordial compression was initiated after 7 minutes of untreated ventricular fibrillation. The animals were randomized to one of four groups: (1) balloon occlusion with proximal infusion of oxygenated saline, (2) balloon occlusion alone, (3) proximal aortic infusion together with epinephrine without balloon occlusion, and (4) injection of epinephrine without balloon occlusion or proximal infusion. For balloon occlusion, the balloon was inflated for 30 seconds during each minute of cardiopulmonary resuscitation. In the subsets of animals that received infusions, oxygenated saline (30 mL) was injected into the proximal aorta immediately after balloon occlusion. Epinephrine was used in two subsets: It was injected as a bolus in amounts of 30 μg/kg into the right atrium at 30 seconds after start of precordial compression and repeated as required to maintain coronary perfusion pressure within the range of 25 to 30 mmHg. Defibrillation was attempted at 1 minute after start of precordial compression and at 1-minute intervals thereafter. Resuscitation attempts were continued until there was return of spontaneous circulation or for a total of 30 minutes after start of precordial compression. Coronary perfusion pressure generated by precordial compression was significantly increased after balloon occlusion. Each of 10 animals was successfully resuscitated and survived for 48 hours after balloon occlusion whether or not it was combined with infusion. Three of five animals were resuscitated by a combination of infusion and epinephrine in the absence of aortic occlusion, but none survived for 48 hours (P=.02). Only one epinephrine-treated animal was successfully resuscitated and survived for 48 hours in the absence of balloon occlusion or infusion (P<.05) ConclusionsAscending aortic balloon occlusion with or without proximal aortic infusion strikingly increased resuscitability and 48-hour survival after cardiac arrest under conditions when conventional methods failed.

Simultaneous aortic, jugular bulb, and right atrial pressures during cardiopulmonary resuscitation in humans.

4) Safety of high-dose dipyridamole infusion. We have previously reported preliminary data on the safety of high-dose DET in 952 studies.5 More recently, data on the updated experience derived from a large-scale multicenter trial involving 12 echocardiography laboratories in Italy have become available.0 Until now (and in full accord with the preliminary experience reported from our group5), 2,401 high-dose DET studies have been performed according to the protocol proposed in 1986.4 This protocol requires that 1) two-dimensional echocardiographic monitoring be continuously performed throughout the test and that aminophylline be immediately given whenever obvious dyssynergy is detected and that 2) the high dose (0.28 mg/kg during a 2-minute period) be given only when the test is still negative for echocardiographic criteria at the fourth minute after the low standard dose (0.56 mg/kg during a 4-minute period). It was found that no major side effects occurred (i.e., death, myocardial infarction, or severe arrhythmias) and that more severe forms of myocardial ischemia (aminophylline-resistant ischemia and ST segment elevation in the absence of resting Q wave) were always elicited by the lower standard dose (0.56 mg/kg during 4 minutes). Of note, 305 studies were performed early (< 15 days) after an acute myocardial infarction.10 When continuous echocardiographic monitoring is combined with graded administration of dipyridamole, the higher dose did not imply a greater risk.0 5) Study population. As clearly shown in Table 7 of our study,1 the prognostic value of DET is apparent also in the subset of patients without myocardial infarction, insofar as hard end points are concerned. Using the Cox model, we found that in this subset the most significant predictor of subsequent events (death and myocardial infarction) was a positive DET (A)=7.3, p<0.01). Finally, we thank Dr. Gerson for acknowledging that we have made a series of new and potentially important observations about DET. We cannot share his concerns on the supposed major limitations of the study but certainly agree that we need much larger study populations and multicenter experience on various patient subsets, as well as more follow-up information, to have a clearer idea about the safety, usefulness, and prognostic accuracy of DET. Our view is that, at the moment, high-dose DET is midway on the bridge that links a promising test to an extensively applied diagnostic procedure. Substantial, further information is required for community hospital use, but no real stepup in information will be provided until larger scale application is made. Please do not forget DET is only 5 years old, and answers to all questions are not yet available. Eugenio Picano, MD CNR, Clinical Physiology Institute University of Pisa Pisa, Italy

Effect of arrest time on the hemodynamic efficacy of precordial compression

OBJECTIVESnTo evaluate the efficacy of conventional threshold levels of coronary perfusion pressure and end-tidal CO2 as predictors of resuscitability after prolonged cardiac arrest.nnnDESIGNnProspective, randomized, controlled animal study.nnnSETTINGnUniversity research laboratory.nnnSUBJECTSnTwenty-one Sprague-Dawley rats, including three groups of seven animals in each group.nnnINTERVENTIONSnVentricular fibrillation was untreated for 9, 12, or 15 mins. After an additional 5-min interval of precordial compression, external direct current defibrillation was attempted.nnnMEASUREMENTS AND MAIN RESULTSnAll animals were successfully resuscitated after 9 mins of ventricular fibrillation but less than one half of the animals were successfully resuscitated after 15 mins of ventricular fibrillation. Each of seven animals survived for 24 hrs after 9 mins of untreated ventricular fibrillation but none of the animals survived after 15 mins of ventricular fibrillation. In this experimental setting, neither coronary perfusion pressure nor end-tidal CO2 produced by precordial compression was predictive of outcomes when the animals underwent progressively longer intervals of untreated cardiac arrest.nnnCONCLUSIONSnThe efficacy of precordial compression--as measured by coronary perfusion pressure and end-tidal CO2 concentration after prolongation of untreated cardiac arrest--was not overtly compromised. However, the previously established critical threshold levels of coronary perfusion pressure and end-tidal CO2 failed as predictors of resuscitability after prolonged intervals of untreated cardiac arrest.

Mechanisms of myocardial hypercarbic acidosis during cardiac arrest

During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.