Max Harry Weil

Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation.

Objectives:Both epinephrine and vasopressin increase aortic and carotid arterial pressure when administered during cardiopulmonary resuscitation. However, we recently demonstrated that epinephrine reduces cerebral cortical microcirculatory blood flow. Accordingly, we compared the effects of nonadrenergic vasopressin with those of epinephrine on cerebral cortical microvascular flow together with cortical tissue Po2 and Pco2 as indicators of cortical tissue ischemia. Design:Randomized, prospective animal study. Setting:University-affiliated research laboratory. Subjects:Domestic pigs. Measurements and Main Results:The tracheae of ten domestic male pigs, weighing 40 ± 2 kg, were noninvasively intubated, and the animals were mechanically ventilated. A frontoparietal bilateral craniotomy was created. Microcirculatory blood flow was quantitated with orthogonal polarization spectral imaging. Blood flow velocity in pial and cortical penetrating vessels measuring <20 μm was graded from 0 (no flow) to 3 (normal). Cerebral cortical tissue carbon dioxide and oxygen tensions (Pbco2 and Pbo2) were measured concurrently using miniature optical sensors. Ventricular fibrillation, induced with an alternating current delivered to the right ventricular endocardium, was untreated for 3 mins. Animals were then randomized to receive central venous injections of equipressor doses of epinephrine (30 μg/kg) or vasopressin (0.4 units/kg) at 1 min after the start of cardiopulmonary resuscitation. After 4 mins of cardiopulmonary resuscitation, defibrillation was attempted. Spontaneous circulation was restored in each animal. However, postresuscitation microvascular flows and Pbo2 were greater and Pbco2 less after vasopressin when compared with epinephrine. We observed that a significantly greater number of cortical microvessels were perfused after vasopressin. Conclusions:Cortical microcirculatory blood flow was markedly reduced after epinephrine, resulting in a greater severity of brain ischemia after the restoration of spontaneous circulation in contrast to the more benign effects of vasopressin.

The Public Access Defibrillation (PAD) trial: study design and rationale.

The PAD Trial is a prospective, multicenter, randomized clinical study testing whether volunteer, non-medical responders can improve survival from out-of-hospital cardiac arrest (OOH-CA) by using automated external defibrillators (AEDs). These lay volunteers, who have no traditional responsibility to respond to a medical emergency as part of their primary job description, will form part of a comprehensive, integrated community approach to the treatment of OOH-CA. The study is being conducted at 24 field centers in the United States and Canada. Approximately 1000 community units (e.g. apartment or office buildings, gated communities, sports facilities, senior centers, shopping malls, etc.) were randomized to treatment by trained laypersons who will provide either cardiopulmonary resuscitation (CPR) alone or CPR plus use of an AED, while awaiting arrival of the communitys emergency medical services responders. The primary endpoint is the number of OOH-CA victims who survive to hospital discharge. Secondary endpoints include neurological status, health-related quality of life (HRQL), cost, and cost-effectiveness. Data collection will last approximately 15 months and is expected to be completed in September 2003.

An Algorithm Used for Ventricular Fibrillation Detection Without Interrupting Chest Compression

Ventricular fibrillation (VF) is the primary arrhythmic event in the majority of patients suffering from sudden cardiac arrest. Attention has been focused on this particular rhythm since it is recognized that prompt therapy, especially electrical defibrillation, may lead to a successful outcome. However, current versions of automated external defibrillators (AEDs) mandate repetitive interruptions of chest compression for rhythm analyses since artifacts produced by chest compression during cardiopulmonary resuscitation (CPR) preclude reliable electrocardiographic (ECG) rhythm analysis. Yet, repetitive interruptions in chest compression are detrimental to the success of defibrillation. The capability for rhythm analysis without requiring “hands-off” intervals will allow for more effective resuscitation. In this paper, a novel continuous-wavelet-transformation-based morphology consistency evaluation algorithm was developed for the detection of disorganized VF from organized sinus rhythm (SR) without interrupting the ongoing chest compression. The performance of this method was evaluated on both uncorrupted and corrupted ECG signals recorded from AEDs obtained from out-of-hospital victims of cardiac arrest. A total of 232 patients and 31 092 episodes of either VF or SR were accessed, in which 8195 episodes were corrupted by artifacts produced by chest compressions. We also compared the performance of this method with three other established algorithms, including VF filter, spectrum analysis, and complexity measurement. Even though there was a modest decrease in specificity and accuracy when chest compression artifact was present, the performance of this method was still superior to other reported methods for VF detection during uninterrupted CPR.

The first documented cardiac arrest rhythm in hospitalized patients with heart failure.

BACKGROUNDnPatients with heart failure (HF) have abnormal cellular anatomy and myocardial mechanics that may impact the initial rhythm and subsequent outcomes in cardiac arrest (CA).nnnHYPOTHESISnPatients with pre-existing HF are less likely to have ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) as the first documented rhythm in CA and have poorer survival than patients without pre-existing HF.nnnPURPOSEnIdentify the first documented cardiac arrest rhythm (FDR) in hospitalized patients with and without a pre-existing history of HF.nnnMETHODSnWe evaluated 60,389 consecutive, adult, index, pulseless CA events with documented initial rhythm in the National Registry of Cardiopulmonary Resuscitation. The primary endpoint was the FDR in patients with and without a history of pre-existing HF. Secondary endpoints were return of spontaneous circulation (ROSC), survival to discharge, and neurological outcome.nnnRESULTSnThirty three percent of patients had a pre-existing diagnosis of HF. HF patients were more likely to have VF/pVT (25.9 vs. 23.2%) and less likely to have asystole (34.4 vs. 35.3%, p=<.0001) than non-HF. There was no difference in survival to discharge (18.3 vs. 18.2%, p=.66), or good neurological outcomes (82.2 vs. 83.2%, p=.23) between the groups. Women were less likely to have VF/pVT as the first documented rhythm in both HF and non-HF groups.nnnCONCLUSIONSnHospitalized patients with HF are more likely than those without HF to have VF/pVT as the FDR in CA, however the clinical magnitude of this difference is small. Overall survival and neurological outcomes are no different than hospitalized arrest patients without HF.

Clinical correlates of arterial lactate levels in STEMI patients

Increases in blood lactate reflect decreases in systemic blood flows associated with low blood flow states characteristic of circulatory shock. Accordingly, the report by Vermeulen and colleagues documents the use of the blood lactate measurement as a prognostic indicator in settings of ST elevation myocardial infarction. That lactate value therefore identified high-risk patients as a complication, often with clinical signs of cardiogenic shock of corresponding severities.

Challenging the rationale of routine vasopressor therapy for management of hypotension.

There is persuasive evidence, including the present report by Dubin and colleagues, of a dissociation between increases in arterial pressure produced by vasopressor agents and improvement in microvascular perfusion and delivery of vital substrates. Especially in settings of septic shock, the current routine administration of adrenergic vasopressor therapy therefore may fail to reverse the primary defect.

Letter by Tang et al Regarding Article, “BIPHASIC Trial: A Randomized Comparison of Fixed Lower Versus Escalating Higher Energy Levels for Defibrillation in Out-of-Hospital Cardiac Arrest”

To the Editor:nnWe read with interest the article by Stiell and colleagues1 in which the efficacy of defibrillation with fixed low energy was compared with escalating high-energy biphasic waveforms in out-of-hospital cardiac arrest settings. When patients received multiple shocks, the likelihood of converting ventricular fibrillation was reportedly greater with high-energy escalating shocks.nnThe study addresses important issues. However, the devices that were compared did not take into consideration differences in waveforms and, most especially, the time duration of the currents delivered. The comparisons were made with the commercially available biphasic waveform device …

Tissue partial pressure of carbon dioxide tension measurements and microcirculation visualisation. New techniques for the study of low flow states

Microcirculation is 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 ismadeup of the smallest blood vessels: arterioles, capillaries and venules [1] (Fig. 1). The previous techniques used for studying microcirculation (microscopes, laser Doppler or plethysmography) were able to provide only a global measurement of microvascular blood flow; a measurement expressed as an average value of whatever was the diameter or direction of single vessels. Recent technological developments allow more precise and direct investigation of the tissue perfusion, and especially of the microcirculatory blood flow. The new techniques are basically noninvasive measurements of tissue carbon dioxide tension (PCO2), for example at the oral cavity mucosa, and the orthogonal polarisation spectral (OPS) imaging techniques, which have allowed direct visualisation and monitoring of microcirculation at the bedside [2, 3] (Fig. 2).

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.