Assessing the short-term outcomes of a community-based intervention for overweight and obese children: The MEND 5-7 programme.

OBJECTIVE: The aim of this study was to report outcomes of the UK service level delivery of MEND (Mind,Exercise,Nutrition...Do it!) 5-7, a multicomponent, community-based, healthy lifestyle intervention designed for overweight and obese children aged 5-7 years and their families. DESIGN: Repeated measures. SETTING: Community venues at 37 locations across the UK. PARTICIPANTS: 440 overweight or obese children (42% boys; mean age 6.1 years; body mass index (BMI) z-score 2.86) and their parents/carers participated in the intervention. INTERVENTION: MEND 5-7 is a 10-week, family-based, child weight-management intervention consisting of weekly group sessions. It includes positive parenting, active play, nutrition education and behaviour change strategies. The intervention is designed to be scalable and delivered by a range of health and social care professionals. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was BMI z-score. Secondary outcome measures included BMI, waist circumference, waist circumference z-score, children's psychological symptoms, parenting self-efficacy, physical activity and sedentary behaviours and the proportion of parents and children eating five or more portions of fruit and vegetables. RESULTS: 274 (62%) children were measured preintervention and post-intervention (baseline; 10-weeks). Post-intervention, mean BMI and waist circumference decreased by 0.5 kg/m(2) and 0.9 cm, while z-scores decreased by 0.20 and 0.20, respectively (p<0.0001). Improvements were found in children's psychological symptoms (-1.6 units, p<0.0001), parent self-efficacy (p<0.0001), physical activity (+2.9 h/week, p<0.01), sedentary activities (-4.1 h/week, p<0.0001) and the proportion of parents and children eating five or more portions of fruit and vegetables per day (both p<0.0001). Attendance at the 10 sessions was 73% with a 70% retention rate. CONCLUSIONS: Participation in the MEND 5-7 programme was associated with beneficial changes in physical, behavioural and psychological outcomes for children with complete sets of measurement data, when implemented in UK community settings under service level conditions. Further investigation is warranted to establish if these findings are replicable under controlled conditions.

Comparison of defibrillation efficacy using biphasic waveforms delivered from various capacitances/pulse widths.

The efficacy of the biphasic waveform shock for the defibrillation of the ventricular myocardium has been reported by researchers and physicians. Although many authors have suggested that biphasic waveforms delivered from lower capacitances and shorter pulse widths could result in the reduction of the energy required for successful defibrillation, no report has described the smallest capacitance and pulse width yielding the lowest DFT. In this study, we compared efficacies of the biphasic waveform shocks and DFT safety margins among five different capacitances (175 mu f, 125 mu f. 100 mu f. 75 mu f, and 50 mu f) combined with 1-3 pulse widths. These experiments performed in six dogs used an endocardial lead/subcutaneous patch defibrillation electrode system. The average DFTs at E50 for 175 mu f (6.5/3.5 ms), 125 mu f (6.5/3.5 ms), 100 mu f (6.0/3.0 ms), 75 mu f (4.0/2.0) ms, and 50 mu f (3.0/2.0 ms) were 8.5, 10.0, 11.0, 14.0, and 16.5), respectively. These results indicate that a biphasic waveform delivered from a larger capacitance with a proper pulse width could achieve a higher defibrillation efficacy. All DFTs at E50 for all waveforms were compared to their deliverable energies and maximum stored energies. This comparison indicated a narrow DFT safety margin with capacitances below 100 mu f. Therefore, it is concluded that higher energy and higher leading edge voltage are required for a biphasic waveform delivered from a smaller capacitance with a shorter pulse width. Since the current capacitor technology provides a maximum voltage of 750 V using two capacitors in series, with the electrode impedance system used in this study, smaller capacitors appear to have a decreased probability of defibrillation success at a given energy.

Renal function following cardiac arrest and resuscitation in the canine.

Organ malfunction often occurs following cardiac arrest and resuscitation. Renal function, inulin clearance (Cln), was examined in 27 dogs before and after (days 2, 4, and 6) cardiac arrest and resuscitation. Group A (n = 7) had no ventricular fibrillation (VF), but cardiopulmonary support was applied for 20 min, and three transthoracic countershocks were delivered. In groups B (n = 7), C (n = 7), and D (n = 6) VF was induced for 2.5, 5.0, and 7.5 min, respectively, followed by cardiopulmonary support for 20, 20, and 15 min, respectively. When necessary, epinephrine and sodium bicarbonate were given during resuscitation. Countershock was applied for defibrillation. Kidneys were examined histologically in groups C and D. Following cardiac arrest, Cln was significantly less in the arrested groups compared to the nonarrested group. Within group C, which received the most epinephrine, Cln correlated negatively with epinephrine administration, and with the energy applied for defibrillation. Histologically, group C showed the highest incidence of cortical tubular cytoplasmic vacuolization, regeneration, inflammation, and tubular casts. Groups C and D showed outer medullary tubular cytoplasmic vacuolization, renal vascular changes, and calcification. In conclusion, cardiac arrest and resuscitation may precipitate acute renal hypofunction as well as reversible and irreversible morphological changes in normal functioning canine kidneys. The confounding effect of pre-existing renal disease remains to be examined experimentally.

Hemodynamic determinants of subdiaphragmatic venous return during closed-chest CPR in a canine cardiac arrest model.

OBJECTIVE: To assess the hemodynamic determinates of peripheral subdiaphragmatic venous-to-right-heart return during closed-chest CPR. MODEL: Seven anesthetized dogs subjected to electrically induced ventricular fibrillation for five minutes. INTERVENTIONS: Conventional closed-chest CPR and closed-chest CPR with continuous abdominal binding at a chest compression rate of 60 per minute, a compression-to-relaxation ratio of 50:50, and a ventilation-to-compression ratio of 1:5. METHODS: Solid-state catheters were positioned in the ascending aorta, right atrium (RA), and inferior vena cava (IVC). Cannulating electromagnetic flow probes were inserted into the IVC and a carotid artery. Analog-to-digital conversion was performed electronically. Five minutes after ventricular fibrillation was induced, interventions were performed in an alternating sequence. Systolic, diastolic, and mean pressures and flows were measured and compared. STATISTICAL METHODS: Two-tailed, unpaired t test applied to equal sample size, linear regression analysis, and multiple regression analysis. RESULTS: Abdominal binding during CPR significantly increased (P less than .05) all measured systolic and diastolic CPR intravascular pressures compared with CPR without abdominal binding but did not affect IVC-to-right-heart venous return. During conventional CPR without abdominal binding, venous return was dependent on the diastolic IVC pressure (r = .86, P = .014), mean IVC pressure (r = .80, P = .03), and carotid blood flow (r = .99, P = .001) but not on the IVC-to-RA pressure gradient. With abdominal binding, venous return was not correlated with any study hemodynamic variable, including the peripheral venous-to-RA pressure gradient. CONCLUSION: Venous return from the subdiaphragmatic venous bed during CPR is dependent on venous pressure, not on the peripheral venous-to-right-heart pressure gradient. Abdominal binding during CPR does not affect venous return. Venous return during CPR diastole is highly dependent on central venous capacitance (left heart outflow during CPR systole).

Atelectasis affects the rate of arterial desaturation during obstructive apnea.

Chronic hemodynamic disturbances are more profound in patients with obstructive sleep apnea when underlying lung disease with abnormal gas exchange (low arterial PO2) is present. Previous studies suggest that pulmonary gas exchange could influence the rate of fall of arterial oxygen saturation (dSaO2/dt) in obstructive sleep apnea. We postulated that abnormal gas exchange in the form of atelectasis would steepen dSaO2/dt and thereby lower nadir arterial oxyhemoglobin saturation (SaO2) for the same duration of apnea. Apneas were created by clamping an indwelling cuffed endotracheal tube at end expiration in eight spontaneously breathing adult baboons. Apneas of the same duration were then repeated during temporary endobronchial occlusion of one lobe of the lung. SaO2 and mixed venous O2 saturation were continuously monitored, and cardiac output was calculated. Worsening of pulmonary gas exchange during atelectasis was documented by an increase in calculated venous admixture from 10.5 +/- 0.8 to 25.0 +/- 0.7% (P less than 0.001). The dSaO2/dt was independent of apnea duration at 30, 45, and 60 s. During endobronchial occlusion, apnea dSaO2/dt increased 20%, and nadir SaO2 was significantly lower. Possible mechanisms for steepening of dSaO2/dt during atelectasis are discussed.

Non-invasive cardiopulmonary support: a canine survival model.

A canine model (group A = 7, B = 7, C = 6) was developed for the study of post-resuscitative disease following untreated ventricular fibrillation with ventilatory arrest (2.5, 5.0, and 7.5 min, respectively). Non-invasive circulatory support (pneumatic vest/binder), with accompanying ventilatory support, was administered for 20.0, 20.0 and 15.0 min, respectively, followed by defibrillation, recovery and elective euthanasia. Sodium bicarbonate and epinephrine were administered during support and early recovery. Group A received the least amount of sodium bicarbonate during cardiopulmonary support and had the highest mean arterial pressure during early recovery. Group B received the most epinephrine during cardiopulmonary support and in total. There were no significant differences in total energy applied during defibrillation. In group A, there was a positive correlation between the total energy applied during defibrillation and the amount of epinephrine administered during early recovery. In group B, there was a positive correlation between the amount of epinephrine administered during cardiopulmonary support and the total energy applied during defibrillation and a negative correlation between the total energy applied and the mean arterial pressure during early recovery. The neurological quality of survival in this model will permit the protracted study of organ dysfunction(s) following prolonged cardiopulmonary arrest and support.

Central venous O2 saturation and rate of arterial desaturation during obstructive apnea.

We examined the rate of fall of arterial O2 saturation (dSao2/dt) after apnea onset in four spontaneously breathing adult male baboons. We postulated that a lower mixed venous O2 saturation (Svo2) would steepen dSao2/dt by more rapid depletion of alveolar O2. Single isolated (NREP) and five or more sequential repetitive apneas (REP) were created by clamping an indwelling cuffed endotracheal tube at end expiration. Fiberoptic catheters were used for continuous monitoring of Sao2, Svo2, and cardiac output. The mean dSao2/dt for all duration NREP apneas was 0.60%/s. Mean dSao2/dt increased above base line for each consecutive REP apnea and was higher in 60 s than in 45 and 30 s REP apnea series. The increase in dSao2/dt corresponded closely with the fall in preapneic Svo2. Preapneic arterial O2 content fell during successive REP apneas but the maximal decrement from base line (1.3 ml/dl) was much less than the maximal decrement in preapneic mixed venous O2 content of 5.1 ml/dl. Preapneic cardiac output for NREP apneas and nadir cardiac output for REP apneas remained constant. Nadir cardiac output for NREP apneas showed higher values for longer duration apneas. We concluded that dSao2/dt is inversely related to preapneic Svo2.

Renal function in conscious dogs: potential effect of gender on measurement.

Conscious dogs were studied to determine the repeatability of and the agreement between conventional inulin clearance (CIn), a urineless or alternative inulin clearance (CInALT), and endogenous creatinine clearance (CCr). Although, the repeatability of the three clearance methods was satisfactory, tests of agreement within gender indicated that CInALT and CCr were not interchangeable numerically with CIn in either males or females. CInALT was significantly higher than CIn in females, and CIn was significantly higher than CCr in both genders. Between genders, there were no significant differences in individual clearance methods, plasma creatinine (PCr), or electrolytes and osmolality. However, urinary osmolality, U/P inulin and U/P creatinine were significantly higher in males. Over the normal range of clearances studied it was not possible to substitute one clearance method for the other regardless of gender. However, the enhanced repeatability of CIn and CInALT in the females suggests that their use in experimental renal studies may be more desirable than males.

Immunogenicity and efficacy of orally administered inactivated influenza virus vaccine in mice.

The immunogenicity and protective efficacy of formalin-inactivated whole influenza A/Bangkok/79 virus vaccine given to unprimed Swiss mice orally in capsules, in their drinking water, or by direct injection into the duodenum were studied. Virus-specific IgG and IgA antibody responses to all these methods were dose-dependent and varied according to immunization conditions. Following intranasal challenge with live A/Bangkok influenza virus, mice given greater than or equal to 66 micrograms haemagglutinin (HA) of vaccine in drinking water or capsules, and mice injected into the duodenum with greater than or equal to 0.66 microgram HA, had significantly lower virus titres in their noses and lungs than control mice comparably inoculated.

Continuous external counterpressure during closed-chest resuscitation: a critical appraisal of the military antishock trouser garment and abdominal binder.

Blood flow during closed-chest CPR may result from variations in intrathoracic pressure rather than selective compression of the cardiac ventricles. During chest compression, the thoracic and abdominal cavities are subjected to positive pressure fluctuations. It has been suggested that compression of the abdomen may improve left heart outflow during CPR by limiting diaphragmatic movement or improving venous return. Abdominal compression has been performed experimentally with pneumatic abdominal binders and with the abdominal compartment of the conventional military antishock trouser (MAST) garment. The MAST garment might also improve cardiac output with CPR through an "autotransfusion" effect. In animal studies, MAST-augmented CPR has improved systolic pressures; it has not been shown to improve vital organ perfusion. In the only available clinical study, CPR with the MAST did not improve survival from prehospital cardiac arrest when compared with conventional CPR alone. If inflation of the MAST does produce blood displacement from the peripheral to the central venous circulation, such an effect may be detrimental in that the arteriovenous pressure gradients necessary for vital organ flow may be adversely affected. Inflation of the MAST during CPR may also adversely effect artificial ventilation. Selective abdominal binding also increases systolic pressures during CPR but does not improve subdiaphragmatic venous return. Although abdominal binding may increase common carotid flow, it has not been shown to improve cerebral or myocardial perfusion when compared with conventional CPR alone. These CPR adjunct techniques have not been shown to improve outcome from cardiac arrest and should remain experimental until further well-designed studies addressing regional vital organ flow and outcome of resuscitation are performed.

Modifications of cardiopulmonary resuscitation based on the cough.

The ability of cardiopulmonary resuscitation (CPR) to provide adequate vital organ blood flow during prolonged resuscitation has long been questioned, as has the mechanism of blood flow during CPR. Because coughing during cardiac arrest has been shown to produce adequate anterograde flow to maintain consciousness in man without compressing the heart, cough CPR has been used as a model of a pure "thoracic pump" mechanism on which to base modifications of CPR. In the thoracic pump mechanism, the left heart is a passive conduit for blood expressed from the pulmonary vasculature to the aorta, and there is selective flow to the brachiocephalic vascular bed because of its low pressure veins, which are protected by closure of thoracic inlet venous valves. Right heart flow from systemic veins to the lungs occurs between applications of pressure. Four alternative modalities exploiting the thoracic pump concept were studied in dogs during ventricular fibrillation with angiographic and pressure recordings: cough CPR, simultaneous chest compression and lung inflation, abdominal compression with lung inflation, and inflation of a vest and binder. The latter technique was associated with successful defibrillation and recovery after more than 30 min of circulatory support during ventricular fibrillation. Preliminary studies in a primate preparation indicate that this technique might be useful for prolonged circulatory support in man when defibrillation is not initially available or successful.

Endocardial and transcutaneous cardiac pacing, calcium chloride, and epinephrine in postcountershock asystole and bradycardias.

Clinically, asystole or a bradyarrhythmia may follow countershock of ventricular fibrillation (VF) in up to 40% of attempts. This study evaluated the effects of artificial cardiac pacing, calcium chloride (CaCl2), and epinephrine in postcountershock asystole/bradycardia. Micromanometer catheters were positioned in the aorta (Ao) and right atrium (RA) of ten dogs and VF induced by right ventricular (RV) stimulation. After 2 min of VF, a 400-J countershock was given. In six animals, asystole or a pulseless bradyarrhythmia followed one countershock. In four animals, up to three countershocks were needed to terminate VF and resulted in asystole or a pulseless bradyarrhythmia. Thirty seconds after termination of VF, cardiac pacing was begun in all animals using conventional RV endocardial pacing (RVEP) or a transcutaneous transthoracic pacing (TTP) technique. RVEP and TTP produced ventricular depolarizations, but electrical capture was never associated with Ao pressure fluctuations. After 2 min of pacing, CaCl2 was given and chest compressions and artificial ventilations (CPR) initiated. CaCl2 had no effect on CPR pressures. After 2 min of CPR, RVEP and TTP were again studied; capture without Ao pressure fluctuations was seen in all animals. Epinephrine was then given and CPR reinstituted. Epinephrine produced a significant increase in CPR Ao systolic pressure (58 +/- 13 to 84 +/- 24 mm Hg, p less than .001) and end-diastolic coronary perfusion pressure (Ao-RA) (9 +/- 4 to 34 +/- 8 mm Hg, p less than .001). Within 94 +/- 53 sec after epinephrine, spontaneous circulation was restored in eight animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Predictive indices of successful cardiac resuscitation after prolonged arrest and experimental cardiopulmonary resuscitation.

To determine if clinically accessible hemodynamic and blood gas measurements are of value in predicting outcome of countershock after prolonged ventricular fibrillation (VF) and artificial cardiopulmonary support, 14 dogs were studied during 30 minutes of VF using two randomly assigned closed-chest techniques. Seven dogs underwent conventional CPR; the other seven were supported with a pneumatic thoracic vest and abdominal binder, which were inflated synchronously with the airway. Ascending aortic (Ao), right atrial (RA), and instantaneous coronary perfusion pressures (Ao - RA) were measured at five-minute intervals. Ao and RA blood samples were analyzed at 10, 20, 25 and 30 minutes for PO2, PCO2, and pH. After 25 minutes, 1 mg epinephrine was given intravenously, and five minutes later defibrillation was attempted. If unsuccessful, repeated countershocks, conventional pharmacologic therapy, and artificial support were continued. If a perfusing spontaneous cardiac rhythm did not result within an additional 30 minutes, the experiment was terminated. Six animals developed a perfusing cardiac rhythm after one or more countershocks (Group 1); eight failed to develop a perfusing rhythm after repeated countershocks and an additional 30 minutes of resuscitative effort (Group 2). Five Group 1 dogs received vest/binder artificial support. When measured values were averaged over the study period, Group 1 was found to have a significantly greater Ao end-diastolic pressure (AoEDP) and peak diastolic coronary perfusion pressure (CPP) when compared to Group 2 (23 +/- 6 vs 14 +/- 8 mm Hg, P less than .05; and 22 +/- 6 vs 5 +/- 10 mm Hg, P less than .01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Use of naloxone during cardiac arrest and CPR: potential adjunct for postcountershock electrical-mechanical dissociation.

Naloxone has been shown to increase arterial pressure in hemorrhagic and septic shock. To determine if naloxone has salutary effects during cardiac arrest with conventional closed-chest cardiopulmonary resuscitation (CPR), ten dogs were studied during 20 minutes of ventricular fibrillation (VF) and CPR and during a 30-minute postcountershock period. Central aortic (Ao) and right atrial (RA) systolic and end-diastolic (EDP) pressures, instantaneous Ao-RA pressure difference (coronary perfusion pressure), and electromagnetic Ao flow were measured. Ao and RA samples were analyzed during a control period and at five-minute intervals during CPR for PO2, PCO2, and pH. During VF, a piston-cylinder device was used to perform anteroposterior sternal depressions and positive pressure ventilations (100% O2) at standard rates and ratios. After 15 minutes of CPR, animals were randomized and given either naloxone (5 mg/kg) or epinephrine (1 mg). Defibrillation was attempted five minutes later using 1 J/kg and then, if necessary, 2, 4, 8, 12, and 16 J/kg until VF was terminated or the maximum energy dose was reached. If VF persisted or if countershock resulted in asystole or a nonperfusing rhythm (electrical-mechanical dissociation [EMD]), the alternate drug (naloxone or epinephrine) was then given. Measured systolic pressures, coronary perfusion pressures, aortic flow, and blood gases were not significantly different during the control period or at five, ten, and 15 minutes of VF and CPR between animal groups prior to drug administration. When compared to hemodynamic values measured at 15 minutes, naloxone had no significant effect on pressures or aortic flow measured five minutes after administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanical "cough" cardiopulmonary resuscitation during cardiac arrest in dogs.

Hemodynamic findings during ventricular fibrillation (VF) and closed-chest cardiopulmonary resuscitation (CPR) are similar to those described during VF and vigorous coughing. Interventions during CPR that mimic the physiologic events of coughing (high intrathoracic pressure and high intraabdominal pressure) improve perfusion during VF and CPR. An external circulatory assist apparatus was devised to emulate cough physiology, i.e., simultaneous pulsatile increases in intrathoracic pressure (pneumatic vest), intraabdominal pressure (abdominal binder) and airway pressure (high-pressure airway inflation). In this study, vest/binder CPR was compared with conventional CPR during 30 minutes of VF and artificial support in 18 randomized dogs. Defibrillation and long-term (more than 24 hours) survival were chosen as end points. During VF and artificial support, aortic and right atrial (RA) pressures, the instantaneous aortic-RA pressure difference (coronary perfusion pressure) and blood gas levels were measured. After 30 minutes of VF and administration of 1 mg of epinephrine, countershock was attempted. Systolic aortic and RA pressures, mean aortic-RA pressure difference and blood gas levels were not significantly different between dogs that were successfully resuscitated and those that were not. However, peak diastolic coronary perfusion pressure (peak diastolic aortic-RA pressure) for survivors averaged 23 +/- 6 mm Hg, but only 6 +/- 10 mm Hg for nonsurvivors (p less than 0.001). A peak diastolic coronary perfusion pressure 16 mm Hg or greater had a positive and negative predictive value for a successful outcome of 1.00. Only 1 of 9 conventional CPR dogs survived 24 hours; 7 of 9 dogs supported with the vest/binder device were alive and neurologically normal at 24 hours (p = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary resuscitation research 1960-1984: discoveries and advances.

The 24-year history of cardiopulmonary resuscitation (CPR) can be divided into four eras. The first (1960-1962) was the era of serendipitous discovery and description of "closed-chest cardiac massage" by Kouwenhoven and colleagues. Closed-chest heart massage was combined with artificial ventilation, and became known as CPR. The second (1962-1968) was the era of skepticism, in which CPR was challenged by investigators whose observations of hemodynamics were not in concert with the proposed mechanism of blood flow. The equality of arterial and central venous pressures during chest compression seemingly belied the proposed mechanism of blood flow during CPR, and raised questions about the effectiveness of the technique. The third era (1968-1976) was one of acceptance and complacency. The effectiveness had become established through widespread use in coronary care units, catheterization laboratories, and prehospital emergency systems, and open-chest cardiac massage was completely supplanted by CPR in virtually every resuscitation effort. The current era (1976-present) is the era of rediscovery and refinement, beginning with the observation that blood flow and pressure can be generated during cardiac arrest by coughing ("cough CPR"), without actual compression of the chest or heart, and that augmentation of arterial pressure and carotid blood flow resulted from simultaneous compression and ventilation (SCV-CPR or "new CPR"). The current era has provided a new explanation of the mechanism of blood flow during CPR and alternative methods of maintaining perfusion during cardiac arrest.(ABSTRACT TRUNCATED AT 250 WORDS)

Circulatory support during cardiac arrest using a pneumatic vest and abdominal binder with simultaneous high-pressure airway inflation.

Animal and clinical studies suggest that blood flow during closed-chest cardiopulmonary resuscitation (CPR) results from phasic intrathoracic pressure fluctuations produced by rhythmic sternal depressions rather than from cardiac compression. Using physiologic observations made in animals and human beings during circulatory collapse and vigorous coughing, a pneumatic thoracic vest garment and abdominal binder device has been designed to emulate "cough CPR." Hemodynamic findings and microsphere regional perfusion observed during cardiac arrest and airway/vest/binder inflation are comparable to those observed during simultaneous chest compression and pulmonary ventilation CPR (SCV-CPR). Resuscitation and survival using the device has been compared to survival rates using conventional closed-chest CPR. The vest/binder apparatus significantly improved the coronary perfusion gradient and survival. Further studies are in progress to determine the clinical utility of this promising resuscitation adjunct.

Atropine: animal models.

Bradyarrhythmias, with or without hypotension, may be associated with acute myocardial infarction, especially inferior. The early use of atropine in the management of sinus bradycardia, with associated hypotension, spurred a continuing controversy that has found only partial solution in animal models. Experimentally there is increased sensory and autonomic motor activity with acute coronary occlusion. For example, in the cat, increased cholinergic activity was evidenced by the absence of bradycardia with atropinization and vagotomy, although these pretreatments accelerated the onset of significant ventricular arrhythmias. Atropine in experimentally infarcted dogs increased ischemia, while elevated heart rates reduced the threshold for ventricular fibrillation (VF) and vagal stimulation increased the threshold for VF, largely independent of heart rate. Specific clinical studies failed to support much of the animal data, although reports of tachyarrhythmias and VF resulting from the administration of atropine extended the controversy. The animal models, in the main, failed to mimic the clinical situation, for: 1) pentobarbital, with its propensity to alter some autonomic reflexes, dominated earlier work; 2) relatively large doses of atropine were employed; 3) the animals were presumed to be free of coronary and cardiac disease, factors known to influence autonomic reflexes; and 4) vagotomy and atropinization commonly preceded the acute occlusion.

Effects of acidemia and sodium bicarbonate therapy in advanced cardiac life support.

Cardiac output using the currently recommended closed-chest cardiopulmonary resuscitation (CPR) technique is marginal (less than 30% of control), and eventually will result in tissue hypoperfusion and lactic acidemia. Intermittent sodium bicarbonate administration currently is recommended for treatment of this metabolic acidemia, and based on available data recommended dosages are empiric but sound. In this review the potential complications of acidemia and sodium bicarbonate administration are considered from the viewpoint of resuscitation outcome. In our opinion, available data are limited, and further evaluation and consideration of sodium bicarbonate requirements in the resuscitation setting are required.

The pharyngeo-tracheal lumen airway: preliminary investigation of a new adjunct.

The technique of prehospital airway management is determined largely by the level of training and expertise of the prehospital care provider. We report preliminary observations and data in experimental animals and patients using a new airway adjunct--the pharyngeo-tracheal lumen (PTL) airway. The PTL airway employs a two-tube, two-cuff system that is inserted in a "blind" fashion. The airway's design allows it to function as an endotracheal tube if the trachea is entered or as an esophageal obturator airway (EOA) if the esophagus is intubated. In the esophageal position, a face-to-mask seal is not required. Preliminary data in 23 experimental animals suggest that the PTL (in the esophageal position) is as effective as a conventional cuffed endotracheal tube. Volumetric efficiency at optimal cuff inflation pressures was 100%, and arterial blood gas values obtained during PTL ventilation were not significantly different from those measured during ventilation with an endotracheal tube at comparable minute ventilations. In six arrest patients undergoing cardiopulmonary resuscitation, arterial PO2 and PCO2 using the PTL airway (176 +/- 105 mm Hg and 36 +/- 12 mm Hg, respectively) were not significantly different from those measured during artificial ventilation with an endotracheal tube (PO2, 162 +/- 124 mm Hg; PCO2, 34 +/- 10 mm Hg). Although the numbers are small, the data suggest that the PTL airway may be an alternative method of emergency airway management when endotracheal intubation cannot be performed.