Exhaled tidal volume overestimation in mechanically ventilated patients with large cardiogenic oscillation

OBJECTIVES: In postcardiac surgery patients, we often noticed that monitored tidal volumes exceeded the ventilator settings. We investigated whether cardiogenic oscillation causes overestimation of tidal volume. DESIGN: Prospective, observational, clinical study. SETTING: Surgical intensive care unit in a national heart institute. PATIENTS: Eight postcardiac surgery patients (age 13-70). INTERVENTIONS: Patients were paralyzed and received flow-triggered volume-controlled ventilation with a tidal volume of 10 mL/kg. In random order, two types of ventilator (Bird 8400 STi and Servo-300) and two respiratory rates (5 and 10 breaths/min) were applied to each patient via a disposal ventilatory circuit and heat-and-moisture exchanger. For each ventilator, we adjusted the flow-triggering sensitivity to prevent autotriggering due to cardiogenic oscillation: 10 L/min for the Bird 8400 STi and green zone for the Servo-300. MEASUREMENTS AND MAIN RESULTS: The magnitude of cardiogenic oscillation during mechanical ventilation was defined as peak expiratory flow fluctuation at end-expiration. We recorded tidal volume using the monitoring devices on the ventilators and calculated the discrepancy from the set tidal volume.Cardiogenic oscillation was significantly greater with the Bird 8400STi (4.0 +/- 1.8 L/min) than with the Servo-300 (1.7 +/- 0.8 L/min). With the Bird 8400 STi, the discrepancy between monitored tidal volume and set tidal volume ranged from 15 to 260 mL when the respiratory rate was 5 breaths/min and from -9 to 75 mL at 10 breaths/min; there was a linear correlation between the overestimation of tidal volume and the magnitude of cardiogenic oscillation. In contrast, with the Servo-300, the discrepancy was relatively small (-36 to 14 mL). CONCLUSIONS: In mechanically ventilated patients with large cardiogenic oscillation, exhaled tidal volume is overestimated on at least one model of ventilator.     

Inadvertent triggering of the ventilator caused by surgically placed pacer wires

Inadvertent ventilator triggering can occur for various reasons. Leaks in the ventilator circuit, endotracheal tube leaks, tracheal cuff leaks, cardiac oscillations, water condensate causing oscillations in the circuit tubing, ventilator expiratory valve integrity, and overly sensitive triggering mechanism settings may precipitate this phenomena. We present a case of inadvertent ventilator triggering caused by electrical stimulation of the diaphragm from surgically placed pacing wires post cardiothoracic surgery. A 47-year-old woman underwent surgical placement of a left (LVAD) and right (RVAD) ventricular assist device for severe end stage cardiomyopathy, as a bridge to cardiac transplantation. The patient was observed to have inadvertent ventilator triggering while deeply sedated postoperatively. The ventilator set respiratory rate was 16 breaths/min, with patient respiratory rate of 30 breaths/min while deeply sedated. Upon assessment of ventilator waveforms and arterial blood gas revealing a profound respiratory alkalosis, the pressure/time waveform demonstrated a -2 cm H(2)O decrease in pressure prior to each cycled breath. The ventilator was subsequently changed from flow trigger sensitivity of 3 L/min to pressure trigger sensitivity of -3 cm H(2)O to eliminate the autotriggering. Later in the patient's ICU stay, inadvertent ventilator triggering was again observed. Further adjustment of the pressure trigger sensitivity to -3 cm H(2)O eliminated the autotriggering. Clinical assessment found the pacing wires were responsible for stimulating the patient's diaphragm, therefore causing airway pressure decreases and premature breath delivery. Once the electrical amplitude of the pacemaker was decreased, the inadvertent ventilator triggering resolved and normal trigger sensitivity and pH was restored.     

Comparison of a 10-breaths-per-minute versus a 2-breaths-per-minute strategy during cardiopulmonary resuscitation in a porcine model of cardiac arrest

BACKGROUND: Hyperventilation during cardiopulmonary resuscitation (CPR) is harmful. METHODS: We tested the hypotheses that, during CPR, 2 breaths/min would result in higher cerebral perfusion pressure and brain-tissue oxygen tension than 10 breaths/min, and an impedance threshold device (known to increase circulation) would further enhance cerebral perfusion and brain-tissue oxygen tension, especially with 2 breaths/min. RESULTS: Female pigs (30.4 +/- 1.3 kg) anesthetized with propofol were subjected to 6 min of untreated ventricular fibrillation, followed by 5 min of CPR (100 compressions/min, compression depth of 25% of the anterior-posterior chest diameter), and ventilated with either 10 breaths/min or 2 breaths/min, while receiving 100% oxygen and a tidal volume of 12 mL/kg. Brain-tissue oxygen tension was measured with a probe in the parietal lobe. The impedance threshold device was then used during an 5 additional min of CPR. During CPR the mean +/- SD calculated coronary and cerebral perfusion pressures with 10 breaths/min versus 2 breaths/min, respectively, were 17.6 +/- 9.3 mm Hg versus 14.3 +/- 6.5 mm Hg (p = 0.20) and 16.0 +/- 9.5 mm Hg versus 9.3 +/- 12.5 mm Hg (p = 0.25). Carotid artery blood flow, which was prospectively designated as the primary end point, was 65.0 +/- 49.6 mL/min in the 10-breaths/min group, versus 34.0 +/- 17.1 mL/min in the 2-breaths/min group (p = 0.037). Brain-tissue oxygen tension was 3.0 +/- 3.3 mm Hg in the 10-breaths/min group, versus 0.5 +/- 0.5 mm Hg in the 2-breaths/min group (p = 0.036). After 5 min of CPR there were no significant differences in arterial pH, PO2, or PCO2 between the groups. During CPR with the impedance threshold device, the mean carotid blood flow and brain-tissue oxygen tension in the 10-breaths/min group and the 2-breaths/min group, respectively, were 102.5 +/- 67.9 mm Hg versus 38.8 +/- 23.7 mm Hg (p = 0.006) and 4.5 +/- 6.0 mm Hg versus 0.7 +/- 0.7 mm Hg (p = 0.032). CONCLUSIONS: Contrary to our initial hypothesis, during the first 5 min of CPR, 2 breaths/min resulted in significantly lower carotid blood flow and brain-tissue oxygen tension than did 10 breaths/min. Subsequent addition of an impedance threshold device significantly enhanced carotid flow and brain-tissue oxygen tension, especially in the 10-breaths/min group.     

Microvascular response in patients with cardiogenic shock

OBJECTIVE: To examine the mechanisms contributing to decreased microvascular blood flow in cardiogenic shock by comparing patients with cardiogenic shock with critically ill controls and with patients with septic shock. DESIGN: Prospective, consecutive entry of patients meeting the criteria for septic shock, cardiogenic shock, and critical illness without coexisting infection or shock. SETTING: University hospital, medical intensive care unit, coronary care unit, and respiratory care unit. PATIENTS: Eight patients with cardiogenic shock secondary to acute myocardial infarction, six critically ill controls, and six patients with septic shock. MEASUREMENTS AND MAIN RESULTS: Forearm blood flow was measured at rest and during reactive hyperemia by venous air plethysmography. Red cell deformability was determined by filtration. Leukocyte aggregation was detected by the leukergy test. Neutrophil CD11b/CD18 expression and soluble intercellular adhesion molecule-1 levels were also measured. In cardiogenic shock, forearm arterial resistance was significantly increased at rest and during reactive hyperemia compared with controls and patients with septic shock. The response to reactive hyperemia was attenuated in cardiogenic and septic shock patients, as measured by the absolute change in forearm blood flow from baseline, which was significantly less as compared with controls (p < .01). The percent change in forearm blood flow during reactive hyperemia compared with forearm blood flow at rest was significantly lower in cardiogenic shock (60+/-10) and in septic shock (50+/-11) compared with controls at baseline (145+/-20; p < .01). Red cell deformability was significantly decreased in cardiogenic shock (1.2+/-0.2 mL/min; p < .05) and septic shock (1.1+/-0.2 mL/min; p < .05), compared with controls (1.8+/-0.1 mL/min). Neutrophil CD11b/CD18 expression, leukergy, and serum intercellular adhesion molecule-1 levels in cardiogenic shock patients were not significantly different from controls. CONCLUSION: These data suggest that the response to reactive hyperemia is attenuated in cardiogenic shock. This appears to reflect increased vasoconstriction and an impaired capacity for vasodilation. Decreased erythrocyte deformability may also be important in limiting systemic microvascular flow. However, evidence supporting a role for neutrophil-endothelial cell interactions was not observed.     

Effects of cardiogenic shock on lactate and glucose metabolism after heart surgery

BACKGROUND: Hyperlactatemia is a prominent feature of cardiogenic shock. It can be attributed to increased tissue production of lactate related to dysoxia and to impaired utilization of lactate caused by liver and tissue underperfusion. The aim of this prospective observational study was to determine the relative importance of these mechanisms during cardiogenic shock. PATIENTS: Two groups of subjects were compared: seven cardiac surgery patients with postoperative cardiogenic shock and seven healthy volunteers. METHODS: Lactate metabolism was assessed by using two independent methods: a) a pharmacokinetic approach based on lactate plasma level decay after the infusion of 2.5 mmol x kg(-1) of sodium lactate; and b) an isotope dilution technique for which the transformation of [13C]lactate into [13C]glucose and 13CO2 was measured. Glucose turnover was determined using 6,62H2-glucose. RESULTS: All patients suffered from profound shock requiring high doses of inotropes and vasopressors. Mean arterial lactate amounted to 7.8 +/- 3.4 mmol x L(-1) and mean pH to 7.25 +/- 0.07. Lactate clearance was not different in the patients and controls (7.8 +/- 3.4 vs. 10.3 +/- 2.1 mL x kg(-1) x min(-1)). By contrast, lactate production was markedly enhanced in the patients (33.6 +/- 16.4 vs. 9.6 +/- 2.2 micromol x kg(-1) x min(-1); p < .01). Exogenous [13C]lactate oxidation was not different (107 +/- 37 vs. 103 +/- 4 mmol), and transformation of [13C]lactate into [13C]glucose was not different (20.0 +/- 13.7 vs. 15.2% +/- 6.0% of exogenous lactate). Endogenous glucose production was markedly increased in the patients (1.95 +/- 0.26 vs. 5.3 +/- 3.0 mg x kg(-1) x min(-1); p < .05 [10.8 +/- 1.4 vs. 29.4 +/- 16.7 micromol x kg(-1) x min(-1)]), whereas net carbohydrate oxidation was not different (1.7 +/- 0.5 vs. 1.3 +/- 0.3 mg x kg(-1) x min(-1) [9.4 +/- 2.8 vs. 7.2 +/- 1.7 micromol x kg(-1) x min(-1)]). CONCLUSIONS: Hyperlactatemia in early postoperative cardiogenic shock was mainly related to increased tissue lactate production, whereas alterations of lactate utilization played only a minor role. Patients had hyperglycemia and increased nonoxidative glucose disposal, suggesting that glucose-induced stimulation of tissue glucose uptake and glycolysis may contribute significantly to hyperlactatemia.     

Lactate and glucose metabolism in severe sepsis and cardiogenic shock

OBJECTIVE: To evaluate the relative importance of increased lactate production as opposed to decreased utilization in hyperlactatemic patients, as well as their relation to glucose metabolism. DESIGN: Prospective observational study. SETTING: Surgical intensive care unit of a university hospital. PATIENTS: Seven patients with severe sepsis or septic shock, seven patients with cardiogenic shock, and seven healthy volunteers. INTERVENTIONS: C-labeled sodium lactate was infused at 10 micromol/kg/min and then at 20 micromol/kg/min over 120 mins each. H-labeled glucose was infused throughout. MEASUREMENTS AND MAIN RESULTS: Baseline arterial lactate was higher in septic (3.2 +/- 2.6) and cardiogenic shock patients (2.8 +/- 0.4) than in healthy volunteers (0.9 +/- 0.20 mmol/L, p < .05). Lactate clearance, computed using pharmacokinetic calculations, was similar in septic, cardiogenic shock, and controls, respectively: 10.8 +/- 5.4, 9.6 +/- 2.1, and 12.0 +/- 2.6 mL/kg/min. Endogenous lactate production was determined as the initial lactate concentration multiplied by lactate clearance. It was markedly enhanced in the patients (septic 26.2 +/- 10.5; cardiogenic shock 26.6 +/- 5.1) compared with controls (11.2 +/- 2.7 micromol/kg/min, p < .01). C-lactate oxidation (septic 54 +/- 25; cardiogenic shock 43 +/- 16; controls 65 +/- 15% of a lactate load of 10 micromol/kg/min) and transformation of C-lactate into C-glucose were not different (respectively, 15 +/- 15, 9 +/- 18, and 10 +/- 7%). Endogenous glucose production was markedly increased in the patients (septic 14.8 +/- 1.8; cardiogenic shock 15.0 +/- 1.5) compared with controls (7.2 +/- 1.1 micromol/kg/min, p < .01) and was not influenced by lactate infusion. CONCLUSIONS: In patients suffering from septic or cardiogenic shock, hyperlactatemia was mainly related to increased production, whereas lactate clearance was similar to healthy subjects. Increased lactate production was concomitant to hyperglycemia and increased glucose turnover, suggesting that the latter substantially influences lactate metabolism during critical illness.     

Myocardial ischemia and weaning failure in patients with coronary artery disease: an update.

OBJECTIVE: To determine the frequency and effects of weaning-related myocardial ischemia on weaning outcomes in patients with coronary artery disease. DESIGN: Prospective cohort study. SETTING: Medical and cardiac intensive care units of a 300-bed teaching community hospital. MEASUREMENTS AND MAIN RESULTS: Three-lead ST segments, heart rate-systolic blood pressure products, and respiratory rate/tidal volume ratios were obtained for patients with coronary artery disease just before and during their initial trials of weaning from mechanical ventilation. ST segments were interpreted by a blinded cardiologist. Eighty-three patients with a mean age of 72.4 +/- 1.1 years (mean +/- SEM), a mean Acute Physiology and Chronic Health Evaluation II score of 16.4 +/- 0.8, and a mean duration of mechanical ventilation of 4.6 +/- 0.9 days were studied. Eight patients showed electrocardiographic evidence of ischemia during weaning, and seven of these patients failed to be liberated on their first day of weaning. The presence of ischemia significantly increased the risk of weaning failure (risk ratio, 2.1; 95% confidence interval, 1.4-3.1). The rate-pressure product for the group as a whole increased significantly during weaning, from 11.9 +/- 0.4 to 13.5 +/- 0.5 mm Hg x beats/min x 10(3) (p < .01). The increase in rate-pressure product tended to be greater in patients who became ischemic (12.8 +/- 0.9 to 17.3 +/- 2.0 mm Hg x beats/min x 10(3)) than in patients who were not ischemic during weaning (11.8 +/- 0.4 to 13.0 +/- 0.5 mm Hg x beats/min x 10(3); p = .05). The rate/volume ratio did not change significantly during weaning, but the rate/volume ratios after both 1 min (65.6 +/- 4.6 vs. 98.0 +/- 9.4 breaths/min/L; p < .05) and 30 mins (68.6 +/- 4.3 vs. 91.1 +/- 8.9 breaths/min/L; p < .05) of unassisted breathing were lower in successful than in unsuccessful patients. CONCLUSION: Electrocardiographic evidence of myocardial ischemia occurs frequently and is associated with significantly increased risk of first-day weaning failure in patients with coronary artery disease.     

Relationship Between Atrioventricular Delay and Oxygen Consumption in Patients with Sick Sinus Syndrome: Relevance to Rate Responsive Pacing

To develop a dromotropic-controlled rate adaptive algorithm for patients with sick sinus syndrome (SSS) and intact AV conduction, 14 pace-maker patients with SSS underwent cardiopulmonary exercise testing (CPX). During exercise, the pace-maker was programmed in an AAT mode without rate adaptation, whereby 3 patients developed supraventricular arrhythmia and 11 patients kept sinus rhythm. Chronotropic incompetence (CI) at heart rate (HR) < 95 beats/min at the anaerobic threshold (AT) was found in five patients. In patients with chronotropic competence (CC), the HR increase was significantly greater than in CI patients (rest: 73.2 +/- 12.6 vs. 64.2 +/- 4.0 beats/min;AT:101.2 +/- 6.2 vs. 82.0 +/- 5.1 beats/min;peak: 135.2 +/- 10.7 vs. 103.2 +/- 10.9 beats/min). There was no significant difference in the AVD between CC and CI patients (rest: 167.7 +/- 38.6 vs. 170.8 +/- 22.5 ms, AT: 156.2 +/- 30.7 vs. 163.6 +/- 21.6 ms, peak: 144.7 +/- 29.0 vs. 152.4 +/- 15.0 ms). The correlation coefficient between HR increase and VO2 was +1.0 and between AVD decrease and VO2 - 1.0 in both groups. An increase in pacing rate from 75 beats/min to 120 beats/min without exercise (overpacing) led to a prolongation of the AV interval of about 30.6 +/- 14.2 ms. Based on this closed loop control with negative feedback, a dromotropic rate adaptive algorithm for patients with SSS and intact AV conduction could be developed.     

Effects of captopril on blood pressure, placental blood flow and uterine oxygen consumption in pregnant rabbits.

Uterine renin may regulate uteroplacental blood flow locally through changes in vascular resistance or systemically by supporting arterial blood pressure. Captopril (5 mg/kg) was given i.v. to 14 conscious pregnant rabbits at day 27.5 +/- 0.3 of gestation for the purpose of investigating the effects of angiotensin converting enzyme inhibition on uteroplacental blood flow and oxygen consumption. Control measurements (mean +/- S.E.M.) were compared to measurements made at 1 hr (n = 14) and at 3 to 4 hr (n = 7). Arterial blood pressure decreased from 80 +/- 3 to 66 +/- 3 mm Hg, P less than .01, and then declined further to 56 +/- 4 mm Hg, P less than .01. Cardiac output was unchanged at 1 hr, 799 +/- 79 vs. 705 +/- 61 ml/min, but was decreased to 634 +/- 29 ml/min by 3 to 4 hr, P less than .01. There was no change in renal blood flow from 102 +/- 13 ml/min. Total uterine blood flow decreased from 37 +/- 5 to 29 +/- 5 ml/min, P less than .01, and then to 23 +/- 1 ml/min, P less than .01, whereas placental blood flow decreased from 25 +/- 4 to 19 +/- 3 to 15 +/- 3 ml/min, P less than .01; there was no significant change in myoendometrial flow. Oxygen delivery per uterine horn decreased from 2.4 +/- 0.3 to 1.8 +/- 0.4 to 1.6 +/- 0.2 ml/min, P less than .005. Oxygen consumption per horn decreased from 1.31 +/- 0.14 to 1.05 +/- 0.15 ml/min by 1 hr, P less than .05, and there was no further decrease.(ABSTRACT TRUNCATED AT 250 WORDS)     

The stroke upper-limb activity monitor: its sensitivity to measure hemiplegic upper-limb activity during daily life

OBJECTIVE: To test the Stroke Upper-Limb Activity Monitor (Stroke-ULAM), which uses electrogoniometry and accelerometry to measure the amount of upper-limb usage in stroke patients in daily life conditions, for its sensitivity to discriminate between moderately recovered and well-recovered stroke patients and control subjects. DESIGN: Cross-sectional study. SETTING: At home or a rehabilitation center. PARTICIPANTS: Seventeen patients with stroke and 5 control subjects. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: Level of usage of upper limb and the percentage of affected upper-limb activity compared with unaffected upper-limb activity (proportion). RESULTS: The level of usage of the affected upper limb of stroke patients was lower than that of the nondominant upper limb of control subjects (electrogoniometry, 97.8 degrees+/-92.3 degrees/min vs 286.2 degrees+/-46.5 degrees/min, P<.01; accelerometry 1.0+/-0.5 g/min vs 2.4+/-0.8 g/min, P<.01). Stroke patients had lower proportions than control subjects in both electrogoniometry (22.6%+/-18.0% vs 84.6%+/-9.8%, P<.01) and accelerometry (39.2%+/-21.4% vs 93.3%+/-5.0%, P<.01). Well-recovered stroke patients had significantly higher proportions compared with moderately recovered patients on both electrogoniometry and accelerometry. CONCLUSIONS: The Stroke-ULAM sensitively measures actual performance, and therefore can be a valuable addition to the mostly capacity-oriented tools currently used to evaluate upper-limb function. Proportion is preferred to the level of usage.     

Increasing respiratory rate to improve CO2 clearance during mechanical ventilation is not a panacea in acute respiratory failure

BACKGROUND: Increasing respiratory rate has recently been proposed to improve CO2 clearance in patients with acute respiratory failure who are receiving mechanical ventilation. However, the efficacy of this strategy may be limited by deadspace ventilation, and it might induce adverse hemodynamic effects related to dynamic hyperinflation. SETTING: An intensive care unit of a university hospital. PATIENTS: We studied 14 patients with acute respiratory failure during the adjustment of ventilator settings on the first day of mechanical ventilation in volume-controlled mode. MEASUREMENTS: After determining the positive end-expiratory pressure that suppresses any intrinsic positive end-expiratory pressure at a respiratory rate of 15 breaths/min, we compared blood gas analysis, respiratory measurements, and Doppler evaluation of right ventricular systolic function by using two different respiratory strategies with the same airway pressure limitation (plateau pressure, < or =25 cm H2O), a low-rate conventional respiratory strategy with a respiratory rate of 15 breaths/min, and a high-rate strategy with a respiratory rate of 30 breaths/min. RESULTS: Compared with the low-rate strategy, the high-rate strategy neither significantly reduced PaCO2 (47 +/- 8 vs. 51 +/- 7 mm Hg with the low-rate strategy) nor significantly improved PaO2 (99 +/- 40 vs. 95 +/- 35 mm Hg with the low-rate strategy). It significantly increased alveolar deadspace to tidal volume ratio (21% +/- 8%, vs. 14% +/- 6% with the low-rate strategy) and produced dynamic hyperinflation, resulting in a substantial intrinsic positive end-expiratory pressure (6.4 +/- 2.7 cm H2O). Right ventricular outflow impedance was increased, resulting in a significant drop in the cardiac index (2.9 +/- 0.6 vs. 3.3 +/- 0.7 L/min/m with the low-rate strategy). CONCLUSION: We conclude that a high respiratory rate strategy during mechanical ventilation in patients with acute respiratory failure did not improve CO2 clearance, produced dynamic hyperinflation, and impaired right ventricular ejection.     

Cardiorespiratory effects of naloxone in children

BACKGROUND: Data on the cardiorespiratory changes and complications following administration of naloxone in children are limited. OBJECTIVE: To evaluate the cardiorespiratory changes and complications following naloxone treatment in children. METHODS: The maximal changes in respiratory rate (RR), heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure, and any complications within 1 and 2 hours following naloxone were tabulated. RESULTS: One hundred ninety-five children received naloxone over 3 years. The mean +/- SD age was 9.7 +/- 6 years. The total doses of naloxone ranged from 0.01 to 7 mg (0.001-0.5 mg/kg body weight), with a median dose of 0.1 mg. Group 1 patients consisted of 116 (60%) children who were postoperative and had been given naloxone by an anesthesiologist; group 2 patients consisted of 79 (40%) children who received naloxone in the emergency department or pediatric intensive care unit. Patients in group 1 were older: 10.6 +/- 5.3 versus 8.2 +/- 6.7 years (p < 0.006), but received significantly lower doses of naloxone (0.09 +/- 0.2 vs. 1.1 +/- 0.76 mg; p < 0.001). When the entire cohort was evaluated, a significant increase in RR (15 +/- 7 vs. 21 +/- 8 breaths/min; p < 0.001), HR (102 +/- 29 vs.107 +/- 29 beats/min; p < 0.001), SBP (109 +/- 17 vs. 115 +/- 15 mm Hg; p < 0.001), and DBP (56 +/- 10 vs. 60 +/- 13 mm Hg; p < 0.001) within 1 hour following naloxone was noted. When the 2 groups were compared, only the changes in RR were greater in group 2 patients (6.8 +/- 7.9 vs. 4.7 +/- 5 breaths/min; p < 0.001) following naloxone. Systolic hypertension occurred in 33 of 195 (16.9%) of all patients, while diastolic hypertension occurred in 13 (6.6%) of all patients after naloxone. Only the incidence of diastolic hypertension was higher in group 2 compared with group 1 patients following naloxone (16% vs. 2%; p < 0.001). Hypertension resolved spontaneously. One child developed pulmonary edema and required positive pressure ventilation for 22 hours. CONCLUSIONS: Moderate increases in RR, HR, and BP occur after naloxone administration to children, but development of more serious complications is rare.     

Comparison of epinephrine and vasopressin in a pediatric porcine model of asphyxial cardiac arrest

OBJECTIVE: This study was designed to compare the effects of vasopressin vs. epinephrine vs. the combination of epinephrine with vasopressin on vital organ blood flow and return of spontaneous circulation in a pediatric porcine model of asphyxial arrest. DESIGN: Prospective, randomized laboratory investigation using an established porcine model for measurement of hemodynamic variables, organ blood flow, blood gases, and return of spontaneous circulation. SETTING: University hospital laboratory. SUBJECTS: Eighteen piglets weighing 8-11 kg. INTERVENTIONS: Asphyxial cardiac arrest was induced by clamping the endotracheal tube. After 8 mins of cardiac arrest and 8 mins of cardiopulmonary resuscitation, a bolus dose of either 0.8 units/kg vasopressin (n = 6), 200 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered in a randomized manner. Defibrillation was attempted 6 mins after drug administration. MEASUREMENTS AND MAIN RESULTS: Mean +/- SEM coronary perfusion pressure, before and 2 mins after drug administration, was 13 +/- 2 and 23 +/- 6 mm Hg in the vasopressin group; 14 +/- 2 and 31 +/- 4 mm Hg in the epinephrine group; and 13 +/- 1 and 33 +/- 6 mm Hg in the epinephrine-vasopressin group, respectively (p = NS). At the same time points, mean +/- SEM left ventricular myocardial blood flow was 44 +/- 31 and 44 +/- 25 mL x min-(1) x 100 g(-1) in the vasopressin group; 30 +/- 18 and 233 +/- 61 mL x min(-1) x 100 g(-1) in the epinephrine group; and 36 +/- 10 and 142 +/- 57 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p < .01 epinephrine vs. vasopressin; p < .02 epinephrine-vasopressin vs. vasopressin). Total cerebral blood flow trended toward higher values after epinephrine-vasopressin (60 +/- 19 mL x min(-1) x 100 g(-1)) than after vasopressin (36 +/- 17 mL x min(-1) x 100 g(-1)) or epinephrine alone (31 +/- 7 mL x min(-1) x 100 g(-1); p = .07, respectively). One of six vasopressin, six of six epinephrine, and four of six epinephrine-vasopressin-treated animals had return of spontaneous circulation (p < .01, vasopressin vs. epinephrine). CONCLUSIONS: Administration of epinephrine, either alone or in combination with vasopressin, significantly improved left ventricular myocardial blood flow during cardiopulmonary resuscitation. Return of spontaneous circulation was significantly more likely in epinephrine-treated pigs than in animals resuscitated with vasopressin alone.     

Enhancing liver blood flow after cardiopulmonary bypass: the effects of dopamine and dopexamine

Liver blood flow is reduced after cardiopulmonary bypass (CPB) and both dopamine and dopexamine are used to overcome this. This study compares the effects of these agents on liver blood flow. Thirty patients undergoing elective coronary artery bypass graft surgery were randomized into three groups (n = 10 per group). Six hours after surgery baseline liver blood flow was determined by the percentage disappearance rate of indocyanine green measured by dichromatic auricular densitometery. Patients then received infusions of either: (1) placebo (dextrose 5%); (2) dopamine (4 micrograms/kg/min); (3) dopexamine (1 microgram/kg/min increasing to 2 micrograms/kg/min). One hour after infusion, liver blood flow measurements were repeated. In the dopexamine group the infusion was increased and the measurements repeated another hour later. We found that patient-specific variables and operative details were similar for all groups. Postoperative cardiac index and heart rate were increased significantly by dopamine (cardiac index 2.82 +/- 0.46 l/m/m2 vs 3.28 +/- 0.67 l/m/m2: p < 0.001 and heart rate 87.5 +/- 13.2 vs 96 +/- 16: p < 0.05) and dopexamine at 2 micrograms/kg/min (cardiac index 2.71 +/- 0.53 l/m/m2 vs 3.45 +/- 0.67 l/m/m2: p < 0.05 and heart rate 89.0 +/- 18.9 vs 107.4 +/- 13.6: p < 0.001) compared to placebo (cardiac index 2.97 +/- 0.8 l/m/m2 vs 3.18 +/- 0.9 l/m/m2: p > 0.05 and heart rate 77.2 +/- 7.4 vs 77.3 +/- 8: p > 0.05) despite similar atrial and systemic arterial pressures. The disappearance rate of indocyanine green was not altered during infusion of placebo group (9.0 +/- 3.2%/min vs 7.9 +/- 3.0%/min: p > 0.05) or dopexamine at 1 microgram/kg/min (9.7 +/- 3.1%/min vs 11.2 +/- 4.1%/min: p > 0.05). The disappearance rate was increased with dopamine (6.7 +/- 3.7%/min vs 11.8 +/- 3.0%/min: p < 0.05) and dopexamine 2 micrograms/kg/min (9.7 +/- 3.1%/min vs 13.5 +/- 3.2%/min: p < 0.05). This indicates a 76% increase in liver blood flow with dopamine and a 38% increase with dopexamine. We conclude that dopamine 4 micrograms/kg/min and dopexamine 2 micrograms/kg/min increase liver blood flow, although this may, in part, be related to an increase in cardiac output. Dopexamine shows no advantage over dopamine in enhancing liver blood flow after CPB.     

Propofol infusion is associated with a higher rapid shallow breathing index in patients preparing to wean from mechanical ventilation.

OBJECTIVE: To determine whether propofol affects spontaneous breathing patterns in critically ill patients recovering from respiratory failure during initial attempts at liberation from mechanical ventilation. DESIGN: Observational cohort study. PATIENTS: Ten critically ill patients in the medical intensive care unit of a 300-bed community teaching hospital. MEASUREMENTS: Demographic and physiologic variables, including respiratory frequency and minute volume, were recorded while patients breathed on continuous positive airway pressure (of 5 cm H(2)O) during and 20-30 min after cessation of propofol infusion. The ratio of respiratory frequency to tidal volume (rapid shallow breathing index or RSBI) was computed for both sets of measurements and values measured during and after propofol infusion were compared. RESULTS: The mean (+/- SEM) age was 54.0 +/- 5.2 years and the mean (+/- SEM) APACHE II (Acute Physiology and Chronic Health Evaluation) score was 18.4 +/- 2.0. During propofol infusion, patients breathed with a significantly lower tidal volume (0.245 vs 0.342 L, p = 0.006), higher RSBI (155.6 vs 114.8 breaths/min/L, p = 0.004), and tended to breathe more rapidly (34.3 vs 31.7 breaths/min, p = 0.18) than at 20-30 min after stopping propofol infusion. Three of 10 patients had RSBIs that were unfavorable (> 105 breaths/min/L) for weaning while on propofol but that became favorable (< 105 breaths/min/L) 20-30 min following cessation of propofol. The weight-adjusted dose of propofol was not correlated with the changes in any of the variables. CONCLUSIONS: Propofol causes changes in breathing pattern that could lead a caregiver to erroneously conclude that a patient is not ready to begin spontaneous breathing trials. Since this effect has also been noted following benzodiazepine infusion, the clinician should consider the patient's "sedation history" when using RSBI to guide weaning decisions.     

Cardiorespiratory exercise capacity and its relation to a new Doppler index in children previously treated with anthracycline.

The purpose of this study was to assess the exercise capacity of patients treated with anthracycline and to evaluate the relation between the exercise capacity and a new Doppler index. The study patients consisted of 70 subjects: 41 healthy subjects and 29 who had been treated with various cumulative doses of anthracycline (range 45 to 873 mg per body surface area). The following conventional echocardiographic parameters were measured: rate-corrected mean velocity of fiber shortening (mVcfc), end-systolic wall stress (ESS), stress-velocity index, and early and late diastolic mitral inflow velocities and their ratio. A new Doppler index, the Tei index, was calculated as the sum of isovolumic contraction time and isovolumic relaxation time divided by the ejection time. Peak oxygen uptake (pVo(2)) and anaerobic threshold (AT) were measured during an upright bicycle exercise test. The pVo(2) and AT in the patient group were significantly lower than those in the control group (pVo(2): 22.0 +/- 3.7 versus 28.5 +/- 7.1 mL/min/kg; AT: 12.7 +/- 1.9 versus 17.3 +/- 4.3 mL/min/kg, respectively; P <.01). There were no significant differences in the mVcfc, ESS, stress-velocity index, E wave, A wave, or E/A wave ratio between the two groups. However, the mean Tei index of the patients was significantly greater than that of the controls (0.41 +/- 0.11 versus 0.33 +/- 0.04, P <.01). The pVo(2) and AT decreased significantly with an increase in the Tei index (r = -0.64 and -0.60, respectively; P <.01). A weak positive correlation was found between the AT and E/A wave ratio (r = 0.54, P <.05). However, no significant correlations were seen between the exercise parameters and the mVcfc, ESS, stress velocity index, or transmitral velocities. Our findings suggest that cardiopulmonary exercise testing revealed an inverse correlation between exercise capacity and the Tei index.     

急性心肌梗死并发心源性休克的临床特征与救治

目的　评价急性心肌梗死 (AMI)并心源性休克的临床特征 ,总结救治经验。方法　 10 8例 AMI患者 ,分为休克组 (11例 )与非休克组 (97例 ) ,对比分析两组患者的临床特征、处理与近期预后的异同。结果　两组患者年龄、性别、糖尿病、冠心病、高脂血症、陈旧性心肌梗死病史及梗死部位无显著性差异 (P均 >0 .0 5 )。与非休克组比较 ,休克组肌酸磷酸激酶和心肌肌钙蛋白 I升高〔(31979.7± 2 2 2 71.1) nm ol· s- 1· L- 1比 (17795 .2± 14 979.7) nmol· s- 1· L- 1和 (90 .7± 6 1.1) μg/ L 比 (39.9± 5 2 .1) μg/ L,P均 <0 .0 5〕,左室射血分数降低 (0 .4 6± 0 .12比 0 .5 5± 0 .12 ,P<0 .0 5 ) ,急性肺水肿、心律失常和肺炎合并症增多 (6 4 %比 14 % ,P<0 .0 0 1;5 5 %比 2 1% ,P<0 .0 5 ;4 6 %比 12 % ,P<0 .0 1) ,采用溶栓治疗、冠状动脉造影、主动脉内气囊反搏者多 (46 %比 18% ,73%比 2 6 %和 36 %比 4 % ,P均 <0 .0 5 )。两组住院期病死率无显著性差异 (0比 4 % ,P>0 .0 5 )。结论　 AMI并休克者心肌梗死面积大 ,急性肺水肿、心律失常和肺炎合并症多 ,需主动脉内气囊反搏者多。正确判断、严密监测、及时有效处理 ,可明显改善患者的早期预后。     

Boussignac continuous positive airway pressure device in the emergency care of acute cardiogenic pulmonary oedema: a randomized pilot study.

This study aimed to assess the short-term respiratory effects of a new portable device that delivers a continuous positive airway pressure via a face mask (Boussignac-CPAP) in patients with severe acute cardiogenic pulmonary oedema, and the feasibility of using this technique in an emergency department. We prospectively studied 30 consecutive patients with acute cardiogenic pulmonary oedema. They were randomly assigned either to the Boussignac-CPAP valve, which delivered oxygen, or to standard oxygen delivery for a duration of 30 min. The end-expiratory pressure reached 9.3+/-0.3 cm H2O with the Boussignac-CPAP valve. At the end of the 30 min period, the decreases in respiratory rate and muscular activity were significantly greater among patients assigned to the Boussignac-CPAP valve compared with those on standard oxygen delivery [24+/-1.6 breaths/min, median 24 (15-37) versus 28.5+/-1.9, median 27 (16-38) and 1.3+/-0.2, median 1 (0-4) versus 2.7+/-0.3, median 2 (0-4), respectively]. Moreover, the arterial oxygen tension to inspired oxygen concentration ratio and tidal volume were improved at the end of the 30 min Boussignac-CPAP period compared with baseline. Boussignac-CPAP was easily implemented and no side-effects were reported. Continuous positive pressure delivered using the Boussignac-CPAP device is feasible in an emergency care setting. It can quickly improve respiratory distress in acute cardiogenic pulmonary oedema patients. A larger trial should be initiated in such an emergency care setting to demonstrate the effectiveness of the Boussignac-CPAP device.