The Effect of Compression Duration on Hemodynamics during Mechanical High-impulse CPR

Objective: To determine whether shorter compression durations combined with fixed increased compression velocity during mechanical high-impulse CPR (HI-CPR) improve resuscitation hemodynamics, compared with mechanical standard CPR (SCPR).
Methods: A porcine model of ventricular fibrillation was used, with each animal serving as its own control. Twelve anesthetized swine (20–25 kg each) were instrumented for hemodynamic monitoring. Ventricular fibrillation was induced and followed, after 3 minutes, by mechanical SCPR (50% duty cycle) for 10 minutes. Mechanical HI-CPR was then applied, with compression durations varied randomly at 2-minute intervals for 20% (COM20), 30% (COM30), and 40% (COM40) of the CPR cycle. A 2-minute mechanical SCPR control phase completed the experiment.
Results: Hemodynamic measurements were significantly better for COM20 and COM30 vs SCPR, including, respectively: mean arterial pressure (MAP), 45 ± 8 and 43 ± 7 vs 36 ± 7 torr; coronary perfusion pressure (CPP), 21± 6 and 21 ± 8 vs 16 ± 6 torr; and end-tidal CO₂ (ETCO₂), 7 ± 2 and 6.6± 2 vs 5 ± 1.4 torr. MAP, CPP, and ETCO₂ during COM40 were not significantly different from those during SCPR, and there was no difference between COM20 and COM30 for any hemodynamic parameter. Aortic flow velocity was significantly better in COM20, COM30, and COM40 vs SCPR: 2.3± 0.7, 2.1± 0.9, and 1.95 ± 0.9 vs 1.3 ± 0.5 cm/sec, respectively.
Conclusion: In a swine model of mechanical HI-CPR, shorter compression durations combined with fixed increased compression velocity significantly improve resuscitation hemodynamics, compared with those afforded by mechanical SCPR.     

Timing of the Left Ventricular Electrogram and Acute Hemodynamic Changes During Implant of Cardiac Resynchronization Therapy Devices

Study Objective: To examine the relationship between timing of the left ventricular (LV) electrogram (EGM) and its acute hemodynamic effect on instantaneous change in LV pressure (LVdP/dt_MAX).
Patients and Methods: In 30 patients (mean = age 67 ± 7.9 years) who underwent implant of cardiac resynchronization therapy systems, the right ventricular (RV) lead was implanted at the RV apex (n = 23) or RV septum (n = 7). The LV lead was placed in a posterior (n = 14) or posterolateral (n = 16) coronary sinus tributary. QRS duration, interval from Q wave to intrinsic deflection of the LV EGM (Q-LV), and interval between intrinsic deflection of RV EGM and LV EGM (RV-LV interval) were measured. The measurements were correlated with the hemodynamic effects of optimized biventricular (BiV) stimulation, using the Pearson correlation coefficient.
Results: The mean LVdP/dt_MAX at baseline was 734 ± 180 mmHg/s, and increased to 905 ± 165 mmHg/s during simultaneous BiV pacing, and to 933 ± 172 mmHg/s after V-V interval optimization. The Pearson correlation coefficient R between QRS duration, the Q-LV interval, and the RV-LV interval at the respective LVdP/dt_MAX was 0.291 (P = 0.66), 0.348 (P = 0.030), and 0.340 (P = 0.033).
Conclusions: Similar significant correlations were observed between the acute hemodynamic effect of optimized BiV stimulation and the Q-LV and the RV-LV intervals. However, individual measurements showed an 80-ms cut-off for the Q-LV interval, beyond which the increase in LVdP/dt_MAX was <10%._.     

Time course of effects of cardiac resynchronization therapy in chronic heart failure: benefits in patients with preserved exercise capacity

Objectives: To assess in patients with chronic heart failure the effect of cardiac resynchronization therapy (CRT) over 12 months' follow-up the time course of the changes in functional and neurohormonal indices and to identify responders to CRT.
Methods: Eighty-nine patients (74.1 ± 1 years, left ventricular ejection fraction [LVEF] < 35%), QRS complex duration >150 ms, in stable New York Heart Association (NYHA) class III or IV on optimal medical treatment were prospectively randomized either in a control (n = 45) or CRT (n = 44) group and underwent clinical evaluation, cardiopulmonary exercise testing (CPET), 2D-Echo, heart rate variability (HRV), carotid baroreflex (BRS), and BNP assessments before and at 6- and 12-month follow-up.
Results: In the CRT group, improvement of cardiac indices and BNP concentration were evident at medium term (over 6 months) follow-up, and these changes persisted on a longer term (12 months) (all P < 0.05). Instead CPET indices and NYHA class improved after 12 months associated with restoration of HRV and BRS (all P < 0.05). We identified 26 responders to CRT according to changes in LVEF and diameters. Responders presented less depressed hemodynamic (LVEF 25 ± 1.0 vs 22 ± 0.1%), functional (peak VO₂ 10.2 ± 0.2 vs 6.9 ± 0.3 ml/kg/min), and neurohormonal indices (HRV 203.6 ± 15.7 vs 147.6 ± 10.ms, BRS 4.9 ± 0.2 vs 3.6 ± 0.3 ms/mmHg) (all P < 0.05). In the multivariate analysis, peak VO₂ was the strongest predictor of responders.
Conclusions: Improvement in functional status is associated with restoration of neurohormonal reflex control at medium term. Less depressed functional status (peak VO₂) was the strongest predictor of responders to CRT.     

The Effects of Endothelin–1 on Coronary Perfusion Pressure during Cardiopulmonary Resuscitation in a Canine Model

Objective: To study the hemodynamic effects of exogenously administered endothelin–1 (ET–1), a peptide produced by endothelial cells with potent non–adrenergically mediated vasoconstrictor properties.
Methods: A prospective drug intervention study was carried out in a resuscitation research laboratory.
Fifteen mixed–breed dogs were anesthetized and instrumented for hemodynamic monitoring. Asphyxia arrest was produced by clamping the endotracheal tube. Hemodynamic data were collected continuously.
Following loss of aortic fluctuations monitored by thoracic aortic catheter, the animals remained in pulseless electrical activity (PEA) for 10 minutes. After 10 minutes of no–flow PEA, closed–chest CPR was begun and the animals were randomized to one of three treatment groups (epi, 0. 02 mg/kg epinephrine IV every 3 minutes; endo, 100 μg ET–1 IV at 0 minutes; and epi/endo, a combination of the epi and endo treatments).
Results: endo and epi alone produced similar coronary perfusion pressures (CPPs). The epi/endo combination produced significantly improved CPP compared with that of either epi or endo alone. In the epi group, the best mean CPP was 16 ± 14 mm Hg and occurred 7 minutes after drug administration. In the endo group, the best mean CPP was 28 ± 7 mm Hg and occurred 13 minutes after drug administration. In the epi/endo combination group, the best mean CPP was 61 ± 37 mm Hg and occurred 7 minutes after drug administration (p < 0. 05 compared with the epi and endo groups alone).
Conclusion: ET–1 is a potent vasoconstrictor. The combination of epi and endo significantly improved CPP compared with that for either agent alone. ET–1 should be investigated further as a vasoconstrictor in cardiac arrest.     

The Effects of Rate-Adaptive Atrial Pacing Versus Ventricular Backup Pacing on Exercise Capacity in Patients with Left Ventricular Dysfunction

Background: Atrial rate-adaptive pacing may improve cardiopulmonary reserve in patients with left ventricular dysfunction.
Methods: A randomized, blinded, single-crossover design enrolled dual-chamber implantable defibrillator recipients without pacing indications and an ejection fraction ≤40% to undergo cardiopulmonary exercise treadmill stress testing in both atrial rate-adaptive pacing (AAIR) and ventricular demand pacing (VVI) pacing modes. The primary endpoint was change in peak oxygen consumption (VO₂). Secondary endpoints were changes in anaerobic threshold, perceived exertion, exercise duration, and peak blood pressure.
Results: Ten patients, nine males, eight with New York Heart Association class I, mean ejection fraction 24 ± 7%, were analyzed. Baseline VO₂ was 3.6 ± 0.5 mL/kg/min. Heart rate at peak exercise was significantly higher during AAIR versus VVI pacing (142 ± 18 vs 130 ± 23 bpm; P = 0.05). However, there was no difference in peak VO₂ (AAIR 23.7 ± 6.1 vs VVI 23.8 ± 6.3 mL/kg/min; P = 0.8), anaerobic threshold (AAIR 1.3 ± 0.3 vs VVI 1.2 ± 0.2 L/min; P = 0.11), rate of perceived exertion (AAIR 7.3 ± 1.5 vs VVI 7.8 ± 1.2; P = 0.46), exercise duration (AAIR 15 minutes, 46 seconds ± 2 minutes, 54 seconds vs VVI 16 minutes, 3 seconds ± 2 minutes, 48 seconds; P = 0.38), or peak systolic blood pressure (AAIR 155 ± 22 vs VVI 153 ± 21; P = 0.61) between the two pacing modes.
Conclusion: In this study, AAIR pacing did not improve peak VO_2, anaerobic threshold, rate of perceived exertion, or exercise duration compared to VVI backup pacing in patients with left ventricular dysfunction and no pacing indications.     

Hepatic vein oxygenation, liver blood flow, and the rate of ethanol metabolism in recently abstinent alcoholic patients

Abstract. To determine whether hepatic hypoxia is associated with hepatocellular necrosis in alcoholics, oxygen tension in the hepatic vein and hepatic blood flow were determined in thirteen patients without overt clinical liver disease. Ethanol metabolic rate was also assayed as an index of liver metabolism. Hepatic blood flow and ethanol metabolic rate were also determined in six normal volunteers. According to liver histology patients were separated into two groups, with and without hepatocellular necrosis. Alcoholics with necrosis showed a higher ( P < 0–002) ethanol metabolic rate (405±0–23 mmol/kg/h) than those without necrosis (2–46±0–34). Hepatic blood flow in the total group of alcoholics was not significantly different from controls; in the group with necrosis it was lower (651-7±44-6 ml/min/m²) than in the group without necrosis (878-3±81-6; P < 0025). Hepatic vein pO₂ was lower ( P < 001) in patients with hepatocellular necrosis (31-7±0–68 mmHg) than in patients without necrosis (35-7±0–99). In the whole group, a significant negative correlation ( r = -0 76, P < 0–003) was observed between hepatic vein pO₂ and ethanol metabolic rate. Acute administration of ethanol (21-7 mmol/kg) did not alter hepatic blood flow in six normal individuals nor in five alcoholic patients, although an increase in hepatic vein pO₂ was observed in the latter. The changes observed in hepatic vein pO₂, functional hepatic blood flow, and ethanol metabolic rate which correlate with hepatocellular necrosis, may be of pathogenic importance in alcoholic liver disease.     

Hepatic vein oxygenation, liver blood flow, and the rate of ethanol metabolism in recently abstinent alcoholic patients

Abstract To determine whether hepatic hypoxia is associated with hepatocellular necrosis in alcoholics, oxygen tension in the hepatic vein and hepatic blood flow were determined in thirteen patients without overt clinical liver disease. Ethanol metabolic rate was also assayed as an index of liver metabolism. Hepatic blood flow and ethanol metabolic rate were also determined in six normal volunteers. According to liver histology patients were separated into two groups, with and without hepatocellular necrosis. Alcoholics with necrosis showed a higher ( P < 0–002) ethanol metabolic rate (405 ± 0–23 mmol/kg/h) than those without necrosis (2–46 ± 0–34). Hepatic blood flow in the total group of alcoholics was not significantly different from controls; in the group with necrosis it was lower (651–7 ± 44–6 ml/min/m²) than in the group without necrosis (878–3 ± 81–6; P < 0025). Hepatic vein pO₂ was lower ( P < 001) in patients with hepatocellular necrosis (31–7 ± 0–68 mmHg) than in patients without necrosis (35–7 ± 0–99). In the whole group, a significant negative correlation ( r = -0 76, P < 0–003) was observed between hepatic vein pO₂ and ethanol metabolic rate. Acute administration of ethanol (21–7 mmol/kg) did not alter hepatic blood flow in six normal individuals nor in five alcoholic patients, although an increase in hepatic vein pO₂ was observed in the latter. The changes observed in hepatic vein pO₂, functional hepatic blood flow, and ethanol metabolic rate which correlate with hepatocellular necrosis, may be of pathogenic importance in alcoholic liver disease.     

Noninvasive Hemodynamic Monitoring of Critical Patients in the Emergency Department

Objective : To evaluate the feasibility of multicomponent noninvasive hemodynamic monitoring in critical emergency patients and to compare this technique with simultaneous invasive monitoring by the pulmonary artery thermodilution catheter.
Methods : A prospective observational study was done comparing invasive monitoring and noninvasive monitoring in 60 critically ill or injured patients who required hemodynamic monitoring shortly after entering the ED of a university-affiliated county hospital. Cardiac output (CO) values measured by the standard thennodilution pulmonary artery catheter technique were compared with simultaneously obtained measurements using a noninvasive bioimpedance method. Concurrent measurements were made of pulse oximetry to screen pulmonary function and transcutaneous oximetry to assess tissue perfusion.
Results : The impedance CO values closely approximated those for the thermodilution method; r 0.81, p < 0.001. Significant circulatory abnormalities, including hypotension, reduced cardiac index, arterial hemoglobin desaturation, tissue hypoxia, reduced O₂ delivery, and consumption, were found in 54 of the 60 (90%) patients. The cardiac index decreased in 44% of the patients, the transcutaneous O₂ decreased in 39%. and the O₂ saturation by pulse oximetry fell in 22% during the observation period in the ED (commonly lasting 2–8 hours).
Conclusions: Noninvasive monitoring can provide hemodynamic and perfusion information previously available only by invasive thermodilution catheters. Such noninvasive monitoring can display continuous on-line real-time data, allowing immediate recognition of circulatory abnormalities and providing a means to titrate therapy to appropriate therapeutic goals.     

Effects of the location of myocardial infarction on the spectral characteristics of ventricular fibrillation

Background: The location of the myocardial infarction (MI) might modify the spectral characteristics of ventricular fibrillation (VF) in humans.
Objective: To evaluate the effect of the location of the infarcted area on the spectral parameters of VF.
Methods: Patients with chronic MI (29 anterior, 32 inferior) and induced VF during cardioverter defibrillator implant were retrospectively studied. Dominant frequency (f_d), organization index (OI), and power of the harmonic peaks were calculated in the device-stored electrograms (EGM) during sinus rhythm (SR) and VF.
Results: The f_d of the VF was not affected by the left ventricular ejection fraction (LVEF) or the MI location (anterior: 4.54 ± 0.74 Hz, inferior: 4.77 ± 0.48 Hz, n.s.). The OI was also similar in both groups. However, in patients with inferior MIs, normalized peak power at f_d was higher (118.3 ± 18.5 vs 100.6 ± 28.2, P < 0.01) and the normalized peak power of the harmonics was lower than in the anterior MI group. The analysis of EGM during SR showed similar results. The size of the necrotic area and its distance to the recording electrode might partially explain these results.
Conclusion: In our series, the spectral characteristics of the EGMs during VF showed significant differences depending on the MI localization. A higher fraction of energy (in the low-frequency region) was seen in inferior MIs, whereas the peak power at the harmonics increased in anterior MIs. A similar effect was seen during SR and VF, suggesting that it is caused by local electrophysiology abnormalities induced by the MI rather than by different intrinsic characteristics of the VF.     

Pharmacokinetics of amikacin in intensive care unit patients

Objective: To characterize the population pharmacokinetics of amikacin in intensive care unit (ICU) patients and to analyse whether these patients show different kinetic behaviour on the basis of their clinical diagnoses.
Method: The patient population comprised 104 medical ICU patients on amikacin treatment for several presumed or documented Gram-negative infections. Four study groups were defined according to patients' clinical diagnosis: sepsis group ( n = 39), trauma group ( n = 20), pneumonia group ( n = 21) and 'other diagnosis' group ( n = 24). The pharmacokinetic parameters for amikacin in these patients were then compared.
Results: The ICU patients were found to have increased values for the amikacin volume of distribution (0.52 ± 0.21 litres/kg), whereas total amikacin clearance expressed as a linear function of creatinine clearance was Cl (ml/min/kg)= 0.13 ± 0.86 Cl _CR which is not significantly different from other estimations reported in the literature. However, this relationship revealed statistically significant differences among the four groups of ICU patients. Moreover, the septic and trauma patients showed higher (but not statistically significant) values for the amikacin volume of distribution.
Conclusion: The amikacin pharmacokinetic parameters obtained should allow Bayesian individualization of amikacin doses in patients admitted to medical ICUs, on the basis of their clinical diagnoses.     

Morphology of the RV electrogram during LV pacing is related to the hemodynamic effect in cardiac resynchronization therapy

Background: Biventricular (BiV) pacing and left ventricular (LV) pacing both improve LV function in patients with heart failure and LV dyssynchrony. We studied the hemodynamic effect of the atrioventricular (AV) interval and the associated changes in the right ventricular (RV) electrogram (EGM) during LV pacing and compared this with the hemodynamic effect of optimized sequential BiV pacing.
Methods: In 16 patients with New York Heart Association (NYHA) class II to IV, sinus rhythm with normal AV conduction, left bundle branch block (LBBB), QRS > 130 ms, and optimal medical therapy, the changes in RV EGM during LV pacing with varying AV intervals were studied. The hemodynamic effect associated with these changes was evaluated by invasive measurement of LVdP/dt_max and compared with the result of optimized sequential BiV pacing in the same patient.
Results: All patients showed electrocardiographic fusion during LV pacing. The morphology of the RV EGM showed changes in the RV activation that indicated a shift in the extent of fusion from LV pacing. These changes were associated with significant changes in LVdP/dt_max. Baseline LV dP/dt_max was 734 ± 177 mmHg/s, which increased to 927 ± 202 mmHg/s (P<0.0001) with optimized LV pacing and to 920 ± 209 mmHg/s (P<0.0001) with optimized sequential BiV pacing.
Conclusion: The RV EGM is a proper indicator for intrinsic activation over the right bundle during LV pacing and reveals the transition to fusion in the RV EGM that is associated with a decrease in LVdP/dt_max. The hemodynamic effect of optimized LV pacing is equal to optimized sequential BiV pacing.     

Padded vs Unpadded Spine Board for Cervical Spine Immobilization

Objectives: To determine whether padding the long spine board improves patient comfort, affects cervical spine (c-spine) immobilization, or increases sacral transcutaneous O₂ tension.
Methods: A prospective randomized, controlled crossover study of healthy volunteers was conducted over a two-week period. Participants included 30 volunteers with no previous history of c-spine injury or disease. The subjects were randomized to either padded or unpadded long spine board immobilization with serial measurements of discomfort (using a visual analog scale) and transcutaneous tissue O₂ tension obtained at zero and 30 minutes. Measurements of ability to flex, extend, rotate, and laterally bend the c-spine were made using a goniometer. The subjects then returned a minimum of three days later to complete the opposite half of the study (padded vs unpadded boards).
Results: Subject discomfort was significantly reduced in the padded group compared with the unpadded group (p = 0.024). There was no significant difference in flexion (p = 0.410), extension (p = 0.231), rotation (p = 0.891), or lateral bending (p = 0.230) for the two groups. There was no significant difference in the actual drop in sacral transcutaneous O₂ tension from time zero to 30 minutes for the padded and the unpadded groups (mean drop = 14.8% ± 17.5% vs 12.2% ± 16.8%, respectively; p = 0.906).
Conclusion: Adding closed-cell foam padding to a long spine board significantly improves comfort without compromising c-spine immobilization. Sacral tissue oxygenation does not appear affected by such padding for healthy volunteers.     

Regional cerebral blood flow (rCBF) in migraine during the interictal period: different rCBF patterns in patients with and without aura

The aim of this study was to evaluate the rCBF (¹³³Xe clearance method) in migrainous patients free from attack. Fifty patients suffering from migraine without aura (group M) and 20 suffering from migraine with aura (group MA) (age range 20-50 years) were submitted to 32 channel rCBF mapping during the interictal period. The rCBF data of patients were compared with those obtained from 60 healthy control subjects (group C) and 21 patients suffering from tension-type headache (group TH). The mean (average of all channels) rCBF values were: group M=70.5 ± 13.7ml/100g/min; group MA=56.6 ± 11.4ml/100g/min; group C=62.3 ± 8.3ml/100g/min; group TH=62.1 ± 8.4ml/100g/min (F=11.93; p <0.001). As expected, patients belonging to group TH had a normal rCBF. The mean rCBF of group M was significantly higher than that of groups C and TH, while in group MA it was significantly lower than in groups C and TH. Group M showed a diffuse hyperemia, while group MA showed rCBF values significantly lower than normal in posterior regions, according to aura. Our results suggest that: (a) the rCBF pattern in migrainous patients is different from that in both controls and TH patients, even during the interictal period; (b) patients suffering from migraine with and without aura are two distinct subpopulations with opposite rCBF deviations.     

Hemicranial Disorder of Vasomotor Adrenoceptors in Migraine and Cluster Headache

SYNOPSIS
Regional cerebral blood flow (rCBF) and cerebral vasomotor responses to 5% CO₂ inhalation were measured before and after pharmacologic μ- or β-adrenoceptor manipulation in Migraine (M) and Cluster headaches (C). Responses of 77 vascular headache patients (M =66 and C = 11) were compared to those of 15 Muscle contraction headache (MCH) and 64 normal volunteers. Oral drugs were: Peripheral μ-adrenoceptor stimulator:isometheptene (Midrin(r)), peripheral μ-blocker:dihydroergotoxin (Hydergine(r)), centrally acting μ-blocker:clonidine (Catapres(r)), peripheral β-blocker:propranolol (Inderal(r)), peripheral β-stimulator:isoproterenol (Isuprel(r)). Peripheral μ stimulation markedly reduced rCBF during headache but effect lessened after headache subsided in M and C. Peripheral μ-blockade and β-stimulation increased CBF in M and C. Peripheral β-blockade markedly decreased CBF during headache in M but caused only small CBF reductions when headache-free. Peripheral adrenoceptor effects on rCBF in M and C were greatest on most recent headache side. Central effects of clonidine were opposite (greatest on non-headache side). Excessive CO₂ responses were greatest on side of headache. After peripheral μ-stimulation, peripheral μ-blockade, peripheral β-stimulation or blockade, CO₂ responses were restored toward normal but not after central μ-blockade. In MCH. contrary to M and C, μ-stimulation had no effect on CBF or CO₂ responses. There appears to be an asymmetrical adrenoceptor disorder in M and C possibly due to sympathetic denervation-hypersensitivity.     

超声评估大脑中动脉慢性闭塞患者侧支循环的临床意义

目的探讨经颅多普勒超声（TCD）和（或）经颅彩色多普勒超声（TCCS）检查评估单侧大脑中动脉慢性闭塞（CMCAO）患者侧支循环的临床意义。 方法回顾性连续纳入2015年8月至2018年4月苏州大学附属第一医院由TCD和（或）TCCS诊断为单侧CMCAO并经数字减影血管造影（DSA）证实的患者54例,记录患者DSA上软脑膜侧支（LMA）分级。TCD和（或）TCCS检测并记录大脑前动脉（ACA）、大脑后动脉（PCA）的平均流速（MV）,并计算其患侧（i）与健侧（c）MV比值（MV_iACA/MV_cACA、MV_iPCA/MV_cPCA）。采用Spearman相关分析法分析ACA及PCA血流动力学参数与LMA分级的相关性。根据临床症状将患者分无症状组（8例）,短暂性脑缺血发作（TIA）组（19例）和脑梗死（CI）组（27例）,比较3组患者ACA及PCA血流参数差异及相对CT灌注参数的差异。 结果MV_iACA、MV_iACA/MV_cACA与LMA分级均呈显著正相关（r=0.568,P=0.000;r=0.757,P=0.000）;MV_iPCA、MV_iPCA/MV_cPCA与LMA分级均呈正相关（r=0.383,P=0.004;r=0.624,P=0.000）。无症状组、TIA组患者MV_iACA、MV_iPCA、MV_iACA/MV_cACA、MV_iPCA/MV_cPCA均高于脑梗死组,且差异均有统计学意义（P<0.05）。无症状组、TIA组患者相对脑血流量（rCBF）、相对脑血容量（rCBV）均高于脑梗死组患者,且差异均有统计学意义（P<0.05）;相对平均通过时间（rMTT）、相对达峰时间（rTTP）均低于脑梗死组患者,且差异均有统计学意义（P<0.05）。 结论TCD和（或）TCCS上ACA及PCA血流动力学参数与DSA上LMA分级具有明显相关性,且与CT灌注成像结果有良好的一致性,对于指导单侧CMCAO患者选择个体化治疗方案具有重要意义。     

Artificial Surfactant Administration in an Animal Model of Near Drowning

Objective: To study the use of exogenous surfactant in a rabbit freshwater near-drowning model.
Methods: In a randomized, placebo-controlled experiment, 21 rabbits were anesthetized, paralyzed, and subjected to near drowning with 6 mL/kg of distilled water. Vital signs, arterial blood gases, and pulmonary compliance were measured at predetermined intervals. The animals were randomized into two groups: a normal O₂ group that had their pO₂ levels adjusted to 75–150 torr using supplemental O₂ as needed, and a high O₂ group ventilated with an Fi_O2 = 100%. Ventilator settings were further adjusted to normalize pH and pCO₂ levels prior to instillation of distilled water. The two groups were further divided and 15 minutes after simulated near drowning, the animals were either treated with surfactant (5 mL/kg instilled en-dotracheally) or not treated. Data were analyzed by repeated-measures analysis of variance.
Results: Near drowning had no significant effect on heart rate or blood pressure. Acidosis was not changed by surfactant; hypoxia was worsened by surfactant: 158 ± 54 torr before and 66 ± 19 torr after administration (p < 0.01). Compliance did not change as a result of surfactant administration. Only the animals (n = 3) in the normal O₂ plus surfactant group died during the 90-minute post-near-drowning period of the study.
Conclusions: Surfactant administration (5 mL/kg) in this animal model of freshwater near drowning offers no benefit over simple ventilation. Assessment of the merit of smaller volumes of surfactant should be investigated because administration of this solution may represent a second pulmonary insult, given current volume recommendations.     

QT Variability Before and After Episodes of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

This study examined the changes in QT dynamics occurring during 5-minute intervals sampled immediately before and 1 hour after episodes of nonsustained ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM). Twenty-four hour Holter recordings were performed in 10 patients with HCM in the absence of antiarrhythmic medications and processed by the ELA Medical QT analysis software. All sinus complexes were averaged over 30-second segments and 2,880 templates were created. For each template, a mean corrected QT_ec (time interval between the onset of QRS and the end of the T wave) and QT_ac (time interval between the onset of the QRS and the peak of the T wave) were calculated, with their standard deviations (SDQT_e and SDQT_a) taken as indices of QT variability. The slopes of the regression line for the QT_e and QT_a against the corresponding RR also were calculated. Forty 5-minute segments were analyzed immediately before (sample A) and 1 hour after (sample B) 20 episodes of nonsustained VT. QT_ac was significantly longer in group A than in group R (321 ± 20 vs 312 ± 22, P < 0.0001) and SDQT_a was significantly lower (2.8 ± 1.2 vs 4.7 ± 3.7, P < 0.03). There were no significant differences in QT_ec, SDQT_e, QTe/RR and QT_a/RR before and after the episodes. Our data indicate that in patients with HCM, the averaged QT_ac is significantly longer and the QT_a variability significantly lower before episodes of nonsustained VT.     

Assessing Acute Ventricular Volume Changes by Intracardiac Impedance in a Chronic Heart Failure Animal Model

Background: Implantable device diagnostics may play an essential role in simplifying the care of heart failure patients by providing fundamental insights into their complex clinical patterns. Early recognition of heart failure progression by a continuous hemodynamic monitoring would allow for timely therapeutic interventions to prevent decompensation and hospitalization. In this study, the feasibility of assessing ventricular volume changes by implant-based measurements of intracardiac impedance was tested in a heart failure animal model.
Methods: Heart failure was induced in five minipigs by high-rate pacing over 3 weeks. During a final open-chest examination a graded dobutamine stress test was performed. Stroke volume (SV) was measured by an ultrasonic flow probe at the ascending aorta. End diastolic pressure (EDP) and maximum pressure slope (dP/dt_max) were calculated from a left ventricular microtip catheter signal. Impedance was measured by an implanted pacemaker between biventricular leads. Stroke impedance (SZ) was calculated as the difference between end-systolic and end-diastolic impedance (EDZ).
Results: Administration of dobutamine led to an increase in SV (55 ± 16%), dP/dt_max (107 ± 89%), and SZ (56 ± 30%). EDP changed by 37 ± 21% whereas EDZ changed by 7.4 ± 4%. Significant correlations were found between SZ and SV (r = 0.88), and between EDZ and EDP (r =−0.82).
Conclusion: The strong correlation with SV allows the application of intracardiac impedance measurements for an implant-based continuous monitoring of cardiac function. Impedance may also be used for hemodynamic optimization of cardiac resynchronization therapy.     

低强度激光鼻腔内照射对脑梗死患者脑血流灌注的影响

目的研究低强度半导体激光鼻腔内照射对脑梗死患者脑血流灌注和脑细胞功能的影响。方法将39例脑梗死患者分为血管内照射(ILIB)组18例与鼻腔内照射(LINC)组21例。ILIB组患者仰卧于检查床上固定头位,先做SPECT基础脑灌注显像,随即行半导体激光血管内照射,时间30min,治疗后再做SPECT脑灌注显像。LINC组同样先做SPECT基础脑灌注显像,随即行半导体激光鼻腔内照射,时间30min,治疗后再做SPECT脑灌注显像。采用脑血流功能变化率(BFCR%)数学模型对患者病灶区和镜像区进行定量分析。结果2组激光治疗30min后,SPECT显示其全脑血流灌注和脑细胞功能状态均有明显改善,以病灶区局部脑血流量和脑细胞功能改善更为显著。治疗后病灶区局部/全脑灌注比值较治疗前明显增高,差异有统计学意义(P<0.01);镜像区局部/全脑灌注比值较治疗前增高,但差异无统计学意义(P>0.05);病灶区BFCR%明显高于镜像区,差异有统计学意义(P<0.01)。2组治疗后组间病灶区局部/全脑灌注比值及BFCR%比较,差异均无统计学意义(P>0.05)。结论低强度激光鼻腔内照射能改善脑梗死患者局部病灶脑血流量,激活脑细胞功能,有着较为广泛的临床应用前景。     

Does once-daily dosing of aminoglycosides affect neuromuscular function?

Objective: Aminoglycosides have been reported to produce a curare-like neuromuscular blockade in animals at serum concentrations higher than those obtained with traditional dosing (1–2 mg/kg every 8 h) in humans. Aminoglycoside-induced neuromuscular blockade is rarely, if ever, seen in humans with traditional dosing. The recent adoption of once-daily dosing of aminoglycosides has raised concerns about increased potential for this adverse effect because higher serum concentrations are produced. The objective of this study was to determine if once-daily dosing of aminoglycosides inhibits respiratory muscle function.
Method: Nine mechanically ventilated ICU patients on once-daily dosing of gentamicin 6 mg/ kg/day were assessed for respiratory muscle strength by measuring maximum inspiratory pressure (MIP). MIP is a measurement of the maximal negative pressure generated by repeated inhalations against an occluded airway over 20 s. This was measured within 1 hour before (MIP_pre) and within 1 hour after each aminoglycoside dose (MIP_post).
Results: Mean values for MIP_pre and MIP_post were −26.7 cm H₂O and − 26.5 cm H₂O, respectively. The mean difference between MIP_pre and MIP_post was − 0.2 cm H₂O, which was not statistically significant ( P >0.05).
Conclusion: The effect of gentamicin (6 mg/kg/day) on respiratory muscle function was not statistically, nor clinically significant, and weaning from mechanical ventilation does not seem to be inhibited by once-daily dosing of aminoglycosides as detectable by measurement of MIP.