Intrathoracic pressure fluctuations move blood during CPR: Comparison of hemodynamic data with predictions from a mathematical model

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21–32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was <0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378–426 N), flow was significantly increased when the duration of compression was increased from short (13%–19% of the cycle) to long (40%–47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures. Thus vital organ perfusion pressures and flow for manual external chest compression are dependent on the duration of compression, but not on rates of compression of 60 and 150/min. These data are of course similar to those produced by vest CPR, where intrathoracic pressure is manipulated without sternal displacement, and to those predicted for movement of blood by intrathoracic pressure changes. These data are, however, opposite to those produced by cardiac deformation and to those predicted for movement blood by direct cardiac compression. We conclude that intrathoracic pressure fluctuations generate blood flow during manual CPR.     

脚压测量用传感器

本文讨论了用于脚压测量的四类压力传感器，电阻式传感器、压电式传感器，光电式传感器，电容式传感器介绍了其结构、原理和特点，并分析了几种典型的测量接口电路。     

Glibenclamide treatment in a Cantú syndrome patient with a pathogenic ABCC9 gain‐of‐function variant: Initial experience

Cantú syndrome (CS), characterized by hypertrichosis, distinctive facial features, and complex cardiovascular abnormalities, is caused by pathogenic variants in ABCC9 and KCNJ8 genes. These genes encode gain‐of‐function mutations in the regulatory (SUR2) and pore‐forming (Kir6.1) subunits of K_ATP channels, respectively, suggesting that channel‐blocking sulfonylureas could be a viable therapy. Here we report a neonate with CS, carrying a heterozygous ABCC9 variant (c.3347G>A, p.Arg1116His), born prematurely at 32 weeks gestation. Initial echocardiogram revealed a large patent ductus arteriosus (PDA), and high pulmonary pressures with enlarged right ventricle. He initially received surfactant and continuous positive airway pressure ventilation and was invasively ventilated for 4 weeks, until PDA ligation. After surgery, he still had ongoing bilevel positive airway pressure (BiPAP) requirement, but was subsequently weaned to nocturnal BiPAP. He was treated for pulmonary hypertension with Sildenafil, but failed to make further clinical improvement. A therapeutic glibenclamide trial was commenced in week 11 (initial dose of 0.05 mg^–1 kg^–1 day^–1 in two divided doses). After 1 week of treatment, he began to tolerate time off BiPAP when awake, and edema improved. Glibenclamide was well tolerated, and the dose was slowly increased to 0.15 mg^?1 kg^?1day^?1 over the next 12 weeks. Mild transient hypoglycemia was observed, but there was no cardiovascular dysfunction. Confirmation of therapeutic benefit will require studies of more CS patients but, based on this limited experience, consideration should be given to glibenclamide as CS therapy, although problems associated with prematurity, and complications of hypoglycemia, might limit outcome in critically ill neonates with CS.     

Sympathetic a-adrenergic control of large-bore arterial vessels,arterioles and veins,and of capillary pressure and fluid exchange in whole-organ cat skeletal muscle

The sympathetic nervous control of the vascular bed of cat gastrocnemius muscle was studied with a new whole-organ technique which permits simultaneous, continuous and quantitative measurements of capillary pressure (P_c), capillary fluid exchange and resistance reactions in the whole vascular bed and in its three consecutive sections: large-bore arterial vessels (> 25 μm), arterioles (< 25 μm) and veins. The results demonstrated a distinct neural control of all three consecutive vascular sections, graded in relation to the rate of nerve excitation up to maximum at 16 Hz. Stimulation at high rates, which in the steady state caused an average rise of overall regional resistance from 15.3 to 120 PRU (7.8-fold increase), thus raised large-bore arterial vessel resistance from 8.8 to 64 PRU (7.3-fold increase), arteriolar resistance from 4.5 to 49 PRU (10.9-fold increase) and venous resistance from 2.0 to 7 PRU (3.5-fold increase). The rate of resistance development (PRU s^-1) of the sympathetic constrictor response was much higher in the arteriolar than in the other sections, which indicates that the neural control is especially prompt and efficient in the arterioles. A passive component was shown to contribute to the described responses only on the venous side, but in no case by more than 10% of the total sympathetic venous resistance response, which thus is mainly active. Of special functional importance was that the new technique provided information about the adrenergic control of P_c, in absolute figures. From the control value of 19 mmHg, graded sympathetic stimulation caused a graded decline in P_c, at maximum constriction by about 7 mmHg. This resulted in marked net transcapillary fluid absorption, in turn increasing plasma volume.     

Maximal dynamic expiratory pressures with fast and slow inspirations

Maximal dynamic expiratory pressures are higher when forced expiration is preceded by a fast inspiration to total lung capacity (TLC) than when preceded by a slow inspiration and a few seconds pause at TLC. We hypothesized that these pressure differences are due to the stretch-shorten cycle (SSC), which refers to enhancement of muscle force when a concentric muscle contraction is immediately preceded by an eccentric contraction. Seven volunteers [36 (2) years; mean (SEM)] performed maximal forced expirations against minimal resistance with fast (F) or slow (S) maneuvers. F maneuvers consisted of a fast inspiration to TLC followed immediately by a fast expiration, whereas S consisted of a slow inspiration to TLC and a 4- to 5-s pause at TLC prior to forced expiration. We measured esophageal pressure (P _es), peak expiratory flow rate (PEFR), and the EMG activity of the transversus abdominis (Tr) by means of intramuscular fine-wire electrodes. The subjects performed several runs of each maneuver in a random order, and runs with the greatest expiratory P _es were analyzed. In comparison with S, F yielded greater P _es [182 (15) versus 167 (15) cmH₂O; P=0.003)] but similar PEFR [9.8 (0.7) versus 9.6 (0.7) l/s, P>0.05] and EMG activity of the Tr during forced expiration [221 (31) versus 208 (34) a.u., P>0.05]. Further analysis revealed significant EMG activity of Tr during end-inspiration (eccentric contraction) with F maneuvers only [73 (22) versus 32 (17) a.u., P<0.05]. We conclude that the ability of expiratory muscles to generate greater P _es with F maneuvers is related to the sequence of an eccentric contraction, which is followed immediately by concentric contraction in a manner analogous to SSC described in skeletal muscles. Electronic Publication     

Noninvasive,automatic 24-h ambulatory blood pressure monitoring in normotensive subjects

Summary The reliability of noninvasive, automatic blood pressure monitoring is not yet clearly established. A 24-h ambulatory blood pressure profile was obtained in 9 healthy, normotensive subjects with an automatic, noninvasive device. The blood pressure profile showed the typical circadian pattern with lower systolic and diastolic values during sleep, although pulse pressure was fairly constant (about 40 mm Hg). The systolic blood pressure rose steeply in the early morning hours — before waking up. The results were compared with simultaneous hourly readings using the auscultatory method. There were no statistically significant differences between the automatic and auscultatory readings, 13 of the 18 mean values at. different time points being within 2 mm Hg of each other. All the auscultatory means fell within the 95% confidence limits of those measured hourly by the automatic method. Although the automatic method seemed to be reliable compared with the auscultatory method, its sensitivity to motion artifacts is a disadvantage in a truly ambulatory setting.     

血液灌流对硫线磷和硫酸阿托品的吸附作用

Objective To study on adsorption effect of cadusafos and atropine sulfate by hemoperfusion.Method Hemoperfusions were performed for sheep blood samples with cadusafos and atropineby through imitated extracorporeal closed circulating perfusion apparatus.Residual cadusafos was determined by gas chromatography and residual atropine was determined by high performance liquid chromatography.Result Dose of adsorption agent was 0.5,1.0 and 1.5 g,respectively.Two hours after hemoperfusion with membrane coated activated charcoal,clearance rate of cadusafos in 3 groups all exceeded 90%.and clearance rate of atropine sulfate was 61.9%,84.9%,88.9%,respectively.One and a half hours after hemoperfusion with HA230 absorption resin,clearance rate of eadusafos in 3 groups all exceeded 90%,and clearance rate of atropine sulfate was 88.0%,97.2%,98.4%,respectively.Three hours after hemoperfusion with membrane coated activated charcoal,The concentration ratio of cadusafos and atropine sulfate in blood promoted to 10.1 times,and the ratio was 6.7 times after hemoperfusion with HA230 absorption resin.Conclusion It suggested that cadusafos were mostly removed from blood after 1.5～2.0hours hemoperfusion with membrane activated charcoal or HA230 absorption resin.The concentration ratio of cadusafos and atropine sulfate in blood will increased after hemoperfusion.     

高血压急诊患者降压前后脑电图变化及临床意义

目的:观察高血压急诊快速降血压对大脑功能的影响情况。方法:监测56例病人含服 降压药前后的脑电活动和血压情况,并对所获资料进行分析。结果:2 h内收缩压(SBP)下降>5.33 kPa (40 mmHg)或舒张压(DBP)下降>4.00 kPa(30 mmHg)时,脑电图异常程度增加,θ及δ频段功率值明 显升高(P<0.01)。结论:降压急骤,可能会造成大脑功能损害     

Contribution of adrenomedullin to homeostatic response to cold stress in rat model

Acute stress known to stimulate sympathetic activity as well as the hypothalamo-pituitary–adrenal (HPA) axis, produces a significant increase in adrenomedullin (ADM) levels in the pituitary gland, plasma and adrenal glands, all of which are key components of HPA axis, suggesting a regulatory or protective role for ADM in countering HPA activation following a variety of physiological and psychological stressors. This study was conducted to assess a rat model for in depth investigation of biochemical mechanisms and consequences of cold stress. Four groups of Sprague–Dawley rats were observed for their serum total protein, glucose, trigliceride and cholesterol levels as well as their blood pressures after housing at room temperature, administration of ADM (1.0 nm/kg), exposing to cold stress (8 °C for 48 h) and exposing to ADM injection in addition to cold stress. The results suggest that application of ADM in addition to cold stress may act via receptors on different end-organs and causes altered metabolic regulation taking partial or total occupation of ADM receptors, stimulated in response to cold application induced physiologic ADM release before pharmacological ADM administration.