Simultaneous Ventilation Research Articles

A novel quantitative dual-isotope method for simultaneous ventilation and perfusion lung SPET.

A quantitative dual-isotope single-photon emission tomography (SPET) technique for the assessment of lung ventilation (V) and perfusion (Q) using, respectively, technetium-99m labelled Technegas (140 keV) and indium-113m labelled macro-aggregated albumin (392 keV), is presented, validated and clinically tested in a healthy volunteer. In order to assess V, Q and V/Q distributions in quantitative terms, algorithms which correct for down scattering, photon scattering and attenuation, as well as an organ outline algorithm, were implemented. Scatter and down-scatter correction were made in the spatial domain by pixel-wise image subtraction of projection-dependent global scattering factors obtained from the energy domain. The attenuation correction was based on an iterative projection/back-projection method. All studies were made on a three-headed SPET system (Trionix) with medium-energy parallel-hole collimators. The set of input data for quantification was based on SPET acquisition of emission data in four separate energy windows, the associated cumulative energy spectra and transmission data. The attenuation correction routine as well as the edge detection algorithm utilized data from (99m)Tc transmission tomography. Attenuation data for (113m)In were obtained by linear scaling of the (99m)Tc attenuation maps. The correction algorithms were experimentally validated with a stack phantom system and applied on a healthy volunteer. The mean difference between the corrected SPET data of the dense stack lung phantom and those obtained from the corresponding scatter- and attenuation-"free" version was only 1.9% for (99m)Tc and 0.9% for (113m)In. The estimated fractional V/Q distribution in the 3-D lung phantom volume had its peak at V/Q=1, with a width (FWHM) of 0.31 due to noise, particularly in the (113m)In images, and to partial volume effects. For a healthy volunteer, the corresponding values were 0.9 and 0.35, respectively. This method allows accurate assessment of radionuclide distribution on a regional basis. For basic lung physiology and clinical practice, the method allows assessment of the global frequency functions of the V, Q and V/Q distributions.

Robust controllers for simultaneous control of temperature and CO 2 concentration in greenhouses

The present work focuses on the control of greenhouse air temperature and CO 2 concentration by means of simultaneous ventilation and enrichment. Such an operation, which may a priori seem contradictory, was shown by several authors to be required to maintain optimal temperature and CO 2 setpoints. The control process is divided into two distinct control loops, the first maintaining the temperature by adjusting the ventilation, and the second maintaining the CO 2 concentration by adjusting the enrichment. The CO 2 concentration controller assumes the ventilation rate to be constant and approximately known over 2-min intervals. Implementation in an experimental greenhouse shows the ability of the controllers to meet the requirements.

Alternating versus synchronous ventilation of left and right lungs in piglets

We tested whether alternating ventilation (AV) of each lung (i.e. with a phase difference of half a ventilatory cycle) would decrease central venous pressure and so increase cardiac output when compared with simultaneous ventilation (SV) of both lungs. If, during AV, the inflated lung expands partly via compression of the opposite lung, mean lung volume will be smaller during AV than SV. As a consequence, mean intrathoracic pressure (as cited in the literature), and therefore, central venous pressure will be smaller. The experiments were performed in seven anaesthetized and paralyzed piglets using a double-piston ventilator. Minute ventilation was the same during AV and SV. Starting at SV, we alternated three times between AV and SV for periods of 10 min. During AV, central venous pressure was decreased by 0.7 mmHg and cardiac output was increased by 10 +/- 4.4% (mean, +/-SD) compared with SV. AV also resulted in increased arterial pressure. During one-sided inflation with closed outlet of the opposite lung, a pressure rise occurred in the opposite lung, indicating compression. The higher cardiac output during AV than SV can be explained by the fact that central venous pressure is lower during AV. This lower central venous pressure is very probably due to the lower mean intrathoracic pressure caused by compression of the opposite lung during unilateral inflation.

Expanding the Envelope of Neonatal Endoscopic Tracheal and Bronchial Surgery

Diagnostic evaluation of the neonatal airway requires special training and instrumentation. The subglottis of a normal full-term infant will allow passage of a 3.0 bronchoscope (outer diameter 5.0 mm, inner diameter 4.3 mm). On occasion, diagnostic rigid endoscopy with simultaneous ventilation in premature infants necessitates use of a 2.5 bronchoscope (outer diameter 4.2 mm, inner diameter 3.5 mm). Although flexible bronchoscopy can be done through an endotracheal tube, surgical manipulation of the airway is limited. Rigid pediatric bronchoscopic optical forceps are too large for use in neonatal bronchoscopes. Therefore, performance of endoscopic tracheal and bronchial procedures in the premature infant requires innovative techniques with thorough knowledge of instrumentation and anesthetic management, generally including apneic techniques. As advances in neonatology result in survival of smaller and smaller patients, otolaryngologists must keep pace to provide adequate support. A case report of endoscopic removal of a granuloma totally obstructing the right primary bronchus in a 1 kg premature infant illustrates these concepts in neonatal endoscopy.

Sub-optimal CO 2 Enrichment of Greenhouses

Greenhouse CO 2 enrichment in warm climates is restricted by the need to ventilate, leading some growers to intermittent enrichment, where enrichment and ventilation alternate several times an hour. This strategy relies on the heat and CO 2 capacity of the system, characterized by a heating time constant of the order of 10 min, during which period ventilation may be suspended. It is shown that, for slowly changing weather, the optimal CO 2 enrichment is basically not intermittent (bang-bang control), but rather quasi steady state (smoothly varying singular control). As the disturbance (weather) frequency increases, the quasi steady-state (QSS) solution becomes less and less optimal. Nevertheless, due to the difficulties involved in implementing a truly optimal control (the need for accurate weather forecast and high control fluxes), the sub-optimal QSS control may be a better choice. We chose to try a controller which aims to follow the QSS temperature and CO 2 setpoints at all disturbance frequencies. The performance of this controller for high disturbance frequencies is a few per cent lower than the truly optimal solution, but over the whole season this effect may not be significant. On the other hand, the controller is likely to be more robust. Implementation of the QSS solution requires simultaneous ventilation and enrichment, properly balanced. This, in turn, requires proportional control, or at least two levels of ventilation, as well as fast on-off switching of fan and CO 2 generator.

Interfering with gaol mail; prisoners' legal letters and the courts

In 1983, a report by the organisation JUSTICE into the state of prisons considered that the ability of convicted prisoners to communicate with those outside prison, by letters or visits was, as prison regulations then stood, ‘severely restricted’. Recent years have, however, witnessed a relaxation in the controls imposed on prisoners’ legal and non-legal correspondence, including the abolition of the prior and simultaneous ventilation rules and many restrictions affecting those convicted of less serious offences. Despite this fact, a number of restrictions remain, and the practices of prison authorities in opening, examining, reading and stopping legal mail continue to occupy domestic and international courts.

Action of carbon dioxide on hypoxic pulmonary vasoconstriction in the rat lung: evidence against specific endothelium-derived relaxing factor-mediated vasodilation.

The effect of hypercapnia on pulmonary vascular tone is controversial with evidence for both a vasoconstrictor and vasodilator action. The objective of this study was to investigate the possibility that this dual response to CO2 could be explained by a direct constrictor action on smooth muscle and an indirect dilator action via the release of endothelium-derived relaxing factor. The effect of ventilation with hypercapnia (FICO2 0.15) on pulmonary pressor response to hypoxia (FIO2 0.3) was investigated. Prospective, randomized study. The National Heart and Lung Institute, UK. The isolated, blood-perfused rat lung. Angiotensin-II and a blocker of endothelium-derived relaxing factor synthesis, NG-monomethyl-L-arginine (L-NMMA). The vasomotor effect of hypercapnia depended on pulmonary arterial pressure. Under resting tone, CO2 acted as a mild constrictor (change in mean pulmonary arterial pressure from 14 +/- 2 to 15 +/- 2 mm Hg, n = 4; p < .05. At increased tone, induced either by hypoxia or Angiotensin-II, CO2 was a vasodilator. Thus, hypoxia increased mean pulmonary arterial pressure from 17 +/- 2 to 32 +/- 2 mm Hg (n = 8; p < .01), but simultaneous ventilation with hypoxia and hypercapnia reduced this by 16 +/- 1% (p < .01). Angiotensin-II (1 microgram) increased pulmonary arterial pressure from 14 +/- 2 to 39 +/- 5 mm Hg (n = 8; p < .01), but with hypercapnia, this angiotensin-induced pulmonary vasoconstriction was reduced by 18 +/- 6% (p < .001). The reduction in hypoxic pulmonary vasoconstriction induced by hypercapnia was not significantly different from that seen with Angiotensin-II hypercapnia. Blocking endothelium-derived relaxing factor synthesis using 30 microM NG-monomethyl-L-arginine did not significantly change either basal pulmonary arterial pressure or the response to hypercapnia, but increased hypoxic pulmonary vasoconstrictor by 24 +/- 4% (n = 4; p < .01). There was no significant difference between the change in hypoxic pulmonary vasoconstriction induced by hypercapnia after saline control (21 +/- 8% decrease) and the change in hypoxic pulmonary vasoconstriction caused by CO2 after 30 microM L-NMMA (25 +/- 10% decrease, p < .05, n = 8). Endothelium-derived relaxing factor seems unlikely to specifically modulate CO2-induced vasodilation in the rat pulmonary circulation.

The functional significance of ventilation frequency, and its relationship to oxygen demand in the resting brown long-eared bat, Plecotus auritus

Mean oxygen consumption and simultaneous ventilation frequency of nine non-reproductive brown long-eared bats (body mass 8.53-13.33 g) were measured on 159 occasions. Ambient (chamber) temperature at which the measurements were made ranged from 10.8 to 41.1 degrees C. Apneic ventilation occurred in 22 of the 59 measurements made when mean oxygen consumption was less than 0.5 ml.min-1. No records of apneic ventilation were obtained when it was over 0.5 ml.min-1. The relationship between ventilation frequency and mean oxygen consumption depended on whether ventilation was apneic or non-apneic. When ventilation was non-apneic the relationship was positive and log-linear. When ventilation was apneic the relationship was log-log. Within the thermoneutral zone ventilation frequency was not significantly different from that predicted from allometric equations for a terrestrial mammal of equivalent body mass, but was significantly greater than that predicted for a bird. A reduction in the amount of oxygen consumed per breath occurred at ambient temperatures above the upper critical temperature (39 degrees C).

Simultaneous Independent Lung Ventilation in Pediatric Patients

Current methods of ventilation do not allow adequate ventilation of the affected lungs in the presence of unilateral disease, e.g., unilateral atelectasis, diaphragmatic hernia, or lobar emphysema. Using a bilumen endotracheal tube and two independent ventilators, synchronized simultaneous independent lung ventilation (SILV) can be achieved. This technique provides a method of treating unilobar, unilateral, or multifocal lung disease effectively. This article describes the author's methodology and clinical experience with SILV.

RESECTION FOR CONGENITAL TRACHEAL STENOSIS

A case of congenital tracheal stenosis is reported. The diagnosis was made on plain X-ray, tomography and computerized axial tomography of the trachea when the child was 8 years old. The operative approach was via a median sternotomy and anaesthesia maintained with dual simultaneous ventilation of the right upper lobe bronchus and distal trachea. Histology of the stenotic area revealed the cartilaginous rings to be completely encircling the trachea.

Effect of withdrawal of respiratory CO2 oscillations on respiratory control at rest

We examined the effect of sudden withdrawal of respiratory oscillations of arterial PCO2 (CO2 oscillations) at resting metabolic rate on the control of respiration in 11 anesthetized paralyzed vagotomized dogs in normoxic normocapnia. A double-lumen endotracheal tube was inserted so that the left and right lungs were ventilated independently. By alternately ventilating each lung, we could completely abolish CO2 oscillations without affecting the mean blood gas levels (withdrawal of CO2 oscillations). The CO2 oscillation was calculated from arterial pH oscillation measured by a rapidly responding intra-arterial pH electrode. Respiratory center output was monitored by use of a moving time average of the phrenic neurogram. A 3-min period of withdrawal of CO2 oscillations was bracketed by two control periods (simultaneous ventilation of lungs for 3 min) to avoid the confounding effect of the baseline drift in the respiratory center output. The amplitude of the CO2 oscillations in the control was 2.33 +/- 0.89 (SD) Torr. When the difference in the mean level of arterial PCO2 between the control and withdrawal of CO2 oscillations was minimized (-0.09 +/- 0.54 Torr; P greater than 0.25), we found negligible change in the minute phrenic activity during withdrawal of CO2 oscillations (-0.02 +/- 6.11% of the control, P greater than 0.98, n = 49; 99% confidence interval -2.36 to 2.32%). Thus we conclude that the maintenance of normal respiration at rest is not critically dependent on a phasic afferent input to the respiratory center arising from respiratory CO2 oscillations.

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.

Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation.

High-fidelity hemodynamic recordings of aortic and right atrial pressures and the coronary perfusion gradient (the difference between aortic and atrial pressure) were made in nine patients during cardiopulmonary resuscitation (CPR). Findings during conventional manual CPR were compared with those during high-impulse CPR (rate, 120 cycles/min with a shorter compression:relaxation ratio) as well as during pneumatic vest CPR with and without simultaneous ventilation and abdominal binding. Aortic peak pressure during conventional CPR averaged 61 +/- 29 mm Hg but varied widely (range, 39-126 mm Hg) among patients. Although the magnitude of improvement was modest, the high-impulse method was the only technique tested that significantly elevated both aortic peak pressure and the coronary perfusion gradient during cardiac arrest. During conventional CPR, aortic pressure rose from 61 +/- 29 to 80 +/- 39 mm Hg during high-impulse CPR, and the gradient rose from 9 +/- 11 to 14 +/- 15 mm Hg, respectively; p less than 0.01. The pneumatic vest method significantly improved peak aortic pressure but not the coronary perfusion gradient. Simultaneous ventilation and chest compression created high end-expiratory pressure and lowered the coronary perfusion gradient. Abdominal binding had no significant hemodynamic effects. This evaluation of experimental resuscitation methods in humans shows that the high-impulse chest compression method augments aortic pressure over levels achieved during conventional CPR methods; however, the improvement in pressure is modest and may not be clinically important. Simultaneous ventilation as well as abdominal binding during CPR were associated with no benefit; in fact, simultaneous ventilation appears to adversely affect cardiac perfusion and, therefore, should not be used during clinical resuscitation.

A physiologic comparison of external cardiac massage techniques

On the basis of recent investigation, controversy has arisen regarding which of several cardiopulmonary resuscitation methods optimizes hemodynamics. The present study was designed to compare five recently described chest compression techniques: high-impulse manual chest compression at 150/min, mechanical compression at 60/min with simultaneous ventilation, mechanical compression at 60/min with simultaneous ventilation and either systolic or diastolic abdominal compression, and pneumatic vest compression at 60/min. Eight dogs were chronically instrumented with electromagnetic flow probes in the ascending and descending aorta while matched micromanometers measured aortic, left ventricular, and pleural pressures. At study, each dog was anesthetized with morphine, intubated, and the heart was fibrillated by rapid ventricular pacing. The five cardiopulmonary resuscitation methods were performed randomly in each preparation within 7 to 10 minutes of arrest. In four dogs, brachiocephalic blood flow was computed as total cardiac output minus descending aortic blood flow, and in all dogs coronary perfusion pressure was calculated as mean diastolic aortic pressure minus mean diastolic left ventricular pressure. Average cardiac output for seven studies was 662 +/- 61 ml/min with high-impulse manual compression, 340 +/- 46 ml/min with mechanical compression and simultaneous ventilation, 336 +/- 45 ml/min with mechanical compression and simultaneous ventilation with systolic abdominal compression, 366 +/- 52 ml/min with mechanical compression and simultaneous ventilation with diastolic abdominal compression, and 196 +/- 29 ml/min with vest resuscitation (high-impulse manual compression significantly greater than other techniques by multivariate analysis, p less than 0.05). Brachiocephalic blood flow generally followed cardiac output and was statistically the greatest with high-impulse manual compression at 273 +/- 47 ml/min (p less than 0.05). Finally, high-impulse manual compression provided the highest coronary perfusion pressure of 31 +/- 4 mm Hg (p less than 0.05) compared to 23 +/- 2 mm Hg for mechanical compression and simultaneous ventilation, 23 +/- 2 mm Hg for mechanical compression and simultaneous ventilation with systolic abdominal compression, 23 +/- 3 mm Hg for mechanical compression and simultaneous ventilation with diastolic abdominal compression, and 11 +/- 2 mm Hg for vest resuscitation. These data demonstrate that high-impulse manual compression generated physiologically and statistically superior hemodynamics when compared with other methods in this model of cardiopulmonary resuscitation.

Programmable pneumatic generator for manipulation of intrathoracic pressure.

The determination that blood can move during cardiopulmonary resuscitation because of imposed changes in intrathoracic pressure has led to the construction and testing of mechanical devices for increasing intrathoracic pressure fluctuations over those obtained by manual means. These mechanical systems have required high-pressure ventilation simultaneous with compression of the chest to augment blood flow. Their usefulness has been limited, however, because of the requirement for endotracheal intubation and complex devices. Similar systems have also been used to generate intrathoracic pressure changes timed to the cardiac cycle to aid the failing, but beating, heart. A system was developed that can produce high intrathoracic pressure without simultaneous ventilation by using a vest that is placed around the thorax. The vest contains a bladder that is rapidly inflated and deflated by the programmable pneumatic generator. Air flows into and out of the bladder by the proper sequencing of large-bore three-way and two-way solenoid valves that are connected in series. A microcomputer-based controller is used to sequence the valves. The programmable pneumatic generator inflates the bladder more rapidly and to higher pressures than previous systems. The programmable pneumatic generator has been used in studies of cardiopulmonary resuscitation (heart arrested) and circulatory assistance (heart beating, but function depressed).

Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs.

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, 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, 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. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 +/- 1% to 46 +/- 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 150/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration 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%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression.(ABSTRACT TRUNCATED AT 400 WORDS)

Aortic and right atrial pressures during standard and simultaneous ventilation and compression CPR in human beings

Aortic and right atrial pressures during standard and simultaneous ventilation and compression CPR in human beings

A Comparison of Standard and “New” Cardiopulmonary Resuscitation (CPR) in Dogs

Standard CPR, consisting of 60 chest compressions per min with a ventilation interposed after every fifth compression, often allows restoration of spontaneous circulation but cannot be relied upon to preserve the brain during resuscitation attempts. In experimental models, it produces only one-third to one-half of normal cerebral blood flow and cannot sustain EEG activity. Many attempts have been made to augment overall cardiac output during CPR and presumably thereby increase cerebral blood flow. Crile used a pneumatic pressure suit to bind the abdomen and legs, but subsequent investigations found a high risk of hepatic trauma with abdominal binding. Both Wilder and Harris showed in dogs that simultaneous ventilation and compression augment carotid flow. Birch showed in an animal model that prolonged compression increased mean arterial pressure during CPR. Weisfeldt and colleagues of Baltimore have recently extended these findings to man, and combined them into a so-called “New” CPR, which consists of:a) high pressure ventilation simultaneous with sternal compression;b) 40 compressions per min;c) 60% compression duration; andd) abdominal binding.

Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs.

Recent studies have demonstrated that for the same chest compression force during mechanical cardiopulmonary resuscitation (CPR), the carotid artery-to-jugular vein pressure gradient and carotid blood flow are increased when the phasic rise of intrathoracic pressure is enhanced by abdominal binding and simultaneous ventilation at high airway pressure with each chest compression (SCV). The objective of the present study was to assess whether cerebral blood flow is also enhanced, since it is known that fluctuations in intrathoracic pressure are transmitted to the intracranial space and affect intracranial pressure (ICP). In two series of pentobarbital-anesthetized dogs, one of two CPR techniques was initiated immediately after inducing ventricular fibrillation. Brain blood flow was measured by the radiolabeled microsphere technique immediately before cardiac arrest and at 1 and 3 minutes after commencing CPR. Evidence of adequate mixing of spheres and lack of sedimentation under these low-flow conditions was verified by correlation with brain venous outflow, comparison of the arterial concentration-time profile of spheres and a nonsedimentary marker (thallium-201 in solution), and use of multiple arterial sampling sites. During SCV CPR with abdominal binding, mean carotid artery pressure (60 +/- 3 mm Hg) was higher than that during conventional CPR (25 +/- 2 mm HG). Pulsations of ICP occurred that were in phase with chest compression and greater than jugular venous pressure. Mean ICP was higher during SCV (46 +/- 2 mm Hg) than conventional CPR (20 +/- 2 mm Hg). However, the net brain perfusion pressure gradient (carotid artery pressure - ICP) was greater with SCV (14 +/- 3 mm Hg) than with conventional CPR (5 +/- 0.4 mm Hg). Cerebral blood flow was significantly greater during SCV CPR (32 +/- 7% of prearrest cerebral flow) than during conventional CPR (3 +/- 2%). We conclude that SCV CPR combined with abdominal binding substantially improved brain perfusion by enhancing cerebral perfusion pressure in this experimental model.

Failure of one method of simultaneous chest compression, ventilation, and abnormal binding during CPR

Some modified methods of CPR improve carotid blood flow, but there are no studies to show that these modified techniques improve survival, Accordingly, an experimental CPR technique using simultaneous chest compression, ventilation (SCV-CPR), and abdominal binding was compared to standard CPR in beagle dogs. The modified technique utilized a broad-based bellows device that was mechanically compressed, producing chest compression, delivering a volume of air to the endotracheal tube, and pressurizing an abdominal binder. The duration of ventricular fibrillation and CPR was 5 min. Five of the 6 dogs could be resuscitated with standard CPR. None of 6 dogs could be resuscitated using this modified method of SCV-CPR and abdominal binding. The aortic diastolic pressure and the diastolic gradient between the aorta and right atrium was significantly different between the 2 groups. Because these pressures relate to the coronary perfusion pressure, they may explain the discrepancy in the survival rate. This study suggests increasing carotid blood flow during CPR will not necessarily improve survival.