Search

Objectives. Vasopressors have been routinely used in cardiopulmonary resuscitation. Recent data show that terlipressin may restore blood pressure in asphyxial and prolonged arrests but its potential role in ventricular fibrillation (VF) remains unknown. The aim of this study was to compare coronary (CorPP) and cerebral (CPP) perfusion pressures achieved by terlipressin/adrenaline versus placebo/adrenaline in VF. Methods. Fourteen domestic pigs were randomly assigned into group A and B. After 5 min of untreated VF, compressiononly resuscitation was applied for 10 min, followed by advanced life support. Terlipressin in a single-dose of 30 μg.kg-1 was added to the first dose of adrenaline in group A, while placebo was given in group B. CorPP and CPP were calculated from right atrial, aortic and intracerebral pressures. Data were analyzed using repeated measurements ANOVA and a Fisher's protected LSD post hoc test. Results. Terlipressin/adrenaline maintained CorPP above 10 mmHg for 17.7 min longer than adrenaline alone (P=0.003) unable to prevent refractory hypotension. CorPP (mean±SD) measured at 35, 45, and 55 min after the onset of VF was 12 ± 4, 11 ± 6, and 10 ± 5 mmHg in the terlipressin group A; and 6 ± 4, 1 ± 5, and -1 ± 5 mmHg in placebo group B (P=0.03, <0.001, and <0.001). CPP measured at the same times was 23 ± 7, 20 ± 7, and 23 ± 7 mmHg in group A; and 13 ± 7, 6 ± 5, and 6 ± 7 mmHg in group B (P=0.01, <0.001, and <0.001). Conclusion. The study showed that a single dose of terlipressin, when added to adrenaline, was effective for achievement of higher vital organ perfusion pressures compared to adrenaline alone. [ABSTRACT FROM AUTHOR]

Background: The use of mechanical cardiopulmonary resuscitation (CPR) has great potential for the clinical setting. The purpose of present study is to compare the hemodynamics and ventilation during and after the load-distributing band CPR, versus the manual CPR in a porcine model of prolonged cardiac arrest, and to investigate the influence of rescue breathing in different CPR protocols. Methods: Sixty-four male pigs (n = 16/group), weighing 30 ± 2 kg, were induced ventricular fibrillation and randomized into four resuscitation groups: continuous load-distributing band CPR without rescue ventilation (C-CPR), load-distributing band 30:2 CPR (A-CPR), load-distributing band CPR with continuous rescue breathing (10/min) (V-CPR) or manual 30:2 CPR (M-CPR). Respiratory variables and hemodynamics were recorded continuously; blood gas was analyzed. Results: Tidal volume produced by compressions in the A-, C- and V-CPR groups were significantly higher compared with the M-CPR group (all p < 0.05). Coronary perfusion pressure of the V-CPR group was significantly lower than the C-CPR group (p < 0.01), but higher than the M-CPR group. The increasing of lung dead space after restoration of spontaneous circulation was significantly greater in the M-CPR group compared with the A-, C- and V-CPR groups (p < 0.01). Blood pH gradually decreased and was lower in the M-CPR group than that in the A-, Cand V-CPR groups (p < 0.01). PaO2 of the A-, C- and V-CPR groups were significantly higher and PaCO2 were significantly lower compared with the M-CPR (both p < 0.05). Cerebral performance categories were better in the A-, C- and V-CPR groups compared with the M-CPR group (p < 0.0001). Conclusions: The load-distributing band CPR significantly improved respiratory parameters during resuscitation by augmenting passive ventilation, and significantly improved coronary perfusion pressure. The volume of ventilation produced by the load-distributing band CPR was adequate to maintain sufficient gas exchange independent of rescue breathing. [ABSTRACT FROM AUTHOR]

Objective:Vasoactive drugs are used in cardiopulmonary resuscitation to increase vital organ perfusion. The aim of this study was to compare the haemodynamic effects of synergistically acting terlipressin and adrenaline vs. adrenaline alone in a porcine model of ventricular fibrillation (VF). Design: Randomized, double-blinded, placebo controlled experimental study. Setting: Department of Anaesthesiology and Intensive Care Medicine, University Hospital; Animal Research Laboratory, Faculty of Military Health Sciences Materials and methods: Fourteen domestic pigs were randomly assigned into group TER (n = 7) and ADR (n = 7). VF was induced using an intra-cardiac pacing lead. After 5 min of untreated arrest, compression-only resuscitation was applied for 10 min, followed by advanced life support. Terlipressin in a single-dose of 30 µg ⋅kg-1 was added to the first dose of adrenaline in group TER, while placebo was given in group ADR. Coronary (CorPP) and cerebral (CPP) perfusion pressures were calculated from the right atrial, aortic and intracerebral pressures. Data were analysed using repeated measurements ANOVA and a Fisher's protected LSD post hoc test. Results: Terlipressin/adrenaline maintained CorPP higher than 10 mm Hg for 17.7 min longer than adrenaline alone (P = 0.003). CorPP (mean ± SD) measured at 35, 45, and 55 min after the onset of VF was 12.2 ± 4.0, 11.0 ± 6.2, and 9.6 ± 4.5 mm Hg in group TER; and 5.8 ± 3.8, 0.6 ± 4.9, and -1.0 ± 4.5 mm Hg in group ADR (P = 0.03, < 0.001, and < 0.001). CPP measured at the same times was 23.0 ± 7.2, 20.4 ±6.9, and 23.1 ± 6.7 mm Hg in group TER; and 13.3 ± 6.5, 6.2 ± 5.3, and 5.6 ± 6.5 mm Hg in group ADR (P = 0.01, < 0.001, and < 0.001). Conclusion: A single dose of terlipressin, when added to adrenaline in cardiopulmonary resuscitation, was effective for achieving significantly higher cerebral and coronary perfusion pressures compared to adrenaline alone, which was unable to prevent severe refractory hypoperfusion. [ABSTRACT FROM AUTHOR]

To review the use of impedance threshold devices (ITD) during CPCR, their proposed mechanism of action, and their application in veterinary medicine. Data sources include scientific reviews and original research publications using the PubMed search engine with the following keywords: 'impedance threshold device' and 'resuscitation' and the Veterinary Information Network search function using the keywords 'impedance threshold device.' Studies in human medicine have demonstrated that the use of an ITD during CPCR in patients during out-of-hospital cardiac arrest improves coronary perfusion pressure and cerebral perfusion pressure. This improvement in vital organ blood flow results in increased cardiac output and faster return of spontaneous circulation. The use of an ITD has been studied in people and currently holds a class IIb level of recommendation according to the 2010 American Heart Association Guidelines for CPR and Emergency Cardiovascular Care. This device is recommended as a way to improve hemodynamics during CPCR by enhancing venous return and avoiding hyperventilation, thereby increasing the likelihood of a successful resuscitation. Multiple controlled studies using pigs with ventricular fibrillation induced cardiopulmonary arrest have demonstrated increased myocardial and cerebral perfusion with the use of an ITD. These studies have emphasized the importance of decreasing intrathoracic pressures during the decompression phase of CPCR and avoiding hyperventilation in order to maximize vital organ blood flow. Use of an ITD during CPCR in human and animal studies has demonstrated improved vital organ perfusion and faster return of spontaneous circulation. However, the majority of these studies have been carried out in people during out-of-hospital cardiac arrest and ventricular fibrillation cardiopulmonary arrest pig models. Further studies evaluating the use of an ITD during CPCR in the veterinary hospital setting are warranted. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Coronary perfusion pressure (CPP) during resuscitation from cardiac arrest has been shown to correlate with return of spontaneous circulation. Adrenergic blockade of beta-1 and alpha-1 receptors is common in the long-term management of ischemic heart disease and congestive heart failure. We sought to compare the CPP response to vasopressin vs. epinephrine in a swine model of cardiac arrest following pre-arrest adrenergic blockade. Methods: Eight anesthetized and instrumented swine were administered 0.1mg epinephrine and arterial pressure and heart rate response were measured. An infusion of labetalol was then initiated and animals periodically challenged with epinephrine until adrenergic blockade was confirmed. The left anterior descending coronary artery was occluded to produce ventricular fibrillation (VF). After 7min of untreated VF, mechanical chest compressions were initiated. After 1min of compressions, 1mg epinephrine was given while CPP was recorded. When CPP values had returned to pre-epinephrine levels, 40U of bolus vasopressin was given. Differences in CPP (post-vasopressor–pre-vasopressor) were compared within animals for the epinephrine and vasopressin response and with eight, non-adrenergically blocked, historical controls using Bayesian statistics with a non-informative prior. Results: The CPP response following epinephrine was 15.1mmHg lower in adrenergically blocked animals compared to non-adrenergically blocked animals (95% Highest Posterior Density [HPD] 2.9–27.2mmHg lower). CPP went up 18.4mmHg more following vasopressin when compared to epinephrine (95% HPD 8.2–29.1mmHg). The posterior probability of a higher CPP response from vasopressin (vs. epinephrine) in these animals was 0.999. Conclusions: Pre-arrest adrenergic blockade blunts the CPP response to epinephrine. Superior augmentation of CPP is attained with vasopressin under these conditions. [ABSTRACT FROM AUTHOR]

Abstract: Background: During manual chest compressions for cardiac arrest the waveforms of chest compressions are generally sinusoidal, whereas mechanical chest compression devices can have different waveforms, including trapezoidal. We studied the haemodynamic differences of such waveforms in a porcine model of cardiac arrest. Methods: Eight domestic pigs (weight 31±3kg) were anaesthetised and instrumented to continuously monitor aortic (AP) and right atrial pressure (RAP), carotid (CF) and cerebral cortical microcirculation blood flow (CCF). Coronary perfusion pressure (CPP) was calculated as the maximal difference between AP and RAP during diastole or decompression phase. After 4min of electrically induced ventricular fibrillation, mechanical chest compressions were performed with four different waveforms in a factorial design, and in randomized sequence for 3min each. Resulting differences are presented as mean with 95% confidence intervals. Results: Mean AP and RAP were higher with trapezoid than sinusoid chest compressions, difference 5.7 (0.7, 11) and 6.3 (2.1, 11)mmHg, respectively. Flow measured as CF and CCF was also improved with trapezoidal waveform, difference 14 (2.8, 26)ml/min and 11 (5.6, 17)% of baseline, respectively, with a parallel, non-significant (P =0.08) trend for CPP. Active vs. passive decompression to zero level improved CF, but without even a trend for CPP. Conclusion: Trapezoid chest compressions and active decompression to zero level improved blood flow to the brain. The compression waveform is an additional factor to consider when comparing mechanical and manual chest compressions and when comparing different compression devices. [ABSTRACT FROM AUTHOR]

Abstract: Background: The rationale for a compression to ventilation ratio of 3:1 in neonates with primary hypoxic, hypercapnic cardiac arrest is to emphasize the importance of ventilation; however, there are no published studies testing this approach against alternative methods. An extended series of cardiac compressions offers the theoretical advantage of improving coronary perfusion pressures and hence, we aimed to explore the impact of compression cycles of two different durations. Materials and methods: Newborn swine (n =32, age 12–36h, weight 2.0–2.7kg) were progressively asphyxiated until asystole occurred. Animals were randomized to receive compressions:ventilations 3:1 (n =16) or 9:3 (n =16). Return of spontaneous circulation (ROSC) was defined as a heart rate ≥100beatsmin−1. Results: All animals except one in the 9:3 group achieved ROSC. One animal in the 3:1 group suffered bradycardia at baseline, and was excluded, leaving us with 15 animals in each group surviving to completion of protocol. Time to ROSC (median and interquartile range) was 150s (115–180) vs. 148s (116–195) for 3:1 and 9:3, respectively (P =0.74). There were no differences in diastolic blood pressure during compression cycles or in markers of hypoxia and inflammation. The temporal changes in mean arterial blood pressure, heart rate, arterial blood gas parameters, and systemic and regional oxygen saturation were comparable between groups. Conclusion: Neonatal pigs with asphyxia-induced cardiac arrest did not respond to a compression:ventilation ratio of 9:3 better than to 3:1. Future research should address if alternative compression:ventilation ratios offer advantages over the current gold standard of 3:1. [Copyright &y& Elsevier]

Abstract: Patients with pulseless electrical activity or refractory ventricular fibrillation have a very bad prognosis. Coronary angiography and angioplasty may be required to restore an effective circulation, but this must be performed whilst chest compressions are continued. The LUCAS chest compression device is suitable for this purpose. So far there are no reports on the effect of this device on coronary circulation in humans. We monitored the coronary perfusion pressure assessed invasively as the difference between the diastolic pressures at the coronary ostium and right atrium, and compared these pressures with coronary flow graded using the TIMI scale in 6 patients. In 4 out of 6 we found a satisfactory coronary artery perfusion pressure and TIMI grade 3 flow (normal) on coronary angiography. Two of these patients survived the first 24h. Two patients did not have a satisfactory perfusion pressure and adequate flow rate was not seen. [Copyright &y& Elsevier]

Abstract: Aims: As the duration of untreated cardiac arrest increases, the effectiveness of standard therapies declines, and may be more harmful than helpful. We investigated the hemodynamic, metabolic and anti-inflammatory effects of Ringer''s ethyl pyruvate solution (REPS) versus Ringer''s solution (RS) in the acute model of prolonged porcine arrest. Methods: Seventeen mixed-breed swine were induced into ventricular fibrillation (VF) and left untreated for 8min. CPR was begun using a mechanical chest compression device at a rate of 100 per minute. At the onset of CPR, animals were randomly assigned to treatment with either 25mL/kg of RS or 25mL/kg of REPS containing 40mg/kg of ethyl pyruvate, infused over 5min in blinded fashion. CPR continued with administration of a drug cocktail at 2min and the first rescue shock was delivered at minute 13 of VF. Animals having ROSC were supported with standardized care for 2h. Results: Both groups had 100% ROSC and 100% 2-h survival. The REPS group exhibited higher median CPP (27.3mmHg) than the control group (16.5mmHg) by 3min of CPR, which continued throughout the duration of CPR (p =0.02). The median time to hypotension following ROSC was 9.64min in the REPS group and 7.25min in controls (p =0.04) and there was a non-significant trend of decreased use of vasopressors for the duration of resuscitation. There was no difference in systemic or cerebral metabolism between groups. There were non-significant trends of decreased IL-6, increased Il-10 and decreased mesenteric bacterial colony growth in those treated with REPS when compared to RS. Conclusions: The administration of REPS with CPR significantly improved intra- and post-resuscitation hemodynamics in this swine model of prolonged cardiac arrest, but did not definitely change the metabolic or inflammatory profile during the acute resuscitation period. [Copyright &y& Elsevier]

Abstract: Background: Cardiac arrest remains one of the leading causes of death worldwide. European Resuscitation Council Guidelines for Resuscitation 2005 recommend epinephrine for its treatment. Objectives: To estimate whether the administration of a vasodilatator such as nitroglycerin in combination with epinephrine during cardiopulmonary resuscitation would improve resuscitation outcome in an established model of ventricular fibrillation. Methods: Design: Prospective, randomized, blinded, controlled study. Setting: Animal research laboratory. Ventricular fibrillation was induced in 20 Landrace/Large-White pigs. It remained untreated for 8 min before attempting resuscitation precordial compressions, mechanical ventilation, and electrical defibrillation. Animals were randomized into two groups, 10 animals each. Group A received saline as placebo (10 mL dilution, bolus) and epinephrine (0.02 mg/kg). Group B received nitroglycerin (50 μg/kg) and epinephrine (0.02 mg/kg) during cardiopulmonary resuscitation. Electrical defibrillation was attempted after 10 min of ventricular fibrillation. Results: Four animals in group A restored spontaneous circulation in comparison to eight in Group B. Coronary perfusion pressure (p < 0.0001) was significantly increased in Group B during cardiopulmonary resuscitation. Conclusion: A vasodilatator, when administered in combination with a vasopressor such as epinephrine during cardiopulmonary resuscitation, increases coronary perfusion pressure. [Copyright &y& Elsevier]

Abstract: Objective: To explore in detail the expected magnitude of systemic perfusion pressure during standard CPR as a function of compression frequency for different sized people from neonate to adult. Method: A 7-compartment mathematical model of the human cardiopulmonary system – upgraded to include inertance of blood columns in the aorta and vena cavae – was exercised with parameters scaled to reflect changes in body weight from 1 to 70kg. Results: Maximal systemic perfusion pressure occurs at chest compression rates near 60, 120, 180, and 250/min for subjects weighing 70, 10, 3, and 1kg, respectively. Such maxima are predicted by analytical models describing the dependence of stroke volume on pump-filling time in the presence of blood inertia. This mathematical analysis reproduces earlier experimental results of Fitzgerald et al. in 10kg dogs. Conclusions: Fundamental geometry and physics suggest that the most effective chest compression frequency in CPR depends upon body size and weight. In neonates there is room for improvement at the top of the compression frequency scale at rates >120/min. In adults there may be benefit from lower compression frequencies near 60/min. [Copyright &y& Elsevier]

Objective. We sought to determine the effect of the preshock pause (PSP) on coronary perfusion pressure (CPP) decay and subsequent rescue shock (RS) outcome in porcine ventricular fibrillation (VF). Methods. Retrospective analysis of digitally recorded CPP tracings was performed. Ventricular fibrillation was electrically induced in all animals and resuscitation was standardized in all experiments. The first RS was delivered after an average of 10.8 minutes of VF (7.4 minutes of nontreatment and 3.4 minutes of resuscitation). The continuous CPP tracing segments, during the hands-off period prior to the first two rescue shocks, were imported into a spreadsheet and analyzed using descriptive statistics as well as univariate and multivariate statistical methods. The RS outcome for each animal was recorded as failed or return of spontaneous circulation (ROSC) (a systolic blood pressure of 80 mmHg or greater, sustained continuously for at least 1 minute). Results. We included 196 rescue shocks (120 first RS [RS1], 76 second RS [RS2]) from 120 swine. The mean CPP following the last compression before RS was 23.4 mmHg (standard error of the mean [SEM]: 1.3). The median PSP duration was 4.1 seconds (interquartile range [IQR]: 3.3, 6.1). The mean CPP just prior to RS was 7.6 mmHg (SEM: 0.6). Overall, the RS was successful (ROSC) in 57 of 120 (0.47 [95% confidence interval (CI): 0.38, 0.56]) attempts. Univariate results showed a counterintuitive positive correlation between PSP and maximum CPP for RS1 (r = 0.548, p < 0.001). Conclusion. During the resuscitation PSP in these porcine studies of prolonged VF, CPP dropped precipitously, but RS outcome was not adversely affected. [ABSTRACT FROM AUTHOR]

Summary: The new resuscitation guidelines permit compressions before delayed, defibrillation, a change that has generally been welcomed. The benefits are generally assumed to relate to the immediate provision of limited coronary perfusion with protection or replenishment of myocardial metabolic reserves. In this paper we argue that the concept is inadequate to explain many experimental and clinical observations made during resuscitation attempts. We argue that changes in the size and shape of the ventricles are the most important reason for the narrow window of opportunity for defibrillation alone and for the value of compressions in extending this period. We also draw attention to the implication for clinical resuscitation and to one aspect of the current guidelines of the European Resuscitation Council that we believe to be inconsistent with the evidence that we review. [Copyright &y& Elsevier]

Summary: Aim of study: After cardiac arrest, uninterrupted chest compressions with restoration of myocardial blood flow facilitates restoration of spontaneous circulation. We recognized that this may best be accomplished with a mechanical device and especially so during transport. We therefore sought to develop a lightweight, portable chest compressor which may be carried on the belt or attached to the oxygen tank typically carried on the back of the first response rescuer. A miniaturized pneumatic chest compressor (MCC) weighing less than 2kg was developed and compared with a currently marketed “Michigan Thumper®”, which weighed 19kg. We hypothesized that the 2kg, low profile, portable device will be as effective as the standard pneumatic Thumper® for restoring circulation during CPR. Material and methods: Ventricular fibrillation was electrically induced in 10 domestic male pigs weighing 39±2kg, and untreated for 5min. Animals were then randomized to receive chest compressions with either the MCC or the Thumper®. After 5min of mechanical chest compression, defibrillation was attempted with a 150J biphasic shock. Coronary perfusion pressure (CPP) and end tidal PCO2 (EtPCO2) were measured by conventional techniques together with right carotid artery blood flow (CBF). Results: Four of five animals compressed with the Thumper® and each animal compressed with the MCC were successfully resuscitated. No significant differences in CPP, EtPCO2, CBF and post-resuscitation myocardial function were observed between groups. Resuscitated animals survived for more than 72h without neurological impairment. Conclusion: The low profile, 2kg miniaturized chest compressor is as effective as the conventional Thumper® in an experimental model of CPR. [Copyright &y& Elsevier]

1. The role of haemodynamic changes in left ventricular remodelling has been poorly investigated, especially in the context of volume overload cardiac hypertrophy. Low diastolic blood pressure and high left ventricular filling pressure are expected to affect coronary driving pressure negatively and thereby put in jeopardy subendocardial perfusion in particular. The consequences to global left ventricular remodelling remain undetermined. The aim of the present study was to investigate the role of coronary driving pressure in the development of subendocardial remodelling and the conceivable effects on cardiac function, using a rat model of aortocaval fistula. 2. Wistar rats, weighing 330–350 g, were submitted to aortocaval fistula (ACF group) or sham (control group) operations. Two haemodynamic measurements were determined following surgery, the initial measurement at week 1 and the final measurement at week 8. Cytokine expression, myeloperoxidase (MPO) activity, metalloproteinase expression and activity and fibrosis were assessed in two distinct left ventricular myocardial layers: the subendocardium (SE) and the non-subendocardium (non-SE). 3. The ACF group showed lower initial and final coronary driving pressure and lower final +dP/dt and –dP/dt compared with the control group. Multivariate analyses disclosed initial coronary driving pressure as the only haemodynamic parameter independently associated with SE fibrosis ( R2 = 0.76; P < 0.0001) and with +dP/dt ( R2 = 0.55; P = 0.0004) and –dP/dt ( R2 = 0.91; P < 0.0001). Matrix metalloproteinase (MMP)-2 expression and activity predominated in the SE of ACF animals, particularly in those with low coronary driving pressure. Increased levels of interleukin (IL)-6 and IL-1β also predominated in the SE of the ACF group. Otherwise, MPO activity and levels of tumour necrosis factor-α and IL-10 were similar in both groups. Final coronary driving pressure correlated with both the expression and activity of MMP-2. 4. Low coronary driving pressure early in the course of ACF determines SE damage and, by this mechanism, interferes negatively in left ventricular function. [ABSTRACT FROM AUTHOR]

Background: Cardiac arrest remains the leading cause of death in Western societies. Advanced Life Support guidelines propose epinephrine (adrenaline) for its treatment. The aim of this study was to assess whether a calcium sensitizer agent, such as levosimendan, administered in combination with epinephrine during cardiopulmonary resuscitation, would improve the initial resuscitation success. Methods: Ventricular fibrillation was induced in 20 Landrace/Large-White piglets, and left untreated for 8 min. Resuscitation was then attempted with precordial compressions, mechanical ventilation and electrical defibrillation. The animals were randomized into two groups (10 animals each): animals in Group A received saline as placebo (10 ml dilution, bolus) + epinephrine (0.02 mg/kg), and animals in Group B received levosimendan (0.012 mg/kg/10 ml dilution, bolus) + epinephrine (0.02 mg/kg) during cardiopulmonary resuscitation. Electrical defibrillation was attempted after 10 min of ventricular fibrillation. Results: Four animals in Group A showed restoration of spontaneous circulation and 10 in Group B ( P = 0.011). The coronary perfusion pressure, saturation of peripheral oxygenation and brain regional oxygen saturation were significantly higher during cardiopulmonary resuscitation in Group B. Conclusions: A calcium sensitizer agent, when administered during cardiopulmonary resuscitation, significantly improves initial resuscitation success and increases coronary perfusion pressure during cardiopulmonary resuscitation. [ABSTRACT FROM AUTHOR]

Copyright of Notfall & Rettungsmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Summary: An intrathoracic pressure regulator (ITPR) is a device that can be added to the external end of a tracheal tube to create controlled negative airway pressure between positive pressure ventilations. The resulting downward bias of the airway pressure baseline promotes increased venous return and enhanced circulation during CPR and also during hypovolemic shock. In the present study, we exercised a mathematical model of the human cardiopulmonary system, including airways, lungs, a four chambered heart, great vessels, peripheral vascular beds, and the biomechanics of chest compression and recoil, to determine the relationship between systemic perfusion pressure during CPR and the value of baseline negative airway pressure in an ITPR. Perfusion pressure increases approximately 50% as baseline airway pressure falls from zero to −10cm H2O. Thereafter perfusion pressure plateaus. Negative bias pressures exceeding −10cm H2O are not needed in ITPR-CPR. [Copyright &y& Elsevier]

Summary: There is growing evidence that microcirculatory blood flow is the ultimate determinant of the outcome in circulatory shock states. We therefore examined changes in the microcirculation accompanying the most severe form of circulatory failure, namely cardiac arrest and the effects of subsequent cardiopulmonary resuscitation. Ventricular fibrillation was electrically induced in nine pigs and untreated for 5min prior to beginning closed chest cardiac compression and attempting electrical defibrillation. Orthogonal polarization spectral imaging was utilized for visualization of the sublingual microcirculation at baseline, 0.5, 1, 3 and 5min after onset of ventricular fibrillation and at 1 and 5min after start of chest compression. Images were also obtained 1 and 5min after restoration of spontaneous circulation. Microvascular flow was graded from 0 (no flow) to 3 (normal flow). Aortic and right atrial pressures were measured and coronary perfusion pressure was computed continuously. Microcirculatory blood flow decreased to less than one-fourth within 0.5min after inducing ventricular fibrillation. Precordial compression partially restored microvascular flow in each animal. In animals that were successfully resuscitated, microvascular flow was significantly greater after 1 and 5min of chest compression than in animals with failed resuscitation attempts. Microvascular blood flow was highly correlated with coronary perfusion pressure (r =0.82, p <0.01). Microvascular blood flow in the sublingual mucosa is therefore closely related to coronary perfusion pressure during cardiopulmonary resuscitation and both are predictive of outcome. [Copyright &y& Elsevier]

Summary: Background: A new device, the intrathoracic pressure regulator (ITPR), was developed to generate continuous negative intrathoracic pressure during cardiopulmonary resuscitation (CPR) and allow for intermittent positive pressure ventilation. Use of the ITPR has been shown to increase vital organ perfusion and short-term survival rates in pigs. The purpose of this study was to investigate the hemodynamic and blood gas effects of more prolonged (15min) use of the ITPR during CPR in a porcine model of cardiac arrest. Methods: After 8min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15min of either ITPR-CPR or standard (STD) CPR. Compressions were delivered at a rate of 100/min with a compression to ventilation ratio of 15:2. Ventilations were delivered with a resuscitator bag. Tracheal, aortic, right atrial, intracranial pressures (ICP), common carotid blood flow and respiratory variables were recorded continuously. Arterial and venous blood gases were collected at baseline, and after 5, 10, and 15min of CPR. Coronary perfusion pressure (CPP) was calculated as diastolic aortic pressure—right atrial pressure. Cerebral perfusion pressure (CerPP) was calculated as mean arterial pressure (MAP)—intracranial pressure. Statistical analysis was performed with unpaired t-test and Friedman''s Repeated Measures Analysis. Results: ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (−9±0.6mmHg versus −3±0.3mmHg, p <0.001), diastolic right atrial pressure (DRAP) (−0.1±0.2mmHg versus 2.3±0.2mmHg, p <0.001) and intracranial pressure (20.8±0.6mmHg versus 23±0.5mmHg, respectively, p =0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO2), (p <0.001). Common carotid artery blood flow was increased by an average of 70%, p <0.001. ABGs showed progressive metabolic acidosis in the ITPR-CPR group, but PaCO2 remained stable at 34mmHg for 15min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO2 values remaining <20mmHg (p <0.001). PaO2 was not different between groups. Following 23min of cardiac arrest (15min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p =0.3. Conclusion: ITPR-CPR significantly improved hemodynamics, vital organ perfusion pressures and common carotid blood flow compared to STD-CPR in a porcine model of prolonged cardiac arrest and basic life support. The beneficial hemodynamic effects of ITPR-CPR were sustained at least 15min without any compromise in oxygenation. [Copyright &y& Elsevier]

Summary: Background: Elevated coronary perfusion pressure (CPP) during CPR is associated with return of spontaneous circulation (ROSC). We compared CPP achieved with three methods of chest compression: manual (MAN), mechanical (MECH) and high-impulse mechanical (HI) in a porcine model of prolonged ventricular fibrillation (VF). We hypothesized that HI (very rapid acceleration of the down-stroke) would produce greater CPPs than MAN or MECH, and that HI would also produce a higher rate of ROSC. Methods: Twenty-eight domestic swine (mean 27.8kg) were randomly assigned to three methods of chest compression. Animals were instrumented under anesthesia, and VF was induced and untreated for 8min. After 2min of CPR, epinephrine (adrenaline) (0.1mg/kg), vasopressin (40U) and propranolol (1.0mg) were administered. CPR continued for three more minutes, after which up to three rescue shocks were delivered. CPP was determined in an automated fashion by measuring the difference between aortic and right atrial pressures 0.1s prior to the down-stroke of each compression (i.e. end-relaxation). ROSC was defined as a systolic pressure greater than 80mmHg sustained for at least 1min. We analyzed CPP and ROSC using repeated measures ANOVA and Fisher''s exact test. Results: Over the 5min of CPR, CPP increased more with HI compression than with MAN compression (p =0.017). ROSC was attained in 4/9 MAN, 6/9 MECH and 10/10 HI (HI versus MAN p =0.01). Conclusions: Over the course of CPR, HI compression increased CPP more than MAN compression. HI compression produced a significantly higher rate of ROSC than MAN, but not MECH compression. [Copyright &y& Elsevier]

Summary: Periodic z-axis acceleration (pGz)-CPR involves an oscillating motion of a whole patient in the head-to-foot dimension on a mechanized table. The method is able to sustain blood flow and long-term survival during and after prolonged cardiac arrest in anesthetized pigs. However, the exact mechanism by which circulation of blood is created has remained unknown. Objectives: To explain the hemodynamic mechanism of pGz-CPR and to suggest some theoretically useful improvements. Method: Computer modeling using a hybrid analytical–numerical approach, based upon Newton''s second law of motion for fluid columns in the aorta and vena cavae, Ohm''s law for resistive flow through vascular beds, and a 10-compartment representation of the adult human circulation. This idealized 70-kg human model is exercised to explore the effects upon systemic perfusion pressure of whole body z-axis acceleration at frequencies ranging from 0.5 to 5Hz. The results, in turn, suggested studies of abdominal compression at these frequencies. Results and conclusions: Blood motion induced in great vessels by periodic z-axis acceleration causes systemic perfusion when cardiac valves are competent. Blood flow is a function of the frequency of oscillation. At 3.5Hz, periodic acceleration using ±0.6G and ±1.2cm oscillations induces forward blood flow of 2.1L/min and systemic perfusion pressure of 47mmHg. A form of resonance occurs at the frequency for peak-flow, in which the period of oscillation matches the round-trip transit time for reflected pulse waves in the aorta. For ±1.0G acceleration at 3.5Hz, systemic perfusion pressure is 80mmHg and forward flow is 3.8L/min in the adult human model with longitudinal z-axis motion of only ±2cm. Similar results can be obtained using abdominal compression to excite resonant pressure–volume waves in the aorta. For 20mmHg abdominal pressure pulses at 3.8Hz, systemic perfusion pressure is 71mmHg and forward flow is 2.8L/min. pGz-CPR and high-frequency abdominal CPR are the physically realistic means of generating artificial circulation during cardiac arrest. These techniques have fundamental mechanisms and practical features quite different from those of conventional CPR and the potential to generate superior systemic perfusion. [Copyright &y& Elsevier]

Summary: Objective: Blood flow during conventional cardiopulmonary resuscitation (CPR) is usually less than adequate to sustain vital organ perfusion. A new chest compression device (LifeBelt™) which compresses both the sternum and the lateral thoraces (compression and thoracic constraint) has been developed. The device is light weight, portable, manually powered and mechanically advantaged to minimize user fatigue. The purpose of this study was to evaluate the mechanism of blood flow with the device, determine the optimal compression force and compare the device to standard manual CPR in a swine arrest model. Methods: Following anesthesia and instrumentation, intravascular contrast injections were performed in four animals and the performance characteristics of the device were evaluated in eight animals. In a comparative outcome study, 42 anesthetized and instrumented swine were randomized to receive LifeBelt™ or manual CPR. Ventricular fibrillation (VF) was induced electrically and was untreated for 7.5min. After 7.5min, countershocks were administered and chest compressions initiated. Pulseless electrical activity (PEA) was observed after one to three shocks in all animals. CPR was continued until restoration of spontaneous circulation (ROSC) or for 10min after the first shock. If ROSC had not occurred within 5min of beginning CPR, 0.01mg/kg of epinephrine (adrenaline) was administered. During CPR, peak systolic aortic pressure (Ao), diastolic coronary perfusion pressure (CPP-diastolic aortic minus diastolic right pressure) and end-tidal CO2 were measured. Results: Angiographic studies demonstrated cardiac compression as the mechanism of blood flow. Optimal performance, determined by coronary perfusion pressure, was observed at a sternal force of 100–130lb (45–59kg). In the comparative trial, significant differences in the measured CPP were observed between LifeBelt™ and manual CPR both at 1min (15±8mmHg versus 10±6mmHg, p <0.05) and 5min (17±4mmHg versus 13±7mmHg, p <0.02) of chest compression. A greater (p <0.05) ETCO2, a marker of cardiac output and systemic perfusion, was observed with LifeBelt™ CPR (20±7mmHg) than with manual CPR (15±5mmHg) at 1min. Peak Ao pressures were not different between methods. With the device, 86% of animals were resuscitated compared to 76% in the manual group. Conclusions: Blood flow with the LifeBelt™ device is primarily the result of cardiac compression. At a sternal force of 100–130lb (45–59kg), the device produces greater CPP than well-performed manual CPR during resuscitation from prolonged VF. [Copyright &y& Elsevier]

Summary: Objective: To discover design principles underlying the optimal waveforms for external chest and abdominal compression and decompression during cardiac arrest and cardiopulmonary resuscitation (CPR). Method: A 14-compartment mathematical model of the human cardiopulmonary system is used to test successive generations of randomly mutated external compression waveforms during cardiac arrest and resuscitation. Mutated waveforms that produced superior mean perfusion pressure became parents for the next generation. Selection was based upon either systemic perfusion pressure (SPP=thoracic aortic minus right atrial pressure) or upon coronary perfusion pressure (CPP=thoracic aortic pressure minus myocardial wall pressure). After simulations of 64,414 individual CPR episodes, 40 highly evolved waveforms were characterized in terms of frequency, duty cycle, and phase. A simple, practical compression technique was then designed by combining evolved features with a constant rate of 80min−1 and duty cycle of 50%. Results: All ultimate surviving waveforms included reciprocal compression and decompression of the chest and the abdomen to the maximum allowable extent. The evolved waveforms produced 1.5–3 times the mean perfusion pressure of standard CPR and greater perfusion pressure than other forms of modified CPR reported heretofore, including active compression–decompression (ACD)+ITV and interposed abdominal compression (IAC)–CPR. When SPP was maximized by evolution, the chest compression/abdominal decompression phase was near 70% of cycle time. When CPP was maximized, the abdominal compression/chest decompression phase was near 30% of cycle time. Near-maximal SPP/CPP of 60/21mmHg (forward flow 3.8L/min) occurred at a compromise compression frequency of 80min−1 and duty cycle for chest compression of 50%. Conclusions: Optimized waveforms for thoraco-abdominal compression and decompression include previously discovered features of active decompression and interposed abdominal compression. These waveforms can be used by manual (Lifestick-like) and mechanical (vest-like) devices to achieve short periods of near normal blood perfusion non-invasively during cardiac arrest. [Copyright &y& Elsevier]

Abstract: Interposed abdominal compression, IAC-CPR incorporates alternating chest and abdominal compressions to generate enhanced artificial circulation during cardiac arrest. The technique has been generally successful in improving blood flow and survival compared to standard CPR; however, some questions remain. Objective:: To determine “why does IAC-CPR produce more apparent benefit in some subjects than in others?” and “what is the proper compression rate, given that there are actually two compressions (chest and abdomen) in each cycle?” Method:: Computer models provide a means to search for subtle effects in complex systems. The present study employs a validated 12-compartment mathematical model of the human circulation to explore the effects upon systemic perfusion pressure of changes in 35 different variables, including vascular resistances, vascular compliances, and rescuer technique. CPR with and without IAC was modeled. Results and conclusions:: Computed results show that the effect of 100mmHg abdominal compressions on systemic perfusion pressure is relatively constant (about 16mmHg augmentation). However, the effect of chest compression depends strongly upon chest compression frequency and technique. When chest compression is less effective, as is often true in adults, the addition of IAC produces relatively dramatic augmentation (e.g. from 24 to 40mmHg). When chest compression is more effective, the apparent augmentation with IAC is relatively less (e.g. from 60 to 76mmHg). The optimal frequency for uninterrupted IAC-CPR is near 50 complete cycles/min with very little change in efficacy over 20–100 cycles/min. In theory, the modest increase in systemic perfusion pressure produced by IAC can make up in part for poor or ineffective chest compressions in CPR. IAC appears relatively less effective in circumstances when chest pump output is high. [Copyright &y& Elsevier]

Abstract: An impedance threshold valve (ITV) is a new airway adjunct for resuscitation that permits generation of a small vacuum in the chest during the recoil phase of chest compression. Objectives:: To explore in detail the expected magnitude and the hemodynamic mechanisms of circulatory augmentation by an ITV in Standard CPR. Method:: A 14-compartment mathematical model of the human cardiopulmonary system—upgraded to include applied chest compression force, elastic recoil of the chest wall, anatomic details of the heart and lungs, and the biomechanics of mediastinal compression—is exercised to explore the conditions required for circulatory augmentation by an ITV during various modes of CPR. Results:: The ITV augments systemic perfusion pressure by about 5mmHg compared to any particular baseline perfusion pressure without the ITV. When baseline perfusion is low, owing to either diminished chest compression force, the existence of a thoracic pump mechanism of blood flow, or the presence of an effective compression threshold, then the relative improvement produced by an ITV is significant. With an ITV the heart expands into soft pericardiac tissue, which makes the heart easier to compress. Conclusions:: An ITV can augment perfusion during CPR. The observed effectiveness of ITVs in the laboratory and in the clinic suggests a thoracic pump mechanism for Standard CPR, and perhaps also an effective compression threshold that must be exceeded to generate blood flow by external chest compression. [Copyright &y& Elsevier]

Abstract: Introduction:: Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival. Hypothesis:: Incomplete chest wall recoil during the decompression phase of standard CPR increases intrathoracic pressure and right atrial pressure, impedes venous return, decreases compression-induced aortic pressures and results in a decrease of mean arterial pressure, coronary and cerebral perfusion pressure. Methods:: Nine pigs in ventricular fibrillation (VF) for 6min, were treated with an automated compression/decompression device with a compression rate of 100min-1, a depth of 25% of the anterior–posterior diameter, and a compression to ventilation ratio of 15:2 with 100% decompression (standard CPR) for 3min. Compression was then reduced to 75% of complete decompression for 1min of CPR and then restored for another 1min of CPR to 100% full decompression. Coronary perfusion pressure (CPP) was calculated as the diastolic (aortic (Ao)–right atrial (RA) pressure). Cerebral perfusion pressure (CerPP) was calculated multiple ways: (1) the positive area (in mmHgs) between aortic pressure and intracranial pressure (ICP) waveforms, (2) the coincident difference in systolic and diastolic aortic and intracranial pressures (mmHg), and (3) CerPP=MAP-ICP. ANOVA was used for statistical analysis and all values were expressed as mean±S.E.M. The power of the study for an alpha level of significance set at 0.05 was >0.90. Results:: With CPR performed with 100%–75%–100% of complete chest wall recoil, respectively, the CPP was 23.3±1.9, 15.1±1.6, 16.6±1.9, p=0.003; CerPP was: (1) area: 313.8±104, 89.2±39, 170.5±42.9, p=0.03, (2) systolic aortic minus intracranial pressure difference: 22.8±3.6, 16.5±4, 23.7±4.5, p=n.s., and diastolic pressure difference: 5.7±3, -2.4±2.4, 3.2±2.5, p=0.04 and (3) mean: 14.3±3, 7±2.9, 12.4±2.9, p=0.03, diastolic aortic pressure was 28.1±2.5, 20.7±1.9, 20.9±2.1, p=0.0125; ICP during decompression was 22.8±1.7, 23±1.5, 19.7±1.7, p=n.s. and mean ICP was 37.1±2.3, 35.5±2.2, 35.2±2.4, p=n.s.; RA diastolic pressure 4.8±1.3, 5.6±1.2, 4.3±1.2 p=0.1; MAP was 52±2.9, 43.3±3, 48.3±2.9, p=0.04; decompression endotracheal pressure, -0.7±0.1, -0.3±0.1, -0.75±0.1, p=0.045. Conclusions:: Incomplete chest wall recoil during the decompression phase of CPR increases endotracheal pressure, impedes venous return and decreases mean arterial pressure, and coronary and cerebral perfusion pressures. [Copyright &y& Elsevier]

Abstract: Although arginine vasopressin (AVP) has been shown to be a promising drug during cardiopulmonary resuscitation (CPR), concern has been raised about the potential for AVP-mediated vasoconstriction of the coronary arteries. In a prospective, randomized laboratory investigation employing an established porcine model, the effects of AVP on haemodynamic variables, left anterior descending (LAD) coronary artery cross sectional area employing intravascular ultrasound (IVUS), and return of spontaneous circulation were studied. During sinus rhythm, the LAD coronary artery cross sectional area was measured by IVUS at baseline, and 90s and 5min after AVP (0.4U/kg IV). Following a 60min recovery, ventricular fibrillation was induced. At 4min, chest compressions were initiated; AVP (0.4U/kg IV) was injected at 5.5min, and defibrillation performed at 8min. LAD coronary artery cross sectional area was measured by IVUS at the pre-arrest baseline, 90s after drug injection during CPR, and 5min after return of spontaneous circulation. Compared with baseline, the mid-LAD coronary artery cross sectional area increased significantly (P<.05) 90s and 5min after AVP administration (9.2±.5mm2 versus 10.7±.6mm2 versus 11.7±.6mm2, respectively) during normal sinus rhythm. Similarly during ventricular fibrillation and CPR plus AVP, the mid-LAD coronary artery cross sectional area increased at 90s after AVP compared with baseline (9.5±.6mm2 versus 11.0±.7mm2; P<.05). Moreover, the cross sectional area increased further 5min after return of spontaneous circulation (9.5±.6mm2 versus 14.0±.8mm2, P<.05). In conclusion, in this experimental model with normal coronary arteries, AVP resulted in significantly increased LAD coronary artery cross sectional area during normal sinus rhythm, during ventricular fibrillation with CPR, and after return of spontaneous circulation. [Copyright &y& Elsevier]

1. The aim of the present study was to evaluate the contribution of disturbance of coronary perfusion to myocardial depression in hearts isolated from lipopolysaccharide (LPS)-treated rats and to investigate the involvement of endothelin (ET)-1 and nitric oxide (NO).2. Rats were treated with LPS (10 mg/kg, i.p.) and, 4 h later, plasma ET-1 concentrations were measured by radioimmunoassay and hearts were excised for perfusion at a constant perfusion flow. The selective ETA receptor antagonist BQ-123, in the absence or presence of aminoguanidine, a specific inhibitor of inducible NO synthase, was given 15 min before LPS challenge. Coronary perfusion pressure (CPP) and measures of myocardial contractile function were recorded.3. In hearts isolated from LPS-treated rats, there was a marked increase in CPP that was abolished by pretreatment with BQ-123. In parallel, an increase in plasma ET-1 concentrations was seen in these rats. Lipopolysaccharide also induced decreases in left ventricular developed pressure (LVDP), the product of LVDP and heart rate and maximal rate of rise/fall of left ventricular pressure (+/– dP/dtmax). Single treatment with BQ-123 or aminoguanidine attenuated LPS-induced myocardial depression. However, when these two drugs were given simultaneously, myocardial depression elicited by LPS was blocked significantly.4. Endothelin-1-mediated coronary vasoconstriction, together with NO, contributes to myocardial depression in hearts isolated from LPS-treated rats. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effects of a bolus dose of vasopressin compared to continuous adrenaline (epinephrine) infusion on vital organ blood flow during cardiopulmonary resuscitation (CPR). Methods: Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. After 2 min of CPR the animals were randomly assigned to receive either vasopressin (0.4 U/kg) or adrenaline (bolus of 20 μg/kg followed by continuous infusion of 10 μg/(kg min)). Defibrillation was attempted after 9 min of CPR. Results: Vasopressin generated higher cortical cerebral blood flow (P<0.001) and lower cerebral oxygen extraction (P<0.001) during CPR compared to continuous adrenaline. Coronary perfusion pressure during CPR was higher in vasopressin-treated pigs (P<0.001) and successful resuscitation was achieved in 12/12 in the vasopressin group versus 5/12 in the adrenaline group (P=0.005). Conclusions: In this experimental model, vasopressin caused a greater increase in cortical cerebral blood flow and lower cerebral oxygen extraction during CPR compared to continuous adrenaline. Furthermore, vasopressin generated higher coronary perfusion pressure and increased the likelihood of restoring spontaneous circulation. [Copyright &y& Elsevier]

Introduction: The purpose of this pilot clinical study was to determine if a novel chest compression device would improve hemodynamics when compared to manual chest compression during cardiopulmonary resuscitation (CPR) in humans. The device is an automated self-adjusting electromechanical chest compressor based on AutoPulse™ technology (Revivant Corporation) that uses a load distributing compression band (A-CPR) to compress the anterior chest. Methods: A total of 31 sequential subjects with in-hospital sudden cardiac arrest were screened with institutional review board approval. All subjects had received prior treatment for cardiac disease and most had co-morbidities. Subjects were included following 10 min of failed standard advanced life support (ALS) protocol. Fluid-filled catheters were advanced into the thoracic aorta and the right atrium and placement was confirmed by pressure waveforms and chest radiograph. The coronary perfusion pressure (CPP) was measured as the difference between the aortic and right atrial pressure during the chest compression’s decompressed state. Following 10 min of failed ALS and catheter placement, subjects received alternating manual and A-CPR chest compressions for 90 s each. Chest compressions were administered without ventilation pauses at 100 compressions/min for manual CPR and 60 compressions/min for A-CPR. All subjects were intubated and ventilated by bag-valve at 12 breaths/min between compressions. Epinephrine (adrenaline) (1 mg i.v. bolus) was given at the request of the attending physician at 3–5 min intervals. Usable pressure signals were present in 16 patients (68±6 years, 5 female), and data are reported from those patients only. A-CPR chest compressions increased peak aortic pressure when compared to manual chest compression (153±28 mmHg versus 115±42 mmHg, P<0.0001, mean±S.D.). Similarly, A-CPR increased peak right atrial pressure when compared to manual chest compression (129±32 mmHg versus 83±40 mmHg, P<0.0001). Furthermore, A-CPR increased CPP over manual chest compression (20±12 mmHg versus 15±11 mmHg, P<0.015). Manual chest compressions were of consistent high quality (51±20 kg) and in all cases met or exceeded American Heart Association guidelines for depth of compression. Conclusion: Previous research has shown that increased CPP is correlated to increased coronary blood flow and increased rates of restored native circulation from sudden cardiac arrest. The A-CPR system using AutoPulse technology demonstrated increased coronary perfusion pressure over manual chest compression during CPR in this terminally ill patient population. [Copyright &y& Elsevier]

Objective: To estimate the optimum ratio of chest compressions to ventilations for one-rescuer CPR that maximizes systemic oxygen delivery in children. Method: Equations describing oxygen delivery and blood flow during CPR as functions of the number of compressions and the number of ventilations delivered over time were adapted from the former work of Babbs and Kern. These equations were solved explicitly as a function of body weight, using scaling algorithms based upon principles of developmental anatomy and physiology. Results: The optimal compression to ventilation (C/V) ratios for infants and younger children increase sharply as a function of body weight. Optimal C/V ratios are lower for professional rescuers, who take less time to deliver a rescue breath, than for lay rescuers, who interrupt chest compressions for longer to perform ventilations. For professional rescuers the optimal C/V ratio, x*, is approximately 1.6√ of W where the W is the patient’s body weight in kg. For lay rescuers the optimum C/V ratio is approximately 2.8√ of W. These values can be approximated for children and teens by the following rules of thumb, based upon the age of the victim: “5 + one half the age in years” for professional rescuers and “5 + age in years” for lay rescuers. Conclusions: Compression to ventilation ratios in CPR should be smaller for children than for adults and gradually increase as a function of body weight. Optimal CPR in children requires relatively more ventilation than optimal CPR in adults. A universal compression/ventilation ratio of 50:2, targeted to optimize adult resuscitation, would not be appropriate for infants and young children. [Copyright &y& Elsevier]

Background: The basic premise that frequent ventilations during cardiopulmonary resuscitation (CPR) are a necessity for tissue oxygenation has recently been challenged. An inspiratory impedance threshold device (ITD) recently has also been shown to increase CPR efficiency, principally by augmenting circulation with little impact on ventilation. The optimal compression to ventilation (C/V) is not known for this new device. The purpose of this study was to compare the currently recommended C/V ratio of 5:1 with a 10:1 ratio, ± the ITD, to optimize circulation and oxygenation during CPR. Methods: Thirty-two adult pigs weighing 26–31 kg were randomized to CPR with varying C/V ratios ± the ITD as follows: A=5:1, B=5:1+ITD, C=10:1, D=10:1+ITD. After 6 min of untreated ventricular fibrillation (VF), closed-chest standard CPR was performed with an automatic piston device that does not impede passive chest wall recoil, at a continuous compression rate of 100 min−1. Synchronous breaths were given every 5 or 10 compressions during the decompression phase depending on the group. CPR was performed for 6 min and physiological variables were measured throughout the experimental protocol. Results: A reduction in the frequency of ventilation from 5:1 to 10:1 resulted in significantly improved arterial and coronary perfusion pressure in a pig model of cardiac arrest. Addition of an ITD resulted in further increases in arterial and coronary perfusion pressures with both 5:1 and 10:1 C/V ratios, without compromising oxygenation. Conclusion: CPR efficiency can be optimized by changing the compression: ventilation ratio from 5:1 to 10:1 and with concurrent use of the inspiratory threshold device. [Copyright &y& Elsevier]

The present study was designed to investigate the protective effects of calcitonin gene-related peptide (CGRP) in a porcine model of cardiopulmonary resuscitation (CPR). Twelve pigs were anesthetized, paralyzed, mechanically ventilated with oxygen, and were monitored for electrocardiograph (ECG), arterial pressure, right atrial pressure, airway pressure. Ventricular fibrillation (VF) was induced in all animals by the application of 30 V of alternating current (60 Hz) across the heart, and remained untreated for 3 min, followed by conventional CPR with pneumatic piston device (Thumper) for 15 min. At 18 min of VF a single dose of vasopressin was given, and followed by defibrillation attempts. Two groups were studied. Group 1: Six pigs were used as saline control. Group 2: 0.3 nmol/kg CGRP was given 15 min prior to induction of VF. All animals in the CGRP pretreated group achieved a return of spontaneous circulation (ROSC) and survived more than 2 h (100%), whereas none of the saline control animals achieved ROSC. Blood gases were not significantly different between the groups. However, CGRP group had significantly higher arterial blood pressure and coronary perfusion pressure than control group during CPR. Pretreatment with CGRP affords a cardioprotective effect in this model of whole body ischemia. [Copyright &y& Elsevier]

Outcome after prehospital defibrillation remains dire. The aim of the present study was to elucidate the pathophysiology of cardiac arrest and to suggest ways to improve outcome. Ventricular fibrillation (VF) was induced in air-ventilated pigs, after which ventilation was withdrawn. After 6.5 min of VF, ventilation with 100% oxygen was initiated. In six pigs (group I), defibrillation was the only treatment carried out. In another six pigs (group II), mechanical chest compression–decompression CPR (mCPR) was carried out for 3.5 min followed by a 40-s hands-off period before defibrillation. If unsuccessful, mCPR was resumed for a further 30 s before a second or a third, 40-s delayed, shock was given. In a final six pigs (group III) mCPR was applied for 3.5 min after which up to three shocks (if needed) were given during on-going mCPR. Return of spontaneous circulation (ROSC) occurred in none of the pigs in group I (0%), in 1 of six pigs in group II (17%) and in five of six pigs in group III (83%). During the first 3 min of VF arterial blood was transported to the venous circulation, with the consequence that the left ventricle emptied and the right ventricle became greatly distended. It took 2 min of mCPR to establish an adequate coronary perfusion pressure, which was lost when the mCPR was interrupted. During 30 s of mCPR coronary perfusion pressure was negative, but a carotid flow of about 25% of basal value was obtained. In this pig model, VF caused venous congestion, an empty left heart, and a greatly distended right heart within 3 min. Adequate heart massage before and during defibrillation greatly improved the likelihood of return of spontaneous circulation (ROSC). [Copyright &y& Elsevier]

Objective: Amiodarone has been shown to be superior to both placebo and lidocaine in improving survival to hospital admission for victims of out-of-hospital refractory ventricular fibrillation. Concern had been expressed about the known vasodilatatory effects of amiodarone if given without precedent vasoconstrictive medications. The haemodynamic effects of intravenous amiodarone administered during ongoing CPR have not been systemically investigated. Our intention was to verify if amiodarone alone produced significantly lower resuscitation haemodynamics than did either adrenaline (epinephrine) alone or the combination of amiodarone and adrenaline.Design: Prospective, randomized, comparative study.Setting: Research laboratory of a medical school.Subjects: Thirty mongrel dogs.Interventions: After 8 min of untreated VF, defibrillation was attempted once at 3 J/kg and external chest compressions and ventilation started. Those animals resistant to the defibrillation attempt were randomized, ten to an adrenaline (0.02 mg/kg) group, ten to an amiodarone (5 mg/kg) group, and ten to a group receiving a combination of both drugs.Measurements and Main Results: Aortic systolic and diastolic, and coronary perfusion pressures were all significantly lower in the group receiving amiodarone alone than in the other two groups. Amiodarone combined with adrenaline produced pressures during CPR similar to adrenaline alone.Conclusion: Amiodarone can be safely administered simultaneously in combination with adrenaline and such a combination results in similar haemodynamic support as adrenaline alone. Amiodarone administered alone produces significantly lower coronary perfusion pressure than when combined with adrenaline. [ABSTRACT FROM AUTHOR]

Personal exposure to mercury vapor and the release of mercury from or during removal of amalgam dental fillings increases its blood and plasma concentration. However, it is not known if these very small amounts affect cardiac function. The effects of continuous exposure to 5 and 20 nM of HgCl2 on the cardiac contractility were investigated in isometric and tetanic contractions of right ventricular strips and in Langendorff perfused rat hearts. The continuous exposure for 2 h produced a small but significant reduction of the isometric twitch force and time to peak tension shortened. Relative post-rest potentiation was not affected by this concentration of HgCl2 suggesting a lack of action of the metal on the sarcoplasmic reticulum activity. Tetanic tension, in contrast to twitch force, was intensively reduced suggesting an important depressant action on the activity of contractile proteins. In perfused hearts beating spontaneously, isovolumic systolic pressure reduced progressively and the diastolic pressure increased. Although occurring heart rate reduction, it was similar for both controls and mercury treated hearts. Also, time dependent changes in coronary perfusion pressure were similar to controls. Results suggested that cardiac effects may be observed after continuous exposure to very small concentrations of mercury, probably as a result of the cell capacity to concentrate mercury. These results also indicate that continuous professional exposure to mercury followed by its absorption might have toxicological consequences affecting cardiac function, and being considered hazardous. [Copyright &y& Elsevier]