Organ Perfusion Pressure Research Articles

Hemodynamic improvement of a LUCAS 2 automated device by addition of an impedance threshold device in a pig model of cardiac arrest

IntroductionThe combination of the LUCAS 2 (L-CPR) automated CPR device and an impedance threshold device (ITD) has been widely implemented in the clinical field. This animal study tested the hypothesis that the addition of an ITD on L-CPR would enhance cerebral and coronary perfusion pressures. MethodsTen female pigs (39.0±2.0kg) were sedated, intubated, anesthetized with isofluorane, and paralyzed with succinylcholine (93.3μg/kg/min) to inhibit the potential confounding effect of gasping. After 4min of untreated ventricular fibrillation, 4min of L-CPR+an active ITD or L-CPR+a sham ITD was initiated and followed by another 4min of the alternative method of CPR. Systolic blood pressure (SBP), diastolic blood pressure (DBP), diastolic right atrial pressure (RAP), intracranial pressure (ICP), airway pressure, and end tidal CO2 (ETCO2) were recorded continuously. Data expressed as mean mmHg±SD. ResultsDecompression phase airway pressure was significantly lower with L-CPR+active ITD versus L-CPR+sham ITD (−5.3±2.2 vs. −0.5±0.6; p<0.001). L-CPR+active ITD treatment resulted in significantly improved hemodynamics versus L-CPR+sham ITD: ETCO2, 35±6 vs. 29±7 (p=0.015); SBP, 99±9 vs. 93±15 (p=0.050); DBP, 24±12 vs. 19±15 (p=0.006); coronary perfusion pressure, 29±8 vs. 26±7 (p=0.004) and cerebral perfusion pressure, 24±13 vs. 21±12 (p=0.028). ConclusionsIn pigs undergoing L-CPR the addition of the active ITD significantly reduced intrathoracic pressure and increased vital organ perfusion pressures.

Use of Advanced Bleeding Control Mechanisms in Athletic Training: A Shift in the Thought Process of Prehospital Care—Part 1: Tourniquets

Two other competencies(Table 1), although not necessarily new to the list ofimmediate emergency management care skills, do requirefurther examination based on the current available scienceand standard of care in prehospital medicine. The purposeof this column is to provide athletic training educators(ATE) with evidence regarding the use of tourniquets in theprehospital setting as well as to be a resource on how toteach the management of external hemorrhage usingtourniquets.Trauma resulting in disruption of soft tissue is classified asan open or closed wound, and any significant loss ofintravascular volume may lead sequentially to hemodynam-ic instability, decreased tissue perfusion, cellular hypoxia,organ damage, and death.

Ventriculoarterial decoupling in human septic shock.

IntroductionSeptic shock is the most severe manifestation of sepsis. It is characterized as a hypotensive cardiovascular state associated with multiorgan dysfunction and metabolic disturbances. Management of septic shock is targeted at preserving adequate organ perfusion pressure without precipitating pulmonary edema or massive volume overload. Cardiac dysfunction often occurs in septic shock patients and can significantly affect outcomes. One physiologic approach to detect the interaction between the heart and the circulation when both are affected is to examine ventriculoarterial coupling, which is defined by the ratio of arterial elastance (Ea) to left ventricular end-systolic elastance (Ees). In this study, we analyzed ventriculoarterial coupling in a cohort of patients admitted to ICUs who presented with vs without septic shock.MethodsIn this retrospective cross-sectional opportunity study, we measured routine hemodynamics using indwelling arterial and pulmonary arterial catheters and transthoracic echocardiograms in 25 septic patients (group S) and 25 non–septic shock patients (group C) upon ICU admission. Ees was measured by echocardiography using a single-beat (EesSB) method. Ea was calculated as 0.9 systolic arterial pressure/stroke volume, and then the Ea/EesSB ratio was calculated (normal value <1.36).ResultsIn group S, 21 patients had an Ea/EesSB ratio >1.36 (uncoupled). The four patients with Ea/EesSB ratios ≤1.36 had higher EesSB values than patients with Ea/EesSB ratios >1.36 (P = 0.007), although Ea measurements were similar in both groups (P = 0.4). In group C, five patients had uncoupled Ea/EesSB ratios. No correlation was found between EesSB and left ventricular ejection fraction and between Ea/EesSB ratio and mixed venous oxygen saturation in septic shock patients.ConclusionsUpon admission to the ICU, patients in septic shock often display significant ventriculoarterial decoupling that is associated with impaired left ventricular performance. Because Ea/Ees decoupling alters cardiovascular efficiency and cardiac energetic requirements independently of Ea or Ees, we speculate that septic patients with ventriculoarterial uncoupling may benefit from therapy aimed at normalizing the Ea/Ees ratio.

Terlipressin/adrenaline is better than adrenaline alone in a porcine model of prolonged ventricular fibrillationA randomized controlled study

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, compression-only resuscitation was applied for 10 min, followed by advanced life support. Terlipressin in a single-dose of 30 􀀁g·kg-1 was added to the first dose of adrenaline in group A, while placebo was given in group B. CorPP and CPP were calcula-ted 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.

Oxidants as important determinants of renal apoptosis during pneumoperitoneum: a study in an isolated perfused rat kidney model

Pneumoperitoneum-associated ischemia-reperfusion (IR) may initiate renal dysfunction. Whether oxidants are responsible for renal structural damage, such as cell apoptosis, has not yet been evaluated. We investigated such eventuality in an isolated rat kidney model. Thirty-five rat kidneys with their vessels and ureter were harvested and perfused within a closed environment at flow of 15 ml min(-1). After stabilization, kidneys were assigned to one of five groups (n = 7 per group): CO(2)-induced intrachamber pressure of 8, 12, or 0 mmHg (control), and 8 or 12 mmHg pressure applied to kidneys from rats treated pre-experimentally with tungsten for 14 days. Pressurization lasted 60 min. Organ perfusion pressure raised as intrachamber pressure increased. Urinary output decreased in the two pressurized nonpretreated groups. Intrachamber pressure was directly associated with an increase in postexperimental xanthine oxidase tissue levels. Twofold apoptosis was documented (p < 0.05) in cortex of nonpretreated kidney in the 12 mmHg group compared with the 8 or 0 mmHg groups. Tungsten pretreatment significantly (p < 0.05) attenuated the abnormalities documented in the 12 mmHg group, but less so in the 8 mmHg pressurized nontreated counterparts. Pneumoperitoneal pressure applied to isolated perfused kidney is associated with renal apoptosis. This rapidly induced structural renal damage is oxidant dependent and can be attenuated by antioxidants. Further studies may shed more light on the role of antioxidants in preventing pneumoperitoneum-induced kidney dysfunction.

Sodium nitroprusside enhanced cardiopulmonary resuscitation (SNPeCPR) improves vital organ perfusion pressures and carotid blood flow in a porcine model of cardiac arrest

Purpose of the studyTo describe a new method of CPR that optimizes vital organ perfusion pressures and carotid blood flow. We tested the hypothesis that a combination of high dose sodium nitroprusside (SNP) as well as non-invasive devices and techniques known independently to enhance circulation would significantly improve carotid blood flow (CBF) and return of spontaneous circulation (ROSC) rates in a porcine model of cardiac arrest. Methods15 isofluorane anesthetized pigs (30±1kg), after 6min of untreated ventricular fibrillation, were subsequently randomized to receive either 15min of standard CPR (S-CPR) (8 animals) or 5min epochs of S-CPR followed by active compression–decompression (ACD)+inspiratory impedance threshold device (ITD) CPR followed by ACD+ITD+abdominal binding (AB) with 1mg of SNP administered at minutes 2, 7, 12 of CPR (7 animals). Primary endpoints were CBF and ROSC rates. ANOVA and Fisher's exact test were used for comparisons. Results/conclusionThere was significant improvement in the hemodynamic parameters in the SNP animals. ROSC was achieved in 7/7 animals that received SNP and in 2/8 in the S-CPR (p=0.007). CBF and end tidal CO2 (ETCO2) were significantly higher in the ACD+ITD+AB+SNP (SNPeCPR) animals during CPR. Bolus doses of SNP, when used in conjunction with ACD+ITD+AB CPR, significantly improve CBF and ROSC rates compared to S-CPR.

Advances in Cardiopulmonary Resuscitation

This article focuses on important advances in the science of cardiopulmonary resuscitation in the last decade that have led to a significant improvement in understanding the complex physiology of cardiac arrest and critical interventions for the initial management of cardiac arrest and postresuscitation treatment. Special emphasis is given to the basic simple ways to improve circulation, vital organ perfusion pressures, and the grave prognosis of sudden cardiac death.

Defining the adequate arterial pressure target during septic shock: not a 'micro' issue but the microcirculation can help

The Surviving Sepsis Campaign guidelines suggest targeting a mean arterial pressure of at least 65 mm Hg to maintain organ perfusion pressure during septic shock. However, the optimal mean arterial pressure can be higher in patients with a history of hypertension or other vascular comorbidities or in those with increased abdominal pressure. In a given individual, the adequate mean arterial pressure target can be difficult to define with the routine hemodynamic parameters (for example, cardiac output, central or mixed venous blood oxygen saturation, and urine output). Near-infrared spectroscopy and sidestream dark field imaging have emerged as promising technologies for monitoring the microcirculation at the bedside. These new methods could provide additional clues to help define the adequate blood pressure to target during the resuscitation phase of septic shock.

Kardiogener Schock - Pharmakologische und mechanische Maßnahmen in der Akutphase

Der kardiogene Schock ist in mehr als 3/4 der Fälle durch einen akuten Myokardinfarkt bedingt. Mit einer Latenz von bis zu 12 Stunden tritt der Schock nach akutem Gefäßverschluss meist erst nach Aufnahme in die Klinik auf. Die Mortalität liegt bei 50–70 % und kann durch eine rasche Diagnosestellung, die sofortige Revaskularisation des Infarktgefäßes und eine effektive hämodynamische Stabilisierung gesenkt werden. Pharmaka und mechanische Kreislaufunterstützungssysteme können zur Aufrechterhaltung eines ausreichenden Organperfusionsdruckes eingesetzt werden, um ein Multiorgandysfunktionssyndrom, welches prognoselimitierend ist, zu vermeiden. Entsprechend den aktuellen Leitlinien sollten im kardiogenen Schock Dobutamin und Noradrenalin bevorzugt werden.

Effect of the Addition of Vasopressin or Vasopressin Plus Nitroglycerin to Epinephrine on Arterial Blood Pressure during Cardiopulmonary Resuscitation in Humans

Background: Infusion of a vasopressor during cardiopulmonary resuscitation (CPR) in humans increases end decompression (diastolic) arterial blood pressure, and consequently increases vital organ perfusion pressure and survival. Several vasoactive drugs have been tested alone or in combination, but their hemodynamic effects have not been investigated clinically in humans. Study Objective: We tested the hypothesis that epinephrine (1 mg) co-administered with vasopressin (40 IU) ± nitroglycerin (300 μg) results in higher diastolic blood pressure than epinephrine alone. Study Design: A prospective, randomized, double-blinded controlled trial in the prehospital setting. The study included 48 patients with witnessed cardiac arrest. Patients received either epinephrine alone (E alone) or epinephrine plus vasopressin (E+V) or epinephrine plus vasopressin plus nitroglycerin (E+V+N). A femoral arterial catheter was inserted for arterial pressure measurement. Outcome Measures: The primary end point was diastolic blood pressure during CPR, 15 min after the first drug administration (T = 15 min). Results: After exclusions, a total of 44 patients were enrolled. Diastolic blood pressures (mm Hg) at T = 15 min were not statistically different between groups (median [interquartile range]: 20 [10], 15 [6], and 15 [13] for E alone, E+V, and E+V+N, respectively. The rate of return of spontaneous circulation was 63% (n = 10) in the epinephrine group, 43% (n = 6) in the epinephrine plus vasopressin group, and 36% (n = 5) in the triple therapy group (NS). Conclusions: Addition of vasopressin or vasopressin plus nitroglycerin to epinephrine did not increase perfusion blood pressure compared to epinephrine alone in humans in cardiac arrest, suggesting the absence of benefit in using these drug combination(s).

Advances in Cardiopulmonary Resuscitation.

This article focuses on important advances in the science of cardiopulmonary resuscitation (CPR) in the last decade that have led to a significant improvement in understanding the complex physiology of cardiac arrest and critical interventions for the initial management of cardiac arrest and postresuscitation treatment. Special emphasis is given to the basic simple ways to improve circulation, vital organ perfusion pressures, and the grave prognosis of sudden cardiac death.

Non‐invasive and quantitative evaluation of peripheral vascular resistances in rats by combined NMR measurements of perfusion and blood pressure using ASL and dynamic angiography

The in vivo determination of peripheral vascular resistances (VR) is crucial for the assessment of arteriolar function. It requires simultaneous determination of organ perfusion (F) and arterial blood pressure (BP). A fully non-invasive method was developed to measure systolic and diastolic BP in the caudal artery of rats based on dynamic NMR angiography. A good agreement was found between the NMR approach and the gold standard techniques (linear regression slope = 0.98, R(2) = 0.96). This method and the ASL-MRI measurement of skeletal muscle perfusion were combined into one single NMR experiment to quantitatively evaluate the local vascular resistances in the calf muscle of anaesthetized rats, in vivo and non-invasively 1) at rest: VR = 7.0 +/- 1.0 mmHg x min 100 g x ml(-1), F = 13 +/- 3 ml min(-1) x 100 g(-1) and mean BP (MBP) = 88 +/- 10 mmHg; 2) under vasodilator challenge (milrinone): VR = 3.7 +/- 1.1 mmHg min x 100 g ml(-1), F = 21 +/- 4 ml min(-1) x 100 g(-1) and MBP = 75 +/- 14 mmHg; 3) under vasopressor challenge (norepinephrine): VR = 9.8 +/- 1.2 mmHg min 100 g ml(-1), F = 14 +/- 3 ml min(-1) x 100 g(-1) and MBP = 137 +/- 2 mmHg.

A New Internal Cardiac Massage Technique

Classical internal cardiac massage mostly can increase systolic blood pressure to maintain sufficient brain and systemic organ perfusion but diastolic blood pressure commonly remains below 10 mmHg. To be able to increase the diastolic blood pressure sufficiently, the surgeon grabs the distal part of the ascending aorta between the thumb and index finger of the left hand and squeezes it during the diastolic time period to increase the diastolic pressure. Ascending aorta is released during ventricular squeezing, and subsequently ascending aorta is squeezed during the ventricular relaxation.

Therapie des kardiogenen Schocks bei akutem Herzinfarkt

The therapy of infarct related cardiogenic shock should primarily focus on fastest possible revascularization. In addition, rapid restoration of sufficient organ perfusion pressure is recommended for the prevention of a multi-organ dysfunction syndrome (MODS). This can be achieved by mechanical circulatory assist devices as well as individual catecholamine therapy. Since assist devices require specially trained physicians, their use is limited to specialized cardiac care centers. However, future technologies such as portable heart-lung-machines may help to further improve transfer to specialized centers and therapy of shock patients.

Cardiac arrest with continuous mechanical chest compression during percutaneous coronary intervention: A report on the use of the LUCAS device

Mechanical chest compression may be necessary to make coronary intervention possible during resuscitation. We report our experience using the Lund University Cardiac Arrest System (LUCAS, Jolife, Lund, Sweden) which is a gas-driven sternal compression device that incorporates a suction cup for active decompression. During the last 13 months LUCAS has been used in our catheterisation laboratory to maintain adequate organ perfusion pressure in 13 patients with cardiac arrest or severe hypotension and bradycardia (male/female ratio 1.6, mean age 59+/-19). The mean compression time was 105+/-60min (range 45-240), and the mean systolic and diastolic blood pressure obtained was 81+/-23 and 34+/-21mmHg, respectively. Angiography and eventually percutanous coronary intervention was possible in all cases during ongoing automatic chest compression. Three patients survived the procedure, but no patients were discharged alive. In two cases we found inadequate flow in the anterior descending artery, and in one case the invasive measurements revealed inadequate coronary perfusion pressure. There were no excessive intra-thoracic or intra-abdominal injuries. We conclude that the LUCAS device is suitable during cardiac catheterisation and intervention, and the device ensures an adequate systemic blood pressure in most patients without life-threatening injuries.

Multiple organ procurement

Liver transplantation is the most demanding of all solid organ tranplantations. It requires perfect organization and motivation of health care professionals, patients and their families. This article deals with the procedure for multiple organ procurement, reviews criteria for organ donation and describes the surgical tehnique for multiple organ procurement. Adequate selection and evaluation of cadaveric donors and of organs for transplantation should include early identification of potential donors, and early diagnosis of brain death. The procurement of the highest number of viable organs jbfor transplantation requires excellence in each of the phases. Early and aggressive physiologic support in the maintenance of fotential donors can reduce organ donor loss due to irreversible asystole or multiorgan jafiure (it is almost always possible to maintain organ perfusion pressure) and increase the number of organs without increasing post-transplant morbidity or mortality. The ideal donor is a young, previously healthy, brain dead, victim of an accident. The surgical procedure for multiple organ procurement from brain death donors must be performed without intraopertive organ damage.

Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs

The intrathoracic pressure regulator (ITPR) was created to improve hemodynamics by generating continuous negative airway pressure between positive pressure ventilations to enhance cardiac preload in apnoeic animals. In normovolemic and hypovolemic pigs, we tested the hypothesis that continuous negative intrathoracic pressure set at -5 or -10mmHg, interrupted only for intermittent positive pressure ventilations, would decrease intracranial (ICP) and right atrial (RAP) pressure, and increase mean arterial pressure (MAP). Twelve pigs were anesthetized with propofol and ventilated with a bag. The ITPR was used to vary baseline endotracheal pressures (ETPs) for 5min periods in the following sequence: 0, -5, 0, -10, 0mmHg under normovolemic conditions. Six pigs were bled 50% (32.5+/-mL/kg) of their estimated blood volume and the airway pressure sequence was repeated. Six other pigs were bled 35% (22.75+/-mL/kg) of their estimated blood volume and the same airway pressure sequence was repeated. Intracranial, aortic, right atrial pressures, arterial blood gases, end tidal CO(2) (ETCO(2)), were measured. ANOVA was used for statistical analysis. Linear regression analysis was performed for ETP and ICP. Mean arterial and vital organ perfusion pressures were significantly improved and RA pressure significantly decreased with the use of the ITPR; the effect was greater with the more negative ETPs and lower circulating blood volume. The change of ICP was linearly related to the ETP and blood loss: DeltaICP=[1.22-0.84(1-%blood loss/100)]xETP, r(2)=0.88 (in mmHg), p<0.001. There were no adverse device effects and there was a significant increase of ETCO(2) with the use of ITPR. The ITPR decreased RAP and ICP significantly and improved mean arterial and cerebral and coronary perfusion pressures without affecting acid base balance severely. The decrease in ICP was directly proportional to the reduction in intrathoracic pressure. The effects were more pronounced in severe hypovolemic and hypotensive states with more negative ETP pressure.

Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs

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 (15 min) use of the ITPR during CPR in a porcine model of cardiac arrest. After 8 min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15 min 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 15 min 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. ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (-9+/-0.6 mmHg versus -3+/-0.3 mmHg, p<0.001), diastolic right atrial pressure (DRAP) (-0.1+/-0.2 mmHg versus 2.3+/-0.2 mmHg, p<0.001) and intracranial pressure (20.8+/-0.6 mmHg versus 23+/-0.5 mmHg, respectively, p=0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO(2)), (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 PaCO(2) remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO(2) values remaining <20 mmHg (p<0.001). PaO(2) was not different between groups. Following 23 min of cardiac arrest (15 min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p=0.3. 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 15 min without any compromise in oxygenation.

Monitoring arterial pressure

Monitoring arterial pressure is an important aspect of providing clinical care to the anaesthetized and critically ill patient. Because auto-regulation of major organ blood flow may be impaired in these patients, maintenance of an adequate organ perfusion pressure is essential, particularly to vital areas such as the brain, heart and kidneys. It is imperative that those patients experiencing or at risk of cardiovascular instability and inadequate organ perfusion are selected for direct continuous monitoring with beat-to-beat variation. Other patients still requiring routine cardiovascular monitoring may be adequately monitored with intermittent indirect blood pressure measurement. This article outlines the different types of arterial monitoring seen in the intensive care and operating theatre environment.

Intrathoracic Pressure Regulator During Continuous-Chest-Compression Advanced Cardiac Resuscitation Improves Vital Organ Perfusion Pressures in a Porcine Model of Cardiac Arrest

A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled -10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. In protocol 1, 20 pigs (weight, 30+/-0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of ITPR-CPR. This sequence was repeated. In protocol 3, 6 animals after 8 minutes of untreated VF were treated with ITPR-CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10, and 15 of CPR. A newer, leak-proof ITPR device was used. Aortic, right atrial, endotracheal pressure, intracranial pressure, and end-tidal CO2 values were measured (mm Hg); common carotid arterial flow also was measured (mL/min). Coronary perfusion pressure (diastolic; aortic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean intracranial pressure) were calculated. Unpaired Student t test and Friedman's repeated-measures ANOVA of ranks were used in protocols 1 and 3. A 2-tailed Wilcoxon signed-rank test was used for analysis in protocol 2. Fischer's exact test was used for survival. Significance was set at P<0.05. Vital organ perfusion pressures and end-tidal CO2 were significantly improved with ITPR-CPR in both protocols. In protocol 1, 1-hour survival was 100% with ITPR-CPR and 10% with STD-CPR (P=0.001). Arterial blood pH was significantly lower and Paco2 was significantly higher with ITPR-CPR in protocol 1. Arterial oxygen saturation was 100% throughout the study in both protocols. Paco2 and Pao2 remained stable, but metabolic acidosis progressed, as expected, throughout the 15 minutes of CPR in protocol 3. Compared with STD-CPR, use of ITPR-CPR improved hemodynamics and short-term survival rates after cardiac arrest.