Laura Puertas

Enhanced perfusion during advanced life support improves survival with favorable neurologic function in a porcine model of refractory cardiac arrest.

Objective: To improve the likelihood for survival with favorable neurologic function after cardiac arrest, we assessed a new advanced life support approach using active compression-decompression cardiopulmonary resuscitation plus an intrathoracic pressure regulator. Design: Prospective animal investigation. Setting: Animal laboratory. Subjects: Female farm pigs (n = 25) (39 ± 3 kg). Interventions: Protocol A: After 12 minutes of untreated ventricular fibrillation, 18 pigs were randomized to group A—3 minutes of basic life support with standard cardiopulmonary resuscitation, defibrillation, and if needed 2 minutes of advanced life support with standard cardiopulmonary resuscitation; group B—3 minutes of basic life support with standard cardiopulmonary resuscitation, defibrillation, and if needed 2 minutes of advanced life support with active compression-decompression plus intrathoracic pressure regulator; and group C—3 minutes of basic life support with active compression-decompression cardiopulmonary resuscitation plus an impedance threshold device, defibrillation, and if needed 2 minutes of advanced life support with active compression-decompression plus intrathoracic pressure regulator. Advanced life support always included IV epinephrine (0.05 &mgr;g/kg). The primary endpoint was the 24-hour Cerebral Performance Category score. Protocol B: Myocardial and cerebral blood flow were measured in seven pigs before ventricular fibrillation and then following 6 minutes of untreated ventricular fibrillation during sequential 5 minutes treatments with active compression-decompression plus impedance threshold device, active compression-decompression plus intrathoracic pressure regulator, and active compression-decompression plus intrathoracic pressure regulator plus epinephrine. Measurements and Main Results: Protocol A: One of six pigs survived for 24 hours in group A versus six of six in groups B and C (p = 0.002) and Cerebral Performance Category scores were 4.7 ± 0.8, 1.7 ± 0.8, and 1.0 ± 0, respectively (p = 0.001). Protocol B: Brain blood flow was significantly higher with active compression-decompression plus intrathoracic pressure regulator compared with active compression-decompression plus impedance threshold device (0.39 ± 0.23 vs 0.27 ± 0.14 mL/min/g; p = 0.03), whereas differences in myocardial perfusion were not statistically significant (0.65 ± 0.81 vs 0.42 ± 0.36 mL/min/g; p = 0.23). Brain and myocardial blood flow with active compression-decompression plus intrathoracic pressure regulator plus epinephrine were significantly increased versus active compression-decompression plus impedance threshold device (0.40 ± 0.22 and 0.84 ± 0.60 mL/min/g; p = 0.02 for both). Conclusion: Advanced life support with active compression-decompression plus intrathoracic pressure regulator significantly improved cerebral perfusion and 24-hour survival with favorable neurologic function. These findings support further evaluation of this new advanced life support methodology in humans.

Reperfusion injury protection during Basic Life Support improves circulation and survival outcomes in a porcine model of prolonged cardiac arrest.

OBJECTIVE Ischemic postconditioning (PC) using three intentional pauses at the start of cardiopulmonary resuscitation (CPR) improves outcomes after cardiac arrest in pigs when epinephrine (epi) is used before defibrillation. We hypothesized PC, performed during basic life support (BLS) in the absence of epinephrine, would reduce reperfusion injury and enhance 24h functional recovery. DESIGN Prospective animal investigation. SETTING Animal laboratory SUBJECTS Female farm pigs (n=46, 39±1kg). INTERVENTIONS Protocol A: After 12min of ventricular fibrillation (VF), 28 pigs were randomized to four groups: (A) Standard CPR (SCPR), (B) active compression-decompression CPR with an impedance threshold device (ACD-ITD), (C) SCPR+PC (SCPR+PC) and (D) ACD-ITD CPR+PC. Protocol B: After 15min of VF, 18 pigs were randomized to ACD-ITD CPR or ACD-ITD+PC. The BLS duration was 2.75min in Protocol A and 5min in Protocol B. Following BLS, up to three shocks were delivered. Without return of spontaneous circulation (ROSC), CPR was resumed and epi (0.5mg) and defibrillation delivered. The primary end point was survival without major adverse events. Hemodynamic parameters and left ventricular ejection fraction (LVEF) were also measured. Data are presented as mean±SEM. MEASUREMENTS AND MAIN RESULTS Protocol A: ACD-ITD+PC (group D) improved coronary perfusion pressure after 3min of BLS versus the three other groups (28±6, 35±7, 23±5 and 47±7 for groups A, B, C, D respectively, p=0.05). There were no significant differences in 24h survival between groups. PROTOCOL B LVEF 4h post ROSC was significantly higher with ACD-ITD+PC vs ACD-ITD alone (52.5±3% vs. 37.5±6.6%, p=0.045). Survival rates were significantly higher with ACD-ITD+PC vs. ACD-ITD alone (p=0.027). CONCLUSIONS BLS using ACD-ITD+PC reduced post resuscitation cardiac dysfunction and improved functional recovery after prolonged untreated VF in pigs. PROTOCOL NUMBER 12-11.

Intrathoracic pressure regulation to treat intraoperative hypotension: A phase II pilot study.

BACKGROUND Intraoperative hypotension secondary to acute blood loss and fluid shifts increases morbidity and mortality. Intrathoracic pressure regulation (IPR) is a new therapy that enhances circulation by increasing venous return with a negative intrathoracic pressure created noninvasively, either actively (vacuum source or patient inspiration) or passively (chest recoil during cardiopulmonary resuscitation). OBJECTIVE In this Phase II pilot study, we tested the hypothesis that active IPR therapy would improve the haemodynamic status of patients who developed clinically significant hypotension during abdominal surgery. DESIGN A phase II, single cohort, interventional pilot study. SETTING University of Minnesota Fairview Hospital. PATIENTS Twenty-two patients [American Society of Anesthesiologists (ASA) physical status I to III] were enrolled prospectively of whom 15 experienced intraoperative hypotension. INTERVENTION If intraoperative hypotension occurred more than 10 min after induction, the IPR device was applied immediately for a minimum of 10 min. MAIN OUTCOME MEASURE The hypotensive SBP immediately before the start of IPR treatment was compared with the SBP obtained at the end of IPR therapy. The paired Students t-test was used to determine statistical significance (P < 0.05). RESULTS Fifteen of the 22 patients enrolled experienced 18 hypotensive episodes, which were treated with at least 10 min of IPR therapy. Fourteen episodes responded to IPR alone and four episodes (four patients) required additional fluid and vasopressor therapy to treat the hypotension. The group mean ± SD SBPs at the onset of the IPR treatment and at the end of IPR treatment were 90.7 ± 9.7 and 98.4 ± 17.4 mmHg (P = 0.02), respectively. The maximum SBP reached during the treatment was 105.6 ± 19.6 mmHg. Pulse pressure increased from 36.8 ± 8.5  mmHg immediately before IPR treatment to 41.5 ± 11.1 mmHg (P = 0.02) at the end of IPR treatment. Mean arterial pressure (MAP) increased from 66.3 ± 9.4 mmHg immediately before IPR treatment to 71.5 ± 14.4 mmHg (P = 0.03) at the end of IPR treatment. No adverse events were identified with use of the IPR device. CONCLUSION IPR may be useful in treating intraoperative hypotension without additional fluid or vasopressor therapy. No significant adverse events were observed. On the basis of this phase II pilot study, a larger study is justified.