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 Student's 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.

The effects of temperature on cardiac pacing thresholds.

BACKGROUND: Human core body temperature can fluctuate between 36 degrees C (sleep) and 42 degrees C (intense exercise). Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. METHODS: Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabeculae were suspended in temperature-controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength-duration curves were determined at 37 degrees C, then at randomized temperatures ranging from 35 degrees C to 42 degrees C. Final thresholds were repeated at 37 degrees C to confirm baseline responses. All threshold data were normalized to a baseline average. RESULTS: Both canine and swine trabeculae elicited significant decreases in thresholds (10-14%) at pacing stimulus durations (pulsewidths) of 0.02 ms (P < 0.01) and 0.10 ms (P < 0.05) between the temperatures of 38 degrees C and 41 degrees C, compared to baseline. Thresholds at 42 degrees C trended back to baseline for both canine (NS) and swine trabeculae (P < 0.05 compared to 38 degrees C-41 degrees C). Human trabeculae thresholds increased >35% (P < 0.05) at 42 degrees C relative to baseline with no significant differences at other temperatures. CONCLUSIONS: Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. Our data for the diseased human trabeculae indicate that cases where cardiac heating may occur (e.g., radiofrequency energy due to MRI scans, febrile events), patients without adequate VPCT safety margin may be at higher risk of loss of proper function of an implanted pacing or defibrillation system.