Biomedical subjects

John P Rosborough

Publications and source records attributed to John P Rosborough.

4 recordsLinked to original sources

PubMed2006

A new device producing manual sternal compression with thoracic constraint for cardiopulmonary resuscitation.

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 7.5 min. After 7.5 min, 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 10 min after the first shock. If ROSC had not occurred within 5 min of beginning CPR, 0.01 mg/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 CO(2) 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 100-130 lb (45-59 kg). In the comparative trial, significant differences in the measured CPP were observed between LifeBelt and manual CPR both at 1 min (15+/-8 mmHg versus 10+/-6 mmHg, p<0.05) and 5 min (17+/-4 mmHg versus 13+/-7 mmHg, p<0.02) of chest compression. A greater (p<0.05) ETCO(2), a marker of cardiac output and systemic perfusion, was observed with LifeBelt CPR (20+/-7 mmHg) than with manual CPR (15+/-5 mmHg) at 1 min. 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 100-130 lb (45-59 kg), the device produces greater CPP than well-performed manual CPR during resuscitation from prolonged VF.

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PubMed2005

Intracardiac voltage gradients during transthoracic defibrillation: implications for postshock myocardial injury.

UNLABELLED: In-vitro studies indicate that the electric-field intensity, or voltage gradient (VG), generated by a defibrillation shock is a determinant of defibrillation success as well as potential shock-induced cardiac injury. It is not clear how common descriptors of shock dose, e.g., joules (J), relate to VGs. OBJECTIVES: To assess the relationships between shock energy descriptors and VG. METHODS: One monophasic and three biphasic waveforms were compared using transthoracic shocks and standard electrodes in five swine. VG measurements via intracavitary multielectrode-tipped catheters were compared with delivered energy and peak current. Shock variables were recorded at native transthoracic impedance and an adjusted impedance approximating that of typical humans. RESULTS: For shocks at the same energy setting, peak current and VGs varied widely among the four defibrillators. At simulated human impedance (75 Omega), shocks at each device's maximum energy setting produced similar VGs among the three biphasic defibrillators, despite different delivered energies. For both native impedance (35 Omega) and at 75 Omega, VG correlated with peak current (r = 0.81 and 0.77, respectively) but not energy setting (r = 0.61, 0.52) or delivered energy (r = 0.58, 0.56). At the maximum energy setting of each device, maximum recorded VGs for both monophasic (33 V/cm) and biphasic (24 V/cm) defibrillators were less than those reported to cause myocardial injury (>60 to 80 V/cm). CONCLUSIONS: Energy descriptors correlate poorly to actual shock intensities. When compared with reported VG thresholds of myocardial injury, this study suggests that risk of injury from critically strong VGs is low for all of these defibrillators and equivalent among tested biphasic waveforms.

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PubMed2004

Electrical therapy for post defibrillatory pulseless electrical activity.

BACKGROUND: Defibrillation may convert ventricular fibrillation (VF) only to reveal profound mechanical dysfunction. Survival following this dysfunction, known as pulseless electrical activity (PEA) and electromechanical dissociation (EMD), is uncommon. We sought to evaluate an electrical therapy for primary post shock PEA following short duration VF. METHODS AND RESULTS: Forty-eight episodes of VF, lasting 110 +/- 25 s, were induced in 16 anesthetized dogs. Following defibrillation, 35 episodes met PEA criteria (ABP < or = 36 mmHg diastolic and pulse pressure < or = 14 mmHg in the first 20 s post shock). These post defibrillation PEA episodes were either Not Treated (NT) or Treated (T) with packets of 4-20 monophasic 0.2 ms 50-100 Hz pulses of 20-60 V applied across the tip and coil of an integrated bipolar transvenous defibrillation lead positioned in the right ventricle. The therapeutic endpoint was return of spontaneous circulation (ROSC; self-sustained ABP > or = 60 mmHg diastolic and/or > or = 100 mmHg systolic) for over 2 min. In the Not Treated group, only 4 of 19 (21%) episodes spontaneously recovered to ROSC in 123 +/- 49 s while in the Treated group, 11 of 16 (69%) of the PEA episodes achieved ROSC in 102 +/- 92 s. CONCLUSIONS: Electrical therapy increased the likelihood of ROSC in primary post defibrillation PEA three-fold (P < 0.01). Recovery occurred in the absence of thoracic compression, mechanical ventilation, or adjunctive drug therapy.

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PubMed2004

A model of ischemically induced ventricular fibrillation for comparison of fixed-dose and escalating-dose defibrillation strategies.

OBJECTIVES: Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation. METHODS: Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J-300 J-360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with < or =3 shocks. RESULTS: VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with < or =3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with < or =3 shocks (p < 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with < or =3 shocks ranging from 200 to 360 J. CONCLUSIONS: In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks.

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