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Biomedical subjects

A F DiMarco

Publications and source records attributed to A F DiMarco.

At least 19 recordsLinked to original sources

The learning curve for investigational surgery: lessons learned from laparoscopic diaphragm pacing for chronic ventilator dependence.

BACKGROUND: Electrical stimulation of the phrenic nerve motor point of the diaphragm through laparoscopic implantation of a pacing system is an option for high spinal cord-injured patients with chronic respiratory insufficiency. This study assesses the operative learning curve for the initial series of patients. METHOD: A series of six patients underwent laparoscopic placement of a diaphragm pacing system. The operative procedure was divided into the following four steps for analysis and rapid adjustment after each operation: exposure of the diaphragm, mapping of the phrenic nerve motor point, implantation of the pacing electrodes, and final routing of the wires to the external system. RESULTS: The first case required two operations, and the second case was unsuccessful because of a nonfunctioning phrenic nerve that led to a change in the preoperative screening criteria. The operative time decreased from 469 min for the first operation to 165 min for the sixth operation. The significant time decrease can be attributed to changes in the mapping and routing aspects of the operation. Key changes during this series that helped to reduce the operative time include abandonment of a software-dependent mapping technique, development of a grid algorithm for mapping, software improvement to increase the speed of stimulation and mapping, refinement of the mapping probe to maintain adequate suction on the diaphragm, shortening of the electrode lengths, and experience with the implantation of connections to the external electrodes. Presently, all five of the successfully implanted patients can be maintained on prolonged ventilatory support with the device. CONCLUSION: Analysis of every step of this investigational procedure enabled us to make rapid changes in surgical protocol, leading to decreases in operative times and expectant improvements in patient safety and efficacy. In this series, analysis was the key to developing a low-risk cost-effective outpatient diaphragm pacing system.

Adult↗

Gas exchange during separate diaphragm and intercostal muscle breathing.

In patients with diaphragm paralysis, ventilation to the basal lung zones is reduced, whereas in patients with paralysis of the rib cage muscles, ventilation to the upper lung zones in reduced. Inspiration produced by either rib cage muscle or diaphragm contraction alone, therefore, may result in mismatching of ventilation and perfusion and in gas-exchange impairment. To test this hypothesis, we assessed gas exchange in 11 anesthetized dogs during ventilation produced by either diaphragm or intercostal muscle contraction alone. Diaphragm activation was achieved by phrenic nerve stimulation. Intercostal muscle activation was accomplished by electrical stimulation by using electrodes positioned epidurally at the T(2) spinal cord level. Stimulation parameters were adjusted to provide a constant tidal volume and inspiratory flow rate. During diaphragm (D) and intercostal muscle breathing (IC), mean arterial Po(2) was 97.1 +/- 2.1 and 88.1 +/- 2.7 Torr, respectively (P < 0.01). Arterial Pco(2) was lower during D than during IC (32.6 +/- 1.4 and 36.6 +/- 1.8 Torr, respectively; P < 0.05). During IC, oxygen consumption was also higher than that during D (0.13 +/- 0.01 and 0.09 +/- 0.01 l/min, respectively; P < 0.05). The alveolar-arterial oxygen difference was 11.3 +/- 1.9 and 7.7 +/- 1.0 Torr (P < 0.01) during IC and D, respectively. These results indicate that diaphragm breathing is significantly more efficient than intercostal muscle breathing. However, despite marked differences in the pattern of inspiratory muscle contraction, the distribution of ventilation remains well matched to pulmonary perfusion resulting in preservation of normal gas exchange.

Animals↗

Mechanism of expiratory muscle activation during lower thoracic spinal cord stimulation.

Lower thoracic spinal cord stimulation (SCS) may be a useful method to restore an effective cough mechanism. In dogs, two groups of studies were performed to evaluate the mechanism of the expiratory muscle activation during stimulation at the T(9)-T(10) level, which results in the greatest changes in airway pressure. In one group, expiratory muscle activation was monitored by evoked muscle compound action potentials (CAPs) from the internal intercostal muscles in the 10th, 11th, and 12th interspaces and from portions of the external oblique innervated by the L(1) and L(2) motor roots. SCS, applied with single shocks, resulted in short-latency CAPs at T(10) but not at more caudal levels. SCS resulted in long-latency CAPs at each of the more caudal caudal recording sites. Bilateral dorsal column sectioning, just below the T(11) spinal cord level, did not affect the short-latency CAPs but abolished the long-latency CAPs and also resulted in a fall in airway pressure generation. In the second group, sequential spinal root sectioning was performed to assess their individual mechanical contribution to pressure generation. Section of the ventral roots from T(8) through T(10) resulted in negligible changes, whereas section of more caudal roots resulted in a progressive reduction in pressure generation. We conclude that 1) SCS at the T(9)-T(10) level results in direct activation of spinal cord roots within two to three segments of the stimulating electrode and activation of more distal roots via spinal cord pathways, and 2) pathway activation of motor roots makes a substantial contribution to pressure generation.

Animals↗

Effects of lung volume on parasternal pressure-generating capacity in dogs.

Previous studies have suggested that the optimum length for force generation of the parasternal intercostal (PS) muscles is well above functional residual capacity (FRC). We further explored this issue by examining the pressure-generating capacity of the PS muscles as a function of lung volume in anaesthetized dogs. Upper thoracic spinal cord stimulation (SCS) was used to electrically activate the PS muscles. Changes in airway pressure and parasternal resting length (LR) during airway occlusion were monitored over a wide range of lung volumes during SCS. To assess the effects of parasternal contraction alone, SCS was performed following phrenicotomy and section of the external intercostal, levator costae and triangularis sterni muscles. With increasing lung volume, there were progressive decrements in the capacity of the PS muscles to produce changes in airway pressure. The relationship between PS pressure generation and lung volume was similar to a previous comparable assessment of the external intercostal muscles. The PS muscles shortened during passive inflation and also shortened further (by > 20 % of LR) during SCS. Total shortening (passive plus active) increased progressively with increasing lung volume. Our results indicate that the capacity of the PS muscles to produce changes in airway pressure (a) falls progressively with increasing lung volume and (b) is similar to that of the external intercostal muscles. We speculate that the fall in PS pressure-generating capacity is related, in part, to progressive reductions in end-inspiratory length.

Animals↗

Pattern of expiratory muscle activation during lower thoracic spinal cord stimulation.

Large positive airway pressures (Paws) can be generated by lower thoracic spinal cord stimulation (SCS), which may be a useful method of restoring cough in spinal cord-injured patients. Optimal electrode placement, however, requires an assessment of the pattern of current spread during SCS. Studies were performed in anesthetized dogs to assess the pattern of expiratory muscle recruitment during SCS applied at different spinal cord levels. A multicontact stimulating electrode was positioned over the surface of the lower thoracic and upper lumbar spinal cord. Recording electromyographic electrodes were placed at several locations in the abdominal and internal intercostal muscles. SCS was applied at each lead, in separate trials, with single shocks of 0.2-ms duration. The intensity of stimulation was adjusted to determine the threshold for development of the compound action potential at each electrode lead. The values of current threshold for activation of each muscle formed parabolas with minimum values at specific spinal root levels. The slopes of the parabolas were relatively steep, indicating that the threshold for muscle activation increases rapidly at more cephalad and caudal sites. These results were compared with the effectiveness of SCS (50 Hz; train duration, 1-2 s) at different spinal cord levels to produce changes in Paw. Stimulation at the T9 and T10 spinal cord level resulted in the largest positive Paws with a single lead. At these sites, threshold values for activation of the internal intercostal (7-11th interspaces) upper portions of external oblique, rectus abdominis, and transversus abdominis were near their minimum. Threshold values for activation of the caudal portions of the abdominal muscles were high (>50 mA). Our results indicate that 1) activation of the more cephalad portions of the abdominal muscles is more important than activation of caudal regions in the generation of positive Paws and 2) it is not possible to achieve complete activation of the expiratory muscles with a single electrode lead by using modest current levels. In support of this latter conclusion, a two-electrode lead system results in more uniform expiratory muscle activation and significantly greater changes in Paw.

Action Potentials↗

Mechanical contribution of expiratory muscles to pressure generation during spinal cord stimulation.

Lower thoracic spinal cord stimulation (SCS) results in the generation of large positive airway pressures (Paw) and may be a useful method of restoring cough in patients with spinal cord injury. The purpose of the present study was to assess the mechanical contribution of individual respiratory muscles to pressure generation during SCS. In anesthetized dogs, SCS was applied at different spinal cord levels by using a 15-lead multicontact electrode before and after sequential ablation of the external and internal obliques, transversus abdominis (TA), rectus abdominis, and internal intercostal muscles. Paw was monitored after tracheal occlusion. SCS at the T(9) spinal cord level resulted in maximal changes in Paw (60 +/- 3 cmH(2)O). Section of the oblique muscles resulted in a fall in Paw to 29 +/- 2 cmH(2)O. After subsequent section of the rectus abdominis and TA, Paw fell to 25 +/- 2 and 12 +/- 1 cmH(2)O respectively. There was a small remaining Paw (4 +/- 1 cmH(2)O) after section of the internal intercostal nerves. Stimulation with a two-electrode lead system (T(9) + T(13)) resulted in significantly greater pressure generation compared with a single-electrode lead due to increased contributions from the obliques and transversus muscles. In a separate group of animals, Paw generation was monitored after section of the abdominal muscles and again after section of the external intercostal and levator costae muscles. These studies demonstrated that inspiratory intercostal muscle stimulation resulted in only a small opposing inspiratory action (</=3 cmH(2)O). We conclude that, during SCS, 1) contraction of the obliques and TA muscles makes the largest contribution to changes in Paw, and 2) stimulation with a two-electrode lead system results in more complete abdominal muscle activation and enhanced mechanical actions of the obliques and transversus muscles.

Abdominal Muscles↗

Functional magnetic stimulation of the respiratory muscles in dogs.

This study assessed the ability of functional magnetic stimulation (FMS) to activate the respiratory muscles in dogs. With the animal supine, FMS of the phrenic nerves using a high-speed magnetic stimulator was performed by placing a round magnetic coil (MC) at the carotid triangle. Following hyperventilation-induced apnea, changes in volume (deltaV) and airway pressure (deltaP) against an occluded airway were determined. FMS of the phrenic nerves produced substantial inspired function (deltaV = 373 +/- 20.5 mL and deltaP = -20 +/- 2.0 cm H2O). After bilateral phrenectomies, maximal inspired deltaV (219 +/- 12.2 mL) and deltaP (-10 +/- 1.0 cm H2O) were produced when the MC was placed near the C6-C7 spinous processes, while maximal expired deltaV (-199 +/- 22.5 mL) and deltaP (11 +/- 2.3 cm H2O) were produced following stimulation near the T9-T10 spinous processes. We conclude: (1) FMS of either the phrenic or upper intercostal nerves results in inspired volume production; (2) FMS of the lower intercostal nerves generates expired volume production; and (3) FMS of the respiratory muscles may be a useful noninvasive tool for artificial ventilation and assisted cough in patients with spinal cord injuries or other neurological disorders.

Animals↗

Efficacy of combined inspiratory intercostal and expiratory muscle pacing to maintain artificial ventilation.

Many patients with ventilator-dependent quadriplegia have coincident phrenic nerve injury and therefore cannot be offered phrenic nerve pacing. The purpose of this study was to assess the utility of combined inspiratory intercostal and expiratory muscle pacing to provide complete ventilatory support. Studies were performed in 15 anesthetized dogs. An electrode was positioned on the epidural surface of the upper thoracic spinal cord to activate the inspiratory intercostal muscles; a separate electrode was positioned on the epidural surface of the lower thoracic spinal cord to activate the expiratory muscles. In an attempt to replicate the effects of inspiratory intercostal pacing alone in humans, stimulus parameters during upper thoracic spinal cord stimulation were adjusted to provide suboptimal levels of ventilation (end-tidal PCO2 of 55 to 60 mm Hg). Expiratory muscle activation was triggered electrically by the inspiratory signal with a 4.2-s delay resulting in alternate inspiratory and expiratory muscle pacing at a combined rate of 14 breaths/min. Combined pacing was maintained for an arbitrary period of 3 h. Initial intercostal muscle pacing alone resulted in an end-tidal PCO2 of 57.1 +/- 1.1 mm Hg. After the addition of expiratory muscle pacing, end-tidal PCO2 fell to 36.3 +/- 1.2 mm Hg. Tidal volume during both inspiratory and expiratory muscle pacing and end-tidal PCO2 remained stable throughout the study period. Our results suggest that combined alternate inspiratory and expiratory muscle pacing may be a viable alternative method of artificial ventilation in ventilator-dependent quadriplegic patients.

Animals↗

Effect of upper respiratory tract infection in patients with neuromuscular disease.

Respiratory muscle strength during acute upper respiratory tract infection (URI) was assessed in patients with various forms of neuromuscular disease. Vital capacity (VC), oxygen saturation, end-tidal PCO2, maximal inspiratory pressure (MIP), and maximal expiratory pressure (MEP) were determined in 25 stable patients with various forms of neuromuscular disease. Thirteen episodes of URI developed in 10 patients. Respiratory parameters were reassessed within 24-36 h following the onset of symptoms in each patient. In patients with URI, mean baseline VC, MIP, and MEP were 1.16 L +/- 0.14, 49.2 cm H2O +/- 6.8, and 35.5 cm H2O +/- 3.8 and fell to 1.01 L +/- 0.15, 37.1 cm H2O +/- 6.2, and 25.5 cm H2O +/- 3.0 during URI (p < 0.05 for each), respectively. Mean baseline PCO2 and oxygen saturation were 39.1 mm Hg +/- 1.1 and 95.1% +/- 1.0, and during URI, 43.9 mm Hg +/- 2.1 (p < 0.05) and 95.0% +/- 1.0 (NS), respectively. Five episodes of significant hypercapnia were observed in 4 patients. All parameters returned to near baseline values following recovery. We conclude that patients with various forms of neuromuscular disease develop reductions in respiratory muscle strength in association with URI. Unlike normal subjects, however, these decrements in respiratory muscle function may result in symptoms of shortness of breath, reductions in vital capacity, and acute hypercapnia in this patient population.

Acute Disease↗

Survey of physicians' attitudes about risks and benefits of chest computed tomography.

To investigate physicians' use of computed tomography (CT) of the chest and their attitudes regarding the risks and benefits of chest CT, we conducted a nationwide survey of 1,000 board certified physicians from several specialties of medicine, using a self-administered mail questionnaire. Three hundred thirteen surveys were completed. Overall, CT ordering practices varied with specialty. While the majority of physicians believed that CT provided new information (64%) and influenced patient management (62%), fewer physicians (30%) perceived that CT improved patient outcome. More than 90% of physicians either did not know or significantly underestimated the degree of radiation associated with CT (equivalent to 100 posteroanterior chest radiographs). We conclude that, given the paucity of prospective controlled trials establishing clear indications for the use of chest CT, physicians across all specialties should give careful consideration to the anticipated benefits and potential risks of chest CT before using this test.

Female↗

Electrical activation of the expiratory muscles to restore cough.

Many patients with spinal cord injury have paralysis of their expiratory muscles and, consequently, lack an effective cough. The purpose of the present study was to evaluate the utility of lower thoracic spinal cord stimulation (SCS) to activate the expiratory muscles. Studies were performed on 15 anesthetized dogs. A quadripolar stimulating electrode (Medtronic Model 3586) was inserted epidurally and on the ventral surface of the lower thoracic spinal cord. Changes in airway pressure, airflow, and internal intercostal and abdominal muscle length were monitored to assess the effects of electrical stimulation. Spinal stimulation applied at the T9-T10 spinal level provided maximal changes in airway pressure generation in preliminary experiments. All subsequent studies were therefore performed with the electrode positioned at this level. The expiratory muscles were stimulated supramaximally over a wide range of lung volumes which were expressed as the corresponding change in airway pressure. The pressure-generating capacity of the expiratory muscles was evaluated by the change in airway pressure produced by SCS during airway occlusion. Peak expiratory airflow was also monitored following release of occlusion. At FRC, deflation (-10 cm H2O) and inflation (+ 30 cm H2O), SCS resulted in positive airway pressures of 44 cm H2O +/- 4 SE, 28 cm H2O +/- 3 SE, and 82 cm H2O +/- 7 SE. The relationship between airway pressure expiratory airflow generation and lung volume was linear (slope = 1.34 +/- 0.04) over the entire vital capacity range. Our results indicate that: (1) a major portion of the expiratory muscles can be activated reproducibly and in concert by electrical stimulation, and (2) this technique may be a clinically useful method of restoring cough in spinal cord injured patients.

Animals↗

Lung herniation. A cause of chronic chest pain following thoracotomy.

Chronic chest pain is a common complication following thoracotomy, which is generally attributed to intercostal neuritis or neuralgia. Response to medical treatment is poor. We report a case of persistent chest pain following open lung biopsy, which was found to result from lung herniation, a rare, but surgically correctable complication of thoracotomy. Since lung herniation may be easily overlooked, this disorder should be considered more often in the differential diagnosis of persistent postthoracotomy chest pain.

Chest Pain↗

Effects of pentobarbital anesthesia on intercostal muscle activation and shortening.

Although pentobarbital (PB) is a commonly used anesthetic in animal studies examining respiratory motor control, there are virtually no studies that have examined the differential effects of deepening anesthesia on the activation of the various intercostal muscles. In dogs, anesthetized initially with 25 mg/kg of PB, the effects of additional doses of PB (20 mg) provided every 15 min on intercostal electromyogram (EMG) were monitored. In each animal, peak external intercostal (EI) and levator costae (LC) activation progressively decreased with additional doses of PB and were eventually abolished, at which point peak parasternal (PA) EMG had increased to 127 +/- 13% (SE) of control values; peak diaphragm EMG was unaffected. The reductions in EI activation were associated with progressive reductions in EI muscle shortening that, in turn, were associated with progressive reductions in lateral rib cage expansion. PA shortening was not significantly affected. Similar results were obtained in animals breathing supplemental oxygen. These results indicate that 1) activation of EI and LC compared with PA have divergent responses, with EI and LC decreasing and PA increasing; 2) the fall in EI activation results in decrements in EI shortening and lateral rib cage motion; and 3) anesthetic depth is an important variable that must be controlled in studies assessing intercostal muscle activation.

Anesthesia↗

Evaluation of intercostal pacing to provide artificial ventilation in quadriplegics.

The purpose of this study was to assess the utility of intercostal muscle pacing by spinal cord stimulation (SCS) to provide artificial ventilation in ventilator-dependent quadriplegic patients. Five ventilator-dependent quadriplegics with phrenic nerve injury (and therefore not candidates for phrenic nerve pacing) were studied. During an initial surgical procedure, a quadripolar epidural disc electrode was positioned on the ventral portion of the upper thoracic spinal cord via a hemilaminectomy and subsequently connected to a radio-frequency receiver implanted subcutaneously over the anterior rib cage. In four of the five patients, initial SCS stimulation resulted in inspired volumes between 150 and 240 ml. Stimulation resulted in no effect in one patient, due to probable cystic degeneration of the thoracic spinal cord. Reconditioning of the intercostal muscles caused substantial increases in inspired volume in three of four patients of 670 to 850 ml. In one patient, reconditioning resulted in a much smaller increase (to 470 ml). The maximum duration that ventilation could be sustained by low-frequency (13 Hz) intercostal pacing ranged between 20 min and 2 3/4 h. Our findings indicate that intercostal pacing via SCS does not result in sufficient inspired volume production to support ventilation for prolonged periods. However, this modality may be a useful adjunct to enhance tidal volume in patients with suboptimal inspired volume by phrenic nerve pacing.

Chronic Disease↗

Respiratory muscle rest using nasal BiPAP ventilation in patients with stable severe COPD.

To more systematically evaluate the effect of respiratory muscle rest on indices of ventilatory function, nine outpatients with stable, severe COPD were treated with nasal pressure-support ventilation delivered via a nasal ventilatory support system (BiPAP, Respironics, Inc) for 2 h a day for 5 consecutive days. An additional eight control patients were treated with sham-BiPAP. Maximum inspiratory pressure (MIP), maximum expiratory pressure (MEP), maximum voluntary ventilation (MVV), arterial blood gas values, Borg dyspnea score, dyspnea-associated functional impairment scales, and distance walked in 6 min were measured in subjects prior to and following the week-long trial. Nasal BiPAP produced a 66.3 +/- 6 percent reduction in peak integrated diaphragmatic electromyographic (EMG) activity. There were no statistically significant changes in MIP, MEP, MVV, arterial pH, PaCO2, or PaO2 or in objective measures of functional impairment from dyspnea in either group after ventilator or sham treatment. However, nasal BiPAP reduced the Borg category score during resting, spontaneous breathing from 2.0 +/- 0.4 to 0.7 +/- 0.3 (p < 0.01) after 5 days of treatment. In contrast, sham BiPAP-treated patients had no change in their dyspnea score, which was 1.8 +/- 0.4 and 1.3 +/- 0.4 before and after sham treatment, respectively. Nasal BiPAP also increased distance walked in 6 min from 780 +/- 155 to 888 +/- 151 ft (p < 0.01) (23,400 +/- 4,650 to 26,640 +/- 4,530 cm) (p < 0.01), whereas sham-BiPAP had no effect (768 +/- 96 and 762 +/- 106 ft [23,040 +/- 2,880 and 22,860 +/- 3,180 cm]) before and after sham treatment, respectively). In conclusion, these results indicate that nasal pressure-support ventilation, delivered via nasal BiPAP, improves exercise capacity and reduces dyspnea over the short term in selected outpatients with stable severe COPD. Whether such short-term improvement can be sustained merits further study.

Activities of Daily Living↗

Failure of vasodilator administration to increase blood flow to the fatiguing diaphragm.

Recent studies have suggested that coronary and limb muscle vessels do not maximally vasodilate under conditions in which cardiac and limb muscle contractile function is dependent on the level of blood flow but, rather, maintain a "vasodilator reserve." If a vasodilator reserve is also present in the fatiguing diaphragm, it may be possible to augment flow to this muscle with vasodilator administration, improving muscle function. The purpose of the present study was therefore to examine the effect of administration of a potent vasodilator, nitroprusside, on the blood flow and contractile function of the fatiguing diaphragm. Studies were performed using an in situ canine diaphragmatic strip preparation that permitted direct measurement of force and blood flow; cardiac output was monitored with a thermodilution catheter. The effects of nitroprusside were examined with the diaphragm rhythmically contracting in response to both subfatiguing and fatiguing stimulation paradigms. For both contraction paradigms, nitroprusside infusions elicited appreciable increases in cardiac output. Nitroprusside infusions also produced significant increases in diaphragmatic blood flow during subfatiguing diaphragmatic contractions but had no effect on flow during fatiguing contractions. Nitroprusside also had no effect on the rate of diaphragmatic fatigue. These data suggest that, under the conditions examined, the diaphragm exhausts its vasodilator reserve during the development of fatigue and vasodilator administration has no appreciable effect on diaphragm blood flow and function. Moreover, although vasodilator drugs with actions similar to nitroprusside are used clinically to augment flow to vital organs, our data would indicate that these drugs have no functionally significant effect on blood flow to the fatiguing diaphragm.

Animals↗

Effects of intraphrenic injection of potassium on diaphragm activation.

The purpose of the present study was to determine whether potassium, injected into the arterial supply of the diaphragm, would reflexly alter efferent diaphragmatic motor outflow and systemic arterial pressure. Studies were performed using in situ canine diaphragm muscle strips in which the inferior phrenic artery and vein were cannulated and all other sources of strip blood flow were ligated. Injection of potassium (0.1 meq) into the inferior phrenic artery elicited a small transient (1-2 breaths) decrease in the peak strip tension developed during spontaneous muscle contractions, in peak integrated strip electromyographic (EMG) activity, and in the peak integrated EMG activity of the contralateral hemidiaphragm. This was followed by a more pronounced and more sustained increase in each of these parameters as well as an increase in systemic arterial pressure. This latter excitatory response was qualitatively similar to that induced by the injection of capsaicin (5 and 25 micrograms) into the phrenic artery. Section of the left phrenic nerve abolished the effects of intra-arterial potassium and capsaicin on systemic arterial pressure and right hemidiaphragm EMG activity. These data support the existence of a potent excitatory phrenic-to-phrenic reflex that can be activated by potassium injection into the diaphragm. Activation of this pathway increases diaphragm motor activation and augments systemic arterial pressure.

Afferent Pathways↗