Foot force direction control during leg pushes against fixed and moving pedals in persons post-stroke.

The component of foot force generated by muscle action (F(m)) during pedaling in healthy humans has a nearly constant direction with increasing force magnitude. The present study investigated the effect of stroke on the control of foot force. Ten individuals with hemiparesis secondary to a cerebral vascular accident performed pushing efforts against translationally fixed and moving pedals on a custom stationary cycle ergometer. We found that while F(m) direction remained constant with increasing effort in both the fixed- and moving-crank conditions for both limbs, the orientation of that force component differed between limbs. The non-paretic limb produced the same F(m) orientation as seen previously in healthy humans. However, relative to the non-paretic limb, the paretic limb force line-of-action was shifted away from the hip and closer to the knee in the sagittal-plane for both pedal motion conditions. In the frontal plane, the paretic limb force line-of-action was shifted laterally, closer to parallel to the midline, for both pedal motion conditions. These shifts were consistent with previously reported lower limb muscle weakness and alterations in muscle activation observed during pedaling tasks following stroke. The finding of similar orientations for static and dynamic pushing efforts suggests that limb posture could be a trigger for relative muscle activation levels. The preservation of a constant direction in F(m) with increasing force magnitude post-stroke, despite an orientation shift, suggests that control of lower limb force may be organized by magnitude and direction and that these two aspects are differentially affected by stroke.

Foot force direction in an isometric pushing task: prediction by kinematic and musculoskeletal models.

The abilities of a kinematic model and a muscle model of the human lower limb to predict the stereotyped direction of the muscular component of foot force produced by seated subjects in a static task were tested and compared. Human subjects ( n=11) performed a quasi-static, lower-limb pushing task against an instrumented bicycle pedal, free to rotate about its own axis, but with the crank fixed. Each pushing trial consisted of applying a force from the resting level to a force magnitude target with the right foot. Ten force target magnitudes were used (200, 250, ..., 650 N) along with 12 pedal positions. For each pushing effort, the muscular contribution to the measured foot force was determined from push onset to peak attained force. This segment was well characterized by a straight line across subjects, pedal positions, and force target magnitudes. The linear nature of the muscular component allowed a characteristic direction to be determined for each trial. A three-joint (hip, knee, and ankle) and a two-joint (hip and knee) net joint torque optimization was applied to a sagittal-plane kinematic model to predict the characteristic force direction. A musculoskeletal model was also used to create a feasible force space (FFS) for the lower limb. This FFS represents the range of possible forces the lower limb could theoretically produce. From this FFS, the direction of the maximum feasible foot force was determined and compared with the characteristic direction of subject performance. The muscle model proved to be the most effective in predicting subject force direction, followed by the three-joint and two-joint net joint torques optimizations. Similarities between the predictions of the kinematic and muscle model were also found.

Circulatory responses to voluntary and electrically induced muscle contractions in humans.

BACKGROUND AND PURPOSE: Transcutaneous electrical nerve stimulation (TENS) increases regional blood flow when applied at intensities sufficient to cause skeletal muscle contraction. It is not known whether increases in blood flow elicited by TENS differ from those caused by voluntary muscle contraction. The purpose of this study, therefore, was to compare the hemodynamic effects of these 2 types of muscle contraction. SUBJECTS AND METHODS: Fourteen people with no known pathology, aged 18 to 49 years (mean=28, SD=8), served as subjects. Calf blood flow (venous occlusion plethysmography), heart rate (electrocardiogram), blood pressure (automated sphygmomanometry), and force (footplate transducer) were measured during electrically induced and voluntary contractions. RESULTS: Both modes of exercise caused rapid, but short-lived vasodilation (calf vascular resistance [mean(SEM]: (53%(3% for voluntary contractions versus (57%(4% for electrically induced contractions). The vasodilation caused by electrically induced contractions persisted for at least 15 seconds in the postexercise period, whereas the vasodilation elicited by voluntary contractions had resolved by this time point. CONCLUSION AND DISCUSSION: The hemodynamic changes elicited by voluntary and electrically induced muscle contractions are similar in magnitude but different in duration.

Characteristics of the force applied to a pedal during human pushing efforts: emergent linearity.

The force seated humans exert on a translationally fixed pedal (foot force) may be directed at any angle because the fixed distance between the seat and the pedal axis kinematically constrains the lower limb. The authors' objective in the present work was to characterize such force. Participants (N = 7) generated force with their lower limb by pushing against the pedal in the most comfortable manner. Pushing efforts were repeated randomly 3 times at each of 97 sagittal-plane pedal axis positions and 10 additional times in 9 of those positions (2,895 total pushes). In 87% of the pushes, the measured sagittal-plane force exerted on the pedal by the foot changed magnitude and direction through time, such that the path of the head of the force vector traced a straight line. The linearity of the foot force paths reflected directional invariance in the changes of the foot force vector as the magnitude of the vector increased. The orientation of those linear force paths varied with limb posture in a similar manner across participants. The authors conclude that the emergent linearity of the force path is consistent with minimization of path length in foot force space. Alternatively, the linearity of the force paths suggests a motor control strategy that simplifies the control to a monoparametric form.

Canine sternal force-displacement relationship during cardiopulmonary resuscitation.

A viscoelastic model developed to model human sternal response to the cyclic loading of manual cardiopulmonary resuscitation (CPR) [8] was used to evaluate the properties of canine chests during CPR. Sternal compressions with ventilations after every fifth compression were applied to supine canines (n = 7) with a mechanical resuscitation device. The compressions were applied at a nominal rate of 90/min with a peak force near 400 N. From measurements of sternal force, sternal displacement, and tracheal airflow, model parameters were estimated and their dependence on time and lung volume evaluated. The position to which the chest recoiled between compressions changed with time at a mean rate of 1.0 mm/min. Within each ventilation cycle (five compressions) the sternal recoil position decreased by 2.0 cm for each liter of decrease in lung volume. The elastic force and damping decreased with time and decreasing lung volume. Canine and human [8] model parameters were found to be similar despite the notable differences in thoracic anatomy between the species, supporting the continued use of canines as models for human CPR. These parameters may be useful in the development of a model relating sternal compression forces to blood flow during CPR.

Observations of ventilation during resuscitation in a canine model.

BACKGROUND: Fear of infection limits the willingness of laymen to do cardiopulmonary resuscitation (CPR). This study assessed the time course of change in arterial blood gases during resuscitation with only chest compression (no ventilation) in an effort to identify the time for which ventilation could be deferred. METHODS AND RESULTS: Aortic pressures and arterial blood gases were monitored in seven 20- to 30-kg dogs in ventricular fibrillation (VF) at 2-minute intervals during chest compression alone (no ventilation) at 80 to 100 compressions per minute. Before the induction of ventricular fibrillation, all animals were intubated and ventilated with room air, 10 mL/kg. The endotracheal tube was removed when VF was induced. Pre-VF arterial pH, PCO2, and O2 saturation were (mean +/- SEM) 7.39 +/- 0.02, 27.0 +/- 1.5 mm Hg, and 97.5 +/- 0.5%, respectively, with aortic pressures being 143.2 +/- 5.7/116.2 +/- 4.6 mm Hg. At 4 minutes of chest compression alone, the corresponding values were 7.39 +/- 0.03, 24.3 +/- 3.1 mm Hg, and 93.9 +/- 3.0%, with an arterial pressure of 48.1 +/- 7.7/22.6 +/- 3.9 mm Hg. Mean minute ventilation during the fourth minute of CPR, measured with a face mask-pneumotachometer, was 5.2 +/- 1.1 L/min. CONCLUSIONS: These data suggest that in the dog model of witnessed arrest, chest compression alone during CPR can maintain adequate gas exchange to sustain O2 saturation > 90% for > 4 minutes. The need for immediate ventilation during witnessed arrest should be reexamined.

A preliminary study of cardiopulmonary resuscitation by circumferential compression of the chest with use of a pneumatic vest.

BACKGROUND: More than 300,000 people die each year of cardiac arrest. Studies have shown that raising vascular pressures during cardiopulmonary resuscitation (CPR) can improve survival and that vascular pressures can be raised by increasing intrathoracic pressure. METHODS: To produce periodic increases in intrathoracic pressure, we developed a pneumatically cycled circumferential thoracic vest system and compared the results of the use of this system in CPR (vest CPR) with those of manual CPR. In phase 1 of the study, aortic and right-atrial pressures were measured during both vest CPR (60 inflations per minute) and manual CPR in 15 patients in whom a mean (+/- SD) of 42 +/- 16 minutes of initial manual CPR had been unsuccessful. Vest CPR was also carried out on 14 other patients in whom pressure measurements were not made. In phase 2 of the study, short-term survival was assessed in 34 additional patients randomly assigned to undergo vest CPR (17 patients) or continued manual CPR (17 patients) after initial manual CPR (duration, 11 +/- 4 minutes) had been unsuccessful. RESULTS: In phase 1 of the study, vest CPR increased the peak aortic pressure from 78 +/- 26 mm Hg to 138 +/- 28 mm Hg (P < 0.001) and the coronary perfusion pressure from 15 +/- 8 mm Hg to 23 +/- 11 mm Hg (P < 0.003). Despite prolonged unsuccessful manual CPR, spontaneous circulation returned with vest CPR in 4 of the 29 patients. In phase 2 of the study, spontaneous circulation returned in 8 of the 17 patients who underwent vest CPR as compared with only 3 of the 17 patients who received continued manual CPR (P = 0.14). More patients in the vest-CPR group than in the manual-CPR group were alive 6 hours after attempted resuscitation (6 of 17 vs. 1 of 17) and 24 hours after attempted resuscitation (3 of 17 vs. 1 of 17), but none survived to leave the hospital. CONCLUSIONS: In this preliminary study, vest CPR, despite its late application, successfully increased aortic pressure and coronary perfusion pressure, and there was an insignificant trend toward a greater likelihood of the return of spontaneous circulation with vest CPR than with continued manual CPR. The effect of vest CPR on survival, however, is currently unknown and will require further study.

Sternal force-displacement relationship during cardiopulmonary resuscitation.

A viscoelastic model is presented to describe the dynamic response of the human chest to cyclic loading during manual cardiopulmonary resuscitation (CPR). Sternal force and displacement were measured during 16 clinical resuscitation attempts and during compressions on five CPR training manikins. The model was developed to describe the clinical data and consists of the parallel combination of a spring and dashpot. The human chests' elastic and damping properties were both augmented with increasing displacement. The manikins' elastic properties were stiffer and both elastic and damping properties were less dependent on displacement than the humans'.

System for mechanical measurements during cardiopulmonary resuscitation in humans.

Effective study of CPR requires measurement of the mechanical properties of the human chest and the resultant vascular pressures. A computer-based mobile data acquisition system was designed and built for this purpose. During manual CPR a short cylindrical module was placed between the rescuer's hands and the patient's chest. This module, which was attached to an easily manipulated position-sensing arm, measured force and acceleration at the sternum. Three-dimensional position and orientation of the module were measured, as well as the component of the applied force which was perpendicular to the sternum. The central venous and aortic pressures were measured by high fidelity pressure transducers. All transducer signals were recorded by digital computer. Real-time feedback of sternal force and displacement, and vascular pressures was provided to the rescue team via chart recordings. An audible signal was produced as an aid in maintaining desired compression rate and duration. The system's mobility permitted rapid implementation at any hospital location. In conclusion, this system was capable of measuring, recording, and displaying multiple physical quantities during manual CPR in humans.

Identification of dynamic mechanical parameters of the human chest during manual cardiopulmonary resuscitation.

Survival from cardiac arrest is dependent on timely cardiopulmonary resuscitation (CPR). Since CPR is often unsuccessful, the outcome may be improved by a better understanding of the relationship between force applied to the sternum and the resulting hemodynamic effects. The first step in this complex chain of interactions is the mechanical response of the chest wall to cyclical compression. We formulated a dynamic mechanical model of the chest response and developed a method of identification of the model parameters based on force, displacement, and acceleration data acquired during cyclical compressions. The elasticity, damping, and equivalent mass of the human chest were estimated with a constrained nonlinear least-mean-square identification technique. The method was validated on data acquired from a test apparatus built for this purpose. The model fit was measured with the normalized chi-square statistic on residuals obtained between recorded force and force predicted by the model. In the analysis of one human chest, the elasticity was found to be nonlinear and statistically different during compression and release. A considerable amount of damping was found, with no significant difference between compression and release. The equivalent mass was too small to be determined accurately. This method can be used to obtain the dynamic mechanical parameters of the human chest and may lead to a better understanding of CPR.