Acute Lower Extremity Fracture Management in Chronic Spinal Cord Injury: 2022 Delphi Consensus Recommendations.

Our objective was to develop a clinical practice guideline (CPG) for the treatment of acute lower extremity fractures in persons with a chronic spinal cord injury (SCI). Methods: Information from a previous systematic review that addressed lower extremity fracture care in persons with an SCI as well as information from interviews of physical and occupational therapists, searches of the literature, and expert opinion were used to develop this CPG. The Grading of Recommendations, Assessment, Development and Evaluations (GRADE) system was used to determine the quality of evidence and the strength of the recommendations. An overall GRADE quality rating was applied to the evidence. Conclusions: Individuals with a chronic SCI who sustain an acute lower extremity fracture should be provided with education regarding the risks and benefits of operative and nonoperative management, and shared decision-making for acute fracture management should be used. Nonoperative management historically has been the default preference; however, with the advent of greater patient independence, improved surgical techniques, and advanced therapeutics and rehabilitation, increased use of surgical management should be considered. Physical therapists, kinesiotherapists, and/or occupational therapists should assess equipment needs, skills training, and caregiver assistance due to changes in mobility resulting from a lower extremity fracture. Therapists should be involved in fracture management as soon as possible following fracture identification. Pressure injuries, compartment syndrome, heterotopic ossification, nonunion, malunion, thromboembolism, pain, and autonomic dysreflexia are fracture-related complications that clinicians caring for patients who have an SCI and a lower extremity fracture may encounter. Strategies for their treatment are discussed. The underlying goal is to return the patient as closely as possible to their pre-fracture functional level with operative or nonoperative management.

Ventricular tachycardias mimicking those arising from the right ventricular outflow tract.

INTRODUCTION: Ablation of ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) has proven highly successful, yet VTs with similar ECG features may originate outside the RVOT. METHODS AND RESULTS: We reviewed the clinical, echocardiographic, and ECG findings of 29 consecutive patients referred for ablation of monomorphic VT having a left bundle branch block pattern in lead V1 and tall monophasic R waves inferiorly. Nineteen patients (group A) had VTs ablated from the RVOT, and 10 patients (group B) had VTs that could not be ablated from the RVOT. The QRS morphology during VT or frequent ventricular premature complexes was the only variable that distinguished the two groups. During the target arrhythmia, ECGs of group B patients displayed earlier precordial transition zones (median V3 vs V5; P < 0.001), more rightward axes (90 +/- 4 vs 83 +/- 5; P = 0.002), taller R waves inferiorly (aVF: 1.9 +/- 1.0 vs 2.4 +/- 0.5; P = 0.020) and small R waves in lead V1 (10/10 vs 9/19; P = 0.011). Radiofrequency catheter ablation from the RVOT failed to eliminate VT in any group B patient, but ablation from the left ventricular outflow tract (LVOT) eliminated VT in 2 of 6 patients in whom left ventricular ablation was attempted. CONCLUSION: The absence of an R wave in lead V1 and a late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes VTs that mimic an RVOT origin. The latter VTs occasionally can be ablated from the LVOT. Recognition of these ECG features may help the physician advise patients and direct one's approach to ablation.

The force-velocity curve in passive whole muscle is asymmetric about zero velocity.

The force-velocity property of passive muscle was investigated to determine if a discontinuity of slope occurred at zero velocity. Isolated, unstimulated whole frog sartorius muscles were subjected to constant-velocity stretches and releases using a servo-controlled lever. The force due to damping (delta T) was calculated by subtracting the tension measured at a very low speed (1.0 mm s-1) from the tension measured at the same length while the muscle was shortening or lengthening at a particular test speed. The experiments were performed over a range of speeds at each of several lengths and at two temperatures. For comparison, the same experiments were performed using a strip of pure latex rubber and a steel spring. Curves showing the magnitude of delta T vs velocity were nearly symmetric about the zero-velocity axis for the steel spring and the rubber strip, but were markedly asymmetric for passive muscle, showing a positive delta T for lengthening at all speeds that was between four and 11 times the negative delta T for shortening at the same speed, depending on the temperature and initial stretch length. The force due to damping at a given speed increased with extension above the rest length in passive muscle but decreased with increasing length in experiments using the latex strip. Predictions obtained from a mathematical model based on a damping element in series with a lightly damped spring were fitted to the experimental measurements of delta T vs velocity. The damping parameter provisionally representing interfilamentary sliding was between six and 12 times larger for lengthening than for shortening.(ABSTRACT TRUNCATED AT 250 WORDS)

Negative developed tension in rapidly shortening whole frog muscles.

High speed isovelocity shortening using a servo-controlled lever was performed on isolated whole frog sartorius muscles at long lengths to ensure substantial passive tension. The tension records of unstimulated control experiments were subtracted from the tension records of fully-tetanized experiments on the same muscles to yield the developed tension exerted by the contractile proteins alone. There are several main results: (1) the positive developed tension had the same relation with shortening speed observed by other researchers in single fibres with no passive tension present; (2) negative developed tension was always measured at velocities of shortening above Vmax, where Vmax (typically 1.5 muscle-lengths s-1 at 2 degrees C) is defined as the velocity of shortening observed to yield zero developed tension; (3) negative developed tension was roughly asymptotic to -0.05 T(o), where T(o) is the developed isometric tetanic tension for the muscle length at which the developed tension was measured during steady shortening; (4) negative developed tension diminished in magnitude at velocities of shortening above approximately 2.5 Vmax; (5) a 10 degrees C increase in temperature from 2 degrees C to 12 degrees C had no significant effect on the shape of the normalized force-velocity curve (%T(o) versus %Vmax), but did increase Vmax by a factor of 2.6 in agreement with the results of previous studies measuring Vmax in the absence of passive tension; (6) addition of curare in the saline bath did not affect the results.

Characteristics of Ca(2+)-activated K+ channels isolated from the left ventricle of a patient with idiopathic long QT syndrome.

Early afterdepolarizations (EADs), possibly caused by reduced K+ conductance, have been hypothesized to cause the long QTU interval and ventricular tachyarrhythmias (VT) in patients with the long QT syndrome (LQTS). In a 26-year-old woman with aborted sudden death as a consequence of the idiopathic LQTS, we recorded with a contact electrode left ventricular endocardial EADs that were enhanced by epinephrine and phenylephrine. Because of uncertain efficacy and side effects achieved with beta-adrenoceptor blockade, the patient underwent left-sided cardiac sympathectomy, at which time we obtained left ventricular biopsy tissue. Crude membrane vesicles were prepared from this tissue and single-channel activity was studied after incorporation of the vesicles in an artificial lipid bilayer (phosphatidylserine, phosphatidylethanolamine, 4:5 weight ratio in decane) in the tip of a patch clamp pipette. Bath and pipette contained 100 mmol/L KCI and 25 mmol/L N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) at pH 7.4. We recorded K+ conducting channels with a mean slope conductance of 49.9 +/- 4.7 picosiemens (pS) (n = 5). Channel open probability was increased by the addition of 1 to 10 mumol/L Ca2+ to the experimental chamber. Addition of charybdotoxin (1-3 nmol/L), a known specific inhibitor of Ca(2+)-activated K+ channels, blocked channel activity. These results are the first to demonstrate Ca(2+)-activated K+ channels from a patient with idiopathic LQTS. These channels appear to show normal characteristics when studied in an artificial planar lipid bilayer.

Electrophysiologic alterations produced by hypoxia in the canine heart.

The purpose of this study was to test whether hypoxia caused simultaneous stimulation of sympathetic and vagal cardiac nerves. To do this, we determined in chloralose-anesthetized, open-chest dogs, changes in sinus cycle length (SCL), atrioventricular nodal conduction time (AH interval), and effective refractory periods (ERP) of the right atrium (RA) and left ventricle (LV) during hypoxia induced by either hypoventilation or by breathing 10% oxygen in nitrogen. We found that hypoventilation decreased arterial pH (mean +/- SE: 7.365 +/- 0.011 versus 7.244 +/- 0.013, p less than 0.001) and Po2 (105.2 +/- 3.6 versus 50.5 +/- 2.0 mm Hg, p less than 0.001), and increased Pco2 (24.4 +/- 0.7 versus 41.9 +/- 1.1 mm Hg, p less than 0.001). SCL (373 +/- 19 versus 485 +/- 35 msec, p less than 0.001), AH interval (92 +/- 4 versus 111 +/- 6 msec, p less than 0.005), and LVERP (159.8 +/- 3.2 versus 162.0 +/- 3.3, p less than 0.05) lengthened, while RAERP shortened (137.7 +/- 2.6 versus 128.8 +/- 3.5, p less than 0.001). After bilateral vagotomy, these electrophysiologic changes were attenuated, and transection of ansae subclaviae following vagotomy did not affect hypoventilation-induced changes that were present after vagotomy alone. In contrast, breathing 10% oxygen decreased Po2 (104.2 +/- 3.3 versus 48.1 +/- 1.7, p less than 0.001) but did not change pH and Pco2. SCL lengthened slightly (444 +/- 15 versus 463 +/- 17, p less than 0.001), but other measured electrophysiologic parameters were not affected. The norepinephrine concentration in the coronary sinus blood increased by 109% to 121% during hypoxia induced by both methods. Hypoventilatory hypoxia blunted sympathetic-induced shortening of LVERP and potentiated vagally-induced SCL lengthening. Neither type of hypoxia affected induction of atrial and ventricular tachyarrhythmias by programmed electrical stimulation. We conclude that the electrophysiologic response during hypoventilatory hypoxia is due primarily to heightened vagal tone. Norepinephrine concentration in the coronary sinus blood more than doubled, but did not alter cardiac electrophysiologic properties, possibly because of simultaneous increase in vagal tone, or possibly due to the release of adenosine or other factors that impaired cardiac electrophysiologic response to elevated norepinephrine levels.

An inspiration-triggered delivery system for oxygen therapy via a nasal cannula.

Therapy for severe chronic lung disease currently includes the administration of supplemental oxygen to prevent breathlessness and tissue hypoxia. Although effective, this therapy is unnecessarily costly, because oxygen is administered to the patient during expiration as well as inspiration. To eliminate this inefficiency, a delivery system that senses the inspiratory effort and delivers oxygen to the patient only during inspiration was developed. The 11 X 5 X 8-cm flow control unit attaches easily to a portable oxygen supply. The components of the system have an expected life of five years, and the 9-V battery provides power for about one month of use. Manual controls permit accommodation to the respiratory pattern of the patient. Preliminary evaluation of the system showed that its effectiveness in producing tissue oxygenation is similar to that of continuous oxygen systems. The system has potential applications in ambulatory oxygen therapy and in other clinical settings to improve the cost/benefit ratio of oxygen treatment.