. Arterial blood pressure response to heavy resistance exercise. J. Appl. Physiol. 58(3): 785-790, 1985.-The purpose of this study was to record the blood pressure response to heavy weight-lifting exercise in five experienced body builders. Blood pressure was directly recorded by means of a capacitance transducer connected to a catheter in the brachial artery. Intrathoracic pressure with the Valsalva maneuver was recorded as mouth pressure by having the subject maintain an open glottis while expiring against a column of Hg during the lifts. Exercises included single-arm curls, overhead presses, and both double-and single-leg presses performed to failure at 80, 90, 95, and 100% of maximum. Systolic and diastolic blood pressures rose rapidly to extremely high values during the concentric contraction phase for each lift and declined with the eccentric contraction. The greatest peak pressures occurred during the double-leg press where the mean value for the group was 320/250 mmHg, with pressures in one subject exceeding 480/350 mmHg. Peak pressures with the single-arm curl exercise reached a mean group value of 255,' 190 mmHg when repetitions were continued to failure. Mouth pressures of 30-50 Torr during a single maximum lift, or as subjects approached failure with a submaximal weight, indicate that a portion of the observed increase in blood pressure was caused by a Valsalva maneuver. It was concluded that when healthy young subjects perform weight-lifting exercises the mechanical compression of blood vessels combines with a potent pressor response and a Valsalva response to produce extreme elevations in blood pressure. Pressures are extreme even when exercise is performed with a relatively small muscle mass.weight-lifting exercise; blood pressure; static contraction; small versus large muscle mass; Valsalva maneuver SEVERAL STUDIES HAVE NOW demonstratedthatregular resistance training or weight lifting is associated with ventricular wall hypertrophy (11, 12, 14, 20). Such findings are considered to be a normal adaptation to a systemic pressure overload induced by such exercise. METHODSFive healthy male volunteers (22-28 yr) served as subjects. All were experienced body builders and were fully informed of the purposes of the study and the associated risks in accordance with the institution's ethics committee.The left brachial artery of each subject was cannulated under local anesthesia with a 24-gauge Angiocath that was connected to a pressure transducer (Bell and Howell, Pasadena, CA) as illustrated in Fig. 1. The response of the transducer was verified to be linear within the range O-500 mmHg, and the system was statically calibrated against an Hg manometer by means of a calibration syringe. In addition, the system was dynamically calibrated by using square-wave pressure signals that were rapidly switched into the arterial line. These signals were then critically damped by adjusting the height of an air column in a section of low-compliance tubing inserted into the line (Fig. 1). Arterial blood pressure was cons...
IntroductionTidal volume and plateau pressure minimisation are the standard components of a protective lung ventilation strategy for patients with acute respiratory distress syndrome (ARDS). Open lung strategies, including higher positive end-expiratory pressure (PEEP) and recruitment manoeuvres to date have not proven efficacious. This study examines the effectiveness and safety of a novel open lung strategy, which includes permissive hypercapnia, staircase recruitment manoeuvres (SRM) and low airway pressure with PEEP titration.MethodTwenty ARDS patients were randomised to treatment or ARDSnet control ventilation strategies. The treatment group received SRM with decremental PEEP titration and targeted plateau pressure < 30 cm H2O. Gas exchange and lung compliance were measured daily for 7 days and plasma cytokines in the first 24 hours and on days 1, 3, 5 and 7 (mean ± SE). Duration of ventilation, ICU stay and hospital stay (median and interquartile range) and hospital survival were determined.ResultsThere were significant overall differences between groups when considering plasma IL-8 and TNF-α. For plasma IL-8, the control group was 41% higher than the treatment group over the seven-day period (ratio 1.41 (1.11 to 1.79), P = 0.01), while for TNF-α the control group was 20% higher over the seven-day period (ratio 1.20 (1.01 to 1.42) P = 0.05). PaO2/FIO2 (204 ± 9 versus 165 ± 9 mmHg, P = 0.005) and static lung compliance (49.1 ± 2.9 versus 33.7 ± 2.7 mls/cm H2O, P < 0.001) were higher in the treatment group than the control group over seven days. There was no difference in duration of ventilation (180 (87 to 298) versus 341 (131 to 351) hrs, P = 0.13), duration of ICU stay (9.9 (5.6 to 14.8) versus 16.0 (8.1 to 19.3) days, P = 0.19) and duration of hospital stay (17.9 (13.7 to 34.5) versus 24.7 (20.5 to 39.8) days, P = 0.16) between the treatment and control groups.ConclusionsThis open lung strategy was associated with greater amelioration in some systemic cytokines, improved oxygenation and lung compliance over seven days. A larger trial powered to examine clinically-meaningful outcomes is warranted.Trial registrationACTRN12607000465459
Patients with severe air-flow obstruction receiving mechanical ventilation are at risk of inadvertent pulmonary hyperinflation with morbidity and mortality caused by pneumothorax and circulatory depression. Nine patients with severe air-flow obstruction (5 asthma, 4 chronic air-flow obstruction) requiring mechanical ventilation were studied while sedated and therapeutically paralyzed. Pulmonary hyperinflation during steady-state ventilation was quantified by measuring total exhaled volume during 20- to 40-s apnea (end-inspiratory lung volume, VEI). Patients were studied at 3 levels of minute ventilation (VE) (10, 16, and 26 L/min) and at each VE, 3 levels of tidal volume (VT) (0.6, 1.0, and 1.6 L) and 3 levels of inspiratory flow (VI) (40, 70, and 100 L/min for VT = 1.0 L). There were progressive increases in VEI when VT was increased or when expiratory time (TE) was decreased either by an increase in rate (and hence VE) or by a decrease in VI (at a constant VE) reaching lung volumes as high as 3.6 +/- 0.4 L above FRC. Alveolar, central venous, and esophageal pressure rose in parallel with lung volumes, and hypotension was seen in most patients at highest lung volumes. Peak airway pressure (Ppk) was predominantly related to inspiratory flow and did not reflect changes in lung volume. Levels of ventilation required for normocapnia prior to paralysis (15.7 +/- 2.3 L/min) were associated with hypotension in 7 patients and probable hyperinflation in excess of 1.96 +/- 0.17 L above FRC. VEI is a simple, reproducible measurement of pulmonary hyperinflation and may be more important than Ppk in the causation of barotrauma.(ABSTRACT TRUNCATED AT 250 WORDS)
Myopathy complicating the therapy of severe asthma has been recently described in several case reports. Twenty-five consecutive patients admitted to the intensive care unit (ICU) at this hospital for mechanical ventilation for severe asthma were studied for the incidence of creatine kinase (CK) enzyme rise and for the development of clinical myopathy. Pharmacologic therapy was standardized, every patient receiving corticosteroids and aminophylline intravenously and salbutamol both nebulized and intravenously. Twenty-two patients received muscle relaxant therapy with vecuronium. In 19 of 25 (76%) of patients there was elevation of CK levels to a median of 1,575 U/L (range, 66 to 7,430) occurring 3.6 +/- 1.5 days after admission. In nine patients there was clinically detectable myopathy. The presence of either myopathy or CK enzyme rise was associated with a significant prolongation of ventilation time. Arterial blood gas measurements on admission to the ICU revealed a pH (mean +/- SD) of 7.07 +/- 0.21, a PaCO2 of 87.2 +/- 32.7, and a PaO2 (with a high FIO2) of 129 +/- 97 mm Hg; however, no correlation was found between the severity of initial metabolic disturbance and the subsequent development of myopathy. There was no association between the type of corticosteroid administered and the subsequent development of myopathy. Patients with myopathy had received a significantly higher total dose of vecuronium when compared with those who did not develop myopathy (p < 0.001, Kruskal Wallis test). We have therefore found a surprisingly high incidence of CK enzyme rise and myopathy in this group of mechanically ventilated patients with severe asthma.(ABSTRACT TRUNCATED AT 250 WORDS)
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