By M Jones; F Moffatt
content material: part 1: evaluate instruments part 2: Pathophysiology part three: Physiotherapy suggestions and Adjuncts part four: Case stories and Self-Assessment
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Extra resources for Cardiopulmonary physiotherapy
F. oxygen therapy). Related topics ACBT +/- manual techniques (p. 71); CPAP (p. 76); GAP (p. 129); IPPB (p. 99); Mobilization (p. 113); Mechanical ventilation (p. 109); NIPPV (p. 118); Oxygen therapy (p. 122); Positioning to maximize ventilation-perfusion ratio (p. 136). J. and Liu SF. (1995) Regulation of pulmonary vascular tone. Pharmacol Rev 47:87–131. , Harris T. et al. (1985) Early predictors of ARDS reversal in patients with established ARDS. Am Rev Resp Dis 131: A143 (abstract). P. (1961) Respiratory gases in the regulation of the pulmonary circulation.
1995) Pulmonary Pathophysiology. 5th edition. Williams and Wilkins, Baltimore. B. (2000) Respiratory Physiology—The Essentials. 6th edition. Lippincott, Williams and Wilkins, Philadelphia. CHEST WALL DEFORMITY OR DISRUPTION Description Collectively, the sternum, thoracic vertebrae, 12 pairs of ribs and the interposing intercostal muscles form the outer chest wall. The chest wall plays a multiple role in maintaining effective ventilation. Any disruption to the chest wall may lead to mechanical dysfunction and ineffi-cient ventilation.
The release of aldosterone stimulates the retention of salt and water by the kidney, further increasing circulating volume, which may compound the problem of increased preload. Higher centers in the brain are also sensitive to a fall in cardiac output, via highand lowpressure baroreceptors which stimulate activation of the sympathetic nervous system (SNS). The production of norepinephrine (noradrenaline) is increased, producing both inotropic (strength of contraction) and chronotropic (frequency of contraction) effects on the heart in an attempt to compensate for the reduced cardiac output.