Cardiopulmonary Physical Therapy, Volume 1Scot Irwin, Jan Stephen Tecklin Mosby, 1985 - 473 pagine |
Dall'interno del libro
Risultati 1-3 di 59
Pagina 186
... alveolar air because carbon dioxide is constantly being added to the alveolar air by the blood . During normal breathing the av- erage partial pressure of alveolar carbon dioxide ( PACO2 ) is 40 mm Hg . If the carbon dioxide production ...
... alveolar air because carbon dioxide is constantly being added to the alveolar air by the blood . During normal breathing the av- erage partial pressure of alveolar carbon dioxide ( PACO2 ) is 40 mm Hg . If the carbon dioxide production ...
Pagina 190
... alveolar septa . The short , wide , intersect- ing capillaries maximize the exposure of the blood to the alveolar air . Finally , oxygenated blood is collected by the pulmonary veins and emptied into the left atrium . The veins are ...
... alveolar septa . The short , wide , intersect- ing capillaries maximize the exposure of the blood to the alveolar air . Finally , oxygenated blood is collected by the pulmonary veins and emptied into the left atrium . The veins are ...
Pagina 191
... alveolar air . With advancement toward the more dependent portions of the lung , the intracapillary pressures increase , and flow increases . In zone III , or the dependent portion of the lung , venous hydrostatic pres- sures exceed ...
... alveolar air . With advancement toward the more dependent portions of the lung , the intracapillary pressures increase , and flow increases . In zone III , or the dependent portion of the lung , venous hydrostatic pres- sures exceed ...
Sommario
an overview of the basic mechanism | 6 |
Physical therapy for the child with respiratory 21 Respiratory rehabilitation of the patient with a spinal | 18 |
Hemodynamics | 19 |
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abnormal activity acute addition airway alveolar alveoli angina arrhythmias assessment associated blood pressure breathing capacity cardiac output cardiac rehabilitation cause cells changes Chapter chest chronic Circulation clinical complete complications continued contraction coronary artery disease decrease depression determined develop discussed disease drainage drugs effects evaluation exercise testing factors failure flow force function further heart rate hypertension important improve increased indicate initial inspiration intensity involved less limited load lower lung major maximal measured mechanical minutes monitored muscle myocardial infarction normal obstructive occur oxygen pain patient peak performed peripheral phase physical therapy position prevent produce progression pulmonary reduced resistance respiratory response Resting rise risk secretions segment severe significant signs sounds surgery symptoms systolic Table therapist thoracotomy tients tion tissue tolerance treatment usually vascular venous ventilation ventricular volume wall