Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 14: Physiological Basis for Oxygenation and Lung Protection Strategies

14-1	Oxygen therapy is less effective in absolute shunt than in /  mismatch because areas of absolute shunt in the lungs receive no ventilation at all; therefore blood perfusing these areas cannot become oxygenated, no matter how high the administered FIO2. On the other hand, in /  mismatch alveoli are still ventilated, even though they are underventilated; this means that supplemental oxygen can still reach these alveoli, raise their PO2, and subsequently, raise the blood PO2.

14-2	Pulmonary edema of congestive heart failure is of the hydrostatic (high pressure) type; there is no damage to the alveolar-capillary (AC) membrane in this type of edema. High pressure drives intravascular fluid across an intact AC membrane that is impermeable to large plasma protein molecules. Thus edema fluid has a relatively low osmotic pressure. In contrast, in acute respiratory distress syndrome (ARDS) the AC membrane is damaged and highly permeable to intravascular fluids, including large-molecular-weight proteins. The high protein content of ARDS edema fluid increases its osmotic pressure, causing even more intravascular fluids to be drawn across the AC membrane. Thus pulmonary edema in ARDS (high-permeability edema) is generally more severe and more difficult to treat than hydrostatic edema.

14-3	Even though acute respiratory distress syndrome is more of an oxygenation problem than a ventilation problem, the processes that produce the oxygenation problem (pulmonary edema, alveolar flooding, and atelectasis) greatly decrease lung compliance and increase the work of breathing. Ultimately mechanical assistance is required to administer end-expiratory pressure therapy, which reduces alveolar collapse, improves lung compliance, and eases the work of breathing. Mechanical ventilation may also be required to forestall overt ventilatory failure due to fatigue of the ventilatory muscles.

14-4	In absolute shunt the alveoli are completely airless, often because they are collapsed. Continuous positive airway pressure and positive end-expiratory pressure can prevent alveolar collapse and possibly reopen them, thus improving oxygenation. In /  mismatch, the affected alveoli are still open and ventilated; thus therapy aimed at reopening alveoli is not appropriate in treating nonshunt oxygenation problems such as pure /  mismatch; instead, therapy should be aimed at improving airway patency to improve ventilation (e.g., secretion mobilization techniques, bronchodilator administration).

14-1	
14-5	A given force is required to inflate an individual’s lungs to 1000 mL; for example, if a distending pressure of 10 cm H2O is required to inflate the lungs to 1000 mL, it does not matter how that pressure is generated; it is simply necessary to create a pressure difference of 10 cm H2O across the lung (i.e., the PA  Ppl must equal 10 cm H2O). A spontaneous breath that inflates the lung to 1000 mL must of necessity generate precisely the same pressure difference across the lung as a mechanically induced lung inflation of 1000 mL; it should be apparent that in this example both types of breaths place exactly the same stress on the alveolar epithelium.

14-6	When chest wall and diaphragm movements are abnormally restricted, the pleural pressure rises in proportion to the alveolar pressure during mechanical lung inflation; thus the pressure that distends the lung (i.e., the PA  Ppl) is not unduly increased, and absolute alveolar pressures higher than 30 cm H2O can be tolerated safely.

14-7	Alveolar epithelial injury in acute respiratory distress syndrome causes local inflammatory mediators to be released into the blood, such as tumor necrosis factor-alpha (TNF-alpha), a key cytokine that mediates the effects of sepsis. Such inflammatory mediators affect not only the lung but may also affect the function of distal body organs and lead to multisystem organ dysfunction syndrome (MODS).

14-8	Sodium bicarbonate infusion can lead to higher PaCO2 if ventilation is not increased to accommodate the additional CO2 generated by bicarbonate buffering of H+ ions.

14-9	Patients with acute respiratory distress syndrome with lobar and patchy distributions of atelectasis and infiltration are more likely to respond positively to prone positioning than are patients with diffuse uniform patterns of atelectasis and infiltration. The effectiveness of prone positioning depends on the redistribution of densities, such that previously unventilated units with blood flow become ventilated; this phenomenon is less likely to occur in patients with a widespread, diffuse pattern of density.

14-10	The inspiratory flow pattern produced by pressure-targeted mechanical ventilation is called a decelerating or a descending ramp pattern; it is created by a progressively decreasing flow rate as inspiration proceeds. In pressure-targeted ventilation, the maximum ventilation pressure is abruptly applied to the airway opening and held constant at that level for the duration of the inspiratory phase. (The newest ventilators allow the operator to select a less abrupt, more gradual rise to the maximum pressure; i.e., the rise time is adjustable.) During lung inflation the alveolar pressure rises until it equalizes with the pressure held at the airway opening, creating a progressively decreasing difference between endotracheal tube pressure and alveolar pressure (i.e., the pressure that drives flow into the lungs decreases steadily as inspiration proceeds). Hence, inspiratory flow begins at a relatively high rate and falls steadily toward zero as alveolar pressure equalizes with endotracheal tube pressure; this explains the creation of the descending ramp flow pattern.