Chapter 29 - Disorders of Ventilation & Gas Exchange

• tension pneumothorax occurs when the intrapleural pressure exceeds atmospheric pressure
• the scenario of tension pneumothorax describes an injury to the chest that permits air to enter but not to leave the pleural space, which results in a rapid increase in pressure in the chest with compression atelectasis of the unaffected lung, a shift in the mediastinum to the opposite side of the chest, and compression of the vena cava with impairment of venous return to the heart and reduced cardiac output
• tension pneumothorax is a life-threatening condition
• emergency treatment of tension pneumothorax involves the prompt insertion of a large-bore needle or chest tube into the affected side of the chest along with one-way valve drainage or continuous chest suction to aid in lung reexpansion
• during an asthma attack, the airways narrow because of bronchospasm, edema of bronchial mucosa, and mucus plugging
• expiration during an asthma attack becomes prolonged because of progressive airway obstruction and, due to a narrowed airway and ineffective gas exchange, wheezing is noted
• during a prolonged asthma attack, air becomes trapped behind the occluded and narrowed airways, causing hyperinflation of the lungs
• as a result of hyperinflation of the lungs due to a prolonged asthma attack, more energy is needed to overcome the tension already present in the lungs, and the accessory muscles are used to maintain ventilation and gas exchange, which causes dyspnea and fatigue
• symptomatology of asthma is substantial
• the physical signs of bronchial asthma vary with the severity of the attack
• respiratory tract infections, especially those caused by viruses, may produce their effects by causing epithelial damage and stimulating the production of IgE antibodies to ward the viral antigens
• in addition to precipitating an asthmatic attack, viral respiratory infections increase airway responsiveness to other asthma triggers that may persist for weeks beyond the original infection
• severe hypoxemia causes reflex vasoconstriction of the pulmonary vessels and further impairment of gas exchange in the lungs
• severe hypoxemia is more common in persons with the chronic bronchitis form of COPD
• hypoxemia stimulates RBC production, causing an increase in RBC and hematocrit values
• in severe hypoxemia, the increase in pulmonary vasoconstriction and subsequent elevation in pulmonary artery pressure further increase the work of the right ventricle; as a result, persons with COPD may develop right-sided heart failure with peripheral edema (i.e., cor pulmonale)
• oxygen therapy is prescribed for selected persons with significant hypoxemia
• administration of continuous low-flow oxygen (1 to 2 L/min) to maintain arterial PO2 levels decreases dyspnea and pulmonary hypertension and improves neuropsychological function and activity tolerance
• because the ventilatory drive associated with hypoxic stimulation of the peripheral chemoreceptors does not occur until the arterial PO2 has been reduced to about 60 mmHg or less, increasing the arterial PO2 level above 60 mmHg tends to depress the hypoxic stimulus for ventilation and often leads to hypoventilation and CO2 retention
• hypoventilation due to the decreased respiratory rate of 4 to 6 breaths/min can cause high PCO2 and low PO2
• hypoventilation almost always causes an increase in PCO2
• the increase in PCO2 due to hypoventilation is directly related to the level of ventilation
• if reduction of ventilation is by one half, this will cause the doubling of PCO2