Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 12: Ventilation-Perfusion Relationships and Arterial Blood Gases

12-1	A decrease in  with respect to  represents hypoventilation, which increases the PaCO2.

12-2	Hyperventilation is located on the high  side (i.e., the right side of the continuum). This represents ventilation in excess of blood flow.

12-3	A mixture of the end-capillary blood from all alveoli in the lungs comprises the pulmonary venous blood, which flows to the left atrium, and then to the left ventricle where it is pumped into the systemic circulation; this blood is commonly called arterial blood.

12-4	In the hypothetical situation in which no shunt exists (the “ideal” lung), breathing 100% oxygen would maximally saturate the hemoglobin of arterial blood. (This situation never exists in reality.) Even poorly ventilated regions eventually attain high PO2s if 100% oxygen is breathed.

12-5	Blood perfusing absolute shunt units (nonventilated alveoli) cannot acquire additional oxygen and thus remains identical to venous blood. This “venous” blood then mixes with the oxygenated blood coming from normal, ventilated lung units, ultimately lowering the arterial PO2. Alveolar gas PO2, on the other hand, remains fixed because it is determined by the FIO2 (i.e., the PAO2 remains unchanged as long as FIO2 stays constant). Thus if the number of nonventilated or shunt units increases, the difference between alveolar PO2 and arterial PO2 (P[A-a]O2) also increases.

12-6	Overall hypoventilation uniformly lowers the PO2 in all alveoli. The PO2 of blood perfusing hypoventilated alveoli equilibrates with this low alveolar PO2, producing arterial hypoxemia. In this situation the PaO2 decreases proportionally with the PAO2, and the difference between these two PO2s does not change.

12-7	Any condition that causes alveoli to become airless creates shunt. Such conditions include alveolar collapse (atelectasis) and alveolar filling or consolidating processes (e.g., pneumonia).

12-8	When compliance varies from region to region throughout the lungs, inspired gas selectively flows to the most compliant areas, leaving low-compliance regions underventilated. These underventilated regions have low  ratios, which means blood passing through these areas is hypoxemic. This hypoxemic blood mixes with oxygenated blood from well-ventilated lung units, causing some degree of arterial hypoxemia (depending on the number of underventilated alveoli).

12-1	
12-9	Alveolar dead space would decrease the mixed expired gas PCO2. Alveolar carbon dioxide originates from the pulmonary capillary blood. Alveoli with no blood flow thus have extremely low PCO2s; gas exhaled from these dead-space alveoli mixes with gas coming from normal alveoli that contain carbon dioxide; the end-result is a mixed expired PCO2 below normal.

12-10	Consider the following shunt equation:

The numerator is directly influenced by the number of nonventilated alveoli present (i.e., as this number increases,  decreases because of the increased blood contribution from nonventilated alveoli). Thus atelectasis affects the numerator. Changes in  directly influence the denominator. The oxygen delivery rate (cardiac output) and tissue oxygen consumption rate determine ; as cardiac output decreases, the tissues extract more oxygen from each deciliter of blood, lowering the . Thus low cardiac output affects the denominator.