Beachey: Respiratory Care Anatomy and Physiology, 2nd Edition

Answers to Concept Questions

Chapter 13: Clinical Assessment of Acid-Base and Oxygenation Status

13-1	A pH of 7.50 indicates alkalemia. The PaCO2 of 38 mm Hg (respiratory component) is in the normal range and therefore cannot be responsible for the alkalemia. The alkalemia must be of metabolic origin.

13-2	A pH of 7.25 indicates acidemia. The HCO3 of 24 mEq/L is in the normal range and therefore cannot be responsible for the acidemia. The acidemia must be of respiratory origin.

13-3	The pH of 7.44 is in the normal range but on the alkalotic side of normal. Therefore the primary cause of the original acid-base disturbance is the component that would by itself cause alkalosis. The [HCO3] of 33 mEq/L (metabolic component) is the only component that can cause alkalosis. Therefore this blood gas is classified as a compensated metabolic alkalosis. The PaCO2 of 50 mm Hg (hypoventilation) is the appropriate compensatory response.

13-4	Compensation refers to the body’s natural response to an acid-base imbalance. Correction refers to therapeutic action taken by health care personnel to restore normal acid-base balance.

13-5	Arterial hypoxemia (PaO2 lower than 60 mm Hg) stimulates the carotid body chemoreceptors, increasing ventilation. In the process, hyperventilation may occur, creating respiratory alkalosis.

13-6	Such a misinterpretation would draw attention away from the underlying respiratory problem (i.e., some process is producing an increased drive to breathe), resulting in hyperventilation. One must focus on possible causes for an increased ventilatory drive. What is the probable source of respiratory distress? If the problem is misinterpreted as a primary metabolic alkalosis, health care personnel may inappropriately take action to reduce the arterial pH.

13-7	When the H+ ions of fixed acids accumulate, they react with HCO3 ions, which reduces plasma HCO3 concentration. Thus the total number of routinely measured plasma anions decreases, creating an apparent “anion gap.” Anion gap = [Na+]  ([Cl] + [HCO3]).

13-8	The intravenous administration of NaHCO3 (a base) in the severely acidotic person would cause HCO3 to buffer H+ ions and drive the hydrolysis reaction to the left, ultimately generating CO2. This situation would call for an increased minute ventilation to rid the body of the excess CO2.

13-9	The measured in vitro standard bicarbonate (SB) is falsely low in the hypercapnic person for this reason: When the blood sample’s PCO2 is lowered to 40 mm Hg in the laboratory setting, the [HCO3] falls slightly due to the hydrolysis effect. If this decrease in [HCO3] were to occur in the body’s capillaries, extravascular HCO3 would diffuse into the blood. But in the laboratory in vitro setting there is no “extravascular” HCO3 that can diffuse into the plasma; thus a measured in vitro laboratory SB is lower than the [HCO3] would be in actual in vivo conditions. On the other hand, the measured in vitro SB is falsely high in the hypocapnic person; in this case the blood sample’s PCO2 would be increased to 40 mm Hg in the laboratory setting. The resulting increase in HCO3 ions stays in the blood sample because they obviously cannot diffuse into extravascular space as they would in the body.

13-10	The body’s tissue cells cannot take up oxygen from the blood in histotoxic poisoning (e.g., cyanide poisoning); thus venous blood oxygen content is abnormally high, decreasing the difference between arterial and venous oxygen contents.

13-11	If the PaO2 is 100 mm Hg, but the blood’s hemoglobin concentration is only 5 g/dL, the blood would have a very low oxygen content and tissue oxygenation would suffer. Likewise, even with a normal CaO2 a very low cardiac output would decrease the amount of oxygen delivered to the tissues each minute, and again tissue oxygenation could suffer.

13-12	Rapidly flowing blood spends less time in contact with the oxygen-consuming tissues than more slowly flowing blood. Therefore each deciliter of blood perfusing the tissues loses less oxygen than it would if blood were flowing more slowly. Thus C{vbar}O2 rises as cardiac output increases.