Question 6.
The physiological dead space is:The PCO2 is used, not the PO2.The answer is C. - often increased in lung disease
Back to Questions
Question 7.
Hypoxic pulmonary vasoconstriction:Although the mechanism of hypoxic pulmonary vasoconstriction is not fully understood, we know that central nervous connections are not required because the phenomenon can be demonstrated in isolated lungs. Therefore, choice A is incorrect.The answer is B. - improves matching of ventilation and blood flow in some lung diseases.
Choice B is correct. Suppose a lobe or lobule of lung is poorly ventilated because of partial bronchial obstruction. The resulting alveolar hypoxia will reduce the blood flow through the mechanism of hypoxic pulmonary vasoconstriction. The result is improvement in the matching of ventilation and blood flow.
Choice C is incorrect. Reducing the PO2 of the blood entering the lung results much less vasoconstriction than reducing the PO2 of alveolar gas.
Choice D is incorrect. Hypoxic pulmonary vasoconstriction is important in the perinatal period. When the newborn baby makes the transition from placental to air breathing, it is important for pulmonary vascular resistance to fall precipitously within a few seconds. As a consequence, pulmonary blood flow dramatically increases from its value of only about 15% of the cardiac output in utero. The increase in pulmonary blood flow is assisted by closure of both the ductus arteriosus and the foramen ovale.
Back to Questions
Question 8.
Pulmonary vascular resistance increases:Pulmonary vascular resistance increases at high altitude as a result of the global alveolar hypoxia. The exact mechanism is still unknown but is apparently a local effect on the smooth muscle of the pulmonary arterial wall. The increase causes right ventricular hypertrophy with characteristic ECG changes.The answer is A. - at high altitude.
Pulmonary vascular resistance during space flight would, if anything decrease as blood flow becomes more uniform. Anemia would decrease viscosity - a term in the resistance formula during exercise, pulmonary capillaries would distend causing resistance to fall.
With exercise, pulmonary arterial pressure tends to rise causing recruitment and distension of pulmonary vessels leading to a fall in pulmonary vascular resistance.
Back to Questions
Question 9.
In a subject with normal lungs, which of the following (acting alone) would have the greatest effect on O2 delivery (arterial o2 concentration x cardiac output)?Halving alveolar ventilation would double alveolar PCO2 and therefore reduce alveolar and arterial PO2 but not enough to halve arterial O2 content. Also, hypoxia would stimulate cardiac output via sympathetic stimulation of heart rate.The answer is D. - hemoglobin reduced to 50% of normal.
A 50% right to left shunt would also lower arterial O2 content but not by 50% since the shunted blood (venous blood) has a significant amount of oxygen (normally about 75% saturated).
Doubling inspired O2 - if you picked this choice …………@#$%!!!!.
Reducing hemoglobin concentration to half normal would reduce arterial O2 content (at any saturation) to half normal, therefore choice D is correct.
Back to Questions
Question 10.
A patient is breathing air at sea level and has a respiratory exchange ratio of 1.0. The arterial blood values are:The alveolar PO2 is found from the alveolar gas equation:PO2 90 mm Hg PCO2 20 mm Hg pH 7.30These indicate that the:The answer is E. - all of the above.
PAO2 = PIO2 - PACO2/R
We can assume that the inspired PO2 is the sea level normal value of 149 mm Hg. Therefore, neglecting the small correction factor, the alveolar PO2 is 149 - 20/1 or 129 mm Hg. Thus the alveolar-arterial PO2 diffusion is 129 - 90 = 39 mm Hg.
The PCO2 of 20 mm Hg means that the patient is hyperventilating. The combination of the low PCO2 and low pH means that plasma bicarbonate concentration is reduced (Henderson-Hasselbalch equation
pH = pK’ = log [HCO3-]/(PCO2 x a)
The data would fit a metabolic acidosis with partial respiration compensation.
Back to Questions
Question 11.
In a patient with anemia and normal lungs:A patient with anemia and normal lungs typically has a normal arterial PO2. Thus, choice A is incorrect. Because the position of the oxygen dissociation curve is typically normal, the arterial oxygen saturation is also normal and thus, choice C is incorrect.The answer is D. - PO2 of mixed venous blood is reduced.
From the Fick principle:
O2 = x (CaO2 - CO2)If the oxygen consumption and cardiac output are normal, the arterial-venous O2 concentration difference will also be normal. Thus, choice B is incorrect. As a matter of fact, cardiac output is sometimes reflexly increased in anemia, and if this occurs, the arterial-venous O2 concentration difference will be decreased.
Choice D is correct. Although the arterial PO2 is typically normal, the PO2 of mixed venous blood must fall. This is because the venous oxygen concentration falls to a very low level as the normal amount of oxygen is extracted, and thus the venous PO is abnormally low.
Back to Questions
Question 12.
Features of mild carbon monoxide poisoning include:Carbon monoxide poisoning causes some of the hemoglobin in the blood to be combined with CO to give carboxyhemoglobin. As a result, there is a decreased arterial O2 concentration (choice D is correct). However, it is important to realize that this does not decrease the arterial PO2. In this respect, carbon monoxide poisoning is similar to anemia where again the arterial PO2 is typically normal but the arterial oxygen concentration is reduced.The answer is D. - decreased arterial O2 concentration.
Choice B is not correct. There is an increase in the affinity of the hemoglobin for oxygen as evidenced by the leftward shift of the oxygen dissociation curve. Thus, carbon monoxide poisoning causes a fall in tissue PO2 for two reasons: first less oxygen is carried in the arterial blood, and second the unloading is impeded by the higher hemoglobin affinity.
Choice C is incorrect. Ventilation is unaffected in mild carbon monoxide poisoning; the chemoreceptors respond primarily to the arterial PO2 and, because this is normal, ventilation remains essentially unchanged.
The word “mild” is included in the stem of the question because with very severe carbon monoxide poisoning there may be brain damage which may alter ventilation.
Back to Questions
Question 13.
The increase in ventilation which occurs immediately following ascent to high altitude:The increase in ventilation which occurs immediately following ascent to high altitude is caused by stimulation of the peripheral chemoreceptors by the arterial hypoxemia. Because of the very high blood flow per tissue mass of the carotid chemoreceptors, they essentially respond to arterial PO2 and therefore choice C is incorrect.The answer is D. - increases still further over the course in the next 1-3 days.
The increase in ventilation is partly inhibited by the resulting fall in PCO2 which causes a rise in pH of the CSF. This reduces the stimulation of the central chemoreceptors which works against the increased drive from the peripheral chemoreceptors. However, after a day or so, the pH of the CSF is reduced to some extent by the outward movement of bicarbonate and thus this inhibitory effect on the central chemoreceptors is diminished. Consequently, ventilation increases still further over the course of the 1-3 days.
The increase in ventilation is not caused by the reduced work of breathing the less dense air though it is true that the work of breathing is reduced to some extent at high altitude. If a subject is asked to breathe as fast and as deeply as he can for 15 seconds, it can be shown that the amount of air that is exhaled (measured at BTPS) is greater at high altitude than at sea level, but this does not cause increased ventilation.
Back to Questions
Question 14.
In a patient with stable chronic lung disease, elevated PaCO2 and decreased PaO2:Many patients with chronic lung disease have chronic hypoxemia and chronic CO2 retention with an elevated arterial PCO2. Typical values might be an arterial PO2 in the 40s or 50s and an arterial PCO2 in the 50s. Such a patient may have the pH of his CSF near the normal value of about 7.32. Although the pH may have fallen in the initial stages of hypercapnia, the arterial PCO2 is often stable at the high value for so long that the pH of the CSF returns to near normal as a result of an increase in CSF bicarbonate concentration. Therefore, choice A is correctThe answer is D. - All of these.
Such a patient has a reduced ventilatory response to CO2. Indeed this is one reason why there is chronic CO2 retention. Part of the reason for the reduced ventilatory response is the near normal value of the CSF pH. Another reason is that such a patient often has severe airway obstruction with a markedly increased airway resistance. In this case, even if a raised arterial PCO2 causes an increase in the number of impulses to the ventilatory muscles from the respiratory center, they are unable to increase ventilation in the normal way because of the airway obstruction. Thus, choice B is correct.
C is correct. In these patients, the hypoxic ventilatory drive from the peripheral chemoreceptors is often the most important stimulus to ventilation. This has important practical consequences. If such a patient is brought into the emergency room and given oxygen to relieve his arterial hypoxemia, his main stimulus to breathing may be abolished, an he may develop lethal CO2 retention and respiratory acidosis. The best way to manage these patients is to give relatively small increases in oxygen concentration (typically 24 to 28 %) and to monitor the arterial PO2, PCO2 and pH carefully for signs of additional CO2 retention and respiratory acidosis.
Choice D is correct. These patients typically have an almost fully compensated respiratory acidosis, but the arterial hydrogen ion concentration is usually slightly increased.