CPR 57-58 - Ventilation Perfusion Inequality, Hypoxaemia, Buffers, and pH Homeostasis Flashcards
List the normal values for alveolar ventilation, perfusion, V/Q ratio, and the alveolar-arterial oxygen gradient.
VA - 4 L/min
Q - 5 L/min
V/Q ratio = 0.8
A-a O2 gradient - 5 to 15 mm Hg
Why does an A-a O2 gradient exist?
Venous admixture from shunts and variations in the V/Q ratio
Differentiate physiological dead space from a physiological shunt.
Physiological dead space results in some air not participating in gas exchange
A physiological shunt results in some blood not being fully oxygenated
Where in the lung is gas exchange most efficient and why?
Gas exchange is most efficient at the apex because of the high V/Q ratio. There isn’t enough Q to mop up all the O2 from the high V so the blood that does go through the apex gets the best oxygenation.
List the two primary ways the lungs try to normalize the V/Q ratio.
If the V/Q ratio is low then hypoxic vasoconstriction will decrease Q, causing blood to be redirected to other parts of the lung.
If the V/Q ratio is high then bronchoconstriction will decrease V to the poorly perfused areas
Providing supplemental oxygen to a patient with hypoxemia would be most useful if the patient’s hypoxemia was caused by which of the following:
Increased Dead Space
High V/Q
Low V/Q
V/Q = 0
V/Q = infinity
Low V/Q
Write out the alveolar gas equation.
Write out the hypoxemia diagnosis flow chart.
What is the general effect on pCO2 and PO2 when the V/Q ratio is increased or decreased?
V/Q > 1 leads to increased pO2 and decreased pCO2
V/Q < 1 leads to decreased pO2 and increased pCO2
Describe what occurs within the body over a 3 day period after a rapid ascent to 12,500 feet.
Hypoxemia develops initially which stimulates ventilation. This causes pCO2 to decline and a respiratory alkalosis to develop which counters the increase in ventilation caused by the initial hypoxemia.
Over 2-3 days, HCO3- secreation by the kidneys and choroid plexus bring blood and CSF pH back to normal. This then allows the hypoxia to increase ventilatory drive again.
Describe how the body adapts to high altitudes in the long term.
The low pO2 stimulates the kidneys to release EPO which stimulates RBC production by the bone marrow
2,3-BPG levels rise resulting in an increase in the P50 of hemoglobin
Describe the pulmonary effects of moutain sickness.
Pulmonary hypoxic vasoconstriction increases pulmonary vascular resistance. This coupled with increased CO drastically increases pulmonary BP which leads to pulmonary edema.
Describe the cerebral effects of mountain sickness.
Cerebral circulation is sensitive to hypocapnia and it causes cerebral vasoconstriction. Combine this with low blood pO2 and headaches and confusion develops. Eventually the low pO2 will lead to cerebral vessel dilation and hyperperfusion of vessels which increases the likelihood of cerebral edema.
What is normal blood pH and [H+]?
pH = 7.35 - 7.45
[H+] = 35-45 nmol/L
At what pH range is a buffer effective?
plus or minus one pH unit of the buffer’s pKa
What does it mean when the pH of a solution is equal to the pKa of a buffer?
That the [HA] = [A-]
When/Where are acidic and basic drugs best absorbed and excreted?
Acidic drugs are best absorbed in the stomach and basic drugs are best absorbed in the intestine because they are neutral at those pHs.
Acidic drugs are best excreted in alkaline urine and basic drugs are best excreted in acidic urine because of ion trapping.
What are the major buffer systems of the body?
- Bicarbonate-carbonic acid buffer system
- Hemoglobin (histidine)
- Phosphate buffer system
- Other proteins with histidine residues
What is the pKa of bicarbonate? What is the ratio of [HCO3-] to [H2CO3] at physiological pH?
pKa - 6.1
20:1
What is normal [HCO3-]?
22-25 mEq/L
How is the value of [H2CO3] calculated?
0.03 x pCO2
Why is it that the bicarbonate buffer system can be used to fix respiratory acidosis since respiration is the initial problem?
The respiratory system actually only regulates the pCO2, it is the renal system that regulates HCO3-. It is because of this that HCO3- functions as the most important physiological buffer
What happens to most of the H+ created by the CA reaction?
The histidines on Hb mop it up
What drives the CA reaction in the reverse direction?
In the lungs, the high pO2 forces oxygen to bind HHb which forms oxyHb and the release of H+. Combine this with the decreasing pCO2 and the CA reaction begins to react in reverse.
Briefly describe how the kidneys can regulate blood pH.
- Filtered HCO3- is almost completely reabsorbed
- Kidneys can secrete H+
- Kidnes can synthesize new HCO3- to replenish HCO3- lost by buffering of nonvolatile acids (sulfate/lactate)
Describe how the kidneys reabsorb filtered bicarbonate and which drug can inhibit this process.
- The CA rxn converts bicarb back into CO2 in the tubular lumen
- CO2 is reabsorbed
- The CA rxn, in the cell, converts CO2 back into bicarb and H+
- H+ is secreted back into the lumen and bicarb is reabsorbed
The drug acetazolamide inhibits CA which would preven the reabsorption of bicard.
Describe how the kidneys secrete H+ without drastically lowering urine pH. What drug can inhibit this process?
The kidneys also filter HPO4-2 which acts as a buffer. This allows the kidneys to secrete H+ as acid phosphate, H2PO4-, without drastically lowering urine pH.
Since acetazolamide is a CA inhibitor it can inhibit the secretion of H+ as well
Describe the two ways the kidneys can create “new” bicarb to add to the blood.
- When H+ is secreted into the lumen using the phosphate buffer system, bicarb is also reabsorbed
- During periods of prolonged acidosis, the tubular cells will use glutaminase to cleave ammonia off of glutamine. Ammonia will freely difuse into the tubular lumen where H+, created by the CA reaction in the tubular cells, will react with it to form ammonium which will be excreted as ammonium chloride. During this process, HCO3- is also made and reabsorbed. Acetazolamide can also inhibit this process.
