Ventilation Perfusion Matching copy

Ventilation Perfusion Matching- Dean 02/25/11 The low PO2 may be due to: **know 4 causes 1. Hypoventilation 2. Impairment of diff d iffusion usion 3. Intrapulmonar y shunting (R-L shunting) 4. V/Q mismatching 1. Hypoventilation- Alveolar ventilation lower than relative metabo lic demands. Due to over- anesthesia, narcotics, neuromuscular disorders (weak so

no

vent ilation on in parts) pumping action), lung diseases(reduced ventilati 2. Diffusion impairment- think Fick eq. Increased thickness will decrease diffusion. Due to: fibrosis, fibrosis, sarcoidosis- inflammation that produces tiny lumps of  cells, asbestosis (chronic inflammatory and fibrotic medical condition brought on by inhaling asbestos fibers), edema 3. Intrapulmonar y shunting(venous admixture)- Alveoli not ve ntilated. High CO2 blood bypasses lung and mixes with the O2 rich blood so get mixed venous and arterial blood. Cannot be fixed with pure O2. Due to airway blockage (mucus), lung diseases (bronchospasm, alveolar edema) 4.Ventilation/Perfusion 4.Ventilation/Perfusion Mismatching ± Low PO2 and high CO2 in that area of  lung due to low gas exchange. Low PO2 relative to blood flow so low V/Q. Normal value= 1. ***This is the most common cause of hypoxemia in patients with lung diseases. When in doubt, answe is V/Q mismatch Ventilation/Pefusion Ratio (V/Q): (V/Q): The pressures of gases(O2 and CO2) in the blood blood depends on the V/Q ratio and not on o n the individual amount of perfusion and vent ilation. ilation. Effect of Altering V/Q Ratio on PO2 and PCO2: Normal V/Q- value is 1. The PO2 becomes becomes 100 mm Hg and PCO2 becomes 40 mm Hg in the blood and in the aveloli after equili equ ilibrium brium is reached. is decreased by obstructing ventilation. Alveolar gas will be the sa me as Low V/Q- The V/Q ratio is the deoxygenated arterial blood with PO2 = 40 and PCO2 = 45. High V/Q- The V/Q ratio is increased by obstructing blood flow. Alveolar gas w ill be the same as the inhaled air so PO2 = 150 and PCO2 = 0. The left correlates to low V/Q and match the blood- PO2 = 40 and PCO2 = 45. The right correlates to high V/Q with PO2/CO2 values matching air- PO2 = 150 and PCO2 = 0. In an upright lung, the apex has a high V/Q ratio and there fore has a high PO2, low PCO2,. The base has

a low V/Q ratio and there for has a low PO2, high PCO2. The base also has more ventilation and more perfusion than the apex. But the slopes at which Q and V change are different and therefore the rate are different. The rate of change of perfusion is much greater than the rate of change of vent ilation (more of a slope) because fluid is heavy than blood so it pools at the base more.

V/Q inequality in normal lungs results in depression of arterial PO2. A-a gradient is due to V/Q mismatch and anatomical shunting. It is normally around 10 mm Hg. Low V/Q units -5 mmHg Anatomical shunting- 5 mmHg. ±Systemic venous blood mixes with systemic arterial blood. - bronchial circulation  pulmonar y vein  systemic arterial blood (now with a lower O2) -coronar y circulation  thebesian veins  L ventricle and atrium(now goes to the body) Large A-a difference and V/Q mismatch =main cause of hypoxmia. A-a gradient increases with age and lung diseases. **peripheral chemoreceptor respond to O2, CO2, and pH while central chemorceptors are more sensitive to CO2. Effect of V/Q Inequality on O2 & CO2 Exchange in Diseased Lungs- low V/Q units increase in number  PO2 decreases and the PCO2 increases stimulates chemoreceptors  increase alveolar ventilation CO2 back to normal BUT O2 will remain low. How is an increase in vent ilation to lungs with V/Q inequality effective at reducing the PCO2 of arterial blood but ineffective at raising its PO2? Can be explained by the shapes of the O2 and CO2 dissociation curves.

O2 Example- Alveolus A has no ventilation due to a shunt. Alveolus B is normal. The blood from both of  these alveoli is mixing together to lower the PO2. Hyperventilation is caused due to peripheral can only affect alveolus B. But alveoli B is lying on the platau stage of the O2 dissociation curve so increase ventilation does not make a huge difference. Therefore the mixed bloods are still hypoxic even though ventilation was increased. The increase from alveolus B is so small that is cannot pull the mixture up even though Alveolus A sits on the steep part of the curve.

CO2 Example: Alveolus A has no ventilation, alveolus B is normal. A small change makes a big difference due to the linear curve. So CO2 is more readily compensated for.

Increase in ventilation to normal or high V/Q units can compensate for low or zero V/Q units and return arterial CO2 to normal (or below), but cannot return O2 to normal.Because of the transport characteristics of  O2 and CO2 in the blood, as represented by their dissociation curves. Elevated arterial CO2 is observed only when alveolar ventilation is severely impaired (hypoventilation) so high CO2 is not an issue unless there are lots of shunts in lung. Hypoxic vasoconstriction occurs when there is low amount of PO2 in the alveolus. It is beneficial in early to middle stages of lung disease because it redirects blood flow from poorly ventilated area to a better  ventilated area. But pulmonar y vascular resistance increases eventually leading to right side heart failure. Low alveolar CO2 will cause constriction of airway smooth muscle. This is useful when there is a blocked arter y and no blood getting to the alveolus. It compensates for a high V/Q by constricted the smooth muscle in the alveolus and redirecting air to areas with more blood flow.

1. Pure O2 will not fix a. Hypoventilation b. Impairment of diffusion c. Intrapulmonar y shunting (R-L shunting) d. V/Q mismatching

2. Most common cause of hypoxemia a. Hypoventilation b. Impairment of diffusion c. Intrapulmonar y shunting (R-L shunting) d. V/Q mismatching

1. C 2. D Objectives: Discuss changes in lung function that can lead to low O2 in systemic arterial blood (hypoxemia). Explain regional gas exchange in normal lungs. Describe how V/Q mismatching can lead to arterial hypoxemia and only minor changes in arterial CO2.