3.1.3 Ventilation-Perfusion Match Flashcards
Inadequate matching of ventilation and perfusion leads to?
Decrease in the efficiency of the lung as a gas exchanger
When is the efficiency of the lung greatest?
The efficiency of the lung is greatest when the ventilation/perfusion (VA/Q) ratio is the same in all regions of the lung.
What are characteristics of the ‘ideal’ lung?
What is the difference between the characteristics of the ideal lung and the real lung?
What is Pc’ ?
Gas pressure at the arterial end of the pulmonary capillary
How will an increase in the VA/Q ratio effect PAO2 and Pc’O2?
O2 is delivered to the alveolo-capillary unit by the ventilation, and removed from the unit by the blood flow. An increase in the VA/Q ratio will raise PAO2 and Pc’O2; a decrease in VA/Q will have the opposite effect.
High VA/Q (hyperventilation) = high PAO2, low PACO2;
How will an increase in VA/Q affect PACO2 and Pc’O2 levels?
CO2 is delivered to the alveolo-capillary unit by the perfusion, and removed by the ventilation, accordingly, and increase in VA/Q will lower PACO2 and Pc’CO2 ‘ a decrease in VA/Q will have the opposite effect.
How does VA/Q change in altering levels of PCO2 and PO2?
As VA/Q increases from the ideal value, the composition approaches that of inspired air. You can see that PO2 increases and PCO2 decreases in roughly the same proportion.
Going on the other direction, as VA/Q decreases from the ideal, the composition approaches that of venous blood. In this case, large decreases in PO2 are accompanied by relatively small increases in PCO2. This means that pathological conditions associated with an increase of shunt units will result in larger decreases in PO2 and consequently in low arterial blood O2 content, while PCO2 will increase relatively less.
Blood flow and ventilation are highest in areas where V/Q is closest to what?
Under resting conditions, the normal lung as a whole has a VA/Q ratio close to 1: both alveolar ventilation and cardiac output are 5-6 L /min
This shows that most V and Q go to areas of the lung that have a VA/Q near 1, and that very little air or blood flow go to areas with VA/Q >> 5 or lower than 0.05.
What are the differences in VA/Q, PACO2, and PO2 in the top, bottom, and overall sections of the lung?
What are the two examples of VA/Q mismatch?
No ventilation with blood flow
Ventilation with no blood flow
What can occur if a section of lung receives blood flow but no ventilation?
The drawing on the left side, shows an area of the lung that does not receive ventilation but receives blood flow. This could be due to obstruction of a bronchus, or to atelectasis as in ARDS or pneumonia. As a result, blood flowing through this area does not pick up any O2 and does not loose any CO2 , and leaves the unventilated area with the same composition of the venous blood entering the lungs. When this stream of blood mixes with the blood leaving the well ventilated areas of the lungs, it tends to lower the PO2 and increase the PCO2 of the mixture. Blood flowing through unventilated areas has the same effect on blood oxygenation as a veno-arterial shunt that bypasses the lung.
What can occur if a section of the lung receives ventilation but no blood flow?
The drawing on the right shows the mirror image of the shunt: in this case an area of the lung receives ventilation but no blood flow. In this case the air ventilating the unperfused area does not exchange gas with blood and does not change in composition compared with the inspired air. The alveoli of the unperfused area behave as an extension of the airways, and constitute an additional dead space. The problem in this case is that blood is diverted to the rest of the lung, and ventilation in the rest of the lung must increase to adequately oxygenate the blood. Since we can not selectively alter ventilation to different portions of the lung, these patients must increase the ventilation to adequately oxygenate the blood. This is also an inefficient system because the air going to the unperfused area is wasted,
How can increased airway resistance affect VA/Q?
The left side shows a lung where airway resistance is greater in one side (A) than in another. Narrowing of airway occurs, for instance, in chronic bronchitis in which there is increased mucus secretion and swelling of the bronchial mucosa. The severity of these changes may vary throughout the lung. In this case, the airflow in and out of A will be lower than in B, and VA will be lower in A.
How can decreased compliance affect VA/Q?
If there are areas with different compliance (right side), the change in volume induced by a given increase in PTP will be lower in B (low compliance, stiff lungs) than in A, and VA will be lower in B
What can be common causes of abnormal pulmonary blood flow in disease?
What is the effect of increased number of dead space units on gas exchange ie ventilation and no blood flow?
Ventilation perfusion units with a high VA/Q ratio behave as an extension of the anatomic dead space. An extreme example is occlusion of a pulmonary artery branch (pulmonary embolism). This could happen when a blood clot in the venous side of the circulation dislodges and is carried by the blood to the lungs. The air ventilating the affected area does not loose O2 or gain CO2 because there is no blood flow with which gases can be exchanged. Cardiac output will be redirected to the open vessels. Ventilation to the perfused areas of the lung will increase, and, depending on the extent of the occlusion, blood may be relatively well oxygenated. The air coming from the non-perfused zone contains no CO2, and, when mixed with the air coming from the perfused area, will “dilute” the CO2 in the mixed expired air. The value of arterial PCO2 will reflect the PCO2 of the alveoli that receive blood (and CO2); accordingly, PECO2 will decrease, the difference between PaCO2 and PECO2 will increase, and the calculated VD/VE will increase.
Pulmonary embolism causing increased dead space will have what effect?
In this case a branch of the pulmonary artery is occluded, so blood flow to a sizable portion of the lung stops. Ventilation is increased and the section of lung that does have blood flow is able to ventilate well enough to maintain a normal PaCO2. The fraction of air coming from alveoli without capillary blood flow reduces the mixed expired PCO2 to one half. In other words, in this case, half of the air comes from areas without CO2; some of it is from the airways (anatomical dead space) but some is from the “alveolar” dead space.
The effect of this condition on arterial blood gases depends on whether the remainder of the lung is able to maintain a level of ventilation that will adequately oxygenate the blood and eliminate CO2; this, in turn, depends on the size if the unperfused area, and on the overall condition of the lung; this could occur in a healthy person with normal lungs (blood clot in a pregnant woman with varicose veins) or in a person with lung disease. When VD/VT is >0.6, patients are usually ventilated artificially because they can not maintain adequate ventilation.
Typically these patients show relatively low PaO2 (70-80 mmHg) without much of an increase in PaCO2 or even low PaCO2. The drop in PaO2 may be due to diffusion impairment brought about by the decrease in pulmonary transit time: as blood flows through a smaller vascular bed, blood velocity increases and the time for diffusion decreases.
The characteristic feature, however, is an increase in VD/VT >> 0.35.
What is the effect of increased number of shunts on O2 exchange ie blood flow and no ventilation?
Shunt units behave as veno-arterial shunts, i.e. as a stream of venous blood that bypasses the ventilated area of the lung and does not change PO2 or PCO2. An extreme example is bronchial occlusion, where blood draining from the non-ventilated area does not undergo gas exchange and maintains the same composition of venous blood. When both blood streams mix in the left atrium, the result will be a lower PO2 and a higher PCO2 than those of the blood draining the well ventilated area. However, due to the difference in the shapes of the ODC and the CO2 dissociation curve, PO2 will be much more affected than PCO2.
A shunt will produce what type of effect on arterial PO2?
How will shunting of blood from alveoli B to A affect the PAO2?
The blood flowing through A has a high O2 saturation, so increasing PAO2 (i.e. hyperventilation or increasing inspired O2) does not increase the blood O2 content by much. The increased PAO2 does not affect the blood flowing through B, since the area has no ventilation; accordingly the increase in PO2 of the blood leaving the lungs is relatively small. The lack of significant effect of increasing PIO2 on PaO2 is a hallmark of these type of conditions.
Shunts have what effect on PaCO2? How is this compensated for?
Besides decreasing PaO2, shunts tend to increase PaCO2. However, the effect on PaCO2 is much smaller than the effect on PaO2.
A large number of low VA/Q units will result in?›
