(4) PULMONARY CIRCULATION notes Flashcards

1
Q

Pressures in pulmonary circulation (Fig. 1a)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In pulmonary circuit (Fig. 2)

A

A) Mean capillary pressure estimated to be 7 mmHg - halfway between mean pulmonary artery pressure (13 mmHg) and left atrial pressure (2 mmHg). Therefore, arterial and venous resistances in the lungs are about equal.

B)Left atrial is about 5 mmHg; varies from 1-5 mmHg. Left atrial pressure is not measured directly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Blood volume in lungs fig 2

A
  1. Only about 450mL blood is in lungs at any moment in time; of this total only approx. 70mL is in capillaries. Thus, this 70mL is distributed over an area of approximately 100m2 !!!
  2. Can vary under both physiological and pathological conditions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Blood flow and its distribution fig 2

A

1) Equal to cardiac output and therefore peripheral factors that affect cardiac output in systemic circuit also control flow in pulmonary circuit. Why must this be so? What would be the consequences if it were not so?
2) Under most conditions pulmonary vessels act as passive distensible tubes that enlarge with increasing pressure and narrow with decreasing pressure.
3) Adequate gas exchange requires blood be distributed to those parts of the lungs where the alveoli are best ventilated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypoxic pulmonary vasoconstriction

A

A) Nervous influences have not been shown to affect blood flow distribution

B) At high altitude, generalized pulmonary vasoconstriction may occur leading to rise in pulmonary arterial pressure and workload on right heart.

c) Fetal life and first breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effect of hydrostatic pressure gradients in the lungs on regional pulmonary blood flow (see Figs. 3, 4 and explanation).

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effect of increased cardiac output on pulmonary circulation during heavy exercise.

A

During heavy exercise lungs are frequently called upon to absorb up to 20 times as much O2 into blood as they normally do.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Effect of increased cardiac output on pulmonary circulation during heavy exercise. This absorption is achieved in three ways:

A

By increasing cardiac output

By increasing the number of open capillaries - Recruitment

Distension - see #5 below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cardiac output can increase up to

A

4-6 times normal before pulmonary arterial pressure becomes excessively elevated (Fig. 5).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

As blood flow to lungs increases, what happens?

A

more and more capillaries open up; pulmonary arterioles and capillaries also expand.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ability of lungs to accommodate the greatly
increased blood flow during exercise, with relatively little increase in pulmonary vascular pressure, is important for at least two reasons:

A

It conserves energy of right heart

It prevents significant rise in pulmonary capillary pressure; this prevents development of pulmonary edema during periods of increased cardiac output, e.g. exercise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Effects of lung volumes of pulmonary vascular resistance

A

Recall that extra-alveolar vessels are the pulmonary arteries and arterioles - they are not exposed to the alveolar pressure because they are not in the walls of the alveoli; intra-alveolar vessels are the pulmonary capillaries - they are exposed to the alveolar pressures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Effects of lung volumes of pulmonary vascular resistance, At low lung volumes

A

Extra-alveolar vessels collapse and increase resistance whereas

Intra-alveolar vessels are less compressed by alveolar gas pressure and therefore decrease resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Effects of lung volumes of pulmonary vascular resistance At high lung volumes

A

A)Extra-alveolar vessels expand and decrease resistance

B)Intra-alveolar vessels are more compressed by alveolar gas pressure and therefore increase resistance

c)Since the two sets of vessels are in series, changes in total pulmonary resistance (TPR) is determined by the sum of the resistance of the two sets of vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Although much of the control of pulmonary circulation is passive, endothelial generated substances can have a profound effect, especially in a clinical setting.

A

1) NO derived from endothelial NOS (eNOS) action on L-arginine has a vasodilatory action
2) endothelin-1 (ET-1) and Thromboxane A2 (TXA2) derived from arachidonic acid by the action of endothelial cyclooxygenase are potent vasoconstrictors
3) In either of the above cases, attention is now being given to the use of agonists (of eNOS) or antagonists (of COX) to produce therapies to alleviate pulmonary congestion, a significant problem in congestive heart failure patients
4. Such vasoactive substances, of course, play a homeostatic role in maintaining flow in the pulmonary arterial tree and thereby keeping flow to the capillaries relatively steady and gas exchange relatively undisturbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinically, understanding the impact of lung volume on pulmonary vascular resistance is very important. Using mechanical ventilation to support a patient with obstructive lung disease who is in respiratory failure, there is a high risk of causing severe hyperinflation with gas trapping and high alveolar pressures. This increase in lung volume and alveolar pressure causes compression of intra-alveolar vessels leading to (1) increase in pulmonary vascular resistance which strains the right heart and leads to decreased cardiac output with potential for right heart failure and (2) compression of intra-alveolar vessels, which would create of Zone I regions and increase dead space.

A

Clearly, this increase in dead space would cause alveolar ventilation to decrease, CO2 exchange to decrease and the patient to develop increased arterial carbon dioxide (PaCO2). In turn this would lead to a respiratory acidosis. Thus, a supposed therapy can lead to a derangement of homeostasis and the development of pathology!

17
Q

The volume of blood passing through lungs each minute (Q) can be calculated using Fick’s principle. This states that O2 consumption per minute (Vo2) is equal to amount of O2 taken up by blood per minute. Since O2 concentration in blood entering lungs is CvO2, and that in blood leaving is CaO2 we have

A

Vo2 is measured by collecting expired gas in a large spirometer and measuring its O2 concentration. Mixed venous blood is taken via a catheter in pulmonary artery, and arterial blood from brachial or radial artery.

18
Q

Pulmonary blood flow can also be measured by

A

the indicator dilution technique.

19
Q

The Fick and dye methods give the average flow over a number of heart cycles. It is also possible to measure instantaneous pulmonary blood flow using the body plethysmograph (Fig. 6).

A
  1. The subject inhales a mixture of gas containing 79% nitrous oxide (N2O) and 21% O2 from a rubber bag inside box.
  2. As N2O, a very soluble gas, is taken up by blood, box pressure falls in a series of small steps, which are synchronous with the heartbeat.
  3. Since the uptake of N2O is flow limited, instantaneous blood flow can be calculated.
  4. In normal subjects there is considerable pulsatility of pulmonary blood flow and this is altered by disease.
20
Q

Water Balance in Lungs

Since only 0.3 - 0.5 μm of tissue separates the capillary blood from the air in the lung, the problem of keeping the alveoli free of fluid is critical.

A
  1. Fluid exchange across the capillary walls is believed to obey Starling’s Law.
  2. It is probable that net pressure of the Starling equation is outward causing a small lymph flow of perhaps 20 mL/hr in man under normal conditions.
    a. This is assisted by the slight negative pressure that exists in lung (-5 cmH2O)
21
Q

Water Balance in Lungs

Where does fluid go when it leaves the capillaries?

A
  1. Fig. 7 shows that fluid that leaks out into the interstitium of the alveolar wall passes through the interstitial space into the perivascular and peribronchial spaces within the lung
  2. Numerous lymphatics in the perivascular and peribronchial spaces help to transport fluid to the hilar lymph nodes.
  3. Pressure in these perivascular spaces is low, thus forming a natural sump for the drainage of fluid. 4. The earliest form of pulmonary edema is interstitial edema.
22
Q

In a later stage of pulmonary edema, fluid crosses the alveolar epithelium into the alveolar spaces.

A
  1. Alveoli fill with fluid one by one and since they are then unventilated, no oxygenation of the blood passing through is possible.
  2. What causes the fluid to start moving across into the alveolar spaces is not clear.
23
Q

Water Balance in Lungs

The normal rate of lymph flow from the lung is only a few mm/hr but it

A

can be shown to increase greatly if the capillary pressure is raised over a long period.

24
Q

can be shown to increase greatly if the capillary pressure is raised over a long period.

A