FUNCTIONAL CONSEQUENCES OF LOW PULMONARY BLOOD PRESSURE

Gas diffusion

In systemic capillaries the balance between oncotic and hydrostatic pressures mean that small increases in hydrostatic pressure caused, for example, by reduced arteriolar resistance will result in significant movement of plasma water into the interstitium. When a large tissue mass, such as skeletal muscle, is involved, this movement will cause a substantial reduction of plasma volume (see Chapter 9, p. 112), but the increased interstitial volume does not prejudice diffusion of solutes between cells and bloodstream because the intercellular connective tissue minimizes tissue expansion. In the lung, by contrast, there is little supporting tissue. If water moves into the interstitial space separating the pulmonary capillaries from the alveoli, it pushes these two structures further apart and increases the distance over which gases must diffuse between air and plasma.

The speed of this diffusional process decreases very rapidly with increased distance, so efficient lung function depends on minimizing the interstitial space by keeping it free of extra water. A pulmonary capillary hydrostatic pressure of 7–8 mmHg is three times less than plasma oncotic pressure. Therefore, there is normally quite a large net inward osmotic gradient to maintain this situation. If, however, capillary pressure rises to levels similar to those in systemic capillaries, then interstitial water starts to accumulate (pulmonary oedema) and gas exchange may become compromised.

This situation results commonly from damage to the mitral valve that separates left atrium and ventricle. Either valvular stenosis or incompetence will elevate left atrial pressure and this will cause a proportionate change in capillary pressure, which may rise as high as 40–50 mmHg with severe valve damage. Paradoxically, patients in whom chronic valve damage has led to a progressive, slow rise in left atrial pressure often have far less pulmonary oedema than would be expected from the absolute pressure changes. This seems to be because, under these circumstances, the lymphatic system within the lung becomes more efficient in recycling fluid from the interstitial spaces.

The practising exercise physiologist is most likely to encounter pulmonary oedema as a consequence of high altitude, since it occurs in many healthy individuals who ascend to heights greater than 3000 m, well below the altitude of many ski resorts and permanent settlements. We will return to examine the reasons for this response to altitude in Chapter 12 (p. 151).

Left ventricular perfusion occurs only during diastole because during systole the left coronary vessels are compressed by the surrounding cardiac muscle (see Chapter 2, p. 6). By contrast, since right ventricular pressure does not normally rise above 25 mmHg, the coronary vasculature supplying the right ventricle is not compressed at any stage of the cardiac cycle and coronary flow is continuous. The increased efficiency of coronary oxygen delivery is reflected in a lower density of coronary blood vessels in the right heart. However, this design feature has potentially disadvantageous results if left atrial pressure becomes chronically elevated and right ventricular pressure rises in response to this higher afterload.

Under these circumstances, right coronary perfusion during systole becomes progressively reduced and the metabolic demands of the right-side cardiac muscle cells are less efficiently serviced. Over time, the right ventricle will respond to the high afterload by muscle hypertrophy. This will exaggerate the coronary insufficiency, both by providing greater metabolic demand for oxygen delivery and by producing more coronary compression. As a result, chronic hypoxic damage to the muscle of the right heart, with an inability to increase contraction appropriately in response to increased filling (right cardiac failure) is a common long-term effect of elevated pulmonary blood pressure (see Chapter 12, p. 148).