The Euler-Liljestrand mechanism causes contraction of the vascular muscles in the pulmonary tracts when there is an insufficient supply of oxygen, which improves the ventilation-perfusion quotient of the lungs. The mechanism is a natural reflex that involves the lungs exclusively. The Euler-Liljestrand mechanism is pathologic at high altitudes, for example, where it promotes pulmonary edema.
What is the Euler-Liljestrand mechanism?
The Euler-Liljestrand mechanism is a natural reflex that affects only the lungs. During vasoconstriction, blood vessels constrict. As a result, the vascular cross-section narrows and blood pressure changes. Vascular smooth muscle is responsible for vasoconstriction and, if necessary, also conducts relaxation and thus dilation of the vessels with vasodilation. The state of tension of the vascular muscles is mediated by various substances, for example, in vasoconstriction by so-called vasoconstrictors. A reflex vasoconstriction characterizes the Euler-Liljestrand mechanism. This natural body process occurs during hypoxia, i.e. when the tissue is supplied with a reduced amount of oxygen. Both global and local oxygen depletion can trigger the Euler-Liljestrand reflex, causing hypoxic pulmonary vasoconstriction or hypoxic pulmonary vascular response. The reflex increases airway resistance locally. Vasoconstriction in the context of the Euler-Liljestrand mechanism affects only the pulmonary circulation. In all other vessels of the body, hypoxia causes vasodilation. Thus, while the pulmonary circulation contracts, all other vessels dilate to allow more oxygen-carrying blood to pass through.
Function and purpose
The flow of blood through the lungs is locally determined. The same is true for the degree of lung ventilation. Thus, lung tissue is locally differentially ventilated and perfused. Because of physical relationships, such as gravity, blood flow is higher in the basal portions, so the basal lung has better perfusion. In addition, because the basal lung portions are less stretched, ventilation is also at a higher level in these portions. Thus, the apical lung portions have poorer perfusion and ventilation in direct comparison to the basal areas. In particular, perfusion decreases extremely from basal to apical. Ventilation decreases as well, but compared to perfusion, the ventilation decrease toward apical is much smaller. The ventilation-perfusion quotient indicates the ratio of lung ventilation to lung perfusion and thus cardiac output. Because of the local differences of basal and apical fractions, the apical ventilation-perfusion quotient is greater than one. In contrast, the basal ventilation-perfusion quotient is less than one. The optimal ventilation-perfusion ratio is again one. This ratio is not reached by the local differences. Therefore, the oxygen uptake of the blood does not correspond to the absolute optimum. Naturally, the perfusion and ventilation differences in the individual lung areas result in blood fractions, such as the intrapulmonary right-to-left shunt, not being supplied with oxygen. To resolve this relationship, the Euler-Liljestrand mechanism reduces the affected shunts. The reflex adjusts the perfusion of the lungs in the relevant areas to match ventilation, thereby improving the ventilation-perfusion ratio. The Euler-Liljestrand reflex achieves this goal with contraction of the vascular muscles in the pulmonary circulation as mediated by oxygen deprivation. For example, in ventilatory disorders associated with pneumonia, vasoconstriction by the Euler-Liljestrand mechanism redistributes blood. In this case, poorly ventilated sections receive less blood flow than better ventilated areas. This effect is relevant in cases of doubt for maintaining oxygen supply in individual tissues and results in redistribution of blood.
Diseases and ailments
The Euler-Liljestrand mechanism is a natural reflex, but in certain contexts also has negative consequences for human health. This is true, for example, in the development of pulmonary hypertension in the setting of chronic obstructive bronchitis or bronchial asthma.The Euler-Liljestrand reflex is significantly involved in the development of this pathological increase in vascular resistance and blood pressure in the pulmonary circulation. The vasoconstriction mediated by the reflex increases the afterload of the right heart and at the same time evokes a ventricular pressure load. The heart responds by compensating. As a result, concentric hypertrophy occurs in the right ventricle. This tissue enlargement of the right ventricle can result in right heart failure. In this phenomenon, the right heart no longer has sufficient pumping power to return enough blood to the circulation. Another disease phenomenon related to the Euler-Liljestrand mechanism is the pulmonary edema of altitude sickness. Altitude sickness afflicts mountaineers who travel at altitudes higher than 2000 meters above sea level. The disease is an adaptation disorder of the organism, which results in dysfunctions of the body. Athletes who set out to climb at speed and have not acclimatized sufficiently beforehand are particularly at risk. The first symptoms of altitude sickness include retinopathy, in which the blood vessels of the retina become prominent, causing a progressive decrease in visual acuity. Pulmonary edema does not occur until acute altitude sickness and is caused by hypoxic vasoconstriction resulting from the Euler-Liljestrand reflex. The increase in perfusion pressure leads to high-altitude pulmonary edema during exertion at high altitudes because of increased leakage of fluid from the vessels of the lungs into the alveolar space. High-altitude pulmonary edema is associated with acute danger to life and should be evaluated and treated immediately if in doubt. High-altitude mountaineers ideally turn back as soon as retinopathy is present and begin the descent or at least remain at the current altitude for acclimatization to still prevent the development of pulmonary edema.
