: Immediately after birth the liquid-filled fetal lung is transformed to one containing air. High distending forces are needed in the first few breaths to overcome the high surface tension that opposed alveolar expansion with air. With successful air inflation, more surfactant is recruited into the air-liquid interface, so that FRC stabilizes and the work of breathing is diminished.
In respiratory distress syndrome, type II alveolar cells fail to secrete surfactant. While the lungs are somewhat more difficult to inflate, the main problem is that during deflation the alveoli readily collapse because surface tension does not fall. Thus, the deflation limb of the pressure-volume curve is similar to the inflation curve. Therefore, each lung inflation is like the first breath of air after birth, when the liquid-filled lungs have to be inflated with air. The increased work required to inflate the lungs fatigues the diaphragm. In the infant this is called infant respiratory distress syndrome.
Pulmonary vascular resistance is very high in the fetus because the vessels are as constricted with smooth muscle as systemic vessels. Less than 10% of C.O. passes through the fetal pulmonary capillaries.
The premature baby has a less well developed response to CO2. As a result frequent apneic (Apnea = cessation of breathing) episodes are seen. As a defense mechanism against hypoxia, premature babies may reduce their basal metabolism. Further, preterm babies and normal birth-weight babies respond to hypoxia with a transient increase in ventilation followed by a sustained depression. This response may be explained by initial stimulation of the peripheral chemoreceptors, followed by an overriding depression of the brainstem respiratory controllers.
Lastly, the Hering-Breuer reflex, is more prominent in newborns than adults. In response to a small but sustained increase in lung volume in newborns this reflex shuts off inspiration, prolongs expiration, and decreases the breathing frequency. This is mediated by the lung stretch receptors. Conversely, lung deflation reflexly increases the respiratory rate via stimulation of lung deflation receptors.
Respiratory Changes in the Elderly
: Pulmonary performance declines with age.
As lung elasticity decreases, and lung compliance increases, the transpulmonary pressure (PA-PPl) at a given lung volume decreases. Thus, the bronchi collapse at higher lung volumes (dynamic airway compression, i.e. equal pressure point). These changes account for the elevated FRC in the elderly.
Elderly and emphysema patients have INCREASED LUNG COMPLIANCE due to loss of supportive tissue around the airways. While a normal lung has a high passive elastic recoil, the sick lung has a decreased elasticity (i.e. decreased transpulmonary pressure). Therefore, while a normal person doesnt have to use much muscle contraction while exhaling, an old/emphysemic person has to depend somewhat more on their internal intercostal expiratory muscles at high lung volumes. By having to use more expiratory muscles the PLEURAL PRESSURE (Ppl) BECOMES MORE POSITIVE THAN NORMAL thus allowing the equal pressure point (Ppl>PA) to be reached more easily, resulting in bronchi collapse at higher lung volumes.
Another consequence of age is stiffening of the chest wall. This happens due to structural changes in the rib cage. Note that the decrease of compliance in the chest wall makes the consequences of the above-mentioned increase of compliance in the lung even worse.
As muscle strength decreases in the elderly, vital capacity and forced expiratory flow rates decrease.
The internal surface area of the lung decreases as the alveoli become wider and shallower due to the loss of elastic fibers in the alveolar walls and alveolar ducts.
Ventilation/Perfusion ratios become more variable with advancing age, and as a result arterial PO2 falls about 3 mm Hg per decade. The arterial PCO2, however, is still regulated at 40 mm Hg, but the ventilatory responses to both hypercapnia and hypoxia are reduced.
High altitude and adaptive responses
High Altitude Effects as you climb up a mountain the barometric pressure and PO2 decrease. As a result your PAO2 will also decrease = hypoxemia. This elicits a variety of compensatory responses, some quick and some gradual.
Adaptive Responses to high altitudes
(1) Initial hyperventilation
this occurs because of stimulation of the peripheral chemoreceptors. The increase in ventilation reduces PaCO2 and [H+]. These decreases in turn reduce the excitation of central chemoreceptors, thus limiting the increase in ventilation.
(2) Acclimatization process
after 2-3 days ventilation increases steadily by the following mechanisms:
the renal excretion of sodium bicarbonate reduces plasma [HCO3-] and returns the blood [H+] toward normal.
The [HCO3-] is decreased in brain interstitial fluid, probably by a metabolic process that moves sodium ions from the brain interstitial fluid into the blood (reducing the strong ion difference that normally maintains plasma bicarbonate).
A modest amount of anaerobic metabolism occurs in the hypoxic brain this metabolic change permits lactate ions to substitute for the reduced bicarbonate ions.
(3) Response to CO2
at high altitudes another alteration is an increase in sensitivity of the ventilatory response to CO2. Consequently, the threshold for a stimulatory effect occurs at a lower PCO2.
(4) Hematocrit changes
hemoglobin concentration increases to augment the blood oxygen-carrying capacity. This happens because more RBCs are produced in response to increased secretion of erythropoietin from the kidney.
the concentration of DPG increases thus decreasing the affinity of O2 to hemoglobin. With a shift of the hemoglobin saturation curve to the right oxygen delivery is improved.
People who are chronically hypoxic (live at high altitudes, right atrium to left atrium shunt, etc.) slowly lose some of their ventilatory response to hypoxia. Etiology is unknown.
Chronic mountain sickness
- occasionally, tolerance of high altitude disappears completely and serious symptoms develop, such as ventilatory depression, polycythemia (due to the increased production of RBCs, blood viscosity increases thus increasing the work of the heart), and heart failure. Once this develops the person has to get off the mountain and/or get 100% O2 administration.