The Structure and Function of Lungs

The essential job of the lungs is to remove from the bloodstream a waste gas (carbon dioxide (CO2) from cell metabolism) and replace it with life-giving oxygen. Their structure follows from this function: spongy and elastic to form a kind of bellows that brings in fresh, sufficiently oxygenated air, then expels the air along with unneeded CO2.

Our body shares, sometimes precariously, a passageway for air and food. Moving downward from the nose or mouth-nasal breathing warms and moistens the inhaled air, making all the subsequent actions easier and more efficient-air typically passes the epiglottis (the flap of cartilage at the root of the tongue) to enter the trachea (windpipe), passing the larynx (voice box) before branching into the bronchi that pipe the air into each of the lungs that flank the heart within the rib cage. These structures are made of smooth muscle connecting cartilage rings; they expand and contract something like an accordion. (Although doctors usually confirm the diagnosis through a particular breathing sound in the lungs, bronchitis sufferers may first pinpoint their condition when they hear and feel a kind of grinding squeakiness in the inflamed cartilage.)

The bronchi continue to divide, into bronchioles and terminate at the microscopic level in alveoli (air sacs). This is the structure that gives the lungs their sponginess. Oxygenation of the bloodstream happens here, at the smallest structural level of both the lungs and the circulatory system (the pulmonary capillaries). The alveoli hold a high concentration of oxygen. When inhalation adds fresh oxygen, the increase in the already-high concentration results in diffusion of the oxygen across the alveolar membrane into the capillaries. By the time it reaches the end of these capillaries, the blood has done its oxygen-delivery work throughout the body. Hemoglobin in the red blood cells has very little oxygen and has been sweeping up carbon dioxide. Given the chemical "choice", hemoglobin will bind to the fresh oxygen and release the carbon dioxide to pass back into the air sac and be expelled on the exhale. The newly oxygenated blood then routes to the heart, which pumps it out throughout the body to oxygenate its cells and pick up their waste CO2.

Obviously this exchange happens pretty quickly in normal breathing. Any number of short-or long-term (acute or chronic) conditions can interfere with it, sometimes fatally:

  • Smoke clogs the alveoli with particles that prevent the exchange of gases. Smoke inhalation is the leading cause of death in fires, which is why dropping to the floor is recommended as the first step toward surviving one.
  • Hemoglobin binds more tightly to carbon monoxide than to either oxygen or carbon dioxide and so effectively and rapidly shuts down the whole respiratory function.
  • Pulmonary fluid, contained by membranes called pleura, normally provides lubrication for the constant and complex mechanical action of the lungs.In pulmonary edema, fluid builds up between the air sacs and the capillaries, impeding the exchange of gases.

On a larger scale, we have the perceptible-though mostly unconscious-actions of the lungs. Inhalation results from a contraction of the diaphragm (a large membranous muscle between the chest cavity and the abdomen) and the intercostal muscles between the ribs. Muscle contraction expands the chest cavity and in turn lowers its air pressure, so that the higher-pressure outside air flows in. Once the lungs are inflated (or in response to certain other conditions), those same muscles relax, constricting the chest cavity and increasing the pressure of the air it holds, so that it flows out the airways to be dispersed into the surrounding air. As at the microscopic level, this mechanical process is subject to breakdowns:

  • Most benignly, overworking of the respiratory function, as in competitive running, creates oxygen demand greater than the supply, resulting in the oxygen debt-in the lungs and throughout muscle tissue-that leaves runners in a deeply gasping state after a race, over and above the elevated respiration that directly sustained the athletic effort.
  • In various kinds of apnea, breathing simply stops. Typically this is caused by a failure of the brain's respiratory controls, although sleep apnea, as one example, can correspond to overweight and can be either exacerbated or alleviated by mouth and body position during sleep
  • Bronchitis and asthma are inflammatory constrictions of, respectively, the bronchi and bronchioles. Both conditions overwork the respiratory muscles. Bronchitis is often transitory and more responsive to treatment, although it can be chronic. Treatment for more-typically chronic asthma is more a question of management and palliation than cure. Either condition can be debilitating and/or fatal.
  • Emphysema is a fibrous stiffening of the lungs. Again, the respiratory muscles work harder to compensate, a response that is not only a strain on the body but typically will eventually not suffice, resulting in dependence on pressured oxygen.
  • Air entering the chest cavity, outside the network of bronchioles and alveoli-usually introduced by injury-can equalize cavity air pressure with the outside air. Either or both lungs can collapse.

Normally our lungs work automatically-or we might say autonomically-in response to the direction of the autonomic nervous system, which runs from the midbrain down the spine and controls the heart, digestive system, and other organs that operate continually without our conscious intervention. The brainstem, or medulla, automatically signals the diaphragm and the intercostal muscles to contract and relax at a typical rate of 15-25 times per minute. This rhythm and "shape" of the contractions also respond to a number of internal or external factors:

  • A central chemoreceptor in the brainstem monitors the level of carbon dioxide in the cerebrospinal fluid (CSF) that bathes the brain and spinal cord, while peripheral receptors monitor blood concentration. At high CO2 levels, the contractions that make up exhalation will speed up and occur deeper in the lungs to flush out the excess, returning to normal with normalization of carbon dioxide.
  • Independently from CO2 monitoring, peripheral chemoreceptors at the trunk lines of the arterial system report on oxygen levels in blood freshly pumped from the heart. When it drops, breathing also speeds up and deepens.
  • Central and peripheral chemoreceptors also monitor the acidity of the blood and CSF; breathing speeds up in response to heightened concentration of hydrogen ion, or pH.
  • Additional specialized receptors transmit data on the degree of stretch in the lungs and chest wall. Response signals from the brain stem trigger an exhalation and regulate inhalation in order to avoid damage from overinflation.
  • When chemical or mechanical irritants are sensed in the airways-dust, water, pollen, irritating gases or particulates from smoke-the respiratory controller sends signals to exhale rapidly and forcefully in the form of sneezing or coughing, in an attempt to expel the intruder.
  • Hiccups are a still unexplained set of seemingly random contractions of the diaphragm, also ordered by the brainstem. We know that fetuses exhibit this kind of contraction-even to the point of being felt by the mother-even before breathing starts.

In addition to these essentially automatic chemo-electro-mechanical operations, the lungs also respond to processes from higher brain centers. The hypothalamus will signal a breathing speed-up in response to pain or strong emotion, as part of the flight-or-fight response. Other regulation of the lungs comes from the complex set of brain activities we call sleep.

In general, we can't consciously direct autonomically controlled organs. The lungs are an interesting (and partial) exception. We can "hold" our breath-stop the automatic regulation of the lungs. Of course, that's not permanent; toddlers may be at risk for choking, but they can't hold their breath till they die. As the receptors that monitor breathing report an increasingly alarming state to the medulla, it responds by forcing expulsion and inhalation. Somewhat more interesting is the willed intervention practiced by yogis and athletes who take the lungs to their limits over a long term and in a regulated way. Their respiration rates may drop to as few as five breaths per minute, because the lungs are being used so efficiently. As breathing slows, so does the heart. A slower heart rate (as well as increased heart rate lability, or ability to rapidly change in response to activity levels) correlates with increased life expectancy. Non-athletes and non-yogis can realize some of these benefits as well-either through a less strenuous regular practice of "mindful breathing" with the body typically in an upright but comfortably relaxed position, or as an intervention in the face of anxiety. The classic methods for stopping hyperventilation come to mind, but even a less dramatic version of the flight-or-fight response to a perceived threat can be "stood down" by slowing and deepening one's breathing and consequently lowering the heart rate-useful in any of the many stressful situations of modern life in which neither flying nor fighting may be the optimal response.

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Published: 2010-09-30