Respiratory Control of Blood pH

Respiratory alkalosis is the rise in pH associated with excessive respiration. Hyperventilation, which can result from anxiety or high fever, is a common cause. The body may control blood pH during hyperventilation by fainting, which results in slower respiration. An intervention that may prevent fainting is to have a hyperventilating person breathe into a paper bag, which allows much of the respired CX)2 to be taken up again. 

As discussed in Chapter 1, at a blood pH of 7.4, the ratio of [HCO3 ] to [H2CO3] is 20 1 and the system s buffering capacity can neutralize a large amount of acid. The system is independently regulated by the kidneys, which control the plasma HCOj level, and by the respiratory rate, which regulates the Pco2- Protein and phosphate buffer systems also operate in plasma and erythrocytes. Proteins are especially important buffers in the intracellular fluid. The hydroxyapatite of bone also acts as a buffer. 

Effector organs are mainly the respiratory muscles, as described previously. Other effectors are muscles located in the airways and tissues for mucus secretion. Control of respiration appears to be based on two criteria (1) removal of excess CO2 and (2) minimization of energy expenditure. It is not the lack of oxygen that stimulates respiration but increased CO2 partial pressure that acts as a powerful respiratory stimulus. Because of the buffering action of blood bicarbonate, blood pH usually falls as more CO2 is produced in the working muscles. Lower blood pH also stimulates respiration. 

Like any closed-loop system, the behavior of the respiratory control system is defined by the continual interaction of the controller and the peripheral processes being controlled. The latter include the respiratory mechanical system and the pulmonary gas exchange process. These peripheral processes have been extensively studied, and their quantitative relationships have been described in detail in previous reviews. Less well understood is the behavior of the respiratory controller and the way in which it processes afferent inputs. A confounding factor is that the controller may manifest itself in many different ways, depending on the modeling and experimental approaches being taken. Traditionally, the respiratory control system has been modeled as a closed-loop feedback/feedforward regulator whereby homeostasis of arterial blood gas and pH is maintained. Alternatively, the respiratory controller may be viewed as a... 

The respiratory mechanism for controlling blood pH begins in the brain with respiratory center neurons that are sensitive to blood CO2 levels and pH. A significant increase in the CO2 of arterial blood, or a decrease below about 7.38 of arterial blood pH, causes the breathing to increase both in rate and depth, resulting in hyperventilation. This increased ventilation eliminates more carbon dioxide, reduces carbonic acid and hydrogen-ion concentrations, and increases the blood pH back toward the normal level (see > Figure 15.11). 

Carbon dioxide is normally present in the atmosphere at about 0.035 percent by volume. It is also a normal end-product of human and animal metabolism. The exhaled breath contains up to 5.6 percent carbon dioxide. The greatest physiological effect of carbon dioxide is to stimulate the respiratory center, thereby controlling the volume and rate of respiration. It is able to cause dilation and constriction of blood vessels and is a vital constituent of the acid-base mechanism that controls the pH of the blood. 

Equation (3-13) shows that the equilibrium pH of the bicarbonate buffer system of plasma can be to some extent controlled by varying the partial pressure of carbon dioxide in the air to which the blood is exposed (i.e. in the lungs). Reduction in partial pressure results in carbon dioxide leaving the blood with a rise in the last term of Equation (3-13) provided that the bicarbonate concentration remains constant. The equilibrium pH of the buffer system and hence the pH of the blood consequently rise. Conversely an increase in partial pressure of carbon dioxide in the alveolar air will result in a fall in the pH of blood plasma. In practice the partial pressure of carbon dioxide in the alveolar air is controlled by the rate of pulmonary ventilation in relation to the rate of production of carbon dioxide by metabolic oxidation within the body. Increased ventilation (i.e. hyperventilation) will lower the partial pressure of carbon dioxide and raise the blood pH, while decreased ventilation raises the partial pressure, making the blood more acid (metabolic acidosis). Normally the respiratory centre controls the rate of ventilation to keep the partial pressure of carbon dioxide close to the normal value of 40 mmHg. 

Bacterial catabolism of oral food residue is probably responsible for a higher [NHj] in the oral cavity than in the rest of the respiratory tract.Ammonia, the by-product of oral bacterial protein catabolism and subsequent ureolysis, desorbs from the fluid lining the oral cavity to the airstream.. Saliva, gingival crevicular fluids, and dental plaque supply urea to oral bacteria and may themselves be sites of bacterial NH3 production, based on the presence of urease in each of these materials.Consequently, oral cavity fNTi3)4 is controlled by factors that influence bacterial protein catabolism and ureolysis. Such factors may include the pH of the surface lining fluid, bacterial nutrient sources (food residue on teeth or on buccal surfaces), saliva production, saliva pH, and the effects of oral surface temperature on bacterial metabolism and wall blood flow. The role of teeth, as structures that facilitate bacterial colonization and food entrapment, in augmenting [NH3J4 is unknown. 

The respiratory center within the hypothalamus, which controls the rate of breathing, is sensitive to changes in pH. As the pH falls, individuals breathe more rapidly and expire more CO2. As the pH rises, they breathe more shallowly. Thus, the rate of breathing contributes to regulation of pH through its effects on the dissolved CO2 content of the blood. 

In man the respiratory factors are usually not markedly changed by morphine. In resting healthy individuals minute volume may be decreased 10-15% and respiratory rate may be unmodified or increased. Oxygen consumption decreases 8-10%. Alveolar carbon dioxide tension increases 2-3 mm. and the blood carbon dioxide capacity remains within 4 vol. % of the control value. The response to carbon dioxide in the inspired air is decreased and the blood remains neutral or shifts 0.05 pH toward the acid side, but experiments are recorded also where respiratory minute volume and oxygen consumption increase and all authors are concordant with respect to a low respiratory quotient after morphine. 

The reverse of alkalosis is a condition known as acidosis. This condition is often caused by a depletion of HCO ions from the blood, which can occur as a result of kidney dysfunction. The kidney controls the excretion of HCO j" ions. If there are too few HCO j" ions in solution, the forward reaction is favored and H3O+ ions accumulate, which lowers the blood s pH. Acidosis can also result from the body s inability to expel CO2, which can occur during pneumonia, emphysema, and other respiratory disorders. Perhaps the single most common cause of acidosis is uncontrolled diabetes, in which acids normally excreted in the urinary system are instead retained by the body. 

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