Ventilation alveolar

Alveolar ventilation supplies O2 to the bloodstream while alveolar capillary perfusion provides alveolar gas with COj. Resting individuals consume approximately 250 mL 02/min and produce approximately 200 ml. COi/min because, stoichiometrically, metabolic processes require a greater supply of O, than the quantity of CO2 produced. Defining the respiratory exchange ratio, R, as... 

Alveolar ventilation Volume of air passing through the alveoli and alveolar... 

Physiologically Based Phamiacokinetic (PBPK) Model—Comprised of a series of compartments representing organs or tissue groups with realistic weights and blood flows. These models require a variety of physiological information tissue volumes, blood flow rates to tissues, cardiac output, alveolar ventilation rates and, possibly membrane permeabilities. The models also utilize biochemical information such as air/blood partition coefficients, and metabolic parameters. PBPK models are also called biologically based tissue dosimetry models. 

Absorption of trichloroethylene in humans is very rapid upon inhalation exposure. Trichloroethylene has a blood/gas partition coefficient that is comparable to some other anesthetic gases (i.e., chloroform, diethylether, and methoxyfluorene), but it is much more lipophilic than these gases. As a consequence of these properties, the initial rate of uptake of inhaled trichloroethylene in humans is quite high, with the rate leveling off after a few hours of exposure (Fernandez et al. 1977). The absorbed dose is proportional to the inhaled trichloroethylene concentration, duration of exposure, and alveolar ventilation rate at a given inhaled air concentration (Astrand and Ovrum 1976). Several studies indicate that 37-64% of inhaled trichloroethylene is taken up from the lungs (Astrand and Ovrum 1976 Bartonicek 1962 Monster et al. 1976). 

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. 

Distinguish between total ventilation and alveolar ventilation... 

Alveolar ventilation. Alveolar ventilation is less than the total ventilation because the last portion of each tidal volume remains in the conducting airways therefore, that air does not participate in gas exchange. As mentioned at the beginning of the chapter, the volume of the conducting airways is referred to as anatomical dead space. The calculation of alveolar ventilation includes the tidal volume adjusted for anatomical dead space and includes only air that actually reaches the respiratory zone ... 

During exercise, the increase in minute ventilation results from increases in tidal volume and breathing frequency. Initially, the increase in tidal volume is greater than the increase in breathing frequency. As discussed earlier in this chapter, increases in tidal volume increase alveolar ventilation more effectively. Subsequently, however, as metabolic acidosis develops, the increase in breathing frequency predominates. 

In early cardiac arrest, adequate alveolar ventilation is the primary means of limiting carbon dioxide accumulation and controlling the acid-base imbalance. With arrests of long duration, buffer therapy is often necessary. 

Respiratory acid-base disorders are caused by altered alveolar ventilation producing changes in arterial carbon dioxide tension (PaC02). Respiratory acidosis is characterized by increased PaC02, whereas respiratory alkalosis is characterized by decreased PaC02. 

The most common cause of acute respiratory failure in COPD is acute exacerbation of bronchitis with an increase in sputum volume and viscosity. This serves to worsen obstruction and further impair alveolar ventilation, resulting in worsening hypoxemia and hypercapnia. Additional causes are pneumonia, pulmonary embolism, left ventricular failure, pneumothorax, and CNS depressants. 

Nitrous oxide (N20), although relatively insoluble, is 20 times more soluble in the blood than nitrogen (N2). The outward diffusion of N20 from the alveolus into the blood is therefore much faster than the inward diffusion of N2 from the blood into the alveolus. Consequently, the alveolus shrinks in volume and the remaining N20 is concentrated within it. This smaller volume has a secondary effect of increasing alveolar ventilation by drawing more gas into the alveolus from the airways in order to replenish the reduced volume. 

The V/Q term describes the imbalance between ventilation (V) and perfusion (Q) in different areas of the lung. Given that alveolar ventilation is 4.5 l.min and pulmonary arterial blood flow is 5.0 l.min 1, the overall V/Q ratio is 0.9. Both ventilation and perfusion increase from top to bottom of the lung, but perfusion by much more than ventilation. 

Hypersensitivity to these agents depressed sodium or potassium serum levels marked kidney and liver disease or dysfunction suprarenal gland failure hyperchloremic acidosis adrenocortical insufficiency severe pulmonary obstruction with inability to increase alveolar ventilation since acidosis may be increased (dichlorphenamide) cirrhosis (acetazolamide, methazolamide) long-term use in chronic noncongestive angle-closure glaucoma. 

Pulmonary conditions These drugs may precipitate or aggravate acidosis. Use with caution in patients with pulmonary obstruction or emphysema when alveolar ventilation may be impaired. 

Frequently it is desirable to overcome the slow rate of rise of alveolar tension associated with such factors as the high blood solubility of some anesthetics and increased pulmonary blood flow. Since both of these factors retard tension development by increasing the uptake of anesthetic, the most effective way to alleviate the problem is to accelerate the input of gas to the alveoli. A useful technique to increase the input of anesthetic to the lung is to elevate the minute alveolar ventilation. This maneuver, which causes a greater quantity of fresh anesthetic gas to be delivered to the patient per unit of time, is most effective with highly soluble agents (Fig. 25.4). 

The alveolar rate of rise toward the inspired concentration (Fa/Fi) is accelerated by an increase in alveolar ventilation from 2 to 4 and from 4 to 8 liters per minute (constant cardiac output). The increase is greatest with the more soluble agent, halothane, and smaller with the least soluble anesthetic, nitrous oxide. (Reprinted with permission from Eger El II [ed.]. Anesthetic Uptake and Action. Baltimore Williams Wilkins, 1974.)... 

Hypoxia. Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. Hypoventilation. Underventilation reduced alveolar ventilation in relation to the oxygen consumption. 

An increase in alveolar ventilation will cause an increase in the alveolar concentration of inhaled agent when semi-closed or open breathing circuits are employed. The effect is most noticeable with a highly soluble anaesthetic, such as diethyl ether. With modern, relatively insoluble agents, such as isoflurane and desflurane, the effects of changes in alveolar ventilation are less pronounced. 

The partial pressure of CO is important in connection with a number of physiological problems. For example, respiratory acidosis is the result of an abnormally high p... CO . The value of arterial pC O varies directly with changes in the metabolic production of CO and indirectly with the amounl of alveolar ventilation. The problem is more commonly ihe result of decreased alveolar ventilation caused by abnormally low CO excretion by the lungs (alveolar /ivpoveniilulion). 

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