Alveolar partial pressure

The phenomenon by which the rise in the alveolar partial pressure of nitrous oxide is disproportionately rapid when it is administered in high concentrations. 

In considering the pharmacokinetics of anesthetics, one important parameter is the speed of anesthetic induction. Anesthesia is produced when anesthetic partial pressure in brain is >MAC. Because the brain is well perfused, anesthetic partial pressure in brain becomes equal to the partial pressure in alveolar gas (and in blood) over the course of several minutes. Therefore, anesthesia is achieved shortly after alveolar partial pressure reaches MAC. WhUe the rate of rise of alveolar partial pressure will be slower for anesthetics that are highly soluble in blood and other tissues, this limitation on speed of induction can be overcome largely by delivering higher inspired partial pressures of the anesthetic. 

Ehmination of inhalational anesthetics is largely the reverse process of uptake. For agents with low blood and tissue solubility, recovery from anesthesia should mirror anesthetic induction, regardless of the duration of administration. For inhalational agents with high blood and tissue solubility, recovery wiU be a function of the duration of administration, because anesthetic accumulated in the fat reservoir will prevent blood (and therefore alveolar) partial pressures from falling rapidly. Patients will be arousable when alveolar partial pressure reaches a partial pres-... 

Oxygen makes up 21% of air, with a partial pressure of 21 kPa (158 mm Hg) at sea level. The partial pressure drives the diffusion of oxygen thus, ascent to elevated altitude reduces the uptake and delivery of oxygen to the tissues. air is delivered to the distal airways and alveoli, the PO2 decreases by dilution with carbon dioxide and water vapor and by uptake into the blood. Under ideal conditions, when ventilation and perfusion are well matched the alveolar PO2 will be -14.6 kPa (110 mm Hg). The corresponding alveolar partial pressures of water and CO2 are 6.2 kPa (47 mm Hg) and 5.3 kPa (40 mm Hg), respectively. Under normal conditions, there is complete equilibration ( alveolar gas and capillary blood. In some diseases, the diffusion barrier for gas transport may be increased during exercise, when high cardiac output reduces capillary transit time, full equilibration may not occur, and the alveolar-end-capillary Po gradient may be increased. 

In a patient in whom there is a sudden rise in the alveolar partial pressure of carbon dioxide, the change in composition of the patient s arterial blood is represented in Figure 3.1 as a move from the normal, represented by point N, along the normal blood line to point A. The increase in the x coordinate represents the rise in the PCO2 of the patient s arterial blood. The increase in the y coordinate represents the rise in bicarbonate concentration the move to a new isohydric contour reflects the increase in hydrogen ion concentration. These changes in composition of the arterial blood are summarized in Table 3.1 Column A. 

Human evolution has taken place close to sea level, and humans are physiologically adjusted to the absolute partial pressure of the oxygen at that point, namely 21.2 kPa (159.2 mm Hg), ie, 20.946% of 101.325 kPa (760 mm Hg). However, humans may become acclimatized to life and work at altitudes as high as 2500—4000 m. At the 3000-m level, the atmospheric pressure drops to 70 kPa (523 mm Hg) and the oxygen partial pressure to 14.61 kPa (110 mm Hg), only slightly above the 13.73 kPa (102.9 mm Hg) for the normal oxygen pressure in alveolar air. To compensate, the individual is forced to breathe much more rapidly to increase the ratio of new air to old in the lung mixture. 

The partial pressure of the water vapor is 47 mmHg and, as a result, the P02 is slightly decreased to 150 mmHg. The PC02 remains at 0 mmHg. By the time the air reaches the alveoli, the POz has decreased to about 100 mmHg. The P02 of the alveolar gas is determined by two processes ... 

As arterial C02 tension is practically identical to alveolar C02 partial pressure, it can be used as a surrogate measurement. This is desirable as measuring arterial C02 tension involves only a simple blood gas analysis. The term Paco2, therefore, becomes Paco2 and so the equation is often written as... 

Minute ventilation versus alveolar oxygen partial pressure... 

Alveolar carbon dioxide partial pressure versus minute ventilation... 

Pulmonary absorption of volatile anesthetics across the alveolar-capillary barrier is very rapid because of the relatively high lipid-water partition coefficients and small molecular radii of such agents. The driving force for diffusion is a combination of the blood-air partition coefficient (which is a measure of the capacity of blood to dissolve drug) and the difference in partial pressure between the alveoli and the arterial and venous blood. Agents with high blood-air partition coefficients require more drug to be dissolved in the blood for equilibrium to be reached. 

Practically speaking, this concept explains the basis for the establishment of partial pressure equilibrium of anesthetic gas between the lung alveoli and the arterial blood. Gas molecules will move across the alveolar membrane until those in the blood, through random molecular motion, exert pressure equal to their counterparts in the lung. Similar gas tension equilibria also will be established between the blood and other tissues. For example, gas molecules in the blood will diffuse down a tension gradient into the brain until equal random molecular motion (equal pressure) occurs in both tissues. 

A Concept of Anesthetic Dose Based on Partial Pressure-Minimum Alveolar Concentration... 

Since the anesthesiologist has control over the partial pressure of anesthetic delivered to the lung, it can be manipulated to control the anesthetic gas concentration in the brain, hence the level of unconsciousness. For this reason, anesthetic dose is usually expressed in terms of the alveolar tension required at equilibrium to produce a defined depth of anesthesia. The dose is determined experimentally as the partial pressure needed... 

The inhalational anesthetics have distinctly different solubility (affinity) characteristics in blood as well as in other tissues. These solubility differences are usually expressed as coefficients and indicate the number of volumes of a particular agent distributed in one phase, as compared with another, when the partial pressure is at equilibrium (Table 25.3). For example, isoflurane has a blood-to-gas partition coefficient (often referred to as the Ostwald solubility coefficient) of approximately 1.4. Thus, when the partial pressure has reached equilibrium, blood will contain 1.4 times as much isoflurane as an equal volume of alveolar air. The volume of the various anesthetics required to saturate blood is similar to that needed to saturate other body tissues (Table 25.3) that is, the blood-tissue partition coefficient is usually not more than 4 (that of adipose tissue is higher). 

Nitrous oxide decreases tidal volume and increases the rate of breathing and minute ventilation. Although arterial carbon dioxide partial pressures tend not to be affected the normal ventilatory responses to carbon dioxide and to hypoxia are depressed. Alveolar collapse in structured lung segments may be more rapid in the presence of nitrous oxide than with oxygen due to its greater solubility. Similarly, it depresses mucous flow and chemotaxis. In theory these factors predispose to postoperative respiratoiy complications. 

The concentration of an inhaled anesthetic in a mixture of gases is proportional to its partial pressure (or tension). These terms are often used interchangeably in discussing the various transfer processes involving anesthetic gases within the body. Achievement of a brain concentration of an inhaled anesthetic necessary to provide an adequate depth of anesthesia requires transfer of the anesthetic from the alveolar air to the blood and from the blood to the brain. The rate at which a therapeutic concentration of the anesthetic is achieved in the brain depends primarily on the solubility properties of the anesthetic, its concentration in the inspired air, the volume of pulmonary ventilation, the pulmonary blood flow, and the partial pressure gradient between arterial and mixed venous blood anesthetic concentrations. 

During inhalation anesthesia, the partial pressure of the inhaled anesthetic in the brain equals that in the lung when steady-state conditions are achieved. Therefore, at a given level (depth) of anesthesia, measurements of the steady-state alveolar concentrations of different anesthetics provide a comparison of their relative potencies. The volatile anesthetic concentration is the percentage of the alveolar gas mixture, or partial pressure of the anesthetic as a percentage of 760 mm Hg (atmospheric pressure at sea level). The minimum alveolar anesthetic concentration (MAC ) is defined as the... 

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). 

Depth of anesthesia is determined by the concentration of anesthetic agent that reaches the brain. Brain concentration, in turn, depends on the solubility and transport of the anesthetic agent in the bloodstream and on its partial pressure in inhaled air. Anesthetic potency is usually expressed as a minimum alveolar concentration (MAC), defined as the percent concentration of anesthetic in inhaled air that results in anesthesia in 50% of patients. As shown in Table 9.6, nitrous oxide, N2O, is the least potent of the common anesthetics. Fewer than 50% of patients are immobilized by breathing an 80 20 mix of nitrous oxide and oxygen. Methoxyflurane is the most potent agent a partial pressure of only 1.2 mm Hg is sufficient to anesthetize 50% of patients, and a partial pressure of 1.4 mm Hg will anesthetize 95%. 

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