Ventilation, minute

TABLE 5.6 Effect of Dead Space Volume, Tidal Volume, and Breathing Frequency on Alveolar >fentllation at a Fixed Minute Ventilation (V = 58.0 Umin). Modified from Chemiack. ... 

Expired minute ventilation, V, defines the gas volume inspired or expired in 1 minute and is given by... 

Typical for normal quiet breathing is approximately 6-8 L/miii. In extreme circumstances, individuals can live for brief periods with minute ventilation rates as low as 1-2 Umin or as high as 300 L/min. Table 5.6 shows the dependence of on Vq, V-p, and / for a given. ... 

Minute ventilation Volume of air expired or inspired during one minute of... 

It is imperative to identify serious causes of respiratory alkalosis and institute effective treatment. In spontaneously breathing patients, respiratory alkalosis is typically only mild or moderate in severity and no specific therapy is indicated. Severe alkalosis generally represents respiratory acidosis imposed on metabolic alkalosis and may improve with sedation. Patients receiving mechanical ventilation are treated with reduced minute ventilation achieved by decreasing the respiratory rate and/or tidal volume. If the alkalosis persists in the ventilated patient, high-level sedation or paralysis is effective. 

Beyond this point, during more severe exercise associated with anaerobic metabolism, minute ventilation increases faster than the rate of oxygen consumption, but proportionally to the increase in carbon dioxide production. The mechanism of the ventilatory response to severe exercise involves metabolic acidosis caused by anaerobic metabolism. The lactic acid produced under these conditions liberates an H+ ion that effectively stimulates the peripheral chemoreceptors to increase ventilation. 

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. 

The AEGL-1 value was based on the observation that exercising healthy human subjects could tolerate exposure to concentrations of 500 or 1,000 ppm for 4 h with no adverse effects on lung function, respiratory symptoms, sensory irritation, or cardiac symptoms (Utell et al. 1997). The exercise, which tripled the subjects minute ventilation, simulates an emergency situation and accelerates pulmonary uptake. Results of the exposure of two subjects for an additional 2 h to the 500-ppm concentration and the exposure of one subject to the 1,000-ppm concentration for an additional 2 h failed to elicit any clear alterations in neurobehavioral parameters. The 4- or 6-h 1,000-ppm concentration is a NOAEL in exercising individuals, there were no indications of response differences among tested subjects, and animal studies indicate that adverse effects occur only at considerably higher concentrations, so the 1,000-ppm value was adjusted by an uncertainty factor (UF) of 1. The intraspecies UF of 1 is supported by the lack of adverse effects in patients with severe... 

Minute ventilation versus alveolar oxygen partial pressure... 

Alveolar carbon dioxide partial pressure versus minute ventilation... 

Scheel et al, exposed 75 rats to ozone at 2 ppm for 3 h and measured pulmonary function immediately after removal of the animals from the exposure chamber. Minute ventilation, tidal volume, and oxygen uptake decreased immediately after exposure and reached minimal recorded values after 8 h. At 20 h after exposure, all measurements had returned to normal. Pulmonary edema may have been responsible for the observations reported. 

One of the principal modifiers of the magnitude of response to ozone is minute ventilation (Vt), which increases proportionally with increase in exercise workload. Studies show that the heavier the workload the greater is the potentiation of ozone effects on the lung. Surprisingly, patients with mild to moderate respiratory disease do not appear to be more sensitive than normal subjects to threshold ozone concentrations. "... 

Adenosine Minute ventilation and heart rate response o... 

Halothane (Fluothane) depresses respiratory function, leading to decreased tidal volume and an increased rate of ventilation. Since the increased rate does not adequately compensate for the decrease in tidal volume, minute ventilation will be reduced plasma PaCOz rises, and hypoxic drive is depressed. With surgical anesthesia, spontaneous ventilation is inadequate, and the patient s ventilation must be controlled. 

N2O (commonly called laughing gas) produces its anesthetic effect without decreasing blood pressure or cardiac output. Although it directly depresses the myocardium, cardiac depression is offset by an N2O-mediated sympathetic stimulation. Likewise, respiration is maintained. Tidal volume falls, but minute ventilation is supported by a centrally mediated increase in respiratory rate. However, since the respiratory depressant effect of N2O are synergistic with drugs such as the opi-... 

Mecfianism of Action A methylxanthine and competitive inhibitor of phosphodiesterase that blocks antagonism of adenosine receptors. Therapeutic Effect Stimulates respiratory center, increases minute ventilation, decreases threshold of or increases response to hypercapnia, increases skeletal muscle tone, decreases diaphragmatic fatigue, increases metabolic rate, and increases oxygen consumption. Pharmacokinetics Protein binding 36%. Widely distributed through the tissues and CSF. Metabolized in liver. Excreted in urine. Half-life 3-7 hr. 

Mechanism of Action A central nervous system stimulant that directly stimulates the respiratorycenterinthemedullaorindirectlybyeffectsonthecarotid. TfterflpeMtIc Effect Increases pulmonary ventilation by increasing resting minute ventilation, tidal volume, respiratory frequency, and inspiratory neuromuscular drive, and enhances the ventilatory response to carbon dioxide. 

Like other volatile agents, sevoflurane causes dose-related respiratory depression. In healthy patients this results in a decrease in tidal volume and an increase in respiratory rate with a net decrease in minute ventilation. At anaesthetic concentrations the degree of depression is greater than that seen with halothane or isoflurane. There is a decline in the slope of the carbon dioxide response curve. Sevoflurane produces the same degree of bronchodilation as isoflurane and enflurane. 

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. 

With the exception of nitrous oxide, all inhaled anesthetics in current use cause a dose-dependent decrease in tidal volume and an increase in respiratory rate. However, the increase in respiratory rate is insufficient to compensate for the decrease in volume, resulting in a decrease in minute ventilation. All volatile anesthetics are respiratory depressants, as indicated by a reduced response to increased levels of carbon dioxide. The degree of ventilatory depression varies among the volatile agents, with isoflurane and enflurane being the most depressant. All volatile anesthetics in current use increase the resting level of Paco2 (the partial pressure of carbon dioxide in arterial blood). 

Metabolic acidosis due to acetazolamide causes increased minute ventilation, which can cause increased intracranial pressure and result in neurological complications (38). 

Endurance and time to exhaustion are also important components of athletic performance. Decreases in either measure were observed in several studies (19,21,38 12). Holland (38) noted a 10% reduction in work performed during all-out cycle ergometer exercise after 24 hr of sleep deprivation. Brodan and Kuhn (39) evaluated subjects (n = 7, sleep debt = 120 hr) with the Harvard step test (reflects cardiorespiratory endurance and recovery) and revealed adaptation during the test but impaired recovery. Martin (41) utilized treadmill testing at 80% V02 max and found decreased time to exhaustion, increased perceived exertion, and increased minute ventilation (n = 8, sleep debt = 36 hr). Martin and Chen (42) revealed a 20% reduction in time to exhaustion after 50 hr of sleep deprivation. Decreased time to exhaustion after 30 hr of sleep deprivation has been demonstrated even when subjects were allowed caffeine intake (21). 

Modern inhalation anesthetics are nonexplosive agents that include the gas nitrous oxide as well as a number of volatile halogenated hydrocarbons. As a group, these agents decrease cerebrovascular resistance, resulting in increased perfusion of the brain. They cause bronchodilation and decrease minute ventilation. Their clinical potency cannot be predicted by their chemical structure, but potency does correlate with their solubility in lipid. The movement of these agents from the lungs to the different body compartments depends upon their solubility in blood and various tissues. Recovery from their effects is due to redistribution from the brain. 

Children have faster respiratory rates than do adults because of their higher metabolic rate, as well as greater minute ventilation. Botentially, infants and children can inhale a higher dosage or amount of toxic substances. 

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