*hematocrit of venous blood is normally 3% greater than that of the arterial blood. In the lungs, the Cl– moves out of the cells and they shrink
Apneustic Center : Apneusis is an abnormal breathing pattern with prolonged inspiratory gasps, followed by brief expiratory movement. Stimulation of the apneustic center in the lower pons produces this breathing pattern in experimental subjects. Stimulation of these neurons apparently excites the inspiratory center in the medulla, prolonging the period of action potentials in the phrenic nerve, and thereby prolonging the contraction of the diaphragm. Pneumotaxic Center : The pneumotaxic center turns off inspiration, limiting the burst of action potentials in the phrenic nerve. In effect, the pneumotaxic center, located in the upper pons, limits the size of the tidal volume, and secondarily, it regulates the respiratory rate. A normal breathing rhythm persists in the absence of this center.
*(as its levels are maintained even with fluctuating Palvo2 while CO2 levels fluctuate appropriately)
*Responses of normal subjects to inhaling O2 and approximately 2, 4, and 6% CO2. The relatively linear increase in respiratory minute volume in response to increased CO2 is due to an increase in both the depth and rate of respiration.**Of course, this linearity has an upper limit. When the PCO 2 of the inspired gas is close to the alveolar PCO 2, elimination of CO2 becomes difficult. When the CO2 content of the inspired gas is more than 7%, the alveolar and arterial PCO 2 begin to rise abruptly in spite of hyperventilation. The resultant accumulation of CO2 in the body (hypercapnia) depresses the central nervous system, including the respiratory center, and produces headache, confusion, and eventually coma (CO2narcosis).
*mediated via peripheral CR
Ventilatory Response to Oxygen LackWhen the O2 content of the inspired air is decreased, respiratory minute volume is increased. The stimulation is slight when the PO2 of the inspired air is more than 60 mm Hg, and marked stimulation of respiration occurs only at lower PO2 values (Figure 37–9). However, any decline in arterial PO2 below 100 mm Hg produces increased discharge in the nerves from the carotid and aortic chemoreceptors. There are two reasons why this increase in impulse traffic does not increase ventilation to any extent in normal individuals until the PO2 is less than 60 mm Hg. Because Hb is a weaker acid than HbO2, there is a slight decrease in the H+ concentration of arterial blood when the arterial PO2 falls and hemoglobin becomes less saturated with O2. The fall in H+ concentration tends to inhibit respiration. In addition, any increase in ventilation that does occur lowers the alveolar PCO2, and this also tends to inhibit respiration. Therefore, the stimulatory effects of hypoxia on ventilation are not clearly manifest until they become strong enough to override the counterbalancing inhibitory effects of a decline in arterial H+ concentration and PCO2.
*in each 2-mg carotid body is about 0.04 mL/min, or 2000 mL/100 g of tissue/min compared with a blood flow 54 mL or 420 mL per 100 g/min in the brain and kidneys, respectively. **in which the amount of dissolved O2 in the blood reaching the receptors is generally normal, even though the combined O2 in the blood is markedly decreased.