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CPR: chapter 41 (9/13/2011) 1. Baseline values for respiratory control a. CO2 = 40 mmHg b.

O2 = 104 mmHg

2. Respiratory center a. Components i. Dorsal respiratory group 1. Location = nucleus of the tractis solitarius in the dorsal medulla 2. Afferent fibers = chemoreceptor, baroreceptor, and various types of lung receptor fibers transmitted by the vagus and glossopharyngeal nerves 3. Main function = inspiration a. Note: even when this area is completely sectioned from incoming fibers, it still maintains a basal rate of discharge such that breathing will occur b. Inspiratory ramp signal = the gradual increase in nerve transmission to the diaphragam during inspiration i. This is graded increase occurs at the phrenic nerve and not at the dorsal respiratory group ii. Importance = allows for a steady increase in the volume of the lungs with inspiration, rather than inspiratory gasps iii. Controlled factors: 1. Rate of increase of the ramp signal 2. Limiting point at which the ramp signal suddenly ceases ii. Pneumotactic center 1. Location = dorsal superior pons within the parabrachial nucleus 2. Main function = switch of the inspiratory ramp signal, thus decreasing the length of inspiration and acting as a trigger for expiration a. Secondary effect = increase the rate of breathing (strong pneumotactic stimulation can increase rate up to 30-40 breaths per minute) iii. Ventral respiratory group of neurons

1. Location = ventrolateral medulla within the nucleus ambiguous and nucleus retroambiguus 2. Main function = contribution of extra inspiratory and expiratory drive during periods of heavy breathing (exercise) iv. Aponeustic center 1. Function = under certain conditions can shut off pneumotactic center, so results in inspiration without expiration (aponeustic breathing) b. Hering Breuer inflation reflex = switch off of the inspiratory ramp signal with increased stretch of the bronchi and bronchioles i. Mechanism = increased stretch within the bronchi and bronchioles is transduced by stretch receptors into inhibitory nerve signals transmitted by the vagus nerve to the dorsal respiratory group ii. Not usually active until tidal volumes increase to about 3x normal, so the point seems to prevent overfilling of the lungs

3. Chemical control of respiration a. Basics i. CO2 and H+ = act directly on the respiratory center ii. Oxygen = acts almost entirely on peripheral chemoreceptors in the carotid and aortic bodies b. Direct control of respiratory center activity by carbon dioxide and hydrogen ions i. Critical idea = hydrogen ions are probably the only direct stimulus for the chemosensitive area of the respiratory center of the medulla, but cannot penetrate the BBB. 1. Chemosensitive area = lies ventrally to the other regions of the respiratory center and transmits signals back to them based up changes in its chemical environment ii. Mechanism = increased CO2 results in shifting the carbonic acid equilibrium back in the direction of water and hydrogen ions. Since increases in blood CO2 are rapidly equilibrated across capillary and cell membrane surfaces, increased CO2 results in increased hydrogen ion production on the brain side of the blood-brain barrier. 1. Note: this means that CO2 increases are quantitatively far more important than hydrogen ion increases in being able to stimulate the chemosensitive area. iii. Decreased stimulation of chemosensitive area by CO2 after 1-2 days

1. Mechanism = increased kidney bicarbonate reabsorption > increased hydrogen ion buffering in the blood and CSF 2. Effectiveness = decreases the effectiveness of increased CO2 to about 1/5 of its initial effect c. Unimportance of oxygen for control of the respiratory center i. Main idea = under normal conditions (pO2 values between 60 and 1000 mmHg) body able to maintain constant level of oxygen delivery to and from tissues with large changes in alveolar concentration. CO2 levels however, can change greatly with changes in ventilation.

4. Peripheral chemoreceptor system for control of respiratory activity role of oxygen in respiratory control a. Components i. Carotid bodies = located at the carotid bifurcation 1. Transmit fibers via CN IX to the dorsal respiratory group 2. Likely to be the more dominant group of chemoreceptors as they act to preserve oxygen flow to the brain ii. Aortic bodies = located along the arch of the aorta 1. Transmit fibers via CN X to the dorsal respiratory group b. Mechanisms of action i. Receptors receive huge blood flows from specialized branches that allow them to detect oxygen and CO2 concentrations in arterial blood ii. increased firing occurs with: 1. Decreased oxygen = most sensitive between 30-60 mmHg as this is the level at which hemoglobin affinity for oxygen drops off rapidly 2. Increased CO2 and H+ a. Important concept here = the effects of these 2 ions on the respiratory center are much more powerful than their effects at the peripheral chemoreceptors, so over the long term their peripheral receptor actions are negligible. However, their actions on the peripheral receptors occur much more rapidly (5x more rapidly) as CO2 reaches these areas faster and no reaction generating hydrogen ions is required. Therefore, CO2 action here is important in increasing responses to CO2 day to day. c. Composite effects of pCO2, pH, and pO2 on alveolar ventilation

i. Critical idea = CO2 concentration is the minute to minute controller of ventilation, so even if hypoxic, ventilation will decrease if CO2 decreases ii. Effects of decreased oxygen with stable levels of CO2 and H+ = little change until arterial pO2 drops to below 60 mmHg 1. Clinical correlation = COPD a. These patients are almost always hypercapnic, so the primary determinant of ventilatory rate becomes oxygen concentration. b. Never want to give someone with COPD high concentrations of oxygen as it will decrease ventilation further, exacerbating the hypercapnia. iii. Acclimization = increased ventilation with chronic exposure to low oxygen concentrations 1. Mechanism = central desensitization to lower CO2 after 2-3 days of increased ventilation. This prevents reflex reductions in ventilatory rate in response to increased blow off of CO2 and allows increases in ventilatory rate of 400-500%. iv. Combined effects of pCO2, pH, and pO2 graphically 1. The lower the partial pressure of oxygen, the greater its effect increasing alveolar ventilation 2. The lower the partial pressure of CO2, the greater its effect on suppressing alveolar ventilation at a given partial pressure of oxygen 3. The lower the pH (higher hydrogen ion concentration), the greater the alveolar ventilation for a given concentration of CO2

5. Regulation of respiration during exercise a. Direct neural control over the respiratory center i. Main idea = motor impulse conduction to active muscles is accompanied by a simultaneous activation of the respiratory center to allow for the required increase in ventilation ii. Interrelation between chemical and neural control of the ventilation 1. Normally, neural control over ventilation allows for compensation for the changing concentrations of oxygen, CO2 and hydrogen ions. Sometimes however, the system is not 100% accurate. For example, increases in ventilation at the onset of exercise due to neural mechanisms may precede increased CO2 concentrations. This results in decreased plasma CO2 which has an inhibitory activity on ventilation.

iii. Idea of the neural mechanism of respiratory control as a learned response = with repeated bouts of exercise an individual becomes more adept at preventing large changes in CO2 concentrations.

6. Other factors that affect respiration a. Voluntary control (i.e. hyper and hypoventilation) b. Lung J receptors = sensory nerve endings in the alveolar walls where they lie adjacent to pulmonary capillaries i. Stimulated during pulmonary edema when capillaries become engorged with blood and result in dyspnea ii. Function = unknown c. Brain edema = results in compression of cerebral arteries, thus blocking blood flow to the chemosensitive area of the brainstem, making the respiratory center insensitive to changes in CO2 concentrations i. Treatment = administration of hypertonic solutions to osmotically remove fluids from the brain d. Anesthesia = overdosage with anesthetics or narcotics is the most common cause of respiratory depression and arrest i. Example drug = sodium pentobarbital (much stronger respiratory depressant than haloethane) e. Periodic breathing (example = Cheyne-Stokes) = alternating periods of increased and decreased respiration as a result of one of two possible mechanisms: i. Increased time for changes in blood concentration to reach the chemosensitive areas of the brain (i.e. severe cardiac failure). In this situation, by the time decreased CO2 has reached the brain, the lungs have exasperated the condition by maintaining the original high respiratory rate that initially caused the problem. This results in an extreme compensation by the respiratory center to suppress ventilation. This in turn results in prolonged decreases in respiratory rate. ii. Increased negative feedback gain by the respiratory center (i.e. brain damage), such that changes in CO2 concentration that would normally elicit only slight responses, now elicit huge responses. f. Sleep apnea i. Definition = prolonged periods of apnea (absence of spontaneous breathing) lasting 10 seconds or longer and occurring 300-500 times per night ii. Types

1. Obstructive sleep apnea = due to the relaxation of pharyngeal muscles and the resultant narrowing of the airway a. Mechanism = snoring and labored breathing followed by periods of apnea. These apnea periods result in greatly increased CO2 and decreased oxygen concentrations, which in turn result in strong stimulation of the respiratory center. The patient then gasps for air and the cycle begins again. b. Most commonly seen in obese patients with excess fat deposited around the pharynx. c. Results in fragmented, restless sleep 2. Central sleep apnea a. Due to one of two possible causes i. Damage to the central respiratory centers ii. Abnormalities of the respiratory neuromuscular apparatus b. Mechanism = decreased ventilation that can be compensated for during awake periods by voluntary breathing. At night the problem is exacerbated and the patient undergoes apnea periods that last as long as it takes for enough CO2 builds up to stimulate the depressed respiratory center. c. These patients are very sensitive to even very small doses of sedatives and narcotics and typically must be treated with CPAP (continuous positive airway pressure) during sleep.