TEAM Educational Module Page 1 of 11

Transcription

1 TEAM Educational Module Page 1 of 11 Control of Breathing during Wakefulness and Sleep Learning Objectives:? Describe the elements of ventilatory control (e.g. central control of rate and depth, chemo- and mechano-receptors, metabolism, and behavior influence)? Demonstrate how each of these elements is affected by sleep? Explain how upper airway patency is maintained (e.g anatomic and functional elements, effects of state and position)? Synthesize how each of these features in ventilatory control impact on normal breathing during sleep Assessment by the audience and by expert opinion. Demonstrated expertise in the subject area A. Clarity of presentation B. Ability to answer questions with appropriate depth of expertise

2 TEAM Educational Module Page 2 of 11 TEXT Physiology of Ventilatory Control Breathing is one part of a control system that operates to provide sufficient O 2 to meet cellular metabolic requirements and to remove enough CO 2 so that cell function is not impaired by excessive change in hydrogen ion concentration. What is remarkable is that in the healthy state the respiratory control system will maintain arterial PO 2 and PCO 2 within a fairly narrow range despite changes in metabolism and environmental conditions with growth, development, and extremes of daily living. Figure 1 illustrates essential components of the system. A controller regulates ventilatory behavior (the controlled system) and operates through efferent neural pathways coordinating contraction and relaxation of the controlled variable (respiratory muscles). A multiplicity of inputs to the controller respiratory neurons ensures that ventilation will be maintained when disease affects one components of this system or when the perception of some sensory cue is blunted by anesthesia, sleep, or neural injury. Conflicting demands, signals, or both from different receptors may be responsible for dyspnea, a common symptom in respiratory disease, or for hiccups, cough, and postural events that also utilize respiratory muscles. The system is also driven by feed forward mechanisms. One example is the anticipation of ventilation that may precede exercise even in the absence of CO 2 sensitivity. Feed forward mechanisms play a critical role in smoothly integrating breathing with swallowing, speaking, singing and defecating. Pontine and medullary respiratory groups initiate ventilatory behavior; these areas regulate the firing pattern of discharge in the motor neurons of the muscles of the upper airway and chest wall in a non-random and sequential fashion. Discharge patterns in

3 TEAM Educational Module Page 3 of 11 some pontine cells appear to be dependent on afferent vagal feedback but become more clearly phasic after vagotomy. Thus, in the adult mammal neither the medulla nor the pons alone generates the respiratory pattern. In addition, there is an interaction between states of alertness and the activity of higher brain centers and the brain stem bulbopontine respiratory neurons that determine respiratory rhythm and depth. A detailed discussion of the theory and the experimental data on the generation of respiratory rate and depth is beyond the scope of the current exercise. Electrical (neural) and mechanical outputs of the central inspiratory activity involve the anatomic structures of the chest wall (to inflate the lungs) and the upper airway (to stabilize the air channel to the lungs). In the diaphragm there is a progressive rate of rise in inspiratory activity that allows the musculature to overcome the progressive increase in the elastic recoil of the lung during inflation. The rate of rise of central inspiratory activity and hence the rate of lung inflation is controlled differently from those mechanisms that terminate inspiration. Hypoxia and hypercapnia increase the steepness of the ramp of inspiratory activity and hence increase the rate of inspiratory airflow and tidal volume, but they have little effect on the duration of inspiration and, therefore, the breathing frequency. This means that ventilatory responses to hypercapnia and hypoxia will depend on the sensitivity of both chemoreceptors and stretch receptors. Chemoreceptor sensitivity, since it influences the rate of increase in central inspiratory activity, is related more closely to the level of average airflow during inspiration than to minute ventilation. The change in the tidal volume/inspiratory time ratio, rather than the change in ventilation itself, more closely reflects chemical drive. On the other hand, the

4 TEAM Educational Module Page 4 of 11 change in inspiratory time as a fraction of total breath duration may relate to afferent feedback such as from the activity of stretch receptors. Additional factors alter the effect of respiratory central drive on tidal volume and frequency. With diseases of the lungs and chest wall, with obstructive apnea during sleep, or during certain stages of sleep when non-respiratory drive is altered in muscles of the chest wall, there can be a mismatch between neural activity and mechanical result. Hence, features of the controlled elements of the chest wall and upper airway can obscure central drive especially if the intervention substantially alters the controlled system. Hence, tidal volume and inspiratory flow are not always a precise copy of central drive. Cortical State Hypothalamic Regulation O 2 Consumption CO 2 Production Weight Pontomedullary Outflow Neural Transmission Carotid Body Medulla (VMS) Frequency Muscle Controlled Variables: O2 content, ph Minute Ventilation Tidal Volume Measured Variables

5 TEAM Educational Module Page 5 of 11 READINESS ASSURANCE TEST INDIVIDAL EXERCISE DO NOT OPEN UNTIL INSTRUCTED TO DO SO.

6 TEAM Educational Module Page 6 of 11 READINESS ASSURANCE TEST 1. Which of the following sequences most accurately describes the pathway for feedback control of ventilation with acute hypoxia? C. Brainstem output => hypoglossal nerve => chest wall => lungs => arterial blood content => carotid body => brainstem D. Brainstem output => chest wall => lungs => phrenic nerve => arterial blood content => carotid body => brainstem E. Brainstem output => phrenic nerve => chest wall => arterial blood content => lungs => ventral medullary surface => brainstem F. Brainstem output => phrenic nerve => chest wall => lungs => carotid body => arterial blood content => brainstem G. Brainstem output => phrenic nerve => chest wall => lungs => arterial blood content => carotid body => Brainstem 2. Which of the following components of the respiratory control determines tidal volume and frequency? A. Brainstem B. Lungs C. Carotid Body D. Vagus nerve afferent activity E. Hypoglossal nerve F. At least two of the above 3. Which of these receptors improve the matching of ventilation to acid-base balance? A. Golgi Tendon organs B. Vagal Stretch receptors C. Laryngeal flow receptors D. Muscle Spindles E. All of the above F. None of the above 4. Which of the following factors will lower PaCO 2? A. Morphine B. Hypoxia C. Dialysis D. Panic Disorder E. B,C, and D correct F. B and D correct 5. Which of the following may occur is there is obstruction at the level of the upper airway or lungs? A. Chronic hypoventilation B. Increased work of breathing C. Hypoxia D. All of the above E. None of the above

7 TEAM Educational Module Page 7 of 11 READINESS ASSURANCE TEST Answer. 1. F. This pathway is appropriate to the question being asked. Acute being 1-3 minutes 2. F. There are at least three and one could argue even four, but clearly the lungs do not produce tidal volume or frequency as they are passive by-standers. 3. F. None of these detect changes in PaCO2 or acid-base basis. 4. The best is F. (B and C), but E. could also be correct. 5. D. All of the above, Sleep apnea, COPD, asthma, or CHF.

8 TEAM Educational Module Page 8 of 11 GROUP ACTIVITY EXERCISE DO NOT OPEN UNTIL INSTRUCTED TO DO SO.

9 TEAM Educational Module Page 9 of 11 Case: Kingman s Mystery One morning in clinic I was presented with a 62 y.o. male golfer who stated that he had been in generally good health except for a nagging knee osteoarthritis until 3 months before seeing me when he had the following. He had a URI during which he experienced a pain in his left shoulder that prevented him from playing golf. He denied trauma. He woke up the next morning acutely short of breath, felt he could not breathe, and called 911. He was admitted from the Emergency Room to Intensive care for asthma and pneumonia, and placed on noninvasive ventilation. He felt somewhat better and was discharged three days later on antibiotics, steroids, and inhalers. No other records are available. He was instructed to see his local physician. He saw him 3 weeks after this hospitalization and in the office did a peak flow (229 with normal of 450) and sent the patient for a blood tests and a blood gas. The later showed a ph of 7.34, PCO2 56, and PO2 57. The rest of the blood tests were normal. The patient came to me with the diagnosis of COPD. I saw him a week later, confirmed his history (he could not breathe when he lay down to sleep). He did smoke in the past (15 year pack history) but no prior history of asthma, wheeze, shortness of breath, snoring, or heart disease (including hypertension). There was no family history of respiratory or cardiovascular problems. There were no allergies and he was on no chronic medications except Aleve; he had completed the course of antibiotics and had stopped the steroids and inhalers. On review of systems, he stated that he complained of some weakness in his left arm and poor range of motion in his shoulder. He was short of breath but felt that he was now out-of-shape. He could not sleep for more than 3 hours at a time; he did not think that he snored; he could not sleep on his back but could sleep on his left side, something new since his hospitalization. He could not play golf because of sleepiness and this shoulder problem. His goal was to play golf again. On physical examination, he was an articulate man, easily understood and without dyspnea. He had pursed lips breathing with active expiration. The HEENT examination was normal. He had a Gr. 1/6 murmur without rubs or gallops. He asked not to lie down for the abdominal examination. He had capsular tenderness on his left shoulder and an inability to raise his left arm over his shoulder. Neurologic examination showed mild weakness and numbness in the left hand; specifically sensation was diminished to pin prick over both radial and ulnar distributions and strength in his hand and upper arm was 4/5. The FVC was 2L and FEV1 1.7L. Lung volumes showed a normal FRC, a low VC, an RV slightly elevated and a RLC at the lower limit of normal. Oxygen saturation was 92%. The DLCO was normal. Chest X-ray was showed heart size at the limit of normal, diaphragms at the same level, but was otherwise normal. Group Activity Question. Which of the following is the most cost-effective action to make a diagnosis? Be prepared to defend your answer. A. Cardiopulmonary Exercise Testing

10 TEAM Educational Module Page 10 of 11 B. Polysomnography C. Examination and VC in the supine position D. High resolution CT E. Sniff test F. Referral for neurologic examination

11 TEAM Educational Module Page 11 of 11 Final diagnosis was bilateral diaphragm paralysis of unknown etiology, presumably viral. The patient recovered function in 5-6 months, something which is reported in the literature as sometimes occurring. The diagnosis was made by observing abdominal paradox with the patient in the supine posture and showing that the VC in the supine position was 1.1L. Polysomnography showed hypoxemia with saturations to the 80 s, with shallow breathing, and an AHI of 5. Although not noted at interpretation, review of the record confirmed paradoxical motion of the abdomen. The patient was placed on bilevel ventilation at night. He underwent successful arthroscopic knee surgery. Eight months later the patient reported he could breathe well and stopped bilevel treatment. VC was now 3L in the upright posture and 2.6L supine. Other points: Sniff test may be interpreted as normal in bilateral diaphragm paralysis. Exercise may be only mildly affects unless there is co-existing lung or heart disease. Dogs with bilateral surgical ablation of the phrenic nerves do fine, as they use active expiration to achieve ventilatory needs. Neurologic examination showed a reduced nerve conduction in the left > right arm consistent with a peripheral neuropathy. CT of neck was normal.