Ventilatory Control Flashcards
- Describe the inputs to and outputs of the central nervous system in controlling breathing.
neural output from the brainstem to respiratory muscles
chemical mechanical and neural act on receptors, which transfer info to integration centers within the brainstem
- **Central Controller
neurons responsible for automaticity an phase switching that make up normal breath
pontine respiratory groups:
median parabrachial nucleus- expiratory control, causes expiration to occur sooner (shorter insp., increase RR
lateral parabrachial nucleus and koliker fuse nucleus- inspiratory neurons increase activity to phrenic nerve
medullary respiratory group:
dorsal respiratory -Nucleus tracts solaris- inspiratory, inhibit expiration neurons in VRG
ventral respiratory group- expiratory and inspiratory (N. Ambiguous, N. Retroambiguous)
Botzinger complex- expiratory, inhibits inspr. decreases phrenic activity
Pre-Botzinger complex- central pattern generator, pacemaker neurons with ability to generate spontaneous activity
- Contrast peripheral and central chemoreceptors in how they sense and respond to changes in respiratory physiology.
peripheral located in the carotid and aortic bodies, sensitive to pH and PaO2 (ventilatory response to hypoxia)
[note the ventilatory response to hypoxia is a curvilinear response while response to CO2 is linear]
central chemo receptors are located on the ventrolateral surface of the medulla, separate from the inspiratory-expiratory neurons of the central controller; receptors are high gain meaning a pH change in 0.01 units causes a increase in alveolar ventilation of 5L/min and are required for rhythmic breathing; response to respiratory acidosis is much faster than the response to metabolic acidosis due to the diffusion rate of H+ much slower than diffusion of CO2 (control mainly ventilatory response to hypercapnia) increased perfusion causes decreased ventilation while decreed perfusion causes a increased ventilation
- Explain how the muscles involved in inspiration and expiration change with increasing levels of ventilation.
inspiratory muscles include the diaphragm, scalene, intercostals and the parasternals
expiratory muscles: abdominal muscles, intercostals and triangular is sternii (recruited at highest levels of exertion)
plus contributions from the upper airway muscles: primary upper airway dilator is the genioglossus, also the levitator and tensor palatine muscles
- Apply the length-tension relationship and force-velocity relationship to lung forces and volumes.
max inspiratory pressure at residual volume is -125 cm H2O
max static expiratory pressure at total lung capacity is +225 cmH2O; achieved at TLC/FRC when ex./in. muscle are most stretched
force-velocity is important to consider in compensation for resistive loads, added resistance will slow the rate of contraction and there by increase the force of contraction
- Appreciate the mechanisms of recognition and response to hypoxia and acidosis.
hypoxia will cause simulation of the peripheral chemoreceptors to innate ventilation, modulated by: 1.hypoxic effects on depression of CNS
- hyperventilation can cause hypocapnia and respiratory alkalosis
- hypoxia increases cerebral blood flow and less hydrogen ion will accumulate at the central chemoreceptor
acute acidosis results in increased ventilation, note delays in accessibility of H+ stimuli to chemoreceptor sites result in a more gradual development of compensatory mechanisms
- List the causes of alveolar hyperventilation.
hyperventilation with low PaCO2 most commonly occurs as a result of stimulus like hypoxemia, metabolic acidosis, or progesterone, most commonly due to lung disease
central neurogenic hyperventilation is “probably uncommon”, it may also be related to anxiety attacks or psychiatric disturbances
- Explain the mechanisms of CO2 retention.
- high metabolic rate
- low minute ventilation (due to high resistive load, high elastic load, weak muscles, low ventilatory drive
- ventilation-perfusion abnormality
- breathing pattern- low TV, high frequency
- List the causes of ventilatory failure.
CNS: drugs, infection, trauma, alveolar hyperventilation
Chest wall: kyphscoliosis, obesity, trauma
Airway obstruction: upper airway, lower airway (COPD)
NM: infection, myasthenia, trauma, myopathy
restrictive disease: interstitial disease, alveolar disease
metabolic: alkalosis, myxedema (hypothyroidism)
- Understand how disease states contribute to respiratory fatigue.
fatigue: energy demands of the fatigue are exceeded by the ability of blood supply determined by work of breathing and strength of respiratory muscle(don’t fatigue as quickly)
(effected by blood supply, oxygenation and nutrition)
- Describe how COPD affects alveolar ventilation, breathing patterns and respiratory muscle function.
inspiratory muscle strength is decreased because diaphragm is at a mechanical disadvantage
weakened inspiratory muscles as well as low oxygen levels; inward abdominal motion during inspiration is observed only in patients with COPD and is associated with poor prognosis
- Appreicate the clinical consequences of quadriplegia in affecting alveolar ventilation, breathing patterns and respiratory muscle function.
inward motion of the rib cage is common due to loss of the stabilizing effect of the intercostal muscles
lax abdominal wall muscles interfere with diaphragm elevating action on the rib cage
patients are at increased risk of muscle fatigue because of weak muscles, increased minute ventilation, chest distortion on inspiration and increased work of breathing
- Apply clinically the importance of diaphragm in ventilation.
diaphragmatic paralysis is most commonly associated with neuromuscular disease; patients present with orthopnea without heart failure, low lung volumes esp. when supine, CO2 retention is often present
patients are especially susceptible to REM sleep-related hypoventilation, REM inhibits intercostal and accessory inspiratory muscles, leaving only the diaphragm
- Describe the afferent input form the airways and what it responds to, the corresponding physiologic changes that occur when afferent systems are activated.
these inputs predominantly affect the pattern of breathing, most apparent with increased demands
airway receptors:
stretch (smooth muscles of airway)- prolong expiratory time
irritation (between epithelial cells in their airway mucosa, stimulated by noxious gases, dust, smoke and cold air- triggering cough, bronchoconstriction and mucous secretion
C receptors determine the level of bronchomotor tone or degree of airway relaxation or constriction
- Describe the afferent receptors of the parenchymal and chest wall muscles as well as what it responds to, the corresponding physiologic changes that occur when afferent systems are activated.
parenchyma: jutxa capillary or J-receptors in the alveolar wall; engorgement of pulmonary capillaries causes rapid shallow breathing
chest wall including diaphragm, intercostal muscles and ribs possess muscle spindles and Golgi apparatus in the tendons of the muscles which reflexively controls the strength or force of muscle contraction (sensation of dyspnea)
