Term
| What is the basic structuring of voluntary/autonomic control of breathing? |
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Definition
1) "Pace-maker" motorneurons in pre-Botzinger complex in brainstem initiate ventilation and inflation by activating the Dorsal (inspiration) and Ventral (expiration) respiratory groups of neurons in the pons and medulla, sending signals to
1a) chest wall (diaphragm and accessory muscles)
1b) upper airway muscles (maintain patency during breathing and protect lungs when swallowing)
2) Peripheral receptors are stimulated and send feedback
3) Motor cortex provides voluntary adjustments |
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Term
| What chemostimuli modulate neural control of breathing? |
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Definition
Can be central (PCO2 sensors) and peripheral (Carotid body and Aortic body)
1) Hypoxia (PaO2)
2) Hypercapnia (PaCO2)
3) pH (H+) |
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Term
| What are the major peripheral chemosensors that regulate breathing? |
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Definition
Aortic body (in arch of aorta) and Carotid Body (at bifurcation).
Consist of Type 1 (Glomus) cells that act as sensors and release catecholamines and Type II (Sheath) support cells.
1) Carotid body is very vascular and senses blood gas tensions (PaO2 NOT oxygen content or oxyhemoglobin saturation) and pH, sending afferent information to the CNS via carotid sinus nerve and CN IX
**Major hypoxemia sensor** |
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Term
| How do peripheral chemoreceptors compensate for hypoxia with hypercapnia? |
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Definition
| Usually, carotid body only augments breathing when PaO2 falls below 60 mmHg, but when hypercapnia is also present, it will augment breathing at values > 60 mmHg |
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Term
| How do central chemoreceptors in the ventrolateral medulla regulate breathing? |
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Definition
70-80% of ventilatory response to PCO2 is centrally mediated, and effects last longer than peripheral receptors.
1) Primarily sense PCO2 (crosses BBB, unlike H and HCO3-), which forms H+ and HCO3- one in the brain (H+ is primary stimulus)
2) Increased H+ stimulates ventilatory drive and alveolar ventilation |
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Term
| What are the 3 major groups of non-chemical receptors that control breathing? |
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Definition
1) Slowly adaptive innervated by myelinated vagal fibers
- Stretch receptors in airway smooth muscle cells are stimulated by inflation, increasing their firing rate and slowly decreasing despite continued stimulus
2) Rapidly adaptive (IRRITANT) innervated by myelinated vagal fibers
- Stretch receptors in airway epithelial cells are stimulated by inflation and exogenous factors, decreasing their firing almost immediately in response to stimulus
- Cause cough, hyperpnea and bronchoconstriction
3) J receptors innervated by un-myelinated C-fibers
- Found in pulmonary interstitial space near pulm/bronchial circulations, and respond to congestion, fibrosis and constriction (asthma) |
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Term
Where are each of the following receptor groups found?
1) Slowly adaptive
2) Rapidly adaptive
3) J receptors |
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Definition
1) Airway smooth muscle (inflation)
2) Airway epithelium (inflation and exogenous compounds)
3) Pulmonary interstitium near pulm/bronchial circulation to sense congestion, fibrosis and constriction. |
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Term
What fibers when stimulated cause each of the following?
1) Apnea followed by rapid shallow breathing, bradycardia and hypotension
2) Apnea following sustained lung inflation
3) Cough, hyperpnea and bronchoconstriction. |
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Definition
1) Pulmonary chemoreflex mediated by J-receptors in pulmonary interstitium in response to CHF, pulmonary fibrosis or asthma
2) Hering-Breuer Inflation Reflex mediated by slowly adaptive stretch receptors in airway smooth muscle in response to prolonged inspiration.
3) Rapidly adaptive stretch (irritant) receptors in airway epithelial cells. |
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Term
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Definition
Loss of automatic control of breathing, with sustained voluntary control usually due to brainstem lesion.
Children require constant ventilation, but in adulthood usually only during sleep. |
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Term
| Why does a lung transplant not significantly alter rate and depth of breathing in most cases? |
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Definition
It is attached above the carina to the recipient's trachea, so tracheal innervation is maintained (all you lose is cough response to lower airways).
This is different from heart transplant, where heart is attached to patient's right atrium and resting rate increases due to lost vagal innervation. |
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Term
What processes are described by each of the following?
1) Deep inspiration followed by forced expiration against a closed glottis
2) Spasmodic contraction of inspiratory muscles timed with sudden glottis closure
3) Series of superimposed inspirations in presence of open glottis
4) Deep inspiration with slow expiration over 5-6 s. |
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Definition
1) Cough
2) Hiccup
3) Sneeze
4) Yawn |
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Term
| Why do patients who were recently in high altitude conditions or who suffer from severe heart failure exhibit waxing and waning periods of hyperventilation and apnea during sleep? |
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Definition
Cheyne-Stokes respiration is usually due to
1) Pulmonary congestion
2) Delay in circulation time between lungs and central chemoreceptors due to cardiac insufficiency
3) Alterations in threshold for PaCO2 to stimulate breathing (might explain occurrence during sleep). |
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Term
| Why might an obese patient present with hypoxia, polycythemia, pulmonary HTN and RHF? |
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Definition
PIckwickian Syndrome where respiratory system cannot compensate for under-ventilation of parts of the lung (PaCO2 is high).
Endocrine-rich fat may explain why only some obese patients can compensate for Pickwickian syndrome** |
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Term
| How can fat directly alter respiratory control mechanisms? |
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Definition
Leptin binds to hypothalamic neurons altering central respiratory control.
Endocrine-rich fat may explain why only some obese patients can compensate for Pickwickian syndrome** |
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Term
| What do the carotid body and central chemoreceptors sense, respectively? |
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Definition
1) Carotid body senses Hypoxemia by detecting PaO2 and sending signals to brain via CN IX and carotid sinus nerve
2) Central chemoreceptors in ventrolateral medulla sense Hypercapnia in the form of H+, which is delivered to the brain as CO2 (CA mediated hydration in neural tissue produces H+ and HCO3-) |
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Term
| What happens to normal breathing during sleep? |
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Definition
Breathe less and responses are blunted.
1) Reduction in tidal volume without increase in frequency
2) Ve falls
3a) Non-REM there is a drop in PaO2 and Hb saturation and an increase in PaCO2. Also decreased sensitivity to PaCO2
3b) REM is more irregular and there is further decreased responsiveness to PaCO2 |
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Term
| Why is there irregular breathing during REM sleep? |
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Definition
| Loss of accessory muscles such as intercostals, making ventilation completely dependent on diaphragm. |
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