Respiratory System Lessons 9-10

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  1. What is control theory of breathing?
    • 1. control systems consist of controller (driver), an effector (output), and a sensor to report the output back to the controller
    • 2. Sensors provide feedback about both mechanical distortion of chest cavity and chemical environment of blood
  2. What is the controller of vent. in control theory of breathing?
    2. central respiratory centers
  3. What is the effector of control theory of breathing?
    3. Effectors are respiratory muscles (diaphragm, abdominal and intercostal muscles)
  4. What are the controllers of the respiratory centers responsible for?
    brain centers control alveolar ventilation by affecting depth (VT) and rate (f) of breathing
  5. Where are controllers located in the brain?
    brainstem (pons/medulla)
  6. What suppresses controllers of respiratory centers?
    • 1. Drugs: heroine
    • 2. anesthetics or trauma resulting in hypoventilation
  7. What can stimulate controllers of respiratory centers?
    • drugs: aspirin
    • fever or progesterone resulting in hyperventilation
  8. What are the central respiratory centers for inspiratory centers?
    1. reticular formation of medulla
  9. What are the central respiratory centers for expiratory centers?
    reticular formation of medulla
  10. What is the pneumotaxic area?
    1. Upper pons: receives input from pulmonary stretch receptors that are stimulated by lung expansion. turns off inspiratory area and regulates inspiratory volume and respiratory rate
  11. Ablation of pneumotaxic area causes what?
    apneusis: prolonged inspriation for many seconds
  12. What are central chemoreceptors and where are they located?
    sensitive to H+ in cerebrospinal fluid. located on vetral surface of medulla
  13. What do central chemoreflexes do?
    • 1. increase H+ (decreases pH) in CSF increases the discharge frequency of receptors. This signal travels to respiratory center causing the cneter to increase the rate and depth of breathing (VA)
    • 2. Increase PaCO2--> H+ CSF --> chemostimulation --> Increase VA --> PaCO2 normal (H+ in plasma can not cross BB barier to stimulate central cehmoreflex
    • 3. Any condition that increases PaCO2 avove normal (hypoventilation) will activate the central chemoreflex to return PaCO2 back to normal level (40 mmHg)
    • 4. Not stimulated by hypoxemia (low PaO2)
    • 5. Larger effect to increase depth of breathing than to increase rate of breathing (Kussmaul's breathing)
  14. What do Peripheral chemoreceptors do?
    • 1. Increase PaCO2 --> carotid Body chemostimulation --> Increase Va --> decrease PaCO2 normal
    • 2. Deacrease PaO2 --> CB chemostimulation --> Increase VA --> PaO2 normal
    • 3. decrease plasma pH --> CB chemostimulation --> Increase VA --> increase pH normal b/c decrease PCO2
  15. Where are peripheral chemoreceptors located?
    carotid and aoritc bodies, travel to medulla by IX and X CNs
  16. What are peripheral chemoreceptors sensitive to?
    PCO2 [H+], and PO2 in arterial blood

    only receptors that respond to hypoxemia (low PaO2)
  17. What are the differences b/t central and peripheral chemeoreceptors?
    • 1. only peripheal chemoreceptors are stimulated by hypoxemia (low PaO2)
    • 2. both respond to changes in arterial PaCO2. 80% of reflex changes in vent. caused by this activation are due to central chemoreflex (central chemoreflex exerts more powerful control over regulation of arterial CO2
    • 3. both respond to chagnes in H+, but b/c H+ cannot cross blood brain barrier, elevation in plasma not related to CO2 would be sensed by peripheral chemoreceptors but not cental chemoreceptors. This occurs in states of metabolic acidosis that porduce acidic end products or renal disease
  18. What do pulmonary stretch receptors do?
    respond to distension of lungs (inspiration). Responsible for Hering-Breuer reflex
  19. What is the Hering-Breuer reflex?
    • 1. inflation of the lung inhibits inspiration
    • 2. Appears to be most effective when VT is increased above normal
    • 3.*** Thought to be a protective mechanism to prevent overinflation of the lungs***
  20. Where are pulmonary stretch receptors and where do they go?
    in airway smooth muslce to medulla (dorsal respiratory group) and pneumotaxic center
  21. What are pulmonary irritant receptors (rapidly adapting receptors)?
    • 1. stimulated by inhalation of irritant substances and inflammatory mediators (histamine, prostaglandins)
    • 2. Causes cough and bronchoconstriction
    • 3. May initiate sighs (large breaths)
    • 4. located in airway epithelium
  22. What are pulmonary J receptors (C-fibers)?
    • 1. located in alveolar walls
    • 2. stimulated by pulmonary edema and irritant substances that gain access to alveoli from inhalation or pulmonary circulation
    • 3. Cause tachypnea, bronchoconstriction, and "burning" sensation in lungs
  23. What are proprioceptors in thoracic cage?
    • 1. located in muscles and joints of respiratory muscles and rib cage
    • 2. respond to contraction of respiratory muscle and movement of rib cage
    • 3. together with pulmonary stretch receptos, these receptors send info back to respiratory centers about degree of inflation of lungs
  24. What is imporatance of cerebral cortex?
    • 1. conscious control of breathing
    • 2. emotional input (anger, stress, fear) often resutls in hyperventialtion
    • 3. exercise (volunatry effort)
    • 4. central command that inititates skeletal muscle contraction also stimulates breathing
  25. What are skeletal muscle receptors (somatic reflex)?
    receptors in muscles of limbs respond to muscle contraction and send a signal to respiratory center to stimulate breathing

    inputs to respiratory centers from central command and muscle receptors make it possible to increase vent. during exercise w/o altering O2 and CO2 content of blood to activate chemoreflexes
  26. What are non-neural inputs to respiratory centers?
    • Fever: alterations in temp. regulation in hypothalamus that produce fever also stimulate respiratory centers resulting in mild hyperventilation
    • Progesterone: elevated lasma progesterone levels in pregnant women stimulate respiratory centers to elvate breathing slightly
  27. What is dyspnea?
    Cognitive feeling of shorness of breath. occurs when vent. is not capable of matcing metabolic activity
  28. What is Tachypnea?
    manifested by rapid breathing. VT is less than normal. thought to be mediated by vagal reflex from lungs caused by stimulation of J receptors. Rapid shallow breathing accompaines stiff lungs of interstitial fibrosis and other restricive diseases, of pulmonary edema, and pulmonary emboli.
  29. What is Kussmaul's breathing?
    manifested as large increases in VT w/ little increase in breathing rate. caused by stimulation of pheripheral or central chemoreceptors. seen in normal individuals during exercise. pt's w/ metabolic acidosis it occurs at rest. feature of obstructive disease
  30. What is apneas?
    most prevalent during sleep b/c of loss of conscious control of breathing that helps to maintain constant breathing while awake
  31. What is central sleep apnea in central hypoventilation (suppressed breathing effort from brainstem)?
    • 1. Congenital (Ondine's curse)
    • 2. Diseases of autonomic system (Shy-Dager, Riley-Day syndromes)
    • 3. Secondary to brain stem trauma, encephalitis, tumors, etc
  32. What are neuromuscular disorders of apneas (impaired resp muscles or chest wall)?
    • 1. muscular dystrophy, neuromyopathies, etc.
    • 2. Chest wall abnormaltieis (obesity, kyphoscoliosis)
    • 3. Secondary to pulmonary diesease (fatigue of respiratory muscles: respiratory failure)
  33. What happens in obstructive sleep apnea (pharyngeal tissue obstructs airways)
    • 1. vent. stops b/c upper airway obstruction despite breathing efforts. Usually due to loss of muscle tone of pharynx
    • 2. frequent in persons who snore and are obese (Pickwickian syndrome)
  34. What are pathophysiological consequences of chronic apneas?
    • 1. pulmonary hypertenstion leading to R heart failure due to hypoxic pulmonary vasoconstriction
    • 2. Polycythemia (overproduction of RBCs due to hypoxemia)
    • 3. Systemic hypertension (high BP) and cardiac arrhythmias due to intense activation of central and peripheral chemoreflex, which elevate sympathetic nerve activity
    • 4. daytime fatigue, narcolepsy, and impaired mental acuity due to arousal from sleep caused by intense chemoreflex activation
  35. What is Biot's breathing?
    cluster breathing is manifested as clusters of irregular breaths alternating with periods of apnea

    caused by trauma/dieseas of pons or medulla
  36. What is Apneusis breathing?
    caused by ablation of pneumotaxic center in pons

    from: trauma/disease of pons
  37. What is Cheyne-Strokes breathing?
    pattern of breathing that waxes and wanes from hyperventilation to near apnea

    L heart failure and deals with VT
  38. What is the Function of the nasal passages?
    • 1. To warm and humidify inspired air
    • 2. To cleanse inspired air of microorganisms and pollutants
    • 3. Olfaction
  39. Blood vessels
    • a. Another unique aspect of the nasal sinuses is that the blood vessels of the nasal mucosa (epithelium) possess sinusoids and arteriovenous anastomoses (shunt vessels).
    • b. The sinusoids allow a large volume of blood to pool near the epithelial surface to enhance heat exchange.
    • c. Changes in blood volume in the sinusoids (capacitance vessels) cause the nasal mucosa to thin or thicken.
    • d. Smooth muscle tone in the capacitance vessels controls their blood volume.
    • e. Smooth muscle tone of resistance vessels controls the rate of blood flow in the mucosa, which indirectly affects blood volume in the sinusoids.
  40. Innervation
    • a. The blood vessels and submucosal glands in the nasal epithelium are innervated by parasympathetic and sympathetic motor nerves.
    • b. Neural motor pathways of the nasal passages
  41. Parasympathetic neural effects on the nasal passage
    • a) Activation of the parasympathetic defense reflex causes nasal resistance and capacitance vessels to dilate (due to acetylcholine release).
    • b) The capacitance vessels swell because the increased rate of blood flow pours more blood into the vessels causing the vessels and thus the epithelial lining to swell.
    • c) Swelling of the nasal mucosa increases resistance to airflow responsible for the sensation of 'stuffiness'
    • d) Relaxation of the precapillary resistance vessels also increases hydrostatic pressure in the nasal capillaries resulting in increased efflux of fluid onto the nasal mucosa.
    • e) Parasympathetic nerves cause increased submucosal gland secretion
    • f): Blockade of the acetylcholine receptor (muscarinic receptor) with atropine-like drugs (e.g. Ipratropium bromide) alleviates congestion and nasal secretions.
  42. Sympathetic neural effects
    • a) Alpha-adrenergic receptors cause contraction of the resistance and capacitance vessels causing decreased blood flow and emptying of blood from capacitance vessels. Thus, the nasal mucosa retracts (alleviates congestion).
    • b): Neosynephrine (an alpha-adrenergic agonist) alleviates nasal congestion due to alpha-adrenergic contraction of nasal blood vessels
    • c) During exercise the nasal passages retract due to increased sympathetic nerve activity (alpha-adrenergic mediated); thus reducing nasal resistance to airflow
    • Decongestants
    • d) Sympathetic nerves do not have major effects on submucosal gland secretion.
  43. Nonadrenergic / noncholinergic nervous system (NANC)
    a) The effects of this neural system on nasal function are unknown
  44. Airway smooth muscle
    a. The nasal passages do not have a layer of smooth muscle beneath the epithelial surface. A subepithelial layer of smooth muscle is typical of the air passages below the larynx
  45. Function of the trachea and lower airway
    • 1. To trap and expel particles that bypass the nasal barrier
    • 2. To protect the lungs from inhaled microorganisms
    • 3. To distribute inspired air to the gas exchange regions
  46. Muco-ciliary escalator
    • a. Goblet cells: secrete mucus
    • b. Serous cells: function unknown (production of sol layer?)
    • c. Submucosal glands: secrete mucus
    • d. Ciliary cells: possess cilia that extend into the mucus layer and propel the mucus toward the pharynx.
    • e. The muco-ciliary escalator operates in the nasal sinuses as well as airways
  47. Proper functioning of the muco-ciliary escalator
    • i. Requires a fine balance between periciliary fluid (sol layer) and mucus (gel layer)
    • a) An adequate sol layer is needed for cilia to beat freely.
    • b) Normally the gel layer floats above the sol layer and is propelled toward the upper airway by the tips of the beating cilia
  48. Abnormality of the muco-ciliary escalator
    • i. In cystic fibrosis, there is an abnormality in Cl- transport in the airway epithelial cells that prevents adequate movement of water onto the epithelial surface (i.e. the sol layer is virtually absent)
    • ii. As a result of an abnormally low sol layer, the cilia cannot beat properly and the thick mucus of the gel layer accumulates in the airways
  49. Function of Airway smooth muscle
    • a. The function of airway smooth muscle is not known for certain. Bronchoconstriction occurs upon irritation of the airways and is thought to help prevent particles from traveling to lower airways .
    • b. Airway smooth muscle is under the control of the autonomic nervous system
  50. Parasympathetic nervous system (vagus)
    • a) Stimulation (cholinergic) causes bronchoconstriction and increased Raw, evoked by airway defense reflex when the airway is irritated.
    • b): Anticholinergic drugs block parasympathetic bronchoconstriction. Ipratropium can provide short-term relief in chronic asthma, but short-acting ß 2 -agonists work more quickly
  51. Sympathetic nervous system
    • a) ß adrenergic receptors on airway smooth muscle cause relaxation (bronchodilation). Their physiological role is not known. Neurotransmitter is epinephrine. The sympathetic system is activated during exercise.
    • b): ß adrenergic agonist drugs (e.g. albuterol, salbutamol) are often effective in alleviating bronchoconstriction of asthma.
  52. Nonadrenergic / noncholinergic nervous system (NANC)
    • a) NANC receptors on airway smooth muscle cause relaxation (bronchodilation).
    • b) The neurotransmitter is not known but thought to be vasoactive intestinal peptide (VIP) or possibly nitric oxide.
    • c) VIP is found in parasympathetic nerve terminals along with acetylcholine.
    • d) The physiological role of NANC is not known.
    • e) A recent theory suggests that people who have abnormally low numbers of NANC receptors on airway smooth muscle are predisposed to asthma.
    • f) Bronchodilators: Agonists of NANC receptors that are easy to administer and effective have not been developed.
  53. Decreasing alveolar CO2 below normal causes what?
    local bronchoconstriction
  54. increasing alveolar CO2 above normal causes what?
  55. Asthma
    • 1. Major disorder of airway smooth muscle.
    • 2. Acute episodes of severe bronchoconstriction resulting in wheezing, dyspnea, cough, sputum formation.
    • 3. Attacks usually triggered by allergens, irritants, exercise, or food/drugs.
    • 4. Airway smooth muscle is very sensitive to bronchoconstricting mediators (e.g. acetylcholine, histamine, leukotrienes, substance P).
    • 5. Cause of asthma is not known. Depletion of VIP in asthmatics suggests that loss of bronchodilator mediators may result in hyper reactivity to constricting substances.
    • 6. Mild asthmatics may not be detected by pulmonary function testing (i.e. asymptomatic) unless they tested during an asthma attack.
    • 7. Methacholine challenge is used to test to hyper reactive airways. Inhalation of methacholine up to 25 mg/ml will decrease FEV1 by more than 20% only in patients who test positive for asthma.
    • 8. Most effective treatments are beta adrenergic and anti-inflammatory drugs.
  56. Catarrhal inflammation
    inflammation of airway epithelium. Inflammation is the result of irritation of the airway lining (epithelium) which stimulates irritant sensory nerve endings that release the neuropeptide substance P. Activation of this axon reflex (neurogenic inflammation) causes degranulation of mast cells. It can occur along the entire respiratory tract.
  57. Mast cell degranulation
    • 1. Cells located beneath the airway epithelium. They release inflammatory substances (degranulation) when stimulated by substance P released from irritant sensory nerves in the epithelium or, in susceptible individuals, by antibodies (IGEs) in response to inhalation of specific antigens ( e.g. pollen, animal dander, etc.).
    • 2. Many inhaled particles are recognized as an antigen (e.g. pollen) in susceptible individuals and cause mast cells to release inflammatory substances. We call this an allergic response.
    • 3. Substances released from mast cells: Histamine, bradykinin, serotonin, prostaglandins (PGx), leukotrienes (LTx, slow reacting substance of anaphylaxis), platelet activating factors, eosinophil chemotactic factor (ECF), neutrophil chemotactic factor (NCF)
  58. Effects of inflammatory substances on the airways
    Contract airway smooth muscle directly b. Stimulate irritant receptors and C-fibers, evoking the irritant reflex c. Enhance mucous secretion from goblet, serous and submucosal gland cells directly d. Increase the beating of ciliary cells (accelerate the muco-ciliary escalator)
  59. Other inflammatory responses caused by these mediators
    • a. Cause vasodilatation of local blood vessels to increase blood flow
    • b. Increase permeability of vascular capillaries to produce interstitial edema and swelling of the tissue
    • c. Promote clotting of plasma in the interstitial spaces
    • d. Promote migration of large numbers of PMNs (polymorphonuclear leukocytes or granulocytes) and monocytes into the tissue (NCF = neutrophil chemotactic factor; ECF = eosinophil chemotactic factor).
    • e. Activate macrophages, neutrophils, and eosinophils
    • f. Effect of swelling, clotting, and edema helps to 'wall off' the injured tissue to retard spread of infectious agents
  60. Other factors contributing to mast cell degranulation
    • a. Complement factors activated by antigen- antibody reactions
    • b. Proteases released from neutrophils and macrophages
    • c. Activated IgE antibodies (the allergic response)
  61. Function of inflammation
    • Cardinal signs of inflammation: rubor, calor, tumor, dolor
    • Hyperemia (increased blood flow) in mucosal vessels (rubor) is to enhance delivery of blood-
    • borne immune cells (monocytes, neutrophils, etc.) to the site of injury.
    • Hyperemia also increases the temperature of the tissue (calor) to impair function of the bacteria/virus.
    • Edema of the epithelium (tumor) retards invasion of bacteria, viruses, etc. into the general circulation via edema formation at the site of injury.
    • Stimulation of irritant receptors (dolor, soreness) alerts the body that the tissue has been injured.
    • Another result of catarrhal inflammation is enhanced muco-ciliary activity, mucous secretion, and bronchoconstriction that help in eliminating the invading irritants.
    • inflammation of the airways results in bronchitis
    • h. i. inflammation of the alveoli results in pneumonia
  62. Pharmacology
    • a. Inhibitors of mast cell degranulation or antagonists to receptors for many of the mediators released from mast cells (anti-inflammatory drugs) are very effective in alleviating nasal congestion and bronchoconstriction.
    • b. Mast cell degranulation: Cromolyn sodium acts to stabilize mast cells and prevent degranulation. Often not very effective.
    • c. Receptor antagonists or synthesis blockers: antihistamines(many, e.g. diphenhydramine), inhibitors of prostaglandin production (e.g. indomethacin). Leukotriene receptor antagonists (e.g. singular)
    • d.Corticosteroids: Glucocorticoids suppress the immune system through inhibition of cytokine production and have an anti-mitotic action on cells of the immune system in addition to other immune suppressing effects. They decrease production of Substance P receptors and increase beta-adrenergic receptors. The accumulative effects are to suppress mast cell degranulation, reduce cytokines, and decrease inflammation. Prednisone is common prescribed glucocorticoid receptor agonist.
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Respiratory System Lessons 9-10
2011-11-06 18:44:35
Respiratory System

Respiratory System Lessons 9-10
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