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Unit 6A Ch. 39 P.

1321 Notes Lower respiratory system function depends on several organ systems: CNS-stimulates and controls breathing Chemoreceptors in brain, aortic arch, carotid bodies which monitor pH and oxygen content of blood. Heart and circulatory system- provide blood supply and gas exchange. Musculoskeletal system- provides intact thorasic cavity capable of expanding and contracting Lungs and bronchial tree- allow air movement and gas exchange. Impaired functioning of any of these systmes effects ventilation and respiration. Tissues become hypoxic with inadequate oxygen to support metabolic activity. Reactive Airway Disease: Asthma and obstructive disorders, air trapping reduces the amount of oxygen available to drive gas exchange. Interstitial Lung Disorders: Affect the ability of the lungs to expand and the work of breathing, again reducing aveolar oxygenation and gas exchange. Pulmonary Vascular Disorders: Affect blood flow to the lungs or a portion of the lungs, reducing gas exchange through their effects on perfusion of the lungs. Respiratory Failure: Is the ultimate consequence of impaired gas exchange. The lungs cannot adequately oxygenate the blood or eliminate carbon dioxide. Neurologic Disorders (head injury, spinal cord trauma or disorders, amyotrophic lateral sclerosis, myasthenia gravis) also can effect gas exchange through their effects on the central or peripheral nervous systems. Aging effects pulmonary ventilation and gas exchange. Number of alveoli decrease, and emphysematious changes (senile emphysema) reduces the surface area for gas excahnge. Alveoli become less elastic, causing increasing air trapping and dead space. For acitve older adults these changes have minimal effects. For those with lung disease age related pulmonary changes increase risk for developing respiratory failure. Reactive Airway Disorders Airways narrow in response to stimulus. Narrowing limits airflow to both into and out of the alveoli. This will increase workload of breathing. And the residual volume of lungs because air is trapped behind narrow airways. Inspired air mixes with abnormally large volume of resudual air, reducing the amount of oxygen available in the alveoli. Decreased aveolar ventilation further reduces oxygen available for exchange. Asthma: Chronic inflammatory disorder of the airways characterized by recurrent episodes of wheezing, breathlessness, chest tightness and coughing. Inflammation causes increased responsiveness of the airways to multiple stimuli. Widespread airflow obstruction. Allergies play strong role in childhood asthma, strong genetic component, environmental factors ; air pollution, occupational hazzards. Respiratoyr viruses rhinovirus and influenza can precipitate asthma attacks. Exercise particularly in cold air and emotional stress. Physiology Review Parasympathetic (cholinergic) stimulation leads to bronchoconstriction, or narrowing of the airways. Sympathetic stimulation through B2 adrenergic receptors causes bronchodilation or expansion of the airways. Slight bronchoconstriction normally predominates. However, when increased airflow is necessary (exercise) the parasympathetic system in inhibited and stimulation of the sympathetic systems causes bronchodilation. Inflammatory mediators (such as histamines) released during an antigen antibody response act directly on bronchial smooth muscle to produce bronchoconstriction. In Asthma the airway is in a persistent state of inflammation. Even when quiet inflammatory cells such as eosinophils , neutrophils, and lymphocytes may be found in airway tissues and edema my be present.

Attack Triggers: inhalation of allergens such as pollen, animal dander, household dust, tobacco, irritant gases ( sulfer dioxide, nitrogen dioxide and ozone) second hand smoke, chemicals. Viral respiratory infections are common internal stimulus for asthma attacks. Asprin, and other nonsteroidal antiinflamatory drugs. Sulfites (in wine, beer, fresh fruit and salads) and beta-blockers. As a result hypoxemia develops. Hypoxemia and increase lung volume due to tapping stimulat the respiratory rate. Hyperventilation causes the Paco2 to fall, leading to respiratory alkalosis. Summary: In an acute attack, inflammatory mediators are released from sensitized airways followed by activation of inflammatory cells. These events lead to bronchoconstriction, airway edema, and impaired mucociliary clearance. Airway narrowing limits airflow and increases the work of breathing; trapped air mixes with inhaled air , impairing gas exchange. Manifestations chest tightness Cough dyspnea wheezing tachypnea and tachycardia anxiety and apprehension