Lesson 1 Chapter 11 – The Respiratory System [Part 2]

Lesson 1 Chapter 11 – The Respiratory System [Part 2] 1 Unit 10 Study Guide Excluded from study: Chapter 11: Respiratory mechanics Pages 454 – 456. Part 2 of The Respiratory System Effect of Exercise and High Altitude on Respiratory Function I. During exercise there is increased ventilation, or hyperpnea (energetic respiration that occurs normally in exercise or abnormally with various fevers), which is matched to the increased metabolic rate so that the arterial blood PCO2 remains normal. o This hyperpnea may be caused by proprioceptor information, cerebral input, and/or changes in arterial PCO2 and pH. o During heavy exercise the anaerobic threshold may be reached at about 55% of the maximal oxygen uptake. At this point, lactic acid is released into the blood by the muscles. o Endurance training enables muscles to utilize oxygen more effectively, so that greater levels of exercise can be performed before the anaerobic threshold is reached. II. Acclimatization to a high altitude involves changes that help to deliver oxygen more effectively to the tissues, despite reduced arterial PO2. o Hyperventilation occurs in response to the low PO2. o The red blood cells produce more 2,3-DPG, which lowers the affinity of hemoglobin for oxygen and improves the unloading reaction. o The kidneys produce the hormone erythropoietin, which stimulates the bone marrow to increase its production of red blood cells, so that more oxygen can be carried by the blood at given values of PO2. Lesson 1 Chapter 11 – The Respiratory System [Part 2] 2 Regulation of Breathing I. The rhythmicity center in the medulla oblongata directly controls the muscles of respiration. o Activity of the inspiratory and expiratory neurons varies in a reciprocal way to produce an automatic breathing cycle. o Activity in the medulla is influenced by the apneustic and pneumotaxic centers in the pons, as well as by sensory feedback information. o Conscious breathing involves direct control by the cerebral cortex via corticospinal tracts. II. Breathing is affected by chemoreceptors sensitive to the PO2, pH, and PO2 of the blood. o The PCO2 of the blood and consequent changes in pH are usually of greater importance than the blood PO2 in the regulation of breathing. Lesson 1 Chapter 11 – The Respiratory System [Part 2] o Central chemoreceptors in the medulla oblongata are sensitive to changes in blood PCO2 because the resultant changes in the pH of the cerebrospinal fluid. o The peripheral chemoreceptors in the aortic and carotid bodies are sensitive to changes in blood PCO2 indirectly, because of consequent changes in blood pH. III. Decreases in blood PO2 directly stimulate breathing only when the blood PO2 is lower than 50 mm Hg. A drop in PO2 also stimulates breathing indirectly, by making the chemoreceptors more sensitive to changes in PCO2 and pH. IV. At tidal volumes of 1 L or more, inspiration is inhibited by stretch receptors in the lungs (the Hering, Breuer reflex). A similar reflex may act to inhibit expiration. • Respiratory centers in brain stem establish a rhythmic breathing pattern – Medullary respiratory centre • Dorsal respiratory group (DRG) – inspiratory neurons • Ventral respiratory group (VRG) – For active inspiration and expiration – Pre-Bötzinger complex (pace-maker) • generate respiratory rhythm – Pneumotaxic centre • Sends impulses to DRG that help “switch off” inspiratory neurons • Dominates over – inhibits apneustic centre – Apneustic centre • Prevents inspiratory neurons from being switched off • Provides extra boost to inspiratory drive – Hering-Breuer reflex • Triggered to prevent over inflation of the lungs 3 Lesson 1 Chapter 11 – The Respiratory System [Part 2] 4 Mechanics of Breathing I. Inspiration and expiration are accomplished by the contraction and relaxation of striated muscles. o During quiet inspiration, the diaphragm and external intercostal muscles contract and thus increase the volume of the thorax. o During quiet expiration, these muscles relax, and the elastic recoil of the lungs and thorax causes a decrease in thoracic volume. o Forced inspiration and expiration are aided by contraction of the accessory respiratory muscles. II. Spirometry aids the diagnosis of a number of pulmonary disorders. o In restrictive disease, such as pulmonary fibrosis, the vital capacity measurement is decreased to below normal. o In obstructive disease, such as asthma and bronchitis, the forced expiratory volume is reduced to below normal because of increased airway resistance to air flow. III. Asthma results from bronchoconstriction; emphysema and chronic bronchitis are frequently referred to collectively as chronic obstructive pulmonary disease. Respiratory Acidosis and Respiratory Alkalosis “ROME” mnemonic R respiratory O opposite pH up, pco2 down = alkalosis pH down, pco2 up = acidosis M metabolic E equal pH up, hco2 up = alkalosis pH down, hco2 down = acidosis Respiratory acidosis: The basic pathophysiology of this is that the patient is not clearing carbon dioxide from their body. Hypoventilation (reduced rate and depth of breathing) causes an Lesson 1 Chapter 11 – The Respiratory System [Part 2] increase in carbon dioxide throughout the cells and tissues of the body. The hypoventilation results in pulmonary congestion and airway obstruction which leads to all the breathing difficulties. Symptoms are: o o o o o o o o o o o pH below 7.35 and pco2 over 45mmhg rapid, shallow respirations hypoventilation dyspnea elevated blood pressure headache hyperkalemia disorientation elevated cardiac output muscle weakness hypoxia Respiratory alkalosis: Hyperventilation, rapid rate of breathing, causes too much carbon dioxide to be exhaled and the pH of the body rises. The cardinal sign of respiratory alkalosis is the deep, rapid breathing, more than 40 breaths per minute, which is similar to kussmaul's respirations (seen in metabolic acidosis). This kind of breathing leads to neuromuscular and central nervous system disturbances. This will occur in pulmonary diseases such as asthma, as well as in pregnancy, fever, at high altitudes and with acute anxiety. Think of the things that would cause a person to breathe very rapidly and cause large losses of carbon dioxide. Symptoms are: o o o o o o o o o o o pH elevated above 7.45 and pco2 below 35mmhg rapid, deep breathing hyperventilation agitation paresthesias seizures confusion hypokalemia lightheadedness dizziness tingling of the extremities [Continued below] 5 Lesson 1 Chapter 11 – The Respiratory System [Part 2] p H < 7 .4 6 A rte ria l b lo o d sa m p le p H > 7 .4 A c id o s is H C O -3 < 2 4 m E q / L A lk a lo s is p C O 2> 4 0 m m H g H C O -3 > 2 4 m E q / L p C O 2< 4 0 m m H g M e ta b o lic a c id o s is R e s p ir a to r y a c id o s is M e ta b o lic a lk a lo s is R e s p ir a to r y a lk a lo s is C ause: A c c u m u la tio n o f a c id in b lo o d , lo s s o f b ic a rb o n a te C o m p e n s a tio n : M o re C O 2 b lo w n -o ff, k id n e y e x c r e te s e x c e s s a c id C ause: H y p o v e n tila tio n , b r e a th in g a ir w ith h ig h C O 2 C o m p e n s a tio n : K id n e y m a k e s m o r e H C O -3 a n d a d d s it to th e b lo o d C ause: A c c u m u l a t i o n o f H C O -3 in b lo o d ( in g e s tio n ) , lo s s o f a c id ( v o m itin g ) C o m p e n s a tio n : L e s s C O 2 b lo w n -o ff, k i d n e y e x c r e t -e s excess H C O 3 C ause: H y p e r v e n tila tio n , h ig h a ltitu d e C o m p e n s a tio n : K i d n e y e x c r e -t e s m o re H C O 3 Respiratory acidosis is an abnormal process characterized by accumulation of CO2. Most often inadequate alveolar ventilation causes accumulation of CO2 in the blood. If CO2 builds up in the blood, the following reactions are pushed to the right: CO2 + H2O  H2CO3  H+ + HCO-3 Retention of CO2 leads to an increase in [H+], and to a fall in pH. The plasma [HCO3-] will also be elevated, but proportionately less than increase in Pco2. The kidneys compensate for respiratory acidosis by increasing the output of H+ ions in the urine. By getting rid of H+ ions the kidneys raise the plasma bicarbonate concentration. Respiratory alkalosis is the opposite of respiratory acidosis. It is produced by alveolar hyperventilation, which results in excessive removal of CO2 from the blood. The kidneys compensate for respiratory alkalosis by increasing the output of bicarbonate ions in the urine. Metabolic acidosis is an abnormal process characterized by gain of fixed acid (i.e., an acid other than H 2CO2), or loss of bicarbonate. In renal failure, the acid end-products of metabolism are not excreted at a rate that keeps up with production. If strong acid is added to the body, the following reactions are pushed to the left: CO2 + H2O  H2CO3  H+ + HCO-3 Lesson 1 Chapter 11 – The Respiratory System [Part 2] 7 [H+] will increase and [HCO3-]will decrease. Pco2 will increase transiently, and in established metabolic acidosis will be below normal due to respiratory compensation Metabolic alkalosis is characterized by gain of strong base or bicarbonate, or loss of acid (other than H 2CO3). Ingestion of excess sodium bicarbonate results in a metabolic alkalosis. Vomiting will also cause metabolic alkalosis. Respiratory compensation is alveolar hypoventilation. Renal compensation involves increased excretion of bicarbonate in the urine. Restrictive Pulmonary Disorders Result from Decreased Lung Expansion • Pulmonary disorders – Tuberculosis (specific type of infection in the lungs) – Pneumonia (a general term for any lung infection caused by a variety of pathogens) – Extra-pulmonary disorders – Chest wall disease • Kyphosis, scoliosis, obesity – Pleural • Pleural effusion (too much fluid in pleural space) • Pneumothorax – Neuromuscular disorders • Myasthenia gravis (an autoimmune disease that causes muscle weakness) • Hemiplegia (paralysis of one side of the body) Pink Bluffer vs Blue Bloater • • • • • • • Chronic bronchitis Blue bloaters Cough with sputum Mismatching of ventilation-perfusion ratio Decreased PaO2 and increased PaCO2 Hypoxemia and cyanosis Polycythemia, Pulmonary hypertension and Corpulmonale common • • • • • • Emphysema Pink puffers Dyspnea Proportionate loss of ventilation-perfusion Decreased PaO2 (slight), normal PaCO2 in early phase, increased later Over-ventilate and maintain relatively normal blood gas levels until late – barrel chest Lesson 1 Chapter 11 – The Respiratory System [Part 2] 8 Lesson 1 Chapter 11 – The Respiratory System [Part 2] 9 A "pink puffer" is a person where emphysema is the primary underlying pathology. As you recall, emphysema results from destruction of the airways distal to the terminal bronchiole-which also includes the gradual destruction of the pulmonary capillary bed and thus decreased inability to oxygenate the blood. So, not only is there less surface area for gas exchange, there is also less vascular bed for gas exchange--but less ventilation-perfusion mismatch than blue bloaters. The body then has to compensate by hyperventilation (the "puffer" part). Their arterial blood gases (ABGs) actually are relatively normal because of this compensatory hyperventilation. Eventually, because of the low cardiac output, people afflicted with this disease develop muscle wasting and weight loss. They actually have less hypoxemia (compared to blue bloaters) and appear to have a "pink" complexion and hence "pink puffer". Some of the pink appearance may also be due to the work (use of neck and chest muscles) these folks put into just drawing a breath. A "blue bloater" is a person where the primary underlying lung pathology is chronic bronchitis. Just a reminder, chronic bronchitis is caused by excessive mucus production with airway obstruction resulting from hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi. Unlike emphysema, the pulmonary capillary bed is undamaged. Instead, the body responds to the increased obstruction by decreasing ventilation and increasing cardiac output. There is a dreadful ventilation to perfusion mismatch leading to hypoxemia and polycythemia. In addition, they also have increased carbon dioxide retention (hypercapnia). Because of increasing obstruction, their residual lung volume gradually increases (the "bloating" part). They are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces--the "blue" part. Bronchial asthma is a chronic inflammatory disease of the airways characterized by bronchial hyperreactivity and a variable degree of airway obstruction. It is diagnosed on the basis of the clinical history, physical examination, and pulmonary function tests, including reversibility testing and measurement of bronchial reactivity. The goal of treatment is to control the symptoms of the disease effectively and in lasting fashion. Long-term treatment with inhaled corticosteroids is the basis of asthma treatment, alongside preventive measures and patient education. Bronchodilators such as beta2 sympathomimetics are used for rapid symptomatic relief of acute attacks. - Can be chronic more acute and intermittent than COPD Lesson 1 Chapter 11 – The Respiratory System [Part 2] 2 types: • • Extrinsic (childhood-onset) – History of allergy (hay fever/eczema) – Family history – Positive skin test Intrinsic (adult-onset) – Respiratory infections/psychological factors – Attacks are sever – Skin test – negative 10 Lesson 1 Chapter 11 – The Respiratory System [Part 2] 11