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RESPIRATORY SYSTEM Ma. Cristina O. Gumangan, MS Phar

Functions of the Respiratory System Respiratory Physiology Ventilation (breathing) External Respiration Transport of gases between the lungs and the rest of the body tissues. Internal Respiration Cellular Respiration Factors that affect gas exchange: Partial pressures of O2 and CO2 1. 2. Thickness and surface area of the respiratory membrane respiratory membrane: alveolar membrane + endothelial membrane + fused basement membrane = 0.5-1.0 um thick Pneumonia - inc. thickness of RM due to mucus build up = dec. diffusion of gases Pulmonary edema fluid in the interstitial spaces, increases diffusion distance Emphsema destruction of the alveoli; less surface area for gas exchange 3. Solubility of O2 and CO2 Solubility in plasma and alveolar fluid: CO2 > O2 4. Temperature high temperature, high kinetic energy, increased movement of gases within the alveoli rate of gas exchange Plasma pH If breathing is shallow and slow High CO2 = high carbonic acid, high H+, low pH = respiratory acidosis = higher

If hyperventilation occurs
CO2: elimination>production Low CO2 = low carbonic acid, high pH = respiratory alkalosis Metabolic Acidosis Low blood pH and blood HCO3- are low Compensatory mechanism: = inc. respiratory rate and depth = dec CO2 = inc pH Metabolic Alkalosis

high blood pH and HCO3Compensatory Mechanism: = slow and shallow respiratory rate and depth = retention of CO2 and production of H+ = lower pH

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Hyperventilation (due to anxiety >>resulting alkalosis = cerebral blood vessel constriction

MANAGEMENT: Breathe into a paper bag =CO2: exhaled air>atmospheric air =inc CO2 Control of Respiration Central Controller: (1) Brainstem 1.Medulla 2.Pons (2)Cortex Limbic system and hypothalamus Effectors: diaphragm, intercostals, abdominal muscles,accessory muscles of respiration COMMON DISORDERS OF THE AIRWAYS I. ASTHMA - is a chronic inflammatory disorder of the airways characterized by: inflammation, obstruction, hyperresponsive airways episodic asthma symptoms due to interactions between cells and inflammatory mediators. PATHOPHYSIOLOGY (Please refer to the slides for visualization) a. Precipitating factors b. Inflammatory cells c. Mediators d. Activity

Hyperresponsiveness
-inc. levels of inflammatory mediators and infiltration by inflammatory cells

Altered autonomic neural control

- inc parasympathetic tone and reflex bronchoconstriction

Airway remodeling
- permanent airway abnormality due to subbasement membrane collagen deposition and fibrosis CLINICAL EVALUATION Physical Findings A. Acute exacerbations - Shortness of breath -Wheezing -Chest tightness

-Cough -Rapid breathing

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B. Chronic, severe asthma -chronic hyperinflation -barrel chest -dec. diaphragmatic excursion Diagnostic Test Results 1.Pulmonary function tests Decreased Forced expiratory volume in 1 second (FEV1) and forced vital capacity Increased Residual volume and total lung capacity Provocation testing with histamine or methacholine challenge 2. Blood Analysis: 3. Sputum analysis: 4. Pulse Oximetry

Oximeter - measures O2 saturation in arterial blood and pulse Normal: 95%-99% oxygen AbN: <95%
5. Arterial blood gas measurements - low PaCO2 6. Chest radiograph - + hyperinflation 7. Allergy skin tests and in vitro test (e.g. radioallergosorbent tests) PHARMACOLOGICAL TREATMENT 1. Bronchodilators a. B2-agonist Classification: 1. rapid acting, short DA 2. rapid acting, long DA 3. Long acting, slow onset SE: tachycardia, development of tolerance b. Methylxanthines c. Anticholinergics 2. Anti-inflammatory a. anti-mediator release b. leukotriene acting agents

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c. steroids classification: 1. locally acting/inhaled steroids 2. Systemic parental steroids 3. systemic oral steroids II. COPD (Chronic Obstructive Pulmonary Disease) - disease state characterized by airflow limitation that is not fully reversible ETIOLOGY OF COPD 1. Cigarette smoking 2. Occupational exposures 3. Acute infections 4. Genetic factor: Emphysema -deficiency of 1-antitrypsin 5. Air pollution CHRONIC BRONCHITIS -characterized by excessive mucus production by the tracheo-bronchial tree = airway obstruction due to edema and bronchial inflammation Pathophysiology of Chronic Bronchitis Respiratory tissue inflammation Changes in tissue Lung infxn: -Streptococcus pneumoniae, -Haemophilus influenzae, -Moraxella catarrhalis, -Staphyloccocus aureus -Pseudomonas aeruginosa sp. reduce ciliary and phagocytic activity inc mucus accumulation weaken the bodys defenses destroy small bronchioles Airways degenerate- overall gas exchange is impaired- exertional dyspnea ACUTE BRONCHITIS results from an infection such as colds or flu CHRONIC BRONCHITIS results usually from exposure to cigarette smoke - Cough: >30ml of sputum in 24 hrs for @ least 3 mos of the year for 2 consecutive years

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EMPHYSEMA -lung disease in which the walls of the alveoli fracture -marked by permanent alveolar enlargement and destructive changes of the alveolar walls. PHARMACOLOGIC TREATMENT 1. Theophylline MOA: bronchodilation inc mucociliary clearance stimulate respiratory drive enhance diaphragmatic contractility improve the ventricular ejection fraction stimulate renal diuresis 2. Antibiotics a. Indications: -tx exacerbations w/ suspected infxn -worsening dyspnea and cough w/ purulent sputum and inc sputum volume 3. Influenza virus vaccine NONPHARMACOLOGIC TREATMENT Oxygen therapy Chest physiotherapy Physical Rehabilitation Physical conditioning Social Psychological Nutritional interventions 4. Quit smoking and avoid other irritants Useful in smoking cessation: Nicotine gum, lozenges Transdermal patches Nicotine Inhalers Bupropion 5. Lung Transplant - restore breathing levels and drastically reduce symptoms 6. Bullectomy - surgical removal of bulla (air pockets)

or

burst

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III. CYSTIC FIBROSIS -an autosomal recessive genetic disease in which the lungs and pancreas produce excessive amounts of thick, sticky mucus The Effects of Cystic Fibrosis Impaired breathing Impaired digestion Life threatening infections How Cystic Fibrosis Develops

mutation in a single gene on chromosome 7 gene contains instructions for building a protein called the cystic fibrosis transmembrane conductance
regulator (CFTR) Early Signs and Symptoms of Cystic Fibrosis Chronic cough or wheeze Recurrent pneumonia/ lung infections No bowel movements (first 24-48 hours of life) Oily-type stools Chronic diarrhea Prolonged jaundice Salty skin Dehydration in hot weather Later Signs and Symptoms of Cystic Fibrosis Liver disease Clubbing of fingers Delayed growth and development Diagnostic test: Pilocarpine Iontophoresis sweat test Children: >60meq/L Adults: >80meq/L Lab Findings: Arterial blood gas: hypoxemia Pulmonary function: Dec forced vital capacity, Dec airflow rates, Dec total lung capacity Management of Cystic Fibrosis a. Physiotheraphy -a way of clearing the thick, sticky mucus that accumulates in the lungs -helps to prevent mucus from blocking air passages, which decreases the possibility of infection and lung damage.

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b. Diet High In Calories and Protein -Supplementing diet w/ tubefeeding

oGastrostomy tube (G-tube) oNasogastric tube (NG-tube)

c. Vitamin Supplements d. Salt supplements e. Pancreatic Enzyme Supplements - Creon and Pancrease Pharmacologic Treatment of CF Antibiotics to treat infection Inhaled bronchodilators Corticosteroids (Prednisone) Cough suppressants and chronic use of mucolytics should be avoided Vaccination against pneumococcal and influenza infxn Recombinant human deoxyribonuclease (rhDNase or dornase alfa) -cleaves the extracellular DNA from neutrophils in sputum -given via aerosol 2.5 mg od or bid

-> 5 y.o
Lung transplantation