Respiratory system Flashcards
List and define the major disorders of the pulmonary system
Understand signs and symptoms of cyanosis
Goals for respiratory lecture
Provides the mechanisms for transport of oxygen from air into blood
Remove carbon dioxide from blood
Purpose of respiratory system
passageways that conduct air between atmosphere and lung
Upper respiratory tract
trachea, bronchial tree, lungs
where gas exchange takes place
Also pulmonary circulation, muscles, nervous system
Lower Respiratory tract
Mucous secreting cells: trap particles
Cilia: sweep mucous and debris out of respiratory tract
Too much mucous or particles: sneeze or cough
Smoking: irritation impairs cilia
Squamous cells replace ciliated epithelium
Respiratory Mucosa
Food and air: separate at esophagus and trachea
Epiglottis: protects opening into larynx
Trachea: is windpipe: composed of smooth muscle and elastic tissue with cartilaginous C rings
Pharynx
Sympathetic stimulation
Relax smooth mm
Dilate/enlarge bronchioles
Bronchiolesalveolar ducts alveoli
Bronchodilation
Single layer of simple squamous epithelial cells
Promotes diffusion of gasses
Respiratory capillary membrane: combined alveolar and capillary wall: gas exchange
Pulmonary capillaries in close contact with alveoli
Macrophages in alveoli: remove foreign material
Alveoli
Detergent action
Decreases surface tension
Facilitates inspiration
Prevents collapse of alveoli when expires
Surfactant
Air flows from high pressure to low pressure area
Pressure change in lungs from alteration in size of thoracic cavity
Ventilation
Ventilatory capacity
Measure air moving in and out of lungs
Disease processes may change this
Pulmonary Volume
Residual volume: volume remaining in lung after maximal expiration (1500ml)
Vital capacity: max amount of air that can be moved in and out of lungs (4000ml)
Dead space: areas where gas exchange cant take place
Tidal volume: air entering lungs with normal breath (500ml)
Inspiratory reserve; max volume air inspired after max expiration (2500ml)
Expiratory reserve: max volume of air expired following passive expiration (1000ml)
Total lung capacity: total volume of air in lung after max inspiration (5500ml)
Forced Expiratory volume in 1 sec (FEV1) volume of air forcibly expired after maximal inspiration in 1 sec (approx 80% of VC) 3200ml
Minute ventilation: Tidal volume x Rate of Ventilation 500 x 15 = 7500
Inspiratory capacity: TV+ IRV
Functional Residual Capacity; ERV+RV-air left after normal exhalation
Vital Capacity: IRV+TV+ERV-max air exhaled after max inhalation
Pulmonary volumes
Measured with peak flow meter
Reached within
100 milliseconds of expiration
Used to evaluate asthma
Peak Expiratory Flow
Medulla and pons
Inspiration: medulla: basic rhythm: phrenic nerve to diaphragm
Expiratory center: used when need forced expiration
Pons: coordination
Depression: meds, shallow breathing, hypothalamus
CO2 levels inhibit voluntary control
Chemo receptors: respond to elevations in CO2 or decrease in oxygen
Control of Ventilation
Must drop significantly (105 to 60mm Hg) before body responds to hypoxemia
Gas exchange: depends on relative concentration of gases
Gases move from high pressure area to low pressure area
Gas exchange can depend on thickness of membrane
Accumulation of fluid: oxygen diffusion is impaired
Extra fluid impairs blood flow
Oxygen levels
Affected by surface area
Decreased surface area, decrease in gas exchange
Emphysema or fibrosis
Most oxygen is carried bound to hemoglobin
Oxygen is released so can absorb into cells
Partial pressure of dissolved oxygen determines how much oxygen is released
CO2 diffuses: easily carried out
Gas exchange
Partial pressure of oxygen in blood Hypercapnia Hypoxemia PaO2: 95-100mmm Hg PaCO2 35-40 mmHg Measure arterial blood gasses in radial artery Pulse oximater Normal pulse ox 96-100%
Arterial blood gasses
pH is usually slightly basic 7.35-7.45
Scale 0-14 (acid-base)
Low pH: acidosis
High pH: alkalosis
High PaCO2: respiratory acidosis: chronic bronchitis
Low PaCO2: respiratory alkalosis: pneumonia
Acid Base Balance of Blood
Radiographs: Change in lungs Opacities: lesions CT: x-rays at various angles Detailed MRI More sophisticated
Chest imaging
Pulmonary arteriography/angiography Blood vessels Detect emboli, vascular abnormalities Use catheter through femoral vein Bronchoscopy Examination of trachea and bronchi Uses flexible tube Can take biopsy Exercise Tolerance
Other testing
Increase in negative pressure
Children, paralysis of intercostal muscles
Intercostal indrawing
Exhalation over trachea: higher pitched, longer than inhalation
Lung: vesicular sounds
Inhale: whoosh
Exhale: quiet
Sounds you might hear
Tracheal sounds over lungs (Pneumonia), absence of sound (effusion, collapsed lung, pneumothrax), crackles, wheezing
Breath sounds
Spirometry: test volumes and airflow
Arterial blood gas: check oxygen, CO2, bicarbonate, serum pH
Exercise tolerance: use with COPD: monitor progress
X-rays: tumors and infections
Bronchoscopy: biopsy check lesion
Culture and sensitivity
Peak expiratory flow: use with asthma
Acid base balance: usually 7.35-7.45 pH
Resp acidosis (pH low) resp alkalosis (pH high)
CT: use to rule out or in several pathologies
MRI:
Pulmonary angiography: look at blood vessels:
Exercise Tolerance
Graded Ex tolerance test: cardio and pulmonary status
Metabolic Equivalent (MET) 1 MET= amnt oxygen required with body at rest in sitting
CBC
Diagnostic Tests
Upper respiratory infection Common cold: Viral Many organisms Usually self limiting Spread by respiratory droplets Mucous membranes red and swollen Increase in secretions Sore throat, fever, headache Treatment: symptomatic: acetaminophen, decongestant
Infectious Disease
Streptococcus pneumoniae
Inflamed, necrotic mucous membranes
Secondary infection
Bacterial? Usually obstructed drainage Pressure builds Haemophilus influenzae, pneumococci, streptococci Nasal congestion Fever Sore throat Treat: decongest, analgesic, antibiotic
Sinusitis
Viral Upper and/or lower respiratory tract Viruses mutate Sudden onset, fever, marked fatigue, aching pain Can get secondary infection
Influenza
Primary infection or secondary to another condition
Aspiration or inflammation of lung
Classify by agent (bacterial, viral, fungal), location, epidemiology, pathophysiologic changes
Lobar pneumonia: usually strep
Manifestations: sudden onset, high fever, chills, fatigue, leukocytosis, dyspnea, tachypnea, tachycardia, pleuritic pain, rales, productive cough
Pneumonia
Diffuse infection
Lower lobes
Pooled secretions
Bronchopneumonia
Atypical pneumonia
Spreads rapidly
High mortality rate
Risk factors: travel to China, Hong Kong, Taiwan
Severe Acute Respiratory Syndrome
At one time considered controlled Now increasing globally Prevalence difficult to estimate Caused by Mycobacterium tuberculosis Hard to kill Primary infection: upper lobe local inflammatory rctn Produce granuloma with caseation: usually wall off Ghon complexes
Miliary TB: progressive form, doesn’t respond well to treatment
Secondary: “active”
Transmitted by oral droplets, milk in some countries
Crowded conditions, situations when resistance is low
Signs/symptoms: anorexia, malaise, fatigue, weight loss
Cough: more severe and productive
Sputum: purulent, blood
Positive TB test, chest x-ray, CT
Tuberculosis
Home or hospital
Combination of drugs
Treat 3 months to a year
Tuberculosis treatment
Cystic Fibrosis Inherited Genetic Thick secretions; mucous is tenacious Obstructs lungs and pancreas Bronchial walls become damaged Infections are common
Obstructive Lung Disease
Salty skin Malabsorption Steatorrhea: bulky, fatty, foul stools Frequent respiratory infections Hypoxia, fatigue, exercise intolerance Diagnose: sweat test Treat: pancreatic enzymes, bile salts, chest therapy, bronchodilators, aggressive treatment when necessary
Cystic Fibrosis
Primary and secondary cancers
3rd most common cancer
90% lung cancer related to smoking
Metastatic cancer: due to lymphatic and venous return
Lung Cancer
Broncho genic carcinoma From bronchial epithelium Most common malignant tumor Oat cell (small cell) carcinoma Rapid growth Usually near major bronchus Very invasive, metastasize early Large cell Found in periphery of lung Rapid growth, metastasize early
Pathophysiology of lung cancer
Most common malignant lung tumor
First change: metaplasia
Chronic irritation
Lung tissue more vulnerable
Tumor: obstruction, inflammation, pleural effusion
Para neoplastic syndrome: secretes hormones (ADH)
Bronchogenic carcinoma: from bronchial epithelium:
Persistent, productive cough Chest x-ray evidence Hemoptysis Chest pain Weight loss, anemia
Signs/symptoms of lung cancer
Chest x-ray
MRI/CT
Mediastinoscopy
Diagnosis for lung cancer
Surgery
Photodynamic therapy
Treatment for lung cancer
Severe/reversible bronchial obstruction
Hypersensitive or hyper responsive airways
Acute or chronic
Rate from mild to severe
Extrinsic: type I hypersensitivity: immune rctn to smoke, perfumes, strong smells, molds, dander
Intrinsic: nonimmune, occur in adults; respiratory infx, exposure to cold, exercise, medications, psychological stress
Asthma
Inflammation of mucosa
Edema
Contraction of smooth muscles
Increase in thick mucous
Partial obstruction of small bronchi, bronchioles: air trapping
Hard to get fresh air in
Pathophysiologic changes in asthma
Total obstruction of airway
Mucus plugs block airflow
Atelectasis occurs
Section of lung can collapse
Oxygen levels are reduced
Vasoconstriction
Reduced blood flow through lungs
Increase workload of right side of heart
Pathophysiologic changes of asthma
May develop irreversible damage to lungs
Bronchial walls thicken
Fibrous tissue in areas of atelectasis
Chronic asthma
Family history of hay fever, asthma, eczema
Viral URI
Air pollution
Sedentary lifestyle with poorly ventilated houses
Etiology of asthma
Cough, dyspnea, tight feeling in chest Wheezing Thick, sticky mucous Tachycardia Hypoxia Hyperventilation Hypoventilation Can lead to respiratory failure
Signs and symptoms of asthma
Check for allergens Avoid triggers Good ventilation Exercise (swimming) Prophylactic medication Inhalers: relax bronchiole smooth muscles Breathing techniques glucocorticoids
Treatment of asthma
Alveolar walls are destroyed
Permanent permanently inflated air spaces
Genetics: alpha1 –antitrypsin: inhibits activity of proteases (present during inflammation)
Cigarette smoking: increases neutrophils and decreases effectiveness of alpha 1 –antitrypsin
Emphysema
Breakdown alveolar walls Surface area for gas exchange decreases Loss of pulmonary capillaries Decreased elastic fibers Alter ventilation/perfusion ratio Decrease support for small bronchi: collapse walls Fibrous thickening of bronchial walls Narrow airways Weakened walls Difficulty with passive expiration
Emphysema
Air trapping
Over inflation of lungs
Barrel chest
Diaphragm flattened
Progressive problems with expiration with emphysema
Large airspaces, blebs Tissue near bleb can rupture Hypercapnia increases Hypoxic drive for inspiration Frequent infections Pulmonary hypertension
Advanced emphysema
Cigarette smoking
Genetics (early development)
Air pollution
Etiology Emphysema
Dyspnea on exertion (DOA) progress to dyspnea at rest
Hyperventilation, use of accessory muscles
Anorexia, fatigue
Clubbed fingers
Signs and symptoms Emphysema
Chest x-ray
Pulmonary function tests:
Increased residual volume
Increased total lung capacity
Diagnostics Emphysema
Avoid irritants
Stop smoking
Immunization against influenza and pneumonia
Pulmonary rehab: appropriate breathing techniques
Pursed lip breathing
Maintain hydration and nutrition
Lung reduction surgery
Treatment Emphysema
Constant irritation from smoking or industrial pollution
Irreversible and progressive
Inflammation of mucous
Hypertrophy of mucous glands: secretions are increased, increase in goblet cells
Decreased ciliated epithelium
Bronchial walls thicken, are fibrosed: leads to obstruction
Secretions pool
Low oxygen levels
Episodes of coughing: may develop cyanosis
Chronic bronchitis
dyspnea, hyperventilation, over inflation- what you may call people with emphysema.
Pink puffer:
low oxygen level, cyanosis, edema- what you may call people with chronic bronchitis.
Blue boater
Cigarette smoking
Industrial area
Heavy smog
Etiology Chronic bronchitis
Chronic productive cough Tachypnea, SOB Cough more severe in morning Hypoxia, cyanosis, hypercapnia Polycythemia Severe weight loss Systemic edema
Signs and symptoms Chronic bronchitis
Reduce exposure to irritants Vaccines Expectorants, bronchodilators Chest therapy to remove mucous Low flow oxygen
Treatment Chronic bronchitis
Bluish color of skin and mucous membranes
Results from large amounts of unoxygenated hemoglobin
Peripheral or generalized
Cardiovascular conditions or Respiratory disease
Not a good early indicatory of hypoxia
Cyanosis
