Module 5 Flashcards
The respiratory system can be divided into what 2 structures
Conducting airways, respiratory tissues
What’s included in conducting airways
nasal passages, mouth and pharynx, larynx, trachea, bronchi, bronchioles
What’s included in respiratory tissues
lungs, respiratory bronchioles, alveolar ducts and sacs (gas exchange)
What are the levels of branching
Trachea, bronchi, bronchioles, alveoli
Where is the site of gas exchange?
Alveoli
What cells are in the alveolar epithelium?
Type 1 and II alveolar cells
(thin squamous; cuboidal, surfactant), macrophages
Describe what happens during inspiration
Inspiration: respiratory muscles expand thoracic cavity which reduces internal pressure allowing environmental air to enter lungs
Describe what happens during expiration
Expiration: respiratory muscles relax, thoracic cavity retracts which increases internal pressure allowing air to move from lungs to area of lower pressure
What occurs with the diaphragm during inspiration and expiration?
The diaphragm is the main muscle of inspiration. When the diaphragm contracts (inspiration), the chest expands. Upon expiration, the chest cavity decreases and pressure inside increases.
What is lung compliance? What factors affect it?
Ease of lung inflation, reliant on water content, elastin, collagen, and surface tension that makes it easier for air to expand a compliant lung.
lung volumes
refers to the amount of air exchanged from a single event during ventilation; tidal volume, inspiratory reserve volume, expiratory reserve volume, residual volume
Tidal volume
normal volume of air inhaled with each breath, 500mL
Inspiratory reserve volume
amount of air that can be forcibly inspired after taking in normal breath, 3100mL
Expiratory reserve volume
amount of air that can be forcibly exhaled after letting out normal breath, 1200mL
residual volume
air remaining in lung after forced expiration, 1200mL
Lung capacities
Calculated using lung volumes; vital capacity, inspiratory capacity, functional residual capacity, total lung capacity
Vital capacity
amount of air exhaled following max inhalation, 4800mL
Inspiratory capacity
max amount of air inhaled following normal expiration, 3600mL
Functional residual capacity
amount of air remaining in lungs after normal expiration, 2400mL
Total lung capacity
Sum of all lung volumes, 6000mL
Pulmonary function tests
Look at pulmonary flow rates in relation to time; max voluntary ventilation, forced vital capacity, forced expiratory volume, forced inspiratory vital flow
Max. voluntary ventilation
measures volume of air a person can move into and out of lungs during max effort lasting 12-15”, L to min
Forced vital capacity
volume of air quickly and forcefully exhaled following full inspiration; lower in obstructive disease
Force expiratory volume
measures expiratory volume in a given time; useful in Dx obstructive lung disorders
Forced inspiratory vital flow
measures respiratory response during rapid max inspiration
ventilation
movement/flow of gases in and out of lungs
Perfusion
low of blood to pulmonary capillaries for gas exchange
Diffusion
movement of gases between alveolar and pulmonary capillaries
Shunt
formed when blood moves from pulmonary circulation to systemic circulation without oxygenation. Anatomic-blood moves from venous to arterial side without moving through lungs. Physiologic shunt blood moves through unventilated parts of lung creating mismatch of ventilation and perfusion
Dead air space
ventilation without perfusion, resulting in high ventilation-perfusion ratio
oxyhemoglobin
Hemoglobin bound to oxygen
affinity
Ability of hemoglobin molecule to bind to oxygen, up to four O2 molecules to become saturated
How is carbon dioxide transported in the blood?
dissolved in blood, attached to hemoglobin, and as bicarbonate
How is breathing controlled?
The automatic regulation is controlled by both chemoreceptors and lung receptors. Chemoreceptors monitor blood levels of oxygen, carbon dioxide, and pH and adjusts ventilation accordingly. Lung receptors monitor breathing patterns and lung function.
What are the characteristics of COPD?
Inflammation and fibrosis of bronchial wall which causes overproduction of mucus and less elasticity of lung tissue. The obstruction of airflow leads to a mismatch in ventilation between ventilation and perfusion which alters the gas exchange at the alveolar level due to decreased surface area.
What is the leading risk factor for COPD?
Smoking
Emphysema
decreased lung elasticity, enlarged airspaces distal to terminal bronchioles, destruction of alveolar walls and capillary beds; hyperinflation of lungs, increased TLC. Main causes smoking and ATT def.
Bronchitis
Hypersecretion of mucus in large airways, hypertrophy of submucosal glands in trachea and bronchi. Chronic irritation from smoking, recurrent infections.CO
COPD
Airflow obstruction, inflammation and fibrosis of bronchial wall, hypertrophy of submucosal glands, overproduction of mucus. Loss of elasticity of lung fibers and alveolar tissue, mismatch in vent. and perfusion, lower surface area for gas exchange
COPD Dx and Tx
H&P, PFTs, chest exray, FVC prolonged and decreased, FEV decreased. Stop smoking, avoid RT infections, vaccines, pulmonary rehab. Inhaled bronchodilators, corticosteroids, O2 therapy to keep sats above 90%.
What are the characteristics of asthma?
Airway obstruction, bronchial hyperresponsiveness, airway inflammation (latter two promoted by IgE), sometimes airway remodeling
What is atopy?
Genetic predisposition for development of IgE mediated hypersensitive reactions as a response to environmental allergens
Asthma risk, pathology, presentation, Dx, Tx
Family Hx, allergies, antenatal exposure to smoke and pollution, GERD, exercise, cold air, AA or Puerto Rican. Inflammatory actions occur in bronchi where no infection, toxins etc exist, causing airflow obstruction (inflammation, hyperresponsiveness, then obstruction). Smooth muscle contraction, increase in inflammatory cells and cytokines which cause epi. injury. Sx wheezing, accessory muscle usage, distant breath sounds, SOB, anxiety. Dx PFTs, H&P. Tx avoid triggers, use of bronchodilators like albuterol or advair.
What is pneumothorax?
Pneumothorax is the presence of air in the pleural space that causes partial or complete collapse of the affected lung. Dx by chest xray or CT scan, pulse ox, ABGs. Sx chest pain, increased resp. rate, SOB, decreased/absent breath sounds.
Spontaneous pneumothorax
rupture of alveolus or air-filled bleb/blister on surface of lung, difference in pleural pressure from top to bottom of lung in taller people that creates blebs. Seen also in people with emphysema.
Traumatic pneumothorax
penetrating chest would or rib fracture puncturing lung. Hemothorax present too. Caused by needle aspirations, central line insertion, intubation, positive pressure vent, CPR
Tension pneumothorax
Air enters pleural space but can’t exit, collapses lung which compresses mediastinal structures and shifts them to unaffected side. HR increases, CO decreased, jugular neck vein distention, subcu. emphysema, shock, hypoxemia. Treated with large bore needle or chest tube inserted into affected side with drainage or suction.
What is atelectasis?
Atelectasis is an incomplete expansion of a lung, or portion of lung, caused by airway obstruction or lung compression.
Atelectasis pathology etc
mucous plug in airway, compression by fluid, tumor, exudate, any obstruction. Risk increases after surgery. Tachypnea, tachycardia, dyspnea, cyanosis, hypoxemia, decreased chest expansion, decreased breath sounds, intercostal retractions. Mediastinum may shift away from affected lung. Dx chest xray/ct scan, Tx reduce obstruction/compression, reinflate collapsed area, O2, ambulation, deep breathing, body positioning.
What type of substance causes a pulmonary embolism?
thrombus, air accidentally injected into an intravenous infusion, fat from the bone marrow after a fracture or trauma, or amniotic fluid that enters the maternal circulation after rupture of membranes.
PE pathology etc
Virchow triad-venous stasis, endothelial injury, hypercoag states. Chest pain, SOB, cough, increased resp rate, hypoxemia, death. Dx H&P, ABGs, venous thrombosis studies, troponin, D dimer, lung scan, ECG, helical chest CT scan. Ultrasonography to locate cause. Tx anticoags (lovenox) or thrombolytic therapy. Increase mobility.
What causes ARDs
aspiration, drugs/toxins (cocaine, heroin, smoke, high concentrations of O2, radiation), infection, trauma/shock (burns, fat emboli, chest trauma), DIC, multiple blood transfusions
ARDs patho
Epi cell injury with increased permeability of alveolar capillary membrane resistant to gas exchange. Lung stiffens, SOB, shunting of blood, impaired gas exchange, hypoxemia, alveolar collapse from inactivated surfactant, fibrosis. Resp. distress, increased RR, resp. failure, hypoxemia, organ failure. Dx chest xray shows diffuse bilateral infiltrates (white out), normal card. Fx. Tx O2, vent support until lungs heal.
Causes and manifestations of respiratory acidosis
Depression of respiratory system (drugs, head injury), lung disease (COPD, asthma, pneumonia), obstruction/disorder of muscles (paralysis of resp. muscles, chest injury, extreme obesity, paralytic drugs), breathing high CO2. pH decreased, PCO2 and HCO3 increased, depressed neural Fx, headache, weakness, confusion, hallucinations, tremors, paralysis, coma, skin warm and flushed, acidic urine
Respiratory acidosis patho
Don’t supplement with too much O2 if on O2 therapy, may suppress resp. drive. Sx of hypoxemia, vasodilation from CO2 crossing BBB. Dx with pH below 7.35, PCO2 >45mmHg. Tx improve ventilation, sometimes mech. vent.
