Test 2- Respiratory Flashcards
Lung Development
- Immaturity of respiratory tract major cause of morbidity and mortality in preme infants
- Surfactant production begins after 20wks
- 25-28 wks of gestation sufficient alveoli present
- At birth 20-50 mil alveoli
- 300 mil at 3-7 yrs
- 700 mil at adulthood
- Lack of stiff structural support make infants more susceptible to lung collapse( atelectasis) and obstruction
Airway Resistance
- Infant airways smaller with more resistance to air flow
- Neonates primarily nose-breathers
- Nasal flaring- sign of increased resp. resistance
- Mucus, edema, airway constriction dramatically reduce airflow
Respiratory disorders in Neonates
-Resp. disorders in infants cause reduced lung compliance( ability to stretch/recoil) or increased airway resistance
Signs of above:
- Tachypnea ( ^ resp. rate)
- grunting
- nasal flaring
- retraction( skin sucked in around ribs)
- stridor (sound of increased turbulence of air moving thru trachea/ large airways)
- wheezing( sound of increased turbulence thru smaller airways)
Airway Structures
Upper airway
- Nasopharynx
- Oropharynx
- Laryngopharynx
Lower Airway
- Larynx
- Trachea
- Bronchi
- Acinus
Nasal Cavity Functions
- Conducts gases to/from lungs
- Filters, warms, humidifies air
- Turbinates convoluted/ vascular
good heat exchanger
water evaporatesfrom surface to humidify air
- Rigid structure prevents collapse
- Vibrissae (large hairs) trap particles
- Mucosal epithelial cilia sweep mucous to nasopharynx then swallowed or expectorated
Sinuses
Four paranasal sinuses: maxillary, frontal, ethymoid, spenoid
- contribute to speech resonance, heat, and water vapor exchange
- mucociliary action (remove bacteria/ debris)
Eustachian Tubes
- Allows pressure equalization of middle ear
- Open during swallowing (closed otherwise)
- Horizontal position/ shorter length in children predisposes to otitis media
Conducting Airways
-Consists of: nasal/oral pharynx, laynx, trachea, bronchi, bronchioles (nonrespiratory/ respiratory)
Functions:
- direct air to respiratory exchange zones of lung
- warm, filter, humidify air
- no gas exchange across conducting airways (only across respiratory bronchi/ alveoli)
Conducting Airway Epithelium
Ciliated columnar mucosal epithelial cells
- cilia beat in sweeping motion
- mucociliary transport (primary defense mech.) move inhaled particles/ mucous to espophogus for swallowing/ coughing
Ciliary function impaired by: smoking, ethanol, cold/ hot air, low humidity, hypo/hyperthermia, anesthetics, corticosteroids, viral infections, excess mucous prod.
Goblet cells: produce mucous
- mucous is 95% water
- hydration status important to production
- children have more goblet cells than adults (more mucous)
Larynx
Functions: sound production, valve to control air mvmnt. out of lungs (expel foreign substances), prevent foreign subs. entering trachea/lungs
-Hyoid bone: horseshoe shaped- from which larynx suspended
Cartilages:
- Thyroid: v-shaped contain vocal folds
- Cricoid: ring shaped- connected to trachea- supports arytenoid posteriorly
- Arythenoid: vocal folds connet on posterior
Vocal Folds: vibrate when air passes- forming sound (longer folds- lower sound/ tighter fold- higher sound)
Lungs: Basic Anatomy
Trachea divides to R/L mainstem bronchi at carina
Right lung: R mainstem bronchus divides to 3 lobular bronchi- RUL, RML, RLL
Left Lung: L mainstem divides to 2 lobular bronchi- LUL, LLL
Lobular bronchi -> segmental bronchi -> bronchopulmonary segments -> terminal bronchioles (smallest units)
Alveoli
Terminal bronchioles lead to alveoli
Alveoli form on respiratory bronchioles
Adults- 350 mil alveoli per lung (700 mil total) and 75 sq. meters of SA
Surface for O2/ CO2 exchange
Alveolar cells
- Type 1: squamous epithelial (pneumocytes) form gas exchange surface
- Type 2: produce surfactant (lowers surface tension/ fascilitate gas exchange)
- Type 3: alveolar macrophages (phagocytize microbes that reach alveoli)
Pleura
- Thin continous membrane covering lungs (visceral) and thoracic cavity (parietal)
- Membranes seperated by small amount of serous fluid to lubricate
- Intrapleural space at negative pressure (keeps lungs pressed against thorax wall)
Nervous Innervation
Autonomic nervous system
- Parasympathetic: vagus nerve (CN10) stimuates bronchioconstriction
- Sympathetic: sympathetic innervation (T1-T4) and epi/norepi causes relaxation of bronchial muscle
- mediated by B-2 adrenergic receptors
Cough Reflex
- Defense against excessive secretions/ foreign substance
- Diminishing cough reflex increases risk of aspiration (cough suppress. meds, brainstem injury, age)
Cough
Initiated by cough receptors in carina and coordinated in brainstem (medulla oblongata)
Cough produced when vocal folds/ epiglottis close against air trapped in lungs
Expiratory muscle contract- increase pressure against closed vocal folds/ epiglottis
High pressure air escapes (ejecting debris/ mucus)
Dual Pulmonary Circulation
Bronchial artery system
- Arise from thoracic aorta (oxygenated arterial blood)
- Supplies oxygenated blood to to bronchi
Dual Pulmonary Circulation (cont.)
Pulmonary artery system
- Arises from pulmonary artery (delivers unoxygenated blood from R ventricle)
- Huge capillary network for gas exchange
–Fewer capillaries in elderly/ infants (less efficient gas exchng)
–Low pressure arterial system
–blood flow increased/ reduced to adjust gas exchng needs
-Oxygenated blood exists thru pulmonary vein into L atrium
Influences on Pulmonary Circulation
Two mechanisms to increase capillary perfusion:
- Recruiting: opening previously closed capillaries
- Increasing arteriolar blood flow
- Pulmonary arterioles constrict in response to alveolar hypoxia (low O2/ high CO2) rerouting blood to alveoli that are well-ventilated
Pulmonary Fluid Balance
Fluid balance in lung tissue regulated by 3 factors:
- Hydrostatic pressure (BP vs tissue pressure)
- Colloid (oncotic) pressure related to protein concntrn)
- Capillary permeability (leakiness between endothelial cells lining capillaries)
Ventilation
- Process of moving air into/out of lungs
- To allow O2 absorption/ removal of CO2
- Ventilation influenced by:
- Age (reduced when old)
- body size/ shape (reduced with obesity)
- body position (reduced in supine)
Measures of Lung Volume
Tidal volume (TV): volume of air breathed in/out without conscious effort (normal)- 500cc
Inspiratory reserve volume (IRV): volume above TV that can be inhaled w/ max effort after normal (3L)
Expiratory reserve volume (ERV): volume above TV that can be forcibly exhaled w/ max effort after normal exhalation (1.2L)
Residual volume (RV): volume left in lungs after max exhalation (1.2L)
Measures of Lung Capacity
Vital capacity (VC): total volume that can be exhaled after max inhalation (VC= TV+IRV+ERV)
Inspiratory capacity (IC): total volume that can be inspired after normal exhalation (IC=TV+IRV)
Functional residual capacity (FRC): total volume in lungs following normal exhalation (FRC=ERV+RV)
Total lung capacity (TLC): amount of air in lungs at max inspiration (TLC= IRV+TV+ERV+RV)
Minute Ventilation
Volume of air thats exchanged each min.
- Respiratory rate (surrogate) 12-18/min normal for healthy adults
- Increased minute ventilation (hyperventilation)- increased need for O2/excess CO2 or increased respiratory drive.
- Decreased (hypoventilation)- reduced need for O2/low CO2 or reduced respiratory drive
Respiratory Function
Primary objective of respiration- get O2 in blood and CO2 out
3 Primary contributors to gas exchange:
- Neuromuscluar function (mechanics of inspiration/expiration)
- Ventilation (gas mvmnt in/out of lungs)
- Diffusion/ perfusion of gases (mvmnt of gas across exchange surfaces)
Alterations of these functions cause pathology
Mechanics of breathing
- Airway resistance affects gas mvmnt in/out of lungs
- Lung compliance (ability to stretch/ recoil when pressure released)- natural response is recoil/collapse (normal compliance)
- Surfactant decreases alveolar surface tension (prevents alveoli fully emptying/ collapsing- atelectasis)
Mechanics of breathing (cont.)
Inspiration (active process)
- diaphragm contracts/ moves downward
- intercostal muscles contract during active inspiration- elevating ribs/ expanding thoracic volume
Expiration (passive process)
- diaphragm/ intercostal muscles relax
- lungs passively recoil
- active expiration requires contraction of different intercostal muscles than used for inspiration
Alveolar ventilation and Blood oxygenation
- slow, deep breathing- increased alveolar ventilation vs. rapid shallow reathing
- partial pressure of O2 in alveoli (100mm Hg) greater than arterial O2 tension (95-100mm Hg)
- large difference between alveolar and arterial O2 indicates poor diffusion of alveolar O2 into blood (caused by fluid in alveoli/ interruption in blood flow)
Ventilation-Perfusion
Anatomic dead space
- pulmonary areas that dont participate in gas exchange (bronchi/ bronchioles)
- increased w/destruction of alveoli (emphysema)
Alveolar dead space
-ventilated but nonperfused (pulmonary embolus)
Physiologic dead space (functional)
-anatomic dead space + alveolar dead space
Airway resistance
Ease of which air moves in/ out of lungs
Influenced by:
- Airway diameter
- Turbulence: turbulent air flow creates more resistance (nose-highest, bronchioles- low)
- Space filling materials/ obstructions: decrease airway diameter- increase turbulence (mucous, tumor, foreign bodies)
Effects of gravity
Upper portion of lungs have:
- less blood flow (less gas exchange)
- larger, partially inflated alveoli
- lesser ventilation capacity (less air mvmnt per alveolus due to partially inflated at all times)
Compliance
How easily lungs expand and contract
- high lung compliance (lung stretches/ passively contracts easily (normal healthy lungs)
- Low lung compliance (lung has difficulty expanding/ doesnt passively contract)
Causes: pulmonary fibrosis, edema, insufficient surfactant, COPD, recurrent infections
O2 and CO2 diffusion
- moving gasses from alveoli blood (O2). blood to alveoli (CO2)
- impaired by decreased SA (emphysema)
- impaired by increased thickness of exchange surface (pulmonary edema)
CO2 Transport
- small amount dissolved in plasma
- some bind to hemoglobin (carbaminohemoglobin)
- Most of CO2 diffuses into RBCs- converted to carbonic acid by carbonic anhydrase
O2 Dissociation
Affinity of hemoglobin for O2 depends on local conditions (oxyhemoglobin)
- Increased tissue metabolism (increased O2 demands) increases pCO2/ H+ (low blood pH)- result in decreased Hb affinity for O2
- Asblood reaches alveolar capillaries CO2 diffuses out of blood into alveoli- increasing blood pH- increasing O2 binding
Affinity of CO binding to Hb higher than O2/CO2
Neurologic control of breathing
Diaphragm doesnt have inherent pacemaker properties
- requires input from resp. center in pons/medulla
- primary regulator low pH (^ CO2)
- secondary is low O2
Suppression of resp. feedback- hypoventilation (opiate OD)
Neurologic control of breathing (cont.)
Chemoreceptors
- Central: affect resp. center
- primary responds to low extracellular pH (^ CO2 cncntrn)- increased ventilation
- Secondary response to reduced O2 cncntrn
- Peripheral: carotid/ aortic bodies
- hypoxia triggers increased resp. center activity
Lung Receptors
-stretch, irritant, hypoxia (decreased O2- increased ventilation)
