Test 2- Respiratory Flashcards

(37 cards)

1
Q

Lung Development

A
  • 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
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2
Q

Airway Resistance

A
  • 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
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3
Q

Respiratory disorders in Neonates

A

-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)
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4
Q

Airway Structures

A

Upper airway

  • Nasopharynx
  • Oropharynx
  • Laryngopharynx

Lower Airway

  • Larynx
  • Trachea
  • Bronchi
  • Acinus
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5
Q

Nasal Cavity Functions

A
  • 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
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6
Q

Sinuses

A

Four paranasal sinuses: maxillary, frontal, ethymoid, spenoid

  • contribute to speech resonance, heat, and water vapor exchange
  • mucociliary action (remove bacteria/ debris)
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7
Q

Eustachian Tubes

A
  • Allows pressure equalization of middle ear
  • Open during swallowing (closed otherwise)
  • Horizontal position/ shorter length in children predisposes to otitis media
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8
Q

Conducting Airways

A

-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)
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9
Q

Conducting Airway Epithelium

A

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)
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10
Q

Larynx

A

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)

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11
Q

Lungs: Basic Anatomy

A

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)

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12
Q

Alveoli

A

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)
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13
Q

Pleura

A
  • 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)
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14
Q

Nervous Innervation

A

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
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15
Q

Cough Reflex

A
  • Defense against excessive secretions/ foreign substance
  • Diminishing cough reflex increases risk of aspiration (cough suppress. meds, brainstem injury, age)
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16
Q

Cough

A

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)

17
Q

Dual Pulmonary Circulation

A

Bronchial artery system

  • Arise from thoracic aorta (oxygenated arterial blood)
  • Supplies oxygenated blood to to bronchi
18
Q

Dual Pulmonary Circulation (cont.)

A

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

19
Q

Influences on Pulmonary Circulation

A

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
20
Q

Pulmonary Fluid Balance

A

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)
21
Q

Ventilation

A
  • 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)
22
Q

Measures of Lung Volume

A

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)

23
Q

Measures of Lung Capacity

A

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)

24
Q

Minute Ventilation

A

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
25
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
26
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)
27
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
28
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)
29
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
30
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)
31
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)
32
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
33
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)
34
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
35
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
36
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)
37
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)