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211 Cards in this Set
- Front
- Back
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what is purpose of upper airway & what consists of UA
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Purpose: conduct, humidify, protect
Mouth, oropharynx, nasopharynx, larynx |
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Trachea is at what vertebrae
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5th
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Tracheobronchial tree divides into what
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R + L mainstem
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Where is aspiration likely & why
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R LL d/t R mainstem bigger & straighter than L
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Identify lower airway
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Tracheobronchial tree
secondary & tertiary bronchus Bronchioles & terminal bronchioles Alveolar ducts Alveoli |
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what is purpose of Lower airway
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protection, gas exchange
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Describe 3 levels of tracheobronchial tree
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0-15 conducting zones
5-15 bronchioles to terminal 16-26 transitional & respiratory |
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How many generations in tracheobronchial tree
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26
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Conducting airways are
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trachea
segmental bronchi subsegmental bronchi (bronchioles) nonrespiratory |
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what is anatomical dead space
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air but no gas exchange
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where is smooth muscle support the most
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prominent into alveolar ducts
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where is columnar epithelium
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glands, cilia, mucus-mucociliary blanket
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where is cuboid epithelium
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bronchioles
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where is squamous epithelium
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alveoli
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smaller radius means what to the resistance
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higher
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bronchioli have a lot of smooth muscle which aids constriction/relaxation which does what to radius
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change radius therefore change resistance & flow
smaller radius higher resistance smaller the flow |
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what is the functional unit of lung
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lobuole
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where does gas exchange occur
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terminal bronchioles, alveolar ducts, alveoli
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name the dual blood supply to lobuole
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1. pulm artery deoxygenated from RV to PA to capillaries to LA
2. bld thru bronchial arteries (branch desc aorta) bring oxygenated blood & nutrients to lung tissue |
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90% of alveolar surface area are made of these cells
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type 1
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Flat, epithelial cells across which gas exchange occurs are these cells
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type 1
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these cells produce surfactant
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type 2
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surfactant from type 2 cells does these 4 things
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reduce surface tension in alveoli
prevent alveoli collapse ease lung inflation prevent fluid accumulation |
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the alveolar has 3 types of cells
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type 1
type 2 macrophage dust cells |
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what are the 3 ventilation respiratory pressures
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intRAalveolar
IntRApleural IntRAthoracic |
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intraalveolar pressure is
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equal to atmospheric P
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Intrapleural pressure is
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always negative & holds lungs agst chest wall
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Intrathoracic pressure is
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equal to intrapleural pressure
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What are the muscles of inspiration
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diaphragm
external intercostal accessory |
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which is the main muscle of inspiration
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diaphragm
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the external intercostal muscles do this
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increase AP diameter of the rib cage
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the accessory muscles are engaged when
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need more volume ie during exercise or stress
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which are the 2 accessory muscles
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scalene raise 1st 2 ribs
SCM raise sternum |
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this is a passive process
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expiration
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expiration is a passive process d/t
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recoil of muscles of inspiration
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accessory muscles of expiration
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abdominal
internal intercostals |
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during inspiration, the diaphragm does this which does this to the lungs
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contracts which pulls down the lungs, the chest expands top to bottom creating more volume, more negative pressure sucks air in
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minute ventilation =
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RR x Vt
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lung compliance refers to
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ease with which lungs are inflated
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compliance =
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change volume/change pressure
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lung compliance is determined by these 3 things
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elastin & collagin fibers of lung
surface tension compliance of rib cage |
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what do elastin fibers do
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keep airway open
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if elastin fibers are replaced by scar tissue as in pul fibrosis/interstitial dz it makes the lungs
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very stiff, non compliant
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if you lose the elastic element of the lungs it causes
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overstretching, loss of recoil
easy to inflate, more difficult to deflate |
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which condition makes it easy to inflate, more difficult to deflate
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emphysema
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which cells produce surfactant
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type 2 alveolar cells
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this is a complex lipoprotein which exerts its effect mainly at end of respiration preventing alveolar collapse
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surfactant (type 2 alveolar cells)
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this forms a film that decreases the contact surface between air & fluid in alveoli thus decreasing surface tension
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surfactant (type 2 alveolar cells)
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distending pressure in alveoli is:
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P = 2T/r (Laplace)
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surfactant has 4 effects on lung inflation
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lowers surface tension (P=2T/r)
Increase lung compliance (ease inflation) stabilize & even inflation of alveoli keeps alveoli dry (prevents p. edema) |
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when do type 2 cells mature
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after 26-28th week of gestation
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premies have respiratory difficulties such as atelectasis & IRDS d/t
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lack of surfactant
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what accelerates maturation of surfactant
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steroids
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volume of air moving is related to pressure differences & related to resistance that the air encounters as it moves thru airway
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directly related
inversely related |
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the sum of resistance in three types of airways (large, medium bronchi & broncioles) is d/t resistance in
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large bronchi
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a small change in caliber of airway means a change in airway resistance
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large
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a small change in caliber of airway causes a large change in airway resistance which is R=1/r4 or law
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Poiseuille
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airway resistance is affected by bronchial smooth muscle via stimulation of these fibers
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parasympathetic & sympathetic
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describe the pressure in the apex
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intrapleural pressure more negative, alveoli more expanded
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describe pressure in base
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d/t gravity the alveoli are less expanded
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work of breathing is determined by the amount of effort
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required to move air thru conducting airway & by compliance of lung
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work of breathing does this during exercise & is this total expenditure
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increases, but <3%
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name 2 causes of increased work of breathing
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increased airway resistance
decreased lung compliance |
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this requires a constant flow
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perfusion of lungs
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Lung perfusion
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requires constant flow
low velocity facilitates exchge hi to low flows bv thinner, compliant, 500 ml blod reservoir for LV |
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distribution of blood flow in apex
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less flow, alveoli bigger-less ventilation bad match
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distribution of blood flow in base
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more blood flow, alveoli smaller, more ventilation better match
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4 shunt conditions
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atelectasis
P edema ARDS PNA |
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3 dead space conditions
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p emboli
low CO excessive PEEP |
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pt has PNA, which side do you position pt so better ventilation/perfusion
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position w/ good side DOWN
always GOOD SIDE DOWN |
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obstruction of local bronchus will cause
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hypoxia & hypercapnia in the area causing vc
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chronic generalized hypoxia seen in
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P HTN
cor pulmonale |
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cor pulmonale is
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damage of RV-HF d/t pulm HTN
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decrease of blood flow causes
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hypocapnia & bronchoconstriction
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Fick's law of diffusion has 4 things
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solubility of gas
surface area thickness of membrane pressure gradient across membrane |
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gas exchange in lungs from from this conc to this
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high to low
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this % of oxygen is dissolved
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3%
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this % of oxygen is on Hgb
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97%
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each gram of Hgb carries oxygen molecules
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4
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when O2 is bound to all 4 heme groups, the Hb molecule is said to be
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saturated
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this curve represents the relationship between HB saturation (HbO2) & Oxygen pressure (PaO2)
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oxyhemoglobin dissociation curve
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factors that affect the ODC
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pH
CO2 Temp 2,3 DPG |
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a shift to the R in the ODC is caused by
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increase 2,3 DPG
increase H+ increase Temp decrease pH |
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a shift to the R in the ODC
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let's go oxygen to tissues easily
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a shift to L in ODC
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hoLd on to O2
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gas exchange in tissue is the
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opposite of what happens in lungs d/t which is high/low conc
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name 3 forms CO2 transport
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10% dissolved in plasma
30% attached to Hb (carbaminohemoglobin) 60% as bicarb (HCO3-)-chloride shift |
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CO2 is this much more soluble in plasma than O2
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20x
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which is more soluble in plasma CO2 or O2
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CO2
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one of CO2 best buffers is
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bicarbonate
hydrated, Cl- enters cell, acid becomes alkanized |
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DRG sends Action Potential to the spinal cord C3-C4 to phrenic nerve which to diaphragm causes
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inhalation
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which nerve is affiliated w/diaphragm
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phrenic nerve
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the chemoreceptor detects H+ in CSF & if high
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breath faster & deeper
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metabolic acidosis causes these breaths
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Kussmauls faster & deeper
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these 2 are peripheral chemo receptors
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carotid & aortic
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the dorsal respiratory center is the of breathing
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pacemaker
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the pneumotaxic center does this to inspiration
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switches off
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this center excites inspiration prolonging it
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apneustic center
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axons are located in this
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phrenic nerve & muscles of respiration
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reflexes are intergrated here
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in level of spinal cord
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central chemoreceptors in the brain stem does this
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monitor H+ level in CSF, which reflects blood CO2
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CO2 combines w/water making H2CO3- which dissociates into
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H+ & HCO3-
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the central chemoreceptors are very sensitive to ST changes in CO2, but this in chronic
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loose sensistivity if CO2 chronically elevated
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these regulate breathing rate
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peripheral chemoreceptors in aortic & carotid bodies
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peripheral chemoreceptors do this
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monitor O2
fully active when PaO2<=60mmHg |
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this is the main stimulus for respiratory center in persons with chronic elevated CO2
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hypoxia
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if you give high oxygen to pt w/COPD this happens
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respiratory depression
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lung receptors respond to stretch by
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inhibiting inspiration
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lung receptors respond to irritants
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cause rapid shallow breathing
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Juxtacapillary Jreceptors do this in response to lung congestion
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tachypnea during p edema
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is there voluntary control of breathing & when
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yes
during talking, eating, singing, blowing... |
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this is difficult or labored breathing in which pt aware of SOB
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dyspnea
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this is the term for increase rate &/depth of respiratory effort
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hyperpnea
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this is rapid, shallow breathing
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tachypnea
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4 mechanisms of dyspnea
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stimulation of lung receptors
increased sensitivity to changes in vent capacity reduced vent capacity (reserve) stimulation of neural receptors in intercostals, diaphragm |
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name the 3 dysfunctions of dyspnea w/examples
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primary pulmonary dysfx: PNA, asthma, emphysema
cardiac dysfx: p. congestion neuromuscular: myasthenia gravis |
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this is the bluish discoloration of skin d/t excess of in small bv
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cyanosis
deoxygenated Hb |
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cyanosis is a sign
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late
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persons w/low Hb will always exhibit cyanosis: true/false
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false
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do the shallow respiratory mvts during fetal life contribute to gas exchange
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no
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what is a major cause of m&m in premature infants
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immaturity of pulmonary system
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by what year of life do the child's lungs have the same amount of alveoli as an adult
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8
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describe compliance of neonate lungs
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chest wall & lungs very compliant so small changes in pressure cause lungs to inflate
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rapid shallow breathing, grunting noise during expiration are signs of
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decrease in lung compliance as seen in PNA, RDS
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upper airway obstruction signs are
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nasal flaring, long inspiration, stridor, retractions
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these are signs of lower airway obstruction
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wheezing, whistling, prolonged expiration
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respiratory d/o involving inflation
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decreased compliance
pleural d/o PNA atelectasis |
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obstructive respiratory d/o
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increased airway resistance
asthma COPD |
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vascular respiratory d/o
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PE
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this is an abnormal collection of fluid in pleural cavity
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pleural effusion
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the pleural cavity normally has a thin layer with approx mLs
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10-20ml
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Name the 5 mechanisms of pleural effusion
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^cap pressure (HF)
^cap permeability (inflamm) vcolloidal osmotic pressure(v albumin) ^negative intrapleural pressure (atelectasis) impaired lymph drainage (CA) |
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what are 3 possible manifestations of pleural effusions
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v lung expansion on affected side
v lung volume mediastinal shift towards UNaffected side |
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towards what side will a mediastinal shift be in pleural effusion
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towards UNaffected side
(pleUral=Unaffected) |
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this is air in the pleural cavity & can be
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pneumothorax
spontaneous, traumatic, tension |
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air in the pleural cavity causes this to happen to the affected lung
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collapse
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a tension pneumothorax causes this
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^pressure pleural space
^intrathoracic pressure collapse affected lung mediastinal shift to OPPosite side of chest compression vena cava v venous return v CO |
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tension pneumo causes a mediastinal shift this way
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OPPosite side of chest
pneumOthorax=Opposite |
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name manifestations of tension pneumo
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chest pain
tachypnea, tachycardia dyspnea hyperresonance decreased bs medialstinal shift to opposite |
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atelectasis is this
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imperfect expansion of alveoli, incomplete expansion
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atelectasis in adults is b/c
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obstruction mucous plug
small seg, entire lobe common post op |
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name manifestations of atelectasis
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tachypnea & tachycardia
fever, hypoxemia(cyanosis) diminised chest expansion absence bs move toward affected side |
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PNA is
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inflammation of parenchymal structures of lung (alveoli, bronchioles)
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this is a significant cause of death in elderly
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PNA
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increase in PNA d/t
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pseudomonas, candida & other resistant strains
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classify PNA based on
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type of agent
distribution setting it occured |
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Lobular vs bronchoPNA distribution
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lobular=lobe
bronchoPNA=all over |
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CAP is caused by these 4 things
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Strep
S Aureus H Flu Chlamydia |
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NAP is caused by these 6 things
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Pseudomonas
S Aureus Enterobacter Klebsiella E coli Serratia |
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immunocompromised PNA is caused by these 4 things
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S Aureus
Aspergillus (fungi) Candida gram negative bacilli |
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which bug is common to all 3 PNAs
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S Aureus
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which is most common route of PNA
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aspiration
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3 ways bugs pass 1st line defense in PNA
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aspiration
inhalation bacteremia |
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what is the 2nd line of defense agst PNA
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alveolar macrophage
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the systemic response is activated in PNA when
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microorganisms are too virulent or large #
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the systemic response to PNA involves these 4 things
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inflammatory mediators released
damage to bronchial & alveolar capillary membranes terminal bronchioles fill with fluid, debris release toxins |
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net result of PNA systemic is:
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dyspnea
V/Q mismatch hypoxemia |
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asthma involves
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airway obstruction
bronchial hyperresponsiveness airway inflammation |
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cells involved in asthma pathology
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mast
eosinophils T lymphocytes epithelial |
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two classes of asthma
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extrinsic & intrinsic
|
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extrinsic asthma is
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type 1 hypersensitivity in response to Ag (IgE)
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intrinsic asthma is
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non immune
r/t exercise, emotions, irritants |
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onset of extrinsic asthma
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childhood
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describe early acute phase extrinsic asthma
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immediate bronchoconstriction (10-20 min)
mediators from IgE coated mast cells |
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describe late phase extrinsic asthma
|
4-8 hrs after exposure
inflammation, increased airway resistance |
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late phase airway inflammation in extrinsic asthma leads to
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edema
epithelial injury impaired mucociliary fx airflow limitation increased airway responsiveness |
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Increased airway responsiveness can lead to
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bronchospasm
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manifestations of intrinsic asthma
|
wheezing
chest tightness prolonged expiration hyperinflation use of accessory muscles dsypnea, fatigue ineffective cough V/Q mismatch (hypoxemia, hypercapnea) |
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treatment of asthma is directed at causes
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avoid triggers
desensitization meds |
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quick relief for attack asthma includes
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short acting B2 agonists, short course corticosteriods
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long term tx of asthma includes
|
inhaled corticosteriods, LT bronchodilators, mast-cell stabilizers(cromolyns), leukotriene modifiers(singulair), IGE blocker (Xolair)
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asthma in children is common & may start
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5-6 years old
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asthma is more prevalent here, & these infections predispose kids for it
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urban, frqt severe viral infections
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this should be monitored in kids on LT corticosteriod therapy
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growth
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in severe cases this may be absent
|
wheezing
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COPD includes 2 types obstructive airway d/o
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emphysema
bronchitis |
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the enlargment of air spaces & destruction of lung is
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emphysema
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the obstruction of small areas chronically is
|
chronic bronchitis
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the pathogenesis of COPD is
|
inflammation, fibrosis bronchial wall
hypertrophy submucosal glands hypersecretion of mucus loss of elastic lung fibers & alveolar tissue |
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elastic fibers are usually protected from this by this
|
elastase by alpha 1-antitrypsin
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the patho of COPD includes these 3 things
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obstruction airflow from inflammation, fibrosis (VQ mismatch)
destruction of alveolar tissue (dec surface area) loss of elastic fibers |
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loss of elastic fibers in COPD does this
|
impairs expiratory flow, increases air trapping, airway collapse
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emphysema is characterized by
|
loss of lung elasticity
abnormal enlargement of air spaces distal to terminal bronchioles destruction of alveolar walls & cap beds |
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|
enlargement of air spaces in emphysema causes
|
hyperinflation of lungs, increased total lung capacity
|
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the primary cause of COPD
|
smoking
|
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chronic bronchitis is airway obstruction caused by
|
inflammation of major & small airways
|
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chronic bronchitis causes
|
edema & hyperplasia of submucosal glands
excess mucous |
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diagnosis of chronic bronchitis
|
hx chronic productive cough >3 months x2 years
|
|
|
type A emphysema is called a
|
pink puffer
|
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|
characteristics of type A emphysema pink puffer:
|
dramatic barrel chest
severe wt loss decreased bs minimal sputum no cyanosis normal ABGs |
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type B chronic bronchitis is aka
|
blue bloater
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type B chronic bronchitis blue bloater characteristics are
|
some barrel chest
some wt loss exp wheezing, crackles bs PROMINENT sputum DRAMATIC cyanosis decreased O2, increased CO2 on ABG |
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if pt has barrel chest, w/severe wt loss & minimal sputum, they are likely to have this type of COPD
|
type A emphysema pink puffer
|
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if pt has a lot of sputum, cyanosis, & hypoxemia & hypercapnia on ABGs, they are likely to have this type of COPD
|
type B chronic bronchitis blue bloater
|
|
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way to remember type B COPD
|
B B B B
type B chronic Bronchitis Blue Bloater |
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PE is an
|
undissolved mass that travels in blood & occludes pulm bv
|
|
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PE can be
|
thrombus (DVT), fat, air
|
|
|
Virchow's Triad is
|
stasis(obese,immobile)
endothelial cell injury(surgery/trauma) hypercoagulability(pregnancy, tumor, birth control pills) |
|
|
if you are on birth control pills & smoke you are at increased risk for this
|
PE
|
|
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the pathophysiology of PE may include these 4 things
|
hypoxic VC
p. HTN RV failure systemic hypotension (decreased CO) |
|
|
clinical manifestations of PE include
|
tachypnea, dyspnea, chest pain, dead space ventilation
VQ mismatch(hypoxemia), decreased CO (hypotension, shock) |
|
|
ALI/ARDS is a syndrome with
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severe dyspnea, hypoxemia, p. infiltrates
|
|
|
mortality with ALI/ARDS is
|
35-60%
|
|
|
etiology of ALI/ARDS includes these things
|
aspiration
blood transfusion (USA) ETOH sepsis, trauma, burns, pancreatitis, high fiO2 |
|
|
name components of pathogenesis of ALI/ARDS
|
local/sys inflammatory
activated neuts release proteolytic enzymes, toxic O2 species etc which damage endo & alvolar epithelium fluid damage to alveolar cells causes surfactant inactivation FORMATION of HYALINE membrane |
|
|
what is distinctive in ALI/ARDS
|
formation of hyaline membrane
|
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|
describe lungs in ALI/ARDS
|
become stiff, increase WOB, less gas exchange, sev dyspnea, hypoxemia
|
|
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ALI/ARDS starts fast & progresses to
|
respiratory failure & MODS
|
|
|
infant RDS is the result of
|
immature type 2 cells, insufficient surfactant
|
|
|
what helps & what inhibits infant RDS
|
cortisol helps
insulin inhibits |
|
|
dx of infant RDS
|
s/s respiratory failure within 24 hrs
central cyanosis, retractions, grunting, increased RR 100 bpm fatigue d/t stiff lungs increased p. pressure might keep ductus arteriosus open |
