exam 2- respiratory Flashcards
pulmonary space
the whole pulmonary cavity (largest)
pleural space
a “potential” space between the 2 vicera (chest wall and lungs)(middle)
pulmonary interstitial space
a “potential” space between the cap mem and the alveolar mem. (smallest)
what do you not want in the pulm. interstitial space
water/fluid
why did they call it surfactant
surface
active
agent
what is surfactant
substance (lipoprotein) produced by the alveoli
what is the purpose of surfactant
reduces the surface tension and allows the alveoli to stay open for gas exchange
what do the pulmonary capillaries of alveolar and cap membrane form
a network around each alveolus so dense that an almost continuous sheet of blood covers the alveoli
how many blood cells can move through ta pulm capp at a time
one, they must move in a single file line
each RBC stays in cap bed for how long and how many alveoli does it exchange with
1 second
2-3 alveoli exchange
normal ventilation stimulates what in the alveoli
surfactant replacement
what happens to the alveoli when a person hyperventilates
leads to alveolar collapse (atelectasis)
normal alveolar unit
normal ventilation
normal perfusion
dead space unit
(pulmonary emboli)
normal ventilation
NO perfusion
shunt unit
NO ventilation
no perfusion
(tumor or fluid blocking the air from reaching alveoli)
silent unit
NO ventilation
NO perfusion
ventilation
movement of atmospheric air into the alveoli
diffusion
movement of o2 across alveolar walls into pulm caps
perfusion
movement of o2 to and into the cells (tissues)
each rbc has how many HG
300
how many o2 molecules can one HG carry
4
how many o3 molecules can one RBC carry
1,200
what are the 7 steps required to transfer O2 from environmental air into cells
ventilation of lungs
transport of o2 from alveoli into plasma
co2 out
circulation of blood
diffusion of o2 from cap into intersitital fluid
diffusion into cells
diffusion of o2 into mitochondria where it synths ATP
if any of the 7 steps of air to cells is interrupted, what happens
tissue becomes hypoxic
hypoxemia
decreased oxygenated of the arterial blood
hypoxia
decreased o2 levels of the cells
why might hypoxia be localized
a blood clot, where the person doesn’t need to be hypoxemic generalized
what are the four major etiologies of hypoxia
reduced transfer of O2 from alveolar (atmospheric) air to blood (hypoxemia)
decreased HgB concentration
decreased inspired O2
Ichemia
what are etiologies of reduced transfer of 02 from alveolar air to blood
hypoventilation
impaired transport of O2 across alveolar membrane
ventilation perfusion mismatch
hypoventilation:
decreased rate and or depressed depth of respirations
risk for those who have undergone anethesia
what two things can impaire transport of 02 across alveolar membrane causing the diffusion capaity of alveolar membrane to be affected
drug overdose
general anesthesia
chest and abdominal pain (surgery or trauma)
surface area available (fluid)
thickened membrane (pulmonary fibrosis)
intestinal space issues (fluid, infection)
what is ventilation perfusion mismatch
ventilation (air into alveoli) and perfusion (pulmonary cap blood flow) normally match but respiratory disease lead to mismatch
what are the etiologies for decreased HGB concentration
anemia
CO poisoning
what is/causes anemia
blood loss
decreased production of RBC’s
decreased iron intake
what is CO poisoning
Co combines with HGB at same site as O2 and blocks sites for O2
HGB likes CO better than O2
what are the etiologies for decreased inspired O2
breathing high altitude air
breathing air from which o2 has been removed (fire)
what are the etiologies of ischemia
decreased blood flow to tissue
why would blood flow decrease to tissues
vasoconstriction
obstruction in BV
decreased cardiac ouput
what causes local or regional ischemia
vasoconstriction
blocking
(ie atherosclerosis of iliac arteries leading to decreased blood flow to legs)
what causes general systemic ischemia
decreased perfusion of o2 to tissues caused by heart not pumping enough
why does hypovolemic shock lead to ischemia
loss of blood volume = lack of blood= lack of O2 perf
what are the manifestations of hypoxia
decreases SaO2, pO2
increased pCO2
decreased pH (respiratory acidosis)
what are the early signs of hypoxia
confusion
lethargy
increased HR
change in behavior
what are the middle signs of hypoxia
dyspnea (sob)
decreased urine output
prolonged cap refill
what are the late signs of hypoxia
decreased BP
cyanosis at lips tounge
what is atelectasis
collapse of alveoli
what are three patho of atelectasis
compression atelectasis
absorption atelectasis
decreased surfactant production
what is compression atelectasisq
external pressure usually caused by tumor or fluid pressing on alveoli
what is absorption atelectasis
in alveoli, internal obstruction usually caused by secretions in alveoli
what causes decreased surfactant production leading to atelectasis
premi babies
anesthesia
prolonged mechanical ventilation
what are the clinical manifestations of atelectasis
crackles (rales) decreased breath sounds dyspnea cough fever decreased pO2, SaO2 increased pCO2
what is pleural effusion
collection of fluid in pleural space
what are the etiologies for pleural effusion
transudate (hydrothorax)
exudate
pus (empymea)
blood (hemothorax)
what is transudate (hydrothorax) in pleural effusion
water accumulation usually under viceral pleura (cardiac/liver/kidney disease)
what is exudate in pleural effusion
fluid is high in proteins from infection or malignancy
what is pus from in pleural effusion
infection
what is blood from in pleural effusion
trauma, thoracic surgery
what are the clinical manifestations of pleural effusion
atelectasis because of fluid displaceing lung tissue
dyspnea
chest pain during respiration
mediastinal shift
what is pneumothorax
the presence of air in pleural space
what are the etiologies of pneumothorax
fractured ribs
rupured bleb (copd)
thoractomy
spontaneous
why do the etiologies cause a pneumothorax
air enters pleural space… negative pressure in pleural space is destroyed, lung collapses
what are the clinical manifestations of pneumothorax
dyspnea
chest pain on breath movts
no breath sounds on effected lung
hypoxia
tension pneumothorax
life threatining
what are the etiologies of tension pneumothorax
usually from trauma
air enters pleural space on inspiration but cannot escape on expiration
wound acts as a one way valve so air continues to build up in pleural space
what are the clinical manifestations of tension pneumothorax
hypoxia
SOB
medistinal shift
decreased BP because of shift in great BV’s
pneumonia
acute infection in lungs (tissue) caused by bacteria, virus, fungus
what is the etiology of pneumonia
lower respiratory tract infection caused by streptococcus (pneumococcal) pneumonia
what are the two types of pneumonia
community acquired
nosocomical (hospital aquried–bacteria ventilator associated– cant cough)
what is the patho chain for pneumonia
aspiration of microb (respiratory droplets) inflammatory response alveoli fill with exudate phagocytosis in alveoli resolution of inflection
what are the clinical manifestations of pneumonia (6)
fever chest pain increased RR rusty, brown, yellow colored sputum increased WBC chest x-ray "infiltrates"
pulmonary emboli
occulsion of a pulmonary artery by an emoblus
what are the four types of emboli in pulmonary emboli
blood clot (thrombus from deep calf)
tissue frag
fat emboli (break in large bone)
air bubble
what are the etiologies of pulmonary emboli
venous statis
vessel injury (trauma, surgery)
history of prior embolus/thrombus
what is venous statis
etiology of PE
blood that doesnt move much
(bedrest, obesity, HF, central venous cath)
what is the patho chain of PE
thrombus(clot) formation
dislodgement of thrombus (becomes emboli)
occlusion of part of pulmonary artery
(can go from this point)
what are the three different chains after occlusion of pulm artery in pulmonary emboli
.. increase in pulm artery pressure right ventricular failure severe shock sudden death.\ .... resolution of clot resulting in absorbed/dissolved or scar tissue from death of tissue in lung
what are the clinical man of PE (7)
depends on severity of PE breathing is silent (dyspnea) fever cough (bloody) tach chest pain hypoxemia
what is acute respiratory failure
inadequate gas exchange to meet tissue oxidation needs at rest
not an actual disease- its a term used to anything demo decreased gas exchange at rest
acute respiratory failure can be applied to any respiratory disorder if it meets what?
pO2 less than 50 mmhg (norm >80)
pCO2 more than 50 mmhg (norm 35-45)
what are the clinical manifestations of acute respiratory failure
depends on specific etiology
acute heart failure leading to pulmonary edema (flash)
accumulation of fluid in the pulmonary interstitial sapce and INTO alveoli
what are the etiologies of acute HF leading to plash pulm edema (4)
left v. heart failure (most common)
mitral stenosis- fluid backs up in pulm inter space
alveolar-cap damage
volume overload
what is the path chain for acute HF leading to plash pulm edema
increase in pulm cap hydrostatis pressure fluid into pulm interstitial space fluid into alveoli dilutes surfactants atelectasis
what are the clinical manifestations of acute HF leading to flash pulm edema (7)
dsypnea sob- orthopnea paroxymal noturnal dyspnea crackles rhonchi hemoptysis hypoxia
what is orthopnea
sob/dyspnea that occurs when laying flat
what is paroxysmal noturnal dyspnea
sob attack when asleep
a sensation athat wakes a person up
what is hemoptysis
pink frothy sputum
tuberculosis
infection caused by mycobacterium tuberculosis bac
what is the patho chain of TB
tb transmitted via airborne droplets inhailed into lung and tb X's inflammation (neurtophils/macrophages) tubercle lesion necrosis of infected tissue either becomes dormant or active tb
what are the clinical manifestations of TB
fatigue weight loss night sweats low grade fever cough (non productive at first, tons (purulent) later (late sign)
how do you diagnos TB
TB skin test
if positive
must have all: +skin test, +sputum culture, + CXR
who get neg TB skin tests
those never exposed and those who were exposed but not infected
who gets positive TB skin tests
active TB
dormant Tb
what is COPT
obstruction of air flow— difficult expiration
chronic broncitis
hypersecretion of muccus and chronic cough (3 mo during winter at least 2 consec. years
what is the etiology of chronic bronchitis
chronic inhailed irritation
cigs, air pollution and infections
what is the patho chain of chronic bronchitis
irritants increase in thick mucus in lungs decrease in cillary function decrease of mucus clearance increase in infection risk inflamed and THICK bronchial walls airway obstruction (esp on expiration)
what are the two major things with chronic bronchitis
mucus build up
thickened bronchial walls
what kind of pts are usually chronic bronchitis
chubby pts
what are the clinical manifestations of chronic bronchitis (7)
wheezing dyspnea productive cough (tons of muccus) decreased exercise tolerance repeated resp infection (yellow green, rusty) hypoxia with resp acidosis cyanosis
emphysema
destruction of alveolar walls - loss of elastic recoil
obstruction is from changes in lung tissue rather than muccus production and inflam
what are the etiologies of emphysema
cig smoking
alpha antitrypsis deficincy- prevents lung tissue from breaking down
what is the patho chain of emphysema
irritants alveolar destruction increase air in alveoli (air trapping) collapse of small airways decrease alveolar diffusing surface area decrease gas exchange (o2 and co2)
what kind of pt are those with emphysema
thin pts
what are the clinical manifestations of emphysema
dyspnea on exp hypoxia with resp acidosis cyanosis no cough- little sputum increased anterior-posterior lateral diameter(barrel chest) freqquent resp infections
pursed lip breathing with what
emphysema
chronic b and emph
occure together a lot cuz of cigs
which two chronic resp issues contribute to COPD
chronic bronchitis
and emphysemia
