Pulmonary Flashcards
Embryonic
weeks 4-7
lung bud –> trachea –> bronchial buds –> mainstem bronchi –> secondary bronchi –> tertiary bronchi
ERROR => tracheoesophageal fistula
Pseudoglandular
Weeks 5-17
endodermal tubules –> terminal bronchioles
surrounded by capillary network
RESPIRATION IMPOSSIBLE
Canalicular
Weeks 16-25
Terminal bronchioles –> respiratory bronchioles –> alveolar ducts
Surrounded by prominent capillary network
airways increase in diameter
Respiration at 25 weeks
Pneumocytes develop at 20 weeks
Saccular
week 26-birth
alveolar ducts –> terminal sacs (separated by sepate)
Alveolar
week 36- 8 years
Terminal sacs –> adult alveoli
in utero breathing via aspiration and expulsion of amniotic fluid –> increase vascular resistance
at birth fluid gets replaced with air –> decrease pulmonary vascular resistance
Pulmonary hypoplasia
poorly developed bronchial tree with abnormal histo
Associated with congenital diaphragmatic hernia (L side), bilateral renal agenesis (potter)
Bronchogenic cysts
caused by abnormal budding of the foregut and dilation of terminal/large bronchi
Discrete round, sharply defined fluid filled density on CXR
asymptomatic, drain poorly –> airway compression or recurrent respiratory infection
club cells
nonciliated low columnar/cuboidal with secretory granules
Located in bronchioles
Degrade toxins, secrete component of surfactant
Type 1 pneumocytes
squamous
thinly line alveoli for optimal gas exchange
Type 2 pneumocytes
cuboidal and clustered
stem cell for Type 1 and Type 2 pneumocytes and secrete surfactant.
Surfactant
decrease alveolar surface tension, decrease alveolar collapse, decrease lung recoil and increase compliance
Composed of lechithins (DPPC)
synthesis begins 20 weeks and achieves mature levels at week 35
CORTICOSTEROIDS –> surfactant
Alveolar macrophages
phagocytes
release cytokines and alveolar proteases
hemosiderin macrophages found in pulmonary edema or alveolar hemorrhage
Neonatal RDS
surfactant deficiency –> high surface tension –> alveolar collapse, ground glas
risk: premature, Maternal DM, C section
Tx: maternal steroids before birth, exogenous surfactant
Therapeutic O2 –> retinopathy, intraventricular hemorrhage, bronchopulmonary dysplasia
L/S >2 is healthy
Conducting zone of Respiratory tree
large airways consist of nose, pharynx, larynx, bronchi
airway resistance highest in large to medium bronchi
Warm, humidifies and filters air BUT NO GAS EXCHANGE
Cartilage and goblet cells extend to bronchi
Pseudostratified ciliated columnar cells= bronchus to beginning of terminal bronchioles then transition to cuboidal cells
Respiratory zone of respiratory tree
lung parenchyma (respiratory bronchioles, alveolar ducts, alveoli.
PARTICIPATE IN GAS EXCHANGE
cuboidal cells in respiratory bronchioles –> simple squamous
cilia terminate in respiratory bronchioles
alveolar macrophages clear debris
Lingula homologous to
right middle lobe
Relation of pulmonary artery to bronchus
Right anterior, Left superior
Carina position
posterior to ascending aorta and anteromedial to descending aorta
Most common site for inhaled foreign bodies
right lung
supine: superior segment of right lower lobe
lying on right side- right upper lobe
upright- enter right lower lobe
T8 Diaphragm
IVC
right phrenic N
T10 Diaphragm
esophagus
Vagus N
T12 Diaphragm
aorta
thoracic duct
azygous vein
Inspiratory reserve volume
air that can still be breathed in after normal inspiration
Tidal volume
air that moves into lung with each quiet inspiration (500)
Expiratory reserve volume
air that can still be breathed out after normal expiration
Residual volume
air in lung after maximal expiration
RV and any lung capacity that includes RV cannot be measured by spirometry
Inspiratory Capacity
IRV+TV
air that be breathed in after normal exhalation
Functional residual capacity
RV + ERV
volume of gas in lungs after normal expiration
Vital capacity
TV + IRV + ERV
Maximum volume of gas that can be expired
Total Lung Capacity
IRV + TV + ERV + RV
volume of gas present in lungs after a maximal inspiration
Elastic recoil
Tendency of lungs to collapse inward and chest wall to spring outward
At FRC airway and alveolar pressure = Patm and intrapleural pressure is negative, PVR at minimum
Compliance
change in lung volume for a change in pressure
inversely proportional to wall stiffness and increased by surfactant
High compliance –> lung easy to fill (emphysema, aging)
Low compliance –> lung hard to fill (pulm fibrosis, pneumonia, ARDS, pulm edema)
Hysteresis
lung inflation follows a different pressure volume curve than lung deflation due to need to overcome surface tension forces in inflation.
Respiratory system changes in the elderly
TLC remains the same
increased compliance, RV, V/G mismatch, A-a gradient
Decreased chest wall compliance, FVC and FEV1, respiratory muscle strength, ventilatory response to hypoxia
CO poisoning
Normal Hb conc
low O2 sat Hb
Normal dissolved O2
low total O2
Anemia
Low Hb conc
Normal O2 sat Hb
Normal Dissolved O2
Low total O2
Polycythemia
High Hb concentration
Normal O2 sat Hb
Normal dissolved O2
High total O2 content
Methemoglobin
Iron in Hb is normally reduced (2+)
oxidized Iron (3+) does not bind O2 readily but has increased affinity to CN- –> tissue hypoxia from low O2 saturation and low O2 content
CYANOSIS AND CHOCOLATE COLORED BLOOD
Shift right on ODC
low Hb affinity for O2 --> high P50 low pH high PCO2 Exercise high 2,3 BPG High altitude high temperature
Shift left on ODC
low O2 unloading --> renal hypoxia --> high EPO synthesis --> compensatory erythrocytosis basic low PCO2 low 2,3 BPG low temp high CO high MetHb high HbF
CN- poisoning
Byproduct of combustion
Tx: hydrocobalamin, nitrites, sodium thiosulfate
Sx: breath has bitter almond odor, CV collapse
ODC normal
CO poisoning
odorless gas from fires, car exhaust or has heaters
Tx: 100% O2
Sx: HA, dizzy, bilateral globus pallidus lesions on MRI
Left shift in curve, bind competitively to Hb
Pulmonary circulation
Low resistance, high compliance
low PaO2 –> hypoxic vasoconstriction that shifts blood away from poorly ventilated region
Perfusion limited
O2, CO2, N2O
gas equilibrates early along the length of the capillary. Exchange can be high only if blood flow high
Diffusion limited
O2, CO
gases does not equilibrate by the time blood reaches the end of the capillary
Ventilation/ perfusion mismatch
High at apex and low at base
with exercise there is vasodilation of apical capillaries so ratio approaches 1
V/Q = 0
obstruction
100% O2 does not improve PaO2
V/Q = infinity
blood flow obstruction
100% O2 improves PaO2
Response to high altitude
low atmospheric oxygen–> low PaO2 –> high ventilation –> low PaCO2 –> respiratory alkalosis –>altitude sickness
increase EPO, 2,3 BPG, mitochondria, renal excretion of HCO3-
Vasoconstriction –> pulmonary HTN and RVH
Response to exercise
High CO2 production, high O2 consumption
Right shift
high ventilation rate meet O2 demand
V/Q ratio from apex to base becomes more uniform
increase pulmonary blood flow due to increased cardiac output
low pH
Rhinosinusitis
obstruction of sinus drainage into nasal cavity –> inflammation and pain over are (Maxillary –> drain against gravity)
superior meatus- drain sphenoid, posterior ethmoid
middle meatus- drain frontal, maxillary and anterior ethmoid
inferior meatus0 drain nasolacrimal duct
VIRAL URI + H. influenz, S. pneumoniae, M. catarrhalis
Epistaxis
most common in anterior segment of nostril
life threatening in posterior segment
caused by foreign body, trauma, allergic rhinitis and nasal angiofibromas