respiratory Flashcards
Lung development
5 stages, lung bud from distal end of respiratory diverticulum during week 4
Every Pulmonologist Can See Aveoli
-Embryonic (weeks 4-7): lung bud–> trachea–> bronchial buds–> mainstem bronchi–> secondary (lobar) bronchi–> tertiary (segmental bronchi), Errors at this stage can lead to a TE fistula
-Pseudoglandular (weeks 5-17): endoermal tubules–> Terminal bronchioles. Surrounded by modest capillary network. Respiration impossible, incompatible with life
- Canalicular (weeks 16-25): terminal bronchioles–> respiratory bronchioles–> alveolar ducts. Surrounded by prominent capillary network (airways increase in diameter, respiration capable at 25 weeks, pneumocytes develop starting at 20 weeks
-Saccular (week 26-birth): Alveolar ducts–> terminal sac, terminal sacs separated by 1’ septae
-Alveolar (week 36 to 8 years): Terminal sacs–> adult alveoli due to 2’ separation, in utero, breathing occurs via aspiration and expulsion of amniotic fluid–> vascular resistance increase through gestation, at birth fluid gets replaced with air and leads to decrease in pulm vascular resistance, at birth 20-70 million alveoli, by 8 years, 300-400 million alveoli
Congenital lung malformations
Pulmonary hypoplasia: poorly developed bronchial tree with abnormal histology, Associated with congenital diaphragmatic hernia (usually left sided), bilateral agenesis (Potter sequence)
Bronchogenic cysts: Caused by abnormal budding of the foregut and dilation of terminal or large bronchi. Discrete, round, sharply defines, fluid filled densities on CXR (air filled if infected). Generally asymptomatic but can drain poorly, causing airway compression and or recurrent respiratory infection
Club cells
Non ciliated, low culumnar cuboidal with secretory granules, located in bronchioles, degrade toxins, secre part of surfactant act as reserve cells
Type 1 pneumocytes
Squamous, 97% of alveolar surfaces, thinly line the alveoli for optimal gas exchange
Type 2 pneumocytes
Cuboidal and clustered
2 functions: stem cells for ty0pe 1 and 2 cells, proliferate during lung damage
Secrete surfactant from lamellar bodies
Surfactant: decreases alveolar surface tension, decrease alveolar collapse, decrease lung recoil and increased compliance
Multiple lecthins (mainly dipalmitoylphosphatidylcholine)
acheives mature levels at week 35
Corticosteroids important for fetal surfactant synthesis and lung development
Law of laplace alveoli have an increased tendency to collapse on expiration as radius decrease
Alveolar macrophages
phagocytose foreign materials, release cytokines and alveolar proteases
Hemosiderin-laden macrophages (HF cells) may be found in the setting of pulmonary edema or alveolar hemorrhage
Neonatal respiratory distress syndrome
Surfactant deficiency-> increase surface tension and multiple alveolar collapse (ground glass appearance of lung fields)
Risk factors: prematurity, maternal diabetes (due to increased fetal insulin, inhibits surfactant), C section delivery (decrease release of fetal glucocorticoids, less stressful than vaginal delivery)
treatment: maternal steroids before birth, exogenous surfactant for infant
Therapeutic supplemental O2 can result in Retinopathy of prematurity, intraventricular hemorrhage, BPD
Lecithin/S ratio should be greater than 2, persisitantly low O2 levels will increase risk of PDA
Respiratory tree conducting zone
large airways consist of the nose, pharynx, larynx, trachea, and bronchi
Airway resistance highest in the large to medium sized bronchi, small airways consist of bronchioles that further divide into terminal bronchioles (large numbers in parallel—> least airway resistance)
Warms, humidifies, and filters air but doesnt participate in gas exchange (anatomic dead space), Cartilage and goblet cells extend to the end of bronchi
Pseudostratifies ciliated columnar cells primarily make up epithelium of bronchus and extend to begining and extend to begining of terminal bronchiols then transition to cuboidal cells, clear mucus and debris from lungs (mucociliary excalator)
Airway smooth muscle cells extend to end of terminal bronchioles
Respiratory zone of tree
lung parenchyma, consists of respiratory bronchioles, alveolar ducts and alveoli, participate in gas exchange
Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli , cilia terminate in respiratory bronchioles, alveolar macrophages clear debris and participate in immne response
Lung anatomy
right lung has 3 lobes left lobe has 2 with the lingula is the right middle lobe due to heart
Relation of the pulmonary artery to the bronchus at each lung hilum is described by RALS (right is anterior to the bronchus, Left is superior)
Carina is posterior to aorta and anteromedial to descending aorta
Right lung is common site for inhaled forein bodies, bronchus is wider, more verticle, and shorter than left
Aspirating while supine- usually enters superior segment of right lower lobe, while lying on right side enters the right upper lobe, while upright- enters right lower lobe
Lungs coverd by 6 ribs in front and 9 in the back
Determination of physiologic dead space
tidal volume x (Paco2-Peco2)/Paco2
Apex is the largest contributor of alveolar dead space
Co2 in arteris- Expiratory Co2
Ventilation s
Minute: volume of gas entering the lungs per minute
Alveolar: (Vt-Vd) x RR
how much gas is reaching the alveoli
Respiratory system changes in the elderly
Aging is associated with progressive decrease in lung function
TLC remains the same
Long compliance increased (loss of elastic recoil), residual volume increased, V/Q mismatch and A-a gradient increases
Decreased: Chest wall compliance decreases (decreased chest wall stiffness, FVC and FEV1 decreases, Respiratory muscle strength can impair cough, Ventrilaroty response to hypoxia
Hemoglobin
Deoxy form has low affinity for O2, and promotes release of O2
Oxy form has high affinity for O2 (Hb exhibits positive cooperativity and positive allosterism
hemoglobin is a H+ ion buffer
O2 content of blood
O2 content = (1.34 x Hb x SaO2) + (.003 x PaO2)
Normally 1 g Hb can bind 1.34 ml O2, normal Hb amount in blood is 15 g/dl
O2 binding capacity= 20 ml O2/dL of blood
With a decrease in Hb there is decreased O2 content of arterial blood, but no change in O2 saturation and PaO@
O2 delivery to tissues= cardiac output x O2 content of blood
CO poisoning- decreased O2 saturation, Notmal hb concentration, PaO2 normal, total O2 is low
Anemia- decreased Hb concentration, normal Hb and saturation and dissoled O2
Poly cythemia- Hb high, O2 saturation normal, PaO2 normal Total O2 content is high
Methemoglobin
Iron in Hb is normally reduced state (frrous 2+ form)
Oxidized form of Hb (ferric Fe3+ doesnt bind O2 but has an increased afinity for cyanide–> tissue hypoxia from decreased O2 saturation and decreased O2 content
Methemoglobinema- cyanosis and chocolate blood
Nitrites from diet or polluted/high altitude and benzocaine cause poisoning by oxidizing iron to Fe 3+
Methemoglobinemia can be treated with methylene blue and vit C
Oxygen hemoglobin dissociation curve
Sigmoidal shape due to positive cooperativity right shift (releases O2; Acid, Co2, Exercise, 23BPG, high altitude, temperature)
Left shift–> dcreased O2 unloading–> renal hypoxia–> EPO -> compensatory erythrocytosis
Fetal Hb (2a and 2y subunits) has lower affinity for 23 BPG
Cyanide vs CO poisoning
both inhibit aerobic metabolism vi inhibition of complex 4 (cytochrome c oxidase)–> hypoxia that does not fully correct with supplemental O2 and increased anaerobic metabolism
Both can lead to pink or cherry red skin (usually post mortem finding), seizures, adn coma
Cyanide: byproduct of synthetic product combustion, ingestion of amygdalin or cyanide (apricot). treat with hydroxyocobalamin (binds cyanide-> cyanocobalamine-> renal excretion
Nitrites (oxidize Hb-> methemoglobin -> binds cyanide very easily-> cyanomethemoglobin (less toxic)
Sodium Thiosulfate (increased cyanide conversition-> thiocyanate-> renal excreation. Breath smells like almonds, leads to cardiovascular collapse, hbO2 curve is normal
Carbon monoxide: gas from fires. Treat with 100% O2 and hyperbaric O2. Leads to headache, dizziness, multi individiuals. Associated with bilateral globus pallidus lesions on MRI. Left shift curve- (increased affinity for O2 decreased , binds carboxy hemoglomin
Pulmonary circulation
Normally low resistance, high-compliance system. A decrease in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of the lung to well ventilated regions
Perfusion limited- O2 (normal health), CO2, N2O cas equilibrates early along the length of the capillary, exchange can be increased only if blood flow increases
Diffusion limited (O2 (in emphysema, fibrosis, exercis), CO (gas does not quilibrate by the time reaches the end of the capillary
Inspiratory reserve volume
air that can still be breathed in after normal inspiration
Tidal volume
Air that moves into lung with each quiet inspiration, typically 500 mls
Expiratory reserve volume
Air that can still be breathed OUT after normal expiration (decreased in COPD)
residual volume
Aith in lung after max expiration, cannot be measure by spirometry
Inspiratory capacity
IRV+TV, Air that can be breathed in after breathing in tidal volume
Functional residual volume
volume of gas in lungs after normal expiration (RV+ERV)
Viral capacity
All the air that can be moved in and out (minus the RV)
Total lung capacity
everything
Oxygen deprivation
Hypoxia (low O2 delivery to tissue) (decreased cardiac output, hypoxia, Ischemia, anemia, CO poisoning)
Hypoxemia (low PaO2)- Normal A-a gradient (high altitiude, hypoventilation (opioids, obesity). Increased A-a gradient (V/Q mismatch, diffusion limitation, right to left shunt)
Ischemia- loss of blood flow (impeded arterial flow, decreased venous drainage
V/Q mismatch
ideally, ventilation is matched to perfusion (1) for adeguate gas exchange
at the apex- v/q=3 (zone 1) wasted ventilation
at the base (zone3), v/1= .06 (wasted perfusion)
Both ventilation and perfusion are highest at the base
With exercise (increased CO)there is vasodilation of apical capillaries--> V/Q gets better Certain organisms that thrive in high O2 flourish in the apex V/Q= 0 oirway 100% o2 doesnt improve O2 (obstruction) V/Q= infinity (blOOd) flow obstruction, physiologic dead space, assuming <100% dead space, 100% O2 does improce PaO2 (you add O2 to all the places that are being perfused
Carbon dioxide transport
CO2 is transport from tissues to lungs in 3 forms
- HCO3 (70%)
- Carbaminohemoglobin (21-25%) CO2 bound to Hb at N terminus of globin (NOT HEME) , CO2 favors deoxy form
- Dissolved CO2 (5-9%)
in lungs, O2 hemoglobin promotes dissociation of H+ from Hb. this shifts equilibrium toward CO2 formation therefore, CO2 is released from RBC (haldane effect)
When there is oxygen, Hgb lets go of H+ and promotes CO2 formation
In peripheral tissues, increased H+ from tissue metabolism shift curve to right to release O2
Majority of CO2 is carried as HCO3+
when HCO3 is released CL is taken in
Response to high altitude
decreased PiO2-> decreased PaO2-> increased ventilation-> decreased CO2-> respiratory Alkalosis, altitude sicness
You need to resp more to get more O2 in–> more CO2 out–> alkalosis
Increased EPO- increased Hct, increased 23 BPG ,, increased mitochondria, increased renal excretion of HcO3- takes a few days to weeks
Chronic hypoxia-> pulmonary vasoconstriction -> RVH
Response to exercise
increased CO2 production, increased O2 consumption, ODC right shift- increased ventilation, V/q mismat better- slight increase in Lactic acidosis
No change in PaO2 or PaCO2, but increase in venous CO2 content and decresed in Venous O2 content
Rhinosinusitis
Obstruction of sinus (maxillary) drainage into nasal cavity–> inflammation and pain over affected area,
Maxillary sinus most common because it drains against gravity due to ostia located superomedially
Superior meatus- drains sphenoid, posterior ethmoid. Middle meatus drains frontal, maxillary and anterior meatious
Inferior meatus drains nasolacrimal duct
Most common acute cause of Rhinosinusitis is viral URI, may lead to superimposed bacterial infection, most commonly H flue, S pneumoniae, M catarrhalis
Paranasal sinus infections may extend to the orbits, cavernous sinus and related complication (oribital cellulitis, cavernous sinus syndrome, meningitis
Epistaxis
nose bleed, most commonly occurs in anterior segment of nostril (Kiesselbach plexus)
Life threatening hemorrhages occurs in posterior segment (sphenopalatine artery (a branch of maxillary artery) , common causes include foreign body, trauma, allergic rhinitis, and nasal angiofibromas (adolescent males
Kiesselbach plexus (drives his Lexus with his Legs) Labial artery, anterior and posterior Ethmoidal arteries, Greater palatine artery, Sphenopalatine artery
head and neck cancer
Mostly squamous cell carcinoma, Risk factors include tobacco, alcohol, HPV 16 (oropharynx), EBV(nasopharyngeal)
Field cancer- carcinogen damage the entire mucosa- multiple tumors
DVT
Blood clot in deep vein> swelling, redness, warmth, pain predisposed by Virchow triad
Stasis (post op, long drive) Hypercoagulability (defect in coagulation cascade such as Factor 5 leiden, oral contraceptive use, pregnancy) Endothelial damage (exposed collagen triggers clotting cascade)
most pulmonary emboli arise from proximal deep veins of lower extremity
D-dimer lab test (used to rule out DVT in low risk pt (high sensitivity, low specificity more likely to have a false pos)
Imaging- compression ultrasound with doppler
use unfractionated heparin or low molecular weight heparin (enoxaparin) for prophylaxis and acute management, use oral anticoagulants (riveroxaban, apixaban) for treatment and longterm prevention
Pulmonary emboli
V/Q mismatch, hypoxia, respiratory alkalosis (start breathing heavy CO2 leaves), sudden onset dyspnea, pleuritic chest pain, tachypnea, tachycardia, large emboli or saddle embolus may cause sudden death due to electromechanical dissociation (pulseless electrical activity). CT pulmonary angiography is imaging test of choid for PE
May have SIQ3T3 abnormality on ECG, Lihns of Zahn are interdigitating areas of pink (platelets, fibrin) and Red RBCs found in thrombi that are formed before death, help distinguish pre and postmortem thrombi
Types Fat Air Thrombus Bacteria, Amniotic fluid, Tumor
Fat embolip long bone fractures, liposuction, classic triad of hypoxemia, neuro abnormalities, petechial rash
Air emboli- nitrogen bubbles precipitate in ascending divers (caisson disease/decompression sickness) treat with hyperbaric O2, or can be iatrogenic to central line placement
Amniotic fluid emboli- during labor and post partum- uterine trauma, can lead to DIC- high mortality
Mediastinal pathology
Normal mediastinum contains heart, thymus, lymph nodes, esophagus(gets innervation from aorta) and aorta
