Carlos Shared "23 Respiratory" - 46 Picmonics

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23 Respiratory

Lung development
Occurs in five stages
Initial development includes development of lung bud from distal end of respiratory diverticulum during week 4.
Embryonic (weeks 4–7)
Lung bud → trachea → bronchial buds → mainstem bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi.
NOTE: Errors at this stage can lead to tracheoesophageal fistula.
Pseudoglandular (weeks 5–17)
Endodermal tubules → terminal bronchioles. Surrounded by modest capillary network.
NOTE: Respiration impossible, incompatible with life.
Canalicular (weeks 16–25)
Terminal bronchioles → respiratory bronchioles → alveolar ducts. Surrounded by prominent capillary network.
Pneumocytes develop starting at 20 weeks
NOTE: Airways increase in diameter. Respiration capable at 25 weeks.
Saccular (week 26–birth)
Alveolar ducts → terminal sacs. Terminal sacs separated by 1° septae.
Alveolar (week 36–8 years)
Terminal sacs → adult alveoli (due to 2° septation).
In utero, “breathing” occurs via aspiration and expulsion of amniotic fluid → ↑ vascular resistance through gestation.
At birth, fluid gets replaced with air → ↓ in pulmonary vascular resistance.
NOTE: 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) and bilateral renal agenesis (Potter sequence).
Bronchogenic cysts
Caused by abnormal budding of the foregut and dilation of terminal or large bronchi.
Discrete, round, sharply defined, fluid-filled densities on CXR (air-filled if infected)
Generally asymptomatic but can drain poorly, causing airway compression and/or recurrent respiratory infections.
Usually found in mediastinum
Diagnostic criteria: Walls contain cartilage
Club cells and Alveolar cell types
Club cells
Nonciliated; low-columnar/cuboidal with secretory granules.
Located in small airways.
Secrete component of surfactant
Degrade toxins
Act as reserve cells
Alveolar cell types
Collapsing pressure (P) = 2 (surface tension) / radius
Alveoli have increased tendency to collapse on expiration as radius decreases (law of Laplace).
Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC).
Surfactant synthesis begins around week 20 of gestation, but mature levels are not achieved until around week 35.
Corticosteroids important for fetus surfactant production and lung development.
Type I pneumocytes
97% of alveolar surfaces.
Line the alveoli
Squamous; thin for optimal gas diffusion.
Type II pneumocytes
Secrete surfactant from lamellar bodies (arrow in image) leads to decreased alveolar surface tension, prevents alveolar collapse, decreased lung recoil, and increased compliance.
Cuboidal and clustered (image)
Also serve as precursors to type I cells and other type II cells.
Proliferate during lung damage, regenerating the alveolar lining after injury.
Alveolar macrophages
Phagocytose foreign materials, release cytokines and alveolar proteases.
Hemosiderin-laden macrophages may be found in the setting of pulmonary edema or alveolar hemorrhage.
Neonatal Respiratory Distress Syndrome
Cause/Mechanism
Fetal Lung Immaturity
Lack of Surfactant
Assessment
Respiratory Distress
Nasal Flaring
Retractions
Grunting
Interventions
Surfactant
Oxygen
Mechanical Ventilation
Considerations
Total Parenteral Nutrition (TPN)
2 mins
Screening tests for fetal lung maturity
Lecithinsphingomyelin (L/S) ratio in amniotic fluid (≥ 2 is healthy; < 1.5 predictive of NRDS)
Foam stability index test
Surfactant-albumin ratio.
Persistently low O2 tension leads to risk of PDA.
Preterm delivery: betamethasone used to stimulate surfactant production in lungs
Preterm delivery: betamethasone used to stimulate surfactant production in lungs
Respiratory tree
Conducting zone
Large airways consist of nose, pharynx, larynx, trachea, and bronchi.
Small airways consist of bronchioles that further divide into terminal bronchioles (large numbers in parallel resulting in the least airway resistance).
Warms, humidifies, and filters air but does not participate in gas exchange, known as “anatomic dead space.”
Cartilage and goblet cells extend to end of bronchi.
Pseudostratified ciliated columnar cells primarily make up epithelium of bronchus and extend to beginning of terminal bronchioles, then transition to cuboidal cells.
Clear mucus and debris from lungs (mucociliary escalator).
Airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point).
Respiratory zone
Lung parenchyma; consists of respiratory bronchioles, alveolar ducts, and alveoli.
Participates 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 immune response.
Lung relations
Right lung has 3 lobes; Left has Less Lobes (2) and Lingula (homolog of right middle lobe).
Instead of a middle lobe, left lung has a space occupied by the heart
Relation of the pulmonary artery to the bronchus at each lung hilum is described by RALS—Right Anterior; Left Superior.
Carina is posterior to ascending aorta and anteromedial to descending aorta (IMAGE)
Right lung is a more common site for inhaled foreign bodies because right main stem bronchus is wider, more vertical, and shorter than the left.
Horizonal fissure is located near the 4th rib
Needle positioning for tension pneumothorax is between 2nd - 3rd rib
Arteries run with the airways at the center of the bronchopulmonary segments
If you aspirate a peanut:
While upright—enters basal segments of right lower lobe. Preferentially on right, but bilateral basal segments can be involved.
While supine—enters superior segment of right upper lobe. Preferentially on right side.
While lying on right side-usually enters right upper lobe
Frequency of location for obstruction is as follows: right main bronchus > left main bronchus > trachea > right lower bronchus > left lower bronchus > bilateral.
Pathways through the Diaphragm
Characteristics
T8 Level (Caval opening)
Inferior Vena Cava
T10 Level (Esophageal Opening)
Esophagus
Vagus Nerve
Esophageal Branches Left Gastric Vessels
T12 Level (Aortic opening)
Aorta
Thoracic Duct
Azygos Vein
2 mins
Physiologic Dead Space (VD)
Tidal Volume (VT)
Partial pressure of arterial CO2 (PaCO2)
Partial pressure of CO2 in expired air (PECO2)
VD = TV x (PaCO2-PECO2) / PaCO2
2 mins
Ventilation
VA = VE − VD
Minute ventilation (VE)
Total volume of gas entering lungs per minute
VE = VT × RR
Alveolar ventilation (VA)
Volume of gas per unit time that reaches alveoli
VA = (VT − VD) × RR
Normal values
Respiratory rate (RR) = 12–20 breaths/min
VT = 500 mL/breath
VD = 150 mL/breath
Lung and chest wall
Elastic recoil
Tendency for lungs to collapse inward and chest wall to spring outward.
At FRC (Functional Residual Capacity), inward pull of lung is balanced by outward pull of chest wall, and system pressure is atmospheric.
Elastic properties of both chest wall and lungs determine their combined volume.
At FRC, airway and alveolar pressures are 0, and intra pleural pressure is negative (prevents atelectasis). PVR is at minimum.
Compliance
Change in lung volume for a change in pressure; expressed as ΔV/ΔP and is inversely proportional to wall stiffness.
High compliance = lung easier to fill (emphysema, normal aging),
Lower compliance = lung harder to fill (pulmonary fibrosis, pneumonia, NRDS, pulmonary edema)
Surfactant increases compliance.
Hysteresis
Lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation.
Hemoglobin development
Embryonic globins: ζ and ε.
Fetal hemoglobin (HbF) = α2γ2
Adult hemoglobin (HbA1) = α2β2
HbF has higher affinity for O2 due to less avid binding of 2,3-BPG, allowing HbF to extract O2 from maternal hemoglobin (HbA1 and HbA2) across the placenta.
HbA2 (α2δ2) is a form of adult hemoglobin present in small amounts.
Hemoglobin
Hemoglobin Has Four Iron Hemes
Lots Of Hemoglobin In Red Blood Cells
High O2 Levels Increase O2 Binding
High Temperature Reduces O2 Binding
High CO2 Levels Reduce O2 Binding
Low pH Reduces O2 Binding
Myoglobin Binds Oxygen in Muscle
2 mins
Hemoglobin modifications (Methemoglobinemia and CO poisoning)
Lead to tissue hypoxia from decreased O2 saturation and decreased O2 content.
Methemoglobin
Oxidized form of Hb (ferric, Fe3+) that does not bind O2 as readily, but has increased affinity for cyanide.
PaO2 normal; SaO2 decreased
Iron in Hb is normally in a reduced state (ferrous, Fe2+). Fe2+ binds O2.
Methemoglobinemia may present with cyanosis and chocolate-colored blood.
Induced methemoglobinemia (using nitrites, followed by thiosulfate) may be used to treat cyanide poisoning.
Nitrites (eg, from dietary intake or polluted/high altitude water sources) and benzocaine cause poisoning by oxidizing Fe2+ to Fe3+.
Methemoglobinemia can also be an inherited disorder. Autosomal recessive. Deficient enzme: Cytochrome b5 reductase (Normally turns methemoglobin to hemoglobin)
Methemoglobinemia can be treated with methylene blue and vitamin C.
Carboxyhemoglobin / CO poisoning
Form of Hb bound to CO in place of O2.
Causes decreased oxygen-binding capacity with left shift in oxygen-hemoglobin dissociation curve.
Pao2 normal; SaO2 decreased
Decreases O2 unloading in tissues.
CO binds competitively to Hb and with 200× greater affinity than O2.
CO poisoning can present with headaches, dizziness, and cherry red skin.
May be caused by fires, car exhaust, or gas heaters.
Early sign of exposure is headache; significant exposure leads to coma and death.
Treatment
Treat with 100% O2 and hyperbaric O2.
Pulmonary circulation
Normally a low-resistance, high-compliance system.
PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation.
A decrease in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung.
Perfusion limited
O2 (normal health), CO2, N2O.
Gas equilibrates early along the length of the capillary.
Diffusion can be increased only if blood flow increases.
Diffusion limited
O2 (emphysema, fibrosis), CO.
Gas does not equilibrate by the time blood reaches the end of the capillary.
Pulmonary Diffusion Equation
Diffusion: V gas = A × Dk × (P1 – P2 / T )
A decreases in emphysema
T increases in pulmonary fibrosis.
DLCO is the extent to which CO, a surrogate for O2, passes from air sacs of lungs into blood.
Pulmonary vascular resistance
PVR = (P pulm artery – P L atrium) / cardiac output
Remember: ΔP = Q × R, so R = ΔP / Q
R = 8ηl / πr4
Alveolar Gas Equation
Equation
Partial Pressure of Alveolar Oxygen (PAO2)
Partial Pressure of Oxygen in the Inspired Air (PIO2)
PIO2 Normally Approximated = 150 mmHg
Arterial Partial Pressure of CO2 (PaCO2)
Respiratory Quotient (R)
R Normally Approximated = 0.8
PAO2 = PIO2 - (PaCO2/R)
1 min
A-a Gradient
Partial pressure of alveolar oxygen (PAO2)
Partial Pressure of Arterial O2 (PaO2)
Normal 10 to 15 mmHg
Hypoxemia with an Abnormal A-a Gradient
Diffusion problem
Shunting (Low V/Q)
Dead space (high V/Q)
1 min
Oxygen deprivation
Hypoxia
Decreased O2 delivery to tissue
Decreased cardiac output
Hypoxemia
Anemia
CO poisoning
Hypoxemia
Decreased PaO2
Normal A-a gradient
High altitude
Hypoventilation (eg, opioid use)
Increased A-a gradient
V/Q mismatch
Diffusion limitation (eg, fibrosis)
Right-to-left shunt
ischemia
Loss of blood flow
Impeded arterial flow
Decreased venous drainage

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