Pulmonology Flashcards
(43 cards)
Conducting zone
Do not participate in gas exchange: warm, humidify, filter air; “anatomic dead space”
Large airways:
- Nose
- Pharynx
- Trachea
- Bronchi (cartilage, goblet cells to end)
Small airways:
- Bronchioles
- Terminal bronchioles (pseudostratified ciliated columnar cells and smooth muscle to end)
Respiratory zone
Gas exchange; NO cilia
Parenchyma:
- Respiratory bronchioles: cuboidal cells
- Alveolar ducts: simple squamous cells up to alveoli
- Alveoli: Type I, Type II pneumocytes, Clara cells, alveolar macrophages
Type II pneumocytes
- Pulmonary surfactant production
Surfactant= dipalmitoylphophatidylcholine
- Begins at week 26
- Mature at week 35: indicated by lecithin-to-sphingomyelin ratio > 2.0 in amniotic fluid
- Glucocorticoids enhance surfactant production in premature babies
- Clara cells= secrete component of surfactant (also degrade toxins, act as reserve cells) - Precursors to Type I pneumocytes (Type I= 97% of alveolar cells)
Inspiratory muscles
Quiet breathing= diaphragm
Exercise inspiration= External intercostals, scalene, sternocleidomastoids
Expiratory muscles
Quiet breathing= passive
Exercise expiration= Abdominals, Obliques, Internal intercostals
Determination of physiologic dead space
Vd/ Vt = (PaCO2-PeCO2)/PaCO2
dead space/tidal volume = (arterial PCO2- expired PCO2)/arterial PCO2
Tidal volume= 500 mL
Total lung capacity ~ 6 L, residual volume= ~1.2 L
* Dead space= conducting airways (think increased in snorkel breathing)
Lung compliance
Change in lung volume for given change in pressure:
- Decreased in pulmonary fibrosis, pneumonia, pulmonary edema
- Increased in Emphysema, normal aging, alpha-1-antitrypsin deficiency
Hemoglobin forms
4 polypeptide subunits (2 alpha, 2 beta):
Taut form= low affinity for O2
- increases in Cl-, H+, CO2, 2,3-BPG, temperature–> taut form (dump O2 in tissue)
- Shifts O2-hemoglobin curve to Right
Relaxed form= high affinity for O2 (300x higher)
- Seen in a decrease in any factor (temp, [H+])
Fetal hemoglobin= 2 alpha, 2 gamma subunits:
- Lower affinity for 2,3-BPG–> higher O2 affinity (doesn’t unload as easily)
- Left-shifted Oxygen-hemoglobin dissociation curve
Methemoglobin
Oxidized hemoglobin (Fe+3) vs normal Fe+2
- Nitrites oxidize iron
- Has increased affinity for cyanide
- Treat methemoglobinemia with methylene blue
Cyanide poisoning:
- Nitrites administered (form methemoglobin)—> bind cyanide; allow cytochrome oxidase to function
- Use thiosyulfate to bind cyanide in methemoglobin–> thiocyanate–> renal excretion
- Convert Methemoglobin back to hemoglobin using methylene blue
Symptoms of Cyanide poisoning: mitochondrial ETC inhibitor
- tachypnea, tachycardia, H/A, cutaneous flushing
- N/V, confusion, weakness
Carboxyhemoglobin
Carbon Monoxide (CO) binds hemoglobin with 200 x affinity as O2 - Decreases O2 binding capacity--> shifts curve to Left--> decreases O2 unloading in tissue
PO2= normal
- Decreased % saturation, blood O2 content
Tx: 100% O2
Pulmonary circulation: Perfusion and Diffusion
Normal:
- Lungs are perfusion limited
- Gas equilibrates early along length of capillary
- Diffusion only increases if blood flow increases
Disease:
- Lungs are diffusion limited: emphysema (decreased area for diffusion), fibrosis (increased thickness of alveolar walls
- Gas does not equilibrate by the time it reaches the end of the capillary
- In exercise, blood moves faster through capillaries (can’t get as much O2)–> therefore rate of respiration increased
** Blood flow (ml/min) ALWAYS= blood flow through systemic circulation
Pulmonary HTN
Normal pulmonary artery pressure= 10-14 mmHg
- Pulmonary HTN= 25+ mmHg or >35 mmHG during exercise
** Endothelial cell dysfunction
Pulmonary HTN–> arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries–> respiratory distress–> cyanosis (deoxygenated Hb > 5g/dL), R ventricular hypertrophy–> death (decompensated cor pulmonale)
Primary= inactivating mutation in BMPR2 gene (normally inhibits vascular smooth m. proliferation)
Severe respiratory distress–> cyanosis, RVH–> death from decompensated cor pulmonale
Causes of Secondary pulmonary HTN
- COPD: hypoxic vasoconstriction–> medial hypertrophy
- Mitral stenosis (increased resistance–> increased pressure)
- Recurrent thromboemboli (decreased cross-sectional area of pulmonary vascular bed)
- Autoimmune disease (inflammation (Sclerosis= T-cells–> TGF-beta)–> intimal fibrosis (collagen, ECM proteins)–> medial hypertrophy)
- Left-Right shunt (increased shear stress–> endothelial injury)
- Sleep apnea/high altitude (hypoxic vasoconstriction–> medial hypertrophy)
- Drugs: diet drugs (fenfluramine, dexfenfluramine, phentamine)
Severe respiratory distress–> cyanosis, RVH–> death from decompensated cor pulmonale
Pulmonary vascular resistance
PVR= P(pulm artery)- P(left atrium= wedge pressure)/ CO
Resistance= (P(pulm artery)- P (wedge pressure))/ Q (flow)
Resistance= [8 x (viscosity of blood=n) x length]/ (pi x r^4)
Alveolar gas equation
PAO2= PIO2 - PaCO2/R
PAO2= alveolar PO2 PIO2= PO2 of inspired air (generally 150mmHg) PaCO2= arterial PCO2 R= respiratory quotient (CO2 produced/O2 consumed) ~ 0.8
A-a gradient= PAO2-PaO2= 10-15 mmHg
- Increased in hypoxemia due to shunting, V/Q mismatch, fibrosis (ventilating fine, but blood can’t get to oxygen!)
V/Q mismatch
Apex: V/Q=3 (wasted ventilation)
- TB thrives here
Base: V/Q= 0.6 (wasted perfusion
- V and Q are greater at base
Exercise: Vasodilation–> V/Q approaches 1
V/Q= 0: airway obstruction (O2 won’t help)
V/Q= infinity: blood flow obstruction (pulmonary embolism)–> improves with 100% O2 administration
CO2 transport
Three forms:
- Bicarb= 90%
- Carbaminohemoglobin (HbCO2)= 5%
- CO2 bound to N-terminus, binding favors taut form of hemoglobin - Dissolved CO2= 5%
Haldane effect: de-oxygenated blood has increased ability to carry CO2 (vice-versa)
RBC contents:
- Carbonic anhydrase (converts CO2 to bicarb)
- Cl-/HCO3- pump:
- RBC is impermeable to H+, but can exchange bicarb (containing H+) for Cl-
- Venous blood therefore has lower Cl- as the increased CO2 in tissue is converted into bicarb (CO2 + H+)–> exchanged out of RBC for Cl- influx
Types of restrictive lung disease
Restricted lung expansion–> decreased lung volumes (decreased FVC and TLC)
- Pulmonary function tests: FEV1/FVC ratio > 80%
- Poor breaching mechanism: extrapulmonary, peripheral hypoventilation, normal A-a gradient:
- Muscular: polio, myasthenia gravis
- Structural: scoliosis, morbid obesity - Interstitial lung disease: pulmonary, lowered diffusion capacity, increased A-a gradient:
- ARDS
- Neonatal RDS (hyaline membrane disease)
- Pneumoconioses (anthracosis, silicosis, asbestosis)
- Sarcoidosis (bilateral hilar adenopathy, noncaseating granulomas; increased ACE and calcium)
- Idiopathic (collagen deposition)
- Goodpasture’s
- Granulomatosis with polyangiitis (Wegener’s)
- Langerhans cell histiocytosis (eosinophilic granuloma)
- Hypersensitivity pneumonitis
- Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)
Neonatal Respiratory distress syndrome (RDS)
Surfactant deficiency–> increased surface tension–> alveolar collapse
- lecithin:sphingomyelin ratio < 1.5 (should be > 2) in amniotic fluid (administer maternal steroids to improve ratio before birth)
- Low O2 tension–> risk of PDA
- Supplemental O2–> retinopathy of prematurity, bronchopulmonary dysplasia (therefore administer artificial surfactant)
Risk factors:
- Prematurity
- maternal diabetes (elevated fetal insulin)
- c-section (decreased fetal glucocorticoid release)
Acute respiratory distress syndrome
ARDS
Caused by:
- Trauma
- Sepsis, shock
- Gastric aspiration
- Uremia
- Acute pancreatitis
- Amniotic fluid embolism
Path:
- Diffuse alveolar damage–> alveolar capillary permeability increases–> protein-rich leakage into alveoli
- Formation of intra-alveolar hyaline membrane (T2 proliferation–> fibrosis)
- Damage due to neutrophilic substances toxic to alveolar wall, coagulation cascade, O2-derived free radicals
Findings:
- Decreased lung compliance
- Increased work of breaching
- Enhanced V/Q mismatch with no change in PCWP
- PaO2/FIO2 < 200
Sleep apnea
Cessation of breathing > 10 seconds during sleep–> disrupted sleep–> daytime somnolence
Central sleep apnea= absent respiratory effeort
Obstructive= no effort against airway obstruction
- Obesity, snoring, systemic/pulmonary HTN, arrhythmias, possible sudden death
Tx: CPAP, weight loss, surgery
** Hypoxia==> increased EPO–> erythropoiesis
Lung cancer complications
SPHERE:
- Superior vena cava syndrome
- Pancoast tumor
- Horner’s syndrome
- Endocrine (paraneoplastic)
- Recurrent laryngeal sx (hoarseness)
- Effusions (pleural/pericardial)
- Leading cause of cancer death
- Most common cause= mets from breast, colon, prostate, bladder
- Metastasizes to: adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly)
Pancoast tumor
Carcinoma that occurs in apex of lung (superior sulcus):
- Affect cervical sympathetic plexus–> Horner’s syndrome (ipsilateral ptosis, miosis, anhidrosis)
- Can invade brachial plexus–> weakness and paresthesias of arm
- Recurrent laryngeal nerve involvement–> hoarseness
Superior Vena Cava (SVC) syndrome
Obstruction of SVC–> impaired drainage from head (“facial plethora”), neck obstruction (Jugular venous distention= JVD), upper extremity edema
- Caused by malignancy and thrombosis of indwelling catheters
- Medical emergency
- Can raise ICP if severe–> H/A, dizziness, increased risk of aneurysm/rupture of cranial aa
