Pulmonary Flashcards
lung function
conducting zone:
trachea, primary bronchus and terminal conducting bronchioles; warms air, traps foreign matter
respiratory zone:
terminal respiratory bronchioles and alveoli
alveoli:
gas exchange
diffusion capacity based on: surface area, thin diffusing area, partial pressure and concentration of gases
low V:Q ratio
V = VENTILATION
Q = PERFUSION
LOW VENTILATION WITH INCREASED OR NORMAL PERFUSION
-low ventilation impairs gas exchange –> dec arterial partial pressure of oxygen and decreased excretion of CO2 –> stim respiratory, increased ventilation to increase ratio towards 1
Physiologic Low V:Q Ratio
-found at base of lungs, due to gravity - receive BOTH greater perfusion and more ventilation (perfuse > vent)
Pathologic Low V:Q Ratio
- ASTHMA, CHRONIC BRONCHITIS, AND ACUTE PULM EDEMA
- HYPOXEMIC RESPONSE TO DEC PaO2 IS LOCAL HYPOXIC VASOCONSTRICTION –> PULM HTN
- right ventricle has to pump against higher pressures –> over time, RIGHT HEART FAILURE (COR PULMONALE)
high V:Q ratio
AREA OF DECREASED PERFUSION COMPARED TO VENTILATION
Physiologic High V:Q Ratio
- at apices of lungs
- reactivation of TB tends to occur here - due to the relatively higher O2 content of lung tissue in apices
Pathologic High V:Q Ratio
- EMPHYSEMA, PULM EMBOLISM OR FOREIGN BODY
- good ventilation but bc decreased blood flow, fails to oxygenate blood
- areas of no perfusion and normal vent = “dead space”
mechanics of breathing
- during quiet breathing, inspiration accounts for most of the work; expiration a passive process
- 90% OF NORMAL WORK OF BREATHING IS DUE TO CONTRACTION OF THE DIAPHRAGM
control of respiration
VENTILATION IS STRICTLY REGULATED PRIMARILY BY CHANGES IN PaCO2
Controlled by:
- CENTRAL CHEMORECEPTROS IN THE MEDULLA - indirectly respond to changes in serum pH via PaCO2 in CSF –> medulla stimulates phrenic nerve –> inc rate/depth of breathing
- PERIPHERAL CHEMORECEPTORS IN CAROTID BODIES AND AORTIC BODIES - respond directly to inc PaCO2 in arterial blood –> stim neurons affecting the medulla –> inc rate and depth of breathing (to lower PaCO2) - sensitive to dec arterial PaO2 but only if significant decline <60
-DKA STIMULATES RESPIRATORY CENTERS, CAUSING KUSSMAUL’S RESPIRATIONS
lung defenses
alveolar cells:
- type I: make up supporting tissue
- type II: PRODUCE SURFACTANT
mucociliary escalator:
-covers nose, bronchi and most of bronchioles
alveolar macrophages
-some evade them: encapsulated organisms, pseudomonas, mycolic acid layer of m.tuberculosis
mast cells
-initiate inflam, repair lung and immunity
pmns
-temporarily present during lung infx; seen in smokers
lung volumes
tidal volume TV - air moved in and out during quiet breathing
residual volume RV- vol of air remains after max expiration
expiratory reserve ERV - vol that can be further exhaled after normal expiration
inspiratory reserve IRV - vol that can be further inhaled after normal inspiration
vital capacity - max vol that can be exhaled after max inhalation IRV + TV + ERV
total lung capacity TLC - vol of lungs at max inspiration
functional residual capacity FRC - vol of gas in lungs at normal tidal volume end-expiration (ERV + RV)
FEV1 (forced expiratory vol in 1 sec) - vol exhaled at end of first second of forced expiration
FVC (forced vital capacity) - vol of air that can be expelled from a max inflated lung with the patient breathing as hard and fast as possible
atypical breath sounds
WHEEZING - high-pitched, whistling, continuous, usually louder during expiration, produced by narrow/obstructed airways - COPD, ASTHMA, bronchiectasis, bronchiolitis, lung ca, sleep apnea, chf, gerd, anaphylaxis, foreign body
RHONCHI - rumbling/rattling, coarse, low pitched sounds, like snoring that may clear w/ cough - INC SECRETIONS
CRACKLES/RALES - non-continuous, heard during inspiration, due to popping open of collapsed alveoli and small airways (from fluid, exudates) - pnm, atelectasis, bronchitis, bronchiectasis, pulmonary edema and fibrosis
STRIDOR - monophonic sound usually loudest over anterior neck due to narrowing of larynx or anywhere over trachea
asthma
- MC CHRONIC CHILDHOOD DZ
- RF: ATOPY
SAMTER’S TRIAD: ASTHMA, NASAL POLYPS, ASA/NSAID ALLERGY
Pathophys:
AIRWAY HYPERREACTIVITY
-extrinsic (allergic) - triggers pollen, dander, dust, mold, etc, MC CHILD/ADOLESCENTS, ASSOC W/ IgE
-intrinsic - triggers infx, pharmacologic (b-blockers, asa, nsaids, acei), occupational, exercise, emo, cold air
BRONCHOCONTSTRICTION
- airway narrowing 2ry to smooth muscle constriction, bronchial wall edema, thick mucus secretion, collagen deposition, air trapping
- OBSTRUX - dec expiratory flow, inc resistance, v/q mismatch
INFLAMMATION
-2ry to cellular infiltration (t-lymphs, neutrophils, eosinophils and cytokines), inc histamine release from mast cells
- sx:
- DYSPNEA, WHEEZING, COUGH (esp at night), chest tight, fatigue
- PROLONGED EXPIRATION W/ WHEEZING, HYPERRESONANCE, dec breath sounds, tachy/tachy, use accessory muscles
- SEVERE - unable to speak full sentences, ams, pulsus paradoxus, cyanosis, tripod, silent chest
- dx:
- PFTs GOLD STANDARD = REVERSIBLE OBSTX
- BRONCHOPROVOCATION - methacholine challenge test, bronchodilator challenge test, exercise challenge test (if PFTs are nondiagnostic)
- PEAK EXPIRATORY FLOW RATE - best and most objective way to assess asthma exacerbation severity and pt response in ED; PEFR >15% from initial attempt = response to tx, normal 400-600
- Pulse Ox - <90% indicative of respiratory distress
- ABG, CXR
- Admission Criteria: PEFR <50% of predicted, ER visit w/in 3 days of exacerbation, status asthmaticus, posttreatment failure, AMS
- Discharge Criteria: PEFR >70% of predicted, >15% since intial, subjective improvement, clear lungs w/ good air movement, adequate fu w/in 24-72 hrs, response sustained for 1 hour post-tx
management of asthma
ACUTE Exacerbations:
B2 AGONISTS SHORT-ACTING (SABA)
- 1ST LINE TX FOR ACUTE
- ALBUTEROL, TERVUTALINE, EPINEPHRINE via NEB
- bronchodilator, dec bronchospasm
ANTICHOLINERGICS (ANTIMUSCARINICS)
- IPRATROPIUM
- bronchodilator
CORTICOSTEROIDS
-anti-inflam, all but mildest should be dc’d on short course oral cortico; dec relapse
LONG-TERM Maintenance:
INHALED CORTICOSTEROIDS
- DRUG OF CHOICE FOR LONG-TERM MAINTENANCE
- BECLOMETHASONE, FLUNISOLIDE, TRIAMCINOLONE
- cytokine and inflam inhibition
LONG-ACTING B2 AGONISTS (LABA)
- SALMEROL, FORMOTEROL
- bronchodilator, prevents sx
MAST CELL MODIFIERS
- CHROMOLYN, NEDOCROMIL
- inhibits mast cell and leukotrien-mediated degranulation; inhibits acute phase response to cold air, exercise, etc
LEUKOTRIENE MODIFIERS/RECEPTOR ANTAGONISTS
- MONTELUKAST, ZAFIRLUKAST, ZILEUTON
- blocks leukotriene-mediated neutrophil migration, smooth muscle contraction
THEOPHYLLINE
- methylxanthine, a bronchodilator that improves respiratory muscle endurance
- higher dose needed for smokers
- narrow therapeutic index - arrhythmias, seizures
OMALIZUMAB
-anti-IgE antibody - used in severe, uncontrolled
asthma classification
Intermittent - SABA prn sx: 0-2x /day 0-2x/week SABA use: 0-2x /day 0-2x/week nighttime awakening: <2x/month interference w/ activity: none exacerbations req steroids: 0-1/yr
Mild Persistent - SABA prn + LOW-DOSE ICS sx: >2 days/week SABA use: >2 days/week nighttime awakening: 3-4x/month interference w/ activity: minor exacerbations req steroids: 2+/yr
Moderate Persistent - SABA prn + MED-DOSE ICS OR LOW ICS + LABA, add LTRA sx: daily SABA use: daily nighttime awakening: >1x/week interference w/ activity: some exacerbations req steroids: 2+/yr
Severe Persistent - HIGH-DOSE ICS + LABA, +/-OMALIZUMAB
sx: throughout day
SABA use: several times/day
nighttime awakening: often, usually nightly
interference w/ activity: extreme
exacerbations req steroids: 2+/yr
*step-wise –> step down if sx controlled for 3+ months
COPD
Irreversible airflow obstx due to: LOSS OF ELASTIC RECOIL, INCREASED AIRWAY RESISTANCE
- chronic bronchitis usually episodic, emphysema steady decline
- RF: SMOKING, a-1 ANTITRYPSIN DEFICIENCY (only genetic dz linked - younger pt <40y, panlobar emphysema)
EMPHYSEMA
- abnormal, permanent enlargement of terminal airspaces
- smoking –> chronic inflam –> loss of elastic recoil and inc compliance –> airway obstruction
CHRONIC BRONCHITIS
- PRODUCTIVE COUGH 3+ MONTHS X 2 CONSECUTIVE YEARS
- chronic inflam –> hypersecretino of mucus, airway narrows, inc resistance –> airway obstx
- mucus plugging and mucociliary escalator destruction makes pt more prone to infx
-sx:
EMPHYSEMA
-DYSPNEA MC
-HYPERINFLATION: hyperresonance, dec breath sounds, dec fremitus, barrel chest, pursed-lip breathing
-respiratory alkalosis, matched v/q defects, mild hypoxemia, cachectic, “PINK PUFFERS”
BRONCHITIS
- PRODUCTIVE COUGH HALLMARK
- RALES, RHONCHI, WHEEZING, signs of cor pulmonale (peripheral edema, cyanosis)
- respiratory acidosis, inc hgb/hct
- severe v/q mismatch, HYPOXEMIA, HYPERCAPNIA
- obese and cyanotic “BLUE BLOATERS”
- dx:
- PFTs/SPIROMETRY - GOLD STD
- CT/CXR
- ECG
management of COPD
BRONCHODILATORS
-COMBO w/ anticholinergics + B2 agonists better
- Anticholinergics: IPRATROPIUM, TIOTROPIUM (preferred over B2 agonists w/ copd)
- B2 Agonists: ALBUTEROL, TERBUTALINE, SALMETEROL
- Theophylline - only used in refractory cases (narrow therapeutic index, monitor levels –> arrhythmias and seizures)
CORTICOSTEROIDS
-may be added to long-acting bronchodilators
OXYGEN
-only med tx proven to dec mortality (dec pulmonary htn and cor pulmonale)
Prevent Exacerbations
- smoking cessation
- vaccinations
- pulmonary rehab
- surgery (lung reduction, transplant)
- abx if increased sputum, change in quality or cxr evidence of infx
- AZITHRO has been shown to have anti-inflam properties in lung
GOLD Criteria - COPD staging
all –> FEV1/FVC <70%
I: Mild
PFT% predicted: FEV1 80+%
Tx: Bronchodilators (short-acting), dec rf
II: Moderate
PFT% predicted: FEV1 50-79%
Tx: Bronchodilators (short-acting) + LONG-ACTING
III: Severe
PFT% predicted: FEV1 30-50%
Tx: Bronchodilators (short-acting) + long-acting + REHAB, steroids if inc exacerbations
IV: Very Severe
Cor pulmonale, respiratory failure, heart failure, FEV1 <30
Tx: Bronchodilators (short-acting) + long-acting + rehab, steroids if inc exacerbations, + O2 THERAPY
bronchiectasis
IRREVERSIBLE BROCNHIATL DILATION 2RY TO TRANSMURAL INFLAMMATION –> destruction of muscular and elastic tissues of bronchial wall, airways collapse easily -> OBSTX AND IMPAIRED CLEARANCE OF MUCUS –> LUNG INFX
Etiologies:
- Recurrent/chronic lung infx
- H.INFLUENZA MC IF NOT CYSTIC FIBROSIS
- PSEUDOMONAS MC IF CYSTIC FIBROSIS
- Hereditary - CF mc cause in US, a-1 antitrypsin deficiency
- Obstx - foreign body aspiration, tumors severe mucus
- sx:
- DAILY CHRONIC COUGH W/ THICK, MUCOPURULENT, FOUL-SMELLING SPUTUM, chest pain, often devo recurrent pneumonia
- HEMOPTYSIS (50-70%) due to erosion into bronchial arteries
- persistent crackles at base, dyspnea, wheeze, rhonchi
- dx:
- HIGH RES CT SCAN - STUDY OF CHOICE: airway dilation, lack of taperiong of bronchi, wall thickening, muco plugs
- PFTs: OBSTRUCTIVE PATTERN
- CXR
- Sputum cultures
- Bronchoscopy
- tx:
- ABX, mucus management (bronchodilators, anti-inflam, sx, embolization for bleed)
- sx in severe, complicated cases
- THICK BROWN SPUTUM –> ASPERGILLUS (ITRA + CORTICO)
- MYCOBACTERIUM AVIUM COMPLEX (MAC) –> CLARITHRO + ETHAMBUTOL
PFTs -obstructive vs restrictive
Obstructive
- INCREASED LUNG VOLUMES
- HYPERINFLATION: INC TLC
- OBSTRUCTION: DEC FEV1, DEC FVC, DEC FEV1/FVC
- inc compliance w/ emphysema
- ASTHMA, COPD, BRONCHIECTASIS, CF, COAL WORKERS PNEUMOCONIOSIS
Restrictive
- DECREASED LUNG VOLUMES
- DEC TLC, FVC
- NORMAL OR INC FEV1/FVC
- dec compliance
- SARCOID, PNEUMOCONIOSIS, IDIOPATHIC FIBROSIS, dec muscle effort: Myasthenia gravis, polio, scoliosis
cystic fibrosis
-defective CF transmembrane receptor (CFTR) –> prevents Cl transport (water mvmt out of cell) –> buildup of thick mucus in lungs, pancreas, liver, intestines –> obstx lung disease and exocrine gland dysfx
- sx:
- YOUNG, W/ BRONCHIECTASIS, PANCREATIC INSUFFICIENCY, GROWTH DELAYS AND INFERTILITY
- GI: MECONIUM ILEUS, PANCREATIC INSUFFICIENCY (dec fat absorption, steatorrhea, vit ADEK deficiency)
- Pulm: RECUR RESP INFX (esp staph and pseudo), chronic sinusitis
- Infertility 95%
- dx:
- ELEVATED SWEAT CHLORIDE TEST - PRIMARY, >60 mmol/L on 2 occasions after Pilocarpine
- CXR: BRONCHIECTASIS, HYPERINFLATION
- PFTs: OBSTRUCTIVE
- DNA definitive
- sputum cultures –> pseudomonas, h.influenzae
- tx:
- AIRWAY CLEARANCE - bronchodilators, mucolytics, abx
- PANCREATIC ENZYME REPLACE - supplement ADEK
- lung and pancreas transplant, vaccinations
sarcoidosis
NON-CASEATING GRANULOMAS, BILAT HILAR LYMPH
CLASSIC PRESENT: YOUNG PT W/ RESPIRATORY AND CONSTITUTIONAL SX, BLURRED VISION AND ERYTHEMA NODOSUM
- inc prevalence in AA, northern europe, female
- onset 20-40y
EXAGGERATED T-CELL RESPONSE to a variety of antigens or self-antigens –> CENTRAL IMMUNE ACTIVATION, PERIPHERAL IMMUNE DEACTIVATION, t-cell accumulation –> GRANULOMA FORMATION
-granulomas take up space, disrupt the normal stx/fx
- sx:
- 50% asymptomatic, most complications are w/ lungs
- Pulmonary 90% - DRY COUGH, DYSPNEA, CHEST PAIN
- Lymphadenopathy - painless, intrathoracic, HILAR NODES
- Skin 25% - ERYTHEMA NODOSUM, LUPUS PERNIO (violet, raised discoloration of nose, ear, cheek, chin), maculopapular rash, subcutaneous nodules
- Vision 20% - ANTERIOR UVEITIS, BLURRED VISION, ocular discomfort, photophobia, ciliary flush, floaters
- Cardiac - arrhythmias, cardiomyopathies
- Rheum - arthralgias, fever, malaise, wl
- Neuro - cranial nerve palsies (esp 7/facial), hypothalamic/pituitary lesions
- dx:
- TISSUE BX: NONCASEATING GRANULOMAS (= no central necrosis) - site skin, nodes, transbronchial
- CXR: BILAT HILAR LYMPHADENOPATHY, INTERSTITIAL LUNG DISEASE
- PFT: RESTRICTIVE (advanced)
- CT: hilar lymphadenopathy, ground glass, fibrosis (adv)
- Gallium scan: inc uptake in affected areas
- Bronchoalveolar lavage: r/o infx, inc CD4:CD8
- labs:
- INC ACE
- hypercalciuria/hypercalcemia (2ry to granuloma, inc vit d)
- Eosinophilia, leukopenia
- Cutaneous anergy - diminished skin reactivity to allergy
- tx:
- OBSERVE - MOST SPONTANEOUS REMISSION IN 2Y
- ORAL CORTICO - TX OF CHOICE IF NEEDED (worsening sx, deteriorating lung fx, decline - r/o tb, infx)
- Methotrexate
- Hydroxychloroquine - may be good for skin lesions
- NSAIDs for msk sx and erythema nodosum
pulmonary fibrosis (idiopathic fibrosing interstitial pneumonia)
CHRONIC PROGRESSIVE INTERSTITIAL SCARRING/FIBROSIS from persistent inflammation –> loss of pulmonary fx w/ restrictive component
-MC MEN 40-50y, smokers, survival <10y @ diagnosis
- sx:
- dyspnea or nonproductive cough (gradual onset)
- fine bibasilar inspiratory crackles, CLUBBING, +/-cyanosis
- dx:
- CXR/CT: DIFFUSE RETICULAR OPACITIES (HONEYCOMBING), GROUND GLASS OPACITIES
- BX: HONEYCOMBING
- PFT: RESTRICTIVE
- tx:
- no effective tx, smoking cessation, O2, steroids in acute exacerbation
- LUNG TRANSPLANT ONLY CURE
pneumoconioses / environmental lung diseases
CHRONIC FIBROTIC LUNG DISEASE SECONDARY TO INHALATION OF MINERAL DUST (ingested by alveolar macrophages, triggering inflam and release of chemical mediators –> parenchymal fibrosis –> restrictive lung disease and dec lung compliance
silicosis
- silica dust inhalation (mining, quarry work w/ granite/slate/quartz, pottery sandblasting)
- sx: asymptomatic +/- dyspnea on exertion, dry cough
- dx:
- CXR: muliple, small, NODULAR OPACITIES IN UPPER LOBES, +EGG SHELL CALCIFICATIONS OF HILAR/MEDIASTINAL NODES
- BX
- tx:
- no proven tx
- supportive: bronchodilators, O2, vaccinations +/-cortico
coal worker’s pneumoconiosis
-inhalation of dust from coal or carbon mines
- dx:
- CXR: SMALL, UPPER LOBE NODULES, HYPERINFLATION
- PFT: MAY BE OBSTRUCTIVE PATTERN
-tx: -supportive - bronchodilators, O2, vaccinations +/-cortico
CAPLAN SYNDROME
COAL WORKER’S PNEUMOCONIOSIS + RHEUMATOID ARTHRITIS
berylliosis
- electronics, aerospace, ceramics, tool and dye manufacturing, fluorescent light bulbs
- sx: dyspnea, cough, arthralgia, wl, fever
-dx:
-CXR: normal 50%, hilar lymphadenopathy, inc interstitial
+exposure, +beryllium lymphocyte proliferation test and noncaseating granulomas on bx
-tx: CORTICO, O2, supportive +/-methotrexate
byssinosis
“brown lung dx” or “monday fever” due to COTTON EXPOSURE in textile industry
-sx: dyspnea, wheezing, cough, chest tightness; worse at beginning of work week, improve over weekend
asbestosis
- seen 15-20 years after long-term exposure to asbestos; smoking inc risk of bronchogenic cancer
- INC RISK: BRONCHOGENIC CARCINOMA MC, MALIGNANT MESOTHELIOMA OF PLEURA
- sx: dyspnea on exertion, nonproductive cough
- dx:
- CXR: PLEURAL PLAQUES (THICKENING), INTERSTITIAL FIBROSIS (HONEYCOMBING), affects lower lobes primarily, +/- shaggy heart signs
- BX: may show linear asbestos bodies
-tx: -supportive, bronchodilators, O2, vaccinations +/-cortico
