Pulmonary Flashcards
COPD general info
two types: chronic bronchitis and emphysema
CB - clinical dx; chronic, productive cough with sputum for at least 3 months per year for at least two consecutive years.
E - pathologic dx w permanent enlargement of air spaces d/t destruction of alveolar walls
Both often coexist, pure dz of either rare
COPD 4th leading cause of death of US
COPD risk factors and causes
Tobacco smoke (90% of cases) alpha 1 antitrypsin deficiency - risk worse w smoking environmental factors (2nd hand smoke) chronic asthma
COPD pathogenesis
Chronic bronchitis - excess mucus productions narrows airways (productive cough); inflammation and scarring in airways, enlargement in mucous glands, smooth muscle hyperplasia lead to obstruction.
Emphysema - destruction of alveolar walls d/t relative excess in protease (elastase) activity or relative deficiency of anti-protease (alpha 1 antitrypsin) activity in lungs. PMNs + macrophages release elastase and digest human lung.
Tobacco smoke increases # of activated PMNs and macrophages, inhibits antitrypsin, and incr oxidative stress on lung by free radical production.
COPD clinical features
Any combo of cough, sputum production, dyspnea, some patients may live sedentary lifestyles with few complaints, avoiding exertional dyspnea.
prolonged expiratory time
end-expiratory wheezes on forced expiration, decr breath sounds, inspiratory crackles
tachypnea, tachycardia
cyanosis
accessory respiratory muscle use
hyper-resonance on percussion
signs of cor pulmonale
chronic resp acidosis + compensatory metabolic alkalosis
COPD diagnosis
PFT - definitive diagnostic test
obstruction evident - decr FEV1, decr FEV1/FVC ratio < 0.70; incr TLC + incr residual vol + incr FRC = air trapping; decr vital capacity
GOLD staging: FEV1 => 80 of predicted value is mild disease.
FEV1 50% - 80% = moderate disease
30% - 50% = severe disease
< 30% = very severe disease
COPD HPI tips
Hx cardiopulmonary diseases
smoking history ( duration, intensity, current smoker)
family history (COPD, heart disease, asthma)
occupation (industrial dusts, fumes)
overall health
history of resp infections (frequency, severity)
pulmonary medications
pulmonary sxs: dyspnea, cough, sputum production, wheezing
clinical monitoring: serial FEV1, pulse ox, exercise tolerance
COPD treatment
smoking cessation most important - improvement in sxs, slows rate of decline, prolongs survival, does not completely reverse
1. inhaled anticholinergic drugs (ipratroprium bromide): bronchodilators
2. inhaled B agonists (albuterol): bronchodilators, provide sx relief, long-acting (salmeterol) for pts using frequently
OR combo of the two above
3. inhaled corticosteroids (budesonide, fluticasone): anti inflammatory
4. theophylline - controversial
5. oxygen therapy - improves survival and quality of life for those with chronic hypoxemia (PaO2 55 mmhg or O2 sat < 88% or PaO2 55-59 + polycythemia or cor pulmonale, despite max med therapy)
6. pulm rehab
7. vaccination
8. surgery
give systemic steroids and abx for acute exacerbations
BBs contraindicated in acute COPD
COPD tx guidelines
mild - mod dz: bronchodilator MDI +- low dose inhaled glucocorticoids
severe dz: above + continuous O2 (if hypoxemic), pulm rehab, triple inhaler therapy (long-acting B agonist, long-acting anticholinergic, inhaled glucocorticoid)
acute COPD exacerbation: bronchodilators, IV methylprednisolone then taper with oral once improved, abx (azithro, levoquin, doxy), supp O2 (90-93% goal), NPPV, intubate or mechanical vent if above doesn’t stabilize (incr RR, incr PaCO2, worsening acidosis)
COPD complications
acute exacerbations (d/t infxns, cardiac dz, noncompliance)
secondary polycythemia
pulm HTN and cor pulmonale
CAP gen info
Two types: community acquired and nosocomial
CAP
- occurs in community or within 72 hrs of hospitalization
- typical or atypical
MC bacterial pathogen: strep pneumoniae (60%) –> H. flu, reg flu, legionella spp
Nosocomial pna
- occurs during hospitalization after 72 hrs
- MC bacterial pathogen: gram neg rods (Ecoli, pseudomonas) and staph aureus
- if vitals entirely normal in OP, probability of pna < 1%
Two rec prevention methods
- influenza vaccine
- pneumococcal vaccine: >65 yo or young ppl at risk (heart disease, scd, etc)
Typical CAP: common agents, sxs, CXR
Common agents
- strep pneumoniae (60%)
- H flu (15%)
- Aerobic gram-negative rods (6-10%) - klebsiella (& other enterobacteriaceae)
- staph aureus (2-10%)
Symptoms
- sudden shaking chills followed by fever
- cough productive of thick, purulent sputum
- pleuritic chest pain (suggests pleural effusion)
- dyspnea
Signs
- tachycardia, tachypnea
- late inspiratory crackles, bronchial breath sounds, increased tactile and vocal fremitus, dullness on percussion
- pleural friction rub (a/w pleural effusion)
Chest xray
- lobar consolidation
- multilobar consolidation indicates very serious illness
Most cases of CAP result from aspiration of oropharyngeal secretions bc majority of organisms that cause CAP are normal inhabitants of the pharynx.
Atypical CAP: common agents, sxs, CXR
Atypical pna - organisms not visible on gram stain & not curable on standard blood agar
Common Agents
- mycoplasma pneumoniae mc
- chlamydia pneumoniae
- chlamydia psittaci
- coxiella burnetti (Q fever)
- legionella spp
- viruses: influenza A or B, adenoviruses, parainfluenza virus, RSV
Symptoms
- insidious onset - sore throat & headache 1st, fatigue, myalgias
- dry cough (no sputum production)
- fevers (chills are uncommon)
Signs
- pulse-temp dissociation; nl pulse in setting of high fever
- wheezing, rhonchi, crackles
CXR
- diffuse reticulonodular infiltrates
- absent or minimal consolidation
CAP diagnosis
1st differentiate lower resp tract infection from upper resp infection and other causes of cough.
- nasal discharge, sore throat, ear pain predominates –> upper
- lower tract infection suss –> differentiate btw pna and acute bronchitis (can’t just with clinical features), need CXR.
CXR, labs (cbc diff, BUN, Cr, glc, lytes or CMP) O2 sat, blood cultures, gram stain/culture, abx therapy)
PA and lat CXR required to confirm dx
- interstitial infiltrates, lobar consolidation, and/or cavitation
- sensitive; if findings not suggestive of pna don’t treat w abx
- false negative cxrs w neutropenia, dehydration, infection w PCP, early dz < 24 hrs
- after treatment, changes on CXR lag behind clinical response (up to 6 wks)
Sputum gram stain (everyone) and culture (hospitalized pts) with cap (low sensitivity + specificity, but done for antimicrobial resistance prob)
- good specimen > 25 [mns and < 10 epithelial cells
Special stains
- acid-fast stain (mycobacterium spp) if TB suss
- silver stain (fungi, p.carinii) for HIV/immunocompromised
Urinary antigen assay for legionella
- very sensitive
- antigen persists in urine for weeks (even after treating)
Consider two blood cultures
CAP pearls
Alcoholics –> klebsiella
Immigrants –> TB
Nursing home residents –> nosocomial pathogen
HIV + –> P. carinii, TB, more likely to have typical infxn
legionella –> organ transplant recipients, renal failure, chronic lung dz, smokers
- presents with GI sxs + hyponatremia
CAP treatment
Hypoxic or hypotensive –> hospitalize (can use PSI, CURB-65 admission if at least 2 points)
Uncomplicated CAP in <60yo, no comorbidities –> macrolide (azithromycin, clarithyromycin) or doxycycline first line
- comorbidities –> FQ
- > 60 yo, comorbidities, or abx tx in last 3 months –> resp FQ (levofloxacin, moxifloxacin) PLUS macrolide or augmentin
OP –> 5 day treatment (don’t stop until patient has been afebrile 48 hrs)
IP –> FQ alone or 3rd gen ceph + macrolide (ceft + azithro)
HAP treatment
tx tailored toward gram-neg rods
cephalosporins w pseudomonal coverage: ceftazidime or cefepime
carbapenems: imipenem
Pip tazo
Macrolides not used as single therapy
CAP complications
Pleural effusion
- > 50%, empyema infrequent
- most w uncomplicated course & resolve w reg abx tx
- thoracentesis if effusion sig > 1 cm on lat decubitus film. Send fluid for gram stain, culture, pH, cell count, glc, protein, LDH levels
Pleural empyema (infected, loculated pleural fluid)
- 1-2% cases
- requires chest tube drainage
Acute resp failure
Pleural Effusion gen info
Caused by one of these mechanisms:
- incr drainage of fluid into pleural space
- incr production of fluid by cells in pleural space
- decr drainage of fluid from pleural space
if patient has minimal lung compromise –> pleural effusions well tolerated vs with lung dz may lead to resp failure.
Transudative effusions - pathophysiology d/t elevated capillary pressure in visceral or parenteral pleura (CHF), or decr plasma oncotic pressure (hypoalbuminemia)
Causes: CHF, cirrhosis, PE, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, atelectasis
Exudative - pathophys d/t incr permeability of pleural surfaces or decr lymphatic flow from pleural surface bc of damage to pleural membranes or vasculature. Any condition a/w infection or inflamm
- if suss, check pleural fluid for diff cell count, total protein, LDH, glc, pH, amylase, TGs, microbiology, cytology
Causes: bacterial pna, TB, malignancy, metastatic dz, viral infection, PE, collagen vascular dz
Light’s criteria
Exudative effusions meet at least one of the following (transudates have none):
protein (pleural)/protein (serum) > 0.5
LDH (pleural)/LDH (serum) > 0.6
Pleural LDH > 2/3s ULN serum LDH
Pleural effusion causes
CHF mc
PNA (bacterial)
Malignancies: lung (36%), breast (25%), lymphoma (10%)
PE
Viral diseases
Cirrhosis with ascites (hepatic hydrothorax)
Pleural effusion clinical features
Symptoms
- often asxs
- dyspnea on exertion
- peripheral edema
- orthopnea, PND
Signs
- dullness to percussion
- decr breath sounds over effusion
- decr tactile fremitus
Pleural effusion diagnosis
Confirm presence/eval size with:
- CXR (PA Lat)
- blunting of costophrenic angle
- about 250 mL pleural fluid must accumulate before it is detectable
- lat decubitus - more reliable than PA and lat cxrs for detecting small effusions & determine if free flowing or loculated - CT chest - more reliable
- Thoracentesis
- ind for eval of all new effusions; diagnostic 70%
- can be therapeutic
- PTX assoc complication, don’t perform on < 10 mm lat decub
Pleural effusion treatment
Transudative effusions
- diuretics and sodium restriction
- therapeutic thoracentesis - only if massive + causing dyspnea
Exudative effusions - tx underlying dz
Parapneumonic effusions (effusion from pna)
- uncomplicated effusions: abx alone
- complicated or empyema: chest tube drainage, intrapleural inj of fibrinolytic agents (stetokinase, urokinase, TPA, to accelerate drainage)
- surgical lysis of adhesions
Empyema causes
Def: pus within pleural space
- untreated exudative pleural effusions
- most cases d/t complication of bacterial pna, can be from other foci of infection I.e. mediastinitis, abscess
Empyema clinical features
those of underlying disease (pna)
Empyema diagnosis
CXR and CT scan
Empyema treatment
Aggressive drainage of pleura (thoracentesis) and abx therapy
Infection is very difficult to eradicate, recurrence common, requiring repeated drainage
For severe, persistent –> rib resection + open drainage
Pleural fluid pearls
elevated pleural fluid amylase: esophageal rupture, pancreatitis, malignancy
milky, opalescent fluid: chylothorax (lymph)
frankly purulent fluid: empyema (pus)
bloody effusion: malignancy
Exudative effusions primarily lymphotic: TB
pH < 7.2: parapneumonic effusion or empyema
glc < 60: rheumatoid arthritis, or empyema, TB, esophageal rupture, malignancy, lupus
NPPV
NPPV delivered as BiPAP or CPAP
BiPAP: can be set at separate inspiratory and expiratory pressures (insp > exp)
Both can be given w nasal mask or full-face mask
NPPV ind in pts with impending resp failure in an attempt to avoid intubation and mechanical ventilation
Success rates highest in pts w hypercapnic resp failure (COPD)
NPPV should not be used for life support ventilation, only to temp support the patient’s own spontaneous breathing
To use NPPV: pt must be neurologically intact, awake and cooperative, able to protect airway,
If no improvement seen, bipap should be discontinued and conventional ET intubation and mech vent initiated.
Pulmonary hypertension gen info
Def: mean pulmonary arterial pressure > 25 mmHg at rest
Can be due to multiple pathophysiologic processes:
- passive d/t resistance in pulm venous system (LHF, mitral stenosis, atrial myxoma)
- hyperkinetic (L to R cardiac shunts like ASD, PDA)
- obstruction (PE, pulm artery stenosis)
- pulmonary vascular obliteration (collagen vascular dz)
- pulm vasoconstriction (chronic hypoxemia, COPD, OSA)
Classification:
Group 1: pulmonary arterial hypertension
- idiopathic, familial, veno-occlusive dz, connective tissue disorders, congenital shunting, HIV, drugs
- abnl incr in pulm arteriolar resistance –> thickening of pulm arteriolar walls –> worsens pulm HTN –> further wall thickening –> vicious cycle
- cause is unknown; young or middle-aged women
- poor prog; mean survival 2-3 yrs from dx
Group 2: left heart disease
- 2ry to any cause of LHF; mitral stenosis, MR
Group 3: lung disease and/or chronic hypoxemia
- ILD, COPD, OSA, etc
Group 4: chronic thromboembolic disease
- recurrent PE (many pts do not have sx of PE), including non thrombotic etiologies (tumor emboli)
Group 5: misc
- pulm vascular compression; tumors, lymphadenopathy; sarcoidosis, langerhans cell histiocytosis, etc
Pulmonary hypertension clinical features
Symptoms DOE Fatigue Chest pain - exertional Syncope - exertional (with severe dz)
Signs
Loud pulmonic component of 2nd heart sound (P2) and subtle lift of sternum (sign of RV dilatation)
RV failure: JVD, hepatosplenomegaly, ascites, peripheral edema
Pulmonary hypertension diagnosis
ECG: RV hypertrophy, R axis deviation, R atrial abnl
CXR: enlarged pulm arteries w/w/o clear lung fields
Echo: dilated pulm artery, dilatation/hypertrophy of RA and RV, abnl movement of IV septum
Right heart cath: required for confirmatory dx - incr mean pulm artery pressure > 25 mmHg
Pulmonary hypertension treatment
If pulm HTN 2ry to another disease process then tx underlying disease
vasoactive agents used in group 1 PAH; right heart cath with trial of vasodilators
Vasoactive agents may lower pulm vascular resistance: inhaled NO, pde5 inhibitors (sildenafil), oral CCBs, prostacyclins (epoprostenol), endothelin receptor antagonists (bosentan)
Many require home O2, diuretics, +- inotropes (digoxin)
Lung transplantation in qualified patients
SIRS
SIRS: 2 or more;
Fever > 38C or hypothermia <36C
Hyperventilation (rate > 20 bpm) or PaCO2 < 32 mmHg
Tachycardia > 90 bpm
Incr WBC count (>12, <4, or >10% band forms)
Sepsis
SIRS + suspected source of infection
Septic shock
hypotension induced by sepsis, persisting despite adequate fluid resuscitation
MODS
altered organ function in an acutely ill patient, usually leading to death
