Pulmonology Flashcards
FRV1/FVC
ratio of air volume expired in 1 second to FVC.
80% is normal,
and this ratio helps us to understand whether the patient has obstructive or restrictive lung disease
80% is +/- restrictive
Total lung capacity
increased in obstructive lung disease
decreased in restrictive lung disease
Functional vital capacity (FVC)
in obstructive versus restrictive lung disease
FVC is the air volume that can be inspired and then expired
decreased in obstructive lung disease because you can’t move air out very well
decreased in restrictive lung disease because you can’t move air in very well
FEV1 in obstructive versus restrictive lung disease
decreased in obstructive as well as in restrictive lung disease
In obstructive lung disease, FEV decreases even more than FVC, so with obstructive lung disease the FEV1/FVC ratio drops more than 70%
In restrictive lung disease the FEV1/FVC ratio is normal or increased because the FEV1 and FVC decrease at a similar rate
DLCO
relative measure of ability to transfer air from pulmonary alveoli to capillary
Alveolar-arterial gradient
What’s a normal value?
When would A-a gradient be increase?
Compares O2 status of alveoli to arterial blood
Normal= 5-15 mmHg
Increased Aa gradient indicates pulmonary embolism, pulmonary edema, right-to-left shunt, higher concentration of inspired oxygen
Aa gradient equation
PAO2-PaO2
(Atmospheric air pressure x FiO2) - (PaCO2/0.8) - (PzO2)= (713nnHg) * (0.21 PaCO2/0 .8)-(PaO2)= 5-15mmHg is considered a normal A-a gradient
PAO2= alveolar O2 content PaO2= Arterial O2 content
Common cold (viral rhinitis)
inflammation of the upper airways
Causes: rhinovirus, coronavirus, adenovirus
H and P: nasal and throat irritation, sneezing, rhinorrhea, nonproductive cough
(Productive cough tends to be more indicative of PNA or bronchitis)
Treatment: supportive, rest, analgesia, hydration, NO antibiotics
Pharyngitis
Inflammation of the throat
viruses: rhinovirus, coronavirus, adenovirus
bacteria: group A beta-hemolytic streptococci (strep pyogenes)
Symptoms: sore throat, lymphadenopathy, nasal congestion
fever, HA, GI symptoms
Red and swollen pharynx
Tonsillar exudates
Pharyngitis diagnosis- Centor criteria
Add one point if: Fever Tonsillar exudates Tender anterior cervical adenopathy Absence of cough 44yo subtract a point
Cough (absence of) Exudates Nodes T (temperature) OR (plus or minus one point for age)
0-1 points= no antibiotic/no throat culture
2-3 points= throat culture/treat if positive
4-5 points= treat empirically
Treatment: self- limited
antibiotics to prevent ARF
(post-strep glomerulonephritis risk does not change with antibiotic use)
Use beta-lactam antibiotics (penicillin, amoxicillin)
What nonbacterial infections present with tonsillar exudates?
infectious mononucleosis
strep pharyngitis
Tonsillar infections
Streptococcal pharyngitis symptoms Ear pain Difficulty swallowing High fever Tonsillar exudates
Treatment: beta- lactam antibiotics (penicillin, amoxicillin)
What are the diagnostic features of peritonsillar abscess? What is the treatment?
Infection between the tonsil and pharyngeal constrictors caused by streptococcus pyogenes, staphylococcus aureus, and/or bacterioides spp.
Severe sore throat, fever, muffled “hot potato” voice
Classic diagnostic feature is obvious abscess on the tonail or deflection of the uvula to the opposite side
Other signs and symptoms include trismus (“lockjaw”) and drooling
Treatment:
Needle aspiration or I&D
Pain meds and antibiotics: amoxicillin/clavulanate, clindamycin
Viral influenza
H and P: arthralgias, myalgias, nasal congestion, nonproductive cough, high fevers, lymphadenopathy
Flu swab
Treatment: symptomatic treatment, fluid intake, zanamivir and oseltamivir which will decrease severity of symptoms
Annual flu vaccine (especially elderly patients, healthcare workers, immunocompromised, lung disease)
Sinusitis- acute
streptococcus pneumoniae
haemophilus influenzae
moraxella catarrhalis
viral infection
associated with barotrauma, allergic rhinitis, prolonged gastric tube placement, asthma and other chronic resp infection
Complications- may spread to CNS and cause meningitis
Sinusitus- chronic
usually caused by sinus obstruction and anaerobic infection
DM predisposes to mucor mycosis
Sinusitis H and P
sinus pain, purulent nasal discharge, maxillary tooth pain, sinus tenderness to palpation, illumination test (unreliable)
CT sinuses for severe sinusitis Treatment: nasal irrigation analgesics oral decongestants intranasal steroids amoxicillin- clavulanate, doxycycline, or levofloxacin
What are the complications of strep pharyngitis, and which can be prevented with antibiotics?
ARF and glomerulonephritis
ARF can be prevented
Signs of a peritonsillar abscess
deviated uvula
trouble opening mouth
muffled “hot potato” voice
look for a bulge in the back of the throat
murmurs that decrease with squatting
HOCM and MVP, because the valve leaflets are further apart with greater afterload
Acute bronchitis
trachea and bronchi
difficult to differentiate from URI in the first few weeks. Generally a clinical diagnosis because the symptoms and radiology are nonspecific. If high fever then evaluate for PNA, and consider influenza
productive cough
shortness of breath
wheezing
sputum culture in persistent cases
Rads- CXR rules out PNA, shows mild congestion
Viruses- MCC
Mycoplasma pneumoniae
Streptococcus pneumoniae
Haemophilus influenzae
Treatment- symptomatic, self- limited Abx if increased risk of bacterial infection (other lung disease, smokers, elderly) fluoroquinolones tetracycline erythromycin azithromycin
PNA
inflammation in the alveoli
- CAP
- HAP
Clinical manifestations can break down into typical and atypical
Features of typical PNA presentation
fever cough malaise purulent sputum chest pain SOB
on xray, lobar infiltrate
common organisms: streptococcus pneumoniae staphylococcus aureus haemophilus influenzae GBS
Features of atypical PNA presentation
less severe symptoms
nonproductive cough
headache fatigue
On CXR, diffuse patchy infiltrates
Common organisms:
mycoplasma pneumonia
legionella pneumophila
chlarmydophila pneumoniae
Viral causes of PNA
influenza parainfluenza adenovirus cytomegalovirus RSV (MCC viral PNA in children)
Streptococcus pneumonaie PNA
MCC PNA in adults
sickle cell patients
high fevers, pleuritic pain, productive cough, rust- colored sputum
Treatment: cephalosporins respiratory fluoroquinolones beta- lactams macrolides preferred- amoxicillin unless you have resistance
Haemophilus influenzae
COPD
SCD
slower onset of symptoms
Treatment: beta- lactams fluoroquinolones doxycycline macrolides
staph aureus PNA
- Nosocomial pneumonia in immunocompromised patients
- Seen in higher rate in patients with influenza
- Abscess formation
Treatment: beta lactams, MRSA coverage (incase resistant)
Klebsiella pneumoniae
Alcoholics, aspiration, hospitalized, sickle cell, currant- jelly sputum
Treatment:
cephalosporins
aminoglycosides
pseudomonas aeruginosa PNA
chronically ill, immunocompromised, cystic fibrosis, chronic ventilator, nosocomial pneumonia, rapid onset of symptoms
(very sick, high mortality)
start empiric antibiotics immediately
- piperacillin- tazobactam
- ceftazidime
- cefepime
- imipenem
- meropenem
- doripenem (beta- lactams)
- ciprofloxicim, levofloxacin (fluoroquinolones)
- aminoglycosides
GBS PNA
neonates and infants
respiratory distress and lethargy
Treatment:
beta- lactams
ampicillin and gentamicin
Enterobacter spp.
Nosocomial pneumonia
elderly patients
3rd generation cephalosporins
-carbapenem
Mycoplasma pneumoniae
walking PNA
MCC in young adults
diffuse bilateral infiltration on CXR
Pt doesn’t appear ill
less severe sx
rash
positive cold- agglutinin test (IgM)
Treatment- macrolides
Legionella pneumophila
aerosolized water, and can be passed from person to person
slow onset
nausea, diarrhea
confusion, ataxia
Treatment: macrolides, fluoroquinolones
Chlamidophile pneumoniae
another atypical pneumonia
- mycoplasma pneumoniae
- legionella pneumophila
- chlamydophila pneumoniae
Very common in the very young and very old
- slow onset of symptoms
- frequent sinusitis
- Treatment with doxycycline, macrolides
Empiric therapy for PNA (cover s. pneumoniae and atypical organisms)
Note: resistance to macrolides is growing
- Resp fluoroquinolone like levofloxicin, moxi, gemifloxifin alone
- or combine a beta-lactam with doxycycline or a macrolide
Most common PNA agent in children
RSV
Most common PNA agent in adults
strep pneumo
PNA with Higher rate after influenza
s. aureus
PNA with currant jelly sputum
klebsiella
PNA with associated with CF
pseudomonas
PNA MC in neonates
GBS
PNA Associated with elderly
enterobacter (Gram negative)
PNA common in young adults
mycoplasma
PNA associated with aerosolized water
legionella
Neonates (first 28 days of life) most common causes of PNA
- GBS is most common
- E. Coli
- Chlamydia trachomatis (long incubation, sx appear 12 weeks later)
- Herpes simplex virus
MCC PNA in children
RSV
Strep pneumoniae
chlamidophila pneumoniae
in older children, think about mycoplasma pneumoniae
MCC PNA in adults
Streptococcus pneumoniae Haemophilus influenza Mycoplasma pneumoniae Chlamydophila pneumoniae Influenza
MCC PNA in elderly
Streptococcus pneumoniae Haemophilus influenzae Influenza Staphylococcus aureus Anaerobes Gram- negative rods
What are the indications for pneumococcal vaccination in adults?
- age 65 and older
- Serious long-term health problems such as heart disease, sickle cell disease, alcoholism, leakage of cerebrospinal fluid, lung disease, diabetes, or cirrhosis
- resistance to infections if lowered due to Hodgkin disease, multiple myeloma, cancer treatment with xrays or drugs, treatment with long-term steroids, bone marrow or organ transplant, kidney failure, HIV/AIDS, lymphoma, leukemia, other cancer, nephrotic syndrome, damaged spleen or no spleen
- Cigarette smokers age 19-54
PNA and gram-positive cocci in clusters
s. aureus
gram- positive cocci in pairs in the context of PNA
s. pneumoniae
gram- negative rods in 80 year-old with PNA
e. coli
gram positive cocci in neonate PNA
GBS
gram neg rods in neonate PNA
e. coli
Fungal PNA with PMHx of travel to SW US
coccidiomycosis
Fungal PNA with PMHx of caves, spelunking, bats
histoplasmosis
Fungal PNA with PMHx of trave l to eastern North America
blastomycosis
Fungal PNA with PMHx of travel to s. America
paracoccidiomycosis
Antifungals used to treat fungal PNA
Amphotericin B
Ketoconazole
Itraconazole
Fluconazole
Pneumocystic jiroveci (PCP)
Immunocompromise
-HIV patients (CD4 count220 (rising LDH despite appropriate treatment portends a poor prognosis)
What is the usual treatment:
21 days of antibiotics with choices including
-TMP-SMX (IV or PO)
-Pentamidine (IV)
-Primaquine (PO) + clindamycin (IV or PO)
Tuberculosis (primary and secondary)
mycobacterium tuberculosis
Primary TB: person who has never been infected with TB contracts disease
Symptoms vary widely: fever, CP, cough common
CXR: hilar lymphadenopathy, or normal, possible Ghon complex
Body often heals from the primary infection by primary fibrosis, allowing the person to move on to latent TB (asymptomatic), which can possibly last for years
Ghon focus vs Ghon complex. Both associated with primary tuberculosis
primary TB focus in a small area of lower lung, granulomatous inflammation
visible on CXR once it has calcified
If seen in combination with hilar lymphadenopathy, a Ghon focus is called a Ghon complex
How do you interpret a positive PPD?
current infection
past exposure
vaccination
5mm PPD is considered positive in
highest risk pop
HIV+
Close contact with TB
CXR findings suggestive of TB
10mm PPD is considered positive in
homeless immigrants IV drug users chronically ill healthcare workers recently incarcerated
15mm PPD is considered positive in
anyone, including low-risk
15mm is always considered positive
Significance of negative PPD skin test
negative no infection anergic malnutrition immunocompromise sarcoidosis
Secondary TB
reactivation of dormant tubercles
fibrocaseous cavitary lesions
symptoms:
fever, hemoptysis, weight loss, night sweats
complications: parenchymal tuberculoma (brain grey matter) Meningitis Pott's disease (vertebral bodies) lymphadenitis renal disease GI disease miliary TB
Labs to confirm TB
sputum culture takes 2-4 weeks
Acid-fast sputum stain every morning for 3 days
negative- probably not TB, discharge, follow up with cultures
positive= TB
Treat TB
Latent- INH (6-9 months) Primary or secondary TB- RIPE Rifampin INH (with B6 to prevent peripheral neuropathy) Pyrazinamide Ethambutol
BCG vaccine
varying efficacy
can have a false positive PPD
in the 1st year of life, after 10 years, should be PPD negative
Causes of ARDS
sepsis, shock, near-drowning, trauma, aspiration, drug overdose, lung infection, etc
Aspiration Acute pancreatitis Air or amniotic embolism Radiation Drug overdose Diffuse lung disease DIC Drowning Shock Sepsis Smoke inhalation
Symptoms and Signs of ARDS
refractory hypoxemia, decreased lung compliance, pulmonary edema
look for a history of acute dyspnea and pulmonary decompensation, cyanosis, tachypnea, wheezing, rales, rhonchi
labs: respiratory alkalosis, decreased O2, decreased CO2, PCWP200
Treat ARDS
Treat underlying diseases, support in ICU
Mechanical ventilation with low tidal volumes (to minimize injury), and adequate PEEP (to recruit collapsed alveoli)
Conservative fluid management to reduce pulmonary edema. Goal CVP 4-6mmHg. (Furosemide and albumin may also be helpful to prevent pulmonary edema)
Prone positioning improves oxygenation but does not improve survival
Minimize oxygen consumption by preventing fever (antipyretics), minimizing anxiety and pain (sedatives and analgesics), and limiting respiratory muscle use (paralytics), particularly in cases of asynchrony of the ventilator and patient’s efforts
Transfuse blood only if hemoglobin drops below 7g/dL, as transfusion may increase risk of death in ARDs patients
What percentage FiO2 does a nasal cannula provide?
24-40% FiO2 (FiO2 increases 3% for every 1L/min up to 6L/min)
What percentage FiO2 does a face mask provide?
50-60% FiO2
What percentage FiO2 does a non-rebreather provide?
60-95% FiO2
What percentage FiO2 does a CPAP provide?
80% FiO2
What perventage FiO2 does mechanical ventilation provide?
up to 100% FiO2
Asthma
reversible airway obstruction secondary to bronchiolar hyperactivity, etc.
Triggers: allergens, illness, exercise, cold temperatures, stress, beta blockers, aspirin (rare), sulfites (rare)
Risk factors: family history, allergies, atopic dermatitis, low socioeconomic status, Churg-Strauss vasculitis
History and physical: cough, dyspnea, wheezing, chest tightness, tachypnea, tachycardia, prolonged expiratory duration, decreased breath sounds, accessory muscle use, pulsus paradoxus, cyanosis, decreased O2 saturation, difficulty talking
Labs: decreased PEFR (pulm exp flow rate), decreased FEV1, ABG shows hypoxemia, respiratory alkalosis
normal CXR, maybe mild hyperinflation
Pulsus paradoxus
deep inspiration causes SBP to drop at least or more than 10mmHg
Definition of mild intermittent asthma
2 or less daytime episodes per week
2 or less nighttime episodes per month
FEV1 greater than or equal to 80%
Treatment: PRN albuterol
Definition of mild persistent asthma
3-6 daytime episodes/week
3-4 nighttime episodes/month
FEV1 > 80%
Management:
Treatment with PRN albuterol
Low dose inhaled steroid
+/- montelukast or cromolyn if pt has high allergy susceptibility
Definition of moderate persistent asthma
daily daytime episodes greater than 1 nighttime episode/week FEV1 60-80% Treatment: PRN albuterol Low to med-dose inhaled steroid \+/- long-acting B2 agonist \+/- montelukast, cromolyn, theophylline if everything else is failing
Definition of severe persistent asthma
continued daytime episodes
frequent nighttime symptoms
FEV1>60%
Treatment: PRN albuterol, High-dose inhaled steroid, long-acting beta2 agonist, daily PO steroid, +/- montelukast, +/- theophylline
Rapid- acting beta2 agonists
bronchodilators
rapid onset of action
albuterol, levalbuterol
Long- acting beta2 agonists
salmeterol, fometerol
bronchodilators, gradual onset, sustained activity
Inhaled corticosteroids
decreased cells involved with airway inflammation, mild persistent and onward, often combined with rapid- acting beta2 agonists
Leukotriene inhibitors
montelukast, zafirlukast, ziluton
block activity or production of leukotrienes (inflammation and bronchospasm), useful in patients with rhinitis- like sx
Mast cell stabilizing agents
cromolyn, etc
stabilizes mast cells
anti-inflammatory prophylaxis
not useful acutely, not used much at all
dosed 3-4 times per day
Theophylline bronchodilator
previously first-line, now replaced in recent years by beta agonists side effects and interactions -hypotension -seizures -tachycardia
treat OD with benzodiazepines, dialysis
adjunct if severe refractory
Anticholinergic agents
block vagal- mediated smooth muscle contraction
used as adjunctive therapy in moderate-to-severe asthma
acute asthma- treatment
3 doses albuterol back to back, ipratropium
systemic steroids
corticosteroids
decreased cells involved with airway inflammation
stronger effect than inhaled preparation
take 4 hours to kick in
PO=IV
status asthmaticus
prolonged, nonresponsive asthma attack, can be fatal
treatment: aggressive bronchodilator therapy corticosteroids O2 intubation
keep SpO2>94%
normal CO2 signals impending decompensation
PCWP cut-off for noncardiogenic pulmonary edema
PCWP18 signals backed up fluids, and this is more likely to be cardiogenic pulmonary edema, or heart failure
ARDS
acute onset of respiratory distress
PaO2:FiO2 ratio
COPD
pulmonary disease that includes airflow limitation and chronic inflammation in the airways and lungs
Chronic bronchitis
chronic productive cough for 3 months
Emphysema
permanent enlargement of airspaces distal to the terminal bronchioles due to destruction of the airspace walls
Asthma
chronic inflammation of the airways resulting in airway responsiveness, wheezing, and SOB that is reversible
COPD H and P, labs
productive cough
recurrent respiratory infection
dyspnea, wheezing, rhonchi
labs: FEV1/FVC
COPD GOLD staging
GOLD 1: FEV1>80% predicted (mild)
may be a gradual, relatively asx progression leading to late diagnosis in stage 2
Gold 2: FEV1 50-80% (moderate)
Gold 3: FEV1 30-50% (severe)
Gold 4: FEV1
COPD management
smoking cessation in all patients, and give flu and pneumovax vaccines
Category A (Gold 1 or 2 with mild or infrequent symptoms) -short-acting bronchodilator- albuterol, atrovent
Category B (Gold 1 or 2 with moderate to severe symptoms)
- short- acting bronchodilator
- long-acting bronchodilator: B2 agonist or anticholinergic (tiotropium, ipratropium)
Category C (GOLD 3 or 4 with mild or infrequent symptoms)
- short- acting bronchodilator
- long-acting bronchodilator
- inhaled steroid
Category D (Gold 3 or 4 with moderate to severe symptoms)
- short- acting bronchodilator
- long-acting bronchodilator
- inhaled steroids
- +/- theophylline
- home oxygen if pulse-ox
Indications for home oxygen
pulse-ox
vaccinations for patients with COPD
yearly influenza vaccine
pneomococcal vaccine
-all smokers between age 19 and 65
-single revaccination after age 65 if greater than 5 years since initial vaccination
Emphysema
Central- from smoking
Panacinar- from A1AT deficiency (alpha 1 antitrypsin inhibits elastase, without it the acini get broken down)
H&P: dyspnea productive cough morning headache barrel- chested pursed-lip breathing prolonged expiratory duration decreased heart sounds decreased breath sounds wheezing rhonchi accessory muscle use JVD
Labs:
PFT: decreased FEV1
decreasd FEV/FVC ratio
increasd TLC
ABG:
decreased O2, increased CO2
CXR: hyperinflated lungs, flat diaphragms, decreased vascular markings
DLCO: decreased in proportion to severity of emphysema, +/-normal in chronic bronchitis
Treatment: inhaled short-acting beta-2 agonist inhaled anticholinergic inhaled corticosteroid alpha- antitrypsin augmentation lung transplantation (severe) home O2 if pulse-ox
Chronic bronchitis
chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded
- procedes or follows changes in FVC
- smoking is often a risk factor
-abx on an individual basis
azithromycin
levofloxacin
amoxicillin with clavulanate
What are the possible etiologies for bronchiectasis?
unknown etiology in 50% of patients
cystic fibrosis
immunodeficiency
dyskinetic cilia: Kartagener syndrome (dextrocardia, sinusitis, bronchiectasis), autosomal dominant polycystic kidney disease (ADPKD)
Pulmonary infections : TB, fungal infection, lung abscess
Obstruction: foreign body aspiration, tumor, lymph nodes
Other etiologies: Young syndrome, foreign body aspiration, rhematoid arthritis, Sjogren syndrome, allergic bronchopulmonary aspergillosis, cigarette smoking
Bronchiectasis H&P, radiology, Treatment, complications
persistent productive cough hemoptysis frequent respiratory infections dyspnea copious sputum wheezing, rales hypoxemia
Radiology: multiple cysts and bronchial crowding
Treatment: Pulmonary hygeine, chest physical therapy, antibiotics, inhaled beta- 2 agonists and corticosteroids, resection of severely diseased regions of the lungs
Complications:
cor pulmonale
massive hemoptysis
abcsess formation
Asbestosis
plumbers
construction workers
demolition workers
Complications:
- malignant mesothelioma
- bronchogenic carcinoma
- synergistic effect with tobacco
Silicosis
sand blasting
increased risk of TB
progressive fibrosis
Coal- worker’s disease
progressive fibrosis
does not increase risk of cancer unless there is radon in the mine
berylliosis
ceramics, electronics, dye- manufacturing
increased risk of lung cancer
may need corticosteroid treatment to maintain respiratory function
Goodpasture syndrome
progressive autoimmune disease of the lungs and kidney 2/2 anti-glomerular basement membrane antibodies
Characterized by intra-alveolar hemorrhage and glomerular nephritis
hemoptysis
dyspnea
recent respiratory infection
diagnosed with +anti-GBM antibodies
UA: proteinuria
granular casts
hematuria
Renal biopsy:
crescent glomerulonephritis
IgG deposition along glomerular capillaries
Treatment: plasmapheresis
corticosteroids
immunosuppressive agents
Granulomatosis with polyangiitis
kidney, lung, upper airway
H and P: hemoptysis dyspnea myalgias chronic sinusitis ulcerations of nasopharynx, saddle nose deformity
labs:
c-ANCA positive
Treatment:
cyclophosphamide
corticosteroids
rapidly fatal if untreated
which pneumoconiosis is associated with progressive fibrosis?
Coal worker’s silicosis
which pneumoconiosis is associated with increased risk of TB?
silicosis
which pneumoconiosis is associated with working with electronics, causes increased cancer risk?
berylliosis
which pneumoconiosis is associated with malignant mesothelioma and bronchogenic carcinoma
asbestosis
Chromosome 22q11 deletion heart defects
truncus arteriosus
tetralogy of fallot
tri21 heart defects
endocardial cushion defects, toF, PDA
Congenital rubella heart defects
PDA, pulmonary artery stenosis
Turner syndrome heart defect
coarctation of the aorta
Marfan syndrome heart defect
aortic regurgitation
PE risk factors
immobilization malignancy recent surgery pregnancy OCP use obesity fractures prior DVT severe burns
PE- what does it look like?
sudden dyspnea pleuritic chest pain cough \+/- syncope feeling of impending doom delirium
Tachypnea and tachycardia on exam
AMS
decreased breath sounds
What tests are helpful to order in PE?
ABG: respiratory alkalosis due to hyperventilation but low PO2 due to hypoxia
D-dimer: normal D-dimer makes PE much less likely, and an elevated d-dimer is non-specific
US of LE veins to rule out DVT: presence of DVT makes PE more likely, absence of DVT does not rule out PE
CXR: usually normal, but may have atelectasis, pleural effusion, or Hampton’s hump (wedge-shaped opacification at the distal lung fields)
EKG changes: most commonly sinus tachycardia +/- nonspecific ST and T-wave changes, and very rarely the classic S1Q3T3 (wide S in lead I, large Q, inverted T in lead III)
V/Q scan: useful and accurate only in confirming low or high clinical probability
CT scan with contrast (CT PE protocol or CT pulmonary angiography), most commonly used method to diagnose or rule out a PE, but not 100% accurate
Pulmonary angiogram: gold standard but mor invasive and rarely performed
PE treatment:
start O2 IV fluids or pressors LMWH (initially) warfarin (3-6 months) IVC filter if meds are contra-indicated or high risk of fall \+/- thrombolytics if massive PE
Pulmonary HTN
HTN of pulmonary vasc
2/2 PE, valvular disease, left-to-right shunts, COPD
idiopathic pulmonary arterial HTN
high mortality rate
Pulmonary HTN- what does it look like?
dyspnea, fatigue, chest pain, cough, syncope, cyanosis, clubbing of fingers, loud S2
valves slam shut
JVD, hepatomegaly
ECG- RVH (cor pulmonale)
CXR: congested pulmonary arteries, enlarged right ventricle
Echocardiogram is how you make this diagnosis! Monitor pulmonary artery pressure noninvasively
Pulm HTN- treatment
O2, Vasodilators, Anticoagulants, Diuretics
Treat the underlying condition
supplemental O2
vasodilators that decrease pulmonary HTN:
Prostanoids: epoprostenol, terprostinil, iloprost
Endothelin receptor antagonists: bosentan, ambrisentan
Cyclic GMP phosphodiesterase inhibitors:sildenafil
CCB: nifedipine
Anticoagulants if primary pulmonary HTN, embolic disease, cardiac causes
Diuretics: pulmonary congestion, JVD
Pulmonary edema:
Increased fluid in lung interstitium (as opposed to in the pleural space as you would see in pleural effusion)
caused by left-sided heart failure, MI, valvular disease, arrhythmia, ARDS, wedge pressure 18 think cardiogenic causes
What does pulmonary edema look like?
symptoms, labs, EKG
dypsnea orthopnea paroxysmal nocturnal dyspnea frothy pink sputum tachycardia wheezing
labs: BNP might be elevated
EKG: T- wave abnormalities, QT prolongation
CXR: cephalization of vasculature, kerley B lines (prominent interstitial markings in lower lung fields), diffuse interstitial fluid
Treat Pulmonary edema
NO LIP
nitrates oxygen until spO2 is in the normal range loop diuretics (go to for PE) inotropic drugs (increase contractility) positioning (legs off the edge of bed to keep fluid out of the chest)
Pulmonary embolism on CXR
Hampton’s hump- wedge shaped pulm infarct
Most helpful imaging studies when PE is suspected
spiral CT with IV contrast
V/Q perfusion scan
Pulmonary angiography
Primary drugs for treating pulmonary htn
vasodilators prostanoids endothelin receptor antagonists phosphodiesterase inhibitors dihydropyridine calcium channel- blockers
indications for repair on an abdominal aneurysm
ruptured
symptomatic
>5.5 cm
rapidly enlarging (>0.5cm in 6 months)
indications for intubating a child with asthma
unable to speak due to the work of breathing
unable to maintain adequate oxygenation despite supplementation
AMS
“count to 10”
What is a pleural effusion?
excess fluid that accumulates in the pleural space
presents with SOB, dyspnea on exertion, pleuritic chest pain, fatigue, weakness
dullness to percussion decreased breath sounds decreased tactile fremitis egophony tracheal deviation away from the effusion
Thoracentesis allows us to analyze the fluid
What is egophony?
Egophony: E to A changes
Bronchophony:
sounds are louder and clearer
Whispered pectoriloquy:
whispered sounds are louder
Tactile fremitus
transmitted vibrations (effusions insulate the sounds)
pathophysiology of a transudate
increased pressure forces filtration across capillary
pathophysiology of an exudate
disruption of lining due to inflammatory process leads to leakage of fluid
Common causes of transudate
CHF, cirrhosis, nephrotic syndrome
common causes of exudate
cancer, infection, vascullitis
Light’s criteria
exudate if any one of the following:
pleural: serum protein ratio >0.5
pleural: serum LDH ratio >0.6
pleural fluid LDH>2/3 of the upper limit of normal for serum LDH
Pleural fluid analysis- what should you order?
Glucose pH Amylase Triglycerides cell count gram stain cytology
How do we treat pleural effusion?
thoracentesis
chest tube if there is a large amount of fluid
pleurodesis (scarring of the surface of the pleura)
Empyema- treatment
chest tube for treatment
recurrent malignant effusion
special catheter
Pneumothorax, causes
spontaneous
trauma
secondary to medical conditions
PTX, types
closed (COPD, TB, blunt chest wall trauma, spontaneous PTX)
open (iatrogenic, central line placement, lung biopsy, thoracentesis)
tension pneumothorax (trauma to the chest wall)
H and P: unilateral chest pain, tiredness, weakness, SOB, decreased wall movement, decreased breath sounds, increased resonance to percussion, decreasd tactile fremitus, hypoxia, JVD, decreased BP, tracheal deviation away from side of pneumothorax
Treatment for PTX
small (15%, chest tube
open PTX: chest tube, occlusive dressing, attempted closure
Treat a tension PTX
hypoxia, low BP
needle decompression immediately into 2nd or 3rd intercostal space, midclavicular line
Treatment for recurrent PTX
pleurodesis
Hemothorax
caused by trauma, malignancy, infection (TB)
H and P: dyspnea, fatigue, pleuritic chest pain, dullness to percussion, decreased tactile fremitus
Labs: thoracentesis, watch H and H
CXR: mediastinal shift
Treatment: O2, chest tube, treat underlying cause
Complications to hemothorax
clot can harden and scar down, and become harder to remove
Malignant mesotheloima
asbestos exposure
H and P: chest pain, dyspnea, dullness to percussion, exudative pleural effusion, chest wall mass
Treatment: poor prognosis
surgery, chemotherapy, radiotherapy, radical surgery
What study helps to determine if a pleural effusion is loculated or free- flowing?
upright CXR
lateral decubitus CXR
sleep apnea
cessation of breathing for at least 10 seconds
3 types:
central
obstructive
mixed
risk factors/ exacerbators for sleep apnea
obesity sedatives intoxication alcohol male gender History and physical: excessive sleeping during the day, snores loudly, awakes gasping for air, morning headaches, overweight or obese, short, fat neck, abnormal palate or pharynx, large adenoids
Labs:
epworth sleepiness scale
polysomnography (apnea index)
increased H/H (hypoxemia)
Treatment for OSA:
weightloss
avoid alcohol and hypnotic medications
continuous positive airway pressure (CPAP) first line, nasal facemask
oral appliance (protrude the mandible forward or hold tongue anterior)
surgical options (uvulopalatopharyngoplasty)
rarely, tracheostomy
stimulants
-modafinil
-armodafinil
What is the treatment for central sleep apnea
CPAP
BiPAP
ASV (adaptive servo- ventilation), which tries to synchronize with the patient’s breathing
Oxygen supplementation
Acetazolamide
Atelectasis
local collapse of lung often occurs post- surgery anesthesia asthmatics foreign bodies mass effect from tumors various pulmonary lesions can lead to increased work of breathing and hypoxemia, may be symptomatic, if persistent can lead to PNA
CXR: fluffy infiltrates, there may be lobar collapse
Treatment: IS, post-op ambulation, upper airway suctioning with bronchoscopy
Intubation
Pre-oxygenate
Pre-treatment:
Lidocaine blunts increase in intracranial pressure- good for head trauma
Fentanyl blunts pain response
Atropine decreases airway secretions, prevents bradycardia
Paralysis induction:
a. sedatives (etomidate, propofol, midazolam, ketamine)
b. paralytics (succinylcholine, rocuronium)
protection and positioning
placing endotracheal tube (end tidal CO2, auscultate)
Complications: tube misplacement
vomiting
aspiration
dental injuries
Longterm tracheostomy may be required if the patient has had an ET tube for several weeks
Ventilation
inspiration by ventilator
expiration spontaneous
ventilation is an art
Controlled mechanical ventilation
machine controls rate and tidal volume, initiates every breath, patient does not use own energy to breath
intermittent mandatory ventilation
machine controls rate and tidal volume
Patient is able to breath in between mechanical breaths
used when weaning patient off of ventilation
Synchronized intermittent mandatory ventilation (SIMV)
synchronizes rate with initiated breaths
delivers tidal volume and rate
patient breaths in between mechanical breaths
used when weaning off mechanical ventilation
Assist controlled ventilation (AC)
wait until the patient attempts to breath, then delivers full tidal volume
machine sets a baseline rate
used when weaning patient off of ventilator
Continuous positive airway pressure (CPAP)
positive pressure to keep airway open
patient is initiating every breath
last step before weaning
Extubation- how do you know when the patient is ready?
max inspiratory pressure 10mL/kg
Minute ventilation 200
Frequency/tidal volume ratio
What substances should be avoided in patients with OSA?
sedatives (benzodiazepines, alcohol, antihistamines)
