Pulmonary Flashcards
air trapping signs in asthma that are ominous
decreased lung sounds
hyperresonance
dx for asthma
decreased PFTs (decreased FEV1/FVC
reversible - with beta agonist - albuterol
inducible - with Ach agonist
ABG - increased A-a gradient
If PFTs in a pt suspected of asthma next step =
methacholine challenge
stages of asthma symptoms
day night FEV1
I <2/wk <2/mon 80%
II <1/day <1/wk . 80%
III . >1/day >1/wk . 60-80%
IV . >1/day >1/wk . <60%
V . refractory to everything so they get oral steroids
stages of asthma tx
I - SABA
II - SABA + ICS (or leukotriene antagonist)
III - SABA + ICS + LABA
IV - SABA + ICS(increase dose) + LABA
LABA without ICS
never ever do this and leukotrine antagonist = ICS
basics of overall asthma tx
always watch pt use their med and add a spacer to make sure meds get in lungs and not just mouth
make sure pts adhere to meds
initial steps during an asthma exacerbation
O2 to maintain SpO2>90%
nebulizers (ipatropium, albuterol)
oral steroids
peak expiration flow rate
Following an acute asthma exacerbation what criteria allows a pt to be discharged home
no O2 requirement
no wheezing
peak expiratory flow rate >70%
following an acute asthma exacerbation what criteria puts them in the ICU
increased O2 demand
rising CO2 on ABG
no wheezing (cant move air)
peak expiratory flow rate <50%
ICU tx of an asthma exacerbation
ventillators
IV methylprednisone
IV magnesium is third line agent
salvage therapy for an asthma exacerbation
racemic Epi
Sub Q Epi
Mg2+
presentation of a pt with lung cancer
fever
weight loss
hemopytosis
(smoking hx)
initial steps to dx cancer
CXR
- if neg -> paraneoplastic syndrome -> if no -> no cancer
- if effusion -> thoracentesis -> if fluid has malignant cells —-> cancer stage 4
if non dx -> CT scan -> 1st Stage with PET scan, 2nd PFs, 3rd Tx
dx techniques for lung cancer
- large proximal lesion
- peripheral lesion
- lesion in the middle of the lung
- large irregular mass in lung
- large proximal -bronchoscopy - EBUS (see thru walls)
- peripheral - CT guided percutaneous biopsy (needle)
- middle of lung - cardiothoracic surgeon - video assisted thorascopic surgery (VATS)
- large, irregular mass in lung - resection
primary prevention of lung cancer
avoid smoking
avoid 2nd hand smoke
what are the requirement for cancer screening with low dose CT scans
55-80
30 pack per year history
quite <15 years ago
nodule criteria that is non cancerous
Size <8mm
Surface - smooth
Smoking - never
Self (age) <45
calcified
nodule criteria that is cancer suspicious
Size >2cm
Surface - spiculated
Smoking - Hx +
Self (age) - >70
pulmonary nodule is found next step is
finding old films
- if no change –> stable
- if new or change –>
- —–> low risk –> serial CT scans
- —–> high risk –> biopsy
small cell lung cancer basics
smoking Hx
centrally located
paraneoplastic syndromes - ACTH (cushing) and SIADH and Lambert Eaton syndrome
tx - chemo and radiation (responds well)
Sqaumous cell cancer lung cancer basics
smoking Hx
centrally located with necrosis and cavitation
More common than small cell cancer
paraneoplastic syndromes - PTH-related peptide (high Ca)
tx - stage related chemo, radiation, resection
adenocarcinoma lung cancer basics
MC primary lung cancer in both smokers and nonsmoker
asbesostosis (non smokers)
peripherally located - can cause pleuritic pain
tx - stage related chemo, radiation, resection
carcinoid lung cancer basics
left sided fibrosis, flushing, wheezing, diarrhea
serotinin syndrome
dx - 5-HIAA in urine
transudate pleural effusion pathophys
fluid falling out of the capillary space due to:
- hydrostatic pressure - CHF
- loss of oncotic pressure (hypoalbuminemia)
exudative pleural effusion pathophys
caused by inflammation - increased permeability of pleural spaces or decreased lymphatic flow from pleural surface because of damage to pleural membranes or vasculature
presentation of pleural effusion
orthopnea
dyspnea on exertion
decreased lung sounds
dullness to percussion in the area of effusion
CXR of pleural effusion
blunting of the costophrenic angle
horizontal meniscus
dx workup of pleural effusion imaging studies
Lateral Decubitus X-ray or US or CT
if small < 1cm watch and wait
if >1cm and no CHF hx –> Tap
if pt has CHF - don’t Tap –> diuresis –> if fails Tap
if pleural effusion suspected and septations/lobes (loculation) present next step =
thoracostomy (+/-) tPA –> if fails then –> thoractomy for debridment
thoracentesis: transudate vs exudate
lights criteria
LDH of fluid —> 2/3 upper nml limits
LDHfluid : LDHserum –> ( >0.6)
total protein (fluid): total protein (serum) –> ( >0.5)
[if any (1) above is + then –> exudate]
all (3) above negative = transudate
what tubes do you send after performing a thoracentesis
1) cell count with diff
2) cytology - cancer (if + stage 4)
3) ADA, glucose, pH, Total protein, LDH , TGL
4) blood cultures - gram stain culture, TB, fungi
breakdown of tube 1 sent s/p thoracentesis
PNA - leukocytosis with PMN (neutrophils)
TB - WBCs with lymphocytosis
RBC - hemothorax or cancer
breakdown of tube 3 sent s/p thoracentesis
ADA - TB
TGL - for chylothorax
DVT causes (vircows triad)
1 - venous stasis - immobility
2 - endothelial injury - central lines, plastics, smoking
3 - hypercoagable stages - hormone replacement therapy, OCPs, factor V leiden, malignancy
DVT presentation
unilateral leg swelling ( >2cm larger than other leg)
tenderness to palpation
dx and tx of DVT
US and anticoagulate
wedge infarct PE pathophys
necrosis dead lung –> hemopytosis
ischemia of pleural –> pleuritic CP
pulm HTN - due to right heart strain
0% perfusion but gas exchagne occurs 100% –> V/Q mismatch –> hypoxemia
platelet derived mediators pathophys on their destruction
vasodilation -> fluid leak out –> increased diffusion barrier for O2 which is diffusion limited -> decreased O2 –> tachypnea and tachycardia (too try and compensate by increasing CO)
but since CO2 is perfusion limited -> pt still able to breath off CO2 which will be worsened by tachypnea
due to poor hypoxia throughout lung –> massive vasoconstriction
ABG findings of PE
increased pH
decreased CO2
decreased O2
CXR and ECG findings in a PE with right heart strain
CXR - nml
ECG - S1, Q1, T3 = right heart strain
and/or elevated troponin
and/or elevated BNP
Wells criteria
<2 –> low probability –> D-dimer
> 4 –> CTA (must have good kidneys) or do V/Q
> 6 –> V/Q scan (must have nml CXR)
when is an IVC filter used for PE
when the next PE will kill the pt and/or if massive bleed (ex: GI bleed) is present and anticoagulants are C/I
cancer pts with PE tx
LMWH
management of an asymptomatic PE
home - LMWH bridge to Warfarin
no right heart strain
vital signs stable
management of a symptomatic PE
admit to floor - LMWH –> warfarin
no right heart strain
vital signs are stable
management of submassive PE
ICU - heparin drip –> warfarin
right heart strain is present
vital signs are stable
management of massive PE
ICU - TPA (if C/I –> thrombectomy)
abnormal vital signs
right heart strain is present
how to assess if there is right heart strain in a PE
elevated troponin or elevated BNP or 2D echo - dilated RV, big RA
chronic thromboembolic pulmonary HTN
pulm HTN with multiple PEs diagnosed
tx - thrombectomy
COPD CXR
barrel shaped chest
Flat Diaphragm
increased radiolucency of lung parenchyma
elongated and narrow heart shadows
COPD pathophys and PFTs
decreased alveolar elasticity in COPD –> lung hyperinflation –> increased TLC, increased FRC, increased RV –> increased work of breathing
reduced inspiratory and expiratory flow rates
ADR of systemic glucocorticoids
leukocytosis with neutrophilic predominance
decreased lymphocytes
decreased eosinophils
MCC of secondary clubbing are
lung malignancy
cystic fibrosis
R->L cardiac shunt
COPD exacerbation management
- O2 - SpO2 target 88-92%
- inhaled bronchodilators
- systemic glucorticoids
- ABX if >1 cardinal sign
- Oseltamavir - if evidence of influenza
- NPPV if ventilatory failure
- Intubate if NPPV fails or if it is contraindicated
cardinal signs of an infectious cause of a COPD exacerbation
increased dyspnea increased cough (frequency or severity) increased sputum production (change in color or volume)
indications for long term home O2 therapy
resting arterial oxygen tension (PaO2) <55mmHg
SaO2 < 88% on room air
pts with cor pulmonale or hematocrit >55% requirements
- SaO2 <89
- PaO2 <59
what are the . most common etiologies of chronic cough
upper airway cough syndrome (post nasal drip)
GERD
Asthma
When can a methachline challenge be given
if no bronchodilator response seen
Lung dz in pts with ankylosing spondylitis
can develop restrictive lung dz due to diminished chest wall and spinal movement
PFTs - decreased VC, decreased TCLl, nml FEV1/FVC
apical cavitary lesion on CXR
reactivation of TB
- fever, night sweats, blood tinged sputum
young pt with SOB, productive cough, evidence of destruction of lower lung lobes
alpha 1 antitrypsin deficiency
panacinar (panlobular) ephysema
<45 y/o
association with liver dz
clinical presentation of interstitial lung dz
progressive exertional dyspnea or persistent cough
half of pts have smoking hx
fine crackles heard during mid to late inspiration
possible digital clubbing
labs/imaging of interstitial lung disease
CXR - reticular or nodular opacities
CT - fibrosis, honeycombing, traction bronchiectasis
PFTs - increased FEV1/FVC
decreased DLCO2, TLC, RV
signficant hypoxemia with exertion due to V/Q mismatch —> increased Alveolar-arterial gradient (A-a)
idiopathic pulmonary fibrosis pathophys
excess collagen deposition in the extracellular matrix around the alveoli –> resultant scarring –> affected PFTs decrease
predisposing factors for aspiration pneumonia
AMS - impaired cough reflex, glottic issues
Dysphagia - due to neuro deficits
GERD
Protracted vomiting
NG-ET tubes
Large volume tube feedings in the recumbent position
Bilateral hilar adenopathy on CXR
increased Ca
erythema nodosum
Sarcoidosis
pts can also have anterior uveitis, arthralgias, arthritis, bells palsy, papilledema, peripheral neuropathy
emphysema presentation
pink puffer
pts are thin - due to increased energy during breathing which is through pursed lips
pts lean forward when sitting
using accesory muscles
bronchitis
blue bloater
overweight and cyanotic (secondary to hypercapnia and hypoxemia)
chronic cough and sputum production
inflammation of airways -> decreased O2
cyanosis and hypoxemia –> vasoconstriction in lungs -> increased resistance in pulmonary arteries -> pulmonary HTN -> RHF –> edema
dx workup of COPD
PFTs
decreased FEV1/FVC
tx of COPD (not an exacerbation)
1 - SABA
2- SABA + LAMA (tiatropium)
3 - SABA + LAMA + LABA
4 - SABA + LAMA + LABA + ICS
5 - SABA + LAMA + LABA +ICS + PDE 4inhbitor
6 - SABA + LAMA + LABA + ICS + PDE4-I + Steroids
tx of chronic COPD
Corticosteroids - inhaled, oral (prednisone), IV
(methylprednisolone)
O2 if SpO2 <88%, PaO2 <55
Prevention (vaccines: flu, streptococcal, smoking
cessation)
Dilators (Short acting - albuterol, tiatropium, long acting
LABA, LAMA, Theophyline, PDE4-I)
Experimental
Rehab
what 2 things decrease mortality in a COPD pt
O2 and smoking cessation
signs and symptoms of a COPD exacerbation
wheezing - especially on forced expiration
cough
sputum production
tachycardia, tachypnea, decreased breath sounds
prolonged expiratory time
pt discharged home on what meds following COPD exacerbations
PO steroids - prednisone
Metered dose inhalers - albuterol
Pathophys behind ARDS
noncardiogenic pulmonary edema
leaky capillaries -> crushes the alveoli –> fluid causes an increased diffusion barrier –> O2 = diffusion limited = less O2 getting in
stiff lungs, increased A-a gradient
presentation of ARDS
sick as shit patient,hypoxemic
acute hypoxemic resp failure = P/A <200
septic shock, transfusion related lung injury , near drowning victim
ARDS CXR
pulmonary edema will be evident
differentiating between ARDS vs HF
CHF - increased PCWP and decreased LV function
ARDS - decreased PCWP and nml to increased LV function
ARDS management
intubation
keep tidal volume low to reduce pressure
keep respiratory rate high so theres no accumulation of CO2
PEEP
treat underlying condition and try diuresis
PEEP pathophys
applies back pressure to maintain recruitment of alveoli which has a small diffusion barrier which allows O2 to get in easier
presentation of diffuse parenchymal lung disease (DPLD) also called interstitial lung disease
chronic and insidious development of hypoxemia
dry hacking cough
dry crackles
restrictive PFTs
tx of DPLD (interstitial lung dz)
steroids
DMARDS
biologics
Idiopathic causes of interstitial lung disease (DPLD)
< 6 wks = acute interstitial pneumonitis
> 6months = idiopathic pulmonary fibrosis
drug induced causes of interstitial lung disease
bleomycin amiodarone radiation nitrofurantoin phenytoin
rheumatological disease that cause interstitial lung disease
SLE
RA
systemic sclerosis
sarcoidosis interstitial lung disease
autoimmune, younger black women
asymptomatic bilateral hilar lymphadenopathy
insidious hypoxemia, blurred vision
heart block, bellsy palsy erythematous nodosum
dx of sarcoidosis
CXR - bilateral hilar lymphadenopathy
CT - (high resolution) - ground glass
PFTs - restrictive pattern
Biopsy = noncasseating granulomas
Trying to rule in cardiac sarcoidosis without pulmonary involvement work up
Cardiac MI followed by a biopsy of endomyocardium with sarcoid in it
conduction disturbances - heart block, arrhythmias
it is the most common cause of death
abestosis interstitial lung disease
increased cancer risk
exposure: shipyard, constructions >30yrs
CXR - pleural plaques on CXR
mesothelioma is dx of
abestosis
biopsy - barbell bodies indicative of abestosis
silicosis of interstitial lung disease
sandblasting, rock quaries, mining, glass manufacturing
upper lungs - looks like TB
pts are at increased risk for TB so need annual TB checks
egg shell calcifications - CXR
berryliosis interstitial lung disease
aeronautic professions
ppl who build or manufacture electronics
coal interstitial lung disease
coal miners caplan syndrome - arthralgias - pulmonary fibrosis ----> check rhematoid factor
hypersensitivity pneumonitis
antigen mediated
person goes to work during week and has pneumonitis symptoms but these disappear over long weekend or on vacation
regional or temporal DPLD
intrapulmonary shunting
examples: pulm edema, PNA, atelectasis
increased A-a gradient
V/Q = O (no ventilation)
diffuse alveolar hypoventilation
uniform fall in ventilation throughout lung
causes: narcotic overdose and neuromuscular weakness
prolonged High FiO2 risks
oxygen toxicity - > formation of proinflammatory oxygen free radicals and predispose atlectasis as nitrogen is displaced
target PaO2 for COPD exacerbation
PaO2 55-80% once this target is reached lower FiO2 <60% which is the safe zone
pt with sick contact, cough, and no upper respiratory symptoms (rhinorrhea, etc) and has right lower lobe cracles on exam
indicates possibly pulmonary consolidation - must do CXR to r/o non viral etiology
pt with an underyling malignancy who presents with acute dyspnea, chest pain, tachycardia, hypoxia, and clear lungs is suggestive of
PE - underlying malignancy (prothrombic state)
they can present with syncope and hemodynamic collapse (RV dysfunction) if massive PE - along with RBBB on ECG
pts with PE can also develop small pleural effusions
new onset LBBB
suggest an acute MI
dyspnea/hypoxia due to pulm edema (crackles on exam)
MCC of orthostatic hypotension in elderly
hypovolemia -> due to decreased renal perfusion -> activation of renin angiotensin aldosterone system -> decreased urine sodium concentration
aspirin exacerbated respiratory dz
non IgE mediated pseudoallergic drug rxn to an imbalance between prostaglandins/ leukotrienes
pts have hx of asthma or chronic rhinosinusitis with nasal polyps
bronchospasm and nasal congestion following aspirin ingestion
tx - montelukast (leukotriene receptor antagonist)
goodpastures disease
lung affects - cough, dyspnea, hemopytosis
renal affects - nephritic range proteinuria, acute renal failure, dysmorphic red cells/red cell casts on UA
pathophys - linear . IgG antibodies along glomerular basement membrane (alpha 3 chain type IV collagen antibodies)
management of ARDS involves avoiding complications of mechanical ventilation such as using lung protective strategies =
low tidal volume ventilation –> lower pulmonary pressures –> decrease likelihood of overdistending alveoli and improve mortality
Pathophys behind ARDS being a complication of pancreatitis
increase serum [ ] of pancreatic enzymes such as phospholipase A2 –> cross pulm capillaries –> damaging lungs and cause inflammatory cascade –> leakage of blood and proteinaceous fluid into alveoli –> alveolar collapse due to surfactant loss and diffuse alveolar damage
complication during the post ictal state
hypoventilation - leading to respiratory acidosis
pancoast tumor (superior pulmonary sulcus tumor)
shoulder pain
C8-T2 neuro issues: weakness and/or atrophy of intrinsice hand muscles, pain and parethesias of 4th and 5th digit, medial forearm and arm
weight loss, supraclavicular lymph node enlargement
horners syndrome association
usually squamous cell cancers