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
primary pulmonary hypertension
presentation
middle aged patients
exertional breathlessness
lungs clear to auscultation
dx of primary pulmonary hypertension
CXR - enlargement of pulmonary arteries with rapid tapering of distal vessels, enlargement of RV
ECG - Right axis deviation
centrilobular emphysema
MC type seen in smokers
predilection for upper lung zones
destruction limited to respiratory bronchioles
panlobular emphysema
pts with alpha 1 antitrypsin deficiency
destruction involves both proximal and distal acini
predilection for lung bases
spirometry values in COPD
FEV1/FVC <0.70 (70%)
FEV1 is decreased
TLC is increased
residual volume is increased
chronic bronchitis timeline
chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years
alpha 1 antitrypsin pathophys
destruction of alveolar walls is due to relative excess in protease (elastase) which is released from PMNs and macrophages and is usually blocked by alpha 1 antitrypsin
tobacco smoke increases number of activated PMNs and macrophages as well as inhibits alpha 1 antitrypsin
emphysema pathophys
pink puffer
permanent enlargement of air spaces distal to the terminal bronchioles due to destruction of alveolar walls
No change in oxygen, no hypoxemia
CO2 retention - compensate by:
- increased AP diameter (barrel chested)
- prolonged expirations
airway obstruction spirometry values
nml or increased TLC with decreased FEV1 (amount of air that can be forced out of lungs in 1 sec)
the lower the FEV1 the more difficulty one has breathing
restrictive lung dz spirometry values
FEV1//FVC = nml to high
TLC = low RV = low to normal
COPD - affect on body pH
leads to chronic resp acidosis with compensatory metabolic alkalosis
also FEV1 measurements for COPD pts have the highest predictive value
what are the only interventions in COPD known to decreased mortality
home oxygen therapy
smoking cessation
what drugs are contraindicated in either a COPD exacerbation or asthma exacerbation
beta blockers
complications of COPD
secondary polycythemia (Hct >55% in men or >47% in women)
signs of acute severe asthma attacks
tachypnea diaphoresis wheezing speaking in incomplete sentences use of accessory muscles
paradoxic movement of abd and diaphragm on inspiration is a sign of
impending respiratory failure
PFTs in asthma
decrease FEV1
decreased FVC
decreased FEV1/FVC ratio
increased FEV1 of 12% with albuterol
decreased FEV1 <20% with methacholine or histamine
In an acute setting (ED) what is the quickest method for dx asthma when a pt is SOB
measuring peak flow (peak expiratory flow rate)
during an acute asthma exacerbation if the PaO2 is nml or elevated
pt is getting fatigued and is no longer performing gas exchange since typically asthmatics hyperventilate and blow off CO2 so respiratory failure is imminent
ADR of inhaled corticosteroids
due to oropharnygeal deposition
- sore throat
- oral candidiasis (thrush)
- hoarseness
tx - using a spacer and rinsing the mouth after use
uses for montelukast and cromolyn sodium/nedocromil sodium
prophylaxis for mild exercise induce asthma
complications of asthma
satus asthmaticus - does not respond to standard meds
acute resp failure - due to resp muscle fatigue
pneumothroax, atelectasis, pneumomediastinum
bronchiectasis basics
permanent, abnormal dilation and destruction of the bronchial walls
chronic inflammation airway
airway collapse
ciliary loss/ dysfunction leading to impaired clearance of secretion
causes of bronchiectasis
recurrent infections
cystic fibrosis
kartagnener syndrome
autoimmune dzs
clinical features of bronchiectasis
cough with large amounts of mucopurulent, foul smelling sputum
dyspnea
hemoptysis - due to ruptured blood vessels near bronchial wall surfaces
dx and tx of bronchiectasis
dx - high res CT, obstructive PFT pattern
tx - abx, bronchial hygiene - hydration and chest physiotherapy, inhaled bronchodilators
the main goal of treating bronchiectasis is to
prevent the complications of PNA and hemoptysis
what type of dx is necessary to differentiate non small cell lung cancer to small cell lung cancer t
tissue diagnosis
local invasion signs for lung cancer
Superior vena cava syndrome phrenic nerve palsy recurrent laryngeal nerve palsy horner syndrome pancoast tumor
superior vena cava syndrome
Most commonly occurs with small cell lung cancer
facial fullness
facial and arm edema
dilated veins over anterior chest , arms and face
JVD
phrenic nerve palsy
courses through the mediastinum where it can be destroyed by a tumor
hemidiaphragmtic paralysis
recurrent laryngeal palsy
causes hoarseness
tx of NSCLC and SCLC
NSCLC - surgery if not metastatic along with adjunct radiation
SCLC - combo os chemo and radiation surgery is not indicated as masses are unresectable
calcification signs in lung cancer
eccentric asymmetric calcification - malignancy
dense central calcification - benign
mediastinal masses
MCC in older pts = metastatic masses
anterior - 4 T’s = thyroid, teratogenic tumors, thymoma, terrible lymphoma
middle - lung cancer, lymphoma, aneurysms
posterior - neurogenic tumors, esophageal masses, enteric cysts, bochdalek hernia
clinical features of mediastinal masses
usually asymptomatic unless compressing adjacent structures
- cough - trachea or bronchi compression
- dysphagia - esophagus compression
- SVC syndrome
- hoarseness - laryngeal
- horners - sympathetic ganglia
- diaphragm paralysis - phrenic
dx of mediastinal mass
CT scan is test of choice
if CT suggests benign and pt is asymptomatic - observation is appropriate
causes of transudative pleural effusions
CHF cirrhosis PE Nephrotic syndrome Peritoneal Dialysis hypoalbuminemia atelectasis
causes of exudative pleural effusions
bacterial pneumonia TB (MCC in developing countries) malignancy, Metastatic dz viral infection PE collagen vascular dzs
elevated pleural fluid amylase
esophageal rupture
pancreatitis malignancy
milky, opalescent fluid seen on thoracentesis drainage of pleural effusion
chylothorax - lymph in the pleural space
frankly purulent fluid seen on thoracentesis
empyema - complication of untreated exudative pleural effusion or bacterial pna
tx - aggressive drainage of pleura and abx - recurrence rate is high if severe and persistent rib resection and open drainage might be necessary
bloody effusion seen with thoracentesis
suspect malignancy
parapneumonic effusion
noninfected pleural effusion secondary to bacterial pneumonia
seen as a complication of rheumatoid pleurisy
low pleural fluid glucose
pH < 7.2 - since its exudative
if pleural fluid on thoracentesis has a glucos elevel < 60 suspect
rheumatoid arthritis in your differential
tx of transudative pleural effusion
diuretics and sodium restriction
therapeutic thoracentesis only if massive effusion is causing dyspnea
pneumothorax
air in the pleural space
2 categories: spontaneous and traumatic
spontaneous pneumothorax
without trauma
primary - healthy persion, spontaneous rupture of subpleural blebs (tall, lean, men), high recurrence rate
secondary (complicated) - underlying lung dz (asthma, interstitial lung dz, CF) life threatening due to lack of pulm reserve
presentation of pneumothorax
sudden onset of ipsy chest pain
dypsnea
cough
decreased breath sounds
hyperresonance over chest
decreased or absent tactile fremitus on affected side
clinical features of a tension pneumothorax
hypotension - due to impaired filling of great veins
distended neck veins
trachea shifted
decreased breath sounds
histiocytosis X
interstitial lung disease
caused by abnormal proliferation of histiocytes (related to langerhans cells of the skin)
smokers
dyspnea and nonproductive cough
spontaneous pneumo, lytic bone lesions, diabetes insipidus
wegener granulomatosis
interstitial lung disease
characterized by necrotizing granulomatous vasculitis
upper and lower resp infections
glomerulonephritis and pulmonary nodules
+ c-ANCA
churg strauss syndrome
interstitial lung disease
granulomatous vasculitis seen in pts with asthma
pulmonary infiltrates, rash, and eosinophilia
+ p-ANCA
tx - systemic glucocrticoids
abestosis increases risk for
bronchogenic carcinoma and malignant mesothelioma
causes of hypersenstivity pneumonitis
farmers lung - moldy hay
bird breeders lung - avian droppings
air condition lug
bagassosis lung - moldy sugar cane
mushroom workers lung - compost
severe hypercapnia (and resp acidosis) can lead to
dyspnea
vasodilation of cerebral vessels (with increased intracranial pressure and subsequent papilledema, HA, and coma)
criteria for respiratory failure
hypoxia - PaO2 <60mmHg
hypercapnia - PCO2 >50mmHg
hypoxemic resp failure
low PaO2 with a PaCO2 that is nml or low
- present when O2 sat < 90% despite FiO2 > 0.6
Causes;
- ARDS, severe pna and pulm edema
hypercapnic resp failure
failure of alveolar ventilation
decrease in mute ventilation or
increase in physiologic dead space leads to CO2 retention –> hypoxemia
Causes: CF, asthma, COPD, severe bronchitis
ventilation is monitored by
PaCO2 - to decrease PaCO2 either increase RR or Tidal volume
oxygenation is monitored by
PaO2 - to decrease PaO2 either decrease FiO2 or decrease PEEP
shunting in resp failure
little or no ventilation in perfused areas (due to collapsed or fluid filled alveoli)
venous blood shunted into arterial circulation without being oxygenated
increased CO2 production: DKA, sepsis, hyperthermia
causes of shunting in resp failure
atelectasis or fluid buildup in alveoli (pneumonia or pulmonary edema),
direct R –> L shunt
supplemental oxygen effect on shunt in resp failure
hypoxia due to a shunt is not responsive to supplemental oxygen
clinical features of respiratory failure
dyspnea - first symptom
maybe cough
inability to speak in complete sentences
use of accessory muscles of respiration
tachypnea, tacycardia
cyanosis
AMS
preferred oxygen delivery system in COPD patients
venturi mask - since you can more precisely control oxygenation
NPPV - noninvasive positive pressure ventilation
BIPA or CPAP
indicated in pts in impending resp failure in an attempt to avoid intubation and mechanical ventilation
pts must be neurologically intact, awake, cooperative and able to protect their airway
dx of ARDS
CXR - bilateral infiltrates on imaging
pulm edema not explained by fluid overload or CHF
PCWP < 18mmHg
PaO2/FiO2 ration:
- 200 to 300 - mild ARDS
- 100 - severe ARDS
complications of ARDS
permanent lung injury - lung scarring or honeycomb lung
barotrauma secondary to high pressure mechanical ventilation - pneumothorax or pneumomediastinum
renal failure - may be due to nephrotoxic medications, sepsis with hypotension
always confirm correct ET placement by
listening for bilateral breath sounds
checking post intubation CXR
- tip of ET should be 2-5cm above the carina
two major goals of mechanical ventilation
maintain alveolar ventilation
correct hypoxemia
pts who require mechanical ventilation
significant resp distress
impaired or reduced LOC with inability to protect airway = absent cough or gag reflex
metabolic acidosis - unable to compensate with ventilation
resp muscle fatigue
significant hypoxemia = PaO2 < 70mmHg or hypercapnia PaCO2 >50mmHg
acceptable ABG ranges with mechanical ventilation
PaO2 = 50 - 60 PaCO2 = 40-50
pH = 7.35 - 7.50
criteria for weaning off from ventilator or extubation
intact cough PaO2/FiO2 >200 PEEP of < 5cm FiO2 <40% RR < 35 minute ventilation < 12
high levels of PEEP increase the risk for
barotrauma (injury to airway = pneumothorax)
+
decreased cardiac output (decreased venous return form increased intathoracic pressure
complications of mechanical ventilation
agitation, anxiety, discomfort
difficulty with tracheal secretions
ventilator associated PNA
barotrauma
tracheomalacia (softening of the tracheal cartilage) due to prolonged presence of ET
when a pt is ventilator dependent for 2 or more weeks a
tracheostomy is performed to prevent tracheomalacia
pulmonary HTN
mean pulmonary arterial pressure > 25mmHg at rest
causes of pulmonary HTN
passive - due to resistance in pulm venous system (LHF, mitral stenosis, atrial myxoma)
hyperkinetic (L –> R cardiac shunt, ASD, PDA)
obstruction (PE, pulm artery stenosis)
pulmonary vascular obliteration (collage vascular dz)
pulmonary arterial HTN
idiopathic, familial
young or middle aged women
abnormal increase in pulmonary arteriolar resistance leads to thickening of pulmonary arteriolar walls
clinical features of pulmonary HTN
dyspnea on exertion
fatigue
chest pain - exertional
syncope - exertional
dx of Pulmonary HTN
loud P2
ECG - RVH and RAD
CXR - enlargend pulm arteries
echo - dilated pulm artery, dilated RA, hypertrophied RV
increase pulmonary artery pressure > 25mmHg
dx of cor pulmonale
CXR - enlargement of RA, RV, and pulm arteries
ECG - RAD, RVH
echo - RV dilatation, nml LV size and function
sources of emboli to the lungs other than the traditional traveling thrombus
fat embolism - long bone fx
amniotic fluid embolism - during or after delivery
air embolism - trauma to thorax, indwelling venous/arterial lines
septic embolism - IV drug use
schistosomniasis
complications of PE
recurrent PEs
pulmonary HTN - in 2/3 of pts
risk factors for PE
age >60
malignancy
prior DVT/PE
hereditary hypercoagulable states - factor V Leidin, protein C and S def, antithrombin III deficiency
prolonged immobilization obesity major surgery (especially pelvic) major trauma pregnancy (OCPs)
sources of emboli
LE - DVTs - iliofemoral DVT
UE - DVT - rare - may be seen in IV drug users
clinical features of a PE
dyspnea
pleuritic chest pain
cough/ hemoptysis
tachypnea, tachycardia (leads to resp alkalosis)
rales
dx of PE
CTA - showing intraluminal filling defects in central, segmental, or lubular pulmonary arteries
[cant be used if pt has renal insufficiency]
+ pulmonary angiogram - definitively proves PE
what dx test and results can rule out a PE
negative (-) D-dimer and low clinical suspicion
low probability V/Q scan and low clinical suspicion
negative pulmonary angiogram (definite)
modified wells criteria
symptoms and sign of DVT = 3.0
alternative dx less likely than PE = 3.0
heart rate > 100 bpm = 1.5
immobilization (>3days) or surgery in prev 4wks = 1.5
previous DVT/PE = 1.5
hemoptysis = 1.0
malignancy = 1.0
score < 5 = unlikely PE
score > 4 = PE likely
contraindications to heparin
active bleeding
uncontrolled HTN
recent stroke
Heparin induced thrombocytopenia (HIT)
tx of aspiration pneumonia
clindamycin (has anaerobic activity)
differential dx of hemopytsis
bronchitis
lung cancer (bronchogenic carcinoma)
TB
bronchiectasis
goodpasture syndrome
Aspergilloma within cavities
nml ABG values
pH = 7.35 - 7.45 PaO = 90 (decreases with age) PaCO2 = 35-45
DLco mechanism
measures the surface area of the alveolar capillary membrane
useful in monitoring conditions such as sarcoidosis and emphysema
causes of low DLco
emphysema
sarcoidosis
interstitial fibrosis
pulmonary vascular dz
lower with anemia
causes of high DLco
asthma obesity intracardiac L --> R shunt exercise pulmonary hemorrhage
if hemoptysis is severe consider
bronchial artery embolization or balloon tamponade of the airway
bronchogenic cysts
middle mediastinum masses
benign
best seen on CT scan
thymoma
anterior mediastinum mass
young male or female
strong association with myasthenia gravis
neurogenic tumors
esophageal leiomyomas
located in posterior mediastinum
indications for noninvasive positive pressure ventilation
COPD (severe exacerbation)
Cardiogenic pulmonary edema
acute resp failure
contraindications for NPPV
inability to protect airway cardiac or respiratory arrest severe acidosis pH < 7.10 ARDS recent esophageal aneursym
pulmonary contusion
presentation
and
dx
< 24hrs after blunt thoracic trauma
tachycardia, tachypnea,
hypoxia
dx - rales, decreased breath sounds, CT or CXR - with patchy, alveolar infiltrates not restricted by anatomical borders
fat embolism
develop resp distress
neurological abnormalities
petechial rash
following a latent period of 12-72hrs after injury
invasive aspergillosis
risk factors and presentation
risk factors - immunocompromised (neutropenias, glucocorticoids, HIV)
triad - fever, cp, hemoptysis
invasive aspergillosis
dx and tx
dx - CXR/ CT - pulmonary nodule with surrounding ground glass opacities (halo sign)
+ cultures
+ cell wall biomarkers (galactomannan, beta D glucan)
tx - voriconazole +/- capsofungin
chronic aspergillosis
risk factors and findings
risk factors - lung dz/damage [cavitary TB]
findings = > 3months - weight loss, cough, hemoptysis, fatigue
chronic aspergillosis
dx and tx
dx - cavitary lesions +/- fungus ball
+ aspergillosis IgG serology
tx - resect, azole meds, embolization if hemoptysis is severe
what decreases the mortality rate of an acute PE
early and affective anticoagulation - should be initiated prior to dx tests being performed - unless a contraindication is present
interstitial lung dz PFTs
TLC
FEV1/FVC
DLco
TLC - decreased
FEV1/FVC - nml or increased
DLco - decreased
COPD PFTs
TLC
FEV1/FVC
DLco
TLC - increased
FEV1/FVC - decreased
DLco - decreased
ASTHMA PFTs
TLC
FEV1/FVC
DLco
TLC - nml/increased
FEV1/FVC - decreased
DLco - nml/increased
Restrictive PFTs
TLC
FEV1/FVC
DLco
TLC - decreased
FEV1/FVC - increased or nml
DLco - nml
DLco in pulmonary artery HTN
decreased
why is the glucose [ ] in an empyema low
due to high metabolic activity and/or leukocytes (and/or) bacteria in the fluid that metabolize the glucose
3 mechanisms for transudative pleural effusion
increased hydrostatic pressure
decreased oncotic pressure
decreased intrapleural pressures
compensatory metabolic alkalosis can lead to what lab affects
decreased Cl- concentration due to bicarbonate retention
both nonallergic rhinitis and allergic rhinitis are managed with
intranasal glucocorticoids
difference between the 2 is that allergic rhinitis pts can ID their trigger and present earlier
exudative pleural effusion mechanisms
increased capillary permeability
pleural membrane permeability
disruption of the lymphatic outflow
chlorpheniramine
H1 antihistamine receptor blocker
decreases allergic response
anti inflammatory -> reduced nasal secretions by limited the secretory response to inflammatory cytokines
histoplasma capsulatum
central, midwestern, and northeastern US
ppl who go in caves who are at increased risk for bat and bird droppings
Coccidiomycosis
Arizona
CP, fatigue, cough and fever
CXR - nml unilateral infiltrate with ipsy hilar lymphadenopathy
biopsy endospores and spherules
bronchiectasis confirmed via
high resolution CT scan
cough with daily mucopurelent sputum production
empiric tx of CAP
outpatient
macrolide or doxycycline (healthy pt)
floroquinolone or beta lactam + macrolide (pt with comorbidities)
empiric tx of CAP
(inpatient)
+
(inpatient in ICU)
inpatient - fluoroquinolone (IV) or beta lactam + macrolide (IV for both)
ICU pt - beta lactam + macrolide (IV) or beta lactam + flouroquinolone (IV)
management of SIADH
fluid restriction +/- salt tablets
hypertonic (3%) saline
granulomatosis with polyangitis
presentation
upper resp issues - sinusitis, saddle nose
lower resp issues - lung nodules/ cavitations
+
renal issues - rapidly progressing glomerulonephritis
skin - non healing ulcers
granulomatosis with polyangitis
dx and tx
dx - CXR - necrotizing pulmonary vasculitis
ANCA - PR3, MPO
leukocytoclastic vasculitis
pauci immune GN
granulomatous vsculitis
tx - corticosteroids + immunomodulators
CO2 retentions leads to what affect on cerebral vasculature
cerebral vasodilation –> seizures, stroke, AMS
complication of pneumocysitis in HIV pts
SIADH - –> decreased Na which can be further worsened by nml saline bolus
CREST syndrome
Scleroderma
C- calcinosis R- raynauds phenomenom E- esophageal dysmotility S-sclerodacytl T- telengiectasias
pathophys of PAH
intimal hyperplasia of pulmonary arteries
progressive dyspnea, exertional syncope, lighthedness –> due to RV failure
alveolar spaces filled with fibroblasts are consistent with
interstitial lung dz
bronchial wall thickening with mucous plugs is consistent with what dx
bronchiectasis
drug induced SLE meds
procainamide
isoniazide
hydralazine
during an acute asthma attack if the PaCO2 begins to normalize or increase
it is a sign of impending resp failure because typically these pts are tachypneic and should be breathing off a lot of CO2 but now they are fatigued and their breaths are not performing gas exchange
exercise induced asthma tx
SABA - such as albuterol 10-20 min before exercise
pH of transudative pleural effusion vs exudative pleural effusion
transudative pleural effusion - pH 7.40 - 7.55
exudative pleural effusion - pH 7.30-.7.45
physical exam findings of lobar pneumonia
increased breath sounds (Crackles and egophony)
increased tactile fremitus
dullness to percussion
physical exam findings of a pleural effusion
decreased breath sounds
decreased tactile fremitus
dullness to percussion
physical exam findings of emphysema
decreased breath sounds
decreased tactile fremitus
hyperresonant to percussion
mediastinum shifting affected by atelectasis
mediastinum will shift towards the side with a large amount of atelectasis
decreased breath sounds
decreased tactile fremitus
dullness to percussion
how does alveolar consolidation in PNA causes hypoxemia
due to R –> L intrapulmonary shunting
dead space ventilation
ventilation of areas of the lung that are not perfused with blood
(ex: PE)
high PaCO2 and low PaO2 levels are suggestive of
alveolar hypoventilation
alveolar gradient formula =
PAO2 - PaO2
CXR showing loculation –>
parapneumonic effusion and empyemas - exudative pleural effusion
high protein - <60 glucose - low pH
development of clubbing and sudden onset joint arthropathy in a chronic smoker is suggestive of
hypertrophic osteoarthropathy - typically associated with cancer so need to perform a CXR to r/o malignancy
Oxygenation of a pt with PaO <60 can be improved by
Increasing FiO2 - usually weaned <60% to avoid O2 toxicity
increased PEEP
- improves mortality in pts with ARDS
dont increase tidal volume as it can lead to increased risk of barotrauma
tx of PE in pts with GFR <30
unfractionated heparin - preferred over LMWH
this is because in renal insufficiency there is reduced clearance of anti Xa leading to increased activity –> increased bleeding risk
mainstay tx of COPD
inhaled antimuscarinic agents
tx of post nasal drip (upper airway cough syndrome)
oral first generation antihistamines
theophylline toxicity
CNS - HA, insomnia, Szs
GI - N/V
Cardiac - arrhythmias, palpitations
Most Common ADR of inhaled corticosteroids therapy
oropharyngeal thrush (oral candidiasis)
complications of positive pressure ventilation
alveolar damage
pneumothorax
hypotension
MCC of cor pulmonale
COPD
causes of increased plateau pressure
pneumothroax
pulm edema
PNA
atelectasis
ADR of beta 2 agonists (albuterol)
reduce K+ levels by driving K+ into cells –> hypokalemia -
- –> muscle weakness, arrhythmias,
- –> EKG changes, tremors, palpitations, HA
Acute PE - pressures
NML PCWP
increased RA pressure
increased pulmonary artery pressure
causes of recurrent PNA in the same location
extrinsic bronchial compression (neoplasm, adenopathy)
intrinsic bronchial obstruction (bronchiectasis, FB)
recurrent aspirations: szs, alcohol, drug use, GERD, dysphagia
workup = CT scan
acute bronchitis
cough > 5days to 3wks (+/- purulent sputum)
preceding resp illness (90% viral)
absent systemic findings (fever, chills)
wheezing or ronchi
chest wall tenderness
dx and tx of acute bronchitis
CXR only if PNA suspected
tx - symptomatic tx - NSAIDs and/or bronchodilators
