Respiratory Flashcards
How much do you expect pH to decrease with increase in CO2?
decrease 0.08 for every 10 mmHg CO2 rise
Infectious insult + Impaired bacterial clearance = dyspnea, hemoptysis, daily mucopurulent sputum, crackles, wheezing
Bronchiectasis
Etiologies of bronchiectasis
- cancer (airway obstruction)
- autoimmune (RA, Sjogrens)
- Aspergillosis, TB
- Hypogammaglobulinemia
- CF, a1at def (congenital)
most common causes of digital clubbing
- Cystic Fibrosis
- Lung Malignancies
- R to L cardiac shunts
most common adverse effect of inhaled steroids
oral thrush
Triad in obesity hypoventilation syndrome
- obesity
- hypercapnia (daytime)
- alveolar hypoventilation (hypoxmia/resp acidosis)
causes of transudate pleural effusions
CHF
Cirrhosis
Nephrotic Syndrome
Peritoneal dialysis
causes of exudative effusions
Infections
Malignancy
Pulmonary Embolism
Connective tissue dz
Inflammatory dz
Fluid from abdomen
CABG
Light’s criteria for exudative effusions
Having at least 1 of the following
Pleural fluid/serum ratio’s:
- -Protein >.5
- -LDH>.6
- -Pleural Fluid LDH > 2/3 of upper limit normal serum LDH
most common cause of pleural effusion
CHF (and thus transudative)
pt has severe asthma exacerbation with impending resp distress. why is a normal/elevated CO2 a poor sign?
asthma exac causes hyperventilation/increased resp drive = decreased CO2. if elevated/normal, shows respiratory muscle fatigue –> inability to meet respiratory demands.
–>these patients require intubation
whats the difference between enoxaparin, rivaroxaban, and fondaparinux?
Enoxaparin = LMWH Rivaroxaban = Oral Factor X inhibitor Fondaparinux = Injection Factor X inhibitor
None of these can be used in patients with poor renal f(x), use unfractionated heparin instead
Why do you need a heparin bridge before warfarin?
Warfarin inhibits Protein C and S, which are anti-thrombogenic..= state of thrombosis (heparin is anti-thrombin)
Criteria for ARDS (4)
- Acute onset (<1 week)
- Bilateral infiltrates on chest imaging
- Pulm edema not explained by fluid overload or CHF (i.e. PCWP <18) –>NONCARDIOGENIC PULM EDEMA
- Abnormal PaO2/FiO2 ratios (<300)
Pathophys behind ARDS
Massive Intrapulmonary shunting of blood, secondary to atelectasis, alveolar collapse and surfactant dysf(x)
–> Increase in lung fluid = stiff lungs, A-a gradient, ineffective gas exchange
Severe hypoxemia that does not improve on 100% oxygen
ARDS
an increase in ____________ causes ARDS, vs _____ causes cardiogenic pulmonary edema
Alveolar capillary permeability (ARDS)
Congestive Hydrostatic Forces (CHF/HF)
T/F: ARDS will have increase in lung fluid and signs of JVD, edema, hepatomegaly
False. ARDS will have increase in lung fluid without any of those cardiogenic signs
Patients with _____ have the highest risk of developing ARDS
sepsis/septic shock
T/F: Pulmonary vasodilators (nitroprusside) help improve tissue oxygenation
False…they should be removed in states of hypoxia
Does ARDS have respiratory alkalosis or acidosis?
Initially have Alkalosis (PaCO2 <40), which switches to acidosis as the work of breathing increases and thus PaCO2 rises
what is the most useful parameter in distinguishing ARDS from cardiogenic pulmonary edema?
PCWP…this refelcts Left heart filling pressures and indirect marker of intravascular V status….<18 points to ARDS
MAP> ____ (at rest) = Pulm HTN
25
clinical signs of pulmonary htn
- Loud P2 (pulmonic component of S2)
- Subtle lift of sternum (RV dilatation)
- if RV failure occurs, will show JVD/hepatomeg/edema etc
how will EKG/Echo help assist in dx of Pulm HTN?
Pulm HTN can lead to RV failure…
-EKG will show RV hypertrophy (Right axis deviation/right atrial abnormality)
-ECHO = dilated pulm artery, dilatation of RA and RV, abnormal movement of ventricular septum
which vasoactive agents can be used in tx of PAH (after R heart cath and trial of vasodilators tried first)
They lower pulm vascular resistance
- PDE inibitors (sildenafil)
- CCB
- Prostacyclins (Epoprostenol)
- Endothelin receptor antagonists (bosentan)
what is cor pulmonale usually secondary to?
COPD!
Defined as RV hypertrophy/failure from pulm htn secondary to pulm disease
PE/Asthma/CF/OSA/ILD also can cause it
Clinical features of cor pulmonale
- decrease exercise tolerance
- Cyanosis and digital clubbing
- RV failure (JVD, edema, hepatomegaly)
- Parasternal lift (RV dilatation)
why is there tachypnea in PE ?
PE causes dead space in areas of the lung because there is ventilation but no perfusion (dec blood flow)
–> causes Hypercarbia and Hypoxemia, which drive respiratory effort
T/F: Most often, PE is clinically silent
True
–>Recurrences are common, leading to chronic pulm HTN and cor pulmonale
What causes most PE-related deaths?
Recurrent PE within first few hours of inital PE…tx with anticoagulatns decreases mortality
Signs of PE
-Tachypnea, Rales, Tachycardia, S4, Increased P2
PaO2 and PaCO2 levels in PE?
Both are low…PaCO2 is low due to hyperventilation (because dec perfusion= hypoxemia and hypercarbia = stimulation to respiratory drive)
=Resp ALKalosis
Initial study of choice for PE
CTa (spiral ct)…only contraindicated if renal dz, for whom V/Q scan works well
Pulmonary angiography = gold standard, but is invasive (rarely performed)
PE clinically likely, do a ______study
PE clinically unlikely, do a ______ study
likely: Spiral CT. if inconclusive, LE ultrasound
Unlikely: D-Dimer. If abnormal, Spiral CT
what should you consider as long term prevention in a patient who had PE but has CI to anticoagulation
IVC filter
Tx for PE
- Heparin drip: start as soon as their is any clinical suspicion (prevent recurrent PE)
- Oxygen
- Consider thrombolytic therapy (not always given tho)
- Consider IVC filter if anticoag CI
where is aspiration most likely to go?
lower portion RUL
upper portion of RLL
most common causes of acute dyspnea
CHF exacerbation pneumonia bronchospasm PE anxiety
causes of high DLCO
- Asthma (increases pulm capillary blood V)
- Obesity
- Intracardiac L-R shunt
- Exercise
- Pulmonary hemorrhage
causes of low DLCO
- Emphysema
- Sarocoidosis
- Fibrosis
- Pulmonary vascular dz
- Anemia (reduced binding of CO to Hgb)
For every 10mm Hg change in PaCO2, there should be a change in pH by ___
.08
- if change is in same direction as change in PaCO2, its metabolic
- if inverse, respiratory
T/F: Restrictive dz has reduced FEV1 and reduced FEV1/FVC ratio
False.
Restrictive has reduced FEV1.
However, ratio is actually normal or increased because of FVC decrease
signs of ILD
- Inspiratory crackles, digital clubbing
- Progressive exertional dyspnea, persistent dry cough
- CXR = reticular/nodular opacities
Pulmonary function tests in ILD
- normal or increased FEV1/FVC
- decreased DLCO
- decreased TLC
- decreased RV
will also see increased A-a gradient
What is the pathophys behind changes to A-a gradient and DLCO in ILD (i.e. pulmonary fibrosis)?
Get peri-alveolar collagen deposition
=decreased gas exchange (A-a) and reduced diffusion capacity of CO
Tx of SIADH
FLUID RESTRICTION +/- salt tablets
Hypertonic saline is only used for severe hyponatremia (sxs of coma, seizure, etc)
Progressive exertional dyspnea + dry cough
ILD ILD ILD ILD ILD ILD ILD ILD
Low FEV1/FVC ratio + increased or decreased DLCO
Low ratio = Obstructive dz
Increased DLCO = Asthma (inc. pulm capillary blood V)
Decreased DLCO = COPD
Normal/high FEV1/FVC ratio + increased or decreased DLCO
Normal/high ratio = Restrictive dz
Increased DLCO = Chest wall weakness
Decreased DLCO = ILD
why is there pulmonary hypertension in ARDS?
hypoxic vasoconstriction
2 ways by which oxygenation can be improved in ARDS pt
- Increasing fraction of inspired O2 (FiO2)
- PEEP (via mechanical ventilator)
–>You want to wean FiO2 to <60% asap to avoid risk of oxygen toxicity (free radicals), so once you’re higher than this you should increase PEEP
most common trigger of COPD exacerbation
URI
Why is FVC decreased in COPD
Air Trapping due to progressive airflow limitation
solitary nodule > ____ likely malignancy
2cm
most common primary lung cancer in smokers and nonsmokers
Adenocarcinoma
non-allergic vs allergic rhinitis
Allergic: predom eye sxs, itching, sneezing, identifiable triggers
NAR: Predominant nasal congestion w/o obvious triggers. antihistamine or glucocorticoids.
in patient tx for CAP (esp in pt >65)
Fluoroquinolone or beta lactam/macrolide (cef/azithro)
Name the mediastinal mass by location:
- Anterior mediastinum
- Middle
- Posterior
Anterior: THYMOMA, retrosternal thyroid, teratoma
Middle: Bronchogenic Cyst, Aortic arch aneurysm
Posterior: all neurogenics i.e. neuroblastoma, esophageal tumor
t/f: panacinar emphysema of a1-antitrypsin def is present diffusely throughout the lungs
false, it is predominantly in the lower bases (vs smoking emphysema which is in upper lobes). Presents in 30-40s
Whats the next step if you suspect CAP based on sxs (few days of fever, cough, and crackles on exam)?
Need CXR to make dx!! Then you can do empiric antibiotics (don’t need cultures)
3 most common causes of chronic cough
- Upper-airway cough syndrome (POSTNASAL DRIP)
- ->responds to anti-histamines - Asthma
- GERD
Simple rule of thumb for pleural effusions (exudative vs transudative)
Transudative: Organs failure…heart (chf), liver (cirrhosis, low albumin), lung (PE, atelectasis), kidneys (nephrotic, low albumin)
Exudative: Infectious, Cancerous (ICE ICE Baby)
If someone has a parapneumonic effusion, what should you be looking out for?
Empyema. Look for a pt who has received antibiotics but continues to be ill.
Empyema vs parapnuemonic effusion
- pH
- Glucose
- Protein
- wbcs
Parapneumonic: Glucose dec, protein inc, pH >7.2, wbc <50k
Empyema: Glucose dec, protein inc, pH <7.2, wbc >50k
orthostatic hypotension usually presents in elder patients, due to _______ ; which lab value should you follow?
Hypovolemia Urine Na (hypovolemia = dec renal perfusion = RAAS = decreased urine Na)
classic triad of fat emboli
Hypoxemia
NEURO dysf(x)
RASH
Why would an asthmatic have elevated wbc’s after an acute exacerbation?
Most likely will get some glucocorticoid therapy, which causes leukocytosis (by released marginated neutrophils)
most common complications of PEEP (i.e. pt in ARDS put on PEEP)
PNEUMOTHORAX
ALVEOLAR DAMAGE
HYPOTENSION
t/f: you suspect PE in a pt, next step is CTa
False, next step is heparin drip! and then CTa
CT findings PE
WEDGE SHAPED infarction = pathogneumonic (don’t call it cancer kid!)
describe why R-L intrapulmonary shunting occurs with pneumonia
Alveoli filled with inflammatory exudate = impaired alveolar ventilation in that portion of lung = R to L shunting, meaning perfusion of lung tissue in absence of alveolar ventilation (extreme V/Q mismatch)
–>characteristically cannot improve hypoxemia with increased FiO2 (due to shunting)
Patient with urticaria and acute-onset difficulty breathing
Laryngeal Edema = Upper Airway Obstruction!!! aka allergic rxn son
Features that make a solitary pulmonary nodule more likely to be malignant
- pt’s age (>50)
- hx of smoking
- > 2cm
- Irregular borders
- Eccentric asymmetric calcification (vs dense, central calcification = benign)
- enlarging
if suspicious for malignancy, BIOPSY/RESECTION
low probability: serial CT scan
Intermediate probability nodule 1cm or larger: PET scan
initial mgmt of acute COPD exacerbation
short acting bronchodilator, glucocorticoids, antibiotic
–>if sxs persist, go to Non-invasive PPV (facemask support instead of intubation)
pathophys behind atelectasis causing pleural effusion
Decreased intrapulmonary effusion (transudative)
other transudative pathophys = increased hydro P (CHF) or dec plasma oncotic p (nephrotic)
what is a positive bronchodilator test for asthma (quantitatively)?
> 12% improvement of FEV1 post-bronchodilator
T/F: Breath sounds and tactile fremitus are decreased with consolidation and pleural effusion
False!
They are increased with consolidation
They are decreased with pleural effusion
Examples of resonance, dullness, and hyperresonance with percussion of lung
Resonant: Normal Lung
Dull: Consolidation, Pleural Effusion, Atelectasis (mucus plugging)
Hyperresonant: Emphysema, Pneumothorax
3 clinical sxs of asbestosis
Progressive dyspnea
Digital Clubbing
End-inspiratory crackles
PFT of asbestosis
Restrictive pattern: decreased lung volume, decreased DLCO, normal FEV1/FVC
Cancer in asbestos patient
Bronchogenic cancer»_space;»> Mesothelioma
Major difference btwn chronic bronchitis and bronchiectasis (both have coughing up of mucus)
CB: Mucus narrows the airways. Seen in smokers, older age.
Bronchiectasis: persistent, abnormal dilation of bronchial walls. Might be a younger patient who doesn’t smoke, signs of cystic fibrosis
most common cause of hemoptysis
Bronchitis lmao fam
In acute COPD exacerbation, do you use inhaled or systemic glucocorticoids?
Systemic!
Inhaled steroids are for long-term albuterol tx; for COPD, dec exacerbation frequency/sxs for do not play a role in acute exacerbation.
cardinal sxs of acute COPD exacerbation
increased dyspnea
increased cough
sputum production (change in volume/color)
–>give antibiotics if at least 2 of these present
T/F: Secondary malignancy is common in patients with Hodgkins lymphoma tx w/chemo and radiation
True
Where does an aspergilloma collect/form?
Previous cavitary lesion
Assist Control (AC) mode delivers a predetermined ____ ____ with every breath
Tidal Volume (6ml/kg body wt)
Hemoptysis + chest pain on inspiration in patient on OCP and recent travel
Pulmonary Embolism (with likely pulm infarction)
Fever, chest pain, and hemoptysis with pulmonary nodules with ground-glass opacities surrounding
Invasive aspergillosis (non-cavitary lesion; seen in transplant, immunocomp, or AIDS patients) -->CT findings = Halo Sign (PCP unlikely with hemoptysis)
lots of cough with production of sputum. How can you tell based on responsiveness to medications and smoking status if its bronchitis or bronchiectasis?
Bronchitis is usually exacerbated by viral infections. Usually a smoker.
Bronchiectasis is usually from recurrent bacterial infections and is responsive to antibiotics. usually a non-smoker.
T/F: CXR is the best dx test for bronchiectasis
False, need high-resolution CT.
CXR will show linear atelectasis, dilated/thickened airways, irregular peripheral opacities.
Increased permeability of the right hemidiaphragm in cirrhosis patients leading to pleural effusion =
Hepatic hydrothorax
low glucose concentrations in empyema are due to:
high metabolic activity of wbcs and/or bacteria
Empyemas and parapneumonic effusions are _____ effusions
exudative
_________ effusions are due to pleural and lung inflammation
Exudative
Patients with COPD are candidates for home oxygen therapy when:
SaO2<88% or PaO2<55mmHg
Obesity and malignancy as risk factors for _______ in a patient with dyspnea and chest pain
Pulmonary Embolism
carcinoma in the apex of the lung that can lead to shoulder/arm pain, hoarseness, and Horner’s syndrome
Pancoast tumor (Superior sulcus tumor) -->typically a squamous cell lung cancer or adenocarcinoma (SMOKERS)
Why would a patient treated for acute asthma exacerbation develop muscle weakness and tremors?
Beta-agonists (albuterol) can cause hypokalemia = muscle weakness, EKG changes, arrythmias, tremors, palpitations, HA
JVD and RBBB on EKG developing few days after operation
Massive pulmonary thromboembolism…PE causing Right heart failure
noncardiogenic pulmonary edema
ARDS
causes of ards
- infection
- trauma
- transfusion
- pancreatitis
tx of ARDS
ventilation: high PEEP, low tidal volume, high FiO2
what is cough in ACE-I due to?
increased substance P, kinins, PGs, Txa2
T/F: Consolidation presents with decreased breath sounds, dullness to percussion
False, dullness to percussion but INCREASED breath sounds…will hear egophany, tactile fremitus etc
PE findings of consolidation vs pleural effusion vs pneumothorax
Consolidation: breaths sounds inc; tactile frem inc; dull
effusion: dec/absent breath sounds; dec tf; dull
pneumo: dec/absent breath sounds; dec tf; hyperresonant
PE findings of emphysema and atelectasis (mucus plugging)
Emphysema: breath sounds dec; tactile frem dec; hyperresonant
Atelectasis: breath sounds dec; tf dec; dull
lung cancer, gynecomastia, galactorrhea
large cell
T/F: JVD on expiration = kussmaul sign = constrictive pericarditis/RCM
False. Kussmaul = jvd on INSPIRATION. JVD on expiration seen in COPD etc
T/F: Infusion of saline may worsen hyponatremia in a patient with SIADH
True (tx is usually fluid restriction)
Why do we tx ARDS patients (tx: ventilation with PEEP) with the tidal volume low?
Low tidal volume prevents overdistention of the alveoli ( a complication of ventilation). this improves mortality
T/F: Pleuritic chest pain is not a feature of pneumonia
False
signs of invasive aspergillosis
-Triad: Chest pain, Fever, Hemoptysis
-Imaging: Solitary nodule with halo sign
cell markers (beta-d-glucan, galactomannan)
causes of low DLCO
Obstructive: Emphysema
Restrictive: ILD; sarcoid, asbestosis, HF
Normal: anemia, PE, Pulm htn
causes of high DLCO
Obstructive: Asthma (can also be normal)
Restrictive: obesity
Normal: pulm hem; polycythemia
normal DLCO
Obstructive: chronic bronchitis, asthma
restrictive: MSK deformity; neuromuscular dz
Smoker with productive cough, DOE, PFT: dec FEV1, normal FVC, dec ratio, normal DLCO
Chronic bronchitis
Why is DLCO normal in chronic bronchitis?
DLCO measures gas exchange btwn alveoli and pulm capillaries. CB has no destruction of alveoli (vs emphysema).( However, CB patients may have worse hypoxemia than E. )
Why is DLCO low in emphysema?
DLCO measures gas exchange btwn alveoli and pulm caps. Emphysema causes destruction of alveolar walls, so decreased diffusion capacity.
CXR dif btwn emphysema and chronic bronchitis
Emphysema: Hyperinflated lungs, dec lung markings
CB: Flattened diaphragm, inc lung markings
T/F: CB is associated with more predominant mucus production than bronchiectasis
False, my mneumonic for CB is misleading. Bronchiectasis is associated with literally buckets of mucus, CB can have mild production
Low FVC (due to airway destruction from repeated infx), dilated conducting airways on CXR, chronic recurring and resolving episodes of lung infection with high amounts of sputum. May have hemoptysis/fever/clubbing
Bronchiectasis
Shoulder pain and Horner’s in a smoker
Pancoast
what are the features of a pancoast tumor?
- horners
- shoulder pain
- c8-t2 involvement: weakness/atrophy of intrinsic hand muscles; pain/paresthesias of 4th/5th digits, medial arm and forearm
- Supraclavicular LN
- weight loss
elevated right atrial pressure, elevated pulmonary artery pressure, normal PCWP in a patient presenting with chest pain/shock/syncope
PE
Wells criteria for PE
+3: signs of DVT
+1.5: hx of PE/DVT; HR>100; recent surg/immob
+1: Hemoptysis; cancer
> 4: PE likely
Empyemas are ___ pleural effusions with ____ glucose due to _____
exudative; low; wbc activity/bacteria
Patient has DOE and CXR shows pleural effusion. What’s the dx standard and when would you do something different?
Diagnostic thoracentesis –> determine whether it is transudative (tx underlying cause) or exudative.
Only time you don’t do this is if you suspect CHF…then, you do ECHO and trial of diuretics.
3 biggest causes of malignant pleural effusions (exudative)
Lung carcinoma, Breast carcinoma, Lymphoma
T/F: Next best step in all pleural effusions = diagnostic thoracentesis
False. This is USUALLY the best next step.
Exception: if the patient has CHF, you do ECHO and diuretics instead
T/F: A patient with 6months of productive cough with mucus and obstructive PFTs likely has chronic bronchitis
False. Need at least 3 consecutive months in 2 successive years
When should you consider A1AT def?
- young patient with COPD
- COPD with minimal smoking hx
- FHx of emphysema or liver dz
- ->LFTs may not be elevated until very late in the dz so don’t be a peasant
airway hyperreactivity is associated with:
asthma
3 most common causes of chronic cough (>8 weeks)
- Post-nasal drip (upper-airway cough syndrome), i.e. allergic rhinitis etc. Improves with H1 blockers (chlorpheniramine)
- Asthma
- GERD
what kind of pleural effusions does a PE cause?
Exudative…usually hemorrhagic or inflammatory. Grossly bloody and painful.
Asthmatic patients typically have a respiratory ______, with ____pCO2
alkalosis; low pCO2 due to hyperventiilation
–>elevated/normal pCO2 indicate increasing severity
Assist control ventilator mode determines a predetermined ____ with every breath
tidal volume (should be 6ml/kg body wt) -->patient can breathe on their own, but if they don't have a minimum resp rate, then that tidal volume is delivered
development of digital clubbing and joint pain (acute onset) in a smoker
Hypertrophic osteoarthropathy (get a CXR). Usually ass. w/underlying lung dz like lung cancer, TB, bronchiectasis, emphysema etc
T/F: All pleural effusions need drainage (i.e. chest tube)
False.
Small ones do NOT need therapy. Use diuretics…especially if CHF related
Large ones , especially infection related (parapneumonic/Empyema!) need a chest tube
What are the options for a recurrent pleural effusion despite chest tube drainage?
Pleurodesis: infuse irritative agent (bleomycin/talcum powder)
Decortication: stripping of pleura from lung
Exudative pleural effusion with low pH (<7.2) and low glucose (<60)
Parapneumonic or Empyema
uncomplicated vs complicated parapneumonic pleural effusions (exudative)
Un: pH>7.2, Glucose >60, wbc <50K, Tx = ABx
C: pH<7.2, Glucose <60, wbc>50k, Tx= drainage (chest tube) and ABx
T/F: Wedge shaped infarct on imaging = PE
True
most common tumors causing Pancoast (superior sulcus) tumor
Squamous cell
Lung adenocarcinoma
T/F: COPD decreased total lung volume, functional residual capacity, and residual volume
false, it actually increases all of these (think increased AP diameter)
Patient with a hx of asthma/chronic sinusitis w/nasal polyps should be careful of _______ potentially causing ____-exacerbated respiratory disease
Aspirinx2, causes nasal congestion/bronchospasm. Avoid NSAID, give LT-R blockers (montelukast)
T/F: In a patient with a hx of asthma and current episode of respiratory distress, absence of wheeze is a positive sign
False, sign of impending resp failure
What levels of FiO2 do you not really want to be above?
Worried about oxygen toxicity when >60%. It can be higher but wean down to below this asap. If patient is having problem with oxygenation, increase PEEP instead.
A-a gradient bullshit
PAO2 = 150 - (PaCO2/.8)
PAO2 - PaO2 = A-a gradient: normal is 10-15.
Increased A-a = V/Q mismatch (PE is a big one), R-L shunt, diffusion limitation
Normal A-a and hypoxemia= hypoventilation, altitude
Tx for hospitalized CAP patient
Either: 1. Beta lactam + Macrolide (ceftriaxone + azithromycin) or 2. Fluoroquinolone (moxifloxacin)
how do you decide if CAP patient needs hospitalization?
Confusion Urea>20 RR>30 BP<90/60 65: (age older than this) Score 0 = outpatient 1-2 = likely inpatient 3-4 = urgent inpatient possibly ICU
What does pulmonary infarction in the setting of PE cause?
Pleuritic pain and hemoptysis (through inflammation and occlusion of peripheral artery)
complications of positive pressure ventilation
- alveolar damage
- PNEUMOTHORAX
- hypotension
Post-op patient with hypotension, distended JVP, and new-onset RBBB
PE
T/F: PE patients usually have tachypnea, tachycardia and hypoexmia, sometimes have loluidw grade fever
true
T/F: Pulmonary contusion is made worse by fluids/intravascular volume expansion
true
Someone comes in with suspected PE. What do you do?
1: supportive stuff (oxygen, fluids)
2: assess for absolute CI to anti-coagulation (active bleeding, recent hemorrhagic stroke)
- ->if yes, do dx testing and then IVC filter
3. No CI then proceed by Wells criteria
- ->low prob of PE: Do dx’ic testing
- ->if PE likely, you don’t wait for a CT you give anticoagulation now
How could blood gases help you distinguish COPD exacerbation from CHF?
COPD: Respiratory ACIDOSIS and hypoxia
CHF: Respiratory alkalosis, hypocapnia and hypoxia
Why does your cystic fibrosis patient bruise easily?
Pancreatic insuff –> Vit k defic
Chronic nasosinopulmonary infxs, digital clubbing, bronchiectasis, and nasal polyps
Either CF or Kartegeners.
Specifics:
CF = FTT and panc insuff, infertility b/c absent vas def
K: situs inversus, infertility b/c immotile sperm
exudative effusion from disruption of the lymphatic flow in the thoracic duct
chylothorax (lots of TGs and leukocytes)
what is the first fucking thing youre going to do in a patient with asthma and they provide ABG?
Check to see if he has hypercarbia and need to intubate the fuck out of him
Restrictive lung dz: decreased DLCO vs normal
decreased: ILD
normal: chest wall weakness
patchy alveolar infiltrate (not necessarily in the anatomical borders), tachypnea/tachycardia/hypoxia within 24 hours of trauma
pulmonary contusion
why do glucocorticoids cause changes in CBC labs?
demargination of neutrophils habibi –> leukocytosis
chronic cough that is worse at night in the absence of major pathology, regardless of age of onset, should be worked up for:
asthma, PFT the homeboy. chronic means >2months
first line for preventing post op pneumonia
incentive spirometry (promotes lung expansion)
young guy with chronic low back pain, worse at night and improved with exercise, elevated ESR
ankylosing spondylitis
_____ exacerbations are associated with wheezing
asthma